Bacterial meningitis is life-threatening: in the United Kingdom, 5–10 per cent of children who contract the disease may die. Most cases of acute bacterial meningitis in the UK are caused by two bacteria: Neisseria meningitidis (meningococcus), and Streptococcus pneumoniae (pneumococcus); other bacteria include Haemophilus in?uenzae (a common cause until virtually wiped out by immunisation), Escherichia coli, Mycobacterium tuberculosis (see TUBERCULOSIS), Treponema pallidum (see SYPHILIS) and Staphylococci spp. Of the bacterial infections, meningococcal group B is the type that causes a large number of cases in the UK, while group A is less common.
Bacterial meningitis may occur by spread from nearby infected foci such as the nasopharynx, middle ear, mastoid and sinuses (see EAR, DISEASES OF). Direct infection may be the result of penetrating injuries of the skull from accidents or gunshot wounds. Meningitis may also be a complication of neurosurgery despite careful aseptic precautions. Immuno-compromised patients – those with AIDS or on CYTOTOXIC drugs – are vulnerable to infections.
Spread to contacts may occur in schools and similar communities. Many people harbour the meningococcus without developing meningitis. In recent years small clusters of cases, mainly in schoolchildren and young people at college, have occurred in Britain.
Symptoms include malaise accompanied by fever, severe headache, PHOTOPHOBIA, vomiting, irritability, rigors, drowsiness and neurological disturbances. Neck sti?ness and a positive KERNIG’S SIGN appearing within a few hours of infection are key diagnostic signs. Meningococcal and pneumococcal meningitis may co-exist with SEPTICAEMIA, a much more serious condition in terms of death rate or organ damage and which constitutes a grave emergency demanding rapid treatment.
Diagnosis and treatment are urgent and, if bacterial meningitis is suspected, antibiotic treatment should be started even before laboratory con?rmation of the infection. Analysis of the CEREBROSPINAL FLUID (CSF) by means of a LUMBAR PUNCTURE is an essential step in diagnosis, except in patients for whom the test would be dangerous as they have signs of raised intracranial pressure. The CSF is clear or turbid in viral meningitis, turbid or viscous in tuberculous infection and turbulent or purulent when meningococci or staphylococci are the infective agents. Cell counts and biochemical make-up of the CSF are other diagnostic pointers. Serological tests are done to identify possible syphilitic infection, which is now rare in Britain.
Patients with suspected meningitis should be admitted to hospital quickly. General pracitioners are encouraged to give a dose of intramuscular penicillin before sending the child to hospital. Treatment in hospital is usually with a cephalosporin, such as ceftazidime or ceftriaxone. Once the sensitivity of the organism is known as a result of laboratory studies on CSF and blood, this may be changed to penicillin or, in the case of H. in?uenzae, to amoxicillin. Local infections such as SINUSITIS or middle-ear infection require treatment, and appropriate surgery for skull fractures or meningeal tears should be carried out as necessary. Tuberculous meningitis is treated for at least nine months with anti-tuberculous drugs (see TUBERCULOSIS). If bacterial meningitis causes CONVULSIONS, these can be controlled with diazepam (see TRANQUILLISERS; BENZODIAZEPINES) and ANALGESICS will be required for the severe headache.
Coexisting septicaemia may require full intensive care with close attention to intravenous ?uid and electrolyte balance, control of blood clotting and blood pressure.
Treatment of close contacts such as family, school friends, medical and nursing sta? is recommended if the patient has H. in?uenzae or N. meningitidis: RIFAMPICIN provides e?ective prophylaxis. Contacts of patients with pneumococcal infection do not need preventive treatment. Vaccines for meningococcal meningitis may be given to family members in small epidemics and to any contacts who are especially at risk such as infants, the elderly and immuno-compromised individuals.
The outlook for a patient with bacterial meningitis depends upon age – the young and old are vulnerable; speed of onset – sudden onset worsens the prognosis; and how quickly treatment is started – hence the urgency of diagnosis and admission to hospital. Recent research has shown that children who suffer meningitis in their ?rst year of life are ten times more likely to develop moderate or severe disability by the age of ?ve than contemporaries who have not been infected. (See British Medical Journal, 8 September 2001, page 523.)
Prevention One type of bacterial meningitis, that caused by Haemophilus, has been largely controlled by IMMUNISATION; meningococcal C vaccine has largely prevented this type of the disease in the UK. So far, no vaccine against group B has been developed, but research continues. Information on meningitis can be obtained from the Meningitis Trust and the Meningitis Research Foundation.... meningitis
The toxin has two components, one having haemagglutinin activity and the other neurotoxic activity which produces most of the symptoms. It has a lethal dose of as little as 1 mg/kg and is highly selective for cholinergic nerves. Thus the symptoms are those of autonomic parasympathetic blockade (dry mouth, constipation, urinary retention, mydriasis, blurred vision) and progress to blockade of somatic cholinergic transmission (muscle weakness). Death results from respiratory muscle paralysis. Treatment consists of supportive measures and 4 aminopyridine and 3, 4 di-aminopyridine, which may antagonise the e?ect of the toxin.... botulism
Incubation period varies from a few hours to ?ve days. Watery diarrhoea may be torrential and the resultant dehydration and electrolyte imbalance, complicated by cardiac failure, commonly causes death. The victim’s skin elasticity is lost, the eyes are sunken, and the radial pulse may be barely perceptible. Urine production may be completely suppressed. Diagnosis is by detection of V. cholerae in a faecal sample. Treatment consists of rapid rehydration. Whereas the intravenous route may be required in a severe case, in the vast majority of patients oral rehydration (using an appropriate solution containing sodium chloride, glucose, sodium bicarbonate, and potassium) gives satisfactory results. Proprietary rehydration ?uids do not always contain adequate sodium for rehydration in a severe case. ANTIBIOTICS, for example, tetracycline and doxycycline, reduce the period during which V. cholerae is excreted (in children and pregnant women, furazolidone is safer); in an epidemic, rapid resistance to these, and other antibiotics, has been clearly demonstrated. Prevention consists of improving public health infrastructure – in particular, the quality of drinking water. When supplies of the latter are satisfactory, the infection fails to thrive. Though there have recently been large epidemics of cholera in much of South America and parts of central Africa and the Indian subcontinent, the risk of tourists and travellers contracting the disease is low if they take simple precautions. These include eating safe food (avoid raw or undercooked seafood, and wash vegetables in clean water) and drinking clean water. There is no cholera vaccine at present available in the UK as it provides little protection and cannot control spread of the disease. Those travelling to countries where it exists should pay scrupulous attention to food and water cleanliness and to personal hygiene.... cholera
Staphylococcal food poisoning occurs after food such as meat products, cold meats, milk, custard and egg products becomes contaminated before or after cooking, usually through incorrect handling by humans who carry S. aureus. The bacteria produce an ENTEROTOXIN which causes the symptoms of food poisoning 1–8 hours after ingestion. The toxin can withstand heat; thus, subsequent cooking of contaminated food will not prevent illness.
Heat-resistant strains of Cl. perfringens cause food poisoning associated with meat dishes, soups or gravy when dishes cooked in bulk are left unrefrigerated for long periods before consumption. The bacteria are anaerobes (see ANAEROBE) and form spores; the anaerobic conditions in these cooked foods allow the germinated spores to multiply rapidly during cooling, resulting in heavy contamination. Once ingested the bacteria produce enterotoxin in the intestine, causing symptoms within 8–24 hours.
Many di?erent types of Salmonella (about 2,000) cause food poisoning or ENTERITIS, from eight hours to three days after ingestion of food in which they have multiplied. S. brendeny, S. enteritidis, S. heidelberg, S. newport and S. thompson are among those commonly causing enteritis. Salmonella infections are common in domesticated animals such as cows, pigs and poultry whose meat and milk may be infected, although the animals may show no symptoms. Duck eggs may harbour Salmonella (usually S. typhimurium), arising from surface contamination with the bird’s faeces, and foods containing uncooked or lightly cooked hen’s eggs, such as mayonnaise, have been associated with enteritis. The incidence of human S. enteritidis infection has been increasing, by more than 15-fold in England and Wales annually, from around 1,100 a year in the early 1980s to more than 32,000 at the end of the 1990s, but has since fallen to about 10,000. A serious source of infection seems to be poultry meat and hen’s eggs.
Although Salmonella are mostly killed by heating at 60 °C for 15 minutes, contaminated food requires considerably longer cooking and, if frozen, must be completely thawed beforehand, to allow even cooking at a su?cient temperature.
Enteritis caused by Campylobacter jejuni is usually self-limiting, lasting 1–3 days. Since reporting of the disease began in 1977, in England and Wales its incidence has increased from around 1,400 cases initially to nearly 13,000 in 1982 and to over 42,000 in 2004. Outbreaks have been associated with unpasteurised milk: the main source seems to be infected poultry.
ESCHERICHIA COLI O157 was ?rst identi?ed as a cause of food poisoning in the early 1980s, but its incidence has increased sharply since, with more than 1,000 cases annually in the United Kingdom in the late 1990s. The illness can be severe, with bloody diarrhoea and life-threatening renal complications. The reservoir for this pathogen is thought to be cattle, and transmission results from consumption of raw or undercooked meat products and raw dairy products. Cross-infection of cooked meat by raw meat is a common cause of outbreaks of Escherichia coli O157 food poisoning. Water and other foods can be contaminated by manure from cattle, and person-to-person spread can occur, especially in children.
Food poisoning associated with fried or boiled rice is caused by Bacillus cereus, whose heat-resistant spores survive cooking. An enterotoxin is responsible for the symptoms, which occur 2–8 hours after ingestion and resolve after 8–24 hours.
Viruses are emerging as an increasing cause of some outbreaks of food poisoning from shell?sh (cockles, mussels and oysters).
The incidence of food poisoning in the UK rose from under 60,000 cases in 1991 to nearly 79,000 in 2004. Public health measures to control this rise include agricultural aspects of food production, implementing standards of hygiene in abattoirs, and regulating the environment and process of industrial food production, handling, transportation and storage.... food poisoning
During a bite by the female mosquito, one or more sporozoites – a stage in the life-cycle of the parasite – are injected into the human circulation; these are taken up by the hepatocytes (liver cells). Following division, merozoites (minute particles resulting from the division) are liberated into the bloodstream where they invade red blood cells. These in turn divide, releasing further merozoites. As merozoites are periodically liberated into the bloodstream, they cause the characteristic fevers, rigors, etc.
Malaria occurs in many tropical and subtropical countries; P. falciparum is, however, con?ned very largely to Africa, Asia and South America. Malaria is present in increasingly large areas; in addition, the parasites are developing resistance to various preventative and treatment drugs. The disease constitutes a signi?cant problem for travellers, who must obtain sound advice on chemoprophylaxis before embarking on tropical trips – especially to a rural area where intense transmission can occur. Transmission has also been recorded at airports, and following blood transfusion.
The World Health Organisation (WHO) has listed malaria as one of Europe’s top ten infectious diseases. In 1992, 20,000 cases were reported: this had risen to more than 200,000 by the late 1990s. The resurgence of malaria has been worldwide, in part the result of the development of resistant strains of the disease, and in part because many countries have failed (or been unable) to implement environmental measures to eliminate mosquitoes. Nearly 40 years ago the WHO forecast that by 1980 only four million people would be affected worldwide; now, at the beginning of the 21st century, around 500 million people a year are contracting malaria with about 3,000 people a day dying from the infection – as many as 70 per cent of them children under the age of ?ve, according to WHO ?gures. The apparently steady advance of global warming means that countries with temperate climates may well warm up su?ciently to enable malaria to become established as an ENDEMIC disease. In any case, the great increase in international air travel has exposed many more people to the risk of malaria, and infected individuals may not exhibit symptoms until they are back home. Doctors seeing a recent traveller with unexplained pyrexia and illness should consider the possibility of malarial infection.
Diagnosis is by demonstration of trophozoites – a stage in the parasite’s life-cycle that takes place in red blood cells – in thick/thin blood-?lms of peripheral blood. Serological tests are of value in deciding whether an individual has had a past infection, but are of no value in acute disease.
P. vivax and P. ovale infections cause less severe disease than P. falciparum (see below), although overall there are many clinical similarities; acute complications are unusual, but chronic ANAEMIA is often present. Primaquine is necessary to eliminate the exoerythrocytic cycle in the hepatocyte (liver cell).
P. falciparum Complications of P. falciparum infection include cerebral involvement (see BRAIN – Cerebrum), due to adhesion of immature trophozoites on to the cerebral vascular endothelium; these lead to a high death rate when inadequately treated. Renal involvement (frequently resulting from HAEMOGLOBINURIA), PULMONARY OEDEMA, HYPOTENSION, HYPOGLYCAEMIA, and complications in pregnancy are also important. In complicated disease, HAEMODIALYSIS and exchange TRANSFUSION have been used. No adequate controlled trial using the latter regimen has been carried out, however, and possible bene?ts must be weighed against numerous potential side-effects – for instance, the introduction of a wide range of infections, overload of the circulatory system with infused ?uids, and other complications.
P. malariae usually produces a chronic infection, and chronic renal disease (nephrotic syndrome) is an occasional sequel, especially in tropical Africa.
Gross SPLENOMEGALY (hyper-reactive malarious splenomegaly, or tropical splenomegaly syndrome) can complicate all four human Plasmodium spp. infections. The syndrome responds to long-term malarial chemoprophylaxis. BURKITT’S LYMPHOMA is found in geographical areas where malaria infection is endemic; the EPSTEIN BARR VIRUS is aetiologically involved.
Prophylaxis Malaria specialists in the United Kingdom have produced guidance for residents travelling to endemic areas for short stays. Drug choice takes account of:
risk of exposure to malaria;
extent of drug resistance;
e?cacy of recommended drugs and their side-effects;
criteria relevant to the individual (e.g. age, pregnancy, kidney or liver impairment). Personal protection against being bitten by
mosquitoes is essential. Permethrinimpregnated nets are an e?ective barrier, while skin barrier protection and vaporised insecticides are helpful. Lotions, sprays or roll-on applicators all containing diethyltoluamide (DEET) are safe and work when put on the skin. Their e?ect, however, lasts only for a few hours. Long sleeves and trousers should be worn after dark.
Drug prophylaxis should be started at least a week before travelling into countries where malaria is endemic (two or three weeks in the case of me?oquine). Drug treatment should be continued for at least four weeks after leaving endemic areas. Even if all recommended antimalarial programmes are followed, it is possible that malaria may occur any time up to three months afterwards. Medical advice should be sought if any illness develops. Chloroquine can be used as a prophylactic drug where the risk of resistant falciparum malaria is low; otherwise, me?oquine or proguanil hydrochloride should be used. Travellers to malaria-infested areas should seek expert advice on appropriate prophylactic treatment well before departing.
Treatment Various chemoprophylactic regimes are widely used. Those commmonly prescribed include: chloroquine + paludrine, me?oquine, and Maloprim (trimethoprim + dapsone); Fansidar (trimethoprim + sulphamethoxazole) has been shown to have signi?cant side-effects, especially when used in conjunction with chloroquine, and is now rarely used. No chemotherapeutic regimen is totally e?ective, so other preventive measures are again being used. These include people avoiding mosquito bites, covering exposed areas of the body between dusk and dawn, and using mosquito repellents.
Chemotherapy was for many years dominated by the synthetic agent chloroquine. However, with the widespread emergence of chloroquine-resistance, quinine is again being widely used. It is given intravenously in severe infections; the oral route is used subsequently and in minor cases. Other agents currently in use include me?oquine, halofantrine, doxycycline, and the artemesinin alkaloids (‘qinghaosu’).
Researchers are working on vaccines against malaria.... malaria
Symptoms: Influenza-like fever, breathlessness, cough.
Prognosis: Chronic lung damage and progressive disability.
Indicated: antifungals, antibiotics.
Alternatives. Teas. Marigold, Ground Ivy, Scarlet Pimpernel, Yarrow. 1 heaped teaspoon to each cup boiling water; infuse 5-15 minutes; 1 cup freely.
Tablets/capsules. Garlic, Echinacea, Goldenseal, Thuja.
Powders. Combine, parts, Echinacea 3; Goldenseal 1; Thuja 1. Dose: 500mg, (two 00 capsules or one- third teaspoon) thrice daily.
Decoction. Irish Moss, to promote expectoration and eliminate debris.
Tinctures. Alternatives. (1) Echinacea 2; Lobelia 1; Liquorice 1. (2) Equal parts: Wild Indigo, Thuja and Pleurisy root. (3) Echinacea 2; Marigold 1; Thuja half; Liquorice half. Dosage: two 5ml teaspoons in water thrice daily. Acute cases: every 2 hours.
Topical. Inhalation of Eucalyptus or Tea Tree oils.
Diet. See: DIET – GENERAL. Yoghurt in place of milk.
Note: Bronchodilators of little value. Those at risk should have an X-ray at regular intervals. ... farmer’s lung
Etiology. Obscure; though cases may be traced to auto-toxaemia, Vitamin B deficiency, menstruation, malaria drugs (chloroquine).
Symptoms: dizziness, nausea, vomiting, tinnitus, sound distortions, heavy sweating, loss of hearing; usually in one ear only. Early diagnosis essential for effective treatment. This may mean reference to a department of otolaryngology or otoneurology.
Treatment. Antispasmodics. Nervines. Sometimes a timely diuretic reduces severity – Uva Ursi, Dandelion root, Wild Carrot.
Alternatives. Current European practice: Betony, German Chamomile, Passion flower, Hawthorn, Hops, Feverfew, White Willow.
Tea. Combine, equal parts: Valerian, Wild Carrot, Agrimony. 2 teaspoons to each cup boiling water; infuse 15 minutes. Half-1 cup every 2 hours during attack; thrice daily thereafter.
Decoction. Mistletoe: 2 teaspoons to each cup cold water steeped overnight. Bring to boil. Allow to cool. Half-1 cup, as above.
Tablets/capsules. Feverfew, Mistletoe, Prickly Ash.
Formula. Ginkgo 2; Dandelion 1; Black Cohosh 1. Dose: Liquid Extracts: 1 teaspoon. Tinctures: 2 teaspoons. Powders: 500mg (two 00 capsules or one-third teaspoon). Thrice daily.
Feverfew tincture. See: FEVERFEW.
Dr J. Christopher: inject into ears, at night, few drops oil of Garlic (or contents of Garlic capsule).
Cider vinegar. 2 teaspoons to glass water: as desired.
Aromatherapy. Inhalants: Eucalyptus or Rosemary oils.
Diet: gluten-free, low salt; good responses observed. High fibre. Avoid dairy products and chocolate. Vitamins: B-complex, B1; B2; B6; E; F. Brewer’s yeast, Niacin.
Minerals: Calcium. Magnesium. Phosphorus. Dolomite. ... meniere’s disease
In the wake of the devastating terrorist attacks on buildings in New York and Washington on 11 September 2001, modi?ed anthrax spores were sent by mail from an unidenti?ed source to some prominent Americans. Several people were infected and a few died. This was the ?rst known use of anthrax as a terror weapon.
Prevention is most important by disinfecting all hides, wool and hair coming from areas of the world. An e?cient vaccine is now available. Treatment consists of the administration of large doses of the broad-spectrum antibiotic, CIPROFLOXACIN. If bioterrorism is thought to be the likely source of anthrax infection, appropriate decontamination procedures must be organised promptly.
Symptoms
EXTERNAL FORM This is the ‘malignant pustule’. After inoculation of some small wound, a few hours or days elapse, and then a red, in?amed swelling appears, which grows larger till it covers half the face or the breadth of the arm, as the case may be. Upon its summit appears a bleb of pus, which bursts and leaves a black scab, perhaps 12 mm (half an inch) wide. The patient is feverish and seriously ill. The in?ammation may last ten days or so, when it slowly subsides and the patient recovers, if surviving the fever and prostration.
INTERNAL FORM This takes the form of pneumonia with haemorrhages, when the spores have been drawn into the lungs, or of ulcers of the stomach and intestines, with gangrene of the SPLEEN, when they have been swallowed.
It is usually fatal in two or three days. Victims may also develop GASTROENTERITIS or MENINGITIS.... anthrax
Uses Its main use is in gout, for which colchicine, the active principle of colchicum, in doses of 0·5 mg every one or two hours until the pain is relieved, followed by 0·5 mg thrice daily for about a week, is the form generally employed.... colchicum
Habitat: Waste places, roadsides.
Features ? Stem weak, straggling, freely branched; line of white hairs along one side only, changing direction at each pair of leaves. Leaves small, ovate, sessile above, flat stalks lower. Flowers white, very small, petals deeply cleft, singly on axils of upper leaves. Taste slightly salty.Part used ? Herb.Action: Demulcent, emollient, pectoral.
Inflammation of the respiratory organs and internal membranes generally. One ounce of herb in 1 1/2 pints of water simmered down to 1 pint. Dose, wineglassful every two or three hours. Used externally as a poultice for inflamed surfaces, boils, burns and skin eruptions.... chickweedBarrier methods These involve a physical barrier which prevents sperm (see SPERMATOZOON) from reaching the cervix (see CERVIX UTERI). Barrier methods reduce the risk of spreading sexually transmitted diseases, and the sheath is the best protection against HIV infection (see AIDS/HIV) for sexually active people. The e?ciency of barrier methods is improved if they are used in conjunction with a spermicidal foam or jelly, but care is needed to ensure that the preparation chosen does not damage the rubber barrier or cause an allergic reaction in the users. CONDOM OR SHEATH This is the most commonly used barrier contraceptive. It consists of a rubber sheath which is placed over the erect penis before intromission and removed after ejaculation. The failure rate, if properly used, is about 4 per cent. DIAPHRAGM OR CAP A rubber dome that is inserted into the vagina before intercourse and ?ts snugly over the cervix. It should be used with an appropriate spermicide and is removed six hours after intercourse. A woman must be measured to ensure that she is supplied with the correct size of diaphragm, and the ?t should be checked annually or after more than about 7 lbs. change in weight. The failure rate, if properly used, is about 2 per cent.
Non-barrier methods These do not provide a physical barrier between sperm and cervix and so do not protect against sexually transmitted diseases, including HIV. COITUS INTERRUPTUS This involves the man’s withdrawing his penis from the vagina before ejaculation. Because some sperm may leak before full ejaculation, the method is not very reliable. SAFE PERIOD This involves avoiding intercourse around the time when the woman ovulates and is at risk of pregnancy. The safe times can be predicted using temperature charts to identify the rise in temperature before ovulation, or by careful assessment of the quality of the cervical mucus. This method works best if the woman has regular menstrual cycles. If used carefully it can be very e?ective but requires a highly disciplined couple to succeed. It is approved by the Catholic church.
SPERMICIDAL GELS, CREAMS, PESSARIES, ETC.
These are supposed to prevent pregnancy by killing sperm before they reach the cervix, but they are unreliable and should be used only in conjunction with a barrier method.
INTRAUTERINE CONTRACEPTIVE DEVICE (COIL) This is a small metal or plastic shape, placed inside the uterus, which prevents pregnancy by disrupting implantation. Some people regard it as a form of abortion, so it is not acceptable to all religious groups. There is a risk of pelvic infection and eventual infertility in women who have used coils, and in many countries their use has declined substantially. Coils must be inserted by a specially trained health worker, but once in place they permit intercourse at any time with no prior planning. Increased pain and bleeding may be caused during menstruation. If severe, such symptoms may indicate that the coil is incorrectly sited, and that its position should be checked. HORMONAL METHODS Steroid hormones have dominated contraceptive developments during the past 40 years, with more than 200 million women worldwide taking or having taken ‘the pill’. In the past 20 years, new developments have included modifying existing methods and devising more e?ective ways of delivering the drugs, such as implants and hormone-releasing devices in the uterus. Established hormonal contraception includes the combined oestrogen and progesterone and progesterone-only contraceptive pills, as well as longer-acting depot preparations. They modify the woman’s hormonal environment and prevent pregnancy by disrupting various stages of the menstrual cycle, especially ovulation. The combined oestrogen and progesterone pills are very e?ective and are the most popular form of contraception. Biphasic and triphasic pills contain di?erent quantities of oestrogen and progesterone taken in two or three phases of the menstrual cycle. A wide range of preparations is available and the British National Formulary contains details of the commonly used varieties.
The main side-e?ect is an increased risk of cardiovascular disease. The lowest possible dose of oestrogen should be used, and many preparations are phasic, with the dose of oestrogen varying with the time of the cycle. The progesterone-only, or ‘mini’, pill does not contain any oestrogen and must be taken at the same time every day. It is not as e?ective as the combined pill, but failure rates of less than 1-per-100 woman years can be achieved. It has few serious side-effects, but may cause menstrual irregularities. It is suitable for use by mothers who are breast feeding.
Depot preparations include intramuscular injections, subcutaneous implants, and intravaginal rings. They are useful in cases where the woman cannot be relied on to take a pill regularly but needs e?ective contraception. Their main side-e?ect is their prolonged action, which means that users cannot suddenly decide that they would like to become pregnant. Skin patches containing a contraceptive that is absorbed through the skin have recently been launched.
HORMONAL CONTRACEPTION FOR MEN There is a growing demand by men worldwide for hormonal contraception. Development of a ‘male pill’, however, has been slow because of the potentially dangerous side-effects of using high doses of TESTOSTERONE (the male hormone) to suppress spermatogenesis. Progress in research to develop a suitable ANDROGEN-based combination product is promising, including the possibility of long-term STEROID implants. STERILISATION See also STERILISATION – Reproductive sterilisation. The operation is easier and safer to perform on men than on women. Although sterilisation can sometimes be reversed, this cannot be guaranteed and couples should be counselled in advance that the method is irreversible. There is a small but definite failure rate with sterilisation, and this should also be made clear before the operation is performed. POSTCOITAL CONTRACEPTION Also known as emergency contraception or the ‘morning after pill’, postcoital contraception can be e?ected by two di?erent hormonal methods. Levonorgesterol (a synthetic hormone similar to the natural female sex hormone PROGESTERONE) can be used alone, with one pill being taken within 72 hours of unprotected intercourse, but preferably as soon as possible, and a second one 12 hours after the ?rst. Alternatively, a combined preparation comprising ETHINYLESTRADIOL and levonorgesterol can be taken, also within 72 hours of unprotected intercourse. The single constituent pill has fewer side-effects than the combined version. Neither version should be taken by women with severe liver disease or acute PORPHYRIAS, but the ethinylestradiol/levonorgesterol combination is unsuitable for women with a history of THROMBOSIS.
In the UK the law allows women over the age of 16 to buy the morning-after pill ‘over the counter’ from a registered pharmacist.... contraception
Symptoms Attacks generally come on at night, following a cold caught during the previous couple of days. The breathing is hoarse and croaking (croup), with a barking cough and harsh respiratory noise. The natural tendency for the laryngeal airway to collapse is increased by the child’s desperate attempts to overcome the obstruction. Parental anxiety, added to that of the child, only exacerbates the situation. After struggling for up to several hours, the child ?nally falls asleep. The condition may recur.
Treatment Most children with croup should be looked after at home if the environment is suitable. Severe episodes may require hospital observation, with treatment by oxygen if needed and usually with a single dose of inhaled steroid or oral PREDNISONE. For the very few children whose illness progresses to respiratory obstruction, intubation and ventilation may be needed for a few days. There is little evidence that putting the child in a mist tent or giving antibiotics is of any value. Of greater importance is the reassurance of the child, and careful observation for signs of deterioration, together with the exclusion of other causes such as foreign-body inhalation and bacterial tracheitis.... croup
Dialysis is available as either haemodialysis or peritoneal dialysis.
Haemodialysis Blood is removed from the circulation either through an arti?cial arteriovenous ?stula (junction) or a temporary or permanent internal catheter in the jugular vein (see CATHETERS). It then passes through an arti?cial kidney (‘dialyser’) to remove toxins (e.g. potassium and urea) by di?usion and excess salt and water by ultra?ltration from the blood into dialysis ?uid prepared in a ‘proportionator’ (often referred to as a ‘kidney machine’). Dialysers vary in design and performance but all work on the principle of a semi-permeable membrane separating blood from dialysis ?uid. Haemodialysis is undertaken two to three times a week for 4–6 hours a session.
Peritoneal dialysis uses the peritoneal lining (see PERITONEUM) as a semi-permeable membrane. Approximately 2 litres of sterile ?uid is run into the peritoneum through the permanent indwelling catheter; the ?uid is left for 3–4 hours; and the cycle is repeated 3–4 times per day. Most patients undertake continuous ambulatory peritoneal dialysis (CAPD), although a few use a machine overnight (continuous cycling peritoneal dialysis, CCPD) which allows greater clearance of toxins.
Disadvantages of haemodialysis include cardiovascular instability, HYPERTENSION, bone disease, ANAEMIA and development of periarticular AMYLOIDOSIS. Disadvantages of peritoneal dialysis include peritonitis, poor drainage of ?uid, and gradual loss of overall e?ciency as endogenous renal function declines. Haemodialysis is usually done in outpatient dialysis clinics by skilled nurses, but some patients can carry out the procedure at home. Both haemodialysis and peritoneal dialysis carry a relatively high morbidity and the ideal treatment for patients with end-stage renal failure is successful renal TRANSPLANTATION.... dialysis
Tea. combine equal parts, German Chamomile, Angelica root, Pennyroyal and Basil; or as many as are available. 1-2 teaspoons to each cup boiling water; infuse 5-15 minutes; 1 cup freely. ... afterbirth
Doctors make the diagnosis of depression when they believe a patient to be ill with the latter condition, which may affect physical health and in some instances be life-threatening. This form of depression is common, with up to 15 per cent of the population suffering from it at any one time, while about 20 per cent of adults have ‘medical’ depression at some time during their lives – such that it is one of the most commonly presenting disorders in general practice. Women seem more liable to develop depression than men, with one in six of the former and one in nine of the latter seeking medical help.
Manic depression is a serious form of the disorder that recurs throughout life and is manifested by bouts of abnormal elation – the manic stage. Both the manic and depressive phases are commonly accompanied by psychotic symptoms such as delusions, hallucinations and a loss of sense of reality. This combination is sometimes termed a manic-depressive psychosis or bipolar affective disorder because of the illness’s division into two parts. Another psychiatric description is the catch-all term ‘affective disorder’.
Symptoms These vary with the illness’s severity. Anxiety and variable moods are the main symptoms in mild depression. The sufferer may cry without any reason or be unresponsive to relatives and friends. In its more severe form, depression presents with a loss of appetite, sleeping problems, lack of interest in and enjoyment of social activities, tiredness for no obvious reason, an indi?erence to sexual activity and a lack of concentration. The individual’s physical and mental activities slow down and he or she may contemplate suicide. Symptoms may vary during the 24 hours, being less troublesome during the latter part of the day and worse at night. Some people get depressed during the winter months, probably a consequence of the long hours of darkness: this disorder – SEASONAL AFFECTIVE DISORDER SYNDROME, or SADS – is thought to be more common in populations living in areas with long winters and limited daylight. Untreated, a person with depressive symptoms may steadily worsen, even withdrawing to bed for much of the time, and allowing his or her personal appearance, hygiene and environment to deteriorate. Children and adolescents may also suffer from depression and the disorder is not always recognised.
Causes A real depressive illness rarely has a single obvious cause, although sometimes the death of a close relative, loss of employment or a broken personal relationship may trigger a bout. Depression probably has a genetic background; for instance, manic depression seems to run in some families. Viral infections sometimes cause depression, and hormonal disorders – for example, HYPOTHYROIDISM or postnatal hormonal disturbances (postnatal depression) – will cause it. Di?cult family or social relations can contribute to the development of the disorder. Depression is believed to occur because of chemical changes in the transmission of signals in the nervous system, with a reduction in the neurochemicals that facilitate the passage of messages throughout the system.
Treatment This depends on the type and severity of the depression. These are three main forms. PSYCHOTHERAPY either on a one-to-one basis or as part of a group: this is valuable for those whose depression is the result of lifestyle or personality problems. Various types of psychotherapy are available. DRUG TREATMENT is the most common method and is particularly helpful for those with physical symptoms. ANTIDEPRESSANT DRUGS are divided into three main groups: TRICYCLIC ANTIDEPRESSANT DRUGS (amitriptyline, imipramine and dothiepin are examples); MONOAMINE OXIDASE INHIBITORS (MAOIS) (phenelzine, isocarboxazid and tranylcypromine are examples); and SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIS) (?uoxetine – well known as Prozac®, ?uvoxamine and paroxetine are examples). For manic depression, lithium carbonate is the main preventive drug and it is also used for persistent depression that fails to respond to other treatments. Long-term lithium treatment reduces the likelihood of relapse in about 80 per cent of manic depressives, but the margin between control and toxic side-effects is narrow, so the drug must be carefully supervised. Indeed, all drug treatment for depression needs regular monitoring as the substances have powerful chemical properties with consequential side-effects in some people. Furthermore, the nature of the illness means that some sufferers forget or do not want to take the medication. ELECTROCONVULSIVE THERAPY (ECT) If drug treatments fail, severely depressed patients may be considered for ECT. This treatment has been used for many years but is now only rarely recommended. Given under general anaesthetic, in appropriate circumstances, ECT is safe and e?ective and may even be life-saving, though temporary impairment of memory may occur. Because the treatment was often misused in the past, it still carries a reputation that worries patients and relatives; hence careful assessment and counselling are essential before use is recommended.
Some patients with depression – particularly those with manic depression or who are a danger to themselves or to the public, or who are suicidal – may need admission to hospital, or in severe cases to a secure unit, in order to initiate treatment. But as far as possible patients are treated in the community (see MENTAL ILLNESS).... depression
alpha-fetoprotein, by ultrasound scanning, by amniocentesis, or by fetoscopy; if anencephaly is detected, termination of the pregnancy may be considered. Anencephaly is due to a failure in the development of the neural tube, which is the nerve tissue in the embryo that normally develops into the spinal cord and brain. (See also neural tube defects.)... anencephaly
Injections of an analgesic drug and an antispasmodic drug may be given to relieve the colic.
Tests such as cholecystography or ultrasound scanning can confirm the presence of gallstones, in which case cholecystectomy (surgical removal of the gallbladder) is possible.... biliary colic
The crisis may be associated with muscle spasm of the tongue, mouth, and neck, and is often triggered by stress.
It may also occur following encephalitis and in parkinsonism, or may be induced by drugs, such as phenothiazine derivatives.... oculogyric crisis
It is a recurrent and paroxysmal disorder starting suddenly and ceasing spontaneously due to occasional sudden excessive rapid and local discharge of the nerve cells in the grey matter (cortex) of the BRAIN. Epilepsy always arises in this way from the brain, but its origin is often of microscopic size. It is diagnosed by the clinical symptoms based on the observations of witnesses. Its cause can sometimes be established by laboratory tests, and brain scanning. Fits can be the ?rst sign of a tumour, or follow a stroke, brain injury or infection, but in the large majority no underlying cause is found – so-called idiopathic epilepsy.
A single epileptic ?t is not epilepsy. Of those people who have a single seizure, a signi?cant minority (20 per cent) have no further attacks.
Major (generalised) seizures have a sudden, often unprovoked onset; the patient emits a cry, then falls to the ground, rigid, blue, and then twitching or jerking both sides of the body: the tonic-clonic convulsion. Drowsiness and confusion may last for some hours after recovering consciousness. Some experience a momentary warning (AURA): a smell, or sensation in the head or abdomen, vision, or déjà vu.
Partial seizures: focal motor (Jacksonian) begin with twitching of the angle of the mouth, the thumb, or the big toe. If the seizure discharge then spreads, the twitching or jerking spreads gradually through the limbs. Consciousness is preserved unless the seizure spreads to produce a secondary generalised ?t. In some attacks the eyes and head may turn, the arm may rise, and the body may turn, while some patients feel tingling in the limbs.
Complex partial seizures (temporal lobe epilepsy) The patient usually appears blank, vacant and may be unable to talk, or may mumble or chatter – though later they often have no memory of this period. They may be able to carry out complex tasks, taking o? gloves or clothes, and may smack their lips or rub repeatedly on one limb (automatisms). A sense of strangeness supervenes: unreality, or a feeling of having experienced it all before (déja vu). There may be a sense of panic. Strange unpleasant smells and tastes are olfactory and gustatory hallucinations. The visual hallucinations evoke complex scenes. An initial rising sense of warmth or discomfort in the stomach, or ‘speeding-up’ of thoughts are common psychomotor symptoms. All these strange symptoms are brief, disappearing within a few seconds or up to 3–4 minutes.
Minor seizures (petit mal) Attacks start in childhood. They last a few seconds. The child ceases what he or she is doing, stares, looks a little pale, and may ?utter the eyelids. The head may drop forwards. Attacks are commonly provoked by overbreathing. The child and parents may be unaware of the attacks
– ‘just daydreaming’. Major ?ts develop in one-third of subjects. By contrast with other types of epilepsy, the ELECTROENCEPHALOGRAM (EEG) is diagnostic.
Precautions Children with epilepsy should take normal school exercises and games, and can swim under supervision. Adults must avoid working at heights, with exposed dangerous machinery, and driving vehicles on public roads. Current legislation allows driving after two years of complete freedom from attacks during waking hours; those who for more than three years have had a history of attacks only while asleep may also drive.
Treatment identi?es, and avoids where possible, any factors (such as shortage of sleep or excessive ?uids) which aggravate or trigger attacks. If ?ts are very infrequent, treatment may not be recommended. However, frequent ?ts may be embarassing, may cause injury or may cause long-term brain damage so treatment is advisable. Anti-epileptic drugs are usually necessary for several years under medical supervision. Carbamazepine and sodium valproate are the most frequently prescribed. The dose is governed by the degree of control of ?ts and sometimes drug levels can be monitored by blood tests to check on dosage. Strict adherence to the drug schedule gives a reasonable chance of total suppression of ?ts, especially in younger patients whose ?ts have started recently. The table summarises anticonvulsant drugs in use. Interactions can occur between anti-epileptics and, if drug treatment is changed, the patient needs careful monitoring. In particular, abrupt withdrawal of a drug should be avoided as this may precipitate severe rebound seizures.
Indications First-choice drugs: Ethosuximide PM, JME Phenobarbitone M, P Phenytoin M, P, CP Carbamazepine M, P, CP Valproate M, PM, JME Second-line drugs: Primidone M, P, CP Clobazam M, CP Vigabatrin M, P, CP Lamotrigine M, P, CP Gabapentin M, P, CP Topirimate P
M = major generalised tonic-clonic; P = partial or focal; CP = complex partial (temporal lobe); PM = petit mal; JME = juvenile myoclonic epilepsy.
Anticonvulsant drugs
As all anticonvulsant drugs have an e?ect on the brain, it is not surprising that there may be side-effects, especially inolving alertness or behaviour. In each case careful assessment is necessary for doctor and patient to agree on the best compromise between stopping ?ts and avoiding ill-effects of medication.
Patients who have an epileptic seizure should not be restrained or have a gag or anything else placed in their mouths; nor should they be moved unless in danger of further injury. Any tight clothing around the neck should be loosened and, when the seizure has passed, the person should be placed in the recovery position to facilitate a return to consciousness (see APPENDIX 1: BASIC FIRST AID).
Patients with epilepsy and their relatives can obtain further advice and information from the British Epilepsy Association or Epilepsy Action Scotland.... epilepsy
It is usually complete after about 12 hours; the stiffness then disappears over the next 48–60 hours.
Physical exertion before death makes rigor mortis begin sooner.
The sooner rigor mortis begins, the quicker it passes.
These facts are used to help assess the time of death.... rigor mortis
Causes The cause of fever is the release of fever-producing proteins (pyrogens) by phagocytic cells called monocytes and macrophages, in response to a variety of infectious, immunological and neoplastic stimuli. The lymphocytes (see LYMPHOCYTE) play a part in fever production because they recognise the antigen and release substances called lymphokines which promote the production of endogenous pyrogen. The pyrogen then acts on the thermoregulatory centre in the HYPOTHALAMUS and this results in an increase in heat generation and a reduction in heat loss, resulting in a rise in body temperature.
The average temperature of the body in health ranges from 36·9 to 37·5 °C (98·4 to 99·5 °F). It is liable to slight variations from such causes as the ingestion of food, the amount of exercise, the menstrual cycle, and the temperature of the surrounding atmosphere. There are, moreover, certain appreciable daily variations, the lowest temperature being between the hours of 01.00 and 07.00 hours, and the highest between 16.00 and 21.00 hours, with tri?ing ?uctuations during these periods.
The development and maintenance of heat within the body depends upon the metabolic oxidation consequent on the changes continually taking place in the processes of nutrition. In health, this constant tissue disintegration is exactly counterbalanced by the consumption of food, whilst the uniform normal temperature is maintained by the adjustment of the heat developed, and of the processes of exhalation and cooling which take place, especially from the lungs and skin. During a fever this balance breaks down, the tissue waste being greatly in excess of the food supply. The body wastes rapidly, the loss to the system being chie?y in the form of nitrogen compounds (e.g. urea). In the early stage of fever a patient excretes about three times the amount of urea that he or she would excrete on the same diet when in health.
Fever is measured by how high the temperature rises above normal. At 41.1 °C (106 °F) the patient is in a dangerous state of hyperpyrexia (abnormally high temperature). If this persists for very long, the patient usually dies.
The body’s temperature will also rise if exposed for too long to a high ambient temperature. (See HEAT STROKE.)
Symptoms The onset of a fever is usually marked by a RIGOR, or shivering. The skin feels hot and dry, and the raised temperature will often be found to show daily variations – namely, an evening rise and a morning fall.
There is a relative increase in the pulse and breathing rates. The tongue is dry and furred; the thirst is intense, while the appetite is gone; the urine is scanty, of high speci?c gravity and containing a large quantity of solid matter, particularly urea. The patient will have a headache and sometimes nausea, and children may develop convulsions (see FEBRILE CONVULSION).
The fever falls by the occurrence of a CRISIS – that is, a sudden termination of the symptoms – or by a more gradual subsidence of the temperature, technically termed a lysis. If death ensues, this is due to failure of the vital centres in the brain or of the heart, as a result of either the infection or hyperpyrexia.
Treatment Fever is a symptom, and the correct treatment is therefore that of the underlying condition. Occasionally, however, it is also necessary to reduce the temperature by more direct methods: physical cooling by, for example, tepid sponging, and the use of antipyretic drugs such as aspirin or paracetamol.... fever
Ben: Kalmegh
Mal: Nilaveppu, Kiriyattu Tam: Nilavempu Kan: KreataImportance: Kalmegh, the Great or Green Chiretta is a branched annual herb. It is useful in hyperdipsia, burning sensation, wounds, ulcers, chronic fever, malarial and intermittent fevers, inflammations, cough, bronchitis, skin diseases, leprosy, pruritis, intestinal worms, dyspepsia, flatulence, colic, diarrhoea, dysentery, haemorrhoids and vitiated conditions of pitta (Warrier et al, 1993). It is used to overcome sannipata type of fever, difficulty in breathing, hemopathy due to the morbidity of kapha and pitta, burning sensation, cough, oedema, thirst, skin diseases, fever, ulcer and worms. It is also useful in acidity and liver complaints (Aiyer and Kolammal, 1962). The important preparations using the drug are Tiktakagheta, Gorocandi gulika, Candanasava, Panchatiktam kasaya, etc. (Sivarajan et al, 1994). A preparation called “Alui” is prepared by mixing powdered cumin (Cuminium cyminum) and large cardamom (Amomum subulatum) in the juice of this plant and administered for the treatment of malaria (Thakur et al, 1989). It is also a rich source of minerals.Distribution: The plant is distributed throughout the tropics. It is found in the plains of India from U.P to Assam, M.P., A.P, Tamil Nadu and Kerala, also cultivated in gardens.Botany: Andrographis paniculata (Burm.f.) Wall ex.Nees belongs to the family Acanthaceae. It is an erect branched annual herb, 0.3-0.9m in height with quadrangular branches. Leaves are simple, lanceolate, acute at both ends, glabrous, with 4-6 pairs of main nerves. Flowers are small, pale but blotched and spotted with brown and purple distant in lax spreading axillary and terminal racemes or panicles. Calyx-lobes are glandular pubescent with anthers bearded at the base. Fruits are linear capsules and acute at both ends. Seeds are numerous, yellowish brown and sub-quadrate (Warrier et al,1993).Another species of Andrographis is A. echioides (Linn.) Nees. It is found in the warmer parts of India. The plant is a febrifuge and diuretic. It contains flavone-echiodinin and its glucoside-echioidin (Husain et al, 1992).Agrotechnology: The best season of planting Andrographis is May-June. The field is to be ploughed well, mixed with compost or dried cowdung and seedbeds of length 3m, breadth 1/2m and 15cm height are to be taken at a distance of 3m. The plant is seed propagated. Seeds are to be soaked in water for 6 hours before sowing. Sowing is to be done at a spacing of 20cm. Seeds may germinate within 15-20 days. Two weedings, first at one month after planting and the second at 2 month after planting are to be carried out. Irrigation during summer months is beneficial. The plant is not attacked by any serious pests or diseases. Flowering commences from third month onwards. At this stage, plant are to be collected, tied into small bundles and sun-dried for 4-5 days. Whole plant is the economic part and the yield is about 1.25t dried plants/ha (Prasad et al, 1997).Properties and activity: Leaves contain two bitter substances lactone “andrographolid” and “kalmeghin”. The ash contains sodium chloride and potassium salts. Plant is very rich in chlorophyte. Kalmeghin is the active principle that contains 0.6% alkaloid of the crude plant. The plant contains diterpenoids, andrographolide, 14-deoxy-11-oxo-andrographolide, 14-deoxy-11,12-dihydroandrographolide, 14-deoxy andrographolide and neoandrographolide (Allison et al, 1968). The roots give flavones-apigenin-7,4-dio-O-methyl ether, 5-hydroxy-7,8,2’,3’- tetramethoxyflavone, andrographin and panicolin and -sitosterol (Ali et al, 1972; Govindachari et al, 1969). Leaves contain homoandrographolide, andrographosterol and andrographone.The plant is vulnerary, antipyretic, antiperiodic, anti-inflammatory, expectorant, depurative, sudorific, anthelmintic, digestive, stomachic, tonic, febrifuge and cholagogue. The plant is antifungal, antityphoid, hepatoprotective, antidiabetic and cholinergic. Shoot is antibacterial and leaf is hypotensive(Garcia et al, 1980). This is used for the inflammation of the respiratory tract. In China, researchers have isolated the andrographolide from which soluble derivative such as 14-deoxy-11, 12-dehydro-andrographolide which forms the subject of current pharmacological and clinical studies. Apigenin 7,4’-O-dimethyl ether isolated from A. paniculata exhibits dose dependent, antiulcer activity in shay rat, histamine induced ulcer in guinea pigs and aspirin induced ulcers in rats. A crude substance isolated from methanolic extract of leaves has shown hypotensive activity. Pre-treatment of rats with leaf (500mg/kg) or andrographolide (5mg/kg) orally prevented the carbon tetrachloride induced increase of blood serum levels of glutamate-oxaloacetate transaminase in liver and prevented hepatocellular membrane.... green chirettaIt usually begins at puberty – although young children can be affected – and tends to stop in middle age: in women, for example, attacks often cease after MENOPAUSE. It frequently disappears during pregnancy. The disorder tends to run in families. In susceptible individuals, attacks may be provoked by a wide variety of causes including: anxiety, emotion, depression, shock, and excitement; physical and mental fatigue; prolonged focusing on computer, television or cinema screens; noise, especially loud and high-pitched sounds; certain foods – such as chocolate, cheese, citrus fruits, pastry; alcohol; prolonged lack of food; irregular meals; menstruation and the pre-menstrual period.
Anything that can provoke a headache in the ordinary individual can probably precipitate an attack in a migrainous subject. It seems as if there is an inherited predispostion that triggers a mechanism whereby in the migrainous subject, the headache and the associated sickness persist for hours, a whole day or even longer.
The precise cause is not known, but the generally accepted view is that in susceptible individuals, one or other of these causes produces spasm or constriction of the blood vessels of the brain. This in turn is followed by dilatation of these blood vessels which also become more permeable and so allow ?uid to pass out into the surrounding tissues. This combination of dilatation and outpouring of ?uid is held to be responsible for the headache.
Two types of migraine have been recognised: classical and common. The former is relatively rare and the headache is preceded by a slowly extending area of blindness in one or both eyes, usually accompanied by intermittent ‘lights’. The phenomenon lasts for up to 30 minutes and is followed by a bad, often unilateral headache with nausea, sometimes vomiting and sensitivity to light. Occasionally, passing neurological symptoms such as weakness in a limb may accompany the attack. The common variety has similar but less severe symptoms. It consists of an intense headache, usually situated over one or other eye. The headache is usually preceded by a feeling of sickness and disturbance of sight. In 15–20 per cent of cases this disturbance of sight takes the form of bright lights: the so-called AURA of migraine. The majority of attacks are accompanied by vomiting. The duration of the headache varies, but in the more severe cases the victim is usually con?ned to bed for 24 hours.
Treatment consists, in the ?rst place, of trying to avoid any precipitating factor. Patients must ?nd out which drug, or drugs, give them most relief, and they must always carry these about with them wherever they go. This is because it is a not uncommon experience to be aware of an attack coming on and to ?nd that there is a critical quarter of an hour or so during which the tablets are e?ective. If not taken within this period, they may be ine?ective and the unfortunate victim ?nds him or herself prostrate with headache and vomiting. In addition, sufferers should immediately lie down; at this stage a few hours’ rest may prevent the development of a full attack.
When an attack is fully developed, rest in bed in a quiet, darkened room is essential; any loud noise or bright light intensi?es the headache or sickness. The less food that is taken during an attack the better, provided that the individual drinks as much ?uid as he or she wants. Group therapy, in which groups of around ten migrainous subjects learn how to relax, is often of help in more severe cases, whilst in others the injection of a local anaesthetic into tender spots in the scalp reduces the number of attacks. Drug treatment can be e?ective and those a?icted by migraine may ?nd a particular drug or combination of drugs more suitable than others. ANALGESICS such as PARACETAMOL, aspirin and CODEINE phosphate sometimes help. A combination of buclizine hydrochloride and analgesics, taken when the visual aura occurs, prevents or diminishes the severity of an attack in some people. A commonly used remedy for the condition is ergotamine tartrate, which causes the dilated blood vessels to contract, but this must only be taken under medical supervision. In many cases METOCLOPRAMIDE (an antiemetic), followed ten minutes later by three tablets of either aspirin or paracetamol, is e?ective if taken early in an attack. In milder attacks, aspirin, with or without codeine and paracetamol, may be of value. SUMATRIPTAN (5-hydroxytryptamine [5HT1] AGONIST – also known as a SEROTONIN agonist) is of value for acute attacks. It is used orally or by subcutaneous injection, but should not be used for patients with ischaemic heart disease. Naratriptan is another 5HT1 agonist that is an e?ective treatment for acute attacks; others are almotriptan, rizariptan and zolmitriptan. Some patients ?nd beta blockers such as propranolol a valuable prophylactic.
People with migraine and their relatives can obtain help and guidance from the Migraine Action Association.... migraine
Symptoms. Attack may be sudden, with acute low right abdominal pain. Lost appetite. Vomiting occurs usually only once. Nausea. Temperature slightly raised (102°). Muscles rigid and boardlike. The sufferer tries to find relief by lying on his back with right leg drawn up. Rapid heartbeat.
May lapse into abscess, perforation or peritonitis. If neglected, gangrene is a possibility, therefore a modern hospital is the safest place. In any case surgical excision may be necessary to prevent a burst when pus would discharge into the surrounding cavity causing peritonitis.
Differential diagnosis. Inflammation of the right ovary, gall bladder or kidney, ileitis, diverticulitis, perforated peptic ulcer.
Skin temperature aids diagnosis. Application of Feverscan thermometer detects local skin temperature over the right iliac fossa and records at least 1°C warmer than that on the left.
An added aid to diagnosis is the facial expression which predominantly conveys an aura of malaise with an obvious upward curving of the upper lip. This is not a wince or grimace but a slower reaction, and occurs on gentle pressure over the appendix. Rectal tenderness may indicate peritonitis.
A practitioner’s prescription would be raised according to the individual requirements of each case; some calling for support of nervous system (Skullcap, Lady’s Slipper) or for the heart (Hawthorn, Motherwort), etc.
To be treated by or in liaison with a qualified medical practitioner.
Treatment. Acute stage – immediate hospitalisation.
Tea. Formula. For non-acute stage: equal parts – German Chamomile, Yarrow, Black Horehound. 1 heaped teaspoon to each cup boiling water; infuse 5-15 minutes. 1 cup thrice daily.
Tea: children. Agrimony.
Tablets/capsules. (non-acute stage), Goldenseal, Blue Flag root, Calamus, Cranesbill, Wild Yam. Juice: Aloe Vera.
Chinese medicine. Fenugreek seeds: 2 teaspoons to each cup water simmer 5 minutes. 1 cup thrice daily, consuming the seeds.
Powders. Formula. Echinacea 2; Myrrh half; Wild Yam half; trace of Cayenne. Dose: 750mg (three 00 capsules or half a teaspoon) thrice daily. Every 2 hours for acute cases.
Tinctures. Formula. Echinacea 2; Wild Yam half; Elderflowers 1; few drops Tincture Capsicum (cayenne). Dose: 1-2 teaspoons in water or herb tea thrice daily or every 2 hours for acute cases.
Finlay Ellingwood MD. Equal parts, Liquid Extract Bryonia and Echinacea. Dose: 20 drops in water, hourly. For prevention of sepsis and pus formation.
Eric F.W. Powell, MNIMH. 1 teaspoon Tincture Echinacea; 10 drops Tincture Myrrh; 2 drops Tincture
Capsicum; in wineglassful hot water. Each wineglass taken in sips; dose repeated hourly until pain eases; then less frequently.
Frank Roberts, MNIMH. Liquid extracts: Equal parts, Wild Yam, Echinacea, Lobelia. Mix. 30-60 drops in wineglassful water, sipped 4 times daily.
John Cooper MD, Waldron, Arkansas, USA. 20 grains Epsom’s salts in hot water every 2 hours until pain ceases, then continue half that quantity. To control pain: Tincture Belladonna, 8 drops in water, when necessary.
Enema. Large enemas are not indicated. Warm strong infusion of German Chamomile proves helpful (50 flowers to 1 pint boiling water). Inject with 1 tablespoon warm olive oil.
Topical. Castor oil packs. Chamomile, Catnep, or Linseed poultices. In France, cases of acute appendicitis are treated with Tea Tree oil by abdominal massage as an alternative to surgery; good results reported.
Diet. No solid food taken as long as raised temperature persists. Herb tea and fruit-juice fast.
Remission of fever or after surgery: Slippery Elm gruel. Convalescent stage requires extra protein to make good muscle wastage and loss of weight. Low fibre.
Supplements. Daily. Beta-carotene 300,000iu. Vitamin C 2-3g. Vitamin E 400-800iu. Child: quarter of adult dose.
Acute stage: until the doctor comes. Do not eat or drink, take laxatives or painkillers. Go to bed. Hot water bottle to ease pain. ... appendicitis
Alternatives: Ginseng, Gotu Kola, Guarana tea, German Chamomile.
Caffeine is the most widely used drug in the world. Studies show that abstinence induces a withdrawal syndrome of fatigue, headache and drowsiness within 24 hours and lasts about a week, on giving up the habit. ... caffeine
Symptoms. Upper abdominal pain, fever, nausea, backache, low blood pressure, high white cell count. Tre atme nt: anti-inflammatories, herbal antibiotics for bacterial infection. Allspice, Bearberry, Elecampane, Goldenseal, Liquorice root, Mullein, Nettles, Wahoo. Others as follows:–
Teas: Haronga Tree, Chamomile, Mullein, Uva Ursi, Burdock leaves, Marigold petals, Liquorice. Cup every 3 hours.
Decoctions: Sarsaparilla (hot). Barberry (cold). See: DECOCTION.
Tablets/capsules. Blue Flag root, Chamomile, Sarsaparilla, Kelp.
Formula. Echinacea 2; Blue Flag root 1; Liquorice root 1. Dose – Liquid extracts: 1 teaspoon. Tinctures: 2 teaspoons. Powders: 500mg (two 00 capsules or one-third teaspoon); every 3 hours for acute cases, otherwise thrice daily.
Goldenseal, tincture: 10 drops once daily maintenance prophylactic dose.
External. Poultice over upper abdomen: Mullein, Chamomile or Castor oil.
Diet. Abundant citrus fruits.
Supplements. Vitamin C, methionine and selenium to mop up free radicals. Without the supplements toxins strike the pancreas, leading to severe pain. In this way they can be used as an alternative to pain-killers. (Researchers, Manchester Royal Infirmary)
Vitamin C. Lack of Vitamin C may trigger acute pancreatitis in susceptible patients. (Mr Patrick Scott, Manchester Royal Infirmary) ... pancreatitis
In adults, chickenpox is rare but usually more severe.
An attack gives lifelong immunity, but the virus remains dormant in nerves and may reappear later in life to cause herpes zoster (shingles).
The cause of chickenpox is the varicella-zoster virus, which is spread in airborne droplets.
A widespread rash develops 2–3 weeks after infection, consisting of clusters of small, red, itchy spots that become fluid-filled blisters within a few hours.
After several days the blisters dry out to form scabs.
Scratching the blisters can lead to secondary infection and scarring.
Paracetamol helps reduce fever and calamine lotion may be used to relieve itching.
In severe cases, aciclovir (an antiviral drug) may be prescribed.... chickenpox
With a dose of 10–30 Gy there is also an early onset of nausea and vomiting, which tends to disappear a few hours later. However, damage to the gastrointestinal tract, which causes severe and frequently bloody diarrhoea (called the gastrointestinal syndrome), and overwhelming infection due to damage to the immune system is likely to result in death 4–14 days after exposure.
Acute exposures of more than 30–100 Gy cause the rapid onset of nausea, vomiting, anxiety, and disorientation.
Within hours, the victim usually dies due to nervous system damage and oedema of the brain; these effects are called the central nervous system syndrome.... radiation sickness
TIAs may be caused by a blood clot (see embolism) temporarily blocking an artery that supplies the brain, or by narrowing of an artery as a result of atherosclerosis.
After a TIA, tests such as CT scanning, blood tests, ultrasound scanning, or angiography may be needed to determine a cause. In some cases, the heart is studied as a possible source of blood clots. Treatment is aimed at preventing stroke, which occurs within 5 years in up to one third of patients with TIA. Treatments include endarterectomy, anticoagulant drugs, or aspirin.... transient ischaemic attack
Urticaria is generally harmless and usually lasts only a few hours. Sometimes a persistent or recurrent form develops. Dermographism is a less common form
of urticaria in which weals form after the skin is stroked. Urticaria sometimes occurs with angioedema.
The cause of urticaria is often unknown. The most common known cause is an allergic reaction (see allergy), often to a particular food, food additive, or drug. Urticaria may also be caused by exposure to heat, cold, or sunlight. Less commonly, it may be associated with another disorder, such as vasculitis, systemic lupus erythematosus, or cancer.
Itching can be relieved by applying calamine lotion or by taking antihistamine drugs. More severe cases may require corticosteroid drugs. Identifying and avoiding known trigger factors can help prevent future reactions. A tendency to urticaria often disappears in time without treatment.... urticaria
Causes The direct cause is various BACTERIA. Sometimes the presence of foreign bodies, such as bullets or splinters, may produce an abscess, but these foreign bodies may remain buried in the tissues without causing any trouble provided that they are not contaminated by bacteria or other micro-organisms.
The micro-organisms most frequently found are staphylococci (see STAPHYLOCOCCUS), and, next to these, streptococci (see STREPTOCOCCUS) – though the latter cause more virulent abscesses. Other abscess-forming organisms are Pseudomonas pyocyanea and Escherichia coli, which live always in the bowels and under certain conditions wander into the surrounding tissues, producing abscesses.
The presence of micro-organisms is not suf?cient in itself to produce suppuration (see IMMUNITY; INFECTION); streptococci can often be found on the skin and in the skin glands of perfectly healthy individuals. Whether they will produce abscesses or not depends upon the virulence of the organism and the individual’s natural resistance.
When bacteria have gained access – for example, to a wound – they rapidly multiply, produce toxins, and cause local dilatation of the blood vessels, slowing of the bloodstream, and exudation of blood corpuscles and ?uid. The LEUCOCYTES, or white corpuscles of the blood, collect around the invaded area and destroy the bacteria either by consuming them (see PHAGOCYTOSIS) or by forming a toxin that kills them. If the body’s local defence mechanisms fail to do this, the abscess will spread and may in severe cases cause generalised infection or SEPTICAEMIA.
Symptoms The classic symptoms of in?ammation are redness, warmth, swelling, pain and fever. The neighbouring lymph nodes may be swollen and tender in an attempt to stop the bacteria spreading to other parts of the body. Infection also causes an increase in the number of leucocytes in the blood (see LEUCOCYTOSIS). Immediately the abscess is opened, or bursts, the pain disappears, the temperature falls rapidly to normal, and healing proceeds. If, however, the abscess discharges into an internal cavity such as the bowel or bladder, it may heal slowly or become chronic, resulting in the patient’s ill-health.
Treatment Most local infections of the skin respond to ANTIBIOTICS. If pus forms, the abscess should be surgically opened and drained.
Abscesses can occur in any tissue in the body, but the principles of treatment are broadly the same: use of an antibiotic and, where appropriate, surgery.... abscess
Both HIV-1 and HIV-2 are predominantly sexually transmitted and both are associated with secondary opportunistic infections. However, HIV-2 seems to result in slower damage to the immune system. HIV-1 is known to mutate rapidly and has given rise to other subtypes.
HIV is thought to have occurred in humans in the 1950s, but whether or not it infected humans from another primate species is uncertain. It became widespread in the 1970s but its latency in causing symptoms meant that the epidemic was not noticed until the following decade. Although it is a sexually transmitted disease, it can also be transmitted by intravenous drug use (through sharing an infected needle), blood transfusions with infected blood (hence the importance of e?ective national blood-screening programmes), organ donation, and occupationally (see health-care workers, below). Babies born of HIV-positive mothers can be infected before or during birth, or through breast feeding.
Although HIV is most likely to occur in blood, semen or vaginal ?uid, it has been found in saliva and tears (but not sweat); however, there is no evidence that the virus can be transmitted from these two body ?uids. There is also no evidence that HIV can be transmitted by biting insects (such as mosquitoes). HIV does not survive well in the environment and is rapidly destroyed through drying.
Prevalence At the end of 2003 an estimated 42 million people globally were infected with HIV – up from 40 million two years earlier. About one-third of those with HIV/AIDS are aged 15–24 and most are unaware that they are carrying the virus. During 2003 it is estimated that 5 million adults and children worldwide were newly infected with HIV, and that 3 million adults and children died. In Africa in 2003,
3.4 million people were newly infected and 2.3 million died, with more than 28 million carrying the virus. HIV/AIDS was the leading cause of death in sub-Saharan Africa where over half of the infections were in women and 90 per cent of cases resulted from heterosexual sex. In some southern African countries, one in three pregnant women had HIV.
In Asia and the Paci?c there were 1.2 million new infections and 435,000 deaths. The area with the fastest-growing epidemic is Eastern Europe, especially the Russian Federation where in 2002 around a million people had HIV and there were an estimated 250,000 new infections, with intravenous drug use a key contributor to this ?gure. Seventy-?ve per cent of cases occurred in men, with male-to-male sexual transmission an important cause of infection, though heterosexual activity is a rising cause of infection.
At the end of 2002 the UK had an estimated 55,900 HIV-infected adults aged between 15 and 59. More than 3,600 individuals were newly diagnosed with the infection in 2000, the highest annual ?gure since the epidemic started
– in 1998 the ?gure was 2,817 and in 1999 just over 3,000 (Department of Health and Communicable Disease Surveillance Centre). The incidence of AIDS in the UK has declined sharply since the introduction of highly active antiretroviral therapy (HAART) and HIV-related deaths have also fallen: in 2002 there were 777 reported new AIDS cases and 395 deaths, compared with 1,769 and 1,719 respectively in 1995. (Sources: UNAIDS and WHO, AIDS Epidemic Update, December 2001; Public Health Laboratory Services AIDS and STD Centre Communicable Disease Surveillance and Scottish Centre for Infection and Environmental Health, Quarterly Surveillance Tables.)
Poverty is strongly linked to the spread of AIDS, for various reasons including lack of health education; lack of e?ective public-health awareness; women having little control over sexual behaviour and contraception; and, by comparison with the developed world, little or no access to antiretroviral drugs.
Pathogenesis The cellular target of HIV infection is a subset of white blood cells called T-lymphocytes (see LYMPHOCYTE) which carry the CD4 surface receptor. These so-called ‘helper T-cells’ are vital to the function of cell-mediated immunity. Infection of these cells leads to their destruction (HIV replicates at an enormous rate – 109) and over the course of several years the body is unable to generate suf?cient new cells to keep pace. This leads to progressive destruction of the body’s immune capabilities, evidenced clinically by the development of opportunistic infection and unusual tumours.
Monitoring of clinical progression It is possible to measure the number of viral particles present in the plasma. This gives an accurate guide to the likely progression rate, which will be slow in those individuals with fewer than 10,000 particles per ml of plasma but progressively more rapid above this ?gure. The main clinical monitoring of the immune system is through the numbers of CD4 lymphocytes in the blood. The normal count is around 850 cells per ml and, without treatment, eventual progression to AIDS is likely in those individuals whose CD4 count falls below 500 per ml. Opportunistic infections occur most frequently when the count falls below 200 per ml: most such infections are treatable, and death is only likely when the CD4 count falls below 50 cells per ml when infection is developed with organisms that are di?cult to treat because of their low intrinsic virulence.
Simple, cheap and highly accurate tests are available to detect HIV antibodies in the serum. These normally occur within three months of infection and remain the cornerstone of the diagnosis.
Clinical features Most infected individuals have a viral illness some three weeks after contact with HIV. The clinical features are often non-speci?c and remain undiagnosed but include a ?ne red rash, large lymph nodes, an in?uenza-like illness, cerebral involvement and sometimes the development of opportunistic infections. The antibody test may be negative at this stage but there are usually high levels of virus particles in the blood. The antibody test is virtually always positive within three months of infection. HIV infection is often subsequently asymptomatic for a period of ten years or more, although in most patients progressive immune destruction is occurring during this time and a variety of minor opportunistic infections such as HERPES ZOSTER or oral thrush (see CANDIDA) do occur. In addition, generalised LYMPHADENOPATHY is present in a third of patients and some suffer from severe malaise, weight loss, night sweats, mild fever, ANAEMIA or easy bruising due to THROMBOCYTOPENIA.
The presentation of opportunistic infection is highly variable but usually involves either the CENTRAL NERVOUS SYSTEM, the gastrointestinal tract or the LUNGS. Patients may present with a sudden onset of a neurological de?cit or EPILEPSY due to a sudden onset of a STROKE-like syndrome, or epilepsy due to a space-occupying lesion in the brain – most commonly TOXOPLASMOSIS. In late disease, HIV infection of the central nervous system itself may produce progressive memory loss, impaired concentration and mental slowness called AIDS DEMENTIA. A wide variety of opportunistic PROTOZOA or viruses produces DYSPHAGIA, DIARRHOEA and wasting. In the respiratory system the commonest opportunistic infection associated with AIDS, pneumonia, produces severe shortness of breath and sometimes CYANOSIS, usually with a striking lack of clinical signs in the chest.
In very late HIV infection, when the CD4 count has fallen below 50 cells per ml, infection with CYTOMEGALOVIRUS may produce progressive retinal necrosis (see EYE, DISORDERS OF) which will lead to blindness if untreated, as well as a variety of gastrointestinal symptoms. At this stage, infection with atypical mycobacteria is also common, producing severe anaemia, wasting and fevers. The commonest tumour associated with HIV is Kaposi’s sarcoma which produces purplish skin lesions. This and nonHodgkin’s lymphoma (see LYMPHOMA), which is a hundred times more frequent among HIV-positive individuals than in the general population, are likely to be associated with or caused by opportunistic viral infections.
Prevention There is, as yet, no vaccine to prevent HIV infection. Vaccine development has been hampered
by the large number of new HIV strains generated through frequent mutation and recombination.
because HIV can be transmitted as free virus and in infected cells.
because HIV infects helper T-cells – the very cells involved in the immune response. There are, however, numerous research pro
grammes underway to develop vaccines that are either prophylactic or therapeutic. Vaccine-development strategies have included: recombinant-vector vaccines, in which a live bacterium or virus is genetically modi?ed to carry one or more of the HIV genes; subunit vaccines, consisting of small regions of the HIV genome designed to induce an immune response without infection; modi?ed live HIV, which has had its disease-promoting genes removed; and DNA vaccines – small loops of DNA (plasmids) containing viral genes – that make the host cells produce non-infectious viral proteins which, in turn, trigger an immune response and prime the immune system against future infection with real virus.
In the absence of an e?ective vaccine, preventing exposure remains the chief strategy in reducing the spread of HIV. Used properly, condoms are an extremely e?ective method of preventing exposure to HIV during sexual intercourse and remain the most important public-health approach to countering the further acceleration of the AIDS epidemic. The spermicide nonoxynol-9, which is often included with condoms, is known to kill HIV in vitro; however, its e?ectiveness in preventing HIV infection during intercourse is not known.
Public-health strategies must be focused on avoiding high-risk behaviour and, particularly in developing countries, empowering women to have more control over their lives, both economically and socially. In many of the poorer regions of the world, women are economically dependent on men and refusing sex, or insisting on condom use, even when they know their partners are HIV positive, is not a straightforward option. Poverty also forces many women into the sex industry where they are at greater risk of infection.
Cultural problems in gaining acceptance for universal condom-use by men in some developing countries suggests that other preventive strategies should also be considered. Microbicides used as vaginal sprays or ‘chemical condoms’ have the potential to give women more direct control over their exposure risk, and research is underway to develop suitable products.
Epidemiological studies suggest that male circumcision may o?er some protection against HIV infection, although more research is needed before this can be an established public-health strategy. Globally, about 70 per cent of infected men have acquired the virus through unprotected vaginal sex; in these men, infection is likely to have occurred through the penis with the mucosal epithelia of the inner surface of the foreskin and the frenulum considered the most likely sites for infection. It is suggested that in circumcised men, the glans may become keratinised and thus less likely to facilitate infection. Circumcision may also reduce the risk of lesions caused by other sexually transmitted disease.
Treatment AIDS/HIV treatment can be categorised as speci?c therapies for the individual opportunistic infections – which ultimately cause death – and highly active antiretroviral therapy (HAART) designed to reduce viral load and replication. HAART is also the most e?ective way of preventing opportunistic infections, and has had a signi?cant impact in delaying the onset of AIDS in HIV-positive individuals in developed countries.
Four classes of drugs are currently in use. Nucleoside analogues, including ZIDOVUDINE and DIDANOSINE, interfere with the activity of the unique enzyme of the retrovirus reverse transcriptase which is essential for replication. Nucleotide analogues, such as tenofovir, act in the same way but require no intracellular activation. Non-nucleoside reverse transcriptase inhibitors, such as nevirapine and EFAVIRENZ, act by a di?erent mechanism on the same enzyme. The most potent single agents against HIV are the protease inhibitors, such as lopinavir, which render a unique viral enzyme ineffective. These drugs are used in a variety of combinations in an attempt to reduce the plasma HIV viral load to below detectable limits, which is achieved in approximately 90 per cent of patients who have not previously received therapy. This usually also produces a profound rise in CD4 count. It is likely, however, that such treatments need to be lifelong – and since they are associated with toxicities, long-term adherence is di?cult. Thus the optimum time for treatment intervention remains controversial, with some clinicians believing that this should be governed by the viral load rising above 10,000 copies, and others that it should primarily be designed to prevent the development of opportunistic infections – thus, that initiation of therapy should be guided more by the CD4 count.
It should be noted that the drug regimens have been devised for infection with HIV-1; it is not known how e?ective they are at treating infection with HIV-2.
HIV and pregnancy An HIV-positive woman can transmit the virus to her fetus, with the risk of infection being particularly high during parturition; however, the risk of perinatal HIV transmission can be reduced by antiviral drug therapy. In the UK, HIV testing is available to all women as part of antenatal care. The bene?ts of antenatal HIV testing in countries where antiviral drugs are not available are questionable. An HIV-positive woman might be advised not to breast feed because of the risks of transmitting HIV via breastmilk, but there may be a greater risk associated with not breast feeding at all. Babies in many poor communities are thought to be at high risk of infectious diseases and malnutrition if they are not breast fed and may thus be at greater overall risk of death during infancy.
Counselling Con?dential counselling is an essential part of AIDS management, both in terms of supporting the psychological wellbeing of the individual and in dealing with issues such as family relations, sexual partners and implications for employment (e.g. for health-care workers). Counsellors must be particularly sensitive to culture and lifestyle issues. Counselling is essential both before an HIV test is taken and when the results are revealed.
Health-care workers Health-care workers may be at risk of occupational exposure to HIV, either through undertaking invasive procedures or through accidental exposure to infected blood from a contaminated needle (needlestick injury). Needlestick injuries are frequent in health care – as many as 600,000 to 800,000 are thought to occur annually in the United States. Transmission is much more likely where the worker has been exposed to HIV through a needlestick injury or deep cut with a contaminated instrument than through exposure of mucous membranes to contaminated blood or body ?uids. However, even where exposure occurs through a needlestick injury, the risk of seroconversion is much lower than with a similar exposure to hepatitis C or hepatitis B. A percutaneous exposure to HIV-infected blood in a health-care setting is thought to carry a risk of about one infection per 300 injuries (one in 1,000 for mucous-membrane exposure), compared with one in 30 for hepatitis C, and one in three for hepatitis B (when the source patient is e-antigen positive).
In the event of an injury, health-care workers are advised to report the incident immediately where, depending on a risk assessment, they may be o?ered post-exposure prophylaxis (PEP). They should also wash the contaminated area with soap and water (but without scrubbing) and, if appropriate, encourage bleeding at the site of injury. PEP, using a combination of antiretroviral drugs (in a similar regimen to HAART – see above), is thought to greatly reduce the chances of seroconversion; it should be commenced as soon as possible, preferably within one or two hours of the injury. Although PEP is available, safe systems of work are considered to o?er the greatest protection. Double-gloving (latex gloves remove much of the blood from the surface of the needle during a needlestick), correct use of sharps containers (for used needles and instruments), avoiding the resheathing of used needles, reduction in the number of blood samples taken from a patient, safer-needle devices (such as needles that self-blunt after use) and needleless drug administration are all thought to reduce the risk of exposure to HIV and other blood-borne viruses. Although there have been numerous cases of health-care workers developing HIV through occupational exposure, there is little evidence of health-care workers passing HIV to their patients through normal medical procedures.... aids/hiv
Nutritional Profile Energy value (calories per serving): Moderate Protein: High Fat: Low Saturated fat: Low Cholesterol: None Carbohydrates: High Fiber: Very high Sodium: Low Major vitamin contribution: Vitamin B6, folate Major mineral contribution: Iron, magnesium, zinc
About the Nutrients in This Food Beans are seeds, high in complex carbohydrates including starch and dietary fiber. They have indigestible sugars (stachyose and raffinose), plus insoluble cellulose and lignin in the seed covering and soluble gums and pectins in the bean. The proteins in beans are limited in the essential amino acids methionine and cystine.* All beans are a good source of the B vitamin folate, and iron. One-half cup canned kidney beans has 7.5 g dietary fiber, 65 mcg folate (15 percent of the R DA), and 1.6 mg iron (11 percent of the R DA for a woman, 20 percent of the R DA for a man). Raw beans contain antinutrient chemicals that inactivate enzymes required to digest proteins and carbohydrates. They also contain factors that inactivate vitamin A and also hemagglutinins, substances that make red blood cells clump together. Cooking beans disarms the enzyme inhibi- tors and the anti-vitamin A factors, but not the hemagglutinins. However, the amount of hemagglutinins in the beans is so small that it has no mea- surable effect in your body. * Soybeans are t he only beans t hat contain proteins considered “complete” because t hey contain sufficient amounts of all t he essent ial amino acids. The Folate Content of ½ Cup Cooked Dried Beans
| Bean | Folate (mcg) |
| Black beans | 129 |
| Chickpeas | 191 |
| Kidney beans canned | 65 |
| Navy beans | 128 |
| Pinto beans | 147 |
The Most Nutritious Way to Serve This Food Cooked, to destroy antinutrients. With grains. The proteins in grains are deficient in the essential amino acids lysine and isoleucine but contain sufficient tryptophan, methionine, and cystine; the proteins in beans are exactly the opposite. Together, these foods provide “complete” proteins. With an iron-rich food (meat) or with a vitamin C-rich food (tomatoes). Both enhance your body’s ability to use the iron in the beans. The meat makes your stomach more acid (acid favors iron absorption); the vitamin C may convert the ferric iron in beans into ferrous iron, which is more easily absorbed by the body.
Diets That May Restrict or Exclude This Food Low-calcium diet Low-fiber diet Low-purine (antigout) diet
Buying This Food Look for: Smooth-skinned, uniformly sized, evenly colored beans that are free of stones and debris. The good news about beans sold in plastic bags is that the transparent material gives you a chance to see the beans inside; the bad news is that pyridoxine and pyridoxal, the natural forms of vitamin B6, are very sensitive to light. Avoid: Beans sold in bulk. Some B vitamins, such as vitamin B6 (pyridoxine and pyridoxal), are very sensitive to light. In addition, open bins allow insects into the beans, indicated by tiny holes showing where the bug has burrowed into or through the bean. If you choose to buy in bulk, be sure to check for smooth skinned, uniformly sized, evenly colored beans free of holes, stones, and other debris.
Storing This Food Store beans in air- and moistureproof containers in a cool, dark cabinet where they are pro- tected from heat, light, and insects.
Preparing This Food Wash dried beans and pick them over carefully, discarding damaged or withered beans and any that float. (Only withered beans are light enough to float in water.) Cover the beans with water, bring them to a boil, and then set them aside to soak. When you are ready to use the beans, discard the water in which beans have been soaked. Some of the indigestible sugars in the beans that cause intestinal gas when you eat the beans will leach out into the water, making the beans less “gassy.”
What Happens When You Cook This Food When beans are cooked in liquid, their cells absorb water, swell, and eventually rupture, releasing the pectins and gums and nutrients inside. In addition, cooking destroys antinutri- ents in beans, making them more nutritious and safe to eat.
How Other Kinds of Processing Affect This Food Canning. The heat of canning destroys some of the B vitamins in the beans. Vitamin B is water-soluble. You can recover all the lost B vitamins simply by using the liquid in the can, but the liquid also contains the indigestible sugars that cause intestinal gas when you eat beans. Preprocessing. Preprocessed dried beans have already been soaked. They take less time to cook but are lower in B vitamins.
Medical Uses and/or Benefits Lower risk of some birth defects. As many as two of every 1,000 babies born in the United States each year may have cleft palate or a neural tube (spinal cord) defect due to their moth- ers’ not having gotten adequate amounts of folate during pregnancy. The current R DA for folate is 180 mcg for a woman and 200 mcg for a man, but the FDA now recommends 400 mcg for a woman who is or may become pregnant. Taking a folate supplement before becoming pregnant and continuing through the first two months of pregnancy reduces the risk of cleft palate; taking folate through the entire pregnancy reduces the risk of neural tube defects. Lower risk of heart attack. In the spring of 1998, an analysis of data from the records for more than 80,000 women enrolled in the long-run ning Nurses Health Study at Har vard School of Public Health/ Brigham and Woman’s Hospital in Boston demonstrated that a diet providing more than 400 mcg folate and 3 mg vitamin B6 a day from either food or supple- ments, more than t wice the current R DA for each, may reduce a woman’s risk of heart attack by almost 50 percent. A lthough men were not included in the analysis, the results are assumed to apply to them as well. NOT E : Beans are high in B6 as well as folate. Fruit, green leaf y vegetables, whole grains, meat, fish, poultr y, and shellfish are good sources of vitamin B6. To reduce the levels of serum cholesterol. The gums and pectins in dried beans and peas appear to lower blood levels of cholesterol. Currently there are two theories to explain how this may happen. The first theory is that the pectins in the beans form a gel in your stomach that sops up fats and keeps them from being absorbed by your body. The second is that bacteria in the gut feed on the bean fiber, producing short-chain fatty acids that inhibit the production of cholesterol in your liver. As a source of carbohydrates for people with diabetes. Beans are digested very slowly, produc- ing only a gradual rise in blood-sugar levels. As a result, the body needs less insulin to control blood sugar after eating beans than after eating some other high-carbohydrate foods (such as bread or potato). In studies at the University of Kentucky, a bean, whole-grain, vegetable, and fruit-rich diet developed at the University of Toronto enabled patients with type 1 dia- betes (who do not produce any insulin themselves) to cut their daily insulin intake by 38 percent. Patients with type 2 diabetes (who can produce some insulin) were able to reduce their insulin injections by 98 percent. This diet is in line with the nutritional guidelines of the American Diabetes Association, but people with diabetes should always consult with their doctors and/or dietitians before altering their diet. As a diet aid. Although beans are high in calories, they are also high in bulk (fiber); even a small serving can make you feel full. And, because they are insulin-sparing, they delay the rise in insulin levels that makes us feel hungry again soon after eating. Research at the University of Toronto suggests the insulin-sparing effect may last for several hours after you eat the beans, perhaps until after the next meal.
Adverse Effects Associated with This Food Intestinal gas. All legumes (beans and peas) contain raffinose and stachyose, complex sug- ars that human beings cannot digest. The sugars sit in the gut and are fermented by intestinal bacteria which then produce gas that distends the intestines and makes us uncomfortable. You can lessen this effect by covering the beans with water, bringing them to a boil for three to five minutes, and then setting them aside to soak for four to six hours so that the indigestible sugars leach out in the soaking water, which can be discarded. Alternatively, you may soak the beans for four hours in nine cups of water for every cup of beans, discard the soaking water, and add new water as your recipe directs. Then cook the beans; drain them before serving. Production of uric acid. Purines are the natural metabolic by-products of protein metabo- lism in the body. They eventually break down into uric acid, sharp cr ystals that may concentrate in joints, a condition known as gout. If uric acid cr ystals collect in the urine, the result may be kidney stones. Eating dried beans, which are rich in proteins, may raise the concentration of purines in your body. Although controlling the amount of purines in the diet does not significantly affect the course of gout (which is treated with allopurinol, a drug that prevents the formation of uric acid cr ystals), limiting these foods is still part of many gout regimens.
Food/Drug Interactions Monoamine oxidase (MAO) inhibitors. Monoamine oxidase inhibitors are drugs used to treat depression. They inactivate naturally occurring enzymes in your body that metabolize tyramine, a substance found in many fermented or aged foods. Tyramine constricts blood vessels and increases blood pressure. If you eat a food containing tyramine while you are taking an M AO inhibitor, you cannot effectively eliminate the tyramine from your body. The result may be a hypertensive crisis. Some nutrition guides list dried beans as a food to avoid while using M AO inhibitors.... beans
Nutritional Profile Energy value (calories per serving): Moderate Protein: High Fat: Moderate Saturated fat: High Cholesterol: Moderate Carbohydrates: None Fiber: None Sodium: Low Major vitamin contribution: B vitamins Major mineral contribution: Iron, phosphorus, zinc
About the Nutrients in This Food Like fish, pork, poultry, milk, and eggs, beef has high-quality proteins, with sufficient amounts of all the essential amino acids. Beef fat is slightly more highly saturated than pork fat, but less saturated than lamb fat. All have about the same amount of cholesterol per serving. Beef is an excellent source of B vitamins, including niacin, vitamin B6, and vitamin B12, which is found only in animal foods. Lean beef pro- vides heme iron, the organic iron that is about five times more useful to the body than nonheme iron, the inorganic form of iron found in plant foods. Beef is also an excellent source of zinc. One four-ounce serving of lean broiled sirloin steak has nine grams fat (3.5 g saturated fat), 101 mg cholesterol, 34 g protein, and 3.81 mg iron (21 percent of the R DA for a woman, 46 percent of the R DA for a man). One four-ounce serving of lean roast beef has 16 g fat (6.6 g saturated fat), 92 mg cholesterol, and 2.96 mg iron (16 percent of the R DA for a woman, 37 percent of the R DA for a man).
The Most Nutritious Way to Serve This Food With a food rich in vitamin C. Ascorbic acid increases the absorption of iron from meat. * These values apply to lean cooked beef.
Diets That May Restrict or Exclude This Food Controlled-fat, low-cholesterol diet Low-protein diet (for some forms of kidney disease)
Buying This Food Look for: Fresh, red beef. The fat should be white, not yellow. Choose lean cuts of beef with as little internal marbling (streaks of fat) as possible. The leanest cuts are flank steak and round steak; rib steaks, brisket, and chuck have the most fat. USDA grading, which is determined by the maturity of the animal and marbling in meat, is also a guide to fat content. U.S. prime has more marbling than U.S. choice, which has more marbling than U.S. good. All are equally nutritious; the difference is how tender they are, which depends on how much fat is present. Choose the cut of meat that is right for your recipe. Generally, the cuts from the cen- ter of the animal’s back—the rib, the T-Bone, the porterhouse steaks—are the most tender. They can be cooked by dry heat—broiling, roasting, pan-frying. Cuts from around the legs, the underbelly, and the neck—the shank, the brisket, the round—contain muscles used for movement. They must be tenderized by stewing or boiling, the long, moist cooking methods that break down the connective tissue that makes meat tough.
Storing This Food Refrigerate raw beef immediately, carefully wrapped to prevent its drippings from contami- nating other foods. Refrigeration prolongs the freshness of beef by slowing the natural multi- plication of bacteria on the meat surface. Unchecked, these bacteria will convert proteins and other substances on the surface of the meat to a slimy film and change meat’s sulfur-contain- ing amino acids methionine and cystine into smelly chemicals called mercaptans. When the mercaptans combine with myoglobin, they produce the greenish pigment that gives spoiled meat its characteristic unpleasant appearance. Fresh ground beef, with many surfaces where bacteria can live, should be used within 24 to 48 hours. Other cuts of beef may stay fresh in the refrigerator for three to five days.
Preparing This Food Trim the beef carefully. By judiciously cutting away all visible fat you can significantly reduce the amount of fat and cholesterol in each serving. When you are done, clean all utensils thoroughly with soap and hot water. Wash your cutting board, wood or plastic, with hot water, soap, and a bleach-and-water solution. For ultimate safety in preventing the transfer of microorganisms from the raw meat to other foods, keep one cutting board exclusively for raw meats, fish, and poultry, and a second one for everything else. Finally, don’t forget to wash your hands.
What Happens When You Cook This Food Cooking changes the appearance and flavor of beef, alters nutritional value, makes it safer, and extends its shelf life. Browning meat after you cook it does not “seal in the juices,” but it does change the fla- vor by caramelizing sugars on the surface. Because beef’s only sugars are the small amounts of glycogen in the muscles, we add sugars in marinades or basting liquids that may also con- tain acids (vinegar, lemon juice, wine) to break down muscle fibers and tenderize the meat. (Browning has one minor nutritional drawback. It breaks amino acids on the surface of the meat into smaller compounds that are no longer useful proteins.) When beef is cooked, it loses water and shrinks. Its pigments, which combine with oxygen, are denatured (broken into fragments) by the heat and turn brown, the natural color of well-done meat. At the same time, the fats in the beef are oxidized. Oxidized fats, whether formed in cooking or when the cooked meat is stored in the refrigerator, give cooked meat a character- istic warmed-over flavor. Cooking and storing meat under a blanket of antioxidants—catsup or a gravy made of tomatoes, peppers, and other vitamin C-rich vegetables—reduces the oxidation of fats and the intensity of warmed-over flavor. Meat reheated in a microwave oven also has less warmed-over flavor. An obvious nutritional benefit of cooking is the fact that heat lowers the fat content of beef by liquif ying the fat so it can run off the meat. One concrete example of how well this works comes from a comparison of the fat content in regular and extra-lean ground beef. According to research at the University of Missouri in 1985, both kinds of beef lose mass when cooked, but the lean beef loses water and the regular beef loses fat and cholesterol. Thus, while regular raw ground beef has about three times as much fat (by weight) as raw ground extra-lean beef, their fat varies by only 5 percent after broiling. To reduce the amount of fat in ground beef, heat the beef in a pan until it browns. Then put the beef in a colander, and pour one cup of warm water over the beef. Repeat with a second cup of warm water to rinse away fat melted by heating the beef. Use the ground beef in sauce and other dishes that do not require it to hold together. Finally, cooking makes beef safer by killing Salmonella and other organisms in the meat. As a result, cooking also serves as a natural preservative. According to the USDA, large pieces of fresh beef can be refrigerated for two or three days, then cooked and held safely for another day or two because the heat of cooking has reduced the number of bacteria on the surface of the meat and temporarily interrupted the natural cycle of deterioration.
How Other Kinds of Processing Affect This Food Aging. Hanging fresh meat exposed to the air, in a refrigerated room, reduces the moisture content and shrinks the meat slightly. As the meat ages enzymes break down muscle pro- teins, “tenderizing” the beef. Canning. Canned beef does not develop a warmed-over flavor because the high tempera- tures in canning food and the long cooking process alter proteins in the meat so that they act as antioxidants. Once the can is open, however, the meat should be protected from oxygen that will change the flavor of the beef. Curing. Salt-curing preserves meat through osmosis, the physical reaction in which liquids flow across a membrane, such as the wall of a cell, from a less dense to a more dense solution. The salt or sugar used in curing dissolves in the liquid on the surface of the meat to make a solution that is more dense than the liquid inside the cells of the meat. Water flows out of the meat and out of the cells of any microorganisms living on the meat, killing the microor- ganisms and protecting the meat from bacterial damage. Salt-cured meat is much higher in sodium than fresh meat. Freezing. When you freeze beef, the water inside its cells freezes into sharp ice crystals that can puncture cell membranes. When the beef thaws, moisture (and some of the B vitamins) will leak out through these torn cell walls. The loss of moisture is irreversible, but some of the vitamins can be saved by using the drippings when the meat is cooked. Freezing may also cause freezer burn—dry spots left when moisture evaporates from the surface of the meat. Waxed freezer paper is designed specifically to hold the moisture in meat; plastic wrap and aluminum foil are less effective. NOTE : Commercially prepared beef, which is frozen very quickly at very low temperatures, is less likely to show changes in texture. Irradiation. Irradiation makes meat safer by exposing it to gamma rays, the kind of high- energy ionizing radiation that kills living cells, including bacteria. Irradiation does not change the way meat looks, feels or tastes, or make the food radioactive, but it does alter the structure of some naturally occurring chemicals in beef, breaking molecules apart to form new com- pounds called radiolytic products (R P). About 90 percent of R Ps are also found in nonirradiated foods. The rest, called unique radiolytic products (UR P), are found only in irradiated foods. There is currently no evidence to suggest that UR Ps are harmful; irradiation is an approved technique in more than 37 countries around the world, including the United States. Smoking. Hanging cured or salted meat over an open fire slowly dries the meat, kills micro- organisms on its surface, and gives the meat a rich, “smoky” flavor that varies with the wood used in the fire. Meats smoked over an open fire are exposed to carcinogenic chemicals in the smoke, including a-benzopyrene. Meats treated with “artificial smoke flavoring” are not, since the flavoring is commercially treated to remove tar and a-benzopyrene.
Medical Uses and/or Benefits Treating and/or preventing iron deficiency. Without meat in the diet, it is virtually impossible for an adult woman to meet her iron requirement without supplements. One cooked 3.5- ounce hamburger provides about 2.9 mg iron, 16 percent of the R DA for an adult woman of childbearing age. Possible anti-diabetes activity. CLA may also prevent type 2 diabetes, also called adult-onset diabetes, a non-insulin-dependent form of the disease. At Purdue University, rats bred to develop diabetes spontaneously between eight and 10 weeks of age stayed healthy when given CLA supplements.
Adverse Effects Associated with This Food Increased risk of heart disease. Like other foods from animals, beef contains cholesterol and saturated fats that increase the amount of cholesterol circulating in your blood, raising your risk of heart disease. To reduce the risk of heart disease, the National Cholesterol Education Project recommends following the Step I and Step II diets. The Step I diet provides no more than 30 percent of total daily calories from fat, no more than 10 percent of total daily calories from saturated fat, and no more than 300 mg of cholesterol per day. It is designed for healthy people whose cholesterol is in the range of 200 –239 mg/dL. The Step II diet provides 25– 35 percent of total calories from fat, less than 7 percent of total calories from saturated fat, up to 10 percent of total calories from polyunsaturated fat, up to 20 percent of total calories from monounsaturated fat, and less than 300 mg cho- lesterol per day. This stricter regimen is designed for people who have one or more of the following conditions: • Existing cardiovascular disease • High levels of low-density lipoproteins (LDLs, or “bad” cholesterol) or low levels of high-density lipoproteins (HDLs, or “good” cholesterol) • Obesity • Type 1 diabetes (insulin-dependent diabetes, or diabetes mellitus) • Metabolic syndrome, a.k.a. insulin resistance syndrome, a cluster of risk fac- tors that includes type 2 diabetes (non-insulin-dependent diabetes) Increased risk of some cancers. According the American Institute for Cancer Research, a diet high in red meat (beef, lamb, pork) increases the risk of developing colorectal cancer by 15 percent for every 1.5 ounces over 18 ounces consumed per week. In 2007, the National Can- cer Institute released data from a survey of 500,000 people, ages 50 to 71, who participated in an eight-year A AR P diet and health study identif ying a higher risk of developing cancer of the esophagus, liver, lung, and pancreas among people eating large amounts of red meats and processed meats. Food-borne illness. Improperly cooked meat contaminated with E. coli O157:H7 has been linked to a number of fatalities in several parts of the United States. In addition, meats con- taminated with other bacteria, viruses, or parasites pose special problems for people with a weakened immune system: the very young, the very old, cancer chemotherapy patients, and people with HIV. Cooking meat to an internal temperature of 140°F should destroy Salmo- nella and Campylobacter jejuni; 165°F, the E. coli organism; and 212°F, Listeria monocytogenes. Antibiotic sensitivity. Cattle in the United States are routinely given antibiotics to protect them from infection. By law, the antibiotic treatment must stop three days to several weeks before the animal is slaughtered. Theoretically, the beef should then be free of antibiotic residues, but some people who are sensitive to penicillin or tetracycline may have an allergic reaction to the meat, although this is rare. Antibiotic-resistant Salmonella and toxoplasmosis. Cattle treated with antibiotics may pro- duce meat contaminated with antibiotic-resistant strains of Salmonella, and all raw beef may harbor ordinary Salmonella as well as T. gondii, the parasite that causes toxoplasmosis. Toxoplasmosis is particularly hazardous for pregnant women. It can be passed on to the fetus and may trigger a series of birth defects including blindness and mental retardation. Both Salmonella and the T. gondii can be eliminated by cooking meat thoroughly and washing all utensils, cutting boards, and counters as well as your hands with hot soapy water before touching any other food. Decline in kidney function. Proteins are nitrogen compounds. When metabolized, they yield ammonia, which is excreted through the kidneys. In laborator y animals, a sustained high-protein diet increases the flow of blood through the kidneys, accelerating the natural age-related decline in kidney function. Some experts suggest that this may also occur in human beings.
Food/Drug Interactions Tetracycline antibiotics (demeclocycline [Declomycin], doxycycline [ Vibtamycin], methacycline [Rondomycin], minocycline [Minocin], oxytetracycline [Terramycin], tetracycline [Achromycin V, Panmycin, Sumycin]). Because meat contains iron, which binds tetracyclines into com- pounds the body cannot absorb, it is best to avoid meat for two hours before and after taking one of these antibiotics. Monoamine oxidase (MAO) inhibitors. Meat “tenderized” with papaya or a papain powder can interact with the class of antidepressant drugs known as monoamine oxidase inhibi- tors. Papain meat tenderizers work by breaking up the long chains of protein molecules. One by-product of this process is tyramine, a substance that constructs blood vessels and raises blood pressure. M AO inhibitors inactivate naturally occurring enzymes in your body that metabolize tyramine. If you eat a food such as papain-tenderized meat, which is high in tyramine, while you are taking a M AO inhibitor, you cannot effectively eliminate the tyramine from your body. The result may be a hypertensive crisis. Theophylline. Charcoal-broiled beef appears to reduce the effectiveness of theophylline because the aromatic chemicals produced by burning fat speed up the metabolism of the- ophylline in the liver.... beef
Nutritional Profile Energy value (calories per serving): Low Protein: Moderate Fat: None Saturated fat: None Cholesterol: None Carbohydrates: High Fiber: None Sodium: Low Major vitamin contribution: B vitamins Major mineral contribution: Phosphorus
About the Nutrients in This Food Beer and ale are fermented beverages created by yeasts that convert the sugars in malted barley and grain to ethyl alcohol (a.k.a. “alcohol,” “drink- ing alcohol”).* The USDA /Health and Human Services Dietary Guidelines for Americans defines one drink as 12 ounces of beer, five ounces of wine, or 1.25 ounces of distilled spirits. One 12-ounce glass of beer has 140 calo- ries, 86 of them (61 percent) from alcohol. But the beverage—sometimes nicknamed “liquid bread”—is more than empty calories. Like wine, beer retains small amounts of some nutrients present in the food from which it was made. * Because yeasts cannot digest t he starches in grains, t he grains to be used in mak ing beer and ale are allowed to germinate ( “malt” ). When it is t ime to make t he beer or ale, t he malted grain is soaked in water, forming a mash in which t he starches are split into simple sugars t hat can be digested (fermented) by t he yeasts. If undisturbed, t he fermentat ion will cont inue unt il all t he sugars have been digested, but it can be halted at any t ime simply by raising or lowering t he temperature of t he liquid. Beer sold in bott les or cans is pasteurized to k ill t he yeasts and stop t he fermentat ion. Draft beer is not pasteurized and must be refrigerated unt il tapped so t hat it will not cont inue to ferment in t he container. The longer t he shipping t ime, t he more likely it is t hat draft beer will be exposed to temperature variat ions t hat may affect its qualit y—which is why draft beer almost always tastes best when consumed near t he place where it was brewed. The Nutrients in Beer (12-ounce glass)
| Nutrients | Beer | %R DA |
| Calcium | 17 mg | 1.7 |
| Magnesium | 28.51 mg | 7–9* |
| Phosphorus | 41.1 mg | 6 |
| Potassium | 85.7 mg | (na) |
| Zinc | 0.06 mg | 0.5– 0.8* |
| Thiamin | 0.02 mg | 1.6 –1.8* |
| R iboflavin | 0.09 mg | 7– 8* |
| Niacin | 1.55 mg | 10 |
| Vitamin B6 | 0.17 mg | 13 |
| Folate | 20.57 mcg | 5 |
Diets That May Restrict or Exclude This Food Bland diet Gluten-free diet Low-purine (antigout) diet
Buying This Food Look for: A popular brand that sells steadily and will be fresh when you buy it. Avoid: Dusty or warm bottles and cans.
Storing This Food Store beer in a cool place. Beer tastes best when consumed within two months of the day it is made. Since you cannot be certain how long it took to ship the beer to the store or how long it has been sitting on the grocery shelves, buy only as much beer as you plan to use within a week or two. Protect bottled beer and open bottles or cans of beer from direct sunlight, which can change sulfur compounds in beer into isopentyl mercaptan, the smelly chemical that gives stale beer its characteristic unpleasant odor.
When You Are Ready to Serve This Food Serve beer only in absolutely clean glasses or mugs. Even the slightest bit of grease on the side of the glass will kill the foam immediately. Wash beer glasses with detergent, not soap, and let them drain dry rather than drying them with a towel that might carry grease from your hands to the glass. If you like a long-lasting head on your beer, serve the brew in tall, tapering glasses to let the foam spread out and stabilize. For full flavor, serve beer and ales cool but not ice-cold. Very low temperatures immo- bilize the molecules that give beer and ale their flavor and aroma.
What Happens When You Cook This Food When beer is heated (in a stew or as a basting liquid), the alcohol evaporates but the flavor- ing agents remain intact. Alcohol, an acid, reacts with metal ions from an aluminum or iron pot to form dark compounds that discolor the pot or the dish you are cooking in. To prevent this, prepare dishes made with beer in glass or enameled pots.
Medical Uses and/or Benefits Reduced risk of heart attack. Data from the American Cancer Society’s Cancer Prevention Study 1, a 12-year survey of more than 1 million Americans in 25 states, shows that men who take one drink a day have a 21 percent lower risk of heart attack and a 22 percent lower risk of stroke than men who do not drink at all. Women who have up to one drink a day also reduce their risk of heart attack. Numerous later studies have confirmed these findings. Lower risk of stroke. In January 1999, the results of a 677-person study published by researchers at New York Presbyterian Hospital-Columbia University showed that moder- ate alcohol consumption reduces the risk of stroke due to a blood clot in the brain among older people (average age: 70). How the alcohol prevents stroke is still unknown, but it is clear that moderate use of alcohol is a key. Heavy drinkers (those who consume more than seven drinks a day) have a higher risk of stroke. People who once drank heavily, but cut their consumption to moderate levels, can also reduce their risk of stroke. Numerous later studies have confirmed these findings. Lower cholesterol levels. Beverage alcohol decreases the body’s production and storage of low-density lipoproteins (LDLs), the protein and fat particles that carr y cholesterol into your arteries. As a result, people who drink moderately tend to have lower cholesterol levels and higher levels of high density lipoproteins (HDLs), the fat and protein particles that carr y cholesterol out of the body. The USDA /Health and Human Services Dietar y Guidelines for Americans defines moderation as two drinks a day for a man, one drink a day for a woman. Stimulating the appetite. Alcoholic beverages stimulate the production of saliva and the gastric acids that cause the stomach contractions we call hunger pangs. Moderate amounts of alcoholic beverages, which may help stimulate appetite, are often prescribed for geriatric patients, convalescents, and people who do not have ulcers or other chronic gastric problems that might be exacerbated by the alcohol. Dilation of blood vessels. Alcohol dilates the capillaries (the tiny blood vessels just under the skin), and moderate amounts of alcoholic beverages produce a pleasant flush that temporar- ily warms the drinker. But drinking is not an effective way to warm up in cold weather since the warm blood that flows up to the capillaries will cool down on the surface of your skin and make you even colder when it circulates back into the center of your body. Then an alco- hol flush will make you perspire, so that you lose more heat. Excessive amounts of beverage alcohol may depress the mechanism that regulates body temperature.
Adverse Effects Associated with This Food Increased risk of breast cancer. In 2008, scientists at the National Cancer Institute released data from a seven-year survey of more than 100,000 postmenopausal women showing that even moderate drinking (one to two drinks a day) may increase by 32 percent a woman’s risk of developing estrogen-receptor positive (ER+) and progesterone-receptor positive (PR+) breast cancer, tumors whose growth is stimulated by hormones. No such link was found between consuming alcohol and the risk of developing ER-/PR- tumors (not fueled by hor- mones). The finding applies to all types of alcohol: beer, wine, and spirits. Increased risk of oral cancer (cancer of the mouth and throat). Numerous studies confirm the American Cancer Society’s warning that men and women who consume more than two drinks a day are at higher risk of oral cancer than are nondrinkers or people who drink less. Note: The Dietary Guidelines for Americans describes one drink as 12 ounces of beer, five ounces of wine, or 1.5 ounces of distilled spirits. Increased risk of cancer of the colon and rectum. In the mid-1990s, studies at the University of Oklahoma suggested that men who drink more than five beers a day are at increased risk of rectal cancer. Later studies suggested that men and women who are heavy beer or spirits drinkers (but not those who are heavy wine drinkers) have a higher risk of colorectal cancers. Further studies are required to confirm these findings. Fetal alcohol syndrome. Fetal alcohol syndrome is a specific pattern of birth defects—low birth weight, heart defects, facial malformations, and mental retardation—first recognized in a study of babies born to alcoholic women who consumed more than six drinks a day while pregnant. Subsequent research has found a consistent pattern of milder defects in babies born to women who consume three to four drinks a day or five drinks on any one occasion while pregnant. To date, there is no evidence of a consistent pattern of birth defects in babies born to women who consume less than one drink a day while pregnant, but two studies at Columbia University have suggested that as few as two drinks a week while preg- nant may raise a woman’s risk of miscarriage. (“One drink” means 12 ounces of beer, five ounces of wine, or 1.25 ounces of distilled spirits.) Alcoholism. Alcoholism is an addiction disease, the inability to control one’s alcohol consumption. It is a potentially life-threatening condition, with a higher risk of death by accident, suicide, malnutrition, or acute alcohol poisoning, a toxic reaction that kills by para- lyzing body organs, including the heart. Malnutrition. While moderate alcohol consumption stimulates appetite, alcohol abuse depresses it. In addition, an alcoholic may drink instead of eating. When an alcoholic does eat, excess alcohol in his/her body prevents absorption of nutrients and reduces the ability to synthesize new tissue. Hangover. Alcohol is absorbed from the stomach and small intestine and carried by the bloodstream to the liver, where it is oxidized to acetaldehyde by alcohol dehydrogenase (ADH), the enzyme our bodies use to metabolize the alcohol we produce when we digest carbohydrates. The acetaldehyde is converted to acetyl coenzyme A and either eliminated from the body or used in the synthesis of cholesterol, fatty acids, and body tissues. Although individuals vary widely in their capacity to metabolize alcohol, on average, normal healthy adults can metabolize the alcohol in one quart of beer in approximately five to six hours. If they drink more than that, they will have more alcohol than the body’s natural supply of ADH can handle. The unmetabolized alcohol will pile up in the bloodstream, interfering with the liver’s metabolic functions. Since alcohol decreases the reabsorption of water from the kidneys and may inhibit the secretion of an antidiuretic hormone, they will begin to urinate copiously, losing magnesium, calcium, and zinc but retaining more irritating uric acid. The level of lactic acid in the body will increase, making them feel tired and out of sorts; their acid-base balance will be out of kilter; the blood vessels in their heads will swell and throb; and their stomachs, with linings irritated by the alcohol, will ache. The ultimate result is a “hangover” whose symptoms will disappear only when enough time has passed to allow their bodies to marshal the ADH needed to metabolize the extra alcohol in their blood. Changes in body temperature. Alcohol dilates capillaries, tiny blood vessels just under the skin, producing a “flush” that temporarily warms the drinker. But drinking is not an effective way to stay warm in cold weather. Warm blood flowing up from the body core to the surface capillaries is quickly chilled, making you even colder when it circulates back into your organs. In addition, an alcohol flush triggers perspiration, further cooling your skin. Finally, very large amounts of alcohol may actually depress the mechanism that regulates body temperature. Impotence. Excessive drinking decreases libido (sexual desire) and interferes with the ability to achieve or sustain an erection. “Beer belly.” Data from a 1995, 12,000 person study at the University of North Carolina in Chapel Hill show that people who consume at least six beers a week have more rounded abdomens than people who do not drink beer. The question left to be answered is which came first: the tummy or the drinking.
Food/Drug Interactions Acetaminophen (Tylenol, etc.). The FDA recommends that people who regularly have three or more drinks a day consult a doctor before using acetaminophen. The alcohol/acetamino- phen combination may cause liver failure. Disulfiram (Antabuse). Taken with alcohol, disulfiram causes flushing, nausea, low blood pressure, faintness, respiratory problems, and confusion. The severity of the reaction gener- ally depends on how much alcohol you drink, how much disulfiram is in your body, and how long ago you took it. Disulfiram is used to help recovering alcoholics avoid alcohol. (If taken with alcohol, metronidazole [Flagyl], procarbazine [Matulane], quinacrine [Atabrine], chlorpropamide (Diabinase), and some species of mushrooms may produce a mild disulfi- ramlike reaction.) Anticoagulants. Alcohol slows the body’s metabolism of anticoagulants (blood thinners) such as warfarin (Coumadin), intensif ying the effect of the drugs and increasing the risk of side effects such as spontaneous nosebleeds. Antidepressants. Alcohol may increase the sedative effects of antidepressants. Drinking alcohol while you are taking a monoamine oxidase (M AO) inhibitor is especially hazard- ous. M AO inhibitors inactivate naturally occurring enzymes in your body that metabolize tyramine, a substance found in many fermented or aged foods. Tyramine constricts blood vessels and increases blood pressure. If you eat a food containing tyramine while you are taking an M AO inhibitor, you cannot effectively eliminate the tyramine from your body. The result may be a hypertensive crisis. Ordinarily, fermentation of beer and ale does not produce tyramine, but some patients have reported tyramine reactions after drinking some imported beers. Beer and ale are usually prohibited to those using M AO inhibitors. Aspirin, ibuprofen, ketoprofen, naproxen, and nonsteroidal anti-inflammatory drugs. Like alcohol, these analgesics irritate the lining of the stomach and may cause gastric bleeding. Combining the two intensifies the effect. Insulin and oral hypoglycemics. Alcohol lowers blood sugar and interferes with the metabo- lism of oral antidiabetics; the combination may cause severe hypoglycemia. Sedatives and other central nervous system depressants (tranquilizers, sleeping pills, antidepres- sants, sinus and cold remedies, analgesics, and medication for motion sickness). Alcohol inten- sifies sedation and, depending on the dose, may cause drowsiness, respiratory depression, coma, or death.... beer
Nutritional Profile Energy value (calories per serving): Moderate Protein: Moderate Fat: Low to moderate Saturated fat: Low to high Cholesterol: Low to high Carbohydrates: High Fiber: Moderate to high Sodium: Moderate to high Major vitamin contribution: B vitamins Major mineral contribution: Calcium, iron, potassium
About the Nutrients in This Food All commercially made yeast breads are approximately equal in nutri- tional value. Enriched white bread contains virtually the same amounts of proteins, fats, and carbohydrates as whole wheat bread, although it may contain only half the dietary fiber (see flour). Bread is a high-carbohydrate food with lots of starch. The exact amount of fiber, fat, and cholesterol in the loaf varies with the recipe. Bread’s proteins, from grain, are low in the essential amino acid lysine. The most important carbohydrate in bread is starch; all breads contain some sugar. Depending on the recipe, the fats may be highly saturated (butter or hydrogenated vegetable fats) or primarily unsaturated (vegetable fat). All bread is a good source of B vitamins (thiamin, riboflavin, niacin), and in 1998, the Food and Drug Administration ordered food manufactur- ers to add folates—which protect against birth defects of the spinal cord and against heart disease—to flour, rice, and other grain products. One year later, data from the Framingham Heart Study, which has followed heart health among residents of a Boston suburb for nearly half a cen- tury, showed a dramatic increase in blood levels of folic acid. Before the fortification of foods, 22 percent of the study participants had a folic acid deficiency; after, the number fell to 2 percent. Bread is a moderately good source of calcium, magnesium, and phos- phorus. (Breads made with milk contain more calcium than breads made without milk.) Although bread is made from grains and grains contain phytic acid, a natural antinutrient that binds calcium ions into insoluble, indigestible compounds, the phytic acid is inactivated by enzyme action during leavening. Bread does not bind calcium. All commercially made breads are moderately high in sodium; some contain more sugar than others. Grains are not usually considered a good source of iodine, but commer- cially made breads often pick up iodine from the iodophors and iodates used to clean the plants and machines in which they are made. Homemade breads share the basic nutritional characteristics of commercially made breads, but you can vary the recipe to suit your own taste, lowering the salt, sugar, or fat and raising the fiber content, as you prefer.
The Most Nutritious Way to Serve This Food As sandwiches, with cheese, milk, eggs, meat, fish, or poultry. These foods supply the essen- tial amino acid lysine to “complete” the proteins in grains. With beans or peas. The proteins in grains are deficient in the essential amino acids lysine and isoleucine and rich in the essential amino acids tryptophan, methionine, and cystine. The proteins in legumes (beans and peas) are exactly the opposite.
Diets That May Restrict or Exclude This Food Gluten-free diet (excludes breads made with wheat, oats, rye, buckwheat and barley flour) Lactose-free diet Low-fiber diet (excludes coarse whole-grain breads) Low-sodium diet
Buying This Food Look for: Fresh bread. Check the date on closed packages of commercial bread.
Storing This Food Store bread at room temperature, in a tightly closed plastic bag (the best protection) or in a breadbox. How long bread stays fresh depends to a great extent on how much fat it contains. Bread made with some butter or other fat will keep for about three days at room tempera- ture. Bread made without fat (Italian bread, French bread) will dry out in just a few hours; for longer storage, wrap it in foil, put it inside a plastic bag, and freeze it. When you are ready to serve the French or Italian bread, you can remove it from the plastic bag and put the foil- wrapped loaf directly into the oven. Throw away moldy bread. The molds that grow on bread may produce carcinogenic toxins. Do not store fresh bread in the refrigerator; bread stales most quickly at temperatures just above freezing. The one exception: In warm, humid weather, refrigerating bread slows the growth of molds.
When You Are Ready to Serve This Food Use a serrated knife to cut bread easily.
What Happens When You Cook This Food Toasting is a chemical process that caramelizes sugars and amino acids (proteins) on the surface of the bread, turning the bread a golden brown. This chemical reaction, known both as the browning reaction and the Maillard reaction (after the French chemist who first identified it), alters the structure of the surface sugars, starches, and amino acids. The sugars become indigestible food fiber; the amino acids break into smaller fragments that are no longer nutritionally useful. Thus toast has more fiber and less protein than plain bread. How- ever, the role of heat-generated fibers in the human diet is poorly understood. Some experts consider them inert and harmless; others believe they may be hazardous.
How Other Kinds of Processing Affect This Food Freezing. Frozen bread releases moisture that collects inside the paper, foil, or plastic bag in which it is wrapped. If you unwrap the bread before defrosting it, the moisture will be lost and the bread will be dry. Always defrost bread in its wrappings so that it can reabsorb the moisture that keeps it tasting fresh. Drying. Since molds require moisture, the less moisture a food contains, the less likely it is support mold growth. That is why bread crumbs and Melba toast, which are relatively mois- ture-free, keep better than fresh bread. Both can be ground fine and used as a toasty-flavored thickener in place of flour or cornstarch.
Medical Uses and/or Benefits A lower risk of some kinds of cancer. In 1998, scientists at Wayne State University in Detroit conducted a meta-analysis of data from more than 30 well-designed animal studies mea- suring the anti-cancer effects of wheat bran, the part of grain with highest amount of the insoluble dietary fibers cellulose and lignin. They found a 32 percent reduction in the risk of colon cancer among animals fed wheat bran; now they plan to conduct a similar meta- analysis of human studies. Breads made with whole grain wheat are a good source of wheat bran. NOTE : The amount of fiber per serving listed on a food package label shows the total amount of fiber (insoluble and soluble). Early in 1999, however, new data from the long-running Nurses Health Study at Brigham Women’s Hospital/Harvard University School of Public Health showed that women who ate a high-fiber diet had a risk of colon cancer similar to that of women who ate a low fiber diet. Because this study contradicts literally hundreds of others conducted over the past 30 years, researchers are awaiting confirming evidence before changing dietary recommendations. Calming effect. Mood is affected by naturally occurring chemicals called neurotransmitters that facilitate transmission of impulses between brain cells. The amino acid tryptophan amino acid is the most important constituent of serotonin, a “calming” neurotransmitter. Foods such as bread, which are high in complex carbohydrates, help move tryptophan into your brain, increasing the availability of serotonin.
Adverse Effects Associated with This Food Allergic reactions and/or gastric distress. Bread contains several ingredients that may trigger allergic reactions, aggravate digestive problems, or upset a specific diet, among them gluten (prohibited on gluten-free diets); milk (prohibited on a lactose- and galactose-free diet or for people who are sensitive to milk proteins); sugar (prohibited on a sucrose-free diet); salt (controlled on a sodium-restricted diet); and fats (restricted or prohibited on a controlled-fat, low-cholesterol diet).... bread
There is little evidence that any one antihistamine is superior to another, and patients vary considerably in their response to them. The antihistamines di?er in their duration of action and in the incidence of side-effects such as drowsiness. Most are short-acting, but some (such as promethazine) work for up to 12 hours. They all cause sedation but promethazine, trimeprazine and dimenhydrinate tend to be more sedating while chlorpheniramine and cyclizine are less so, as are astemizole, oxatomide and terfenadine. Patients should be warned that their ability to drive or operate machinery may be impaired when taking these drugs, and that the effects of ALCOHOL may be increased.... antihistamine drugs
Nutritional Profile Energy value (calories per serving): Moderate to high Protein: Moderate to high Fat: Low to high Saturated fat: High Cholesterol: Low to high Carbohydrates: Low Fiber: None Sodium: High Major vitamin contribution: Vitamin A, vitamin D, B vitamins Major mineral contribution: Calcium
About the Nutrients in This Food Cheese making begins when Lactobacilli and/or Streptococci bacteria are added to milk. The bacteria digest lactose (milk sugar) and release lactic acid, which coagulates casein (milk protein) into curds. Rennet (gastric enzymes extracted from the stomach of calves) is added, and the mixture is put aside to set. The longer the curds are left to set, the firmer the cheese will be. When the curds are properly firm, they are pressed to squeeze out the whey (liquid) and cooked. Cooking evaporates even more liquid and makes the cheese even firmer.* At this point, the product is “fresh” or “green” cheese: cottage cheese, cream cheese, farmer cheese. Making “ripe” cheese requires the addition of salt to pull out more moisture and specific organisms, such as Penicil- lium roquefort for Roquefort cheese, blue cheese, and Stilton, or Penicillium cambembert for Camembert and Brie. The nutritional value of cheese is similar to the milk from which it is made. All cheese is a good source of high quality proteins with sufficient amounts of all the essential amino acids. Cheese is low to high in fat, mod- erate to high in cholesterol. * Natural cheese is cheese made direct ly from milk. Processed cheese is natural cheese melted and combined wit h emulsifiers. Pasteurized process cheese foods contain ingredients t hat allow t hem to spread smoot hly; t hey are lower in fat and higher in moisture t han processed cheese. Cholesterol and Saturated Fat Content of Selected Cheeses Mozzarella Source: USDA, Nutritive Value of Foods, Home and Garden Bullet in No. 72 (USDA, 1989). All cheeses, except cottage cheese, are good sources of vitamin A. Orange and yellow cheeses are colored with carotenoid pigments, including bixin (the carotenoid pigment in annatto) and synthetic beta-carotene. Hard cheeses are an excellent source of calcium; softer cheeses are a good source; cream cheese and cottage cheese are poor sources. The R DA for calcium is 1,000 mg for a woman, 1,200 mg for a man, and 1,500 mg for an older woman who is not on hormone- replacement therapy. All cheese, unless otherwise labeled, is high in sodium.
| Calcium Content of Cheese | ||
| Cheese | Serving | Calcium (mg) |
| Blue | oz. | 150 |
| Camembert | wedge | 147 |
| Cheddar | oz. | 204 |
| Cottage cheese | ||
| creamed | cup | 135 |
| uncreamed | cup | 46 |
| Muenster | oz. | 203 |
| Pasteurized processed American | oz. | 174 |
| Parmesan grated | tbsp. | 69 |
| Provolone | oz. | 214 |
| Swiss | oz. | 272 |
The Most Nutritious Way to Serve This Food With grains, bread, noodles, beans, nuts, or vegetables to add the essential amino acids miss- ing from these foods, “complete” their proteins, and make them more nutritionally valuable.
Diets That May Restrict or Exclude This Food Antiflatulence diet Controlled-fat, low-cholesterol diet Lactose- and galactose-free diet (lactose, a disaccharide [double sugar] is composed of one unit of galactose and one unit of glucose) Low-calcium diet (for patients with kidney disease) Sucrose-free diet (processed cheese)
Buying This Food Look for: Cheese stored in a refrigerated case. Check the date on the package. Avoid: Any cheese with mold that is not an integral part of the food.
Storing This Food Refrigerate all cheese except unopened canned cheeses (such as Camembert in tins) or grated cheeses treated with preservatives and labeled to show that they can be kept outside the refrigerator. Some sealed packages of processed cheeses can be stored at room temperature but must be refrigerated once the package is opened. Wrap cheeses tightly to protect them from contamination by other microorganisms in the air and to keep them from drying out. Well-wrapped, refrigerated hard cheeses that have not been cut or sliced will keep for up to six months; sliced hard cheeses will keep for about two weeks. Soft cheeses (cottage cheese, ricotta, cream cheese, and Neufchatel) should be used within five to seven days. Use all packaged or processed cheeses by the date stamped on the package. Throw out moldy cheese (unless the mold is an integral part of the cheese, as with blue cheese or Stilton).
Preparing This Food To grate cheese, chill the cheese so it won’t stick to the grater. The molecules that give cheese its taste and aroma are largely immobilized when the cheese is cold. When serving cheese with fruit or crackers, bring it to room temperature to activate these molecules.
What Happens When You Cook This Food Heat changes the structure of proteins. The molecules are denatured, which means that they may be broken into smaller fragments or change shape or clump together. All of these changes may force moisture out of the protein tissue, which is why overcooked cheese is often stringy. Whey proteins, which do not clump or string at low temperatures, contain the sulfur atoms that give hot or burned cheese an unpleasant “cooked” odor. To avoid both strings and an unpleasant odor, add cheese to sauces at the last minute and cook just long enough to melt the cheese.
How Other Kinds of Processing Affect This Food Freezing. All cheese loses moisture when frozen, so semisoft cheeses will freeze and thaw better than hard cheeses, which may be crumbly when defrosted. Drying. The less moisture cheese contains, the less able it is to support the growth of organ- isms like mold. Dried cheeses keep significantly longer than ordinary cheeses.
Medical Uses and/or Benefits To strengthen bones and reduce age-related loss of bone density. High-calcium foods protect bone density. The current recommended dietary allowance (R DA) for calcium is still 800 mg for adults 25 and older, but a 1984 National Institutes of Health (NIH) Conference advisory stated that lifelong protection for bones requires an R DA of 1,000 mg for healthy men and women age 25 to 50 ; 1,000 mg for older women using hormone replacement therapy; and 1,500 mg for older women who are not using hormones, and these recommendations have been confirmed in a 1994 NIH Consensus Statement on optimal calcium intake. A diet with adequate amounts of calcium-rich foods helps protect bone density. Low-fat and no-fat cheeses provide calcium without excess fat and cholesterol. Protection against tooth decay. Studies at the University of Iowa (Iowa City) Dental School confirm that a wide variety of cheeses, including aged cheddar, Edam, Gouda, Monterey Jack, Muenster, mozzarella, Port Salut, Roquefort, Romano, Stilton, Swiss, and Tilsit—limit the tooth decay ordinarily expected when sugar becomes trapped in plaque, the sticky film on tooth surfaces where cavity-causing bacteria flourish. In a related experiment using only cheddar cheese, people who ate cheddar four times a day over a two-week period showed a 20 percent buildup of strengthening minerals on the surface of synthetic toothlike material attached to the root surfaces of natural teeth. Protection against periodontal disease. A report in the January 2008 issue of the Journal of Periodontology suggests that consuming adequate amounts of dairy products may reduce the risk of developing periodontal disease. Examining the dental health of 942 subjects ages 40 to 79, researchers at Kyushu University, in Japan, discovered that those whose diets regularly included two ounces (55 g) of foods containing lactic acid (milk, cheese, and yogurt) were significantly less likely to have deep “pockets” (loss of attachment of tooth to gum) than those who consumed fewer dairy products.
Adverse Effects Associated with This Food Increased risk of heart disease. Like other foods from animals, cheese is a source of choles- terol and saturated fats, which increase the amount of cholesterol circulating in your blood and raise your risk of heart disease. To reduce the risk of heart disease, the USDA /Health and Human Services Dietary Guidelines for Americans recommends limiting the amount of cholesterol in your diet to no more than 300 mg a day. The guidelines also recommend limit- ing the amount of fat you consume to no more than 30 percent of your total calories, while holding your consumption of saturated fats to more than 10 percent of your total calories (the calories from saturated fats are counted as part of the total calories from fat). Food poisoning. Cheese made from raw (unpasteurized) milk may contain hazardous microorganisms, including Salmonella and Listeria. Salmonella causes serious gastric upset; Lis- teria, a flulike infection, encephalitis, or blood infection. Both may be life-threatening to the very young, the very old, pregnant women, and those whose immune systems are weakened either by illness (such as AIDS) or drugs (such as cancer chemotherapy). In 1998, the Federal Centers for Disease Control (CDC) released data identif ying Listeria as the cause of nearly half the reported deaths from food poisoning. Allergy to milk proteins. Milk is one of the foods most frequently implicated as a cause of allergic reactions, particularly upset stomach. However, in many cases the reaction is not a true allergy but the result of lactose intolerance (see below). Lactose intolerance. Lactose intolerance—the inability to digest the sugar in milk—is an inherited metabolic deficiency that affects two thirds of all adults, including 90 to 95 percent of all Orientals, 70 to 75 percent of all blacks, and 6 to 8 percent of Caucasians. These people do not have sufficient amounts of lactase, the enzyme that breaks the disaccharide lactose into its easily digested components, galactose and glucose. When they drink milk, the undi- gested sugar is fermented by bacteria in the gut, causing bloating, diarrhea, flatulence, and intestinal discomfort. Some milk is now sold with added lactase to digest the lactose and make the milk usable for lactase-deficient people. In making cheese, most of the lactose in milk is broken down into glucose and galactose. There is very little lactose in cheeses other than the fresh ones—cottage cheese, cream cheese, and farmer cheese. Galactosemia. Galactosemia is an inherited metabolic disorder in which the body lacks the enzymes needed to metabolize galactose, a component of lactose. Galactosemia is a reces- sive trait; you must receive the gene from both parents to develop the condition. Babies born with galactosemia will fail to thrive and may develop brain damage or cataracts if they are given milk. To prevent this, children with galactosemia are usually kept on a protective milk- free diet for several years, until their bodies have developed alternative pathways by which to metabolize galactose. Pregnant women who are known carriers of galactosemia may be advised to give up milk and milk products while pregnant lest the unmetabolized galactose in their bodies cause brain damage to the fetus (damage not detectable by amniocentesis). Genetic counseling is available to identif y galactosemia carriers and assess their chances of producing a baby with the disorder. Penicillin sensitivity. People who experience a sensitivity reaction the first time they take penicillin may have been sensitized by exposure to the Penicillium molds in the environment, including the Penicillium molds used to make brie, blue, camembert, roquefort, Stilton, and other “blue” cheeses.
Food/Drug Interactions Tetracycline. The calcium ions in milk products, including cheese, bind tetracyclines into insoluble compounds. If you take tetracyclines with cheese, your body may not be able to absorb and use the drug efficiently. Monoamine oxidase (MAO) inhibitors. Monoamine oxidase inhibitors are drugs used to treat depression. They inactivate naturally occurring enzymes in your body that metabolize tyra- mine, a substance found in many fermented or aged foods. Tyramine constricts blood ves- sels and increases blood pressure. If you eat a food such as aged or fermented cheese which is high in tyramine while you are taking an M AO inhibitor, your body may not be able to eliminate the tyramine. The result may be a hypertensive crisis.
Tyramine Content of Cheeses High Boursault, Camembert, Cheddar, Emmenthaler, Stilton Medium to high Blue, brick, Brie, Gruyère, mozzarella, Parmesan, Romano, Roquefort Low Processed American cheese Very little or none Cottage and cream cheese Sources: The Medical Letter Handbook of Adverse Drug Interactions (1985); Handbook of Clinical Dietetics ( The A merican Dietet ic Associat ion, 1981). False-positive test for pheochromocytoma. Pheochromocytomas (tumors of the adrenal glands) secrete adrenalin that is converted by the body to vanillyl-mandelic acid ( VM A) and excreted in the urine. Tests for this tumor measure the level of VM A in the urine. Since cheese contains VM A, taking the test after eating cheese may result in a false-positive result. Ordinarily, cheese is prohibited for at least 72 hours before this diagnostic test.... cheese
Nutritional Profile Energy value (calories per serving): Moderate Protein: Low (cocoa powder) High (chocolate) Fat: Moderate Saturated fat: High Cholesterol: None Carbohydrates: Low (chocolate) High (cocoa powder) Fiber: Moderate (chocolate) High (cocoa powder) Sodium: Moderate Major vitamin contribution: B vitamins Major mineral contribution: Calcium, iron, copper
About the Nutrients in This Food Cocoa beans are high-carbohydrate, high-protein food, with less dietary fiber and more fat than all other beans, excepting soy beans. The cocoa bean’s dietary fiber includes pectins and gums. Its proteins are limited in the essential amino acids lysine and isoleucine. Cocoa butter, the fat in cocoa beans, is the second most highly saturated vegetable fat (coconut oil is number one), but it has two redeeming nutritional qualities. First, it rarely turns rancid. Second, it melts at 95°F, the temperature of the human tongue. Cocoa butter has no cholesterol; neither does plain cocoa powder or plain dark chocolate. Cocoa beans have B vitamins (thiamine, riboflavin, niacin) plus min- erals (iron, magnesium, potassium, phosphorus, and copper). All chocolate candy is made from chocolate liquor, a thick paste pro- duce by roasting and grinding cocoa beans. Dark (sweet) chocolate is made of chocolate liquor, cocoa butter, and sugar. Milk chocolate is made of choc- olate liquor, cocoa butter, sugar, milk or milk powder, and vanilla. White * These values apply to plain cocoa powder and plain unsweetened chocolate. Add- ing other foods, such as milk or sugar, changes these values. For example, there is no cholesterol in plain bitter chocolate, but there is cholesterol in milk chocolate. chocolate is made of cocoa butter, sugar, and milk powder. Baking chocolate is unsweetened dark chocolate. The most prominent nutrient in chocolate is its fat. Fat Content in One Ounce of Chocolate
| Saturated fat (g) | Monounsaturated fat (g) | Polyunsaturated fat (g) | Cholesterol (mg) | |
| Dark (sweet) | ||||
| chocolate | 5.6 | 3.2 | 0.3 | 0 |
| Milk chocolate | 5.9 | 4.5 | 0.4 | 6.6 |
| Baking chocolate | 9 | 5.6 | 0.3 | 0 |
| White chocolate | 5.5 | 2.6 | 0.3 | 0 |
The Most Nutritious Way to Serve This Food With low-fat milk to complete the proteins without adding saturated fat and cholesterol. NOTE : Both cocoa and chocolate contain oxalic acid, which binds with calcium to form cal- cium oxalate, an insoluble compound, but milk has so much calcium that the small amount bound to cocoa and chocolate hardly matters. Chocolate skim milk is a source of calcium.
Diets That May Restrict or Exclude This Food Antiflatulence diet Low-calcium and low-oxalate diet (to prevent the formation of calcium oxalate kidney stones) Low-calorie diet Low-carbohydrate diet Low-fat diet Low-fat, controlled-cholesterol diet (milk chocolates) Low-fiber diet Potassium-regulated (low-potassium) diet
Buying This Food Look for: Tightly sealed boxes or bars. When you open a box of chocolates or unwrap a candy bar, the chocolate should be glossy and shiny. Chocolate that looks dull may be stale, or it may be inexpensively made candy without enough cocoa butter to make it gleam and give it the rich creamy mouthfeel we associate with the best chocolate. (Fine chocolate melts evenly on the tongue.) Chocolate should also smell fresh, not dry and powdery, and when you break a bar or piece of chocolate it should break cleanly, not crumble. One exception: If you have stored a bar of chocolate in the refrigerator, it may splinter if you break it without bringing it to room temperature first.
Storing This Food Store chocolate at a constant temperature, preferably below 78°F. At higher temperatures, the fat in the chocolate will rise to the surface and, when the chocolate is cooled, the fat will solidif y into a whitish powdery bloom. Bloom is unsightly but doesn’t change the chocolate’s taste or nutritional value. To get rid of bloom, melt the chocolate. The chocolate will turn dark, rich brown again when its fat recombines with the other ingredients. Chocolate with bloom makes a perfectly satisfactory chocolate sauce. Dark chocolate (bitter chocolate, semisweet chocolate) ages for at least six months after it is made, as its flavor becomes deeper and more intense. Wrapped tightly and stored in a cool, dry cabinet, it can stay fresh for a year or more. Milk chocolate ages only for about a month after it is made and holds its peak flavor for about three to six months, depending on how carefully it is stored. Plain cocoa, with no added milk powder or sugar, will stay fresh for up to a year if you keep it tightly sealed and cool.
What Happens When You Cook This Food Chocolate burns easily. To melt it without mishap, stir the chocolate in a bowl over a pot of hot water or in the top of a double boiler or put the chocolate in a covered dish and melt it in the microwave (which does not get as hot as a pot on the store). Simple chemistry dictates that chocolate cakes be leavened with baking soda rather than baking powder. Chocolate is so acidic that it will upset the delicate balance of acid (cream of tartar) and base (alkali = sodium bicarbonate = baking soda) in baking powder. But it is not acidic enough to balance plain sodium bicarbonate. That’s why we add an acidic sour-milk product such as buttermilk or sour cream or yogurt to a chocolate cake. Without the sour milk, the batter would be so basic that the chocolate would look red, not brown, and taste very bitter.
How Other Kinds of Processing Affect This Food Freezing. Chocolate freezes and thaws well. Pack it in a moistureproof container and defrost it in the same package to let it reabsorb moisture it gave off while frozen.
Medical Uses and/or Benefits Mood elevator. Chocolate’s reputation for making people feel good is based not only on its caffeine content—19 mg caffeine per ounce of dark (sweet) chocolate, which is one-third the amount of caffeine in a five-ounce cup of brewed coffee—but also on its naturally occurring mood altering chemicals phenylethylalanine and anandamide. Phenylethylalanine is found in the blood of people in love. Anandamide stimulates areas of your brain also affected by the active ingredients in marijuana. (NOTE : As noted by the researchers at the Neurosci- ences Institute in San Diego who identified anandamide in chocolate in 1996, to get even the faintest hint of marijuana-like effects from chocolate you would have to eat more than 25 pounds of the candy all at once.) Possible heart health benefits. Chocolate is rich in catechins, the antioxidant chemicals that give tea its reputation as a heart-protective anticancer beverage (see tea). In addition, a series of studies beginning with those at the USDA Agricultural Research Center in Peoria, Illinois, suggest that consuming foods rich in stearic acid like chocolate may reduce rather than raise the risk of a blood clot leading to a heart attack. Possible slowing of the aging process. Chocolate is a relatively good source of copper, a mineral that may play a role in slowing the aging process by decreasing the incidence of “protein glycation,” a reaction in which sugar molecules ( gly = sugar) hook up with protein molecules in the bloodstream, twisting the protein molecules out of shape and rendering them unusable. This can lead to bone loss, rising cholesterol, cardiac abnormalities, and a slew of other unpleasantries. In people with diabetes, excess protein glycation may be one factor involved in complications such as loss of vision. Ordinarily, increased protein glyca- tion is age-related. But at the USDA Grand Forks Human Nutrition Research Center in North Dakota, agricultural research scientist Jack T. Saari has found that rats on copper-deficient diets experience more protein glycation at any age than other rats. A recent USDA survey of American eating patterns says that most of us get about 1.2 mg copper a day, considerably less than the Estimated Safe and Adequate Daily Dietary Intake (ESADDI) or 1.5 mg to 3 mg a day. Vegetarians are less likely to be copper deficient because, as Saari notes, the foods highest in copper are whole grains, nuts, seeds, and beans, including the cocoa bean. One ounce of dark chocolate has .25 mg copper (8 –17 percent of the ESADDI).
Adverse Effects Associated with This Food Possible loss of bone density. In 2008, a team of Australian researchers at Royal Perth Hos- pital, and Sir Charles Gairdner Hospital published a report in the American Journal of Clinical Nutrition suggesting that women who consume chocolate daily had 3.1 percent lower bone density than women who consume chocolate no more than once a week. No explanation for the reaction was proposed; the finding remains to be confirmed. Possible increase in the risk of heart disease. Cocoa beans, cocoa powder, and plain dark chocolate are high in saturated fats. Milk chocolate is high in saturated fats and cholesterol. Eating foods high in saturated fats and cholesterol increases the amount of cholesterol in your blood and raises your risk of heart disease. NOTE : Plain cocoa powder and plain dark chocolate may be exceptions to this rule. In studies at the USDA Agricultural Research Center in Peoria, Illinois, volunteers who consumed foods high in stearic acid, the saturated fat in cocoa beans, cocoa powder, and chocolate, had a lower risk of blood clots. In addition, chocolate is high in flavonoids, the antioxidant chemicals that give red wine its heart-healthy reputation. Mild jitters. There is less caffeine in chocolate than in an equal size serving of coffee: A five- ounce cup of drip-brewed coffee has 110 to 150 mg caffeine; a five-ounce cup of cocoa made with a tablespoon of plain cocoa powder ( 1/3 oz.) has about 18 mg caffeine. Nonetheless, people who are very sensitive to caffeine may find even these small amounts problematic. Allergic reaction. According to the Merck Manual, chocolate is one of the 12 foods most likely to trigger the classic food allergy symptoms: hives, swelling of the lips and eyes, and upset stomach.* The others are berries (blackberries, blueberries, raspberries, strawberries), corn, eggs, fish, legumes (green peas, lima beans, peanuts, soybeans), milk, nuts, peaches, pork, shellfish, and wheat (see wheat cer ea ls).
Food/Drug Interactions Monoamine oxidase (MAO) inhibitors. Monoamine oxidase inhibitors are drugs used to treat depression. They inactivate naturally occurring enzymes in your body that metabolize tyra- mine, a substance found in many fermented or aged foods. Tyramine constricts blood vessels and increases blood pressure. Caffeine is a substance similar to tyramine. If you consume excessive amounts of a caffeinated food, such as cocoa or chocolate, while you are taking an M AO inhibitor, the result may be a hypertensive crisis. False-positive test for pheochromocytoma. Pheochromocytoma, a tumor of the adrenal gland, secretes adrenalin, which the body converts to VM A (vanillylmandelic acid). VM A is excreted in urine, and, until recently, the test for this tumor measured the level of VM A in the urine. In the past, chocolate and cocoa, both of which contain VM A, were eliminated from the patient’s diet prior to the test lest they elevate the level of VM A in the urine and produce a false-positive result. Today, more finely drawn tests usually make this unnecessary. * The evidence link ing chocolate to allergic or migraine headaches is inconsistent. In some people, phenylet hylamine (PEA) seems to cause headaches similar to t hose induced by t yramine, anot her pressor amine. The PEA-induced headache is unusual in t hat it is a delayed react ion t hat usually occurs 12 or more hours after t he chocolate is eaten.... chocolate
Nutritional Profile Energy value (calories per serving): Low Protein: Trace Fat: Trace Saturated fat: None Cholesterol: None Carbohydrates: Trace Fiber: Trace Sodium: Low Major vitamin contribution: None Major mineral contribution: None
About the Nutrients in This Food Coffee beans are roasted seeds from the fruit of the evergreen coffee tree. Like other nuts and seeds, they are high in proteins (11 percent), sucrose and other sugars (8 percent), oils (10 to 15 percent), assorted organic acids (6 percent), B vitamins, iron, and the central nervous system stimulant caffeine (1 to 2 percent). With the exceptions of caffeine, none of these nutrients is found in coffee. Like spinach, rhubarb, and tea, coffee contains oxalic acid (which binds calcium ions into insoluble compounds your body cannot absorb), but this is of no nutritional consequence as long as your diet contains adequate amounts of calcium-rich foods. Coffee’s best known constituent is the methylxanthine central ner- vous system stimulant caffeine. How much caffeine you get in a cup of coffee depends on how the coffee was processed and brewed. Caffeine is Caffeine Content/Coffee Servings Brewed coffee 60 mg/five-ounce cup Brewed/decaffeinated 5 mg/five-ounce cup Espresso 64 mg/one-ounce serving Instant 47 mg/rounded teaspoon
The Most Nutritious Way to Serve This Food In moderation, with high-calcium foods. Like spinach, rhubarb, and tea, coffee has oxalic acid, which binds calcium into insoluble compounds. This will have no important effect as long as you keep your consumption moderate (two to four cups of coffee a day) and your calcium consumption high.
Diets That May Restrict or Exclude This Food Bland diet Gout diet Diet for people with heart disease (regular coffee)
Buying This Food Look for: Ground coffee and coffee beans in tightly sealed, air- and moisture-proof containers. Avoid: Bulk coffees or coffee beans stored in open bins. When coffee is exposed to air, the volatile molecules that give it its distinctive flavor and richness escape, leaving the coffee flavorless and/or bitter.
Storing This Food Store unopened vacuum-packed cans of ground coffee or coffee beans in a cool, dark cabinet—where they will stay fresh for six months to a year. They will lose some flavor in storage, though, because it is impossible to can coffee without trapping some flavor- destroying air inside the can. Once the can or paper sack has been opened, the coffee or beans should be sealed as tight as possible and stored in the refrigerator. Tightly wrapped, refrigerated ground coffee will hold its freshness and flavor for about a week, whole beans for about three weeks. For longer storage, freeze the coffee or beans in an air- and moistureproof container. ( You can brew coffee directly from frozen ground coffee and you can grind frozen beans without thawing them.)
Preparing This Food If you make your coffee with tap water, let the water run for a while to add oxygen. Soft water makes “cleaner”-tasting coffee than mineral-rich hard water. Coffee made with chlorinated water will taste better if you refrigerate the water overnight in a glass (not plastic) bottle so that the chlorine evaporates. Never make coffee with hot tap water or water that has been boiled. Both lack oxygen, which means that your coffee will taste flat. Always brew coffee in a scrupulously clean pot. Each time you make coffee, oils are left on the inside of the pot. If you don’t scrub them off, they will turn rancid and the next pot of coffee you brew will taste bitter. To clean a coffee pot, wash it with detergent, rinse it with water in which you have dissolved a few teaspoons of baking soda, then rinse one more time with boiling water.
What Happens When You Cook This Food In making coffee, your aim is to extract flavorful solids (including coffee oils and sucrose and other sugars) from the ground beans without pulling bitter, astringent tannins along with them. How long you brew the coffee determines how much solid material you extract and how the coffee tastes. The longer the brewing time, the greater the amount of solids extracted. If you brew the coffee long enough to extract more than 30 percent of its solids, you will get bitter compounds along with the flavorful ones. (These will also develop by let- ting coffee sit for a long time after brewing it.) Ordinarily, drip coffee tastes less bitter than percolator coffee because the water in a drip coffeemaker goes through the coffee only once, while the water in the percolator pot is circulated through the coffee several times. To make strong but not bitter coffee, increase the amount of coffee—not the brewing time.
How Other Kinds of Processing Affect This Food Drying. Soluble coffees (freeze-dried, instant) are made by dehydrating concentrated brewed coffee. These coffees are often lower in caffeine than regular ground coffees because caffeine, which dissolves in water, is lost when the coffee is dehydrated. Decaffeinating. Decaffeinated coffee is made with beans from which the caffeine has been extracted, either with an organic solvent (methylene chloride) or with water. How the coffee is decaffeinated has no effect on its taste, but many people prefer water-processed decaf- feinated coffee because it is not a chemically treated food. (Methylene chloride is an animal carcinogen, but the amounts that remain in coffees decaffeinated with methylene chloride are so small that the FDA does not consider them hazardous. The carcinogenic organic sol- vent trichloroethylene [TCE], a chemical that causes liver cancer in laboratory animals, is no longer used to decaffeinate coffee.)
Medical Uses and/or Benefits As a stimulant and mood elevator. Caffeine is a stimulant. It increases alertness and concentra- tion, intensifies muscle responses, quickens heartbeat, and elevates mood. Its effects derive from the fact that its molecular structure is similar to that of adenosine, a natural chemical by-product of normal cell activity. Adenosine is a regular chemical that keeps nerve cell activ- ity within safe limits. When caffeine molecules hook up to sites in the brain when adenosine molecules normally dock, nerve cells continue to fire indiscriminately, producing the jangly feeling sometimes associated with drinking coffee, tea, and other caffeine products. As a rule, it takes five to six hours to metabolize and excrete caffeine from the body. During that time, its effects may vary widely from person to person. Some find its stimu- lation pleasant, even relaxing; others experience restlessness, nervousness, hyperactivity, insomnia, flushing, and upset stomach after as little as one cup a day. It is possible to develop a tolerance for caffeine, so people who drink coffee every day are likely to find it less imme- diately stimulating than those who drink it only once in a while. Changes in blood vessels. Caffeine’s effects on blood vessels depend on site: It dilates coronary and gastrointestinal vessels but constricts blood vessels in your head and may relieve headache, such as migraine, which symptoms include swollen cranial blood vessels. It may also increase pain-free exercise time in patients with angina. However, because it speeds up heartbeat, doc- tors often advise patients with heart disease to avoid caffeinated beverages entirely. As a diuretic. Caffeine is a mild diuretic sometimes included in over-the-counter remedies for premenstrual tension or menstrual discomfort.
Adverse Effects Associated with This Food Stimulation of acid secretion in the stomach. Both regular and decaffeinated coffees increase the secretion of stomach acid, which suggests that the culprit is the oil in coffee, not its caffeine. Elevated blood levels of cholesterol and homocysteine. In the mid-1990s, several studies in the Netherlands and Norway suggested that drinking even moderate amounts of coffee (five cups a day or less) might raise blood levels of cholesterol and homocysteine (by-product of protein metabolism considered an independent risk factor for heart disease), thus increas- ing the risk of cardiovascular disease. Follow-up studies, however, showed the risk limited to drinking unfiltered coffees such as coffee made in a coffee press, or boiled coffees such as Greek, Turkish, or espresso coffee. The unfiltered coffees contain problematic amounts of cafestol and kahweol, two members of a chemical family called diterpenes, which are believed to affect cholesterol and homocysteine levels. Diterpenes are removed by filtering coffee, as in a drip-brew pot. Possible increased risk of miscarriage. Two studies released in 2008 arrived at different conclusions regarding a link between coffee consumption and an increased risk of miscar- riage. The first, at Kaiser Permanente (California), found a higher risk of miscarriage among women consuming even two eight-ounce cups of coffee a day. The second, at Mt. Sinai School of Medicine (New York), found no such link. However, although the authors of the Kaiser Permanente study described it as a “prospective study” (a study in which the research- ers report results that occur after the study begins), in fact nearly two-thirds of the women who suffered a miscarriage miscarried before the study began, thus confusing the results. Increased risk of heartburn /acid reflux. The natural oils in both regular and decaffeinated coffees loosen the lower esophageal sphincter (LES), a muscular valve between the esopha- gus and the stomach. When food is swallowed, the valve opens to let food into the stomach, then closes tightly to keep acidic stomach contents from refluxing (flowing backwards) into the esophagus. If the LES does not close efficiently, the stomach contents reflux and cause heartburn, a burning sensation. Repeated reflux is a risk factor for esophageal cancer. Masking of sleep disorders. Sleep deprivation is a serious problem associated not only with automobile accidents but also with health conditions such as depression and high blood pres- sure. People who rely on the caffeine in a morning cup of coffee to compensate for lack of sleep may put themselves at risk for these disorders. Withdrawal symptoms. Caffeine is a drug for which you develop a tolerance; the more often you use it, the more likely you are to require a larger dose to produce the same effects and the more likely you are to experience withdrawal symptoms (headache, irritation) if you stop using it. The symptoms of coffee-withdrawal can be relieved immediately by drinking a cup of coffee.
Food/Drug Interactions Drugs that make it harder to metabolize caffeine. Some medical drugs slow the body’s metabolism of caffeine, thus increasing its stimulating effect. The list of such drugs includes cimetidine (Tagamet), disulfiram (Antabuse), estrogens, fluoroquinolone antibiotics (e.g., ciprofloxacin, enoxacin, norfloxacin), fluconazole (Diflucan), fluvoxamine (Luvox), mexi- letine (Mexitil), riluzole (R ilutek), terbinafine (Lamisil), and verapamil (Calan). If you are taking one of these medicines, check with your doctor regarding your consumption of caf- feinated beverages. Drugs whose adverse effects increase due to consumption of large amounts of caffeine. This list includes such drugs as metaproterenol (Alupent), clozapine (Clozaril), ephedrine, epinephrine, monoamine oxidase inhibitors, phenylpropanolamine, and theophylline. In addition, suddenly decreasing your caffeine intake may increase blood levels of lithium, a drug used to control mood swings. If you are taking one of these medicines, check with your doctor regarding your consumption of caffeinated beverages. Allopurinol. Coffee and other beverages containing methylxanthine stimulants (caffeine, theophylline, and theobromine) reduce the effectiveness of the antigout drug allopurinol, which is designed to inhibit xanthines. Analgesics. Caffeine strengthens over-the-counter painkillers (acetaminophen, aspirin, and other nonsteroidal anti-inflammatories [NSAIDS] such as ibuprofen and naproxen). But it also makes it more likely that NSAIDS will irritate your stomach lining. Antibiotics. Coffee increases stomach acidity, which reduces the rate at which ampicillin, erythromycin, griseofulvin, penicillin, and tetracyclines are absorbed when they are taken by mouth. (There is no effect when the drugs are administered by injection.) Antiulcer medication. Coffee increases stomach acidity and reduces the effectiveness of nor- mal doses of cimetidine and other antiulcer medication. False-positive test for pheochromocytoma. Pheochromocytoma, a tumor of the adrenal glands, secretes adrenalin, which is converted to VM A (vanillylmandelic acid) by the body and excreted in the urine. Until recently, the test for this tumor measured the levels of VM A in the patient’s urine and coffee, which contains VM A, was eliminated from patients’ diets lest it elevate the level of VM A in the urine, producing a false-positive test result. Today, more finely drawn tests make this unnecessary. Iron supplements. Caffeine binds with iron to form insoluble compounds your body cannot absorb. Ideally, iron supplements and coffee should be taken at least two hours apart. Birth control pills. Using oral contraceptives appears to double the time it takes to eliminate caffeine from the body. Instead of five to six hours, the stimulation of one cup of coffee may last as long as 12 hours. Monoamine oxidase (MAO) inhibitors. Monoamine oxidase inhibitors are drugs used to treat depression. They inactivate naturally occurring enzymes in your body that metabolize tyra- mine, a substance found in many fermented or aged foods. Tyramine constricts blood vessels and increases blood pressure. Caffeine is a substance similar to tyramine. If you consume excessive amounts of a caffeinated beverage such as coffee while you are taking an M AO inhibitor, the result may be a hypertensive crisis. Nonprescription drugs containing caffeine. The caffeine in coffee may add to the stimulant effects of the caffeine in over-the-counter cold remedies, diuretics, pain relievers, stimulants, and weight-control products containing caffeine. Some cold pills contain 30 mg caffeine, some pain relievers 130 mg, and some weight-control products as much as 280 mg caffeine. There are 110 –150 mg caffeine in a five-ounce cup of drip-brewed coffee. Sedatives. The caffeine in coffee may counteract the drowsiness caused by sedative drugs; this may be a boon to people who get sleepy when they take antihistamines. Coffee will not, however, “sober up” people who are experiencing the inebriating effects of alcoholic beverages. Theophylline. Caffeine relaxes the smooth muscle of the bronchi and may intensif y the effects (and/or increase the risk of side effects) of this antiasthmatic drug.... coffee
This technique is used when normal methods of attempted CONCEPTION or ARTIFICIAL INSEMINATION with healthy SEMEN have failed. In the UK, assisted-conception procedures are governed by the Human Fertilisation & Embryology Act 1990, which set up the Human Fertilisation & Embryology Authority (HFEA).
Human Fertilisation & Embryology Act 1990 UK legislation was prompted by the report on in vitro fertilisation produced by a government-appointed committee chaired by Baroness Warnock. This followed the birth, in 1978, of the ?rst ‘test-tube’ baby.
This Act allows regulation monitoring of all treatment centres to ensure that they carry out treatment and research responsibly. It covers any fertilisation that uses donated eggs or sperm (called gametes) – for example, donor insemination or embryos (see EMBRYO) grown outside the human body (known as licensed treatment). The Act also covers research on human embryos with especial emphasis on foolproof labelling and immaculate data collection.
Human Fertilisation & EmbryologyAuthority (HFEA) Set up by the UK government following the Warnock report, the Authority’s 221 members inspect and license centres carrying out fertilisation treatments using donated eggs and sperm. It publishes a code of practice advising centres on how to conduct their activities and maintains a register of information on donors, patients and all treatments. It also reviews routinely progress and research in fertility treatment and the attempted development of human CLONING. Cloning to produce viable embryos (reproductive cloning) is forbidden, but limited licensing of the technique is allowed in specialist centres to enable them to produce cells for medical treatment (therapeutic cloning).
In vitro fertilisation (IVF) In this technique, the female partner receives drugs to enhance OVULATION. Just before the eggs are released from the ovary (see OVARIES), several ripe eggs are collected under ULTRASOUND guidance or through a LAPAROSCOPE. The eggs are incubated with the prepared sperm. About 40 hours later, once the eggs are fertilised, two eggs (three in special circumstances) are transferred into the mother’s UTERUS via the cervix (neck of the womb). Pregnancy should then proceed normally. About one in ?ve IVF pregnancies results in the birth of a child. The success rate is lower in women over 40.
Indications In women with severely damaged FALLOPIAN TUBES, IVF o?ers the only chance of pregnancy. The method is also used in couples with unexplained infertility or with male-factor infertility (where sperms are abnormal or their count low). Women who have had an early or surgically induced MENOPAUSE can become pregnant using donor eggs. A quarter of these pregnancies are multiple – that is, produce twins or more. Twins and triplets are more likely to be premature. The main danger of ovarian stimulation for IVF is hyperstimulation which can cause ovarian cysts. (See OVARIES, DISEASES OF.)... assisted conception
Nutritional Profile Energy value (calories per serving): Low Protein: High Fat: Low Saturated fat: Low Cholesterol: None Carbohydrates: Moderate Fiber: Moderate Sodium: Low Major vitamin contribution: Vitamin A, folate, vitamin C Major mineral contribution: Potassium, iron
About the Nutrients in This Food Asparagus has some dietary fiber, vitamin A, and vitamin C. It is an excel- lent source of the B vitamin folate. A serving of four cooked asparagus spears (½ inch wide at the base) has 1.2 g dietary fiber, 604 IU vitamin A (26 percent of the R DA for a woman, 20 percent of the R DA for a man), 4.5 mg vitamin C (6 percent of the R DA for a woman, 5 percent of the R DA for a man), and 89 mcg folate (22 percent of the R DA).
The Most Nutritious Way to Serve This Food Fresh, boiled and drained. Canned asparagus may have less than half the nutrients found in freshly cooked spears.
Diets That May Restrict or Exclude This Food Low-sodium diet (canned asparagus)
Buying This Food Look for: Bright green stalks. The tips should be purplish and tightly closed; the stalks should be firm. Asparagus is in season from March through August. Avoid: Wilted stalks and asparagus whose buds have opened.
Storing This Food Store fresh asparagus in the refrigerator. To keep it as crisp as possible, wrap it in a damp paper towel and then put the whole package into a plastic bag. Keeping asparagus cool helps it hold onto its vitamins. At 32°F, asparagus will retain all its folic acid for at least two weeks and nearly 80 percent of its vitamin C for up to five days; at room temperature, it would lose up to 75 percent of its folic acid in three days and 50 percent of the vitamin C in 24 hours.
Preparing This Food The white part of the fresh green asparagus stalk is woody and tasteless, so you can bend the stalk and snap it right at the line where the green begins to turn white. If the skin is very thick, peel it, but save the parings for soup stock.
What Happens When You Cook This Food Chlorophyll, the pigment that makes green vegetables green, is sensitive to acids. When you heat asparagus, its chlorophyll will react chemically with acids in the asparagus or in the cooking water to form pheophytin, which is brown. As a result, cooked asparagus is olive-drab. You can prevent this chemical reaction by cooking the asparagus so quickly that there is no time for the chlorophyll to react with acids, or by cooking it in lots of water (which will dilute the acids), or by leaving the lid off the pot so that the volatile acids can float off into the air. Cooking also changes the texture of asparagus: water escapes from its cells and they collapse. Adding salt to the cooking liquid slows the loss of moisture.
How Other Kinds of Processing Affect This Food Canning. The intense heat of can ning makes asparagus soft, robs it of its bright green color, and reduces the vitamin A, B, and C content by at least half. ( White asparagus, which is bleached to remove the green color, contains about 5 percent of the vitamin A in fresh asparagus.) With its liquid, can ned asparagus, green or white, contains about 90 times the sodium in fresh asparagus ( 348 mg in 3.5 oz. can ned against 4 mg in 3.5 oz. fresh boiled asparagus).
Medical Uses and/or Benefits Lower risk of some birth defects. As many as two of every 1,000 babies born in the United States each year may have cleft palate or a neural tube (spinal cord) defect due to their moth- ers’ not having gotten adequate amounts of folate during pregnancy. The R DA for folate is 400 mcg for healthy adult men and women, 600 mcg for pregnant women, and 500 mcg for women who are nursing. Taking folate supplements before becoming pregnant and through the first two months of pregnancy reduces the risk of cleft palate; taking folate through the entire pregnancy reduces the risk of neural tube defects. Lower risk of heart attack. In the spring of 1998, an analysis of data from the records for more than 80,000 women enrolled in the long-running Nurses’ Health Study at Harvard School of Public Health/Brigham and Woman’s Hospital, in Boston, demonstrated that a diet providing more than 400 mcg folate and 3 mg vitamin B6 daily, from either food or supplements, more than twice the current R DA for each, may reduce a woman’s risk of heart attack by almost 50 percent. Although men were not included in the analysis, the results are assumed to apply to them as well. However, data from a meta-analysis published in the Journal of the American Medical Association in December 2006 called this theory into question. Researchers at Tulane Univer- sity examined the results of 12 controlled studies in which 16,958 patients with preexisting cardiovascular disease were given either folic acid supplements or placebos (“look-alike” pills with no folic acid) for at least six months. The scientists, who found no reduction in the risk of further heart disease or overall death rates among those taking folic acid, concluded that further studies will be required to verify whether taking folic acid supplements reduces the risk of cardiovascular disease.
Adverse Effects Associated with This Food Odorous urine. After eating asparagus, we all excrete the sulfur compound methyl mercap- tan, a smelly waste product, in our urine.
Food/Drug Interactions Anticoagulants. Asparagus is high in vitamin K, a vitamin manufactured naturally by bac- teria in our intestines, an adequate supply of which enables blood to clot normally. Eating foods that contain this vitamin may interfere with the effectiveness of anticoagulants such as heparin and warfarin (Coumadin, Dicumarol, Panwarfin) whose job is to thin blood and dissolve clots.... asparagus
In those circumstances professional advice should be sought from a doctor or counsellor.... daydreams
The dependence that most concerns modern society is one in which individuals become dependent on or addicted to certain substances such as alcohol, drugs, tobacco (nicotine), caffeine and solvents. This is often called substance abuse. Some people become addicted to certain foods or activities: examples of the latter include gambling, computer games and use of the Internet.
The 28th report of the World Health Organisation Expert Committee on Drug Dependence in 1993 de?ned drug dependence as: ‘A cluster of physiological, behavioural and cognitive phenomena of variable intensity, in which the use of a psychoactive drug (or drugs) takes on a high priority. The necessary descriptive characteristics are preoccupation with a desire to obtain and take the drug and persistent drug-seeking behaviour. Psychological dependence occurs when the substance abuser craves the drug’s desirable effects. Physical dependence occurs when the user has to continue taking the drug to avoid distressing withdrawal or abstinence symptoms. Thus, determinants and the problematic consequences of drug dependence may be biological, psychological or social and usually interact.’
Di?erent drugs cause di?erent rates of dependence: TOBACCO is the most common substance of addiction; HEROIN and COCAINE cause high rates of addiction; whereas ALCOHOL is much lower, and CANNABIS lower again. Smoking in the western world reached a peak after World War II with almost 80 per cent of the male population smoking. The reports on the link between smoking and cancer in the early 1960s resulted in a decline that has continued so that only around a quarter of the adult populations of the UK and USA smokes. Globally, tobacco consumption continues to grow, particularly in the developing world with multinational tobacco companies marketing their products aggressively.
Accurate ?gures for illegal drug-taking are hard to obtain, but probably approximately 4 per cent of the population is dependent on alcohol and 2 per cent on other drugs, both legal and illegal, at any one time in western countries.
How does dependence occur? More than 40 distinct theories or models of drug misuse have been put forward. One is that the individual consumes drugs to cope with personal problems or diffculties in relations with others. The other main model emphasises environmental in?uences such as drug availability, environmental pressures to consume drugs, and sociocultural in?uences such as peer pressure.
By contrast to these models of why people misuse drugs, models of compulsive drug use – where individuals have a compulsive addiction
– have been amenable to testing in the laboratory. Studies at cellular and nerve-receptor levels are attempting to identify mechanisms of tolerance and dependence for several substances. Classical behaviour theory is a key model for understanding drug dependence. This and current laboratory studies are being used to explain the reinforcing nature of dependent substances and are helping to provide an explanatory framework for dependence. Drug consumption is a learned form of behaviour. Numerous investigators have used conditioning theories to study why people misuse drugs. Laboratory studies are now locating the ‘reward pathways’ in the brain for opiates and stimulants where positive reinforcing mechanisms involve particular sectors of the brain. There is a consensus among experts in addiction that addictive behaviour is amenable to e?ective treatment, and that the extent to which an addict complies with treatment makes it possible to predict a positive outcome. But there is a long way to go before the mechanisms of drug addiction are properly understood or ways of treating it generally agreed.
Effects of drugs Cannabis, derived from the plant Cannabis sativa, is a widely used recreational drug. Its two main forms are marijuana, which comes from the dried leaves, and hashish which comes from the resin. Cannabis may be used in food and drink but is usually smoked in cigarettes to induce relaxation and a feeling of well-being. Heavy use can cause apathy and vagueness and may even cause psychosis. Whether or not cannabis leads people to using harder drugs is arguable, and a national debate is underway on whether its use should be legalised for medicinal use. Cannabis may alleviate the symptoms of some disorders – for example, MULTIPLE SCLEROSIS (MS) – and there are calls to allow the substance to be classi?ed as a prescribable drug.
About one in ten of Britain’s teenagers misuses volatile substances such as toluene at some time, but only about one in 40 does so regularly. These substances are given o? by certain glues, solvents, varnishes, and liquid fuels, all of which can be bought cheaply in shops, although their sale to children under 16 is illegal. They are often inhaled from plastic bags held over the nose and mouth. Central-nervous-system excitation, with euphoria and disinhibition, is followed by depression and lethargy. Unpleasant effects include facial rash, nausea and vomiting, tremor, dizziness, and clumsiness. Death from COMA and acute cardiac toxicity is a serious risk. Chronic heavy use can cause peripheral neuropathy and irreversible cerebellar damage. (See SOLVENT ABUSE (MISUSE).)
The hallucinogenic or psychedelic drugs include LYSERGIC ACID DIETHYLAMIDE (LSD) or acid, magic mushrooms, ecstasy (MDMA), and phencyclidine (PCP or ‘angel’ dust, mainly used in the USA). These drugs have no medicinal uses. Taken by mouth, they produce vivid ‘trips’, with heightened emotions and perceptions and sometimes with hallucinations. They are not physically addictive but can cause nightmarish bad trips during use and ?ashbacks (vivid reruns of trips) after use, and can probably trigger psychosis and even death, especially if drugs are mixed or taken with alcohol.
Stimulant drugs such as amphetamine and cocaine act like adrenaline and speed up the central nervous system, making the user feel con?dent, energetic, and powerful for several hours. They can also cause severe insomnia, anxiety, paranoia, psychosis, and even sudden death due to convulsions or tachycardia. Depression may occur on withdrawal of these drugs, and in some users this is su?ciently deterrent to cause psychological dependence. Amphetamine (‘speed’) is mainly synthesised illegally and may be eaten, sni?ed, or injected. Related drugs, such as dexamphetamine sulphate (Dexedrine), are prescribed pills that enter the black market. ECSTASY is another amphetamine derivative that has become a popular recreational drug; it may have fatal allergic effects. Cocaine and related drugs are used in medicine as local anaesthetics. Illegal supplies of cocaine (‘snow’ or ‘ice’) and its derivative, ‘crack’, come mainly from South America, where they are made from the plant Erythroxylon coca. Cocaine is usually sni?ed (‘snorted’) or rubbed into the gums; crack is burnt and inhaled.
Opiate drugs are derived from the opium poppy, Papaver somniferum. They are described as narcotic because they induce sleep. Their main medical use is as potent oral or injectable analgesics such as MORPHINE, DIAMORPHINE, PETHIDINE HYDROCHLORIDE, and CODEINE. The commonest illegal opiate is heroin, a powdered form of diamorphine that may be smoked, sni?ed, or injected to induce euphoria and drowsiness. Regular opiate misuse leads to tolerance (the need to take ever larger doses to achieve the same e?ect) and marked dependence. A less addictive oral opiate, METHADONE HYDROCHLORIDE, can be prescribed as a substitute that is easier to withdraw.
Some 75,000–150,000 Britons now misuse opiates and other drugs intravenously, and pose a huge public-health problem because injections with shared dirty needles can carry the blood-borne viruses that cause AIDS/HIV and HEPATITIS B. Many clinics now operate schemes to exchange old needles for clean ones, free of charge. Many addicts are often socially disruptive.
For help and advice see APPENDIX 2: ADDRESSES: SOURCES OF INFORMATION, ADVICE, SUPPORT AND SELF-HELP – National Dugs Helpline.
(See ALCOHOL and TOBACCO for detailed entries on those subjects.)... dependence
Insulin-dependent and non-insulindependent diabetes have a varied pathological pattern and are caused by the interaction of several genetic and environmental factors.
Insulin-dependent diabetes mellitus (IDDM) (juvenile-onset diabetes, type 1 diabetes) describes subjects with a severe de?ciency or absence of insulin production. Insulin therapy is essential to prevent KETOSIS – a disturbance of the body’s acid/base balance and an accumulation of ketones in the tissues. The onset is most commonly during childhood, but can occur at any age. Symptoms are acute and weight loss is common.
Non-insulin-dependent diabetes mellitus (NIDDM) (maturity-onset diabetes, type 2 diabetes) may be further sub-divided into obese and non-obese groups. This type usually occurs after the age of 40 years with an insidious onset. Subjects are often overweight and weight loss is uncommon. Ketosis rarely develops. Insulin production is reduced but not absent.
A new hormone has been identi?ed linking obesity to type 2 diabetes. Called resistin – because of its resistance to insulin – it was ?rst found in mice but has since been identi?ed in humans. Researchers in the United States believe that the hormone may, in part, explain how obesity predisposes people to diabetes. Their hypothesis is that a protein in the body’s fat cells triggers insulin resistance around the body. Other research suggests that type 2 diabetes may now be occurring in obese children; this could indicate that children should be eating a more-balanced diet and taking more exercise.
Diabetes associated with other conditions (a) Due to pancreatic disease – for example, chronic pancreatitis (see PANCREAS, DISORDERS OF); (b) secondary to drugs – for example, GLUCOCORTICOIDS (see PANCREAS, DISORDERS OF); (c) excess hormone production
– for example, growth hormone (ACROMEGALY); (d) insulin receptor abnormalities; (e) genetic syndromes (see GENETIC DISORDERS).
Gestational diabetes Diabetes occurring in pregnancy and resolving afterwards.
Aetiology Insulin-dependent diabetes occurs as a result of autoimmune destruction of beta cells within the PANCREAS. Genetic in?uences are important and individuals with certain HLA tissue types (HLA DR3 and HLA DR4) are more at risk; however, the risks associated with the HLA genes are small. If one parent has IDDM, the risk of a child developing IDDM by the age of 25 years is 1·5–2·5 per cent, and the risk of a sibling of an IDDM subject developing diabetes is about 3 per cent.
Non-insulin-dependent diabetes has no HLA association, but the genetic in?uences are much stronger. The risks of developing diabetes vary with di?erent races. Obesity, decreased exercise and ageing increase the risks of disease development. The risk of a sibling of a NIDDM subject developing NIDDM up to the age of 80 years is 30–40 per cent.
Diet Many NIDDM diabetics may be treated with diet alone. For those subjects who are overweight, weight loss is important, although often unsuccessful. A diet high in complex carbohydrate, high in ?bre, low in fat and aiming towards ideal body weight is prescribed. Subjects taking insulin need to eat at regular intervals in relation to their insulin regime and missing meals may result in hypoglycaemia, a lowering of the amount of glucose in the blood, which if untreated can be fatal (see below).
Oral hypoglycaemics are used in the treatment of non-insulin-dependent diabetes in addition to diet, when diet alone fails to control blood-sugar levels. (a) SULPHONYLUREAS act mainly by increasing the production of insulin;
(b) BIGUANIDES, of which only metformin is available, may be used alone or in addition to sulphonylureas. Metformin’s main actions are to lower the production of glucose by the liver and improve its uptake in the peripheral tissues.
Complications The risks of complications increase with duration of disease.
Diabetic hypoglycaemia occurs when amounts of glucose in the blood become low. This may occur in subjects taking sulphonylureas or insulin. Symptoms usually develop when the glucose concentration falls below 2·5 mmol/l. They may, however, occur at higher concentrations in subjects with persistent hyperglycaemia – an excess of glucose – and at lower levels in subjects with persistent hypo-glycaemia. Symptoms include confusion, hunger and sweating, with coma developing if blood-sugar concentrations remain low. Re?ned sugar followed by complex carbohydrate will return the glucose concentration to normal. If the subject is unable to swallow, glucagon may be given intramuscularly or glucose intravenously, followed by oral carbohydrate, once the subject is able to swallow.
Although it has been shown that careful control of the patient’s metabolism prevents late complications in the small blood vessels, the risk of hypoglycaemia is increased and patients need to be well motivated to keep to their dietary and treatment regime. This regime is also very expensive. All risk factors for the patient’s cardiovascular system – not simply controlling hyperglycaemia – may need to be reduced if late complications to the cardiovascular system are to be avoided.
Diabetes is one of the world’s most serious health problems. Recent projections suggest that the disorder will affect nearly 240 million individuals worldwide by 2010 – double its prevalence in 1994. The incidence of insulin-dependent diabetes is rising in young children; they will be liable to develop late complications.
Although there are complications associated with diabetes, many subjects live normal lives and survive to an old age. People with diabetes or their relatives can obtain advice from Diabetes UK (www.diabetes.org.uk).
Increased risks are present of (a) heart disease, (b) peripheral vascular disease, and (c) cerebrovascular disease.
Diabetic eye disease (a) retinopathy, (b) cataract. Regular examination of the fundus enables any abnormalities developing to be detected and treatment given when appropriate to preserve eyesight.
Nephropathy Subjects with diabetes may develop kidney damage which can result in renal failure.
Neuropathy (a) Symmetrical sensory polyneuropathy; damage to the sensory nerves that commonly presents with tingling, numbness of pain in the feet or hands. (b) Asymmetrical motor diabetic neuropathy, presenting as progressive weakness and wasting of the proximal muscles of legs. (c) Mononeuropathy; individual motor or sensory nerves may be affected. (d) Autonomic neuropathy, which affects the autonomic nervous system, has many presentations including IMPOTENCE, diarrhoea or constipation and postural HYPOTENSION.
Skin lesions There are several skin disorders associated with diabetes, including: (a) necrobiosis lipoidica diabeticorum, characterised by one or more yellow atrophic lesions on the legs;
(b) ulcers, which most commonly occur on the feet due to peripheral vascular disease, neuropathy and infection. Foot care is very important.
Diabetic ketoacidosis occurs when there is insu?cient insulin present to prevent KETONE production. This may occur before the diagnosis of IDDM or when insu?cient insulin is being given. The presence of large amounts of ketones in the urine indicates excess ketone production and treatment should be sought immediately. Coma and death may result if the condition is left untreated.
Symptoms Thirst, POLYURIA, GLYCOSURIA, weight loss despite eating, and recurrent infections (e.g. BALANITIS and infections of the VULVA) are the main symptoms.
However, subjects with non-insulindependent diabetes may have the disease for several years without symptoms, and diagnosis is often made incidentally or when presenting with a complication of the disease.
Treatment of diabetes aims to prevent symptoms, restore carbohydrate metabolism to as near normal as possible, and to minimise complications. Concentration of glucose, fructosamine and glycated haemoglobin in the blood are used to give an indication of blood-glucose control.
Insulin-dependent diabetes requires insulin for treatment. Non-insulin-dependent diabetes may be treated with diet, oral HYPOGLYCAEMIC AGENTS or insulin.
Insulin All insulin is injected – mainly by syringe but sometimes by insulin pump – because it is inactivated by gastrointestinal enzymes. There are three main types of insulin preparation: (a) short action (approximately six hours), with rapid onset; (b) intermediate action (approximately 12 hours); (c) long action, with slow onset and lasting for up to 36 hours. Human, porcine and bovine preparations are available. Much of the insulin now used is prepared by genetic engineering techniques from micro-organisms. There are many regimens of insulin treatment involving di?erent combinations of insulin; regimens vary depending on the requirements of the patients, most of whom administer the insulin themselves. Carbohydrate intake, energy expenditure and the presence of infection are important determinants of insulin requirements on a day-to-day basis.
A new treatment for diabetes, pioneered in Canada and entering its preliminary clinical trials in the UK, is the transplantation of islet cells of Langerhans from a healthy person into a patient with the disorder. If the transplantation is successful, the transplanted cells start producing insulin, thus reducing or eliminating the requirement for regular insulin injections. If successful the trials would be a signi?cant advance in the treatment of diabetes.
Scientists in Israel have developed a drug, Dia Pep 277, which stops the body’s immune system from destroying pancratic ? cells as happens in insulin-dependent diabetes. The drug, given by injection, o?ers the possibility of preventing type 1 diabetes in healthy people at genetic risk of developing the disorder, and of checking its progression in affected individuals whose ? cells are already perishing. Trials of the drug are in progress.... diabetes mellitus
Bacteria are classi?ed according to their shape: BACILLUS (rod-like), coccus (spherical – see COCCI), SPIROCHAETE (corkscrew and spiral-shaped), VIBRIO (comma-shaped), and pleomorphic (variable shapes). Some are mobile, possessing slender hairs (?agellae) on the surfaces. As well as having characteristic shapes, the arrangement of the organisms is signi?cant: some occur in chains (streptococci) and some in pairs (see DIPLOCOCCUS), while a few have a ?lamentous grouping. The size of bacteria ranges from around 0.2 to 5 µm and the smallest (MYCOPLASMA) are roughly the same size as the largest viruses (poxviruses – see VIRUS). They are the smallest organisms capable of existing outside their hosts. The longest, rod-shaped bacilli are slightly smaller than the human erythrocyte blood cell (7 µm).
Bacterial cells are surrounded by an outer capsule within which lie the cell wall and plasma membrane; cytoplasm ?lls much of the interior and this contains genetic nucleoid structures containing DNA, mesosomes (invaginations of the cell wall) and ribosomes, containing RNA and proteins. (See illustration.)
Reproduction is usually asexual, each cell dividing into two, these two into four, and so on. In favourable conditions reproduction can be very rapid, with one bacterium multiplying to 250,000 within six hours. This means that bacteria can change their characteristics by evolution relatively quickly, and many bacteria, including Mycobacterium tuberculosis and Staphylococcus aureus, have developed resistance to successive generations of antibiotics produced by man. (METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS (MRSA)) is a serious hazard in some hospitals.
Bacteria may live as single organisms or congregate in colonies. In arduous conditions some bacteria can convert to an inert, cystic state, remaining in their resting form until the environment becomes more favourable. Bacteria have recently been discovered in an inert state in ice estimated to have been formed 250 million years ago.
Bacteria were ?rst discovered by Antonj van Leewenhoek in the 17th century, but it was not until the middle of the 19th century that Louis Pasteur, the famous French scientist, identi?ed bacteria as the cause of many diseases. Some act as harmful PATHOGENS as soon as they enter a host; others may have a neutral or benign e?ect on the host unless the host’s natural immune defence system is damaged (see IMMUNOLOGY) so that it becomes vulnerable to any previously well-behaved parasites. Various benign bacteria that permanently reside in the human body are called normal ?ora and are found at certain sites, especially the SKIN, OROPHARYNX, COLON and VAGINA. The body’s internal organs are usually sterile, as are the blood and cerebrospinal ?uid.
Bacteria are responsible for many human diseases ranging from the relatively minor – for example, a boil or infected ?nger – to the potentially lethal such as CHOLERA, PLAGUE or TUBERCULOSIS. Infectious bacteria enter the body through broken skin or by its ori?ces: by nose and mouth into the lungs or intestinal tract; by the URETHRA into the URINARY TRACT and KIDNEYS; by the vagina into the UTERUS and FALLOPIAN TUBES. Harmful bacteria then cause disease by producing poisonous endotoxins or exotoxins, and by provoking INFLAMMATION in the tissues – for example, abscess or cellulitis. Many, but not all, bacterial infections are communicable – namely, spread from host to host. For example, tuberculosis is spread by airborne droplets, produced by coughing.
Infections caused by bacteria are commonly treated with antibiotics, which were widely introduced in the 1950s. However, the con?ict between science and harmful bacteria remains unresolved, with the overuse and misuse of antibiotics in medicine, veterinary medicine and the animal food industry contributing to the evolution of bacteria that are resistant to antibiotics. (See also MICROBIOLOGY.)... bacteria
Nutritional Profile Energy value (calories per serving): Moderate to high Protein: None Fat: None Saturated fat: None Cholesterol: None Carbohydrates: None (except for cordials which contain added sugar) Fiber: None Sodium: Low Major vitamin contribution: None Major mineral contribution: Phosphorus
About the Nutrients in This Food Spirits are the clear liquids produced by distilling the fermented sugars of grains, fruit, or vegetables. The yeasts that metabolize these sugars and convert them into alcohol stop growing when the concentration of alcohol rises above 12–15 percent. In the United States, the proof of an alcoholic beverage is defined as twice its alcohol content by volume: a beverage with 20 percent alcohol by volume is 40 proof. This is high enough for most wines, but not high enough for most whiskies, gins, vodkas, rums, brandies, and tequilas. To reach the concentra- tion of alcohol required in these beverages, the fermented sugars are heated and distilled. Ethyl alcohol (the alcohol in beer, wine, and spirits) boils at a lower temperature than water. When the fermented sugars are heated, the ethyl alcohol escapes from the distillation vat and condenses in tubes leading from the vat to a collection vessel. The clear liquid that collects in this vessel is called distilled spirits or, more technically, grain neutral spirits. Gins, whiskies, cordials, and many vodkas are made with spirits American whiskeys (which include bourbon, rye, and distilled from grains. blended whiskeys) and Canadian, Irish, and Scotch whiskies are all made from spirits aged in wood barrels. They get their flavor from the grains and their color from the barrels. (Some whiskies are also colored with caramel.) Vodka is made from spirits distilled and filtered to remove all flavor. By law, vodkas made in America must be made with spirits distilled from grains. Imported vodkas may be made with spirits distilled either from grains or potatoes and may contain additional flavoring agents such as citric acid or pepper. Aquavit, for example, is essentially vodka flavored with caraway seeds. Gin is a clear spirit flavored with an infusion of juniper berries and other herbs (botanicals). Cordials (also called liqueurs) and schnapps are flavored spirits; most are sweetened with added sugar. Some cordials contain cream. Rum is made with spirits distilled from sugar cane (molasses). Tequila is made with spirits distilled from the blue agave plant. Brandies are made with spirits distilled from fruit. (Arma- gnac and cognac are distilled from fermented grapes, calvados and applejack from fermented apples, kirsch from fermented cherries, slivovitz from fermented plums.) Unless they contain added sugar or cream, spirits have no nutrients other than alcohol. Unlike food, which has to be metabolized before your body can use it for energy, alcohol can be absorbed into the blood-stream directly from the gastrointestinal tract. Ethyl alcohol provides 7 calories per gram.
The Most Nutritious Way to Serve This Food The USDA /Health and Human Services Dietary Guidelines for Americans defines one drink as 12 ounces of beer, five ounces of wine, or 1.25 ounces of distilled spirits, and “moderate drinking” as two drinks a day for a man, one drink a day for a woman.
Diets That May Restrict or Exclude This Food Bland diet Lactose-free diet (cream cordials made with cream or milk) Low-purine (antigout) diet
Buying This Food Look for: Tightly sealed bottles stored out of direct sunlight, whose energy might disrupt the structure of molecules in the beverage and alter its flavor. Choose spirits sold only by licensed dealers. Products sold in these stores are manufac- tured under the strict supervision of the federal government.
Storing This Food Store sealed or opened bottles of spirits in a cool, dark cabinet.
Preparing This Food All spirits except unflavored vodkas contain volatile molecules that give the beverage its characteristic taste and smell. Warming the liquid excites these molecules and intensifies the flavor and aroma, which is the reason we serve brandy in a round glass with a narrower top that captures the aromatic molecules as they rise toward the air when we warm the glass by holding it in our hands. Whiskies, too, though traditionally served with ice in America, will have a more intense flavor and aroma if served at room temperature.
What Happens When You Cook This Food The heat of cooking evaporates the alcohol in spirits but leaves the flavoring intact. Like other alcoholic beverages, spirits should be added to a recipe near the end of the cooking time to preserve the flavor while cooking away any alcohol bite. Alcohol is an acid. If you cook it in an aluminum or iron pot, it will combine with metal ions to form dark compounds that discolor the pot and the food you are cooking. Any recipe made with spirits should be prepared in an enameled, glass, or stainless-steel pot.
Medical Uses and/or Benefits Reduced risk of heart attack. Data from the American Cancer Society’s Cancer Prevention Study 1, a 12-year survey of more than 1 million Americans in 25 states, shows that men who take one drink a day have a 21 percent lower risk of heart attack and a 22 percent lower risk of stroke than men who do not drink at all. Women who have up to one drink a day also reduce their risk of heart attack. Numerous later studies have confirmed these findings. Lower cholesterol levels. Beverage alcohol decreases the body’s production and storage of low density lipoproteins (LDLs), the protein and fat particles that carry cholesterol into your arteries. As a result, people who drink moderately tend to have lower cholesterol levels and higher levels of high density lipoproteins (HDLs), the fat and protein particles that carry cholesterol out of the body. Numerous later studies have confirmed these findings. Lower risk of stroke. In January 1999, the results of a 677-person study published by researchers at New York Presbyterian Hospital-Columbia University showed that moderate alcohol consumption reduces the risk of stroke due to a blood clot in the brain among older people (average age: 70). How alcohol prevents stroke is still unknown, but it is clear that moderate use is a key. Heavy drinkers (those who consume more than seven drinks a day) have a higher risk of stroke. People who once drank heavily, but cut their consumption to moderate levels, reduce their risk of stroke. Stimulating the appetite. Alcoholic beverages stimulate the production of saliva and the gastric acids that cause the stomach contractions we call hunger pangs. Moderate amounts of alcoholic beverages, which may help stimulate appetite, are often prescribed for geriatric patients, convalescents, and people who do not have ulcers or other chronic gastric problems that might be exacerbated by the alcohol. Dilation of blood vessels. Alcoholic beverages dilate the tiny blood vessels just under the skin, bringing blood up to the surface. That’s why moderate amounts of alcoholic beverages (0.2–1 gram per kilogram of body weight, or two ounces of whiskey for a 150-pound adult) temporarily warm the drinker. But the warm blood that flows up to the surface of the skin will cool down there, making you even colder when it circulates back into the center of your body. Then an alcohol flush will make you perspire, so you lose more heat. Excessive amounts of beverage alcohol may depress the mechanism that regulates body temperature.
Adverse Effects Associated with This Food Alcoholism. Alcoholism is an addiction disease, the inability to control one’s alcohol consumption. It is a potentially life-threatening condition, with a higher risk of death by accident, suicide, malnutrition, or acute alcohol poisoning, a toxic reaction that kills by para- lyzing body organs, including the heart. Fetal alcohol syndrome. Fetal alcohol syndrome is a specific pattern of birth defects—low birth weight, heart defects, facial malformations, learning disabilities, and mental retarda- tion—first recognized in a study of babies born to alcoholic women who consumed more than six drinks a day while pregnant. Subsequent research has found a consistent pattern of milder defects in babies born to women who drink three to four drinks a day or five drinks on any one occasion while pregnant. To date there is no evidence of a consistent pattern of birth defects in babies born to women who consume less than one drink a day while preg- nant, but two studies at Columbia University have suggested that as few as two drinks a week while pregnant may raise a woman’s risk of miscarriage. (One drink is 12 ounces of beer, five ounces of wine, or 1.25 ounces of distilled spirits.) Increased risk of breast cancer. In 2008, scientists at the National Cancer Institute released data from a seven-year survey of more than 100,000 postmenopausal women showing that even moderate drinking (one to two drinks a day) may increase by 32 percent a woman’s risk of developing estrogen-receptor positive (ER+) and progesterone-receptor positive (PR+) breast cancer, tumors whose growth is stimulated by hormones. No such link was found between consuming alcohol and the risk of developing ER-/PR- tumors (not fueled by hor- mones). The finding applies to all types of alcohol: beer, wine, and distilled spirits. Increased risk of oral cancer (cancer of the mouth and throat). Numerous studies confirm the A merican Cancer Societ y’s warn ing that men and women who consume more than t wo drinks a day are at higher risk of oral cancer than are nondrinkers or people who drink less. Increased risk of cancer of the colon and rectum. In the mid-1990s, studies at the University of Oklahoma suggested that men who drink more than five beers a day are at increased risk of rectal cancer. Later studies suggested that men and women who are heavy beer or spirits drinkers (but not those who are heavy wine drinkers) have a higher risk of colorectal cancers. Further studies are required to confirm these findings. Malnutrition. While moderate alcohol consumption stimulates appetite, alcohol abuses depresses it. In addition, an alcoholic may drink instead of eating. When an alcoholic does eat, excess alcohol in his/her body prevents absorption of nutrients and reduces the ability to synthesize new tissue. Hangover. Alcohol is absorbed from the stomach and small intestine and carried by the bloodstream to the liver, where it is oxidized to acetaldehyde by alcohol dehydrogenase (ADH), the enzyme our bodies use every day to metabolize the alcohol we produce when we digest carbohydrates. The acetaldehyde is converted to acetyl coenzyme A and either eliminated from the body or used in the synthesis of cholesterol, fatty acids, and body tis- sues. Although individuals vary widely in their capacity to metabolize alcohol, an adult of average size can metabolize the alcohol in four ounces (120 ml) whiskey in approximately five to six hours. If he or she drinks more than that, the amount of alcohol in the body will exceed the available supply of ADH. The surplus, unmetabolized alcohol will pile up in the bloodstream, interfering with the liver’s metabolic functions. Since alcohol decreases the reabsorption of water from the kidneys and may inhibit the secretion of an antidiuretic hormone, the drinker will begin to urinate copiously, losing magnesium, calcium, and zinc but retaining uric acid, which is irritating. The level of lactic acid in the body will increase, making him or her feel tired and out of sorts; the acid-base balance will be out of kilter; the blood vessels in the head will swell and throb; and the stomach, its lining irritated by the alcohol, will ache. The ultimate result is a hangover whose symptoms will disappear only when enough time has passed to allow the body to marshal the ADH needed to metabolize the extra alcohol in the person’s blood. Changes in body temperature. Alcohol dilates capillaries, tiny blood vessels just under the skin, producing a “flush” that temporarily warms the drinker. But drinking is not an effective way to stay warm in cold weather. Warm blood flowing up from the body core to the surface capillaries is quickly chilled, making you even colder when it circulates back into your organs. In addition, an alcohol flush triggers perspiration, further cooling your skin. Finally, very large amounts of alcohol may actually depress the mechanism that regulates body temperature. Impotence. Excessive drinking decreases libido (sexual desire) and interferes with the ability to achieve or sustain an erection. Migraine headache. Some alcoholic beverages contain chemicals that inhibit PST, an enzyme that breaks down certain alcohols in spirits so that they can be eliminated from the body. If they are not broken down by PST, these alcohols will build up in the bloodstream and may trigger a migraine headache. Gin and vodka appear to be the distilled spirits least likely to trigger headaches, brandy the most likely.
Food/Drug Interactions Acetaminophen (Tylenol, etc.). FDA recommends that people who regularly have three or more drinks a day consult a doctor before using acetaminophen. The alcohol/acetaminophen combination may cause liver failure. Anti-alcohol abuse drugs (disulfiram [Antabuse]). Taken concurrently with alcohol, the anti- alcoholism drug disulfiram can cause flushing, nausea, a drop in blood pressure, breathing difficulty, and confusion. The severity of the symptoms, which may var y among individu- als, generally depends on the amount of alcohol consumed and the amount of disulfiram in the body. Anticoagulants. Alcohol slows the body’s metabolism of anticoagulants (blood thinners), intensif ying the effect of the drugs and increasing the risk of side effects such as spontane- ous nosebleeds. Antidepressants. Alcohol may strengthen the sedative effects of antidepressants. Aspirin, ibuprofen, ketoprofen, naproxen and nonsteroidal anti-inflammatory drugs. Like alco- hol, these analgesics irritate the lining of the stomach and may cause gastric bleeding. Com- bining the two intensifies the effect. Insulin and oral hypoglycemics. Alcohol lowers blood sugar and interferes with the metabo- lism of oral antidiabetics; the combination may cause severe hypoglycemia. Sedatives and other central nervous system depressants (tranquilizers, sleeping pills, antide- pressants, sinus and cold remedies, analgesics, and medication for motion sickness). Alcohol intensifies the sedative effects of these medications and, depending on the dose, may cause drowsiness, sedation, respiratory depression, coma, or death. MAO inhibitors. Monoamine oxidase (M AO) inhibitors are drugs used as antidepressants or antihypertensives. They inhibit the action of natural enzymes that break down tyramine, a substance formed naturally when proteins are metabolized. Tyramine is a pressor amine, a chemical that constricts blood vessel and raises blood pressure. If you eat a food that contains tyramine while you are taking an M AO inhibitor, the pressor amine cannot be eliminated from your body and the result may be a hypertensive crisis (sustained elevated blood pressure). Brandy, a distilled spirit made from wine (which is fermented) contains tyramine. All other distilled spirits may be excluded from your diet when you are taking an M AO inhibitor because the spirits and the drug, which are both sedatives, may be hazard- ous in combination.... distilled spirits
Examination of the ear includes inspection of the external ear. An auriscope is used to examine the external ear canal and the ear drum. If a more detailed inspection is required, a microscope may be used to improve illumination and magni?cation.
Tuning-fork or Rinne tests are performed to identify the presence of DEAFNESS. The examiner tests whether the vibrating fork is audible at the meatus, and then the foot of the fork is placed on the mastoid bone of the ear to discover at which of the two sites the patient can hear the vibrations for the longest time. This can help to di?erentiate between conductive and nerve deafness.
Hearing tests are carried out to determine the level of hearing. An audiometer is used to deliver a series of short tones of varying frequency to the ear, either through a pair of headphones or via a sound transducer applied directly to the skull. The intensity of the sound is gradually reduced until it is no longer heard and this represents the threshold of hearing, at that frequency, through air and bone respectively. It may be necessary to play a masking noise into the opposite ear to prevent that ear from hearing the tones, enabling each ear to be tested independently.
General symptoms The following are some of the chief symptoms of ear disease: DEAFNESS (see DEAFNESS). EARACHE is most commonly due to acute in?ammation of the middle ear. Perceived pain in this region may be referred from other areas, such as the earache commonly experienced after tonsillectomy (removal of the TONSILS) or that caused by carious teeth (see TEETH, DISORDERS OF). The treatment will depend on the underlying cause. TINNITUS or ringing in the ear often accompanies deafness, but is sometimes the only symptom of ear disease. Even normal people sometimes experience tinnitus, particularly if put in soundproofed surroundings. It may be described as hissing, buzzing, the sound of the sea, or of bells. The intensity of the tinnitis usually ?uctuates, sometimes disappearing altogether. It may occur in almost any form of ear disease, but is particularly troublesome in nerve deafness due to ageing and in noise-induced deafness. The symptom seems to originate in the brain’s subcortical regions, high in the central nervous system. It may be a symptom of general diseases such as ANAEMIA, high blood pressure and arterial disease, in which cases it is often synchronous with the pulse, and may also be caused by drugs such as QUININE, salicylates (SALICYLIC ACID and its salts, for example, ASPIRIN) and certain ANTIBIOTICS. Treatment of any underlying ear disorder or systemic disease, including DEPRESSION, may reduce or even cure the tinnitis, but unfortunately in many cases the noises persist. Management involves psychological techniques and initially an explanation of the mechanism and reassurance that tinnitus does not signify brain disease, or an impending STROKE, may help the person. Tinnitus maskers – which look like hearing aids – have long been used with a suitably pitched sound helping to ‘mask’ the condition.
Diseases of the external ear
WAX (cerumen) is produced by specialised glands in the outer part of the ear canal only. Impacted wax within the ear canal can cause deafness, tinnitis and sometimes disturbance of balance. Wax can sometimes be softened with olive oil, 5-per-cent bicarbonate of soda or commercially prepared drops, and it will gradually liquefy and ‘remove itself’. If this is ineffective, syringing by a doctor or nurse will usually remove the wax but sometimes it is necessary for a specialist (otologist) to remove it manually with instruments. Syringing should not be done if perforation of the tympanic membrane (eardrum) is suspected. FOREIGN BODIES such as peas, beads or buttons may be found in the external ear canal, especially in children who have usually introduced them themselves. Live insects may also be trapped in the external canal causing intense irritation and noise, and in such cases spirit drops are ?rst instilled into the ear to kill the insect. Except in foreign bodies of vegetable origin, where swelling and pain may occur, syringing may be used to remove some foreign bodies, but often removal by a specialist using suitable instrumentation and an operating microscope is required. In children, a general anaesthetic may be needed. ACUTE OTITIS EXTERNA may be a di?use in?ammation or a boil (furuncle) occurring in the outer ear canal. The pinna is usually tender on movement (unlike acute otitis media – see below) and a discharge may be present. Initially treatment should be local, using magnesium sulphate paste or glycerine and 10-per-cent ichthaminol. Topical antibiotic drops can be used and sometimes antibiotics by mouth are necessary, especially if infection is acute. Clotrimazole drops are a useful antifungal treatment. Analgesics and locally applied warmth should relieve the pain.
CHRONIC OTITIS EXTERNA producing pain and discharge, can be caused by eczema, seborrhoeic DERMATITIS or PSORIASIS. Hair lotions and cosmetic preparations may trigger local allergic reactions in the external ear, and the chronic disorder may be the result of swimming or use of dirty towels. Careful cleaning of the ear by an ENT (Ear, Nose & Throat) surgeon and topical antibiotic or antifungal agents – along with removal of any precipitating cause – are the usual treatments. TUMOURS of the ear can arise in the skin of the auricle, often as a result of exposure to sunlight, and can be benign or malignant. Within the ear canal itself, the commonest tumours are benign outgrowths from the surrounding bone, said to occur in swimmers as a result of repeated exposure to cold water. Polyps may result from chronic infection of the ear canal and drum, particularly in the presence of a perforation. These polyps are soft and may be large enough to ?ll the ear canal, but may shrink considerably after treatment of the associated infection.
Diseases of the middle ear
OTITIS MEDIA or infection of the middle ear, usually occurs as a result of infection spreading up the Eustachian tubes from the nose, throat or sinuses. It may follow a cold, tonsillitis or sinusitis, and may also be caused by swimming and diving where water and infected secretions are forced up the Eustachian tube into the middle ear. Primarily it is a disease of children, with as many as 1.5 million cases occurring in Britain every year. Pain may be intense and throbbing or sharp in character. The condition is accompanied by deafness, fever and often TINNITUS.
In infants, crying may be the only sign that something is wrong – though this is usually accompanied by some localising manifestation such as rubbing or pulling at the ear. Examination of the ear usually reveals redness, and sometimes bulging, of the ear drum. In the early stages there is no discharge, but in the later stages there may be a discharge from perforation of the ear drum as a result of the pressure created in the middle ear by the accumulated pus. This is usually accompanied by an immediate reduction in pain.
Treatment consists of the immediate administration of an antibiotic, usually one of the penicillins (e.g. amoxicillin). In the majority of cases no further treatment is required, but if this does not quickly bring relief then it may be necessary to perform a myringotomy, or incision of the ear drum, to drain pus from the middle ear. When otitis media is treated immediately with su?cient dosage of the appropriate antibiotic, the chances of any permanent damage to the ear or to hearing are reduced to a negligible degree, as is the risk of any complications such as mastoiditis (discussed later in this section). CHRONIC OTITIS MEDIA WITH EFFUSION or glue ear, is the most common in?ammatory condition of the middle ear in children, to the extent that one in four children in the UK entering school has had an episode of ‘glue ear’. It is characterised by a persistent sticky ?uid in the middle ear (hence the name); this causes a conductive-type deafness. It may be associated with enlarged adenoids (see NOSE, DISORDERS OF) which impair the function of the Eustachian tube. If the hearing impairment is persistent and causes problems, drainage of the ?uid, along with antibiotic treatment, may be needed – possibly in conjunction with removal of the adenoids. The insertion of grommets (ventilation tubes) was for a time standard treatment, but while hearing is often restored, there may be no long-term gain and even a risk of damage to the tympanic membrane, so the operation is less popular than it was a decade or so ago. MASTOIDITIS is a serious complication of in?ammation of the middle ear, the incidence of which has been dramatically reduced by the introduction of antibiotics. In?ammation in this cavity usually arises by direct spread of acute or chronic in?ammation from the middle ear. The signs of this condition include swelling and tenderness of the skin behind the ear, redness and swelling inside the ear, pain in the side of the head, high fever, and a discharge from the ear. The management of this condition in the ?rst instance is with antibiotics, usually given intravenously; however, if the condition fails to improve, surgical treatment is necessary. This involves draining any pus from the middle ear and mastoid, and removing diseased lining and bone from the mastoid.
Diseases of the inner ear
MENIÈRE’S DISEASE is a common idiopathic disorder of ENDOLYMPH control in the semicircular canals (see EAR), characterised by the triad of episodic VERTIGO with deafness and tinnitus. The cause is unknown and usually one ear only is affected at ?rst, but eventually the opposite ear is affected in approximately 50 per cent of cases. The onset of dizziness is often sudden and lasts for up to 24 hours. The hearing loss is temporary in the early stages, but with each attack there may be a progressive nerve deafness. Nausea and vomiting often occur. Treatment during the attacks includes rest and drugs to control sickness. Vasodilator drugs such as betahistine hydrochloride may be helpful. Surgical treatment is sometimes required if crippling attacks of dizziness persist despite these measures. OTOSCLEROSIS A disorder of the middle ear that results in progressive deafness. Often running in families, otosclerosis affects about one person in 200; it customarily occurs early in adult life. An overgrowth of bone ?xes the stapes (the innermost bone of the middle ear) and stops sound vibrations from being transmitted to the inner ear. The result is conductive deafness. The disorder usually affects both ears. Those affected tend to talk quietly and deafness increases over a 10–15 year period. Tinnitus often occurs, and occasionally vertigo.
Abnormal hearing tests point to the diagnosis; the deafness may be partially overcome with a hearing aid but surgery is eventually needed. This involves replacing the stapes bone with a synthetic substitute (stapedectomy). (See also OTIC BAROTRAUMA.)... ear, diseases of
Nutritional Profile Energy value (calories per serving): Moderate Protein: High Fat: Low to moderate Saturated fat: Low to moderate Cholesterol: Moderate Carbohydrates: Low Fiber: None Sodium: Low (fresh fish) High (some canned or salted fish) Major vitamin contribution: Vitamin A, vitamin D Major mineral contribution: Iodine, selenium, phosphorus, potassium, iron, calcium
About the Nutrients in This Food Like meat, poultry, milk, and eggs, fish are an excellent source of high- quality proteins with sufficient amount of all the essential amino acids. While some fish have as much or more fat per serving than some meats, the fat content of fish is always lower in saturated fat and higher in unsaturated fats. For example, 100 g/3.5 ounce cooked pink salmon (a fatty fish) has 4.4 g total fat, but only 0.7 g saturated fat, 1.2 g monounsaturated fat, and 1.7 g polyunsaturated fat; 100 g/3.5 ounce lean top sirloin has four grams fat but twice as much saturated fat (1.5 g), plus 1.6 g monounsatu- rated fat and only 0.2 g polyunsaturated fat. Omega-3 Fatty Acid Content of Various Fish (Continued) Fish Grams/ounce Rainbow trout 0.30 Lake whitefish 0.25 Source: “Food for t he Heart,” American Health, April 1985. Fish oils are one of the few natural food sources of vitamin D. Salmon also has vita- min A derived from carotenoid pigments in the plants eaten by the fish. The soft bones in some canned salmon and sardines are an excellent source of calcium. CAUTION: do not eat the bones in r aw or cook ed fish. the only bones consider ed edible ar e those in the canned products.
The Most Nutritious Way to Serve This Food Cooked, to kill parasites and potentially pathological microorganisms living in raw fish. Broiled, to liquify fat and eliminate the fat-soluble environmental contaminants found in some freshwater fish. With the soft, mashed, calcium-rich bones (in canned salmon and canned sardines).
Diets That May Restrict or Exclude This Food Low-purine (antigout) diet Low-sodium diet (canned, salted, or smoked fish)
Buying This Food Look for: Fresh-smelling whole fish with shiny skin; reddish pink, moist gills; and clear, bulging eyes. The flesh should spring back when you press it lightly. Choose fish fillets that look moist, not dry. Choose tightly sealed, solidly frozen packages of frozen fish. In 1998, the FDA /National Center for Toxicological Research released for testing an inexpensive indicator called “Fresh Tag.” The indicator, to be packed with seafood, changes color if the product spoils. Avoid: Fresh whole fish whose eyes have sunk into the head (a clear sign of aging); fillets that look dry; and packages of frozen fish that are stained (whatever leaked on the package may have seeped through onto the fish) or are coated with ice crystals (the package may have defrosted and been refrozen).
Storing This Food Remove fish from plastic wrap as soon as you get it home. Plastic keeps out air, encouraging the growth of bacteria that make the fish smell bad. If the fish smells bad when you open the package, throw it out. Refrigerate all fresh and smoked fish immediately. Fish spoils quickly because it has a high proportion of polyunsaturated fatty acids (which pick up oxygen much more easily than saturated or monounsaturated fatty acids). Refrigeration also slows the action of microorgan- isms on the surface of the fish that convert proteins and other substances to mucopolysac- charides, leaving a slimy film on the fish. Keep fish frozen until you are ready to use it. Store canned fish in a cool cabinet or in a refrigerator (but not the freezer). The cooler the temperature, the longer the shelf life.
Preparing This Food Fresh fish. Rub the fish with lemon juice, then rinse it under cold running water. The lemon juice (an acid) will convert the nitrogen compounds that make fish smell “fishy” to compounds that break apart easily and can be rinsed off the fish with cool running water. R insing your hands in lemon juice and water will get rid of the fishy smell after you have been preparing fresh fish. Frozen fish. Defrost plain frozen fish in the refrigerator or under cold running water. Pre- pared frozen fish dishes should not be thawed before you cook them since defrosting will make the sauce or coating soggy. Salted dried fish. Salted dried fish should be soaked to remove the salt. How long you have to soak the fish depends on how much salt was added in processing. A reasonable average for salt cod, mackerel, haddock (finnan haddie), or herring is three to six hours, with two or three changes of water. When you are done, clean all utensils thoroughly with hot soap and hot water. Wash your cutting board, wood or plastic, with hot water, soap, and a bleach-and-water solution. For ultimate safety in preventing the transfer of microorganisms from the raw fish to other foods, keep one cutting board exclusively for raw fish, meats, and poultry, and a second one for everything else. Finally, don’t forget to wash your hands.
What Happens When You Cook This Food Heat changes the structure of proteins. It denatures the protein molecules so that they break apart into smaller fragments or change shape or clump together. These changes force moisture out of the tissues so that the fish turns opaque. The longer you cook fish, the more moisture it will lose. Cooked fish flakes because the connective tissue in fish “melts” at a relatively low temperature. Heating fish thoroughly destroys parasites and microorganisms that live in raw fish, making the fish safer to eat.
How Other Kinds of Processing Affect This Food Marinating. Like heat, acids coagulate the proteins in fish, squeezing out moisture. Fish marinated in citrus juices and other acids such as vinegar or wine has a firm texture and looks cooked, but the acid bath may not inactivate parasites in the fish. Canning. Fish is naturally low in sodium, but can ned fish often contains enough added salt to make it a high-sodium food. A 3.5-ounce ser ving of baked, fresh red salmon, for example, has 55 mg sodium, while an equal ser ving of regular can ned salmon has 443 mg. If the fish is can ned in oil it is also much higher in calories than fresh fish. Freezing. When fish is frozen, ice cr ystals form in the flesh and tear its cells so that mois- ture leaks out when the fish is defrosted. Commercial flash-freezing offers some protec- tion by freezing the fish so fast that the ice cr ystals stay small and do less damage, but all defrosted fish tastes drier and less palatable than fresh fish. Freezing slows but does not stop the oxidation of fats that causes fish to deteriorate. Curing. Fish can be cured (preser ved) by smoking, dr ying, salting, or pickling, all of which coagulate the muscle tissue and prevent microorganisms from growing. Each method has its own particular drawbacks. Smoking adds potentially carcinogenic chemicals. Dr ying reduces the water content, concentrates the solids and nutrients, increases the calories per ounce, and raises the amount of sodium.
Medical Uses and/or Benefits Protection against cardiovascular disease. The most important fats in fish are the poly- unsaturated acids k nown as omega-3s. These fatt y acids appear to work their way into heart cells where they seem to help stabilize the heart muscle and prevent potentially fatal arrhythmia (irregular heartbeat). A mong 85,000 women in the long-run n ing Nurses’ Health Study, those who ate fatt y fish at least five times a week were nearly 50 percent less likely to die from heart disease than those who ate fish less frequently. Similar results appeared in men in the equally long-run n ing Physicians’ Health Study. Some studies suggest that people may get similar benefits from omega-3 capsules. Researchers at the Consorzio Mario Negri Sud in Santa Maria Imbaro ( Italy) say that men given a one-gram fish oil capsule once a day have a risk of sudden death 42 percent lower than men given placebos ( “look-alike” pills with no fish oil). However, most nutrition scientists recom- mend food over supplements. Omega-3 Content of Various Food Fish Fish* (3 oz.) Omega-3 (grams) Salmon, Atlantic 1.8 Anchovy, canned* 1.7 Mackerel, Pacific 1.6 Salmon, pink, canned* 1.4 Sardine, Pacific, canned* 1.4 Trout, rainbow 1.0 Tuna, white, canned* 0.7 Mussels 0.7 * cooked, wit hout sauce * drained Source: Nat ional Fisheries Inst itute; USDA Nut rient Data Laborator y. Nat ional Nut ri- ent Database for Standard Reference. Available online. UR L : http://w w w.nal.usda. gov/fnic/foodcomp/search /.
Adverse Effects Associated with This Food Allergic reaction. According to the Merck Manual, fish is one of the 12 foods most likely to trigger classic food allergy symptoms: hives, swelling of the lips and eyes, and upset stom- ach. The others are berries (blackberries, blueberries, raspberries, strawberries), chocolate, corn, eggs, legumes (green peas, lima beans, peanuts, soybeans), milk, nuts, peaches, pork, shellfish, and wheat (see wheat cer ea ls). NOTE : Canned tuna products may contain sulfites in vegetable proteins used to enhance the tuna’s flavor. People sensitive to sulfites may suf- fer serious allergic reactions, including potentially fatal anaphylactic shock, if they eat tuna containing sulfites. In 1997, tuna manufacturers agreed to put warning labels on products with sulfites. Environmental contaminants. Some fish are contaminated with methylmercury, a compound produced by bacteria that chemically alters naturally occurring mercury (a metal found in rock and soil) or mercury released into water through industrial pollution. The methylmer- cury is absorbed by small fish, which are eaten by larger fish, which are then eaten by human beings. The larger the fish and the longer it lives the more methylmercury it absorbs. The measurement used to describe the amount of methylmercury in fish is ppm (parts per mil- lion). Newly-popular tilapia, a small fish, has an average 0.01 ppm, while shark, a big fish, may have up to 4.54 ppm, 450 times as much. That is a relatively small amount of methylmercur y; it will soon make its way harmlessly out of the body. But even small amounts may be hazardous during pregnancy because methylmercur y targets the developing fetal ner vous system. Repeated studies have shown that women who eat lots of high-mercur y fish while pregnant are more likely to deliver babies with developmental problems. As a result, the FDA and the Environ men- tal Protection Agency have now warned that women who may become pregnant, who are pregnant, or who are nursing should avoid shark, swordfish, king mackerel, and tilefish, the fish most likely to contain large amounts of methylmercur y. The same prohibition applies to ver y young children; although there are no studies of newborns and babies, the young brain continues to develop after birth and the logic is that the prohibition during pregnancy should extend into early life. That does not mean no fish at all should be eaten during pregnancy. In fact, a 2003 report in the Journal of Epidemiology and Community Health of data from an 11,585-woman study at the University of Bristol (England) shows that women who don’t eat any fish while pregnant are nearly 40 percent more likely to deliver low birth-weight infants than are women who eat about an ounce of fish a day, the equivalent of 1/3 of a small can of tuna. One theory is that omega-3 fatty acids in the fish may increase the flow of nutrient-rich blood through the placenta to the fetus. University of Southern California researchers say that omega-3s may also protect some children from asthma. Their study found that children born to asthmatic mothers who ate oily fish such as salmon at least once a month while pregnant were less likely to develop asthma before age five than children whose asthmatic pregnant mothers never ate oily fish. The following table lists the estimated levels of mercury in common food fish. For the complete list of mercury levels in fish, click onto www.cfsan.fda.gov/~frf/sea-mehg.html. Mercury Levels in Common Food Fish Low levels (0.01– 0.12 ppm* average) Anchovies, butterfish, catfish, clams, cod, crab (blue, king, snow), crawfish, croaker (Atlantic), flounder, haddock, hake, herring, lobster (spiny/Atlantic) mackerel, mul- let, ocean perch, oysters, pollock, salmon (canned/fresh frozen), sardines, scallops, shad (American), shrimp, sole, squid, tilapia, trout (freshwater), tuna (canned, light), whitefish, whiting Mid levels (0.14 – 0.54 ppm* average) Bass (salt water), bluefish, carp, croaker ( Pacific), freshwater perch, grouper, halibut, lobster (Northern A merican), mackerel (Spanish), marlin, monkfish, orange roughy, skate, snapper, tilefish (Atlantic), tuna (can ned albacore, fresh/frozen), weakfish/ sea trout High levels (0.73 –1.45 ppm* average) King mackerel, shark, swordfish, tilefish * ppm = parts per million, i.e. parts of mercur y to 1,000,000 parts fish Source: U.S. Food and Drug Administ rat ion, Center for Food Safet y and Applied Nut rit ion, “Mercur y Levels in Commercial Fish and Shellfish.” Available online. UR L : w w w.cfsan.fda. gov/~frf/sea-mehg.ht ml. Parasitical, viral, and bacterial infections. Like raw meat, raw fish may carry various pathogens, including fish tapeworm and flukes in freshwater fish and Salmonella or other microorganisms left on the fish by infected foodhandlers. Cooking the fish destroys these organisms. Scombroid poisoning. Bacterial decomposition that occurs after fish is caught produces a his- taminelike toxin in the flesh of mackerel, tuna, bonito, and albacore. This toxin may trigger a number of symptoms, including a flushed face immediately after you eat it. The other signs of scombroid poisoning—nausea, vomiting, stomach pain, and hives—show up a few minutes later. The symptoms usually last 24 hours or less.
Food/Drug Interactions Monoamine oxidase (MAO) inhibitors. Monoamine oxidase inhibitors are drugs used to treat depression. They inactivate naturally occurring enzymes in your body that metabolize tyramine, a substance found in many fermented or aged foods. Tyramine constricts blood vessels and increases blood pressure. If you eat a food such as pickled herring, which is high in tyramine, while you are taking an M AO inhibitor, your body may not be able to eliminate the tyramine and the result may be a hypertensive crisis.... fish
Many snakes are non-venomous (e.g. pythons, garter snakes, king snakes, boa constrictors) but may still in?ict painful bites and cause local swelling. Most venomous snakes belong to the viper and cobra families and are common in Asia, Africa, Australia and South America. Victims of bites may experience various effects including swelling, PARALYSIS of the bitten area, blood-clotting defects, PALPITATION, respiratory di?culty, CONVULSIONS and other neurotoxic and cardiac effects. Victims should be treated as for SHOCK – that is, kept at rest, kept warm, and given oxygen if required but nothing by mouth. The bite site should be immobilised but a TOURNIQUET must not be used. All victims require prompt transfer to a medical facility. When appropriate and available, antivenoms should be administered as soon as possible.
Similar management is appropriate for bites and stings by spiders, scorpions, sea-snakes, venomous ?sh and other marine animals and insects.
Bites and stings in the UK The adder (Vipera berus) is the only venomous snake native to Britain; it is a timid animal that bites only when provoked. Fatal cases are rare, with only 14 deaths recorded in the UK since 1876, the last of these in 1975. Adder bites may result in marked swelling, weakness, collapse, shock, and in severe cases HYPOTENSION, non-speci?c changes in the electrocardiogram and peripheral leucocytosis. Victims of adder bites should be transferred to hospital even if asymptomatic, with the affected limb being immobilised and the bite site left alone. Local incisions, suction, tourniquets, ice packs or permanganate must not be used. Hospital management may include use of a speci?c antivenom, Zagreb®.
The weever ?sh is found in the coastal waters of the British Isles, Europe, the eastern Atlantic, and the Mediterranean Sea. It possesses venomous spines in its dorsal ?n. Stings and envenomation commonly occur when an individual treads on the ?sh. The victim may experience a localised but increasing pain over two hours. As the venom is heat-labile, immersion of the affected area in water at approximately 40 °C or as hot as can be tolerated for 30 minutes should ease the pain. Cold applications will worsen the discomfort. Simple ANALGESICS and ANTIHISTAMINE DRUGS may be given.
Bees, wasps and hornets are insects of the order Hymenoptera and the females possess stinging apparatus at the end of the abdomen. Stings may cause local pain and swelling but rarely cause severe toxicity. Anaphylactic (see ANAPHYLAXIS) reactions can occur in sensitive individuals; these may be fatal. Deaths caused by upper-airway blockage as a result of stings in the mouth or neck regions are reported. In victims of stings, the stinger should be removed as quickly as possible by ?icking, scraping or pulling. The site should be cleaned. Antihistamines and cold applications may bring relief. For anaphylactic reactions ADRENALINE, by intramuscular injection, may be required.... bites and stings
The imaging systems of COMPUTED TOMOGRAPHY (CT) and magnetic resonance imaging (see MRI) have powerful computer techniques underlying them.
Computerised statistical analysis of study data, population databases and disease registries is now routine, leading to enhanced understanding of the interplay between diseases and the population. And the results of research, available on computerised indexes such as MEDLINE, can be obtained in searches that take only seconds, compared with the hours or days necessary to accomplish the same task with its paper incarnation, Index Medicus.
Medical informatics The direct computerisation of those activities which are uniquely medical – history-taking, examination, diagnosis and treatment – has proved an elusive goal, although one hotly pursued by doctors, engineers and scientists working in the discipline of medical informatics. Computer techniques have scored some successes: patients are, for example, more willing to be honest about taboo areas, such as their drug or alcohol consumption, or their sexual proclivities, with a computer than face to face with a clinician; however, the practice of taking a history remains the cornerstone of clinical practice. The examination of the patient is unlikely to be supplanted by technological means in the foreseeable future; visual and tactile recognition systems are still in their infancy. Skilled interpretation of the result by machine rather than the human mind seems equally as remote. Working its way slowly outwards from its starting point in mathematical logic, ARTIFICIAL INTELLIGENCE that in any way mimics its natural counterpart seems a distant prospect. Although there have been successes in computer-supported diagnosis in some specialised areas, such as the diagnosis of abdominal pain, workable systems that could supplant the mind of the generalist are still the dream of the many developers pursuing this goal, rather than a reality available to doctors in their consulting rooms now.
In therapeutics, computerised prescribing systems still require the doctor to make the decision about treatment, but facilitate the process of writing, issuing, and recording the prescription. In so doing, the system can provide automated checks, warning if necessary about allergies, potential drug interactions, or dosing errors. The built-in safety that this process o?ers is enhanced by the superior legibility of the script that ensues, reducing the potential for error when the medicine is dispensed by the nurse or the pharmacist.
Success in these individual applications continues to drive development, although the process has its critics, who are not slow to point to the lengthier consultations that arise when a computer is present in the consulting room and its distracting e?ect on communication with the patient.
Underlying these many software applications lies the ubiquitous personal computer – more powerful today than its mainframe predecessor of only 20 years ago – combined with networking technology that enables interconnection and the sharing of data. As in essence the doctor’s role involves the acquisition, manipulation and application of information – from the individual patient, and from the body of medical knowledge – great excitement surrounds the development of open systems that allow di?erent software and hardware platforms to interact. Many problems remain to be solved, not least the fact that for such systems to work, the whole organisation, and not just a few specialised individuals, must become computer literate. Such systems must be easy to learn to use, which requires an intuitive interface between user(s) and system(s) that is predictable and logical in its ordering and presentation of information.
Many other issues stand in the way of the development towards computerisation: standard systems of nomenclature for medical concepts have proved surprisingly di?cult to develop, but are crucial for successful information-sharing between users. Sharing information between existing legacy systems is a major challenge, often requiring customised software and extensive human intervention to enable the previous investments that an organisation has made in individual systems (e.g. laboratory-result reporting) to be integrated with newer technology. The beginnings of a global solution to this substantial obstacle to networking progress is in sight: the technology that enables the Internet – an international network of telephonically linked personal computers – also enables the establishment of intranets, in which individual servers (computers dedicated to serving information to other computers) act as repositories of ‘published’ data, which other users on the network may ‘browse’ as necessary in a client-server environment.
Systems that support this process are still in early stages of development, but the key conceptualisations are in place. Developments over the next 5–10 years will centre on the electronic patient record available to the clinician on an integrated clinical workstation. The clinical workstation – in essence a personal computer networked to the hospital or practice system – will enable the clinician to record clinical data and diagnoses, automate the ordering of investigations and the collection of the results, and facilitate referral and communication between the many professionals and departments involved in any individual patient’s care.
Once data is digitised – and that includes text, statistical tables, graphs, illustrations and radiological images, etc. – it may be as freely networked globally as locally. Consultations in which live video and sound transmissions are the bonds of the doctor-patient relationship (the techniques of telemedicine) are already reality, and have proved particularly convenient and cost-e?ective in linking the patient and the generalist to specialists in remote areas with low population density.
As with written personal medical records, con?dentiality of personal medical information on computers is essential. Computerised data are covered by the Data Protection Act 1984. This stipulates that data must:
be obtained and processed fairly and lawfully.
be held only for speci?ed lawful purposes.
•not be used in a manner incompatible with those purposes.
•only be recorded where necessary for these purposes.
be accurate and up to date.
not be stored longer than necessary.
be made available to the patient on request.
be protected by appropriate security and backup procedures. As these problems are solved, concerns about
privacy and con?dentiality arise. While paper records were often only con?dential by default, the potential for breaches of security in computerised networks is much graver. External breaches of the system by hackers are one serious concern, but internal breaches by authorised users making unauthorised use of the data are a much greater risk in practice. Governing network security so that clinical users have access on a need-to-know basis is a di?cult business: the software tools to enable this – encryption, and anonymisation (ensuring that clinical information about patients is anonymous to prevent con?dential information about them leaking out) of data collected for management and research processes – exist in the technical domain but remain a complex conundrum for solution in the real world.
The mushroom growth of websites covering myriad subjects has, of course, included health information. This ranges from clinical details on individual diseases to facts about medical organisations and institutes, patient support groups, etc. Some of this information contains comments and advice from orthodox and unorthodox practitioners. This open access to health information has been of great bene?t to patients and health professionals. But web browsers should be aware that not all the medical information, including suggested treatments, has been subject to PEER REVIEW, as is the case with most medical articles in recognised medical journals.... information technology in medicine
Severe head injuries cause unconsciousness for hours or many days, followed by loss of memory before and after that period of unconsciousness. The skull may be fractured; there may be ?ts in the ?rst week; and there may develop a blood clot in the brain (intracerebral haematoma) or within the membranes covering the brain (extradural and subdural haematomata). These clots compress the brain, and the pressure inside the skull – intracranial pressure – rises with urgent, life-threatening consequences. They are identi?ed by neurologists and neurosurgeons, con?rmed by brain scans (see COMPUTED TOMOGRAPHY; MRI), and require urgent surgical removal. Recovery may be complete, or in very severe cases can be marred by physical disabilities, EPILEPSY, and by changes in intelligence, rational judgement and behaviour. Symptoms generally improve in the ?rst two years.
A minority of those with minor head injuries have complaints and disabilities which seem disproportionate to the injury sustained. Referred to as the post-traumatic syndrome, this is not a diagnostic entity. The complaints are headaches, forgetfulness, irritability, slowness, poor concentration, fatigue, dizziness (usually not vertigo), intolerance of alcohol, light and noise, loss of interests and initiative, DEPRESSION, anxiety, and impaired LIBIDO. Reassurance and return to light work help these symptoms to disappear, in most cases within three months. Psychological illness and unresolved compensation-claims feature in many with implacable complaints.
People who have had brain injuries, and their relatives, can obtain help and advice from Headwat and from www.neuro.pmr.vcu.edu and www.biausa.org... brain injuries
Habitat: Dry, hilly wastes.
Features ? The stem is angular, five-sided, dark green, and branches at an acute angle.Yellow pea-like flowers appear in May and June. The lower leaves are on short stalks and consist of three small obovate leaflets, the upper leaves being stalkless and frequently single.Part used ? Tops.Action: Powerfully diuretic.
Broom tops are often used with Agrimony and Dandelion root for dropsy and liver disorders. For this purpose a decoction of 1 ounce each of Broom tops and Agrimony and 1/2 ounce Dandelion root to 3 pints of water simmered down to 1 quart is taken in wineglassful doses every four or five hours.Coffin recommends us to ? "Take of broom-tops, juniper-berries and dandelion-roots, each half-an-ounce, water, a pint and a half, boil down to a pint, strain, and add half-a-teaspoonsful of cayenne pepper. Dose, half- a-wineglassful four times a day."... broomNutritional Profile Energy value (calories per serving): High Protein: High Fat: High Saturated fat: Low Cholesterol: High Carbohydrates: Low Fiber: None Sodium: High Major vitamin contribution: B vitamins Major mineral contribution: Calcium, iron, phosphorus
About the Nutrients in This Food Caviar is a high-fat, high-cholesterol, high-protein, low-carbohydrate food. It is extremely high in sodium (650 mg/oz.) and, ounce for ounce, contains twice as much calcium as milk.
Diets That May Restrict or Exclude This Food Low-cholesterol, controlled-fat diet Low-salt/low-sodium diet
Buying This Food Look for: Shiny, translucent, large-grained gray fresh caviar (sturgeon roe) with a clean aroma. Look for: Tightly sealed tins and jars of less expensive roe. Lumpfish roe is small-grained and usually black. Cod, salmon, carp, pike, and tuna roe are large-grained and orangey red or pinkish.
Storing This Food Store fresh caviar in the coldest part of the refrigerator; it will spoil within hours at tempera- tures above 39°F. Store jars of caviar in a cool, dark place.
Preparing This Food Always serve caviar in a dish (or jar) nestled in ice to keep it safe at room temperature. The roe contains so much salt that it will not freeze. When making canapés, add the caviar last so that the oil does not spread and discolor the other ingredients.
How Other Kinds of Processing Affect This Food Pressing. Pressed caviar is caviar with 10 percent of its moisture removed. As a result it con- tains more nutrients per ounce than regular caviar and is even higher in sodium.
Medical Uses and/or Benefits Omega-3 fish oils. Caviar contains the same protective oils found in other fish (see fish).
Food/Drug Interactions MAO inhibitors. Monoamine oxidase (M AO) inhibitors are drugs used as antidepressants or antihypertensives. They inhibit the action of enzymes that break down tyramine, a natural by-product of protein metabolism. Tyramine is a pressor amine, a chemical that constricts blood vessels and raises blood pressure. If you eat a food that contains tyramine while you are taking an M AO inhibitor, the pressor amine cannot be eliminated from your body and the result could be a hypertensive crisis (sustained elevated blood pressure). Caviar contains small amounts of tyramine.... caviar
Menstruation depends upon a functioning ovary (see OVARIES) and this upon a healthy PITUITARY GLAND. The regular rhythm may depend upon a centre in the HYPOTHALAMUS, which is in close connection with the pituitary. After menstruation, the denuded uterine ENDOMETRIUM is regenerated under the in?uence of the follicular hormone, oestradiol. The epithelium of the endometrium proliferates, and about a fortnight after the beginning of menstruation great development of the endometrial glands takes place under the in?uence of progesterone, the hormone secreted by the CORPUS LUTEUM. These changes are made for the reception of the fertilised OVUM. In the absence of fertilisation the uterine endometrium breaks down in the subsequent menstrual discharge.
Disorders of menstruation In most healthy women, menstruation proceeds regularly for 30 years or more, with the exceptions connected with childbirth. In many women, however, menstruation may be absent, excessive or painful. The term amenorrhoea is applied to the condition of absent menstruation; the terms menorrhagia and metrorrhagia describe excessive menstrual loss – the former if the excess occurs at the regular periods, and the latter if it is irregular. Dysmenorrhoea is the name given to painful menstruation. AMENORRHOEA If menstruation has never occurred, the amenorrhoea is termed primary; if it ceases after having once become established it is known as secondary amenorrhoea. The only value of these terms is that some patients with either chromosomal abnormalities (see CHROMOSOMES) or malformations of the genital tract fall into the primary category. Otherwise, the age of onset of symptoms is more important.
The causes of amenorrhoea are numerous and treatment requires dealing with the primary cause. The commonest cause is pregnancy; psychological stress or eating disorders can cause amenorrhoea, as can poor nutrition or loss of weight by dieting, and any serious underlying disease such as TUBERCULOSIS or MALARIA. The excess secretion of PROLACTIN, whether this is the result of a micro-adenoma of the pituitary gland or whether it is drug induced, will cause amenorrhoea and possibly GALACTORRHOEA as well. Malfunction of the pituitary gland will result in a failure to produce the gonadotrophic hormones (see GONADOTROPHINS) with consequent amenorrhoea. Excessive production of cortisol, as in CUSHING’S SYNDROME, or of androgens (see ANDROGEN) – as in the adreno-genital syndrome or the polycystic ovary syndrome – will result in amenorrhoea. Amenorrhoea occasionally follows use of the oral contraceptive pill and may be associated with both hypothyroidism (see under THYROID GLAND, DISEASES OF) and OBESITY.
Patients should be reassured that amenorrhoea can often be successfully treated and does not necessarily affect their ability to have normal sexual relations and to conceive. When weight loss is the cause of amenorrhoea, restoration of body weight alone can result in spontaneous menstruation (see also EATING DISORDERS – Anorexia nervosa). Patients with raised concentration of serum gonadotrophin hormones have primary ovarian failure, and this is not amenable to treatment. Cyclical oestrogen/progestogen therapy will usually establish withdrawal bleeding. If the amenorrhoea is due to mild pituitary failure, menstruation may return after treatment with clomiphene, a nonsteroidal agent which competes for oestrogen receptors in the hypothalamus. The patients who are most likely to respond to clomiphene are those who have some evidence of endogenous oestrogen and gonadotrophin production. IRREGULAR MENSTRUATION This is a change from the normal monthly cycle of menstruation, the duration of bleeding or the amount of blood lost (see menorrhagia, below). Such changes may be the result of an upset in the balance of oestrogen and progesterone hormones which between them control the cycle. Cycles may be irregular after the MENARCHE and before the menopause. Unsuspected pregnancy may manifest itself as an ‘irregularity’, as can an early miscarriage (see ABORTION). Disorders of the uterus, ovaries or organs in the pelvic cavity can also cause irregular menstruation. Women with the condition should seek medical advice. MENORRHAGIA Abnormal bleeding from the uterus during menstruation. A woman loses on average about 60 ml of blood during her period; in menorrhagia this can rise to 100 ml. Some women have this problem occasionally, some quite frequently and others never. One cause is an imbalance of progesterone and oestrogen hormones which between them control menstruation: the result is an abnormal increase in the lining (endometrium) of the uterus, which increases the amount of ‘bleeding’ tissue. Other causes include ?broids, polyps, pelvic infection or an intrauterine contraceptive device (IUD – see under CONTRACEPTION). Sometimes no physical reason for menorrhagia can be identi?ed.
Treatment of the disorder will depend on how severe the loss of blood is (some women will become anaemic – see ANAEMIA – and require iron-replacement therapy); the woman’s age; the cause of heavy bleeding; and whether or not she wants children. An increase in menstrual bleeding may occur in the months before the menopause, in which case time may produce a cure. Medical or surgical treatments are available. Non-steroidal anti-in?ammatory drugs may help, as may tranexamic acid, which prevents the breakdown of blood clots in the circulation (FIBRINOLYSIS): this drug can be helpful if an IUD is causing bleeding. Hormones such as dydrogesterone (by mouth) may cure the condition, as may an IUD that releases small quantities of a PROGESTOGEN into the lining of the womb.
Traditionally, surgical intervention was either dilatation and curettage of the womb lining (D & C) or removal of the whole uterus (HYSTERECTOMY). Most surgery is now done using minimally invasive techniques. These do not require the abdomen to be cut open, as an ENDOSCOPE is passed via the vagina into the uterus. Using DIATHERMY or a laser, the surgeon then removes the whole lining of the womb. DYSMENORRHOEA This varies from discomfort to serious pain, and sometimes includes vomiting and general malaise. Anaemia is sometimes a cause of painful menstruation as well as of stoppage of this function.
In?ammation of the uterus, ovaries or FALLOPIAN TUBES is a common cause of dysmenorrhoea which comes on for the ?rst time late in life, especially when the trouble follows the birth of a child. In this case the pain exists more or less at all times, but is aggravated at the periods. Treatment with analgesics and remedying the underlying cause is called for.
Many cases of dysmenorrhoea appear with the beginning of menstrual life, and accompany every period. It has been estimated that 5–10 per cent of girls in their late teens or early 20s are severely incapacitated by dysmenorrhoea for several hours each month. Various causes have been suggested for the pain, one being an excessive production of PROSTAGLANDINS. There may be a psychological factor in some sufferers and, whether this is the result of inadequate sex instruction, fear, family, school or work problems, it is important to o?er advice and support, which in itself may resolve the dysmenorrhoea. Symptomatic relief is of value.... menstruation
Tumours All masses cause varying combinations of headache and vomiting – symptoms of raised pressure within the inexpansible bony box formed by the skull; general or localised epileptic ?ts; weakness of limbs or disordered speech; and varied mental changes. Tumours may be primary, arising in the brain, or secondary deposits from tumours arising in the lung, breast or other organs. Some brain tumours are benign and curable by surgery: examples include meningiomas and pituitary tumours. The symptoms depend on the size and situation of the mass. Abscesses or blood clots (see HAEMATOMA) on the surface or within the brain may resemble tumours; some are removable. Gliomas ( see GLIOMA) are primary malignant tumours arising in the glial tissue (see GLIA) which despite surgery, chemotherapy and radiotherapy usually have a bad prognosis, though some astrocytomas and oligodendronogliomas are of low-grade malignancy. A promising line of research in the US (in the animal-testing stage in 2000) suggests that the ability of stem cells from normal brain tissue to ‘home in’ on gliomal cells can be turned to advantage. The stem cells were chemically manipulated to carry a poisonous compound (5-?uorouracil) to the gliomal cells and kill them, without damaging normal cells. Around 80 per cent of the cancerous cells in the experiments were destroyed in this way.
Clinical examination and brain scanning (CT, or COMPUTED TOMOGRAPHY; magnetic resonance imaging (MRI) and functional MRI) are safe, accurate methods of demonstrating the tumour, its size, position and treatability.
Strokes When a blood vessel, usually an artery, is blocked by a clot, thrombus or embolism, the local area of the brain fed by that artery is damaged (see STROKE). The resulting infarct (softening) causes a stroke. The cells die and a patch of brain tissue shrinks. The obstruction in the blood vessel may be in a small artery in the brain, or in a larger artery in the neck. Aspirin and other anti-clotting drugs reduce recurrent attacks, and a small number of people bene?t if a narrowed neck artery is cleaned out by an operation – endarterectomy. Similar symptoms develop abruptly if a blood vessel bursts, causing a cerebral haemorrhage. The symptoms of a stroke are sudden weakness or paralysis of the arm and leg of the opposite side to the damaged area of brain (HEMIPARESIS), and sometimes loss of half of the ?eld of vision to one side (HEMIANOPIA). The speech area is in the left side of the brain controlling language in right-handed people. In 60 per cent of lefthanders the speech area is on the left side, and in 40 per cent on the right side. If the speech area is damaged, diffculties both in understanding words, and in saying them, develops (see DYSPHASIA).
Degenerations (atrophy) For reasons often unknown, various groups of nerve cells degenerate prematurely. The illness resulting is determined by which groups of nerve cells are affected. If those in the deep basal ganglia are affected, a movement disorder occurs, such as Parkinson’s disease, hereditary Huntington’s chorea, or, in children with birth defects of the brain, athetosis and dystonias. Modern drugs, such as DOPAMINE drugs in PARKINSONISM, and other treatments can improve the symptoms and reduce the disabilities of some of these diseases.
Drugs and injury Alcohol in excess, the abuse of many sedative drugs and arti?cial brain stimulants – such as cocaine, LSD and heroin (see DEPENDENCE) – can damage the brain; the effects can be reversible in early cases. Severe head injury can cause localised or di?use brain damage (see HEAD INJURY).
Cerebral palsy Damage to the brain in children can occur in the uterus during pregnancy, or can result from rare hereditary and genetic diseases, or can occur during labour and delivery. Severe neurological illness in the early months of life can also cause this condition in which sti? spastic limbs, movement disorders and speech defects are common. Some of these children are learning-disabled.
Dementias In older people a di?use loss of cells, mainly at the front of the brain, causes ALZHEIMER’S DISEASE – the main feature being loss of memory, attention and reasoned judgement (dementia). This affects about 5 per cent of the over-80s, but is not simply due to ageing processes. Most patients require routine tests and brain scanning to indicate other, treatable causes of dementia.
Response to current treatments is poor, but promising lines of treatment are under development. Like Parkinsonism, Alzheimer’s disease progresses slowly over many years. It is uncommon for these diseases to run in families. Multiple strokes can cause dementia, as can some organic disorders such as cirrhosis of the liver.
Infections in the brain are uncommon. Viruses such as measles, mumps, herpes, human immunode?ciency virus and enteroviruses may cause ENCEPHALITIS – a di?use in?ammation (see also AIDS/HIV).
Bacteria or viruses may infect the membrane covering the brain, causing MENINGITIS. Viral meningitis is normally a mild, self-limiting infection lasting only a few days; however, bacterial meningitis – caused by meningococcal groups B and C, pneumococcus, and (now rarely) haemophilus – is a life-threatening condition. Antibiotics have allowed a cure or good control of symptoms in most cases of meningitis, but early diagnosis is essential. Severe headaches, fever, vomiting and increasing sleepiness are the principal symptoms which demand urgent advice from the doctor, and usually admission to hospital. Group B meningococcus is the commonest of the bacterial infections, but Group C causes more deaths. A vaccine against the latter has been developed and has reduced the incidence of cases by 75 per cent.
If infection spreads from an unusually serious sinusitis or from a chronically infected middle ear, or from a penetrating injury of the skull, an abscess may slowly develop. Brain abscesses cause insidious drowsiness, headaches, and at a late stage, weakness of the limbs or loss of speech; a high temperature is seldom present. Early diagnosis, con?rmed by brain scanning, is followed by antibiotics and surgery in hospital, but the outcome is good in only half of affected patients.
Cerebral oedema Swelling of the brain can occur after injury, due to engorgement of blood vessels or an increase in the volume of the extravascular brain tissue due to abnormal uptake of water by the damaged grey (neurons) matter and white (nerve ?bres) matter. This latter phenomenon is called cerebral oedema and can seriously affect the functioning of the brain. It is a particularly dangerous complication following injury because sometimes an unconscious person whose brain is damaged may seem to be recovering after a few hours, only to have a major relapse. This may be the result of a slow haemorrhage from damaged blood vessels raising intracranial pressure, or because of oedema of the brain tissue in the area surrounding the injury. Such a development is potentially lethal and requires urgent specialist treatment to alleviate the rising intracranial pressure: osmotic agents (see OSMOSIS) such as mannitol or frusemide are given intravenously to remove the excess water from the brain and to lower intracranial pressure, buying time for de?nitive investigation of the cranial damage.... brain, diseases of
Severe and extensive burns are most frequently produced by the clothes – for example, of a child – catching ?re. This applies especially to cotton garments, which blaze up quickly. It should be remembered that such a ?ame can immediately be extinguished by making the individual lie on the ?oor so that the ?ames are uppermost, and wrapping him or her in a rug, mat or blanket. As prevention is always better than cure, particular care should always be exercised with electric ?res and kettles or pots of boiling water in houses where there are young children or old people. Children’s clothes, and especially night-clothes, should be made of non-in?ammable material: pyjamas are also much safer than nightdresses.
Severe scalds are usually produced by escape of steam in boiler explosions. Cigarettes are a common cause of ?res and therefore of burns; people who have fallen asleep in bed or in a chair while smoking may set ?re to the bed or chair. Discarded, unextinguished cigarettes are another cause.
Degrees of burns Burns are referred to as either super?cial (or partial-thickness) burns, when there is su?cient skin tissue left to ensure regrowth of skin over the burned site; and deep (or full-thickness) burns, when the skin is totally destroyed and grafting will be necessary.
Symptoms Whilst many domestic burns are minor and insigni?cant, more severe burns and scalds can prove to be very dangerous to life. The main danger is due to SHOCK, which arises as a result of loss of ?uid from the circulating blood at the site of a serious burn. This loss of ?uid leads to a fall in the volume of the circulating blood. As the maintenance of an adequate blood volume is essential to life, the body attempts to compensate for this loss by withdrawing ?uid from the uninjured areas of the body into the circulation. If carried too far, however, this in turn begins to affect the viability of the body cells. As a sequel, essential body cells, such as those of the liver and kidneys, begin to suffer, and the liver and kidneys cease to function properly. This will show itself by the development of JAUNDICE and the appearance of albumin in the urine (see PROTEINURIA). In addition, the circulation begins to fail with a resultant lack of oxygen (see ANOXIA) in the tissues, and the victim becomes cyanosed (see CYANOSIS), restless and collapsed: in some cases, death ensues. In addition, there is a strong risk of infection occurring. This is the case with severe burns in particular, which leave a large raw surface exposed and very vulnerable to any micro-organisms. The combination of shock and infection can all too often be life-threatening unless expert treatment is immediately available.
The immediate outcome of a burn is largely determined by its extent. This is of more signi?cance than the depth of the burn. To assess the extent of a burn in relation to the surface of the body, what is known as the Rule of Nine has been evolved. The head and each arm cover 9 per cent of the body surface, whilst the front of the body, the back of the body, and each leg each cover 18 per cent, with the perineum (or crutch) accounting for the remaining 1 per cent. The greater the extent of the burn, the more seriously ill will the victim become from loss of ?uid from his or her circulation, and therefore the more prompt should be his or her removal to hospital for expert treatment. The depth of the burn, unless this is very great, is mainly of import when the question arises as to how much surgical treatment, including skin grafting, will be required.
Treatment This depends upon the severity of the burn. In the case of quite minor burns or scalds, all that may be necessary if they are seen immediately is to hold the part under cold running water until the pain is relieved. Cooling is one of the most e?ective ways of relieving the pain of a burn. If the burn involves the distal part of a limb – for example, the hand and forearm – one of the most e?ective ways of relieving pain is to immerse the burned part in lukewarm water and add cold water until the pain disappears. As the water warms and pain returns, more cold water is added. After some three to four hours, pain will not reappear on warming, and the burn may be dressed in the usual way. Thereafter a simple dressing (e.g. a piece of sterile gauze covered by cotton-wool, and on top of this a bandage or adhesive dressing) should be applied. The part should be kept at rest and the dressing kept quite dry until healing takes place. Blisters should be pierced with a sterile needle, but the skin should not be cut away. No ointment or oil should be applied, and an antiseptic is not usually necessary.
In slightly more severe burns or scalds, it is probably advisable to use some antiseptic dressing. These are the cases which should be taken to a doctor – whether a general practitioner, a factory doctor, or to a hospital Accident & Emergency department. There is still no general consensus of expert opinion as to the best ‘antiseptic’ to use. Among those recommended are CHLORHEXIDINE, and antibiotics such as BACITRACIN, NEOMYCIN and polymixin. An alternative is to use a Tulle Gras dressing which has been impregnated with a suitable antibiotic.
In the case of severe burns and scalds, the only sound rule is immediate removal to hospital. Unless there is any need for immediate resuscitation, such as arti?cial respiration, or attention to other injuries there may be, such as fractures or haemorrhage, nothing should be done on the spot to the patient except to make sure that s/he is as comfortable as possible and to keep them warm, and to cover the burn with a sterile (or clean) cloth such as a sheet, pillowcases, or towels wrung out in cold water. If pain is severe, morphine should be given – usually intravenously. Once the victim is in hospital, the primary decision is as to the extent of the burn, and whether or not a transfusion is necessary. If the burn is more than 9 per cent of the body surface in extent, a transfusion is called for. The precise treatment of the burn varies, but the essential is to prevent infection if this has not already occurred, or, if it has, to bring it under control as quickly as possible. The treatment of severe burns has made great advances, with quick transport to specialised burns units, modern resuscitative measures, the use of skin grafting and other arti?cial covering techniques and active rehabilitation programmes, o?ering victims a good chance of returning to normal life.
CHEMICAL BURNS Phenol or lysol can be washed o? promptly before they do much damage. Acid or alkali burns should be neutralised by washing them repeatedly with sodium bicarbonate or 1 per cent acetic acid, respectively. Alternatively, the following bu?er solution may be used for either acid or alkali burns: monobasic potassium phosphate (70 grams), dibasic sodium phosphate (70 grams) in 850 millilitres of water. (See also PHOSPHORUS BURNS.)... burns and scalds
Nutritional Profile Energy value (calories per serving): Low Protein: Moderate Fat: Low Saturated fat: Low Cholesterol: None Carbohydrates: High Fiber: High Sodium: Moderate Major vitamin contribution: Vitamin A Major mineral contribution: Potassium
About the Nutrients in This Food Carrots are high-fiber food, roots whose crispness comes from cell walls stiffened with the insoluble dietary fibers cellulose and lignin. Carrots also contain soluble pectins, plus appreciable amounts of sugar (mostly sucrose) and a little starch. They are an extraordinary source of vitamin A derived from deep yellow carotenoids (including beta-carotene). One raw carrot, about seven inches long, has two grams of dietary fiber and 20,250 IU vitamin A (nine times the R DA for a woman, seven times the R DA for a man).
The Most Nutritious Way to Serve This Food Cooked, so that the cellulose- and hemicellulose-stiffened cell walls of the carrot have partially dissolved and the nutrients inside are more readily available.
Diets That May Restrict or Exclude This Food Disaccharide-intolerance diet (for people who are sucrase- and /or invertase-deficient) Low-fiber diet Low-sodium diet (fresh and canned carrots)
Buying This Food Look for: Firm, bright orange yellow carrots with fresh, crisp green tops. Avoid: Wilted or shriveled carrots, pale carrots, or carrots with brown spots on the skin.
Storing This Food Trim off the green tops before you store carrots. The leaf y tops will wilt and rot long before the sturdy root. Keep carrots cool. They will actually gain vitamin A during their first five months in storage. Protected from heat and light, they can hold to their vitamins at least another two and a half months. Store carrots in perforated plastic bags or containers. Circulating air prevents the for- mation of the terpenoids that make the carrots taste bitter. Do not store carrots near apples or other fruits that manufacture ethylene gas as they continue to ripen; this gas encourages the development of terpenoids. Store peeled carrots in ice water in the refrigerator to keep them crisp for as long as 48 hours.
Preparing This Food Scrape the carrots. Ver y young, tender carrots can be cleaned by scrubbing with a veg- etable brush. Soak carrots that are slightly limp in ice water to firm them up. Don’t discard slightly wilted intact carrots; use them in soups or stews where texture doesn’t matter.
What Happens When You Cook This Food Since carotenes do not dissolve in water and are not affected by the normal heat of cooking, carrots stay yellow and retain their vitamin A when you heat them. But cooking will dissolve some of the hemicellulose in the carrot’s stiff cell walls, changing the vegetable’s texture and making it easier for digestive juices to penetrate the cells and reach the nutrients inside.
How Other Kinds of Processing Affect This Food Freezing. The characteristic crunchy texture of fresh carrots depends on the integrity of its cellulose- and hemicellulose-stiffened cell walls. Freezing cooked carrots creates ice crystals that rupture these membranes so that the carrots usually seem mushy when defrosted. If possible, remove the carrots before freezing a soup or stew and add fresh or canned carrots when you defrost the dish.
Medical Uses and/or Benefits A reduced risk of some kinds of cancer. According to the American Cancer Society, carrots and other foods rich in beta-carotene, a deep yellow pigment that your body converts to a form of vitamin A, may lower the risk of cancers of the larynx, esophagus and lungs. There is no such benefit from beta-carotene supplements; indeed, one controversial study actually showed a higher rate of lung cancer among smokers taking the supplement. Protection against vitamin A-deficiency blindness. In the body, the vitamin A from carrots becomes 11-cis retinol, the essential element in rhodopsin, a protein found in the rods (the cells inside your eyes that let you see in dim light). R hodopsin absorbs light, triggering the chain of chemical reactions known as vision. One raw carrot a day provides more than enough vitamin A to maintain vision in a normal healthy adult.
Adverse Effects Associated with This Food Oddly pigmented skin. The carotenoids in carrots are fat-soluble. If you eat large amounts of carrots day after day, these carotenoids will be stored in your fatty tissues, including the fat just under your skin, and eventually your skin will look yellow. If you eat large amounts of carrots and large amounts of tomatoes (which contain the red pigment lycopene), your skin may be tinted orange. This effect has been seen in people who ate two cups of carrots and two tomatoes a day for several months; when the excessive amounts of these vegetables were eliminated from the diet, skin color returned to normal. False-positive test for occult blood in the stool. The active ingredient in the guaiac slide test for hidden blood in feces is alphaguaiaconic acid, a chemical that turns blue in the presence of blood. Carrots contain peroxidase, a natural chemical that also turns alphaguaiaconic acid blue and may produce a positive test in people who do not actually have blood in the stool.... carrots
Occupational health includes both mental and physical health. It is about compliance with health-and-safety-at-work legislation (and common law duties) and about best practice in providing work environments that reduce risks to health and safety to lowest practicable levels. It includes workers’ ?tness to work, as well as the management of the work environment to accommodate people with disabilities, and procedures to facilitate the return to work of those absent with long-term illness. Occupational health incorporates several professional groups, including occupational physicians, occupational health nurses, occupational hygienists, ergonomists, disability managers, workplace counsellors, health-and-safety practitioners, and workplace physiotherapists.
In the UK, two key statutes provide a framework for occupational health: the Health and Safety at Work, etc. Act 1974 (HSW Act); and the Disability Discrimination Act 1995 (DDA). The HSW Act states that employers have a duty to protect the health, safety and welfare of their employees and to conduct their business in a way that does not expose others to risks to their health and safety. Employees and self-employed people also have duties under the Act. Modern health-and-safety legislation focuses on assessing and controlling risk rather than prescribing speci?c actions in di?erent industrial settings. Various regulations made under the HSW Act, such as the Control of Substances Hazardous to Health Regulations, the Manual Handling Operations Regulations and the Noise at Work Regulations, set out duties with regard to di?erent risks, but apply to all employers and follow the general principles of risk assessment and control. Risks should be controlled principally by removing or reducing the hazard at source (for example, by substituting chemicals with safer alternatives, replacing noisy machinery, or automating tasks to avoid heavy lifting). Personal protective equipment, such as gloves and ear defenders, should be seen as a last line of defence after other control measures have been put in place.
The employment provisions of the DDA require employers to avoid discriminatory practice towards disabled people and to make reasonable adjustments to working arrangements where a disabled person is placed at a substantial disadvantage to a non-disabled person. Although the DDA does not require employers to provide access to rehabilitation services – even for those injured or made ill at work – occupational-health practitioners may become involved in programmes to help people get back to work after injury or long-term illness, and many businesses see the retention of valuable sta? as an attractive alternative to medical retirement or dismissal on health grounds.
Although a major part of occupational-health practice is concerned with statutory compliance, the workplace is also an important venue for health promotion. Many working people rarely see their general practitioner and, even when they do, there is little time to discuss wider health issues. Occupational-health advisers can ?ll in this gap by providing, for example, workplace initiatives on stopping smoking, cardiovascular health, diet and self-examination for breast and testicular cancers. Such initiatives are encouraged because of the perceived bene?ts to sta?, to the employing organisation and to the wider public-health agenda. Occupational psychologists recognise the need for the working population to achieve a ‘work-life balance’ and the promotion of this is an increasing part of occupational health strategies.
The law requires employers to consult with their sta? on health-and-safety matters. However, there is also a growing understanding that successful occupational-health management involves workers directly in the identi?cation of risks and in developing solutions in the workplace. Trade unions play an active role in promoting occupational health through local and national campaigns and by training and advising elected workplace safety representatives.
Occupational medicine The branch of medicine that deals with the control, prevention, diagnosis, treatment and management of ill-health and injuries caused or made worse by work, and with ensuring that workers are ?t for the work they do.
Occupational medicine includes: statutory surveillance of workers’ exposure to hazardous agents; advice to employers and employees on eliminating or reducing risks to health and safety at work; diagnosis and treatment/management of occupational illness; advice on adapting the working environment to suit the worker, particularly those with disabilities or long-term health problems; and advice on the return to work and, if necessary, rehabilitation of workers absent through illness. Occupational physicians may play a wider role in monitoring the health of workplace populations and in advising employers on controlling health hazards where ill-health trends are observed. They may also conduct epidemiological research (see EPIDEMIOLOGY) on workplace diseases.
Because of the occupational physician’s dual role as adviser to both employer and employee, he or she is required to be particularly diligent with regards to the individual worker’s medical CONFIDENTIALITY. Occupational physicians need to recognise in any given situation the context they are working in, and to make sure that all parties are aware of this.
Occupational medicine is a medical discipline and thus is only part of the broader ?eld of occupational health. Although there are some speci?c clinical duties associated with occupational medicine, such as diagnosis of occupational disease and medical screening, occupational physicians are frequently part of a multidisciplinary team that might include, for example, occupational-health nurses, healthand-safety advisers, ergonomists, counsellors and hygienists. Occupational physicians are medical practitioners with a post-registration quali?cation in occupational medicine. They will have completed a period of supervised in-post training. In the UK, the Faculty of Occupational Medicine of the Royal College of Physicians has three categories of membership, depending on quali?cations and experience: associateship (AFOM); membership (MFOM); and fellowship (FFOM).
Occupational diseases Occupational diseases are illnesses that are caused or made worse by work. In their widest sense, they include physical and mental ill-health conditions.
In diagnosing an occupational disease, the clinician will need to examine not just the signs and symptoms of ill-health, but also the occupational history of the patient. This is important not only in discovering the cause, or causes, of the disease (work may be one of a number of factors), but also in making recommendations on how the work should be modi?ed to prevent a recurrence – or, if necessary, in deciding whether or not the worker is able to return to that type of work. The occupational history will help in deciding whether or not other workers are also at risk of developing the condition. It will include information on:
the nature of the work.
how the tasks are performed in practice.
the likelihood of exposure to hazardous agents (physical, chemical, biological and psychosocial).
what control measures are in place and the extent to which these are adhered to.
previous occupational and non-occupational exposures.
whether or not others have reported similar symptoms in relation to the work. Some conditions – certain skin conditions,
for example – may show a close relationship to work, with symptoms appearing directly only after exposure to particular agents or possibly disappearing at weekends or with time away from work. Others, however, may be chronic and can have serious long-term implications for a person’s future health and employment.
Statistical information on the prevalence of occupational disease in the UK comes from a variety of sources, including o?cial ?gures from the Industrial Injuries Scheme (see below) and statutory reporting of occupational disease (also below). Neither of these o?cial schemes provides a representative picture, because the former is restricted to certain prescribed conditions and occupations, and the latter suffers from gross under-reporting. More useful are data from the various schemes that make up the Occupational Diseases Intelligence Network (ODIN) and from the Labour Force Survey (LFS). ODIN data is generated by the systematic reporting of work-related conditions by clinicians and includes several schemes. Under one scheme, more than 80 per cent of all reported diseases by occupational-health physicians fall into just six of the 42 clinical disease categories: upper-limb disorders; anxiety, depression and stress disorders; contact DERMATITIS; lower-back problems; hearing loss (see DEAFNESS); and ASTHMA. Information from the LFS yields a similar pattern in terms of disease frequency. Its most recent survey found that over 2 million people believed that, in the previous 12 months, they had suffered from an illness caused or made worse by work and that
19.5 million working days were lost as a result. The ten most frequently reported disease categories were:
stress and mental ill-health (see MENTAL ILLNESS): 515,000 cases.
back injuries: 508,000.
upper-limb and neck disorders: 375,000.
lower respiratory disease: 202,000.
deafness, TINNITUS or other ear conditions: 170,000.
lower-limb musculoskeletal conditions: 100,000.
skin disease: 66,000.
headache or ‘eyestrain’: 50,000.
traumatic injury (includes wounds and fractures from violent attacks at work): 34,000.
vibration white ?nger (hand-arm vibration syndrome): 36,000. A person who develops a chronic occu
pational disease may be able to sue his or her employer for damages if it can be shown that the employer was negligent in failing to take reasonable care of its employees, or had failed to provide a system of work that would have prevented harmful exposure to a known health hazard. There have been numerous successful claims (either awarded in court, or settled out of court) for damages for back and other musculoskeletal injuries, hand-arm vibration syndrome, noise-induced deafness, asthma, dermatitis, MESOTHELIOMA and ASBESTOSIS. Employers’ liability (workers’ compensation) insurers are predicting that the biggest future rise in damages claims will be for stress-related illness. In a recent study, funded by the Health and Safety Executive, about 20 per cent of all workers – more than 5 million people in the UK – claimed to be ‘very’ or ‘extremely’ stressed at work – a statistic that is likely to have a major impact on the long-term health of the working population.
While victims of occupational disease have the right to sue their employers for damages, many countries also operate a system of no-fault compensation for the victims of prescribed occupational diseases. In the UK, more than 60 diseases are prescribed under the Industrial Injuries Scheme and a person will automatically be entitled to state compensation for disability connected to one of these conditions, provided that he or she works in one of the occupations for which they are prescribed. The following short list gives an indication of the types of diseases and occupations prescribed under the scheme:
CARPAL TUNNEL SYNDROME connected to the use of hand-held vibrating tools.
hearing loss from (amongst others) use of pneumatic percussive tools and chainsaws, working in the vicinity of textile manufacturing or woodworking machines, and work in ships’ engine rooms.
LEPTOSPIROSIS – infection with Leptospira (various listed occupations).
viral HEPATITIS from contact with human blood, blood products or other sources of viral hepatitis.
LEAD POISONING, from any occupation causing exposure to fumes, dust and vapour from lead or lead products.
asthma caused by exposure to, among other listed substances, isocyanates, curing agents, solder ?ux fumes and insects reared for research.
mesothelioma from exposure to asbestos.
In the UK, employers and the self-employed have a duty to report all occupational injuries (if the employee is o? work for three days or more as a result), diseases or dangerous incidents to the relevant enforcing authority (the Health and Safety Executive or local-authority environmental-health department) under the Reporting of Injuries, Diseases and Dangerous Occurrences Regulations 1995 (RIDDOR). Despite this statutory duty, comparatively few diseases are reported so that ?gures generated from RIDDOR reports do not give a useful indication of the scale of occupational diseases in the UK. The statutory reporting of injuries is much better, presumably because of the clear and acute relationship between a workplace accident and the resultant injury. More than 160,000 injuries are reported under RIDDOR every year compared with just 2,500 or so occupational diseases, a gross underestimate of the true ?gure.
There are no precise ?gures for the number of people who die prematurely because of work-related ill-health, and it would be impossible to gauge the exact contribution that work has on, for example, cardiovascular disease and cancers where the causes are multifactorial. The toll would, however, dwarf the number of deaths caused by accidents at work. Around 250 people are killed by accidents at work in the UK each year – mesothelioma, from exposure to asbestos at work, alone kills more than 1,300 people annually.
The following is a sample list of occupational diseases, with brief descriptions of their aetiologies.
Inhaled materials
PNEUMOCONIOSIS covers a group of diseases which cause ?brotic lung disease following the inhalation of dust. Around 250–300 new cases receive bene?t each year – mostly due to coal dust with or without silica contamination. SILICOSIS is the more severe disease. The contraction in the size of the coal-mining industry as well as improved dust suppression in the mines have diminished the importance of this disease, whereas asbestos-related diseases now exceed 1,000 per year. Asbestos ?bres cause a restrictive lung disease but also are responsible for certain malignant conditions such as pleural and peritoneal mesothelioma and lung cancer. The lung-cancer risk is exacerbated by cigarette-smoking.
Even though the use of asbestos is virtually banned in the UK, many workers remain at risk of exposure because of the vast quantities present in buildings (much of which is not listed in building plans). Carpenters, electricians, plumbers, builders and demolition workers are all liable to exposure from work that disturbs existing asbestos. OCCUPATIONAL ASTHMA is of increasing importance – not only because of the recognition of new allergic agents (see ALLERGY), but also in the number of reported cases. The following eight substances are most frequently linked to occupational asthma (key occupations in brackets): isocyanates (spray painters, electrical processors); ?our and grain (bakers and farmers); wood dust (wood workers); glutaraldehyde (nurses, darkroom technicians); solder/colophony (welders, electronic assembly workers); laboratory animals (technicians, scientists); resins and glues (metal and electrical workers, construction, chemical processors); and latex (nurses, auxiliaries, laboratory technicians).
The disease develops after a short, symptomless period of exposure; symptoms are temporally related to work exposures and relieved by absences from work. Removal of the worker from exposure does not necessarily lead to complete cessation of symptoms. For many agents, there is no relationship with a previous history of ATOPY. Occupational asthma accounts for about 10 per cent of all asthma cases. DERMATITIS The risk of dermatitis caused by an allergic or irritant reaction to substances used or handled at work is present in a wide variety of jobs. About three-quarters of cases are irritant contact dermatitis due to such agents as acids, alkalis and solvents. Allergic contact dermatitis is a more speci?c response by susceptible individuals to a range of allergens (see ALLERGEN). The main occupational contact allergens include chromates, nickel, epoxy resins, rubber additives, germicidal agents, dyes, topical anaesthetics and antibiotics as well as certain plants and woods. Latex gloves are a particular cause of occupational dermatitis among health-care and laboratory sta? and have resulted in many workers being forced to leave their profession through ill-health. (See also SKIN, DISEASES OF.)
Musculoskeletal disorders Musculoskeletal injuries are by far the most common conditions related to work (see LFS ?gures, above) and the biggest cause of disability. Although not all work-related, musculoskeletal disorders account for 36.5 per cent of all disabilities among working-age people (compared with less than 4 per cent for sight and hearing impairment). Back pain (all causes – see BACKACHE) has been estimated to cause more than 50 million days lost every year in sickness absence and costs the UK economy up to £5 billion annually as a result of incapacity or disability. Back pain is a particular problem in the health-care sector because of the risk of injury from lifting and moving patients. While the emphasis should be on preventing injuries from occurring, it is now well established that the best way to manage most lower-back injuries is to encourage the patient to continue as normally as possible and to remain at work, or to return as soon as possible even if the patient has some residual back pain. Those who remain o? work on long-term sick leave are far less likely ever to return to work.
Aside from back injuries, there are a whole range of conditions affecting the upper limbs, neck and lower limbs. Some have clear aetiologies and clinical signs, while others are less well de?ned and have multiple causation. Some conditions, such as carpal tunnel syndrome, are prescribed diseases in certain occupations; however, they are not always caused by work (pregnant and older women are more likely to report carpal tunnel syndrome irrespective of work) and clinicians need to be careful when assigning work as the cause without ?rst considering the evidence. Other conditions may be revealed or made worse by work – such as OSTEOARTHRITIS in the hand. Much attention has focused on injuries caused by repeated movement, excessive force, and awkward postures and these include tenosynovitis (in?ammation of a tendon) and epicondylitis. The greatest controversy surrounds upper-limb disorders that do not present obvious tissue or nerve damage but nevertheless give signi?cant pain and discomfort to the individual. These are sometimes referred to as ‘repetitive strain injury’ or ‘di?use RSI’. The diagnosis of such conditions is controversial, making it di?cult for sufferers to pursue claims for compensation through the courts. Psychosocial factors, such as high demands of the job, lack of control and poor social support at work, have been implicated in the development of many upper-limb disorders, and in prevention and management it is important to deal with the psychological as well as the physical risk factors. Occupations known to be at particular risk of work-related upper-limb disorders include poultry processors, packers, electronic assembly workers, data processors, supermarket check-out operators and telephonists. These jobs often contain a number of the relevant exposures of dynamic load, static load, a full or excessive range of movements and awkward postures. (See UPPER LIMB DISORDERS.)
Physical agents A number of physical agents cause occupational ill-health of which the most important is occupational deafness. Workplace noise exposures in excess of 85 decibels for a working day are likely to cause damage to hearing which is initially restricted to the vital frequencies associated with speech – around 3–4 kHz. Protection from such noise is imperative as hearing aids do nothing to ameliorate the neural damage once it has occurred.
Hand-arm vibration syndrome is a disorder of the vascular and/or neural endings in the hands leading to episodic blanching (‘white ?nger’) and numbness which is exacerbated by low temperature. The condition, which is caused by vibrating tools such as chain saws and pneumatic hammers, is akin to RAYNAUD’S DISEASE and can be disabling.
Decompression sickness is caused by a rapid change in ambient pressure and is a disease associated with deep-sea divers, tunnel workers and high-?ying aviators. Apart from the direct effects of pressure change such as ruptured tympanic membrane or sinus pain, the more serious damage is indirectly due to nitrogen bubbles appearing in the blood and blocking small vessels. Central and peripheral nervous-system damage and bone necrosis are the most dangerous sequelae.
Radiation Non-ionising radiation from lasers or microwaves can cause severe localised heating leading to tissue damage of which cataracts (see under EYE, DISORDERS OF) are a particular variety. Ionising radiation from radioactive sources can cause similar acute tissue damage to the eyes as well as cell damage to rapidly dividing cells in the gut and bone marrow. Longer-term effects include genetic damage and various malignant disorders of which LEUKAEMIA and aplastic ANAEMIA are notable. Particular radioactive isotopes may destroy or induce malignant change in target organs, for example, 131I (thyroid), 90Sr (bone). Outdoor workers may also be at risk of sunburn and skin cancers. OTHER OCCUPATIONAL CANCERS Occupation is directly responsible for about 5 per cent of all cancers and contributes to a further 5 per cent. Apart from the cancers caused by asbestos and ionising radiation, a number of other occupational exposures can cause human cancer. The International Agency for Research on Cancer regularly reviews the evidence for carcinogenicity of compounds and industrial processes, and its published list of carcinogens is widely accepted as the current state of knowledge. More than 50 agents and processes are listed as class 1 carcinogens. Important occupational carcinogens include asbestos (mesothelioma, lung cancer); polynuclear aromatic hydrocarbons such as mineral oils, soots, tars (skin and lung cancer); the aromatic amines in dyestu?s (bladder cancer); certain hexavalent chromates, arsenic and nickel re?ning (lung cancer); wood and leather dust (nasal sinus cancer); benzene (leukaemia); and vinyl chloride monomer (angiosarcoma of the liver). It has been estimated that elimination of all known occupational carcinogens, if possible, would lead to an annual saving of 5,000 premature deaths in Britain.
Infections Two broad categories of job carry an occupational risk. These are workers in contact with animals (farmers, veterinary surgeons and slaughtermen) and those in contact with human sources of infection (health-care sta? and sewage workers).
Occupational infections include various zoonoses (pathogens transmissible from animals to humans), such as ANTHRAX, Borrelia burgdorferi (LYME DISEASE), bovine TUBERCULOSIS, BRUCELLOSIS, Chlamydia psittaci, leptospirosis, ORF virus, Q fever, RINGWORM and Streptococcus suis. Human pathogens that may be transmissible at work include tuberculosis, and blood-borne pathogens such as viral hepatitis (B and C) and HIV (see AIDS/HIV). Health-care workers at risk of exposure to infected blood and body ?uids should be immunised against hapatitis B.
Poisoning The incidence of occupational poisonings has diminished with the substitution of noxious chemicals with safer alternatives, and with the advent of improved containment. However, poisonings owing to accidents at work are still reported, sometimes with fatal consequences. Workers involved in the application of pesticides are particularly at risk if safe procedures are not followed or if equipment is faulty. Exposure to organophosphate pesticides, for example, can lead to breathing diffculties, vomiting, diarrhoea and abdominal cramps, and to other neurological effects including confusion and dizziness. Severe poisonings can lead to death. Exposure can be through ingestion, inhalation and dermal (skin) contact.
Stress and mental health Stress is an adverse reaction to excessive pressures or demands and, in occupational-health terms, is di?erent from the motivational impact often associated with challenging work (some refer to this as ‘positive stress’). Stress at work is often linked to increasing demands on workers, although coping can often prevent the development of stress. The causes of occupational stress are multivariate and encompass job characteristics (e.g. long or unsocial working hours, high work demands, imbalance between e?ort and reward, poorly managed organisational change, lack of control over work, poor social support at work, fear of redundancy and bullying), as well as individual factors (such as personality type, personal circumstances, coping strategies, and availability of psychosocial support outside work). Stress may in?uence behaviours such as smoking, alcohol consumption, sleep and diet, which may in turn affect people’s health. Stress may also have direct effects on the immune system (see IMMUNITY) and lead to a decline in health. Stress may also alter the course and response to treatment of conditions such as cardiovascular disease. As well as these general effects of stress, speci?c types of disorder may be observed.
Exposure to extremely traumatic incidents at work – such as dealing with a major accident involving multiple loss of life and serious injury
(e.g. paramedics at the scene of an explosion or rail crash) – may result in a chronic condition known as post-traumatic stress disorder (PTSD). PTSD is an abnormal psychological reaction to a traumatic event and is characterised by extreme psychological discomfort, such as anxiety or panic when reminded of the causative event; sufferers may be plagued with uncontrollable memories and can feel as if they are going through the trauma again. PTSD is a clinically de?ned condition in terms of its symptoms and causes and should not be used to include normal short-term reactions to trauma.... occupational health, medicine and diseases
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