Habitat: Native to China and Japan; cultivated in Indian gardens as an ornamental.
English: Maidenhair tree called Living Fossils (in India), Kew tree.Action: Antagonizes bronchospasm, used as a circulatory stimulant, peripheral vasodilator.
Key application: Standardized dry extract—for symptomatic treatment of disturbed performance in organic brain syndrome within the regimen ofa therapeutic concept in cases of dementia syndromes— memory deficits, disturbance in concentration, depressive emotional conditions, dizziness, tinnitus and headache. (German Commission E, ESCOP, WHO.) As vasoactive and platelet aggregation inhibitor.(The British Herbal Pharmacopoeia.) (For pharmocological studies in humans and clinical studies, see ESCOP.)The majority of pharmacological studies and clinical trials have been conduced using a standardized extract which contains 24% flavonoid glyco- sides (Ginko flavone glycosides) and 6% terpenoids (ginkgolides and bilob- alide).The extract increases tolerance to hypoxia and exhibits anti-ischaemic effect. It simultaneously improves the fluidity of blood, decreases platelet adhesion, decreases platelet and erythro- cyte aggregation and reduces plasma and blood viscosity. The extract protects erythrocytes from haemolysis. The extract also decreases the permeability of capillaries and protects the cell membrane by trapping deleterious free radicals.The extract also increased cerebral blood flow in about 70% patients evaluated (patients between 30-50 year age had 20% increase from the base line, compared with 70% in those 50- to 70- year-olds).A reversal of sexual dysfunction with concurrent use of ginkgo with antidepressant drugs has been reported. (Am J Psychiatry, 2000 157(5), 836837.)The National Centre for Complementary and Alternative Medicine, USA, is conducting a 5-year study of 3000 people aged 75 and older to determine if ginkgo, 240 mg daily, prevents dementia or Alzheimer's disease.... ginkgo bilobaBoth 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
Patchy localised hair loss is commonly caused by fungal infections (tinea capitis – see RINGWORM), especially in the tropics. It may also be due to trauma, such as hair-pulling by children or disturbed adults, or hair-straightening by African or Afro-Caribbean women (traction alopecia). Rarely, diseases of the scalp-skin such as discoid lupus erythematosus (see under LUPUS) or lichen planus (see under LICHEN) may cause patchy alopecia with scarring which is irreversible. The long-term effects of radiotherapy may be similar.
Treatment depends on the cause. Speci?c antifungal drugs cure tinea capitis. Correction of thyroid or iron de?ciency may be dramatic. Male baldness may be modi?ed slightly by long-term use of minoxidil lotion, or improved permanently by various types of hair-follicle grafting of transplants from the occipital scalp. Female balding may be amenable to anti-androgen/oestrogen regimens, but severe forms require a wig.... alopecia
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
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
There are few signi?cant di?erences between the various antimuscarinic drugs available, but some patients may tolerate one drug better than another or ?nd that they need to adjust their drug regimen in relation to food.... benzhexol
Nutritional Profile Energy value (calories per serving): Low Protein: Low Fat: Low Saturated fat: Low Cholesterol: None Carbohydrates: High Fiber: Low Sodium: Moderate Major vitamin contribution: Vitamin C Major mineral contribution: Iron, potassium
About the Nutrients in This Food Cranberries are nearly 90 percent water. The rest is sugars and dietary fiber, including insoluble cellulose in the skin and soluble gums and pectins in the flesh. Pectin dissolves as the fruit ripens; the older and riper the cran- berries, the less pectin they contain. Cranberries also have a bit of protein and a trace of fat, plus moderate amounts of vitamin C. One-half cup cranberries has 1.6 g dietary fiber and 6.5 mg vitamin C (9 percent of the R DA for a woman, 7 percent of the R DA for a man). One-half cup cranberry sauce has 1.5 g dietary fiber and 3 mg vitamin C (4 percent of the R DA for a woman, 3 percent of the R DA for a man).
The Most Nutritious Way to Serve This Food Relish made of fresh, uncooked berries (to preserve the vitamin C, which is destroyed by heat) plus oranges.
Diets That May Restrict or Exclude This Food Low-fiber diet
Buying This Food Look for: Firm, round, plump, bright red berries that feel cool and dry to the touch. Avoid: Shriveled, damp, or moldy cranberries. Moldy cranberries may be contaminated with fusarium molds, which produce toxins that can irritate skin and damage tissues by inhibiting the synthesis of DNA and protein.
Storing This Food Store packaged cranberries, unwashed, in the refrigerator, or freeze unwashed berries in sealed plastic bags for up to one year.
Preparing This Food Wash the berries under running water, drain them, and pick them over carefully to remove shriveled, damaged, or moldy berries. R inse frozen berries. It is not necessary to thaw before cooking.
What Happens When You Cook This Food First, the heat will make the water inside the cranberry swell, so that if you cook it long enough the berry will burst. Next, the anthocyanin pigments that make cranberries red will dissolve and make the cooking water red. Anthocyanins stay bright red in acid solutions and turn bluish if the liquid is basic (alkaline). Cooking cranberries in lemon juice and sugar preserves the color as well as brightens the taste. Finally, the heat of cooking will destroy some of the vitamin C in cranberries. Cranberry sauce has about one-third the vitamin C of an equal amount of fresh cranberries.
Medical Uses and/or Benefits Urinary antiseptic. Cranberr y juice is a long-honored folk remedy for urinar y infections. In 1985, researchers at Youngstown (Ohio) State University found a “special factor” in cran- berries that appeared to keep disease-causing bacteria from adhering to the surface of cells in the bladder and urinar y tract. In 1999, scientists at study at Rutgers University (in New Jersey) identified specific tannins in cranberries as the effective agents. In 2004, research- ers at Beth Israel Medical Center (New York) published a review of 19 recent studies of cranberries. The report, in the journal American Family Physician, suggested that a regimen of eight ounces of unsweetened cranberr y juice or one 300 – 400 mg cranberr y extract tablet twice a day for up to 12 months safely reduced the risk of urinar y tract infections. In 2008, a similar review by scientists at the University of Stirling (Scotland) of 10 studies showed similar results.
Adverse Effects Associated with This Food Increased risk of kidney stones. Long-term use of cranberry products may increase the risk of stone formation among patients known to form oxalate stones (stones composed of calcium and/or other minerals).
Food/Drug Interactions Anticoagulants Anticoagulants (blood thinners) are drugs used to prevent blood clots. They are most commonly prescribed for patients with atrial fibrillation, an irregular heartbeat that allows blood to pool in the heart and possibly clot before being pumped out into the body. In 2006 researchers at the College of Pharmacy and the Antithrombosis Center at the Univer- sity of Illinois (Chicago) reported that consuming cranberry juice while using the anticoagu- lant warafin (Coumadin) might cause fluctuations in blood levels of the anticoagulant, thus reducing the drug’s ability to prevent blood clots.... cranberries
Nutritional Profile Energy value (calories per serving): Moderate Protein: High Fat: High Saturated fat: Moderate Cholesterol: High Carbohydrates: Low Fiber: None Sodium: Moderate to high Major vitamin contribution: Vitamin A, riboflavin, vitamin D Major mineral contribution: Iron, calcium
About the Nutrients in This Food An egg is really three separate foods, the whole egg, the white, and the yolk, each with its own distinct nutritional profile. A whole egg is a high-fat, high-cholesterol, high-quality protein food packaged in a high-calcium shell that can be ground and added to any recipe. The proteins in eggs, with sufficient amounts of all the essential amino acids, are 99 percent digestible, the standard by which all other proteins are judged. The egg white is a high-protein, low-fat food with virtually no cholesterol. Its only important vitamin is riboflavin (vitamin B2), a vis- ible vitamin that gives egg white a slightly greenish cast. Raw egg whites contain avidin, an antinutrient that binds biotin a B complex vitamin for- merly known as vitamin H, into an insoluble compound. Cooking the egg inactivates avidin. An egg yolk is a high-fat, high-cholesterol, high-protein food, a good source of vitamin A derived from carotenes eaten by the laying hen, plus vitamin D, B vitamins, and heme iron, the form of iron most easily absorbed by your body. One large whole egg (50 g/1.8 ounce) has five grams fat (1.5 g satu- rated fat, 1.9 g monounsaturated fat, 0.7 g polyunsaturated fat), 212 mg cholesterol, 244 IU vitamin A (11 percent of the R DA for a woman, 9 percent * Values are for a whole egg. of the R DA for a man), 0.9 mg iron (5 percent of the R DA for a woman, 11 percent of the R DA for a man) and seven grams protein. The fat in the egg is all in the yolk. The protein is divided: four grams in the white, three grams in the yolk.
The Most Nutritious Way to Serve This Food With extra whites and fewer yolks to lower the fat and cholesterol per serving.
Diets That May Restrict or Exclude This Food Controlled-fat, low-cholesterol diet Low-protein diet
Buying This Food Look for: Eggs stored in the refrigerated dair y case. Check the date for freshness. NOTE : In 1998, the FDA and USDA Food Safety and Inspection Service (FSIS) proposed new rules that would require distributors to keep eggs refrigerated on the way to the store and require stores to keep eggs in a refrigerated case. The egg package must have a “refrigera- tion required” label plus safe-handling instructions on eggs that have not been treated to kill Salmonella. Look for: Eggs that fit your needs. Eggs are graded by the size of the yolk and the thick- ness of the white, qualities that affect appearance but not nutritional values. The higher the grade, the thicker the yolk and the thicker the white will be when you cook the egg. A Grade A A egg fried sunny side up will look much more attractive than a Grade B egg prepared the same way, but both will be equally nutritions. Egg sizes ( Jumbo, Extra large, Large, Medium, Small) are determined by how much the eggs weigh per dozen. The color of the egg’s shell depends on the breed of the hen that laid the egg and has nothing to do with the egg’s food value.
Storing This Food Store fresh eggs with the small end down so that the yolk is completely submerged in the egg white (which contains antibacterial properties, nature’s protection for the yolk—or a developing chick embryo in a fertilized egg). Never wash eggs before storing them: The water will make the egg shell more porous, allowing harmful microorganisms to enter. Store separated leftover yolks and whites in small, tightly covered containers in the refrigerator, where they may stay fresh for up to a week. Raw eggs are very susceptible to Salmonella and other bacterial contamination; discard any egg that looks or smells the least bit unusual. Refrigerate hard-cooked eggs, including decorated Easter eggs. They, too, are suscep- tible to Salmonella contamination and should never be left at room temperature.
Preparing This Food First, find out how fresh the eggs really are. The freshest ones are the eggs that sink and lie flat on their sides when submerged in cool water. These eggs can be used for any dish. By the time the egg is a week old, the air pocket inside, near the broad end, has expanded so that the broad end tilts up as the egg is submerged in cool water. The yolk and the white inside have begun to separate; these eggs are easier to peel when hard-cooked. A week or two later, the egg’s air pocket has expanded enough to cause the broad end of the egg to point straight up when you put the egg in water. By now the egg is runny and should be used in sauces where it doesn’t matter if it isn’t picture-perfect. After four weeks, the egg will float. Throw it away. Eggs are easily contaminated with Salmonella microorganisms that can slip through an intact shell. never eat or serve a dish or bever age containing r aw fr esh eggs. sa lmonella is destroyed by cooking eggs to an inter nal temper atur e of 145°f ; egg-milk dishes such as custar ds must be cooked to an inter nal temper atur e of 160°f. If you separate fresh eggs by hand, wash your hands thoroughly before touching other food, dishes, or cooking tools. When you have finished preparing raw eggs, wash your hands and all utensils thoroughly with soap and hot water. never stir cooked eggs with a utensil used on r aw eggs. When you whip an egg white, you change the structure of its protein molecules which unfold, breaking bonds between atoms on the same molecule and forming new bonds to atoms on adjacent molecules. The result is a network of protein molecules that hardens around air trapped in bubbles in the net. If you beat the whites too long, the foam will turn stiff enough to hold its shape even if you don’t cook it, but it will be too stiff to expand natu- rally if you heat it, as in a soufflé. When you do cook properly whipped egg white foam, the hot air inside the bubbles will expand. Ovalbumin, an elastic protein in the white, allows the bubble walls to bulge outward until they are cooked firm and the network is stabilized as a puff y soufflé. The bowl in which you whip the whites should be absolutely free of fat or grease, since the fat molecules will surround the protein molecules in the egg white and keep them from linking up together to form a puff y white foam. Eggs whites will react with metal ions from the surface of an aluminum bowl to form dark particles that discolor the egg-white foam. You can whip eggs successfully in an enamel or glass bowl, but they will do best in a copper bowl because copper ions bind to the egg and stabilize the foam.
What Happens When You Cook This Food When you heat a whole egg, its protein molecules behave exactly as they do when you whip an egg white. They unfold, form new bonds, and create a protein network, this time with molecules of water caught in the net. As the egg cooks, the protein network tightens, squeez- ing out moisture, and the egg becomes opaque. The longer you cook the egg, the tighter the network will be. If you cook the egg too long, the protein network will contract strongly enough to force out all the moisture. That is why overcooked egg custards run and why overcooked eggs are rubbery. If you mix eggs with milk or water before you cook them, the molecules of liquid will surround and separate the egg’s protein molecules so that it takes more energy (higher heat) to make the protein molecules coagulate. Scrambled eggs made with milk are softer than plain scrambled eggs cooked at the same temperature. When you boil an egg in its shell, the air inside expands and begins to escape through the shell as tiny bubbles. Sometimes, however, the force of the air is enough to crack the shell. Since there’s no way for you to tell in advance whether any particular egg is strong enough to resist the pressure of the bubbling air, the best solution is to create a safety vent by sticking a pin through the broad end of the egg before you start to boil it. Or you can slow the rate at which the air inside the shell expands by starting the egg in cold water and letting it warm up naturally as the water warms rather than plunging it cold into boiling water—which makes the air expand so quickly that the shell is virtually certain to crack. As the egg heats, a little bit of the protein in its white will decompose, releasing sulfur that links up with hydrogen in the egg, forming hydrogen sulfide, the gas that gives rot- ten eggs their distinctive smell. The hydrogen sulfide collects near the coolest part of the egg—the yolk. The yolk contains iron, which now displaces the hydrogen in the hydrogen sulfide to form a green iron-sulfide ring around the hard-cooked yolk.
How Other Kinds of Processing Affect This Food Egg substitutes. Fat-free, cholesterol-free egg substitutes are made of pasteurized egg whites, plus artificial or natural colors, flavors, and texturizers (food gums) to make the product look and taste like eggs, plus vitamins and minerals to produce the nutritional equivalent of a full egg. Pasteurized egg substitutes may be used without additional cooking, that is, in salad dressings and eggnog. Drying. Dried eggs have virtually the same nutritive value as fresh eggs. Always refrigerate dried eggs in an air- and moistureproof container. At room temperature, they will lose about a third of their vitamin A in six months.
Medical Uses and/or Benefits Protein source. The protein in eggs, like protein from all animal foods, is complete. That is, protein from animal foods provides all the essential amino acids required by human beings. In fact, the protein from eggs is so well absorbed and utilized by the human body that it is considered the standard by which all other dietary protein is measured. On a scale known as biological value, eggs rank 100 ; milk, 93; beef and fish, 75; and poultry, 72. Vision protection. The egg yolk is a rich source of the yellow-orange carotenoid pigments lutein and zeaxanthin. Both appear to play a role in protecting the eyes from damaging ultraviolet light, thus reducing the risk of cataracts and age-related macular degeneration, a leading cause of vision of loss in one-third of all Americans older than 75. Just 1.3 egg yolks a day appear to increase blood levels of lutein and zeaxanthin by up to 128 percent. Perhaps as a result, data released by the National Eye Institute’s 6,000-person Beaver Dam ( Wisconsin) Eye Study in 2003 indicated that egg consumption was inversely associated with cataract risk in study participants who were younger than 65 years of age when the study started. The relative risk of cataracts was 0.4 for people in the highest category of egg consumption, compared to a risk of 1.0 for those in the lowest category. External cosmetic effects. Beaten egg whites can be used as a facial mask to make your skin look smoother temporarily. The mask works because the egg proteins constrict as they dry on your face, pulling at the dried layer of cells on top of your skin. When you wash off the egg white, you also wash off some of these loose cells. Used in a rinse or shampoo, the pro- tein in a beaten raw egg can make your hair look smoother and shinier temporarily by filling in chinks and notches on the hair shaft.
Adverse Effects Associated with This Food Increased risk of cardiovascular disease. Although egg yolks are high in cholesterol, data from several recent studies suggest that eating eggs may not increase the risk of heart disease. In 2003, a report from a 14-year, 177,000-plus person study at the Harvard School of Public Health showed that people who eat one egg a day have exactly the same risk of heart disease as those who eat one egg or fewer per week. A similar report from the Multiple R isk Factor Intervention Trial showed an inverse relationship between egg consumption and cholesterol levels—that is, people who ate more eggs had lower cholesterol levels. Nonetheless, in 2006 the National Heart, Lung, and Blood Institute still recommends no more than four egg yolks a week (including the yolk in baked goods) for a heart-healthy diet. The American Heart Association says consumers can have one whole egg a day if they limit cholesterol from other sources to the amount suggested by the National Cholesterol Education Project following the Step I and Step II diets. (Both groups permit an unlimited number of egg whites.) 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) Food poisoning. Raw eggs (see above) and egg-rich foods such as custards and cream pies are excellent media for microorganisms, including the ones that cause food poisoning. To protect yourself against egg-related poisoning, always cook eggs thoroughly: poach them five minutes over boiling water or boil at least seven minutes or fry two to three minutes on each side (no runny center) or scramble until firm. Bread with egg coating, such as French toast, should be cooked crisp. Custards should be firm and, once cooked, served very hot or refrigerated and served very cold. Allergic reaction. According to the Merck Manual, eggs are 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), choco- late, corn, fish, legumes (green peas, lima beans, peanuts, soybeans), milk, nuts, peaches, pork, shellfish, and wheat (see wheat cer ea ls).
Food/Drug Interactions Sensitivity to vaccines. Live-virus measles vaccine, live-virus mumps vaccine, and the vac- cines for influenza are grown in either chick embryo or egg culture. They may all contain minute residual amounts of egg proteins that may provoke a hypersensitivity reaction in people with a history of anaphylactic reactions to eggs (hives, swelling of the mouth and throat, difficulty breathing, a drop in blood pressure, or shock).... eggs
Nutritional Profile Energy value (calories per serving): Moderate Protein: High Fat: Low Saturated fat: High Cholesterol: Moderate Carbohydrates: None Fiber: None Sodium: Low Major vitamin contribution: B vitamins Major mineral contribution: Iron, zinc
About the Nutrients in This Food Like other animal foods, game meat has high-quality proteins with suf- ficient amounts of all the essential amino acids. Some game meat has less fat, saturated fat, and cholesterol than beef. All game meat is an excellent source of B vitamins, plus heme iron, the form of iron most easily absorbed by your body, and zinc. For example, one four-ounce serving of roast bison has 28 g protein, 2.7 g fat (1.04 g saturated fat), 93.7 mg cholesterol, 3.88 mg iron (25.8 percent of the R DA for a woman of childbearing age), and 4.1 mg zinc (27 percent of the R DA for a man). The Nutrients in Roasted Game Meat (4-ounce serving)
The Most Nutritious Way to Serve This Food With a food rich in vitamin C. Vitamin C increases the absorption of iron.
Diets That May Restrict or Exclude This Food Low-protein diet (for kidney disease)
Buying This Food In American markets, game meats are usually sold frozen. Choose a package with no leaks or stains to suggest previous defrosting.
Storing This Food Keep frozen game meat well wrapped in the freezer until you are ready to use it. The packaging protects the meat from oxygen that can change its pigments from reddish to brown. Freezing prolongs the freshness of the meat by slowing the natural multiplication of bacteria that digest proteins and other substances on the surface, converting them to a slimy film. The bacteria also change the meat’s sulfur-containing 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. Large cuts of game meat can be safely frozen, at 0°F, for six months to a year.
Preparing This Food Defrost the meat in the refrigerator to protect it from spoilage. Trim the meat to dispose of all visible fat, thus reducing the amount of fat and cholesterol in each serving. 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 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 way meat looks and tastes, alters its nutritional value, makes it safer, and extends its shelf life. Browning meat before you cook it does not “seal in the juices,” but it does change the flavor by caramelizing proteins and sugars on the surface. Because meat’s only sugars are the Game Meat
63 small amounts of glycogen in muscle tissue, we add sugars in marinades or basting liquids that may also contain acids (vinegar, lemon juice, wine) to break down muscle fibers and tenderize the meat. (NOTE : 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 meat is heated, it loses water and shrinks. Its pigments, which combine with oxygen, are denatured (broken into fragments) by the heat. They turn brown, the natural color of well-done meat. At the same time, the fats in the meat are oxidized, a reaction that produces a characteristic warmed-over flavor when the cooked meat is refrigerated and then reheated. Cooking and storing the meat under a blanket of antioxidants—catsup or a gravy made of tomatoes, peppers and other vitamin-C rich vegetables—reduces fat oxidation and lessens the warmed-over flavor. Meat reheated in a microwave oven is also less likely to taste warmed-over.
How Other Kinds of Processing Affect This Food Aging. Hanging fresh meat exposed to air in a cold room evaporates moisture and shrinks the meat slightly. At the same time, bacterial action on the surface of the meat breaks down proteins, producing an “aged” flavor. (See below, Food/drug interactions.) 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 solu- tion. The salt or sugar used in curing dissolve 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 micro-organisms and protecting the meat from bacterial damage. Salt-cured meat is higher in sodium than fresh meat. Smoking. Hanging fresh meat over an open fire slowly dries the meat, kills microorgan- isms on its surface, and gives the meat a rich, smoky flavor. The flavor 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. Artificial smoke 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.
Adverse Effects Associated with This Food Increased risk of cardiovascular disease. Like all foods from animals, game meats are a source of cholesterol. 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) 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, meat con- taminated with other bacteria, viruses, or parasites poses 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; to 165°F, E. coli, and to 212°F, Listeria monocytogenes. Decline in kidney function. Proteins are nitrogen compounds. When metabolized, they yield ammonia that is excreted through the kidneys. In laboratory animals, a sustained high-pro- tein 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 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 an M AO inhibitor, you cannot effectively eliminate the tyramine from your body. The result may be a hypertensive crisis.... game meat
Shigellosis This form is usually caused by Shigella dysenteriae-1 (Shiga’s bacillus), Shigella ?exneri, Shigella boydii, and Shigella sonnei; the latter is the most benign and occurs in temperate climates also. It is transmitted by food and water contamination, by direct contact, and by ?ies; the organisms thrive in the presence of overcrowding and insanitary conditions. The incubation is between one and seven days, and the severity of the illness depends on the strain responsible. Duration of illness varies from a few days to two weeks and can be particularly severe in young, old, and malnourished individuals. Complications include perforation and haemorrhage from the colo-rectum, the haemolytic uraemic syndrome (which includes renal failure), and REITER’S SYNDROME. Diagnosis is dependent on demonstration of Shigella in (a) faecal sample(s) – before or usually after culture.
If dehydration is present, this should be treated accordingly, usually with an oral rehydration technique. Shigella is eradicated by antibiotics such as trimethoprimsulphamethoxazole, trimethoprim, ampicillin, and amoxycillin. Recently, a widespread resistance to many antibiotics has developed, especially in Asia and southern America, where the agent of choice is now a quinolone compound, for example, cipro?oxacin; nalidixic acid is also e?ective. Prevention depends on improved hygiene and sanitation, careful protection of food from ?ies, ?y destruction, and garbage disposal. A Shigella carrier must not be allowed to handle food.
Entamoeba histolytica infection Most cases occur in the tropics and subtropics. Dysentery may be accompanied by weight loss, anaemia, and occasionally DYSPNOEA. E. histolytica contaminates food (e.g. uncooked vegetables) or drinking water. After ingestion of the cyst-stage, and following the action of digestive enzymes, the motile trophozoite emerges in the colon causing local invasive disease (amoebic colitis). On entering the portal system, these organisms may gain access to the liver, causing invasive hepatic disease (amoebic liver ‘abscess’). Other sites of ‘abscess’ formation include the lungs (usually right) and brain. In the colo-rectum an amoeboma may be di?cult to di?erentiate from a carcinoma. Clinical symptoms usually occur within a week, but can be delayed for months, or even years; onset may be acute – as for Shigella spp. infection. Perforation, colo-rectal haemorrhage, and appendicitis are unusual complications. Diagnosis is by demonstration of E. histolytica trophozoites in a fresh faecal sample; other amoebae affecting humans do not invade tissues. Research techniques can be used to di?erentiate between pathogenic (E. dysenteriae) and non-pathogenic strains (E. dispar). Alternatively, several serological tests are of value in diagnosis, but only in the presence of invasive disease.
Treatment consists of one of the 5nitroimidazole compounds – metronidazole, tinidazole, and ornidazole; alcohol avoidance is important during their administration. A ?ve- to ten-day course should be followed by diloxanide furoate for ten days. Other compounds – emetine, chloroquine, iodoquinol, and paromomycin – are now rarely used. Invasive disease involving the liver or other organ(s) usually responds favourably to a similar regimen; aspiration of a liver ‘abscess’ is now rarely indicated, as controlled trials have indicated a similar resolution rate whether this technique is used or not, provided a 5-nitroimidazole compound is administered.... dysentery
Blood pressure is measured using two values. The systolic pressure – the greater of the two – represents the pressure when blood is pumped from the left VENTRICLE of the heart into the AORTA. The diastolic pressure is the measurement when both ventricles relax between beats. The pressures are measured in millimetres (mm) of mercury (Hg). Despite the grey area between normal and raised blood pressure, the World Health Organisation (WHO) has de?ned hypertension as a blood pressure consistently greater than 160 mm Hg (systolic) and 95 mm Hg (diastolic). Young children have readings well below these, but blood pressure rises with age and a healthy person may well live symptom free with a systolic pressure above the WHO ?gure. A useful working de?nition of hypertension is the ?gure at which the bene?ts of treating the condition outweigh the risks and costs of the treatment.
Between 10 and 20 per cent of the adult population in the UK has hypertension, with more men than women affected. Incidence is highest in the middle-aged and elderly. Because most people with hypertension are symptomless, the condition is often ?rst identi?ed during a routine medical examination, otherwise a diagnosis is usually made when complications occur. Many people’s blood pressure rises when they are anxious or after exercise, so if someone’s pressure is above normal at the ?rst testing, it should be taken again after, say, 10 minutes’ rest, by which time the reading should have settled to the person’s regular level. BP measurements should then be taken on two subsequent occasions. If the pressure is still high, the cause needs to be determined: this is done using a combination of personal and family histories (hypertension can run in families), a physical examination and investigations, including an ECG and blood tests for renal disease.
Over 90 per cent of hypertensive people have no immediately identi?able cause for their condition. They are described as having essential hypertension. In those patients with an identi?able cause, the hypertension is described as secondary. Among the causes of secondary hypertension are:
Lifestyle factors such as smoking, alcohol, stress, excessive dietary salt and obesity.
Diseases of the KIDNEYS.
Pregnancy (ECLAMPSIA).
Various ENDOCRINE disorders – for example, PHAEOCHROMOCYTOMA, CUSHING’S DISEASE, ACROMEGALY, thyrotoxicosis (see under THYROID GLAND, DISEASES OF).
COARCTATION OF THE AORTA.
Drugs – for example, oestrogen-containing oral contraceptives (see under CONTRACEPTION), ANABOLIC STEROIDS, CORTICOSTEROIDS, NON-STEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDS).
Treatment People with severe hypertension may need prompt admission to hospital for urgent investigation and treatment. Those with a mild to moderate rise in blood pressure for which no cause is identi?able should be advised to change their lifestyle: smokers should stop the habit, and those with high alcohol consumption should greatly reduce or stop their drinking. Obese people should reduce their food consumption, especially of animal fats, and take more exercise. Everyone with hypertension should follow a low-salt diet and take regular exercise. Patients should also be taught how to relax, which helps to reduce blood pressure and, if they have a stressful life, working patterns should be modi?ed if possible. If these lifestyle changes do not reduce a person’s blood pressure su?ciently, drugs to achieve this will be needed. A wide range of anti-hypertensive drugs are available on prescription.
A ?rst-line treatment is one of the THIAZIDES, e?ective at a low dosage and especially useful in the elderly. Beta blockers (see BETAADRENOCEPTOR-BLOCKING DRUGS), such as oxprenolol, acebutol or atenolol, are also ?rst-line treatments. ACE inhibitors (see ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS) and CALCIUM-CHANNEL BLOCKERS can be used if the ?rst-line choices are not e?ective. The drug treatment of hypertension is complex, and sometimes various drugs or combinations of drugs have to be tried to ?nd what regimen is e?ective and suits the patient. Mild to moderate hypertension can usually be treated in general practice, but patients who do not respond or have complications will normally require specialist advice. Patients on anti-hypertensive treatments require regular monitoring, and, as treatment may be necessary for several years, particular attention should be paid to identifying sideeffects. Nevertheless, e?ective treatment of hypertension does enable affected individuals to live longer and more comfortable lives than would otherwise be the case. Older people with moderately raised blood pressure are often able to live with the condition, and treatment with anti-hypertensive drugs may produce symptoms of HYPOTENSION.
In summary, hypertension is a complex disorder, with di?erent patients responding di?erently to treatment. So the condition sometimes requires careful assessment before the most e?ective therapy for a particular individual is identi?ed, and continued monitoring of patients with the disorder is advisable.
Complications Untreated hypertension may eventually result in serious complications. People with high blood pressure have blood vessels with thickened, less ?exible walls, a narrowed LUMEN and convoluted shape. Sometimes arteries become rigid. ANEURYSM may develop and widespread ATHEROMA (fat deposits) is apparent in the arterial linings. Such changes adversely affect the blood supply to body tissues and organs and so damage their functioning. Patients suffer STROKE (haemorrhage from or thrombosis in the arteries of the BRAIN) and heart attacks (coronary thrombosis
– see HEART, DISEASES OF). Those with hypertension may suffer damage to the retina of the EYE and to the OPTIC DISC. Indeed, the diagnosis of hypertension is sometimes made during a routine eye test, when the doctor or optician notices changes in the retinal arteries or optic disc. Kidney function is often affected, with patients excreting protein and excessive salt in their urine. Occasionally someone with persistent hypertension may suffer an acceleration of damage to the blood vessels – a condition described as ‘malignant’ hypertension, and one requiring urgent hospital treatment.
Hypertension is a potentially dangerous disease because it develops into a cycle of self-perpetuating damage. Faulty blood vessels lead to high blood pressure which in turn aggravates the damage in the vessels and thus in the tissues and organs they supply with blood; this further raises the affected individual’s blood pressure and the pathological cycle continues.... hypertension
Insulin is extracted mainly from pork pancreas and puri?ed by crystallisation; it may be made biosynthetically by recombinant DNA technology using Escherichia coli, or semisynthetically by enzymatic modi?cation of porcine insulin to produce human insulin. The latter is the form now generally used, although some patients ?nd it unsuitable and have to return to porcine insulin.
The hormone acts by enabling the muscles and other tissues requiring sugar for their activity to take up this substance from the blood. All insulin preparations are to a greater or lesser extent immunogenic in humans, but immunological resistance to insulin action is uncommon.
Previously available in three strengths, of 20, 40, and 80 units per millilitre (U/ml), these have now largely been replaced by a standard strength of 100 U/ml (U100). Numerous different insulin preparations are listed; these differ in their speed of onset and duration of action, and hence vary in their suitability for individual patients.
Insulin is inactivated by gastrointestinal enzymes and is therefore generally given by subcutaneous injection, usually into the upper arms, thighs, buttocks, or abdomen. Some insulins are also available in cartridge form, which may be administered by injection devices (‘pens’). The absorption may vary from di?erent sites and with strenuous activity. About 25 per cent of diabetics require insulin treatment: most children from the onset, and all patients presenting with ketoacidosis. Insulin is also often needed by those with a rapid onset of symptoms such as weight loss, weakness, and sometimes vomiting, often associated with ketonuria.
The aim of treatment is to maintain good control of blood glucose concentration, while avoiding severe HYPOGLYCAEMIA; this is usually achieved by a regimen of preprandial injections of short-acting insulin (often with a bedtime injection of long-acting insulin). Insulin may also be given by continuous subcutaneous infusion with an infusion pump. This technique has many disadvantages: patients must be well motivated and able to monitor their own blood glucose, with access to expert advice both day and night; it is therefore rarely used.
Hypoglycaemia is a potential hazard for many patients converting from porcine to human insulin, because human insulin may result in them being unaware of classical hypoglycaemic warning symptoms. Drivers must be particularly careful, and individuals may be forbidden to drive if they have frequent or severe hypoglycaemic attacks. For this reason, insurance companies should be warned, and diabetics should – after taking appropriate medical advice – either return to porcine insulin or consider stopping driving.... insulin
About 80 per cent of patients survive an acute stroke and they are at risk of a further episode within a few weeks and months; about 10 per cent in the ?rst year and 5 per cent a year after that. HYPERTENSION, smoking, HYPERLIPIDAEMIA and raised concentration of blood sugar, along with OBESITY, are signi?cant pointers to further strokes and preventive steps to reduce these factors are worthwhile, although the reduction in risk is hard to assess. Even so, the affected person should stop smoking, greatly reduce alcohol intake, check for and have treated diabetes, reduce weight and exercise regularly. In any case, a diet rich in fresh fruit and vegetables and low in fat and salt, exercise and the avoidance of smoking may reduce the risk of having a ?rst stroke.
The evidence is inconclusive that patients with ischaemic stroke should be treated with antihypertensives. Furthermore, neither the starting blood pressure nor the best drug regimen or its starting time are generally agreed. Studies on the most e?ective methods of preventing and treating stroke are continuing; meanwhile available evidence suggests that an active approach to prevention of primary and secondary hypertension will bene?t patients and usually be cost-e?ective.... ischaemic stroke
Only a small minority of those exposed to M. leprae develop the disease. The incubation period is 3–5 years or longer. The major clinical manifestations involve skin and nerves: the former range from depigmented, often anaesthetic areas, to massive nodules; nerve involvement ranges from localised nerve swelling(s) to extensive areas of anaesthesia. Advanced nerve destruction gives rise to severe deformities: foot-drop, wrist-drop, claw-foot, extensive ulceration of the extremities with loss of ?ngers and toes, and bone changes. Eye involvement can produce blindness. Laryngeal lesions produce hoarseness and more serious sequelae. The diagnosis is essentially a clinical one; however, skin-smears, histological features and the lepromin skin-test help to con?rm the diagnosis and enable the form of disease to be graded.
Although the World Health Organisation had originally hoped to eliminate leprosy worldwide by 2000, that has proved an unrealistic target. The reason is an absence of basic information. Doctors are unable to diagnose the disorder before a patient starts to show symptoms; meanwhile he or she may have already passed on the infection. Doctors do not know exactly how transmission occurs or how it infects humans – nor do they know at what point a carrier of the bacterium may infect others. The incidence of new infections is still more than 650,000 cases a year or about 4.5 cases per 10,000 people in those countries worst affected by the disease.
Treatment Introduction of the sulphone compound, dapsone, revolutionised management of the disease. More recently, rifampicin and clofazimine have been added as ?rst-line drugs for treatment. Second-line drugs include minocycline, o?oxacin and clarithromycin; a number of regimens incorporating several of these compounds (multi-drug regimens – introduced in 1982) are now widely used. A three-drug regime is recommended for multi-bacillary leprosy and a two-drug one for parcibacillary leprosy. Dapsone resistance is a major problem worldwide, but occurs less commonly when multi-drug regimens are used. Older compounds – ethionamide and prothionamide
– are no longer used because they are severely toxic to the liver. Corticosteroids are sometimes required in patients with ‘reversal reaction’. Supportive therapy includes physiotherapy; both plastic and orthopaedic surgery may be necessary in advanced stages of the disease. Improvement in socio-economic conditions, and widespread use of BCG vaccination are of value as preventive strategies. Early diagnosis and prompt institution of chemotherapy should prevent long-term complications.... leprosy
“A good and proper diet in disease is worth a hundred medicines and no amount of medication can do good to a patient who does not observe a strict regimen of diet.” (Charaka Samhita 300AD)
A healthy diet helps maintain the immune system, builds up reserves and hastens recovery from illness.
A good general diet includes foods low in fat, salt and high in fibre. All white sugar and white sugar products (chocolates, sweets, etc) should be replaced with natural sugars (honey, dates, figs, molasses, raisins etc). It should contain plenty of raw fresh fruit and vegetables; best prepared in a juice-press.
Vegetables should be conservatively cooked in very little water with little salt in a covered vessel. At least one mixed raw vegetable salad should be taken daily. Bread can be replaced by jacket potato, Soya- bean flour products or ripe bananas. Puddings, pastry and suety meals should be avoided.
Lean meat should be restricted to two or three parts a week with liberal inclusion of oily fish. Tofu, a Soya bean product, is an excellent alternative to meat. Three or four eggs, only, should be taken weekly.
Dairy produce (milk, butter, cream) contain cholesterol which thickens the blood, blocks arteries and increases resistance against the heart and major blood vessels, and should be taken sparingly.
Accept: Garlic, Onions, Lecithin, Muesli or Oatmeal porridge for breakfast or at other times during the day, yoghurt, honey.
Reject: fried foods, biscuits, confectionery.
Salt: replace with powdered Garlic, Celery or Kelp.
Alcohol: replace with fresh fruit or raw vegetable juices. Coffee is a risk factor raising cholesterol concentration; Dandelion coffee, Rutin or any one of many herbal teas available offer alternatives.
Avoid over-eating and meals when tired. Foods should be well masticated without liquid drinks; dry- feed. Plenty of liquid drinks, water etc should be taken between meals.
Supplements: Vitamin C 200mg, Vitamin E 200iu, morning and evening. Evening Primrose oil. Efamol produce a combined Evening Primrose and Fish oil capsule.
Dietary fibre can prevent certain colonic diseases. Treatment of disease by diet is preferred to drugs because it has the advantage of being free from side-effects. ... diet - general
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
Surgery may be most common, and is often the only treatment, for some gastrointestinal tumours, soft-tissue tumours, gynaecological tumours and advanced cancers of the head and neck.
Radiotherapy uses ionising radiation to kill tumour cells. Radiation is by naturally occurring isotopes (see ISOTOPE) or arti?cially produced X-RAYS. Germ-cell tumours (see SEMINOMA; TERATOMA) and malignant lymphomas (see LYMPHOMA) appear to be particularly sensitive to irradiation, and many head and neck tumours, gynaecological cancers, and localised cancers of the PROSTATE GLAND and URINARY BLADDER are curable with radiotherapy. It is also a valuable means of reducing pain from bone metastases (see METASTASIS). Unpleasant side-effects are common: chie?y lethargy, loss of appetite and dry, itchy skin symptoms.
Chemotherapy is also an important treatment in germ-cell tumours (see above); in some forms of LEUKAEMIA and lymphoma; in ovarian cancer (following surgery – see OVARIES, DISEASES OF); and in small-cell lung cancer (although most patients die within 18 months – see LUNGS, DISEASES OF). It is also used in some breast cancers (see BREASTS, DISEASES OF); advanced myeloma (see MYELOMATOSIS); sarcomas (see under CANCER); and some childhood cancers (such as WILMS’ TUMOUR).
More than 20 substances are in common use, the major classes being ALKYLATING AGENTS (e.g. cyclophosphamide, chlorambucil, busul fan); ANTIMETABOLITES (e.g. methotrexate); VINCA ALKALOIDS (e.g. vincristine, vinblastine); and antitumour ANTIBIOTICS (e.g. actinomycin D). Choice of agent and the appropriate regimen requires expert guidance. Common side-effects include nausea and vomiting, bone-marrow suppression and ALOPECIA, with each substance having its own spectrum of unwanted effects.
Good doctor-patient communication, with the sharing of information and bringing the patient into the decision-making process, is vital even if time-consuming and exhausting.
Equally imortant treatment is PALLIATIVE, for example to ensure e?ective pain or nausea control. Common sources of pain in cancer may involve bone, nerve compression, soft tissue, visceral, myofascial, constipation, muscle spasm, low-back pain, joint pain (e.g. capsulitis) and chronic post-operative pain. Patients may be suffering from more than one pain, all of which should be identi?ed. The aim should be to eliminate pain.
There are three rungs of the analgesic ladder; if one rung fails, the next one should be tried:
(1) non-opioid drugs – for example, aspirin, PARACETAMOL, NON-STEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDS); (2) weak opioids – for example, CODEINE, DIHYDROCODEINE, dextropropoxyphene; (3) strong opioids
– for example, MORPHINE, DIAMORPHINE, buprenorphine. Oral treatment is always preferable, unless prevented by severe vomiting. (See also CANCER; ONCOLOGIST; PAIN; PALLIATIVE CARE.)... oncology
Stage 0: the presence of risk factors and symptoms (e.g. cough and wheeze) with normal *forced expiratory volume in 1 second (FEV1).
Stage 1: FEV1 is normal, but the ratio of FEV1 to forced *vital capacity (FVC) is less than 70%.
Stage 2: FEV1 is less than 80% but more than 50% of the predicted value for the patient’s age and height.
Stage 3: FEV1 less than 50% but more than 30%.
Stage 4: FEV1 less than 30% or the presence of chronic respiratory failure.
The guidelines for COPD recommend different treatment regimens for different stages. Although the response to inhaled corticosteriods is less for COPD than for asthma, these drugs, especially combined with inhaled long-acting beta agonists (e.g. *salmeterol), can improve quality of life and survival in stages 3 and 4. There is also a decrease in the number of acute exacerbations of COPD (AECOPD): increased sputum volume or purulence and/or breathlessness, with or without symptoms (e.g. cough, wheeze, chest pain, malaise, fever).... chronic obstructive pulmonary disease
– an early graded return to activity gives the best long-term results, but doing too much too soon runs the risk of exacerbating the original injury.
Chronic (overuse) injuries affecting the bones (see BONE), tendons (see TENDON) or BURSAE of the JOINTS are common in many sports. Examples include chronic INFLAMMATION of the common extensor tendon where it
attaches to the later EPICONDYLE of the humerus – common in throwers and racquet sportspeople – and stress fractures of the TIBIA or METATARSAL BONES of the foot in runners. After an initial period of rest, management often involves coaching that enables the athlete to perform the repetitive movement in a less injury-susceptible manner.
Exercise physiology is the science of measuring athletic performance and physical ?tness for exercise. This knowledge is applied to devising and supervising training regimens based on scienti?c principles. Physical ?tness depends upon the rate at which the body can deliver oxygen to the muscles, known as the VO2max, which is technically di?cult to measure. The PULSE rate during and after a bout of exercise serves as a good proxy of this measurement.
Regulation of sport Sports medicine’s role is to minimise hazards for participants by, for example, framing rule-changes which forbid collapsing the scrum, which has reduced the risk of neck injury in rugby; and in the detection of the use of drugs taken to enhance athletic performance. Such attempts to gain an edge in competition undermine the sporting ideal and are banned by leading sports regulatory bodies. The Olympic Movement Anti-Doping Code lists prohibited substances and methods that could be used to enhance performance. These include some prohibited in certain circumstances as well as those completely banned. The latter include:
stimulants such as AMPHETAMINES, bromantan, ca?eine, carphedon, COCAINE, EPHEDRINE and certain beta-2 agonists.
NARCOTICS such as DIAMORPHINE (heroin), MORPHINE, METHADONE HYDROCHLORIDE and PETHIDINE HYDROCHLORIDE.
ANABOLIC STEROIDS such as methandione, NANDROLONE, stanazol, TESTOSTERONE, clenbuterol, androstenedone and certain beta-2 agonists.
peptide HORMONES, mimetics and analogues such as GROWTH HORMONE, CORTICOTROPHIN, CHORIONIC GONADOTROPHIC HORMONE, pituitary and synthetic GONADOTROPHINS, ERYTHROPOIETIN and INSULIN. (The list produced above is not comprehen
sive: full details are available from the governing bodies of relevant sports.) Among banned methods are blood doping (pre-competition administration of an athlete’s own previously provided and stored blood), administration of arti?cial oxygen carriers or plasma expanders. Also forbidden is any pharmacological, chemical or physical manipulation to affect the results of authorised testing.
Drug use can be detected by analysis of the URINE, but testing only at the time of competition is unlikely to detect drug use designed to enhance early-season training; hence random testing of competitive athletes is also used.
The increasing professionalism and competitiveness (among amateurs and juveniles as well as professionals) in sports sometimes results in pressures on participants to get ?t quickly after injury or illness. This can lead to
players returning to their activity before they are properly ?t – sometimes by using physical or pharmaceutical aids. This practice can adversely affect their long-term physical capabilities and perhaps their general health.... sports medicine
Constipation is usually due to an underlying condition which requires primary treatment: i.e. anaemia.
The habit of taking purgatives lessens ability of the bowel to do its work. Gentler-acting remedies are advised: Isphagula (Psyllium seeds, light). In prescriptions, it is good practice to include a remedy for the liver (Barberry, Wahoo) and the digestive system (Dandelion, Liquorice). For constipation of pregnancy – see PREGNANCY.
Alternatives. Senna. 1-2 teaspoons leaves or 5-7 pods to cup cold water left to stand overnight. Combined tea. Equal parts: Senna leaves, Chamomile flowers, Fennel seeds. 1-2 teaspoons to each cup boiling water; infuse 15 minutes. 1 cup, evening.
Psyllium seeds (Ispaghula, pale) 1, 2, 3 or more teaspoons aided down with sips of water, morning or evening.
Decoctions. Any of the following: Black root, Blue Flag, Buckthorn, Cascara sag, Dandelion root, Turkey Rhubarb, Wahoo, Yellow Dock.
Tablets/capsules. Dandelion. Calamus. Blue Flag. Seaweed and Sarsaparilla. Turkey Rhubarb. Damiana. Senokot.
“Natural Herb Tablet”: Holy Thistle 60mg; Aloes BP 50mg; Fennel powder BPC 15mg; Myrrh powder BPC 15mg; Extract Skullcap 10mg; Powdered Valerian BPC 30mg; Powdered Lime flowers BPC 1949 30mg. Two or more tablets as necessary. Variations of this formula are on sale throughout Europe and the UK.
Powders. Combinations. Alternatives. (1) Turkey Rhubarb, with trace Cayenne. Use powder, or rubbed Rhubarb root with aid of kitchen grater.
(2) Equal parts: Barberry, Liquorice, Senna pods.
(3) Turkey Rhubarb 6; Slippery Elm 1; Liquorice 1. (4) Senna 70; Buckthorn 5; Fennel 10; Mate 5; Elder 5; Psyllium (pale) 5. Dose: 500-750mg (2-3 00 capsules or one-third-half a teaspoon) once or twice daily, as necessary.
Tinctures. Formulae: (1) Turkey Rhubarb, with trace of Capsicum. (2) Dandelion 2; Cascara sag, 2; Barberry 2; Liquorice 1; Tincture Ginger half. Half-2 teaspoons in hot water, evening.
Standard sales. A large number of preparations are on sale including Potter’s “Lion Cleansing Herbs”, Monastery herbs, Priory herbs. Fybogel Orange to increase bulk in colon. Regulan, for high fibre regimen. Enema or gravity douche: half an ounce Chamomile flowers to 2 pints boiling water allowed to cool. Inject warm; repeat twice weekly until normal function is established.
Diet. Milk-free diet often curative. Teaspoon powdered Agar Agar with meals once or twice daily. Prunes soaked overnight. Yoghurt. Crude black molasses. Increase fibre-foods. Dandelion coffee.
Hay Diet. Impressive results reported.
Supplementation. Cod Liver oil.
Vitamins: A. B-complex, Thiamine, Niacin, C. P (bioflavonoids). Minerals: Calcium. Potassium. Zinc. ... constipation