There are 3 types of such conditions.
In the 1st, there are no tumours present but the condition carries an increased risk of cancer.
In the 2nd, there are noncancerous tumours that tend to become cancerous or are associated with the development of cancerous tumours elsewhere.
The 3rd type comprises disorders which have irregular features from the beginning but do not always become fully cancerous.
Nutritional Profile Energy value (calories per serving): Low Protein: Low Fat: Low Saturated fat: Low Cholesterol: None Carbohydrates: High Fiber: Moderate Sodium: Low Major vitamin contribution: Vitamin C Major mineral contribution: Calcium
About the Nutrients in This Food Blueberries have some protein and a little fat. They have no starch but do contain sugars and dietary fiber—primarily pectin, which dissolves as the fruit matures—and lignin in the seeds. (The difference between blueber- ries and huckleberries is the size of their seeds; blueberries have smaller ones than huckleberries.) One-half cup fresh blueberries has 1.5 g dietary fiber and 9.5 mg. vitamin C (13 percent of the R DA for a woman, 11 percent of the R DA for a man).
The Most Nutritious Way to Serve This Food Fresh, raw, or lightly cooked.
Buying This Food Look for: Plump, firm dark-blue berries. The whitish color on the ber- ries is a natural protective coating. Avoid: Baskets of berries with juice stains or liquid leaking out of the berries. The stains and leaks are signs that there are crushed (and possibly moldy) berries inside.
Storing This Food Cover berries and refrigerate them. Then use them in a day or two. Do not wash berries before storing. The moisture increases the chance that they will mold in the refrigerator. Also, handling the berries can damage them, tearing cells and releas- ing enzymes that will destroy vitamins. Do not store blueberries in metal containers. The anthocyanin pigments in the berries can combine with metal ions to form dark, unattractive pigment/metal compounds that stain the containers and the berries.
Preparing This Food R inse the berries under cool running water, then drain them and pick them over carefully to remove all stems, leaves, and hard (immature) or soft (over-ripe) berries.
What Happens When You Cook This Food Cooking destroys some of the vitamin C in fresh blueberries and lets water-soluble B vitamins leach out. Cooked berries are likely to be mushy because heat dissolves the pectin inside. Blueberries may also change color when cooked. The berries are colored with blue anthocyanin pigments. Ordinarily, anthocyanin-pigmented fruits and vegetables turn red- dish in acids (lemon juice, vinegar) and deeper blue in bases (baking soda). But blueberries also contain yellow pigments (anthoxanthins). In a basic (alkaline) environments, as in a batter with too much baking soda, the yellow and blue pigments will combine, turning the blueberries greenish blue. Adding lemon juice to a blueberry pie stabilizes these pigments; it is a practical way to keep the berries a deep, dark reddish blue.
How Other Kinds of Processing Affect This Food Canning and freezing. The intense heat used in canning the fruit or in blanching it before freezing reduces the vitamin C content of blueberries by half.
Medical Uses and/or Benefits Anticancer activity. According to the U.S. Department of Agriculture, wild blueberries rank first among all fruits in antioxidant content; cultivated blueberries (the ones sold in most food markets) rank second. Antioxidants are natural chemicals that inactivate free radicals, molecule fragments that can link together to form cancer-causing compounds. Several ani- mal studies attest to the ability of blueberries to inhibit the growth of specific cancers. For example, in 2005, scientists at the University of Georgia reported in the journal Food Research International that blueberry extracts inhibited the growth of liver cancer cells in laboratory settings. The following year, researchers at Rutgers University (in New Jersey) delivered data to the national meeting of the American Chemical Society from a study in which laboratory rats fed a diet supplemented with pterostilbene, another compound extracted from blueber- ries, had 57 percent fewer precancerous lesions in the colon than rats whose diet did not contain the supplement. The findings, however, have not been confirmed in humans. Enhanced memory function. In 2008, British researchers at the schools of Food Biosciences and Psychology at the University of Reading and the Institute of Biomedical and Clinical Sciences at the Peninsula Medical School (England) reported that adding blueberries to one’s normal diet appears to improve both long-term and short-term memory, perhaps because anthocyanins and flavonoids (water-soluble pigments in the berries) activate signals in the hippocampus, a part of the brain that controls learning and memory. If confirmed, the data would support the role played by diet in maintaining memory and brain function. Urinary antiseptic. A 1991 study at the Weizmann Institute of Science (Israel) suggests that blueberries, like cr anber r ies, contain a compound that inhibits the ability of Escherichia coli, a bacteria commonly linked to urinary infections, to stick to the wall of the bladder. If it cannot cling to cell walls, the bacteria will not cause an infection. This discovery lends some support to folk medicine, but how the berries work, how well they work, or in what “dos- ages” remains to be proven.
Adverse Effects Associated with This Food Allergic reaction. Hives and angiodemea (swelling of the face, lips, and eyes) are common allergic responses to berries, virtually all of which have been reported to trigger these reac- tions. According to the Merck Manual, berries are one of the 12 foods most likely to trigger classic food allergy symptoms. The others are chocolate, corn, eggs, fish, legumes (peas, lima beans, peanuts, soybeans), milk, nuts, peaches, pork, shellfish, and wheat (see wheat cer ea ls).... blueberries
Acute gastritis is an in?ammatory reaction of the gastric mucosa to various precipitating factors, ranging from physical and chemical injury to infections. Acute gastritis (especially of the antral mucosas) may well represent a reaction to infection by a bacterium called Helicobacter pylori. The in?ammatory changes usually go after appropriate antibiotic treatment for the H. pylori infection. Acute and chronic in?ammation occurs in response to chemical damage of the gastric mucosa. For example, REFLUX of duodenal contents may predispose to in?ammatory acute and chronic gastritis. Similarly, multiple small erosions or single or multiple ulcers have resulted from consumption of chemicals, especialy aspirin and antirheumatic NONSTEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS).
Acute gastritis may cause anorexia, nausea, upper abdominal pain and, if erosive, haemorrhage. Treatment involves removal of the o?ending cause.
Chronic gastritis Accumulation of cells called round cells in the gastric mucosal characterises chronic gastritis. Most patients with chronic gastritis have no symptoms, and treatment of H. pylori infection usually cures the condition.
Atrophic gastritis A few patients with chronic gastritis may develop atrophic gastritis. With or without in?ammatory change, this disorder is common in western countries. The incidence increases with age, and more than 50 per cent of people over 50 may have it. A more complete and uniform type of ATROPHY, called ‘gastric atrophy’, characterises a familial disease called PERNICIOUS ANAEMIA. The cause of the latter disease is not known but it may be an autoimmune disorder.
Since atrophy of the corpus mucosa results in loss of acid- and pepsin-secreting cells, gastric secretion is reduced or absent. Patients with pernicious anaemia or severe atrophic gastritis of the corpus mucosa may secrete too little intrinsic factor for absorption of vitamin B12 and so can develop severe neurological disease (subacute combined degeneration of the spinal cord).
Patients with atrophic gastritis often have bacterial colonisation of the upper alimentary tract, with increased concentration of nitrite and carcinogenic N-nitroso compounds. These, coupled with excess growth of mucosal cells, may be linked to cancer. In chronic corpus gastritis, the risk of gastric cancer is about 3–4 times that of the general population.
Postgastrectomy mucosa The mucosa of the gastric remnant after surgical removal of the distal part of the stomach is usually in?amed and atrophic, and is also premalignant, with the risk of gastric cancer being very much greater than for patients with duodenal ulcer who have not had surgery.
Stress gastritis Acute stress gastritis develops, sometimes within hours, in individuals who have undergone severe physical trauma, BURNS (Curling ulcers), severe SEPSIS or major diseases such as heart attacks, strokes, intracranial trauma or operations (Cushing’s ulcers). The disorder presents with multiple super?cial erosions or ulcers of the gastric mucosa, with HAEMATEMESIS and MELAENA and sometimes with perforation when the acute ulcers erode through the stomach wall. Treatment involves inhibition of gastric secretion with intravenous infusion of an H2-receptorantagonist drug such as RANITIDINE or FAMOTIDINE, so that the gastric contents remain at a near neutral pH. Despite treatment, a few patients continue to bleed and may then require radical gastric surgery.
Gastric ulcer Gastric ulcers were common in young women during the 19th century, markedly fell in frequency in many western countries during the ?rst half of the 20th century, but remained common in coastal northern Norway, Japan, in young Australian women, and in some Andean populations. During the latter half of this century, gastric ulcers have again become more frequent in the West, with a peak incidence between 55 and 65 years.
The cause is not known. The two factors most strongly associated with the development of duodenal ulcers – gastric-acid production and gastric infection with H. pylori bacteria – are not nearly as strongly associated with gastric ulcers. The latter occur with increased frequency in individuals who take aspirin or NSAIDs. In healthy individuals who take NSAIDs, as many as 6 per cent develop a gastric ulcer during the ?rst week of treatment, while in patients with rheumatoid arthritis who are being treated long term with drugs, gastric ulcers occur in 20–40 per cent. The cause is inhibition of the enzyme cyclo-oxygenase, which in turn inhibits the production of repair-promoting PROSTAGLANDINS.
Gastric ulcers occur especially on the lesser curve of the stomach. The ulcers may erode through the whole thickness of the gastric wall, perforating into the peritoneal cavity or penetrating into liver, pancreas or colon.
Gastric ulcers usually present with a history of epigastric pain of less than one year. The pain tends to be associated with anorexia and may be aggravated by food, although patients with ‘prepyloric’ ulcers may obtain relief from eating or taking antacid preparations. Patients with gastric ulcers also complain of nausea and vomiting, and lose weight.
The principal complications of gastric ulcer are haemorrhage from arterial erosion, or perforation into the peritoneal cavity resulting in PERITONITIS, abscess or ?stula.
Aproximately one in two gastric ulcers heal ‘spontaneously’ in 2–3 months; however, up to 80 per cent of the patients relapse within 12 months. Repeated recurrence and rehealing results in scar tissue around the ulcer; this may cause a circumferential narrowing – a condition called ‘hour-glass stomach’.
The diagnosis of gastric ulcer is con?rmed by ENDOSCOPY. All patients with gastric ulcers should have multiple biopsies (see BIOPSY) to exclude the presence of malignant cells. Even after healing, gastric ulcers should be endoscopically monitored for a year.
Treatment of gastric ulcers is relatively simple: a course of one of the H2 RECEPTOR ANTAGONISTS heals gastric ulcers in 3 months. In patients who relapse, long-term inde?nite treatment with an H2 receptor antagonist such as ranitidine may be necessary since the ulcers tend to recur. Recently it has been claimed that gastric ulcers can be healed with a combination of a bismuth salt or a gastric secretory inhibitor
for example, one of the PROTON PUMP INHIBITORS such as omeprazole or lansoprazole
together with two antibiotics such as AMOXYCILLIN and METRONIDAZOLE. The long-term outcome of such treatment is not known. Partial gastrectomy, which used to be a regular treatment for gastric ulcers, is now much more rarely done unless the ulcer(s) contain precancerous cells.
Cancer of the stomach Cancer of the stomach is common and dangerous and, worldwide, accounts for approximately one in six of all deaths from cancer. There are marked geographical di?erences in frequency, with a very high incidence in Japan and low incidence in the USA. In the United Kingdom around 33 cases per 100,000 population are diagnosed annually. Studies have shown that environmental factors, rather than hereditary ones, are mainly responsible for the development of gastric cancer. Diet, including highly salted, pickled and smoked foods, and high concentrations of nitrate in food and drinking water, may well be responsible for the environmental effects.
Most gastric ulcers arise in abnormal gastric mucosa. The three mucosal disorders which especially predispose to gastric cancer include pernicious anaemia, postgastrectomy mucosa, and atrophic gastritis (see above). Around 90 per cent of gastric cancers have the microscopic appearance of abnormal mucosal cells (and are called ‘adenocarcinomas’). Most of the remainder look like endocrine cells of lymphoid tissue, although tumours with mixed microscopic appearance are common.
Early gastric cancer may be symptomless and, in countries like Japan with a high frequency of the disease, is often diagnosed during routine screening of the population. In more advanced cancers, upper abdominal pain, loss of appetite and loss of weight occur. Many present with obstructive symptoms, such as vomiting (when the pylorus is obstructed) or di?culty with swallowing. METASTASIS is obvious in up to two-thirds of patients and its presence contraindicates surgical cure. The diagnosis is made by endoscopic examination of the stomach and biopsy of abnormal-looking areas of mucosa. Treatment is surgical, often with additional chemotherapy and radiotherapy.... stomach, diseases of
There are 2 main types of cervical cancer: the squamous type is the most common and is thought to be associated with the human papilloma virus, acquired during sexual intercourse. Factors that predispose to this type of cancer are smoking, starting to have sex at an early age, and having many sexual partners.
The second, rarer, type of cervical cancer, adenocarcinoma, sometimes occurs in women who have never had sexual intercourse. Its causes are unclear.
Symptoms do not develop until the condition is advanced, when there is vaginal bleeding or a bloodstained discharge at unexpected times, and pain if the cancer has spread within the pelvis.
Following an abnormal smear test result, colposcopy or a cone biopsy may be carried out to diagnose the condition.
A localized early cancer may be destroyed by electrocoagulation, diathermy, laser treatment, or cryosurgery.
If the cancer has spread into the cervical canal, a cone biopsy may be sufficient to remove all the diseased tissue.
In more advanced cases affecting the pelvic organs, radiotherapy may be given.
Radical surgery, in which the bladder, vagina, cervix, uterus, and rectum are removed, may be recommended in certain cases.... cervix, cancer of
In Britain, for instance, preventive medicine is usually taken to encompass a range of activities whose purpose is:
to reduce the chance of a person contracting a disease or becoming disabled.
to identify either an increased susceptibility to develop a disease, or an early manifestation of a disease at a stage which will still allow treatment to be e?ective. The American College of Preventive Medi
cine (1983) de?ned it as ‘a specialised ?eld of medical practice composed of distinct disciplines which utilise skills focusing on the health of de?ned populations in order to promote and maintain health and well-being and to prevent disease, disability and premature death’.
However de?ned, the spectrum of activities encompassed by preventive medicine is wide and includes actions, such as counselling about lifestyle, where there may not be a clear cut-o? between a preventive and a curative act. For example, advice about smoking and exercise to a recent victim of a myocardial infarction (see under HEART, DISEASES OF) is both essential to treatment and preventive against a future attack. Action aimed at a whole population – such as the addition of ?uoride to drinking-water to protect against dental caries (see under TEETH, DISORDERS OF) – is part of a population-based public-health strategy but would also be widely regarded as preventive medicine.
A common and widely accepted classi?cation of preventive medicine is as follows:
Primary prevention which aims at the complete avoidance of a disease (for example, by immunising a child against an infectious disease – see IMMUNISATION).
Secondary prevention which aims at detecting and curing a disease at an early stage before it has caused any symptoms. This requires ‘screening’ procedures to detect either the early pre-symptomatic condition, or a risk factor which may lead to it. (An example of the former is cervical cytology, where a sample of cells is scraped from the cervix of the UTERUS and examined microscopically for abnormality.
An example of the latter is CHOLESTEROL measurement as part of assessing an individual’s risk of developing ischaemic heart disease (see under HEART, DISEASES OF). If it is signi?cantly raised, dietary or drug treatment can be advised.)
Tertiary prevention aims at minimising the consequences for a patient who already has the disease (e.g. advising people to take more exercise and stop smoking after a heart attack).
Many prefer to limit the term ‘preventive medicine’ to primary and secondary prevention, emphasising the focus on risk-reducing interventions targeted at ‘well’ individuals. Others prefer the wider emphasis because of the importance of a preventive approach in reducing further disability by recognising and treating symptoms early. This can be particularly important in older people, where, for example, vigorous treatment of an orthopaedic problem can enable the patient to maintain physical mobility with all the bene?ts to health that brings. Whether primary, secondary or tertiary prevention, some form of screening question or test is normally necessary to identify a problem.
The range and extent of opportunities for prevention are expanding as research identi?es the causes of diseases and more e?ective treatment becomes feasible. Inevitably there is economic and political debate about the cost-e?ectiveness of prevention versus cure, as well as about the ETHICS. The situation varies in relation to the natural history of the speci?c disease. Some conditions can easily be prevented but once contracted cannot be cured
(e.g. RABIES); others are easily cured but are not yet preventable.
Screening Screening involves carrying out tests either to identify a treatable disease at a very early stage, before it has caused symptoms or damage; or to identify a risk factor which can lead to a disease. The tests might be by simple questioning (e.g. ‘Do you smoke cigarettes?’ – this predicts a considerable increase in the risk of chronic bronchitis, heart disease, bronchial cancer and many other diseases, and enables targeted advice and help to stop smoking to be given). Other screening tests involve carrying out complex special investigations such as blood tests or the microscopic investigations of cells – for example, for precancerous changes.
Many conditions can be identi?ed at an early stage before they cause symptoms or signs of disease and in time for e?ective treatment to be carried out. Inevitably, some of the screening tests proposed can be expensive (particularly if used in large populations), painful or inaccurate and may not improve the results of treatment. Screening can also provoke considerable anxiety in those waiting for tests or results. Therefore, over the years considerable research has been carried out into the appropriateness and ethics of screening, and the World Health Organisation in 1968 identi?ed a set of rules for evaluating screening tests:
The condition sought should be an important health problem, for which there should be an accepted treatment for patients with recognised disease.
Facilities for diagnosis and treatment should be available if a case is found.
The screening test or examination must be suitable and valid. A false positive test will cause massive anxiety and also considerable expense in proving that there is no disease. Similarly, false negatives can lead people to be reassured and to ignore serious symptoms until too late. If large numbers of positive tests or false positives occur during a screening programme, health services can be swamped.
The test, and any treatment as a possible result, should be acceptable. For example, there is little point in screening for a fetal abnormality which, if found, would lead to a recommendation for termination if the mother will refuse it on religious or moral grounds.
Screening tests also need to be considered from an economic perspective and the cost of case-?nding (including diagnosis and treatment of patients diagnosed) balanced in relation to possible expenditure on medical care as a whole.
Finally the programme should re?ect the natural history of the disease, and case-?nding should normally be a continuing process and not a ‘once for all’ project. If these rules are followed, considerable
bene?ts can result from well-planned and well-managed screening programmes, and they form an important part of any health-care system. The extent to which manipulation of genetic material will be added to more traditional approaches such as counselling, immunisation and drug treatment cannot yet be predicted but, as time goes by, it is often likely to be ethical and social controls which limit developments rather than technical and scienti?c limits.... preventive medicine
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