Question

What should you write about?

Diet is high in fat, saturated fat, meat, low in fiber; you have a family history of heart disease; you are overweight - You may want to write about Heart Disease

You have a family history of Type I or Type II Diabetes - You may want to write about it.

Your diet is high in fat, saturated fat, low in fiber, low in fruits/vegetables; you have family members who have had cancer (any kind); you are overweight - You may want to write about Cancer.

Your diet is high in sodium, low in calcium, low in magnesium, low in potassium; you have family members how have high blood pressure - You may want to write about Hypertension

You are overweight or you have close family members who are overweight - You may want to write about Obesity.

Your calcium intake is low, you are female, you don't exercise; you have family members (mother, grandmother, aunt) who have osteoporosis - You may want to write about Osteoporosis.

Write a 2 page paper (double spaced, 12 pt font, 1" margins) analyzing your diet and your risk for chronic disease.

Answer 1

1. Cardiovascular disease
   It is now generally agreed that diet governs many situations favouring the onset of "heart-disease", particularly coronary heart disease. Of all the factors associated with CHD (e.g., plasma cholesterol, high blood pressure, cigarette smoking, lack . of physical activity) plasma cholesterol has a very high statistical significance with the incidence of CHD. The risk of CHD appears to increase as the plasma cholesterol concentration rises.
   Various studies have supported the role of elevated blood levels of cholesterol and low-density lipoproteins (LDL) in the development of atherosclerosis. Geographical studies have shown that there is no population in whom CHD is common that does not have a relatively high mean level of plasma total cholesterol (TC) in adults. These observations have been reinforced by metabolic studies.
   Also, trials of the effect of dietary changes on CHD have suggested that altering the fatty acid composition of the diet in favour of greater intake of polyunsaturated fatty acids (PUFA) and less intake of saturated fats, while restricting the intake of fat calories to less than 30 per cent of the. total calories may lower the risk that CHO will subsequently develop.
   The evidence of association is now so strong for cholesterol and CHO that the WHO Expert Committee (1982) considered its effect to be "causal" in populations although this cannot be claimed yet for individuals. The WHO Expert Committee concludes that there is a well established triangular relationship between habitual diet, blood cholesterol levels and CHO.
2. Diabetes
   In a diabetic, there is impaired metabolism of glucose in the body, which leads to an excess of glucose in blood and urine. Insulin helps in checking and maintaining the level of glucose in the blood. Insulin deficiency leads to accelerated utilization of energy reserves from fat stores. The fatty acids are oxidized by the liver to ketone bodies. Excess of ketone bodies leads to their accumulation in urine. This condition is known as ketoacidosis and can result in diabetic coma. Due
   to insulin deficiency excess of fatty acids are converted to triglycerides. In diabetes, these accumulate in the blood. Insulin is also important for the synthesis of proteins and deficiency of insulin leads to muscle wasting.
   Studies in England showed that diabetics ate an average of 1000 kcal per day more than non-diabetics. It was also found that most diabetics were in non-manual occupations than non-diabetics. And the diet of diabetics did not appear to differ in any marked way from that of non-diabetics, except in quantity. There is no sound evidence that any specific dietary factor is diabetogenic.
   It has been suggested that deficiencies of trace elements such as chromium, copper and zinc may play a role in the pathogenesis of diabetes mellitus, but clinical evidence is lacking.
   Malnutrition-related diabetes mellitus has recently attracted attention. Protein deficiency may be involved in the pathogenesis of some forms of diabetes. Exessive consumption of alcohol can increase the risk of diabetes by damaging the pancreas and liver and by promoting obesity.
3. Cancer
   It is postulated that 80 per cent of cancers may be due to environmental factors, and some dietetic factors may be involved. Existing knowledge is reviewed as below:
   (a) Dietary fat:
   Population surveys have shown a strong positive correlation between cancer colon and dietary intake of fat. It has been suggested that the high fat intake accounts for the high incidence of colon cancer in Western communities.
   In Japan, recent increases in fat consumption have been associated with a striking increase in rates of colon cancer. Dietary fat is believed to increase the secretion of bile acids in the bowl which is then metabolized by bacterial flora into carcinogen or co-carcinogens. However, no known carcinogen has yet been identified from faeces and the evidence is thus incomplete.
   A positive correlation between per capita consumption of dietary fat and breast cancer rates. has also been noted. A reduction in dietary fat may alter the risk of breast cancer, perhaps by increasing oestrogen production or prolactin release.
   (b) Dietary fibre:
   Several studies indicate that the risk of colon cancer is inversely related to the consumption of dietary fibre, which may protect against intestinal carcinogens or precursors by dilutional or other effects. Although the available epidemiological data are not entirely consistent, the weight of evidence generally supports the hypothesis that fibre protects against colon cancer.
   (c) Micronutrients:
   Micronutrients may also have a protective influence since cancers of the lung and several other sites have been associated with a low intake of vitamin A.
   The risk of stomach cancer has been related to a deficiency of
   vitamin C, which may act by inhibiting the formation of carcinogenic nitrosamines in the stomach. Trace elements (e.g., selenium) have also been implicated in the aetiology of cancer.
   (d) Food additives and contaminants:
   Food additives and contaminants (e.g., preservatives, artificial colours,· artificial sweeteners, pesticides, flavours, anti-oxidants) have always been under suspicion as possible carcinogens in their long-term effects.
   Food processing involves exposure to high temperature, oxidation, polymerization, production of nitrosamines, polycyclic aromatic hydrocarbons, etc which are injurious to health. It is thought in some quarters that nitrosamines are responsible for certain types of gastric carcinoma.
   Saccharin and cyclamate are weak bladder carcinogens or co-carcinogens in laboratory animals, but the risk in man is very small if present at all.
   Aflatoxin is a carcinogenic metabolite. Coffee intake has been associated
   with bladder cancer and recently with pancreatic cancer but causal relationships have not been established. The mutagenic properties of food additives are under constant surveillance.
   (e) Alcohol:
   Heavy drinking increases the risk of liver cancer. ·It is estimated that alcohol contributes to about 3 per cent of all cancer deaths. Some recent studies have suggested that beer consumption may be related to cancer rectum, but the association has not been confirmed.
4. Obesity:
   In richer countries and some developing countries, obesity is a health problem. The connection between severe obesity and premature death from diabetes, hypertension and CHO is well established.
   The basic cause of obesity is overnutrition. A diet containing more energy than needed may lead to prolonged postprandial hyperlipidaemia and deposition of triglycerides in adipose tissue resulting
   in obesity.
   It is known that a relative insulin resistance takes place in obesity in peripheral tissues, mainly adipose tissues, while the insulin secretion is normal or increased. The demonstrated reduction in the sensitivity to insulin of the large adipocyte can be attributed to the decreased affinity of the insulin receptors or a reduction in their number in the cell membrane. Through a feedback mechanism, the insulin secretion is stepped up', thus leading to a state of hyperinsulinism.
   From a practical point of view, all hypotheses concerning the genesis of obesity could be put down to over-nutrition, to a hyper-energy food intake. This is a sound basis for preventive and therapeutic recommendations.