|Speaker:||Artemis P. Simopoulos, Center for Genetics, Nutrition, and Health|
|Topic:||“Genetic Variation and Nutrition”|
The meeting scheduled February 16, 1996, was cancelled by President Coates because heavy snow would have prevented the speaker G. Charmaine Gilbreath and many members from attending. The President Mr. Coates called the 2056th meeting to order at 8:20 p.m. on March 1, 1996. The Recording Secretary read the minutes of the 2055th meeting and they were approved.
The President introduced Artemis P. Simopoulos of the Center for Genetics, Nutrition, and Health, Washington, DC, to discuss “Genetic Variation and Nutrition”.
The health of the individual depends on genetic endowment, age, environmental exposure and knowledge. Hippocrates in the 5th century BCE advocated what would be called positive health, regimens of diet, exercise, and prevention. Modern research shows why these are important precepts to follow, although his ideas about positioning of houses and influences of prevailing winds are probably not as important as he had thought. As part of the influence of environment on health, the available food supply must be considered along with the genetics of the individual. We are not only what we eat, but also what we are genetically predisposed to metabolize. It is important that the variation among individuals be taken into account when recommendations for healthy diet are formulated and publicized.
The transition of humans from hunting-gathering to agriculture for food production has been been influencing our genetics for only the last 10,000 years. Comparing paleolithic and current diets, as a percentage of calories consumed protein has decreased from 34 to 12%, carbohydrate has changed little from 45 to 46%, while fat has increased from 21 to 42%. The amount of fiber and complex carbohydrates in the diet has decreased significantly. The amount of sodium has increased by a factor of 3 to 10, while the amounts of calcium and ascorbate have decreased by factors 2 to 4. Saturated fatty acids constituted less than 100f calories from 4 million to 100,000 years ago, and has now risen to approximately 20%. We are consuming a diet that is not consistemt with our biochemical and evolutionary predisposition.
While total fat remained constant at approximately 20% of calories till about 1800, it has doubled since then. Of these fats, trans-unsaturated fatty acids that were previously a negligible dietary component are now significant, and omega-6 unsaturated fatty acids have increased while omega-3 unsaturated fatty acids have decreased. Omega-3 unsaturated fatty acids in the diet can reduce platelet aggregation, blood viscosity, blood pressure and cardiac arhythmias, and increase bleed time. Trans-unsaturated fatty acids are physically similar to saturated fatty acids in their extended conformation. The principal good points of the trans-unsaturated fatty acids are that they don't oxidize as easily so they cook or fry better. In the diet however they can decrease serum testosterone levels, while increasing serum LDL (low density lipoprotein) cholesterol levels, platelet aggregation, and sperm abnormalities. In an American 1800 calorie diet, 5% of the calories may be trans unsaturated fatty acids.
Advances in genetics and molecuar biology indicate that susceptibility to chronic diseases such as coronary artery disease (CAD), hypertension, diabetes, obesity, osteoporosis, alcoholism and cancer is genetically determined. Studies have shown that 50% of the variance in plasma choleterol is genetically determined and 3060% of the variance in blood pressure is genetically determined. For fibrinogen, an independent risk factor for CAD, 1550% of the variance is genetically determined. In the UK population the variance for the fibrinogen level is 15%, in the Hawaiian population it is 50%. Among Australians, 75% of the variance in bone density is genetically determined. Genetic studies have demonstrated remarkable genetic diversity in human populations, and more extensive variability has been described at the DNA level. Nutritional health depends on the interaction of diet and the gennetically controlled asspects of digestion, absorption, distribution, transformation, storage and excretion. Genetic variation influences the response to diet. Therefore, to be successful, dietary interventions must be based on the frequency of genes in the population whose effects we are attempting to control or modify.
Consider coronary heart disease, the 1st most important risk factor is a
family history of early heart disease. The 14th most important factor is
homocysteinuria which can be controlled by dietary folic acid. The 4 most
important environmental factors are (1) smoking, (2) sedentary life style and
lack of aerobic exercise, (3) diet with high consumption of saturated fats and
low consumption of omega-3 unsaturated fatty acids, and (4) psychosocial
factors of type A personality and social class. Among more than 20 genetic
factors, one of the most important is which types of apolipoprotein, A2, A3, or
A4, an individual is endowed with. The breakdown of these phenotypes within
the population is as follows:
Each of these phenotypes has a different basic LDL cholesterol level. Dietary oat bran helps lowers blood cholesterol in the A3/A3 phenotypes, but not in the A3/A4 or A4/A4 pheotypes. As another example, bone mineral density homozygotes do not respond to changes in dietary calcium level as much as heterozygotes do. Modern dietary advice must obviously take into account knowledge of an individual's genotype. Interdisciplinary efforts by nutritionists and geneticists are needed to identify individuals susceptible to chronic disease without nutritional intervention early in life.
Ms. Simopoulos kindly answered questions from the audience. The President thanked the speaker on behalf of the Society, announced the speaker for the next meeting, restated the parking policy, and adjourned the 2056th meeting at 9:37 p.m.
|John S. Garavelli|
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