Essentials of Health

Wednesday, June 29, 2005

Low zinc intake may influence exercise performance

In a recent study published in the May 2005 American Journal of Clinical Nutrition, researchers analyzed the effect of restricted dietary zinc on metabolic responses during exercise. Certain zinc-containing enzymes are believed to regulate energy expenditure, but there is limited data on the role of zinc in promoting physiologic function during exercise.

Male study participants received a low-zinc diet (3.8 mg/day) for 9 weeks and after a 6 week wash-out period, the same diet supplemented with 15 mg of zinc for an additional 9 weeks. Using two types of stationary exercise bike tests, researchers tested the subjects' cardiovascular fitness during the second and ninth week of each diet period.

Low dietary zinc resulted in a significant decline in work capacity and performance in the subjects when compared to results during the supplemented period. Blood tests confirmed that the low-zinc regimen resulted in reduced blood zinc concentration and retention, and lowered the activity of specific zinc-dependent enzymes. The lowered activity of these enzymes impacts exercise performance by compromising the body's ability to regulate the increase in blood carbon dioxide that is produced during exercise. These results suggest that adequate zinc is necessary for peak performance and metabolic response during exercise.

Wednesday, June 22, 2005

Inadequate magnesium intake is associated with heart disease risk

Current dietary guidelines recommend a minimum magnesium intake of 310-420 mg per day to maintain health and reduce cardiovascular risk. Recent evidence from both clinical and animal studies suggest that magnesium may be associated with inflammatory processes. In a recent study published in the June volume of the Journal of the American College of Nutrition, researchers determined that dietary magnesium consumption is associated with C-reactive protein (CRP), a marker of inflammation. Participants included a large nationally representative sample of U.S. adults.

Among the U.S. adults, 68% consumed less than the recommended daily allowance (RDA) of magnesium, and 19% consumed less than 50% of the RDA. Adults who consumed less than the RDA of magnesium were 1.48-1.75 times more likely to have elevated CRP than adults who consumed greater levels than the RDA. Overweight adults over age 40 consuming less than 50% RDA for magnesium were 2.24 times more likely to have elevated CRP than adults getting more than the RDA.

Most Americans consume magnesium at levels below the RDA. Since individuals with intakes below the RDA are more likely to have elevated CRP, inadequate intakes of magnesium may contribute to cardiovascular disease risk.

Tuesday, June 14, 2005

Linolenic acid reduces atherosclerotic plaque

Alpha-linolenic acid is an omega-3 fatty acid found in salad dressings, flax and canola oil. A study published in the June 7 2005 issue of the journal Circulation has shown a decreased prevalence of calcified atherosclerotic plaque in the coronary arteries of individuals whose diets included higher amounts of alpha-linolenic acid.

Data from over 2,000 participants in the National Heart, Lung, and Blood Institute Family Heart Study (FHS) were included in this study. The presence and extent of coronary artery calcified atherosclerotic plaque was measured by CT scans during a 7 yr follow up.

Alpha-linolenic intake ranged from 170 milligrams to 3.48 grams per day. The researchers found an inverse association between alpha-linolenic acid consumption and the presence of calcified atherosclerotic plaque. Individuals in the highest 20 percent of alpha-linolenic acid intake experienced a 62 percent lower risk of having the plaques than those with the lowest intakes.

Researchers note that alpha-linolenic acid is a precursor of eicosapentaenoic acid (EPA) which reduces inflammation by inhibiting arachidonic acid metabolism. Alpha-linolenic acid may, therefore, reduce coronary calcification risk by its anti-inflammatory properties.

Wednesday, June 08, 2005

Nutritional supplements improve symptoms of peripheral vascular disease

A new study published in the June 2005 issue of the Journal of Nutrition indicates that a combination of nutrients known to help protect against cardiovascular disease also helps to improve the risk factors and symptoms of peripheral vascular disease (PVD). Peripheral vascular disease is a blockage of the arteries in the legs caused by atherosclerosis. Due to inadequate blood supply, the condition often causes cramping pain in the legs that occurs during walking.

Sixty men with PVD were divided into two groups. The treatment group received a daily fortified milk product that contained 200 milligrams eicosapentaenoic acid (EPA), 130 milligrams docosahexaenoic acid (DHA), 5.12 grams oleic acid, 150 micrograms folic acid, and vitamins A, B6, D, and E. The control group received skimmed milk with added vitamins A and D. Blood samples were drawn at the beginning of the 12 month study and every three months until the study's conclusion.

Pain free walking distance progressively increased after the third month by up to 3.5 times in the group that received the supplements, while the group that received the skim milk experienced nonsignificant improvements. A measurement of blood pressure ratio between the ankle and brachial artery improved in the treatment group, but not in the control group. The treatment group experienced a drop in total cholesterol, ApoB, and homocysteine among those in whom it was previously elevated.

These findings provide evidence for the role of nutrition in reducing the symptoms PVD as well as general cardiovascular disease.

Friday, June 03, 2005

Micronutrient deficiencies likely to be a major cause of cancer

The following abstract and conclusion were published by Dr. Bruce Ames of the University of California, Berkeley. Dr. Ames is a leading expert in Molecular Toxicology and Nutrition. The research was published in two major journals: Micronutrient deficiencies. A major cause of DNA damage Ann N Y Acad Sci. 1999;889:87-106, and DNA damage from micronutrient deficiencies is likely to be a major cause of cancer Mutat Res. 2001 Apr 18;475(1-2):7-20.

ABSTRACT

DNA damage from micronutrient deficiencies is likely to be a major cause of cancer. A deficiency of any of the micronutrients: folic acid, Vitamin B12, Vitamin B6, niacin, Vitamin C, Vitamin E, iron, or zinc, mimics radiation in damaging DNA by causing single- and double-strand breaks, oxidative lesions, or both. For example, the percentage of the US population that has a low intake (<50%>20%. A level of folate deficiency causing chromosome breaks was present in approximately 10% of the US population, and in a much higher percentage of the poor. Folate deficiency causes extensive incorporation of uracil into human DNA (4 million/cell), leading to chromosomal breaks. This mechanism is the likely cause of the increased colon cancer risk associated with low folate intake. Some evidence, and mechanistic considerations, suggest that Vitamin B12 (14% US elderly) and B6 (10% of US) deficiencies also cause high uracil and chromosome breaks. Micronutrient deficiency may explain, in good part, why the quarter of the population that eats the fewest fruits and vegetables (five portions a day is advised) has about double the cancer rate for most types of cancer when compared to the quarter with the highest intake. For example, 80% of American children and adolescents and 68% of adults do not eat five portions a day. Common micronutrient deficiencies are likely to damage DNA by the same mechanism as radiation and many chemicals, appear to be orders of magnitude more important, and should be compared for perspective. Remedying micronutrient deficiencies should lead to a major improvement in health and an increase in longevity at low cost.

CONCLUSION

Optimizing micronutrient intake (through better diets, fortification of foods, or multivitamin-mineral pills) can have a major impact on public health at low cost. Other micronutrients are likely to be added to the list of those whose deficiency causes DNA damage in the coming years. Tuning-up human metabolism, which varies with genetic constitution and changes with age, is likely to be a major way to minimize DNA damage, improve health and prolong healthy lifespan.