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LE Magazine July 2001

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Studies from throughout the world that can help you live longer

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July 2001 Table of Contents

  1. Homocysteine causes DNA damage in nerve cells
  2. Selenium, interleukins and AIDS
  3. Effect of alpha-lipoic acid on brain antioxidants
  4. Alpha-lipoic acid helps cell recovery
  5. Homocysteine and kidney disease
  6. Vitamin supplements and cardiovascular risk
  7. Folic acid supplementation and heart disease

1. Homocysteine causes DNA damage in nerve cells

Elevated blood levels of the sulfur-containing amino acid homocysteine increase the risk for atherosclerosis, stroke and possibly Alzheimer's disease. A recent study shows that homocysteine induces cell death in nerve cells in the brains of rats. DNA strand breaks occur rapidly after exposure to homocysteine and precede mitochondrial dysfunction, oxidative stress and caspase (enzyme that degrades DNA during cell death) activation. Homocysteine increases the vulnerability of neurons in the hippocampus of the brain to excitotoxic and oxidative injury, in cell culture and in vivo. This suggests a mechanism by which homocysteine may contribute to the pathogenesis of neurodegenerative disorders.

JOURNAL OF NEUROSCIENCE, 2000, Vol 20, Iss 18, pp 6920-6926


2. Selenium, interleukins and AIDS

Decreased selenium levels, as found in persons with HIV infection or AIDS, are sensitive markers of disease progression. Selenium deficiency, an independent predictor of mortality in both HIV-l-infected adults and children, is an essential micronutrient that is associated with an improvement of T cell (immune) function and reduced apoptosis (programmed cell death) in animals. In addition, adequate selenium may enhance resistance to infections through modulation of interleukin (IL) production. There are 12 interleukins which are proteins produced by the immune system that modulate inflammation and immunity. Selenium supplementation up-regulates (increases interactions) IL-2 and increases activation, proliferation, differentiation and programmed cell death of T helper cells. Selenium supplementation may down-regulate the abnormally high levels of IL-8 and tumor necrosis factor (TNF, kills tumor cells) as observed in HIV disease, which has been associated with neurological damage, Kaposi's sarcoma, wasting syndrome and increased viral replication. This suggests a new mechanism through which selenium may affect HIV-1 disease progression.

JOURNAL OF INFECTIOUS DISEASES, 2000, Vol 182, Suppl. 1, pp S69-S73


3. Effect of alpha-lipoic acid on brain antioxidants

The effect of alpha-lipoic acid (an antioxidant) on lipid peroxidation and antioxidants were evaluated in the brains of rats. In aged rats, the levels of vitamin C, E and glutathione were low, but the lipid peroxidation rate was high. Alpha-lipoic acid was given for 7 and 14 days. It reduced lipid peroxidation and elevation in the levels of antioxidants in the aged rats. The modulatory effect of alpha-lipoic acid in decreasing age-associated alterations proves its role as a potent brain antioxidant.

PHARMACOLOGICAL RESEARCH, 2000, Vol 42, Iss 3, pp 219-222


4. Alpha-lipoic acid helps cell recovery

A study evaluated the effect of alpha-lipoic acid on nucleic acid and protein contents in young and aged rats. Age-associated decreases in the DNA, RNA and protein contents were observed in aged rats. Alpha-lipoic acid was administered (100 mg/kg body weight/day) to young and aged rats from 7 and 14 days. The results showed that alpha-lipoic acid substantially increased the nucleic acid and protein contents in aged rats. Hence, it can be justified that alpha-lipoic acid is efficient in helping the cell to recover from free radical damage.

PHARMACOLOGICAL RESEARCH, 2000, Vol 42, Iss 3, pp 223-226


5. Homocysteine and kidney disease

Hyperhomocysteinemia (an elevated circulating level of the sulfur-containing amino acid homocysteine) has been shown to be a risk factor for vascular disease in the general population. In those with kidney failure, hyperhomocysteinemia is common. Proposed mechanisms include reduced kidney elimination and impaired non-kidney elimination of homocysteine, possibly because of inhibition of crucial enzymes in the methionine-homocysteine metabolism. Deficiencies of folic acid, vitamin B6, or vitamin B12 may also play a role. Studies have indicated that hyperhomocystenemia is an independent risk factor for atherothrombotic disease (artery plaque buildup and blood clots) in those with predialysis and end-stage kidney disease. In those with kidney disease, blood homocysteine concentration can be reduced by administration of folic acid in doses ranging from 1 to 15 mg per day. Studies are now underway to establish whether homocysteine-lowering therapy will reduce atherothrombotic events in those with kidney failure.

SEMINARS IN THROMBOSIS AND HEMOSTASIS, 2000, Vol 26, Iss 3, pp 313-324


6. Vitamin supplements and cardiovascular risk

Studies have shown that higher blood homocysteine levels appear to be associated with higher risks of coronary, cerebral and peripheral vascular disease. When blood levels of folic acid, vitamin B12 and B6 are high, homocysteine is low, and vice versa. Several studies of vitamin supplements to lower homocysteine levels was carried out to determine the optimal dose of folic acid required to lower homocysteine levels, and to assess whether vitamin B12 or vitamin B6 had additive effects. It was found that dietary folic acid in a daily dosage range of 0.5 to 5 mg reduced homocysteine levels by 25% and Vitamin B12 by 7%. Vitamin B6 (mean 16.5 mg) did not have any significant effect. Thus, in typical populations, daily supplementation with both 0.5 to 5 mg folic acid and about 0.5 mg vitamin B12 would be expected to reduce homocysteine levels by 25%-33% and thus reduce the risk of vascular disease.

SEMINARS IN THROMBOSIS AND HEMOSTASIS, 2000, Vol 26, Iss 3, pp 341-348


7. Folic acid supplementation and heart disease

Folic acid supplementation may help prevent the following three common and important disorders: neural tube defect pregnancies, ischemic heart disease and strokes, and possibly colon cancer. Several studies have irrefutably established that folic acid supplementation in proper doses reduces neural tube defect pregnancies. Several studies have established a close link between hyperhomocysteinemia (elevated homocysteine) and ischemic heart disease (deficiency of blood due to obstruction of vessels). This is supported by evidence obtained from genetic defects leading to elevated blood levels of homocysteine. There is reasonable evidence to conclude that hyperhomocysteinemia is the actual cause of excessive heart diseases. Folic acid supplementation in proper doses could potentially reduce ischemic heart disease by 40%. There is also some evidence to suggest that folic acid treatment reduces the incidence of colon cancer. The reduction in all three health problems is dependent upon the dose of folic acid. The levels needed are rarely supplied by the daily food intake, even under ideal conditions, although breakfast cereals address this problem at least in part.

SEMINARS IN THROMBOSIS AND HEMOSTASIS, 2000, Vol 26, Iss 3, pp 349-352



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