beta-carotene and Vitamin-B-12-Deficiency

In this article we review published studies on the role of serum micronutrient levels in the natural history of HIV infection. Specifically, we have focused on vitamins B12, E, A, and beta-carotene. Deficiencies of one or several of these vitamins have been associated with an accelerated progression of HIV infection to AIDS. Most investigators have used serum micronutrient levels as an indicator of vitamin nutriture. However, serum levels are not always the most sensitive or specific indicators of vitamin status. Nonetheless, serum vitamin levels are relatively easy to obtain and have been studied in various HIV-infected populations in individuals at different stages of disease. Low serum B12 levels have been associated with increased neurologic abnormalities, more rapid HIV disease progression, and increased AZT-related bone marrow toxicity. Low serum vitamin E levels have been associated with an increase in oxidative stress in HIV-infected individuals. However, early studies of vitamin E supplementation suggest that vitamin E may have important immunostimulatory properties. Studies of vitamin A deficiency in HIV-infected populations have shown that low serum vitamin A levels are associated with increased mortality, more rapid disease progression, and increased maternal-fetal transmission. However, there is little evidence that vitamin A supplementation, beyond the correction of deficiency, is beneficial in HIV infection. Finally, several clinical trials of beta-carotene supplementation have failed to show significant or sustained improvements in the immune response of patients with HIV infection or AIDS.

Topics: Avitaminosis; beta Carotene; Disease Progression; HIV Infections; Humans; Micronutrients; Nutrition Assessment; Nutritional Requirements; Vitamin A Deficiency; Vitamin B 12 Deficiency; Vitamin E Deficiency; Vitamins

Routine vitamin supplementation for the elderly has been advocated by many. Specific vitamin deficiencies are rare in free-living elderly, but are not uncommonly encountered in hospitalized and institutionalized patients. Deficiency may result from interactions with medications or overall poor dietary intake. Low blood or plasma vitamin concentration is not necessarily indicative of a deficient state. Specific vitamin supplements are useful in the treatment and prevention of a deficient state. However, there is little, if any benefit from supplementation for reasons other than replacement therapy. The incidence and clinical symptoms of thiamine (vitamin B1), riboflavin (B2), pyridoxine (vitamin B6), vitamin B12, C, D, folate, niacin, vitamin A, E, beta carotene, and K deficiency and their treatment and prevention in the elderly are discussed.

Topics: Aged; Ascorbic Acid Deficiency; beta Carotene; Folic Acid Deficiency; Humans; Niacin; Riboflavin Deficiency; Thiamine Deficiency; Vitamin A Deficiency; Vitamin B 12 Deficiency; Vitamin B 6 Deficiency; Vitamin D; Vitamin E Deficiency; Vitamin K Deficiency; Vitamins

Previous studies have found associations between one-carbon metabolism nutrients and risk of several cancers, but little is known regarding upper gastrointestinal tract (UGI) cancer. We analyzed prediagnostic serum concentrations of several one-carbon metabolism nutrients (vitamin B12, folate, vitamin B6, riboflavin and homocysteine) in a nested case-control study within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study of male smokers, which was undertaken in Finland between 1985 and 1988. We conducted a nested case-control study including 127 noncardia gastric adenocarcinoma (NCGA), 41 esophagogastric junctional adenocarcinoma and 60 esophageal squamous cell carcinoma incident cases identified within ATBC. Controls were matched to cases on age, date of serum collection and follow-up time. One-carbon nutrient concentrations were measured in fasting serum samples collected at baseline (up to 17 years prior to cancer diagnosis). Odds ratios and 95% confidence intervals (CI) were calculated using conditional logistic regression. Lower prediagnostic vitamin B12 concentrations at baseline were associated with a 5.8-fold increased risk of NCGA (95% CI = 2.7-12.6 for lowest compared to highest quartile, p-trend <0.001). This association remained in participants who developed cancer more than 10 years after blood collection, and after restricting the analysis to participants with clinically normal serum vitamin B12 (>300 pmol/L). In contrast, pepsinogen I, a known serologic marker of gastric atrophy, was not associated with NCGA in this population. As vitamin B12 absorption requires intact gastric mucosa to produce acid and intrinsic factor, our findings suggest vitamin B12 as a possible serologic marker for the atrophic gastritis that precedes NCGA, one more strongly associated with subsequent NCGA than pepsinogen.

Topics: Aged; alpha-Tocopherol; beta Carotene; Carcinoma, Squamous Cell; Case-Control Studies; Dietary Supplements; Esophageal Neoplasms; Esophageal Squamous Cell Carcinoma; Finland; Folic Acid; Homocysteine; Humans; Male; Middle Aged; Prospective Studies; Riboflavin; Stomach Neoplasms; Vitamin B 12; Vitamin B 12 Deficiency