beta-carotene and Folic-Acid-Deficiency

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

We have investigated the effect of modest supplementation with alpha-tocopherol (100 mg/day), beta-carotene (6 mg/day), vitamin C (100 mg/day) and selenium (50 microg/day) on oxidative stress and chromosomal damage, and the influence of methylenetetrahydrofolate reductase (MTHFR) genotype on these end-points. Subjects were two groups of middle-aged men differing in cardiovascular risk; 46 survivors of myocardial infarction before age 50 and 60 healthy controls. They were randomly divided into equal groups to receive antioxidants or placebo for 12 weeks. Twenty-eight patients and 58 controls completed the intervention. Micronucleus levels in peripheral lymphocytes and changes seen after intervention were studied in relation to the MTHFR C677T genotype, basal homocysteine and plasma folate levels. Ferric reducing ability of plasma and concentration of malondialdehyde were measured to assess the antioxidant effect of supplementation. There was no association of micronuclei with folate, homocysteine or malondialdehyde levels before supplementation. Micronucleus frequencies and plasma folate levels did not vary significantly with MTHFR genotype. Homocysteine levels in subjects with the TT variant genotype were significantly higher compared with CT or CC (P = 0.001), especially in subjects with low folate (P = 0.012). In the placebo control group an increase in micronuclei (P = 0.04) was detected at the end of the intervention period. This effect was not seen in the supplemented group. In antioxidant-supplemented myocardial infarction survivors we found an increase in the ferric reducing ability of plasma (P < 0.001) and a decrease in malondialdehyde (P = 0.001). Micronucleus frequency showed a decrease, strongest in subjects with normal folate levels (P = 0.015). In subjects with low folate levels, a high correlation was found between micronuclei after supplementation and homocysteine, both before (r = 0.979, P = 0.002) and after supplementation (r = 0.922, P = 0.009). Thus, folate deficiency may amplify the effect of other risk factors such as elevated homocysteine levels or variant MTHFR genotype, as well as influencing the ability of antioxidant supplementation to protect against genetic damage.

Topics: alpha-Tocopherol; Antioxidants; Ascorbic Acid; beta Carotene; Cardiovascular Diseases; Dietary Supplements; DNA Damage; Folic Acid; Folic Acid Deficiency; Genotype; Humans; Male; Methylenetetrahydrofolate Reductase (NADPH2); Micronucleus Tests; Middle Aged; Myocardial Infarction; Oxidative Stress; Selenium

Folate derivatives are important in experimental colorectal carcinogenesis; low folate intake, particularly with substantial alcohol intake, is associated with increased risk. The enzyme 5,10-methylenetetrahydrofolate reductase (MTHFR) catalyzes the conversion of 5,10-methylenetetrahydrofolate, required for purine and thymidine syntheses, to 5-methyltetrahydrofolate, the primary circulatory form of folate necessary for methionine synthesis. A common mutation (677C-->T) in MTHFR reduces enzyme activity, leading to lower levels of 5-methyltetrahydrofolate. To evaluate the role of folate metabolism in human carcinogenesis, we examined the associations of MTHFR mutation, plasma folate levels, and their interaction with risk of colon cancer. We also examined the interaction between genotype and alcohol intake. We used a nested case-control design within the Physicians' Health Study. Participants were ages 40-84 at baseline when alcohol intake was ascertained and blood samples were drawn. During 12 years of follow-up, we identified 202 colorectal cancer cases and matched them to 326 cancer-free controls by age and smoking status. We genotyped for the MTHFR polymorphism and measured plasma folate levels. Men with the homozygous mutation (15% in controls) had half the risk of colorectal cancer [odds ratio (OR), 0.49; 95% confidence interval (CI), 0.27-0.87] compared with the homozygous normal or heterozygous genotypes. Overall, we observed a marginal significant increased risk of colorectal cancer (OR, 1.78; 95% CI, 0.93-3.42) among those whose plasma folate levels indicated deficiency (<3 ng/ml) compared with men with adequate folate levels. Among men with adequate folate levels, we observed a 3-fold decrease in risk (OR, 0.32; 95% CI, 0.15-0.68) among men with the homozygous mutation compared with those with the homozygous normal or heterozygous genotypes. However, the protection due to the mutation was absent in men with folate deficiency. In men with the homozygous normal genotype who drank little or no alcohol as reference, those with the homozygous mutation who drank little or no alcohol had an 8-fold decrease in risk (OR, 0.12; 95% CI, 0.03-0.57), and for moderate drinkers, a 2-fold decrease in risk (OR, 0.42; 95% CI, 0.15-1.20); no decrease in risk was seen in those drinking 1 or more drinks/day. Our findings provide support for an important role of folate metabolism in colon carcinogenesis. In particular, these results suggest that the 677C-->IT mutation

Topics: Adult; Aged; Aged, 80 and over; Alcohol Drinking; Aspirin; beta Carotene; Case-Control Studies; Cocarcinogenesis; Colorectal Neoplasms; Diet; DNA Methylation; DNA Replication; Double-Blind Method; Folic Acid; Folic Acid Deficiency; Genetic Predisposition to Disease; Genotype; Humans; Male; Methylenetetrahydrofolate Reductase (NADPH2); Middle Aged; Odds Ratio; Oxidoreductases Acting on CH-NH Group Donors; Point Mutation; Polymorphism, Genetic; Prospective Studies; Risk; Tetrahydrofolates; United States

Triple negative breast cancer (TNBC) presents clinical challenges due to unknown etiology, lack of treatment targets, and poor prognosis. We examined combined genetic and nutritional risk models of TNBC in 354 breast cancer cases. We evaluated 18 DNA-repair nonsynonymous single nucleotide polymorphisms (nsSNPs) and dietary/nutritional intakes. Multivariate Adaptive Regression Splines models were used to select nutrients of interest and define cut-off values for logistic regression models. Our results suggest that TNBC was associated with 6 DNA-repair nsSNPs, ERCC4 R415Q (rs1800067), MSH3 R940Q (rs184967), MSH6 G39E (rs1042821), POLD1 R119H (rs1726801), XRCC1 R194W (rs1799782), and XPC A499V (rs2228000) and/or deficiencies in 3 micronutrients (zinc, folate, and β-carotene). Combined analyses of these 6 nsSNPs and 3 micronutrients showed significant association with TNBC: odds ratios = 2.77 (95% confidence interval = 1.01-7.64) and 10.89 (95% confidence interval = 3.50-33.89) for 2 and at least 3 risk factors, respectively. To the best of our knowledge, this is the first study to suggest that multiple genetic and nutritional factors are associated with TNBC, particularly in combination. Our findings, if validated in larger studies, will have important clinical implication that dietary modulations and/or micronutrient supplementations may prevent or reverse TNBC phenotype, so tumors can be treated with less toxic therapeutic strategies, particularly in genetically susceptible women.

Topics: Adult; Aged; beta Carotene; Case-Control Studies; Diet; DNA Repair; Energy Intake; Female; Folic Acid; Folic Acid Deficiency; Gene-Environment Interaction; Genetic Predisposition to Disease; Humans; Logistic Models; Malnutrition; Micronutrients; Middle Aged; Multivariate Analysis; Nutrition Assessment; Pilot Projects; Polymorphism, Single Nucleotide; Risk Factors; Surveys and Questionnaires; Triple Negative Breast Neoplasms; Zinc

To estimate the prevalence of optic neuropathy (ON) among prisoners in a provincial prison in Papua New Guinea, and to explore risk factors for this condition among this population.. Cross-sectional observation study of 148 male prisoners aged ≥18 years using an interview-based questionnaire, assessment of visual and nervous system function, ocular examination, and blood analysis (α-tocopherol, β-carotene, lutein, folate, homocysteine, holotranscobalamin II, riboflavin, selenium, thiamin, and vitamins A, B(12) and C). Likelihood of the presence of ON was based on ordered groups determined by weighted combination of optic nerve head appearance and visual dysfunction (acuity, field, color perception). Main outcome measures were prevalence and associations of ON.. Sample prevalence of clinical ON was 10.4% (95% confidence interval [CI], 6.2-16.8). No cases were found of unexplained non-visual nervous system dysfunction, including peripheral neuropathy. Increasing age (p = 0.001), length of current (p = 0.002) and lifetime (p = 0.03) incarceration, and duration of smoking by current smokers (p = 0.001) were associated with increased ON likelihood. However, when age-controlled, the smoking duration association was not maintained (p = 0.6). Prisoners were folate deficient. Adjusting for age and duration of current incarceration, whole blood (p = 0.02) and red blood cell (p = 0.04) folate concentrations were inversely associated with ON likelihood. No association was found for any other assessed demographic, lifestyle or biochemical measure.. A cluster of ON associated with folate deficiency has been identified. Recommendations for dietary change and micronutrient supplementation have been made.

Topics: Adult; alpha-Tocopherol; beta Carotene; Cross-Sectional Studies; Female; Folic Acid; Folic Acid Deficiency; Humans; Lutein; Male; Optic Nerve Diseases; Papua New Guinea; Prevalence; Prisoners; Risk Factors; Selenium; Surveys and Questionnaires; Vision Disorders; Vitamin A; Vitamin B 12

Topics: beta Carotene; Female; Folic Acid Deficiency; Humans; Iodine; Micronutrients; Pregnancy; Pregnancy Complications; Selenium; Vitamin A; Zinc

The presence of HPV, using the Digene Hybrid Capture System, was identified in a group of 324 women with CIN and in 228 women with normal cytological smears. Risk of occurrence of CIN was 40 times higher for high risk HPV types. The serum folic acid level and the level of antioxidant compounds in plasma (retinol, alpha-tocopherol, vitamins C and E) in women of the studied and control group was determined by HPLC (high-performance liquid chromatography-reversed phase). Statistically lower levels of folic acid were found in the women with CIN-HPV (+) (OR: 7.5: 95% CI: 1.2-9.7). Studies have shown that lower levels of antioxidants coexisting with low levels of folic acid increases the risk of CIN development.

Topics: Antioxidants; beta Carotene; Cocarcinogenesis; Female; Folic Acid; Folic Acid Deficiency; Humans; Papillomaviridae; Papillomavirus Infections; Regression Analysis; Risk Factors; Tumor Virus Infections; Uterine Cervical Dysplasia; Uterine Cervical Neoplasms; Vitamin E

Levels of vitamin A, beta-carotene and vitamin E in peripheral venous blood of women in abruptio placentae and in normal pregnancy have been compared. Chemical methods were used for the estimation of these compounds. The results show that levels of all three compounds in abruptio placentae are lower than those found in the normal pregnancy. We have earlier shown that levels of ascorbic acid in these subjects are low while other studies have indicated that levels of folic acid in them are also low. Based on our present and earlier published work it is suggested that abruptio placentae is a condition with multiple vitamin deficiency. Whether this is its cause or effect is however not clear.

Topics: Abruptio Placentae; beta Carotene; Carotenoids; Female; Folic Acid Deficiency; Humans; Intestinal Absorption; Pregnancy; Vitamin A; Vitamin A Deficiency; Vitamin E; Vitamin E Deficiency