beta-carotene and Vitamin-D-Deficiency

The objective of this review was to evaluate the evidence from human studies on the intake of vitamins, either as monotherapies or in combination with other vitamins, as neuroprotective agents that may delay the onset of cognitive decline in older adults.. Evidence-based methodologies were used to capture and evaluate the highest levels of evidence.. The current evidence available showed no association for cognitive benefits of vitamins B6 or B12 as a monotherapy, and recent systematic reviews provide no clear evidence that supplementation with vitamin B6, B12 and/or folic acid improves dementia outcomes or slows cognitive decline, even though it may normalise homocysteine levels. Meta-analyses from systematic reviews have shown an association between low vitamin D levels and diminished cognitive function, although causality cannot be confirmed from the available evidence. There is no convincing evidence for an association of vitamin A, vitamin C or vitamin E either as a monotherapy or in combination with other antioxidant vitamins such as β-carotene and the prevention of cognitive decline. The appraisal of nineteen systematic reviews and meta-analyses has highlighted the heterogeneity between studies, and the need for better consensus on definitions of cognitive decline, duration of testing and agreement on which specific endpoints are clinically relevant.. Evaluation of the totality of the currently available evidence indicates that intake of the above vitamins, either as a monotherapy, or in combination with other vitamins, has no clinically-relevant effect on delaying cognitive decline or delaying the onset of dementia in older adults.

Topics: Aged; Antioxidants; Ascorbic Acid; beta Carotene; Cognition; Cognition Disorders; Dementia; Dietary Supplements; Folic Acid; Homocysteine; Humans; Meta-Analysis as Topic; Vitamin A; Vitamin B 12; Vitamin B 6; Vitamin D; Vitamin D Deficiency; Vitamin E; Vitamins

Background. Vitamins A, D and E and beta-carotene may have a protective function for cognitive health, due to their antioxidant capacities. Methods. We analyzed data from 1334 non-demented participants (mean age 84 years) from the AgeCoDe study, a prospective multicenter-cohort of elderly general-practitioner patients in Germany, of whom n = 250 developed all-cause dementia and n = 209 developed Alzheimer’s dementia (AD) during 7 years of follow-up. We examined whether concentrations of vitamins A (retinol), D (25-hydroxycholecalciferol) and E (alpha-tocopherol) and beta-carotene, would be associated with incident (AD) dementia. Results. In our sample, 33.7% had optimum vitamin D concentrations (≥50 nmol/L). Higher concentrations of vitamin D were associated with lower incidence of all-cause dementia and AD (HR 0.99 (95%CI 0.98; 0.99); HR0.99 (95%CI 0.98; 0.99), respectively). In particular, subjects with vitamin D deficiency (25.3%, <25 nmol/L) were at increased risk for all-cause dementia and AD (HR1.91 (95%CI 1.30; 2.81); HR2.28 (95%CI 1.47; 3.53), respectively). Vitamins A and E and beta-carotene were unrelated to (AD) dementia. Conclusions. Vitamin D deficiency increased the risk to develop (AD) dementia. Our study supports the advice for monitoring vitamin D status in the elderly and vitamin D supplementation in those with vitamin D deficiency. We observed no relationships between the other vitamins with incident (AD) dementia, which is in line with previous observational studies.

Topics: Aged; Aged, 80 and over; Alzheimer Disease; beta Carotene; Dementia; Humans; Prospective Studies; Tocopherols; Vitamin A; Vitamin D; Vitamin D Deficiency; Vitamins

A 4-year-old boy attending the autism assessment service was identified to have a restricted diet. His food diary documented that he ate a narrow range of foods and consumed excessive quantities of carrot juice (excess 2.5 L daily). Physical examination showed that the boy had a florid orange discolouration of his skin, growth parameters were <91st centile for weight, >50th centile for height and head circumference. Blood investigations showed a raised serum carotene level and vitamin D deficiency. He was referred for urgent specialist input from dietetics and the other disciplines within the autism intervention team.

Topics: beta Carotene; Child Development Disorders, Pervasive; Child, Preschool; Daucus carota; Feeding and Eating Disorders of Childhood; Feeding Behavior; Humans; Male; Pigmentation Disorders; Vitamin D Deficiency

Male SD rats were fed a vitamin E- and selenium-deficient diet, a diet supplemented with vitamin E and selenium, and diets supplemented with vitamin E, selenium, trolox C, ascorbic acid palmitate, acetylcysteine, beta-carotene, canthaxanthin, coenzyme Q0, coenzyme Q10, and (+)-catechin. Liver slices were incubated at 37 degrees C with and without CBrCl3, t-butyl-hydroperoxide, Fe+2, or Cu+2. The effect of antioxidant nutrients on the oxidative damage to rat liver was studied by measurement of the production of oxidized heme proteins (OHP) during the oxidative reactions. Diet supplemented with vitamin E and selenium showed a strong protection against heme protein oxidation compared to the antioxidant-deficient diet. Furthermore, increasing the diversity and quantity of antioxidants in the diets provided significantly more protection.

Topics: Acetylcysteine; Animals; Antioxidants; Ascorbic Acid; beta Carotene; Canthaxanthin; Carotenoids; Catechin; Chromans; Dose-Response Relationship, Drug; Hemeproteins; In Vitro Techniques; Male; Oxidants; Oxidation-Reduction; Rats; Rats, Sprague-Dawley; Selenium; Ubiquinone; Vitamin D Deficiency; Vitamin E