TY - JOUR
T1 - B-vitamins for neuroprotection
T2 - Narrowing the evidence gap
AU - Nachum-Biala, Yaarit
AU - Troen, Aron M.
PY - 2012/3
Y1 - 2012/3
N2 - A compelling and extensive epidemiological literature documents the strong association of inadequate status of folate, vitamin B12, and to a lesser degree vitamin B6, with increased risk of neurodegenerative and cerebrovascular disease. Mildly elevated plasma total homocysteine, which is biochemically related to low status of these B-vitamins, is similarly associated with increased risk for these conditions. This, together with experimental data showing that experimental B-vitamin deficiency and/or hyperhomocysteinemia can cause a variety of neurological and vascular deficits in animals, has provided the evidence base and motivation for a growing number of large randomized, double-blind clinical trials aimed at determining the efficacy and safety of B-vitamin supplementation for preserving cognitive function in older adults. Despite some encouraging trials showing benefit of B-vitamins for slowing brain atrophy and cognitive decline, the majority of these studies have not demonstrated that B-vitamin supplementation has protective or therapeutic cognitive benefit. There are many possible explanations for the inconsistency between the clinical trials and for the discrepancy between their findings and the predictions of the epidemiological evidence. Among these are the possibility of inadequate hypotheses guiding the trials, design limitations of the individual trials, and inherent limitations of nutritional randomized clinical trials. Resolving these issues will be crucial for designing definitive trials and ultimately for guiding nutritional interventions for cognitive protection.
AB - A compelling and extensive epidemiological literature documents the strong association of inadequate status of folate, vitamin B12, and to a lesser degree vitamin B6, with increased risk of neurodegenerative and cerebrovascular disease. Mildly elevated plasma total homocysteine, which is biochemically related to low status of these B-vitamins, is similarly associated with increased risk for these conditions. This, together with experimental data showing that experimental B-vitamin deficiency and/or hyperhomocysteinemia can cause a variety of neurological and vascular deficits in animals, has provided the evidence base and motivation for a growing number of large randomized, double-blind clinical trials aimed at determining the efficacy and safety of B-vitamin supplementation for preserving cognitive function in older adults. Despite some encouraging trials showing benefit of B-vitamins for slowing brain atrophy and cognitive decline, the majority of these studies have not demonstrated that B-vitamin supplementation has protective or therapeutic cognitive benefit. There are many possible explanations for the inconsistency between the clinical trials and for the discrepancy between their findings and the predictions of the epidemiological evidence. Among these are the possibility of inadequate hypotheses guiding the trials, design limitations of the individual trials, and inherent limitations of nutritional randomized clinical trials. Resolving these issues will be crucial for designing definitive trials and ultimately for guiding nutritional interventions for cognitive protection.
KW - Clinical trials
KW - Cognition
KW - Dementia
KW - Folate
KW - Homocysteine
KW - Vitamin B12
UR - http://www.scopus.com/inward/record.url?scp=84859433604&partnerID=8YFLogxK
U2 - 10.1002/biof.1006
DO - 10.1002/biof.1006
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C2 - 22419558
AN - SCOPUS:84859433604
SN - 0951-6433
VL - 38
SP - 145
EP - 150
JO - BioFactors
JF - BioFactors
IS - 2
ER -