Experts Criticise ‘Inaccurate’ View That B Vitamins Have No Role In Alzheimer’s Disease Prevention

26 Feb 2015 --- Patients in the very early stages of dementia could miss out on a potentially effective treatment after misleading research was published last year, say medical experts.

The researchers, who claimed that B vitamins were ‘sadly not going to prevent Alzheimer’s disease’, have been strongly criticised.

Clinicians and scientists have labelled the statement ‘inaccurate and misleading’, voicing concerns that the unjustified claim could bias research funding and health policy decisions, as well as having a negative impact on patient welfare.

Dr Peter Garrard, of the Cardiovascular and Cell Sciences Research Institute at St George’s, University of London, said that the analysis of previous clinical trial data published last year cast no doubt whatever on the potential of folic acid and vitamin B-12 to prevent dementia, and that the lead author’s comments were ‘unjustified and misleading’.

Dr Garrard pointed out that taking B vitamins lowers blood levels of a molecule (homocysteine), which in high concentrations acts as a potent risk factor for dementia. He highlighted the ‘first-rate scientific evidence that the use of B vitamins confers both biological and neuropsychological benefits’ on individuals aged over 70 who had noticed a recent decline in their cognitive abilities.

He emphasised the urgent need for a definitive trial to establish whether this simple and safe treatment can slow cognitive deterioration in a similar group of people, as such individuals are known to have a heightened risk of developing full-blown Alzheimer’s disease.

In separate letters to the American Journal of Clinical Nutrition, Dr Garrard and Professor David Smith, of the University of Oxford, pointed out a number of flaws in the new analysis, including: 1) reliance on data from trials of vascular disease prevention rather than dementia; 2) the use of the Mini Mental State Examination (MMSE), which is designed to detect dementia but is unsuitable for assessing small changes in cognitively normal people; and 3) the absence of any cognitive decline in untreated patients, rendering the whole study irrelevant to the question of clinical benefits in cognitive impairment or dementia.