Updated August, 2012
A study was conducted with mice that showed that high doses of vitamin B3 (as niacinamide) caused reversal of Alzheimer's Disease, including re-gaining lost memory.
OK. While this is interesting, it's a mouse study, not a human study.
Well, the results were so exciting that a human study is being conducted at University of Californiat (UC) at Irvine with the co-operation of the very conservative Alzheimer's Association.
I am eager to see the results of that study but rather than wait a year or two to talk about it, I am telling people about this potential effect now.
Niacinamide is not toxic at the dose that this study says would work for humans, 3,000 mg a day, and it's inexpensive so why not see if it helps people - and their loved ones - suffering from this debilitating disease.
Note that because niacinamide blood levels decrease after about 90 minutes, the most effective dosing would likely be 250 mg every 90 minutes.
Or to make life easier 1,500 mg of extended-release niacinamide could be taken two times a day.
The product that is being used for the UCLA human study called Enduramide is available in 500 mg extended-release tablets.
I bought some and am taking it, but not 3,000 mg a day because I don't have Alzheimer's or any symptoms of possible early Alzheimer's.
I sometimes take one or two tablets during the day, and three tablets before sleep because niacinamide has also been shown to have similar actions on the benzodiazepine receptors in the brain to the sleeping medication, Valium, that can make you feel calm and sleepy.
I don't find that it feels like a drug and don't notice it making me feel sleepy during the day, but it does seem to enhance deeper, restful sleep taking 1,500 mg before bedtime.
A HUMAN ALZHEIMER'S STUDY OF A COENZYME THAT NIACINAMIDE CONVERTS TO IN THE BODY
Demarin V, et al. Treatment of Alzheimer's disease with stabilized oral nicotinamide adenide dinucleotide: a randomized, double-blind study. Drugs Exp Clin Res. 2004;30(1):27-33.
Abstract
This study was designed to evaluate the effect of stabilized oral nicotinamide adenine dinucleotide (NADH) on cognitive functioning in patients with Alzheimer's disease (AD). NADH is a coenzyme that plays a key role in cellular energy production and stimulates dopamine production. In previous trials NADH has been shown to improve cognitive functioning in patients with Parkinson's disease, depression and AD. The present trial was a randomized, placebo-controlled, matched-pairs, double-blind, 6-month clinical study. Patients with probable AD (n = 26) were randomized to receive either stabilized oral NADH (10 mg/day) or placebo. Twelve pairs of subjects were matched for age and baseline total score on the Mattis Dementia Rating Scale (MDRS) and the Mini Mental State Examination. After 6 months of treatment, subjects treated with NADH showed no evidence of progressive cognitive deterioration and had significantly higher total scores on the MDRS compared with subjects treated with placebo (p < 0.05). Analysis of MDRS subscales revealed significantly better performance by NADH subjects on measures of verbal fluency (p = 0.019), visual-constructional ability (p = 0.038) and a trend (p = 0.08) to better performance on a measure of abstract verbal reasoning. There were no differences between groups in measures of attention, memory, or in clinician ratings of dementia severity (Clinical Dementia Rating). Consistent with earlier studies, the present findings support NADH as a treatment for AD.
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