Vitamins >> Vitamin B1 - Disease Prevention & Treatment

Because thiamin deficiency can result in a form of dementia (Wernicke-Korsakoff syndrome), its relationship to Alzheimer's disease and other forms of dementia have been investigated. Several investigators found evidence of decreased activity of the thiamin pyrophosphate-dependent enzymes, a-ketoglutarate dehydrogenase and transketolase, in the brains of patients who died of Alzheimer's disease. Such findings are consistent with evidence of reduced glucose metabolism found on PET scans of the brains of Alzheimer's disease patients. The finding of decreased brain levels of thiamin pyrophophosphate (TPP) in the presence of normal levels of free thiamin and thiamin monophosphate (TMP) suggests that the decreased enzyme activity is not likely to be the result of thiamin deficiency, but rather of impaired synthesis of TPP. Presently, there is only slight evidence that thiamin supplements are of benefit in Alzheimer's disease. A double blind placebo-controlled study of 15 patients (10 completed the study) reported no beneficial effect of 3 grams of thiamin/day on cognitive decline over a 12-month period. A preliminary report from another study claimed a mild benefit of 3 to 8 grams of thiamin/day in dementia of Alzheimer's type in 1993, but no additional data from that study are available. A mild beneficial effect in patients with Alzheimer's disease was reported after 12 weeks of treatment with 100 milligrams/day of a thiamin derivative (thiamin tetrahydrofurfuryl disulfide), but this study was not placebo-controlled. A recent systematic review of randomized, double blind, placebo-controlled trials of thiamin in patients with dementia of Alzheimer's type found no evidence that thiamin was a useful treatment for the symptoms of Alzheimer's disease.

Severe thiamin deficiency (wet beriberi) can lead to impaired cardiac function and ultimately congestive heart failure (CHF). Although cardiac manifestations of beriberi are rarely encountered in industrialized countries, CHF due to other causes is common, especially in the elderly. Diuretics used in the treatment of CHF, notably furosemide (Lasix), have been found to increase thiamin excretion, potentially leading to marginal thiamin deficiency. A number of studies have examined thiamin nutritional status in CHF patients and most found a fairly low incidence of thiamin deficiency, as measured by assays of transketolase activity. As in the general population, older CHF patients were found to be at higher risk of thiamin deficiency. An important measure of cardiac function in CHF is the left ventricular ejection fraction (LVEF), which can be assessed by echocardiography. In a randomized double-blind study of 30 CHF patients, all of whom had been taking furosemide for at least 3 months, intravenous (IV) thiamin therapy (200 mg/day) for 7 days resulted in an improved LVEF compared to IV placebo. When all 30 of the CHF patients in that study subsequently received 6 weeks of oral thiamin therapy (200 mg/day) the average LVEF improved by 22%. This finding may be significant because improvements in LVEF have been associated with improved survival in CHF patients. Conclusions that can be drawn from the studies published to date are limited due to small sample sizes, lack of randomization in some studies, and a need for more precise assays of thiamin nutritional status. Presently, the role of thiamin supplementation in maintaining cardiac function in CHF patients remains controversial.