Thiamine Treatment Reportedly Effective in Treating 

Some People with Generalized Anxiety Disorder

A recent paper1 reports on the successful treatment of patients with generalized anxiety disorder who have low blood thiamine (vitamin B1) levels. People with generalized anxiety disorder are reported to be fearful, constantly worried about minor matters, and to expect the worst.

People can have low blood thiamine levels for a variety of reasons. For one thing, the intestinal absorption of thiamine (B1) may decrease with age,1as it requires intestinal alkaline phosphatase (ALP) in the active process of absorbing B1. The activity of ALP has been observed to decrease in old rats and may be due to the reduction in the number of enterocytes (intestinal cells) caused by the age-induced atrophy of intestinal mucosa. (Interestingly, another paper2 reported that oral treatment with intestinal alkaline phosphatase prevented high fat diet-induced endotoxemia (LPS, lipopolysaccharide, is also known as endotoxin) as well as preventing high fat diet-induced metabolic syndrome, both effects observed in a mouse experiment.) Intestinal alkaline phosphatase is known to be a powerful detoxification agent for LPS (endotoxin) and to reduce the inflammatory effects of a high fat diet on the GI tract. Hence, intestinal alkaline phosphatase appears to be important in maintaining gastrointestinal function.)

Another problem is, according to the authors,1 that single oral doses of thiamine above 2.5 mg are mostly unabsorbed (this according to two cited papers, one from 1948 and the other from 1960). This means, the authors believe, that when a patient over 60 is deficient, intramuscular administration of thiamine is required to restore thiamine supplies. When treated in this way, patients are started at 100 mg two to three times a day of thiamine for 1 to 2 weeks. We doubt that many Americans are so severely depleted that they would require this course of treatment and certainly very few people maintaining a nutritional regimen such as those who read this newsletter. Nevertheless, if you are over 60 and suffer from generalized anxiety disorder (or something that sounds like it), it would be a good idea to get your thiamine blood levels measured to make sure they are within the normal range. The two of us take more than the oral amount mention in this paper. Sandy and Durk take 60 mg a day.

Alcohol consumption is a very common cause of thiamine deficiency. Alcohol is metabolized to acetaldehyde (very chemically similar to formaldehyde) in both the gut and the liver. This acetaldehyde can react with thiamine and destroy it—which can promote anxiety and, in turn, promote further excessive alcohol consumption. Indeed, alcoholics may suffer from memory loss and Korsakoff’s psychosis, which is caused at least in part by brain thiamine deficiency due to excess alcohol consumption.3 Peripheral neuropathy can also be caused by thiamine deficiency. Thiamine can provide protection against these adverse effects of acetaldehyde.4-6

In this study,1 9 patients with generalized anxiety disorder were treated with 100 mg. thiamine intramuscularly per day for 2–4 weeks. The patients also had histories of hypertension, type 2 diabetes, or both. The results showed patients with improved scores on the Hamilton Anxiety Rating Scale, increased appetite and general well-being, and decreased fatigue. Impressively, the patients were able to discontinue using anti-anxiety and beta-blocker medications.

As is the case with many reported human clinical trials, the number of subjects was very small and, hence, the results have to be interpreted with caution. Still, thiamine deficiency is easy enough to detect and, if discovered, easy to treat.



  1. Luong K, Nguyen L. The impact of thiamine treatment on generalized anxiety disorder. Int J Clin Med. 2:439-43 (2011).
  2. Kaliannan et al. Intestinal alkaline phosphatase prevents metabolic syndrome in mice. Proc Natl Acad Sci USA. 110(17):7003-8 (2013).
  3. Pekkanen. Effects of thiamin deprivation and antagonism on voluntary ethanol intake in rats. J Nutr. 110:937-44 (1980).
  4. Sprince et al. Protectants against acetaldehyde toxicity: sulfhydryl compounds and ascorbic acid. Fed Proc. 33(3):pt. 1 (March 1974).
  5. Sprince et al. Protective action of ascorbic acid and sulfur compounds against acetaldehyde toxicity: implication in alcoholism and smoking. Agents Actions.5(2):164-73 (1975).
  6. Aberle et al. Acetaldehyde-induced cardiac contractile dysfunction may be alleviated by vitamin B1 but not by vitamins B6 or B12. ALCOHOL ALCOHOL.39(5):450-4 (2004).