Benfotiamine

Two small clinical trials suggest that benfotiamine treatment slows cognitive decline in people with mild cognitive impairment or mild Alzheimer’s disease, but they need to be confirmed by larger, long-term studies. Our search identified:

• 1 phase 2a randomized controlled trial in people with mild cognitive impairment or mild Alzheimer’s disease
• 1 open-label uncontrolled study in Alzheimer’s patients
• 3 preclinical studies

In a randomized controlled trial of 70 people with mild cognitive impairment or mild Alzheimer’s disease, benfotiamine treatment (300 mg, twice daily) for 12 months showed a trend for a slowing of cognitive decline [1]. Advanced glycation end products (AGEs), which are toxic protein modifications indicative of altered glucose metabolism and aging, typically increase in the brains of Alzheimer’s patients, but benfotiamine treatment significantly reduced this increase. No benfotiamine effects were observed for verbal memory or cerebral glucose metabolism in this study. A larger confirmatory trial is needed to extend these preliminary findings.

Benfotiamine is converted to thiamine, which serves as a key factor for three enzymes involved in generating energy from glucose [2]. Preclinical studies have found that benfotiamine enhances cognitive function and reduces biological markers of Alzheimer’s disease [3; 4]. These benefits may be due to benfotiamine’s ability to suppress the activity of an enzyme that promotes the progression of Alzheimer’s [5]. However, these effects have not been confirmed in humans.

For Dementia Patients

In a randomized controlled trial, benfotiamine treatment (300 mg, twice daily) for 12 months showed a trend for a slowing of cognitive decline in people with mild cognitive impairment or mild Alzheimer’s disease [1]. However, benefits were only seen in people who had high cognitive function at baseline. There was also a small open-label, uncontrolled study which showed that benfotiamine treatment for 18 months resulted in improved cognitive function in Alzheimer’s patients [6]. The treatment did not decrease levels of beta-amyloid, a biological marker of Alzheimer’s disease.

Benfotiamine is generally considered safe for most people when taken at standard doses. In clinical trials, side effects were mild and included gastrointestinal issues and skin reactions [7]. A small percentage of people taking benfotiamine may have mild increases in liver enzymes and urinary white blood cells [8]. Because benfotiamine gets converted to thiamine (vitamin B1), and thiamine may cause low blood pressure or low blood glucose, people taking drugs or herbs to lower blood pressure or blood glucose should exercise caution [9].

NOTE: This is not a comprehensive safety evaluation or complete list of potentially harmful drug interactions. It is important to discuss safety issues with your physician before taking any new supplement or medication.

Benfotiamine supplements are available over-the-counter, often in capsules containing 150–300 mg. In a randomized controlled trial in people with mild cognitive impairment or mild Alzheimer’s disease, a benfotiamine dose of 300 mg, orally, twice daily, was tested [1]. Other studies in clinical populations have used doses ranging from 200–600 mg/day [7; 10; 11].

Information on safety and drug interactions with thiamine from the Mayo Clinic

Full scientific report (PDF) on Cognitive Vitality Reports

1. Gibson GE, Luchsinger JA, Cirio R et al. (2020) Benfotiamine and Cognitive Decline in Alzheimer's Disease: Results of a Randomized Placebo-Controlled Phase IIa Clinical Trial. Journal of Alzheimer's disease : JAD 78, 989-1010.
2. Gibson GE, Hirsch JA, Cirio RT et al. (2013) Abnormal thiamine-dependent processes in Alzheimer's Disease. Lessons from diabetes. Mol Cell Neurosci 55, 17-25.
3. Pan X, Gong N, Zhao J et al. (2010) Powerful beneficial effects of benfotiamine on cognitive impairment and beta-amyloid deposition in amyloid precursor protein/presenilin-1 transgenic mice. Brain 133, 1342-1351.
4. Markova N, Bazhenova N, Anthony DC et al. (2017) Thiamine and benfotiamine improve cognition and ameliorate GSK-3beta-associated stress-induced behaviours in mice. Prog Neuropsychopharmacol Biol Psychiatry 75, 148-156.
5. Sun XJ, Zhao L, Zhao N et al. (2012) Benfotiamine prevents increased beta-amyloid production in HEK cells induced by high glucose. Neurosci Bull 28, 561-566.
6. Pan X, Chen Z, Fei G et al. (2016) Long-Term Cognitive Improvement After Benfotiamine Administration in Patients with Alzheimer's Disease. Neurosci Bull 32, 591-596.
7. Stracke H, Gaus W, Achenbach U et al. (2008) Benfotiamine in diabetic polyneuropathy (BENDIP): results of a randomised, double blind, placebo-controlled clinical study. Exp Clin Endocrinol Diabetes 116, 600-605.
8. Sheng L, Cao W, Lin P et al. (2021) Safety, Tolerability and Pharmacokinetics of Single and Multiple Ascending Doses of Benfotiamine in Healthy Subjects. Drug design, development and therapy 15, 1101-1110.
9. (2013) Thiamine (Vitamin B1). Mayo Clinic.
10. Fraser DA, Diep LM, Hovden IA et al. (2012) The effects of long-term oral benfotiamine supplementation on peripheral nerve function and inflammatory markers in patients with type 1 diabetes: a 24-month, double-blind, randomized, placebo-controlled trial. Diabetes Care 35, 1095-1097.
11. Haupt E, Ledermann H, Kopcke W (2005) Benfotiamine in the treatment of diabetic polyneuropathy—a three-week randomized, controlled pilot study (BEDIP study). Int J Clin Pharmacy There 43, 71-77.