Benfotiamine, a synthetic derivative of vitamin B1, shows promise in reducing advanced glycation end-products (AGEs) and may improve cognitive health over time.
In recent discussions surrounding preventative health, benfotiamine—a synthetic form of vitamin B1, also known as thiamine—has gained attention for its potential role in enhancing memory and cognitive function. The Kahn Center, which focuses on long-term cardiac health while assessing risks for cancer, diabetes, and dementia, highlights the accumulation of AGEs as a significant factor in chronic diseases.
Benfotiamine’s Impact on Brain Health
The Kahn Center employs a unique method to measure AGEs through skin autofluorescence (SAF). The clinic suggests that modifying blood sugar levels, altering cooking methods—such as avoiding high-heat and dry cooking techniques for meats—and supplementing with benfotiamine can help mitigate AGE accumulation over time.
Preclinical studies indicate that benfotiamine can effectively address various pathologies associated with Alzheimer’s disease (AD). These include cognitive impairment, the presence of amyloid-β plaques, neurofibrillary tangles, reduced glucose metabolism, oxidative stress, heightened AGEs, and inflammation.
Study Overview
A recent study aimed to assess the feasibility, safety, and efficacy of benfotiamine in improving cognitive function among adults with amnestic mild cognitive impairment (aMCI) or mild dementia due to AD. This placebo-controlled trial involved a twelve-month treatment regimen of benfotiamine at a dosage of 300 mg taken twice daily, comparing outcomes between the benfotiamine group and the placebo group. The primary outcome measure was the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-Cog), while secondary outcomes included the clinical dementia rating (CDR) score and brain fluorodeoxyglucose (FDG) uptake, as measured by positron emission tomography (PET). Blood levels of AGEs were also evaluated as an exploratory outcome.
Study Findings
In the trial, 34 participants received benfotiamine, while 36 were given a placebo. Results showed that benfotiamine treatment was safe, with a 43% lower increase in ADAS-Cog scores among those receiving benfotiamine, indicating a reduced rate of cognitive decline compared to the placebo group. Additionally, the worsening of CDR scores was 77% lower (p = 0.034) in the benfotiamine group, particularly among individuals who were non-carriers of the APOE ε4 allele, a genetic risk factor for Alzheimer’s disease.
Notably, benfotiamine treatment significantly reduced increases in AGEs (p = 0.044), with a more pronounced effect observed in the APOE ε4 non-carriers.
Conclusion
The findings suggest that oral benfotiamine is both safe and potentially effective in improving cognitive outcomes for individuals with MCI and mild AD. This affordable and readily available supplement may provide a valuable option in managing cognitive decline. With advancements in measuring AGEs, particularly through SAF, healthcare providers can better identify patients at heightened risk for Alzheimer’s disease and other chronic conditions, including coronary disease, diabetes, and neuropathy.
At the Kahn Center, patients are advised to avoid high-temperature cooking methods. Instead, methods such as stewing or slow cooking are encouraged, as animal products, especially bacon, are high in AGEs. There is growing evidence supporting the efficacy of benfotiamine, which is utilized alongside lifestyle modifications as a preventive strategy. Regular monitoring of blood sugar levels through fasting glucose, insulin, and HgbA1C tests is standard practice, with continuous glucose monitoring considered for some patients.
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