CLINICIAN ALERT: REVERSING THIAMINE (VITAMIN B1) DEFICIENCY IN THE TREATMENT OF DIABETIC POLYNEUROPATHY: AN IMPORTANT THERAPEUTIC GOAL
SUMMARY: Thiamine deficiency is endemic in diabetics and an etiological factor in diabetic polyneuropathy. Reversing thiamine deficiency is an important therapeutic goal which has been shown to dramatically improve the symptoms associated with diabetic polyneuropathy.
In a seminal paper on thiamine deficiency and diabetes, Thornalley et al. compared plasma thiamine status in diabetic vs. non-diabetic subjects and found plasma thiamine concentration was decreased by 75% in diabetic patients. These findings agree with other studies and confirm that thiamine deficiency is endemic in diabetics. In a related paper, Porta et al. make the case that “diabetes might be considered a thiamine-deficient state…”. They eloquently argue that diabetes, a disease characterized by impaired carbohydrate processing, is intimately related to thiamine deficiency, a condition that impairs carbohydrate processing. Because the most commonly prescribed antidiabetic medication, metformin, inhibits the actions of thiamine transporter molecules in the intestines, diabetics on metformin are at even greater risk of thiamine deficiency than are patients on other antidiabetic medications. The relationship between thiamine deficiency and impaired function of intestinal thiamine transporters may be highly relevant in diabetics.
Although the causes of diabetic polyneuropathy are complex and multifaceted, it is well established that thiamine deficiency contributes to the intensity of the neuropathic symptoms experienced by diabetics. Neurons are a highly energy-dependent cell type. They require tenfold the energy of most other cell types. Thiamine is essential for the production of energy from carbohydrates and its deficiency decreases energy availability to all cells but, because of their high energy requirements, neurons are particularly vulnerable to thiamine deficiency. In peripheral nerves, decreased energy availability is expressed clinically as polyneuropathy. As such, the reversal of thiamine deficiency is an important therapeutic goal which often dramatically improves the symptoms of patients with diabetic polyneuropathy.
Dietary thiamine is water-soluble and poorly absorbed. Its absorption is dependent on the actions of thiamine transporter molecules located on the surface of the intestines. The efficiency of these transporter molecules can be decreased by many factors including metformin and chronic alcohol use. Benfotiamine, a high potency form of thiamine, is lipid soluble. It is absorbed from the intestines via passive diffusion, a process independent of thiamine transporter molecules. Lipid solubility allows for greatly improved absorption when compared to water-soluble thiamine. Benfotiamine is an ideal agent to reverse thiamine deficiency and has been shown in multiple well-constructed scientific studies to be safe and often effective in successfully and rapidly improving the symptoms associated with diabetic polyneuropathy.