Metformin Shown to Inhibit Thiamine (Vitamin B1) Absorption, a Contributing Factor in Diabetic Polyneuropathy
by Dr. Richard Mann, DABPS, ret, Chief Scientific Officer & Founder, Realm Labs®
In a landmark paper, Thornalley et al showed that, due to impaired kidney function, plasma thiamine levels in diabetics are 75% lower than in non-diabetics. Thiamine deficiency is a major contributing factor in the pathobiology of diabetic polyneuropathy and its reversal by a lipid soluble form of thiamine, benfotiamine,is characterized by significant improvement in the symptoms of polyneuropathy including pain, numbness and tingling of the feet and legs. Patients on metformin were recently shown to be at even greater risk of thiamine deficiency than other diabetics. A 2015 study published in the journal Molecular Pharmacology found that metformin, the most commonly prescribed drug in the US for the treatment of diabetes, inhibited thiamine transporter molecule THTR2, decreasing thiamine absorption from the intestines and thiamine availability to peripheral neurons.
Benfotiamine is absorbed via passive diffusion. Unlike most forms of thiamine, the absorption of benfotiamine is independent of transporter molecule THTR2. Benfotiamine is safe, effective and works within a month. It is ideally suited to restore thiamine levels and improve neuropathic symptoms in all diabetics, including those on metformin.
Over the past decade, benfotiamine has revolutionized the management of polyneuropathy in the US and Canada. It is currently dispensed by thousands of clinicians to their patients suffering from polyneuropathy caused by diabetes, prediabetes, alcoholism, advanced age and chemotherapy, all conditions associated with thiamine deficiency. This new data on the inhibition of thiamine absorption by metformin further explains the impressive results reported by these clinicians.
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