Diabetic peripheral neuropathy (DPN) is the most common complication of diabetes and is responsible for substantial deterioration in quality of life. DPN is characterized by damage to nerves and small blood vessels. About 60% to 70% of people with diabetes have nervous system damage. The results of such damage include impaired sensation or pain in the feet or hands, difficulty swallowing, slowed digestion of food in the stomach, carpal tunnel syndrome, numbness and tingling of extremities, diarrhea, urinary incontinence, facial, mouth and eyelid drooping, vision changes, dizziness, muscle weakness, speech impairment, impotence, erectile dysfunction and anorgasmia, burning or electric pain, among others.1
According to current medical guidelines, metformin is the first-line drug of choice for the treatment of type 2 diabetes (DM2) particularly in overweight people with normal kidney function.2 Metformin therapy for more than 6 months in patients with DM2 who are carriers of certain dysfunctional MTHFR polymorphisms could be considered a pharmacogenetic cause for worsening of DPN, suggesting an earlier switch to insulin. This risk appears to be higher in patients with certain MTHFR genotypes, due to higher serum levels of Homocysteine. Methylene-tetrahydrofolate reductase (MTHFR) is an enzyme that is encoded by the MTHFR gene. MTHFR catalyzes the conversion folate (vitamin B9) found naturally in foods, to its active form. Impairment of this process leads to build up of Homocysteine which is a potentially toxic amino acid and cardiovascular risk factor.
Related to:
Diabetes, Metabolic syndrome, Peripheral Neuropathy, Metformin