In order for neurons to successfully perform their primary function of conducting action potentials, their mitochondria produce significantly greater amounts of energy, in the form of ATP, than all other cell types. The inability of the mitochondria in peripheral neurons to generate sufficient quantities of ATP for healthy cellular functioning is believed to be a contributing factor in polyneuropathy. As such, increasing ATP production within the mitochondria of peripheral neurons is a highly desirable goal in the treatment of patients with polyneuropathy.
Ninety percent of cellular thiamine, also known as vitamin B1, is found within the mitochondria. Vitamin B1 is essential for the mitochondrial production of ATP. Thiamine deficiency is well-established in diabetes and alcoholism–two of the leading causes of polyneuropathy. Thiamine replacement with the use of benfotiamine, a highly bioactive form of the vitamin, has been shown to improve the symptoms of polyneuropathy in diabetics and alcoholics. This is likely a consequence of improved mitochondrial function and increased ATP production within peripheral neurons.
Interestingly, appropriate low-level laser light therapy of certain frequencies and intensities has also been shown to reduce neuropathic symptoms. The mechanism by which this occurs is believed to be, in part, the stimulation by light energy ofcytochrome-c-oxidase (complex IV) in the mitochondrial respiratory chain causing increased ATP production within peripheral neurons.
The fact that these disparate therapies both appear to improve mitochondrial ATP production and be beneficial in the treatment of polyneuropathy supports the hypothesis that decreased ATP availability in peripheral neurons is an important contributing factor in polyneuropathy. This would also account for the observation by many clinicians that their clinical success rate in the treatment of polyneuropathy with the use of low-level laser light therapy is improved with the addition of benfotiamine supplementation.