Adenosine Triphosphate (ATP) is the primary intracellular energy carrier of all living organisms on earth. In humans, the vast majority of ATP is produced in the mitochondria through the actions of oxidative phosphorylation–an aerobic metabolic process in which energy is extracted from pyruvate, the end product of glycolysis. The Krebs Cycle is central to this mechanism.
Vitamin B1 is a rate-limiting essential nutrient of the Krebs Cycle. It acts as a coenzyme or allosteric regulator on five of the nine enzymes that either compose the cycle or regulate the entry of pyruvate into the cycle. Cellular ATP availability is dependent on adequate vitamin B1 levels. High levels of vitamin B1 act to maximize ATP production. This is of particular significance in neurons. Nerve cells require about 10 ten times the energy of most all other cell types. Nerve cells are highly sensitive to low ATP levels, and as such, people deficient in vitamin B1 often experience neurological dysfunction.
In the central nervous system (CNS), vitamin B1 deficiency is associated with Alzheimer’s disease. In the peripheral nervous system (PNS), it is associated with diabetic and other polyneuropathies. In the US, Alzheimer’s disease is the most common neurodegenerative disease of the CNS and polyneuropathy is the most common form of neurodegeneration of PNS. The data would thus suggest that vitamin B1 deficiency is associated with a high proportion of cases of neurodegenerative disease in the US. Unfortunately, vitamin B1 deficiency is quite common and most often goes unrecognized. In addition to diabetics and people suffering from Alzheimer’s disease, the elderly, people with a history of chronic alcohol abuse, and the obese, are all known to frequently be vitamin B1 deficient.
Clinicians should consider vitamin B1 supplementation with benfotiamine, a safe and effective vitamin B1 analogue, in cases where a neurodegenerative process, such as diabetic and other polyneuropathies, is suspected. This course of treatment is well supported by the scientific literature as well as the experience of tens of thousands of patients and clinicians.
Preliminary studies suggest that benfotiamine may significantly improve neurological function in Alzheimer’s disease. The powerful beneficial effects observed in these studies resulted recently in a grant of $45 million by the NIH to fund a large-scale, multi-center clinical trial to evaluate benfotiamine as a potentially effective therapy for mild Alzheimer’s disease or mild cognitive impairment. Let’s hope this new study proves the efficacy of this remarkable nutrient in the treatment of this terrible malady. I am extremely hopeful and guardedly optimistic.