Vitamin-dependent Gene Databases
This vitamin-dependent database lists all known gene products with domains using either vitamin B1 (thiamine), B2 (riboflavin), or B3 (niacin) as a co-factor or substrate (Penberthy, 2013).
Genetic polymorphisms that reduce vitamin (derived) co-factor/substrate binding affinity result in individuals whose lives can be saved, improved, or optimized by high-dose vitamin therapy (Ames, 2002). This is true for countless numbers of individuals. It costs almost nothing to do high-dose vitamin therapy and the safety profile is superior to most pharmaceuticals.
It may be a clinically significant to consider genetic polymorphisms in the genes containing NAD, thiamine, and/or riboflavin-binding domains.
These databases were developed from my own research using UniproKB with assistance of Dr. Kristian Axelsen of the Swiss Institute of Bioinformatics, 2012.
Databases are freely available for download at the bottom of this page.
Niacin is particularly impressive for many reasons not limited to the following. The biochemical end-product of niacin consumption, nicotinamide adenine dinucleotide (NAD), is used a co-factor or substrate in more reactions than any other vitamin-derived co-factor, >450 reactions. A polymorphism in the NAD binding for any of these genes can cause an individual to require higher amounts of niacin to provide greater NAD concentrations. NAD is used in phase 1 drug metabolism, including basic alcohol metabolism, where the founder of Alcoholics Anonymous himself, Bill W, was a great proponent of its use in controlling alcoholism (Niacin Therapy as Used by Abram Hoffer). We know more about several mechanisms that specifically and actively trigger the depletion of NAD than we do for most vitamins (Penberthy, 2007; Penberthy, 2009). Niacin-related research continues to amaze, with the PARP, Sirtuin, CD38, drug metabolism fields, and more all giving perennial consideration to this amazing molecule.
Thiamine, while only involved in roughly 30 different reactions, thiamine is essential for several central bioenergetic pathways particularly important in preventing neurodegeneration and powering the heart. Thiamine is distinguished as the heat-sensitive B vitamin. Absence of thiamine essentially causes the brain to rot and favorable results have been seen after high-dose administration for a variety of neurological conditions. Thiamine is routinely administered by injection to treat Wernicke-Korsakoff syndrome, which most frequently occurs in chronic alcoholics. Recovery from nystagmus can occur within minutes of injection. Most unfortunately thiamine research is woefully overlooked, but it makes sense as consideration for neurodegenerative diseases like Alzheimer's.
Riboflavin is the most colorful vitamin. While, it is difficult to achieve high doses of this B vitamin due to poor solubility, something is everything when it is essential. It is used in a wide range of reactions (>200). Unfortunately the mechanisms of riboflavin depletion are poorly understood and this vitamin is generally understudied.
Ames BN, Elson-Schwab I, Silver EA. High-dose vitamin therapy stimulates variant enzymes with decreased coenzyme binding affinity (increased K(m)): relevance to genetic disease and polymorphisms. Am J Clin Nutr. Apr 2002;75(4):616-658.
Penberthy WT. Niacin, Riboflavin, and Thiamine. In: Stipanuk MH, Caudill MA, eds. Biochemical, physiological, and molecular aspects of human nutrition. 3rd ed. St. Louis, Mo.: Elsevier/Saunders; 2013:p.540-564.
Penberthy WT. Pharmacological targeting of IDO-mediated tolerance for treating autoimmune disease. Curr Drug Metab. Apr 2007;8(3):245-266.
Penberthy WT, Tsunoda I. The importance of NAD in multiple sclerosis. Curr Pharm Des. 2009;15(1):64-99.