... Defective oxidative metabolism caused in this patient’s case by thiamine deficiency, causes exaggerated brain perception. The brain induced a pain that gave the false impression that the disease originated in the joints and other parts of the body. Even if the origin of the pain is truly from a joint or muscle, defective oxidative metabolism in the brain will exaggerate the sense of pain perceived by the patient. Although this “phantom” pain is known as “hyperalgesia”, the mechanism is not well known as being due to compromised oxidation in the pain perception brain centers. Thiamine deficiency was responsible for the hyperalgesia experienced by the case of a patient with eosinophilic esophagitis that was posted recently on this website. ...Returning to the case of the 6-year old boy discussed above, we learned over time that his health was dependent on high doses of thiamine to function. Believe it or not, this child required 600 mg of thiamine a day in order to prevent his episodes of illness. If he began to notice the beginning of an infection he would double the dose. The recommended daily allowance for thiamine is between one and 1.5 mg a day. Here, and in many other cases, huge doses of the vitamin are required in order to accomplish the physiologic effect. This represents what I call vitamin dependency.
Thiamine and magnesium, like many other vitamins, are known as cofactors to enzymes. An enzyme without its cofactor works inefficiently if it works at all. The “magic” of evolution has “invented” this cooperative action which is in itself under genetic control. In technical terms, the vitamin has to “bond” with the enzyme. If this bonding mechanism is genetically compromised, the concentration of the corresponding cofactor has to be increased enormously by supplementation in order to prevent the inevitable symptoms. You can see that this requires a clinical perspective tied to unusual biochemical knowledge. This is in complete contrast to what is usually regarded as vitamin deficiency, arising from insufficient concentrations in the diet.
What is perhaps not known sufficiently is that prolonged vitamin deficiency appears to affect this bonding mechanism. For example, it has long been known that to cure chronic beriberi, megadoses of thiamine are required for months. I have concluded that the megadoses of thiamine given by supplementation to a patient with long term symptoms arising from unrecognized deficiency appears to re-activate the inefficient enzyme. It is as though the enzyme has to be repeatedly exposed to megadoses of its cofactor to stimulate it and restore its lost function.