Relative nutritional deficiencies associated with centrally acting monoamines

Abstract

BackgroundTwo primary categories of nutritional deficiency exist. An absolute nutritional deficiency occurs when nutrient intake is not sufficient to meet the normal needs of the system, and a relative nutritional deficiency exists when nutrient intake and systemic levels of nutrients are normal, while a change occurs in the system that induces a nutrient intake requirement that cannot be supplied from diet alone. The purpose of this paper is to demonstrate that the primary component of chronic centrally acting monoamine (serotonin, dopamine, norepinephrine, and epinephrine) disease is a relative nutritional deficiency induced by postsynaptic neuron damage.Materials and methodsMonoamine transporter optimization results were investigated, reevaluated, and correlated with previous publications by the authors under the relative nutritional deficiency hypothesis. Most of those previous publications did not discuss the concept of a relative nutritional deficiency. It is the purpose of this paper to redefine the etiology expressed in these previous writings into the realm of relative nutritional deficiency, as demonstrated by monoamine transporter optimization. The novel and broad range of amino acid precursor dosing values required to address centrally acting monoamine relative nutritional deficiency properly is also discussed.ResultsFour primary etiologies are described for postsynaptic neuron damage leading to a centrally acting monoamine relative nutritional deficiency, all of which require monoamine transporter optimization to define the proper amino acid dosing values of serotonin and dopamine precursors.ConclusionHumans suffering from chronic centrally acting monoamine-related disease are not suffering from a drug deficiency; they are suffering from a relative nutritional deficiency involving serotonin and dopamine amino acid precursors. Whenever low or inadequate levels of monoamine neurotransmitters exist, a relative nutritional deficiency is present. These precursors must be administered simultaneously under the guidance of monoamine transporter optimization in order to achieve optimal relative nutritional deficiency management. Improper administration of these precursors can exacerbate and/or facilitate new onset of centrally acting monoamine-related relative nutritional deficiencies.

Administration of supplemental L-tyrosine with phenelzine: a clinical literature review

“…Total phenelzine with L-tyrosine medical record data on file are approximately 43,532 patient-days. This database was started in 1999, and up to the time of this writing no concerns have been raised regarding concomitant administration of L-tyrosine with phenelzine 15–29…”

Management of L-dopa overdose in the competitive inhibition state

“…L-dopa freely crosses the blood–brain barrier, then is synthesized into dopamine without biochemical feedback inhibition 2. Greater amounts of L-dopa need to be administered if increased synthesis of dopamine in the central nervous system is required 3–12. L-tyrosine does not have this ability, due to norepinephrine biochemical feedback inhibition of tyrosine hydroxylase.…”

“…Their respective conversion to L-dopa and 5-HTP in a normal or optimal diet are inadequate to establish competitive inhibition. This limits the amount of dopamine and serotonin synthesized to levels less than are required to place the system into the competitive inhibition state 12–20. When daily dopamine and dopamine amino acid requirements are higher than can be achieved in a normal or optimal diet, the state is known as a relative nutritional deficiency 12…”

“…Full optimization of the competitive inhibition state requires simultaneous administration of properly balanced 5-HTP, L-dopa, L-tyrosine, a thiol (L-cysteine, glutathione, S-adenosylmethionine, or L-methionine), and cofactors (vitamin C, pyridoxal phosphate, or calcium carbonate). To date, the only published methodology for optimization of the competitive inhibition state is Organic Cation Transporter Type 2 (OCT2) functional status determination 12–20…”

“…The properly balanced competitive inhibition approach avoids the extensive depletion of serotonin, thiols, L-tyrosine, and L-tryptophan that is known to exist with L-dopa monotherapy. It also eliminates the nausea dosing barrier that may occur when L-dopa is administered without the need for a general decarboxylase inhibitor 2,12…”