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L-Dopa Analysis

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The most significant side effects and adverse reactions may occur with long-term use many months or longer. Administration of 5-HTP alone depletes catecholamines dopamine, norepinephrine, and epinephrine. Based on monoamine transporter optimization MTO studies, managing depression and other centrally acting monoamine-related diseases requires a combination of properly balanced dopamine and serotonin amino acid precursors. Dopamine and serotonin amino acid precursor administration must be in proper balance. If only 5-HTP or 5-HTP that dominates dopamine at the enzyme is administered, it will block dopamine synthesis at the AAAD enzyme through competitive inhibition, leading to depletion of dopamine and the rest of the catecholamines.

Metabolism of serotonin and dopamine is catalyzed by monoamine oxidase MAO. The activity level of MAO is not static. Without a properly balanced increase in dopamine there will be increased metabolism of dopamine leading to depletion. The synthesis, metabolism, and transport of serotonin and dopamine, along with their amino acid precursors, are primarily controlled by the functional status of transport, which is carried out by organic cation transporters OCT.

Serotonin, dopamine, and their amino acid precursors must be transported by OCT across cell walls. Transport dominates, controls and regulates synthesis and metabolism. Administration of 5-HTP alone leads to increased unbalanced transport of serotonin. Competitive inhibition at the transporters will inhibit movement of dopamine and its precursors into areas that affect synthesis and metabolism, compromising and depleting dopamine catecholamine levels. Long-term administration of 5-HTP alone, or in an unbalanced manner, facilitates depletion of catecholamines, negatively affecting neurotransmitter-related disease processes. A literature review revealed that more studies have been reported using 5-HTP in combination with another substance than using 5-HTP alone due to the lack of efficacy of 5-HTP alone.

One combination examined includes the use of 5-HTP with carbidopa. Carbidopa inhibits peripheral conversion of 5-HTP to serotonin and l -dopa to dopamine. Additionally, a previous study reported that in animals 5-HTP caused increased turnover of both dopamine and norepinephrine. They hypothesized that 5-HTP is taken up by catecholaminergic neurons, transformed into 5-HT that, in turn, could act as a false transmitter, possibly increasing the turnover of catecholamines. In other words, it is unknown whether 5-HTP augments or reduces catecholaminergic neuronal functions. Serotonin and dopamine systems exist in two distinctly different and separate states. The endogenous state occurs when no supplemental amino acid precursors Figure 1 are administered.

The competitive inhibition state occurs when at least one serotonin and one dopamine amino acid precursor Figure 1 are administered simultaneously. In the unbalanced state, amino acid precursors of serotonin or dopamine dominate the opposite system in synthesis, metabolism, and transport, leading to depletion of nondominant monoamine neurotransmitters Figure 2. Sulfur amino acids may deplete dopamine. Sulfur amino acids may deplete serotonin.

Amino acid precursors of serotonin and dopamine in the competitive inhibition state are intertwined during synthesis, metabolism, and transport to the point that they function as one system. This is a deep-seated interaction as discussed in the novel concept of apical regulatory super system APRESS , published in The paper discusses how the serotonin and dopamine systems, when properly balanced in the competitive inhibition state, function as one system.

In this state, functions regulated only by serotonin in the endogenous state can be regulated by manipulating dopamine levels, and functions regulated only by dopamine in the endogenous state can be regulated by manipulating serotonin. Most importantly, if only one precursor of the serotonin and dopamine system is administered or it is administered in a manner that dominates the other system either serotonin or dopamine in synthesis, metabolism and transport, neurotransmitter depletion of the dominated system will occur. When this depletion of the nondominant system is great enough, any effects observed with administration of the single or dominant amino acid will no longer be observed.

A study involving properly balanced serotonin and dopamine amino acid precursor dosing values guided by MTO published in and documents that administration of properly balanced serotonin and dopamine precursors is not only highly effective for managing depression, but can also be used to differentiate bipolar depression cycling heavily on the depressive pole from unipolar depression major affective disorder. To achieve optimal efficacy, minimal side effects, and prevent depletion of other amino acids and neurotransmitters, 5-HTP must be administered in proper balance with dopamine amino acid precursors along with proper levels of sulfur amino acids.

Synthesis and metabolism are controlled by transporter function. Transporters move serotonin, dopamine and their amino acid precursors into and out of cells to sites where synthesis and metabolism occur. MTO is an in situ method for determining the functional status of OCT responsible for establishing serotonin and dopamine levels throughout the body. Optimization requires establishing serotonin in the Phase 3 optimal range while dopamine is in its Phase 3 optimal range. The Phase 3 optimal ranges of serotonin and dopamine are independent of one another.

When both serotonin and dopamine are in their respective phase 3 optimal ranges, optimization has occurred. Optimal group results cannot be obtained without MTO. The following are group effective therapeutic ranges defined by MTO during simultaneous administration of serotonin and dopamine precursors:. The effective therapeutic ranges listed above are independent of each other. For example, in one patient, a daily 5-HTP dosing value of 2, mg per day with an l -dopa dosing value of 30 mg per day may be required for proper balance of transport to place both serotonin and dopamine in their respective Phase 3 optimal ranges.

Another patient may require 25 mg per day of 5-HTP with 2, mg of l -dopa for Phase 3 optimization. Dosing values required for transporter optimization are highly individualized. To understand the extreme variability in the dosing levels of 5-HTP and the other amino acid precursors, it is important to understand why these transporters react so differently from one individual to the next. Neurotransmitters facilitate the flow of electric signals across the synapse between the pre- and post-synaptic neurons. When a change in the overall flow of electricity across the synapse is needed, a signal is sent throughout the body that encodes the identical transporters to regulate and control neurotransmitter flow in the specific manner required to optimize this flow.

This process may damage areas regulating affect and mood, leading to depression. Since serotonin and dopamine do not cross the blood—brain barrier, the total number of serotonin and dopamine molecules present in the brain is a function of the amount of nutrients amino acid precursors available to be synthesized into new neurotransmitter molecules. If the amount of neurotransmitter molecules is low or inadequate, a relative nutritional deficiency exists. Optimal efficacy and minimized side effects are not a function of achieving sufficiently high amino acid dosing levels; they are a function of achieving a proper balance between serotonin and dopamine.

Intuitively, the potential is extraordinary, but from a practical level efficacy is no better than placebo. In review of the science, effective integration of 5-HTP into a patient management plan is much more complicated than simply giving some 5-HTP in order to have more serotonin throughout the system. Administration of 5-HTP alone is contraindicated for depression and any process involving a catecholamine component due to its ability to facilitate depletion of these neurotransmitters. Administering serotonin or dopamine amino acid precursors should never involve administration of only one amino acid.

Improperly balanced amino acid precursors are associated with decreased efficacy, increased side effects, and depletion of the nondominant system. AS has no disclosures to reveal. National Center for Biotechnology Information , U. Journal List Neuropsychiatr Dis Treat v. Neuropsychiatr Dis Treat. Published online Jul Author information Copyright and License information Disclaimer. This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

An expression of concern has been published for this article. See Neuropsychiatr Dis Treat. This article has been cited by other articles in PMC. Abstract Lhydroxytryptophan 5-HTP is the immediate precursor of serotonin. Introduction In the United States, the nutritional supplement 5-hydroxytryptophan 5-HTP became available over the counter in April of The argument for using 5-HTP When placed in the proper context, the following basic chemical properties 2 — 15 explain the failure of 5-HTP to achieve consistent results. The following scientific facts are generally accepted without dispute: In central nervous system disease states associated with synaptic serotonin dysfunction, synaptic serotonin levels in the brain must be increased to induce optimal outcomes.

Serotonin does not cross the blood—brain barrier. Short-term efficacy of 5-HTP alone Generally, efficacy studies related to 5-HTP fall into one of two categories: open nonblinded and double-blind, placebo-controlled studies. Monoamine depletion by amino acid precursors Serotonin and dopamine systems exist in two distinctly different and separate states. Open in a separate window. Figure 1. Synthesis pathway of serotonin and catecholamines. Abbreviation: 5-HTP, 5-hydroxytryptophan. Figure 2. Effects of 5-HTP when administered in an unbalanced manner Amino acid precursors of serotonin and dopamine in the competitive inhibition state are intertwined during synthesis, metabolism, and transport to the point that they function as one system.

Administration of 5-HTP in a properly balanced manner To achieve optimal efficacy, minimal side effects, and prevent depletion of other amino acids and neurotransmitters, 5-HTP must be administered in proper balance with dopamine amino acid precursors along with proper levels of sulfur amino acids. Conclusion 5-HTP in the treatment of depression has languished for years. References 1. Hinz M. In: Kohlstadt I, editor. Food and Nutrients in Disease Management. Both stimulatory and inhibitory effects of dietary 5-hydroxytryptophan and tyrosine are found on urinary excretion of serotonin and dopamine in a large human population.

The dual-gate lumen model of renal monoamine transport. Neurotransmitter testing of the urine; a comprehensive analysis. Research and Reports in Urology. A pilot study differentiating recurrent major depression from bipolar disorder cycling on the depressive pole. The regulatory nature of the N-terminal domain residues 1— is conferred by its structural flexibility. This lag time is not observed, however, for a truncated PAH lacking the N-terminal domain or if the full-length enzyme is pre-incubated with Phe. Deletion of the N-terminal domain also eliminates the lag time while increasing the affinity for Phe by nearly two-fold; no difference is observed in the V max or K m for the tetrahydrobiopterin cofactor.

Prokaryotic PAH is monomeric, whereas eukaryotic PAH exists in an equilibrium between homotetrameric and homodimeric forms. The resulting distortion of the tetramer symmetry is evident in the differential surface area of the dimerization interfaces and distinguishes PAH from the tetramerically symmetrical tyrosine hydroxylase. In addition to reduced catalytic efficiency, the dimer does not display positive cooperativity toward L-Phe which at high concentrations activates the enzyme , suggesting that L-Phe allosterically regulates PAH by influencing dimer-dimer interaction.

PAH is a critical enzyme in phenylalanine metabolism and catalyzes the rate-limiting step in its complete catabolism to carbon dioxide and water. The principal source of phenylalanine is ingested proteins, but relatively little of this pool is used for protein synthesis. Transamination to phenylpyruvate , whose metabolites are excreted in the urine, represents another pathway of phenylalanine turnover, but catabolism through PAH predominates.

In humans, this enzyme is expressed both in the liver and the kidney, and there is some indication that it may be differentially regulated in these tissues. Deficiency in PAH activity due to mutations in PAH causes hyperphenylalaninemia HPA , and when blood phenylalanine levels increase above 20 times the normal concentration, the metabolic disease phenylketonuria PKU results. Follow-up studies suggest that in the case of certain PAH mutants, excess BH4 4 acts as a pharmacological chaperone to stabilize mutant enzymes with disrupted tetramer assembly and increased sensitivity to proteolytic cleavage and aggregation.

Since phenylketonuria can cause irreversible damage, it is imperative that deficiencies in the phenylalanine hydroxylase are determined early on in development. Originally, this was done using a bacterial inhibition assay known as the Guthrie Test. Now, PKU is part of newborn screening in many countries, and elevated phenylalanine levels are identified shortly after birth by measurement with tandem mass spectrometry.

Placing the individual on a low phenylalanine, high tyrosine diet can help prevent any long-term damage to their development. The three enzymes are homologous, that is, are thought to have evolved from the same ancient hydroxylase. From Wikipedia, the free encyclopedia. Chromosome 12 human [1]. See also: Biopterin-dependent aromatic amino acid hydroxylase. National Center for Biotechnology Information, U. National Library of Medicine. Annual Review of Biochemistry. PMID The Journal of Biological Chemistry. PMC Chemical Reviews. Archives of Biochemistry and Biophysics. Molecular Genetics and Metabolism. Scientific Reports. Journal of the American Chemical Society.

Nature Structural Biology. S2CID Journal of Molecular Biology. European Journal of Biochemistry. Journal of Inherited Metabolic Disease. Human Mutation. Human Genetics. Cotton RG Waters PJ April Metabolism : Protein metabolism , synthesis and catabolism enzymes. Essential amino acids are in Capitals. Saccharopine dehydrogenase Glutaryl-CoA dehydrogenase.

Alanine transaminase. D-cysteine desulfhydrase.

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