Monoamine depletion by reuptake inhibitors

Hinz, Marty; Stein, Alvin; Uncini, Thomas

doi:10.2147/dhps.s24798

Cited by 11 publications

(73 citation statements)

References 29 publications

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“…When the monoamine flows are optimized immediately above the phase 2/phase 3 inflection point, as discussed in this section, there is optimal restoration of postsynaptic electrical flow. However, when a significant RND exists, encoded OCT needs cannot be met by dietary intake alone, and this is the basis of the RND 1–13…”

Section: Methodsmentioning

confidence: 99%

“…Conditions prior to in situ monoamine transporter optimization (MTO, referred to in some previous papers as OCT functional status optimization) made it impossible to achieve consistent results with the administration of monoamine amino acid precursors. With the invention and refinement of MTO, the ability to study, manipulate, and optimally manage monoamine-related RND became clinically possible 1–13…”

Section: Absolute Nutritional Deficiency Versus Rndmentioning

confidence: 99%

“…When the etiology of chronic symptoms is postsynaptic electrical compromise, the system needs to be placed into the competitive inhibition state in order to elevate synaptic monoamines high enough to compensate for the postsynaptic damage. Optimization of synaptic monoamine levels in order to facilitate optimal flow of electricity is only possible with simultaneous administration of serotonin and dopamine precursors guided by MTO 1–8,11–13…”

Section: Endogenous Versus Competitive Inhibition Statementioning

confidence: 99%

“…When unbalanced amino acid precursors and/or monoamines are present at the transporter entrance, systemic monoamine concentrations, which are dependent on transport, will not be optimal. This leads to an amino acid-induced RND along with suboptimal regulation of function 1–8,11–13…”

Section: Synaptic Monoamine Levelsmentioning

confidence: 99%

“…Further research in the areas covered in the previous writings has revealed a relative nutritional deficiency (RND) etiology not previously recognized or reported. The novel concept of a monoamine-related RND is developed in this paper 1–13…”

Section: Introductionmentioning

confidence: 99%

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Relative nutritional deficiencies associated with centrally acting monoamines

Hinz¹,

Stein²,

Uncini³

2012

IJGM

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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.

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Section: Methodsmentioning

confidence: 99%

Section: Absolute Nutritional Deficiency Versus Rndmentioning

confidence: 99%

Section: Endogenous Versus Competitive Inhibition Statementioning

confidence: 99%

Section: Synaptic Monoamine Levelsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Relative nutritional deficiencies associated with centrally acting monoamines

Hinz¹,

Stein²,

Uncini³

2012

IJGM

Self Cite

View full text Add to dashboard Cite

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Dietary intake of tryptophan tied emotion-related impulsivity in humans

Javelle

Zimmer

et al. 2021

International Journal for Vitamin and Nutrition Research

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Abstract. Emotion-related impulsivity, defined as the tendency to say or do things that one later regret during periods of heightened emotion, has been tied to a broad range of psychopathologies. Previous work has suggested that emotion-related impulsivity is tied to an impaired function of the serotonergic system. Central serotonin synthesis relies on the intake of the essential amino acid, tryptophan and its ability to pass through the blood brain barrier. Objective: The aim of this study was to determine the association between emotion-related impulsivity and tryptophan intake. Methods: Undergraduate participants (N = 25, 16 women, 9 men) completed a self-rated measure of impulsivity (Three Factor Impulsivity Index, TFI) and daily logs of their food intake and exercise. These data were coded using the software NutriNote to evaluate intakes of tryptophan, large neutral amino acids, vitamins B6/B12, and exercise. Results: Correlational analyses indicated that higher tryptophan intake was associated with significantly lower scores on two out of three subscales of the TFI, Pervasive Influence of Feelings scores r = –.502, p < . 010, and (lack-of) Follow-Through scores, r = –.407, p < . 050. Conclusion: Findings provide further evidence that emotion-related impulsivity is correlated to serotonergic indices, even when considering only food habits. It also suggests the need for more research on whether tryptophan supplements might be beneficial for impulsive persons suffering from a psychological disorder.

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Effects of 5-hydroxytryptophan on distinct types of depression: a systematic review and meta-analysis

et al. 2019

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Context Serotonergic dysfunction, including reduced central serotonin levels, is associated with different psychiatric syndromes, including depression. As a serotonin precursor, 5-hydroxytryptophan has long been used as a nonpharmacological treatment for depression. Objective A systematic review and meta-analysis was conducted to determine the antidepressant effects of 5-hydroxytryptophan in depressed patients. Data sources MEDLINE (via PubMed) and Google Scholar were searched from inception to May 2018. Data extraction Thirteen investigations were included in the systematic review (using PRISMA guidelines), and 7 in the full meta-analysis (pre-registered on PROSPERO: CRD42018104415). Data analysis Analyses revealed a depression remission rate of 0.65 (95% confidence interval [CI], 0.55–0.78; remission rate [k] = 13), and this was confirmed by the questionnaire results, which revealed a large Hedges’ g (1.11; 95%CI, 0.53–1.69). Methodological variability (in treatment duration, type of depression studied, experimental design, 5-hydroxytryptophan dosage) contributes to heterogeneity in the results (I2 = 76%, τ2 = 0.379). In addition, the OHAT (Office of Health Assessment and Translation risk of bias rating) tool suggested that, on the whole, current studies are relatively weak (few include placebo groups). Conclusion Further trials should overcome these limitations by using placebo-controlled studies that include patients with well-defined depression diagnoses, along with strong characterization of psychological and physiological patient characteristics.

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Monoamine depletion by reuptake inhibitors

Cited by 11 publications

References 29 publications

Relative nutritional deficiencies associated with centrally acting monoamines

Relative nutritional deficiencies associated with centrally acting monoamines

Dietary intake of tryptophan tied emotion-related impulsivity in humans

Effects of 5-hydroxytryptophan on distinct types of depression: a systematic review and meta-analysis

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