Depression

Hinz, Marty

doi:10.1201/9781420067637.ch29

Cited by 11 publications

(112 citation statements)

References 37 publications

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“…Most patients, by history, are simultaneously suffering from three or more monoamine deficiency diseases 9. This etiology is consistent with multifocal RND.…”

Section: Organic Cation Transportersmentioning

confidence: 75%

“…Properly balanced amino acid precursors are necessary; dietary nutrient intake alone is not sufficient to establish high enough monoamine levels to optimize transporter-dependent synaptic monoamines 9,12…”

Section: Discussionmentioning

confidence: 99%

“…While recognizing that any of several monoamines may be involved while displaying identical symptomatology, the exact determination of which ones are primarily involved is not required. The MTO approach simultaneously optimizes levels of all three of these monoamines in transport, based on interpretation of information encoded in the transporters 9,12,13…”

Section: Discussionmentioning

confidence: 99%

“…If proper levels of nutrients are not administered concomitantly with the drug, monoamine neurotransmitter depletion may and often does occur, leading to a drug-induced RND 9,12…”

Section: Discussionmentioning

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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“…Most patients, by history, are simultaneously suffering from three or more monoamine deficiency diseases 9. This etiology is consistent with multifocal RND.…”

Section: Organic Cation Transportersmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…If proper levels of nutrients are not administered concomitantly with the drug, monoamine neurotransmitter depletion may and often does occur, leading to a drug-induced RND 9,12…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Relative nutritional deficiencies associated with centrally acting monoamines

Hinz¹,

Stein²,

Uncini³

2012

IJGM

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“…The concept of reuptake inhibitor tachyphylaxis is controversial. Double-blind, placebo-controlled studies reveal that in depression and ADHD treatment, the placebo response is greater than the drug effect in relief of symptoms 7,8. This leads to the argument that discontinuation of a drug’s clinical effects predominantly represents a placebo relapse rather than drug tachyphylaxis 9,10…”

Section: Introductionmentioning

confidence: 99%

Monoamine depletion by reuptake inhibitors

Hinz¹,

Stein²,

Uncini³

2011

DHPS

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BackgroundDisagreement exists regarding the etiology of cessation of the observed clinical results with administration of reuptake inhibitors. Traditionally, when drug effects wane, it is known as tachyphylaxis. With reuptake inhibitors, the placebo effect is significantly greater than the drug effect in the treatment of depression and attention deficit hyperactivity disorder, leading some to assert that waning of drug effects is placebo relapse, not tachyphylaxis.MethodsTwo groups were retrospectively evaluated. Group 1 was composed of subjects with depression and Group 2 was composed of bariatric subjects treated with reuptake inhibitors for appetite suppression.ResultsIn Group 1, 200 subjects with depression were treated with citalopram 20 mg per day. A total of 46.5% (n = 93) achieved relief of symptoms (Hamilton-D rating score ≤ 7), 37 (39.8%) of whom experienced recurrence of depression symptoms, at which point an amino acid precursor formula was started. Within 1–5 days, 97.3% (n = 36) experienced relief of depression symptoms. In Group 2, 220 subjects were treated with phentermine 30 mg in the morning and citalopram 20 mg at 4 pm. In this group, 90.0% (n = 198) achieved adequate appetite suppression. The appetite suppression ceased in all 198 subjects within 4–48 days. Administration of an amino acid precursor formula restored appetite suppression in 98.5% (n = 195) of subjects within 1–5 days.ConclusionReuptake inhibitors do not increase the total number of monoamine molecules in the central nervous system. Their mechanism of action facilitates redistribution of monoamines from one place to another. In the process, conditions are induced that facilitate depletion of monoamines. The “reuptake inhibitor monoamine depletion theory” of this paper offers a novel and unified explanation for the waning of response seen after a reuptake inhibitor is started, independent of a drug or placebo etiology.

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Amino acid-responsive Crohn's disease: a case study

Stein¹,

Hinz²,

Uncini³

2010

CEG

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Purpose:This paper reviews the clinical course of a case of severe Crohn’s disease and discusses the scientific ramifications of a novel treatment approach.Patients and methods:A case study of a 37-year-old male with a 22-year history of Crohn’s disease whose clinical course had experienced no sustained remissions. The patient was treated with a protocol that utilized serotonin and dopamine amino acid precursors administered under the guidance of organic cation transporter assay interpretation.Results:Within 5 days of achieving the necessary balance of serotonin and dopamine, the patient experienced remission of symptoms. This remission has been sustained without the use of any Crohn’s disease medications.Conclusion:In Crohn’s disease, it is known that there is an increase of both synthesis and tissue levels of serotonin in specific locations. It is asserted that this is prima facie evidence of a significant imbalance in the serotonin–dopamine system, leading to serotonin toxicity. The hypothesis formulated is that improperly balanced serotonin and dopamine transport, synthesis, and metabolism is a primary defect contributing to the pathogenesis of Crohn’s disease.

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Depression

Cited by 11 publications

References 37 publications

Relative nutritional deficiencies associated with centrally acting monoamines

Relative nutritional deficiencies associated with centrally acting monoamines

Monoamine depletion by reuptake inhibitors

Amino acid-responsive Crohn's disease: a case study

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