Central Nervous System Plus Autonomic Nervous System Disorders Responsible for Gastrointestinal and Pancreatobiliary Diseases

Lechín, Fuad; Dijs, Bertha van der

doi:10.1007/s10620-008-0369-9

Cited by 14 publications

(12 citation statements)

References 92 publications

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“…In addition, the neural sympathetic overactivity provoked by amantadine interferes with the parasympathetic drive responsible for the release of intestinal serotonin which redounded in the reduction of both p5-HT and f5-HT circulating levels. With respect to this, we have quoted exhaustive evidence showing the existence of two types of opposite ANS profiles which underlie most diseases: (1) adrenal sympathetic and (2) neural sympathetic (Lechin and van der Dijs 2008, 2009a, b). …”

Section: Discussionmentioning

confidence: 99%

Effects of amantadine on circulating neurotransmitters in healthy subjects

et al. 2010

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Considering that glutamatergic axons innervate the C1(Ad) medullary nuclei, which are responsible for the excitation of the peripheral adrenal glands, we decided to investigate catecholamines (noradrenaline, adrenaline and dopamine) plus indolamines (plasma serotonin and platelet serotonin) at the blood level, before and after a small oral dose of amantadine, a selective NMDA antagonist. We found that the drug provoked a selective enhancement of noradrenaline plus a minimization of adrenaline, dopamine, plasma serotonin and platelet serotonin circulating levels. Significant enhancement of diastolic blood pressure plus reduction of systolic blood pressure and heart rate paralleled the circulating parameter changes. The above findings allow us to postulate that the drug was able to enhance the peripheral neural sympathetic activity. Minimization of both adrenal sympathetic and parasympathetic activities was also registered after the amantadine challenge. The above findings supported the postulation that this drug should be a powerful therapeutic tool for treating diseases affected by adrenal sympathetic hyperactivity.

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Section: Discussionmentioning

confidence: 99%

Effects of amantadine on circulating neurotransmitters in healthy subjects

et al. 2010

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“…Recent work suggests that depression is associated with higher methylation levels in the 5-hydroxytryptamine transporter ( 5-HTT , or SLC6A4 ) gene (Olsson et al, 2010; Philibert et al, 2008), a transporter for serotonin released under the parasympathetic excitation (Lechin & van der Dijs, 2009). Genetic studies suggest that carriers of the short allele of the 5-HTT promoter polymorphism exhibited more depressive symptoms than individuals homozygous for the long allele under high stress conditions (Caspi et al, 2003).…”

Section: Empirical Evidence For the Role Of Epigenetic Mechanisms In mentioning

confidence: 99%

How does the social environment ‘get into the mind’? Epigenetics at the intersection of social and psychiatric epidemiology

Toyokawa

Uddin

Koenen

et al. 2012

Social Science & Medicine

173

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The social environment plays a considerable role in determining major psychiatric disorders. Emerging evidence suggests that features of the social environment modify gene expression independently of the primary DNA sequence through epigenetic processes. Accordingly, dysfunction of epigenetic mechanisms offers a plausible mechanism by which an adverse social environment gets “into the mind” and results in poor mental health. The purpose of this review is to provide an overview of the studies suggesting that epigenetic changes introduced by the social environment then manifest as psychological consequences. Our goal is to build a platform to discuss the ways in which future epidemiologic studies may benefit from including epigenetic measures. We focus on schizophrenia, major depressive disorder, post-traumatic stress disorder, anorexia nervosa, and substance dependence as examples that highlight the ways in which social environmental exposures, mediated through epigenetic processes, affect mental health.

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“…Neuroendocrine and metabolic disorders should also be included into this syndrome, the source of which is located at the medullary C1(Ad) nuclei responsible for the peripheral adrenal sympathetic branch 19,20. The findings presented in this study demonstrate also that an oral dose of amantadine, a N-methyl-D-aspartate antagonist which annuls the firing activity of the C1(Ad) medullary nuclei,11 minimizes systolic blood pressure and heart rate, both of which are cardiovascular parameters positively correlated with adrenal sympathetic activity.…”

Section: Discussionmentioning

confidence: 99%

Anorexia nervosa versus hyperinsulinism: therapeutic effects of neuropharmacological manipulation

Lechín

Dijs²,

Pardey-Maldonado³

et al. 2011

TCRM

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Background:We have demonstrated that anorexia nervosa is underpinned by overwhelming adrenal sympathetic activity which abolishes the neural sympathetic branch of the peripheral autonomic nervous system. This physiological disorder is responsible for gastrointestinal hypomotility, hyperglycemia, raised systolic blood pressure, raised heart rate, and other neuroendocrine disorders. Therefore, we prescribed neuropharmacological therapy to reverse this central and autonomic nervous system disorder, in order to normalize the clinical and neuroendocrine profile. Methods: The study included 22 female patients with anorexia nervosa (10 restricted type, 12 binge-eating type) who received three months of treatment with amantadine 100 mg/day. We measured blood pressure, heart rate, and circulating neurotransmitters, (noradrenaline, adrenaline, dopamine, platelet serotonin, free plasma serotonin) during supine resting, one minute of orthostasis, and a five-minute exercise test before and after one, two, and three months of treatment with amantadine, a drug which abrogates adrenal sympathetic activity by acting at the C1(Ad) medullary nuclei responsible for this branch of the peripheral sympathetic activity. Results: We found the amantadine abolished symptoms of anorexia nervosa from the first oral dose onwards. Normalization of autonomic and cardiovascular parameters was demonstrated within the early days of therapy. Abrupt and sustained increases in the plasma noradrenaline:adrenaline ratio and disappearance of abnormal plasma glucose elevation were registered throughout the three-month duration of the trial. Significant and sustained increases in body weight were documented in all cases. No relapses were observed. Conclusion: We have confirmed our previously published findings showing that the anorexia nervosa syndrome depends on the hypomotility of the gastrointestinal tract plus hyperglycemia, both of which are triggered by adrenal sympathetic hyperactivity. The above neuroendocrine plus neuroautonomic and clinical disorders which underpinned anorexia nervosa were abruptly suppressed since the first oral dose of amantadine, a drug able to revert the C1(Ad) over A5(NA) pontomedullary predominance responsible for adrenal and neural sympathetic activity, respectively.

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Central Nervous System Plus Autonomic Nervous System Disorders Responsible for Gastrointestinal and Pancreatobiliary Diseases

Cited by 14 publications

References 92 publications

Effects of amantadine on circulating neurotransmitters in healthy subjects

Effects of amantadine on circulating neurotransmitters in healthy subjects

How does the social environment ‘get into the mind’? Epigenetics at the intersection of social and psychiatric epidemiology

Anorexia nervosa versus hyperinsulinism: therapeutic effects of neuropharmacological manipulation

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