New Hypothesis Unifies Previous Theories of Psychopathology and Identifies Core Biological Abnormality in Psychiatric Disorders

Michael Raymond Binder

doi:doi:10.11648/j.ajcem.20221001.14

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New Hypothesis Unifies Previous Theories of Psychopathology and Identifies Core Biological Abnormality in Psychiatric Disorders

Michael Raymond Binder

Published in American Journal of Clinical and Experimental Medicine (Volume 10, Issue 1)

Received: 4 January 2022 Accepted: 20 January 2022 Published: 28 January 2022

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Abstract

Despite millennia of philosophical debate and the enormous strides that have been made in neuroscience over the last century, the pathophysiology of psychiatric disorders remains unclear. Although the monoamine hypothesis has, for more than fifty years, provided a strong basis of support for the use of antidepressants in the treatment of depression, the overall success rate with antidepressants has been disappointingly low. Coincidingly, the monoamine hypothesis has come under increasing scrutiny for failing to explain all of the phenomena that characterize mood disorders. Consequently, mental health researchers, in an effort to find new molecular targets for treatment, have been searching for a more comprehensive explanation of the means by which psychiatric symptoms develop. Recently, several new models of depression have been proposed, including the immune, the endocrine, the glutamatergic, the GABAergic, the mitochondrial, and the neuroplastic; but none of them integrate the workings of the mind with the workings of the brain, and none of them explain how abnormalities in brain function actually translate into abnormalities in thought and emotion. However, an emerging hypothesis—one that reconceptualizes the anatomy of the cognitive-emotional system and unifies previous psychological and biological theories of psychopathology—posits that psychiatric symptoms are induced by a vicious cycle of mutual overstimulation between the mind and the brain. According to the Multi-Circuit Neuronal Hyperexcitability Hypothesis of Psychiatric Disorders, the mind, when under stress, overstimulates the associated neurons and circuits. The associated neurons and circuits, in turn, overstimulate the mind, particularly if the neurological system is inherently hyperexcitable. The result is an abnormal increase in the intensity and the duration of the associated thoughts and emotions, a change that distinguishes functionally abnormal thoughts and emotions from normal ones. A more detailed understanding of the mechanism by which psychiatric symptoms develop and perpetuate has important implications for treatment, as it would allow psychotherapists to better visualize what is happening in the cognitive-emotional system; it would allow psychiatrists to better visualize the target for medical interventions; and, by reducing the stigma of mental illness, it would allow patients to be more willing to seek and follow through with mental health care.

Published in	American Journal of Clinical and Experimental Medicine (Volume 10, Issue 1)
DOI	10.11648/j.ajcem.20221001.14
Page(s)	23-37
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2022. Published by Science Publishing Group

Keywords

Pathophysiology of Psychiatric Disorders, Biology of Mental Illness, Neuronal Hyperexcitability, Biomarkers of Disease, Objective Assessments, Anticonvulsants, Mood Stabilizers, Neuroregulators

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Michael Raymond Binder. (2022). New Hypothesis Unifies Previous Theories of Psychopathology and Identifies Core Biological Abnormality in Psychiatric Disorders. American Journal of Clinical and Experimental Medicine, 10(1), 23-37. https://doi.org/10.11648/j.ajcem.20221001.14

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Michael Raymond Binder. New Hypothesis Unifies Previous Theories of Psychopathology and Identifies Core Biological Abnormality in Psychiatric Disorders. Am. J. Clin. Exp. Med. 2022, 10(1), 23-37. doi: 10.11648/j.ajcem.20221001.14

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Michael Raymond Binder. New Hypothesis Unifies Previous Theories of Psychopathology and Identifies Core Biological Abnormality in Psychiatric Disorders. Am J Clin Exp Med. 2022;10(1):23-37. doi: 10.11648/j.ajcem.20221001.14

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@article{10.11648/j.ajcem.20221001.14,
  author = {Michael Raymond Binder},
  title = {New Hypothesis Unifies Previous Theories of Psychopathology and Identifies Core Biological Abnormality in Psychiatric Disorders},
  journal = {American Journal of Clinical and Experimental Medicine},
  volume = {10},
  number = {1},
  pages = {23-37},
  doi = {10.11648/j.ajcem.20221001.14},
  url = {https://doi.org/10.11648/j.ajcem.20221001.14},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20221001.14},
  abstract = {Despite millennia of philosophical debate and the enormous strides that have been made in neuroscience over the last century, the pathophysiology of psychiatric disorders remains unclear. Although the monoamine hypothesis has, for more than fifty years, provided a strong basis of support for the use of antidepressants in the treatment of depression, the overall success rate with antidepressants has been disappointingly low. Coincidingly, the monoamine hypothesis has come under increasing scrutiny for failing to explain all of the phenomena that characterize mood disorders. Consequently, mental health researchers, in an effort to find new molecular targets for treatment, have been searching for a more comprehensive explanation of the means by which psychiatric symptoms develop. Recently, several new models of depression have been proposed, including the immune, the endocrine, the glutamatergic, the GABAergic, the mitochondrial, and the neuroplastic; but none of them integrate the workings of the mind with the workings of the brain, and none of them explain how abnormalities in brain function actually translate into abnormalities in thought and emotion. However, an emerging hypothesis—one that reconceptualizes the anatomy of the cognitive-emotional system and unifies previous psychological and biological theories of psychopathology—posits that psychiatric symptoms are induced by a vicious cycle of mutual overstimulation between the mind and the brain. According to the Multi-Circuit Neuronal Hyperexcitability Hypothesis of Psychiatric Disorders, the mind, when under stress, overstimulates the associated neurons and circuits. The associated neurons and circuits, in turn, overstimulate the mind, particularly if the neurological system is inherently hyperexcitable. The result is an abnormal increase in the intensity and the duration of the associated thoughts and emotions, a change that distinguishes functionally abnormal thoughts and emotions from normal ones. A more detailed understanding of the mechanism by which psychiatric symptoms develop and perpetuate has important implications for treatment, as it would allow psychotherapists to better visualize what is happening in the cognitive-emotional system; it would allow psychiatrists to better visualize the target for medical interventions; and, by reducing the stigma of mental illness, it would allow patients to be more willing to seek and follow through with mental health care.},
 year = {2022}
}

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SN  - 2330-8133
UR  - https://doi.org/10.11648/j.ajcem.20221001.14
AB  - Despite millennia of philosophical debate and the enormous strides that have been made in neuroscience over the last century, the pathophysiology of psychiatric disorders remains unclear. Although the monoamine hypothesis has, for more than fifty years, provided a strong basis of support for the use of antidepressants in the treatment of depression, the overall success rate with antidepressants has been disappointingly low. Coincidingly, the monoamine hypothesis has come under increasing scrutiny for failing to explain all of the phenomena that characterize mood disorders. Consequently, mental health researchers, in an effort to find new molecular targets for treatment, have been searching for a more comprehensive explanation of the means by which psychiatric symptoms develop. Recently, several new models of depression have been proposed, including the immune, the endocrine, the glutamatergic, the GABAergic, the mitochondrial, and the neuroplastic; but none of them integrate the workings of the mind with the workings of the brain, and none of them explain how abnormalities in brain function actually translate into abnormalities in thought and emotion. However, an emerging hypothesis—one that reconceptualizes the anatomy of the cognitive-emotional system and unifies previous psychological and biological theories of psychopathology—posits that psychiatric symptoms are induced by a vicious cycle of mutual overstimulation between the mind and the brain. According to the Multi-Circuit Neuronal Hyperexcitability Hypothesis of Psychiatric Disorders, the mind, when under stress, overstimulates the associated neurons and circuits. The associated neurons and circuits, in turn, overstimulate the mind, particularly if the neurological system is inherently hyperexcitable. The result is an abnormal increase in the intensity and the duration of the associated thoughts and emotions, a change that distinguishes functionally abnormal thoughts and emotions from normal ones. A more detailed understanding of the mechanism by which psychiatric symptoms develop and perpetuate has important implications for treatment, as it would allow psychotherapists to better visualize what is happening in the cognitive-emotional system; it would allow psychiatrists to better visualize the target for medical interventions; and, by reducing the stigma of mental illness, it would allow patients to be more willing to seek and follow through with mental health care.
VL  - 10
IS  - 1
ER  -

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Michael Raymond Binder

NorthShore University HealthSystem, Highland Park Hospital, Highland Park, USA

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Michael Raymond Binder. (2022). New Hypothesis Unifies Previous Theories of Psychopathology and Identifies Core Biological Abnormality in Psychiatric Disorders. American Journal of Clinical and Experimental Medicine, 10(1), 23-37. https://doi.org/10.11648/j.ajcem.20221001.14

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ACS Style

Michael Raymond Binder. New Hypothesis Unifies Previous Theories of Psychopathology and Identifies Core Biological Abnormality in Psychiatric Disorders. Am. J. Clin. Exp. Med. 2022, 10(1), 23-37. doi: 10.11648/j.ajcem.20221001.14

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AMA Style

Michael Raymond Binder. New Hypothesis Unifies Previous Theories of Psychopathology and Identifies Core Biological Abnormality in Psychiatric Disorders. Am J Clin Exp Med. 2022;10(1):23-37. doi: 10.11648/j.ajcem.20221001.14

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@article{10.11648/j.ajcem.20221001.14,
  author = {Michael Raymond Binder},
  title = {New Hypothesis Unifies Previous Theories of Psychopathology and Identifies Core Biological Abnormality in Psychiatric Disorders},
  journal = {American Journal of Clinical and Experimental Medicine},
  volume = {10},
  number = {1},
  pages = {23-37},
  doi = {10.11648/j.ajcem.20221001.14},
  url = {https://doi.org/10.11648/j.ajcem.20221001.14},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20221001.14},
  abstract = {Despite millennia of philosophical debate and the enormous strides that have been made in neuroscience over the last century, the pathophysiology of psychiatric disorders remains unclear. Although the monoamine hypothesis has, for more than fifty years, provided a strong basis of support for the use of antidepressants in the treatment of depression, the overall success rate with antidepressants has been disappointingly low. Coincidingly, the monoamine hypothesis has come under increasing scrutiny for failing to explain all of the phenomena that characterize mood disorders. Consequently, mental health researchers, in an effort to find new molecular targets for treatment, have been searching for a more comprehensive explanation of the means by which psychiatric symptoms develop. Recently, several new models of depression have been proposed, including the immune, the endocrine, the glutamatergic, the GABAergic, the mitochondrial, and the neuroplastic; but none of them integrate the workings of the mind with the workings of the brain, and none of them explain how abnormalities in brain function actually translate into abnormalities in thought and emotion. However, an emerging hypothesis—one that reconceptualizes the anatomy of the cognitive-emotional system and unifies previous psychological and biological theories of psychopathology—posits that psychiatric symptoms are induced by a vicious cycle of mutual overstimulation between the mind and the brain. According to the Multi-Circuit Neuronal Hyperexcitability Hypothesis of Psychiatric Disorders, the mind, when under stress, overstimulates the associated neurons and circuits. The associated neurons and circuits, in turn, overstimulate the mind, particularly if the neurological system is inherently hyperexcitable. The result is an abnormal increase in the intensity and the duration of the associated thoughts and emotions, a change that distinguishes functionally abnormal thoughts and emotions from normal ones. A more detailed understanding of the mechanism by which psychiatric symptoms develop and perpetuate has important implications for treatment, as it would allow psychotherapists to better visualize what is happening in the cognitive-emotional system; it would allow psychiatrists to better visualize the target for medical interventions; and, by reducing the stigma of mental illness, it would allow patients to be more willing to seek and follow through with mental health care.},
 year = {2022}
}

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TY  - JOUR
T1  - New Hypothesis Unifies Previous Theories of Psychopathology and Identifies Core Biological Abnormality in Psychiatric Disorders
AU  - Michael Raymond Binder
Y1  - 2022/01/28
PY  - 2022
N1  - https://doi.org/10.11648/j.ajcem.20221001.14
DO  - 10.11648/j.ajcem.20221001.14
T2  - American Journal of Clinical and Experimental Medicine
JF  - American Journal of Clinical and Experimental Medicine
JO  - American Journal of Clinical and Experimental Medicine
SP  - 23
EP  - 37
PB  - Science Publishing Group
SN  - 2330-8133
UR  - https://doi.org/10.11648/j.ajcem.20221001.14
AB  - Despite millennia of philosophical debate and the enormous strides that have been made in neuroscience over the last century, the pathophysiology of psychiatric disorders remains unclear. Although the monoamine hypothesis has, for more than fifty years, provided a strong basis of support for the use of antidepressants in the treatment of depression, the overall success rate with antidepressants has been disappointingly low. Coincidingly, the monoamine hypothesis has come under increasing scrutiny for failing to explain all of the phenomena that characterize mood disorders. Consequently, mental health researchers, in an effort to find new molecular targets for treatment, have been searching for a more comprehensive explanation of the means by which psychiatric symptoms develop. Recently, several new models of depression have been proposed, including the immune, the endocrine, the glutamatergic, the GABAergic, the mitochondrial, and the neuroplastic; but none of them integrate the workings of the mind with the workings of the brain, and none of them explain how abnormalities in brain function actually translate into abnormalities in thought and emotion. However, an emerging hypothesis—one that reconceptualizes the anatomy of the cognitive-emotional system and unifies previous psychological and biological theories of psychopathology—posits that psychiatric symptoms are induced by a vicious cycle of mutual overstimulation between the mind and the brain. According to the Multi-Circuit Neuronal Hyperexcitability Hypothesis of Psychiatric Disorders, the mind, when under stress, overstimulates the associated neurons and circuits. The associated neurons and circuits, in turn, overstimulate the mind, particularly if the neurological system is inherently hyperexcitable. The result is an abnormal increase in the intensity and the duration of the associated thoughts and emotions, a change that distinguishes functionally abnormal thoughts and emotions from normal ones. A more detailed understanding of the mechanism by which psychiatric symptoms develop and perpetuate has important implications for treatment, as it would allow psychotherapists to better visualize what is happening in the cognitive-emotional system; it would allow psychiatrists to better visualize the target for medical interventions; and, by reducing the stigma of mental illness, it would allow patients to be more willing to seek and follow through with mental health care.
VL  - 10
IS  - 1
ER  -

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