Despite enormous strides in medical diagnostics and the ability to analyze and track disease processes, the underlying cause of most psychiatric and medical disorders remains unclear. Consequently, the treatment of these disorders continues to be more palliative than preventive. However, an emerging hypothesis contends that severe and persistent stress is at the root of most psychiatric and general medical conditions. Although this idea is not new, what is new is the identification of a powerful but elusive endogenous driver of the stress. According to the Multi-Circuit Neuronal Hyperexcitability (MCNH) hypothesis, ordinary daily stressors are abnormally amplified by an inherent hyperexcitability of the neurological system. This pathophysiological trait, which appears to be inherited in an autosomal dominant distribution and expressed through the central and peripheral nervous systems, causes shockwaves to be repeatedly sent through the body, keeping it in fight-or-flight mode much or all of the time. The strain that this commonly-occurring trait places on various organs and systems of the body can cause repeated bouts of mental illness and a gradual progression of physical illnesses such as diabetes mellitus, high blood pressure, cardiovascular disease, autoimmune diseases, cancer, and dementia. Although the etiology of most illnesses is thought to be multifactorial, the genealogical distribution in which they occur and the relationship that they have to one another strongly suggests that among the various psychological, biological, and environmental factors that contribute to their development, the trait of neuronal hyperexcitability is the most important. This observation has enormous implications because neuronal hyperexcitability is a highly modifiable risk factor. Any psychological, behavioral, dietary, or medical intervention that quiets the nervous system can potentially prevent or delay the development of the various illnesses that are thought to be fueled by the neuronal hyperexcitability trait. In addition, there is emerging evidence that the trait can be detected through resting vital-sign measurements. The ease of this objective measurement and the power that it has to incentivize affected persons to take control of their health underscores the importance of recognizing the connection between neuronal hyperexcitability and the pathogenesis of disease.
Published in | American Journal of Clinical and Experimental Medicine (Volume 10, Issue 1) |
DOI | 10.11648/j.ajcem.20221001.11 |
Page(s) | 1-7 |
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 |
Neuronal Hyperexcitability, Biomarkers of Disease, Preventive Medicine, Anticonvulsants, Pathophysiology of Psychiatric Disorders, Genetics of Psychiatric Disorders
[1] | Binder MR. FLASH Syndrome: tapping into the root of chronic illness. AJCEM 2020; 8 (6): 101-109. |
[2] | Binder MR. Gabapentin—the popular but controversial anticonvulsant drug may be zeroing in on the pathophysiology of disease. AJCEM 2021; 9 (4): 122-134. |
[3] | Binder MR. The multi-circuit neuronal hyperexcitability hypothesis of psychiatric disorders. AJCEM 2019; 7 (1): 12-30. |
[4] | Binder MR. Neuronal hyperexcitability: Significance, cause, and diversity of clinical expression. AJCEM 2021; 9 (5): 163-173. |
[5] | Goddard GV. Development of epileptic seizures through brain stimulation at low intensity. Nature 1967; 214: 1020-1021. |
[6] | Rose GM, Diamond DM, Pang K, Dunwiddie TV. Primed burst potentiation: lasting synaptic plasticity invoked by physiologically patterned stimulation. In: Haas HL, Buzsàki G. (eds) Synaptic plasticity in the hippocampus. Springer, Berlin, Heidelberg, 1988. |
[7] | Fleming KC, Volcheck MM. Central sensitization syndrome and the initial evaluation of a patient with fibromyalgia: a review. Rambam Maimonides Med J 2015; 6 (2): e0020. |
[8] | Kenney MJ, Ganta CK. Autonomic nervous system and immune system interactions. Compr Physiol 2014; 4 (3): 1177-1200. |
[9] | Dave ND, Xiang L, Rehm KE, Marshall Jr GD. Stress and allergic diseases. Immunol Allergy Clin North Am 2011; 31 (1): 55-68. |
[10] | Segerstrom SC, Miller GE. Psychological stress and the human immune system: a meta-analytic study of 30 years of inquiry. Psychol Bull 2004; 130 (4): 601-630. |
[11] | Farr M, Mathews J, Zhu D-F, Ambron RT. Inflammation causes a long-term hyperexcitability in the nociceptive sensory neurons of Aplysia. Learn Mem 1999; 6 (3): 331–340. |
[12] | Stojanovich L, Marisavljevich D. Stress as a trigger of autoimmune disease. Autoimmun Rev 2008; 7 (3): 209-213. |
[13] | Ahmeidi AA, Musa A, Ahmed, HS, et al. Inflammatory markers as predictors of mortality in COVID-19 infection. Afr J Lab Med 2020; 9 (1): 1298. |
[14] | Griner T. What's really wrong with you? A revolutionary look at how muscles affect your health. Avery Publishing. New York, NY., 1995. |
[15] | Kassi E, Pervanidou P, Kaltsas G, Chrousos G. Metabolic syndrome: definitions and controversies. BMC Medicine 2011; 9 (48). |
[16] | Murphy R, Carroll RW, Krebs JD. Pathogenesis of the metabolic syndrome: insights from monogenic disorders. Mediators of Inflammation 2013; 2013. |
[17] | Gade W, Schmit J, Collins M, Gade J. Beyond obesity: The diagnosis and pathophysiology of metabolic syndrome. American Society for Clinical Laboratory Science 2010; 23 (1): 51-61. |
[18] | Post RM. (2007) Kindling and sensitization as models for affective episode recurrence, cyclicity, and tolerance phenomena. Neuroscience & Biobehavioral Reviews. 31 (6): 858-873. |
[19] | Binder MR: The neuronal excitability spectrum: A new paradigm in the diagnosis, treatment, and prevention of mental illness and its relation to chronic disease. AJCEM; 2021; 9 (6): 187-203. |
[20] | Latvala A, Kuja-Halkola R, Rick C, et al. Association of resting heart rate and blood pressure in late adolescence with subsequent mental disorders: A longitudinal population study of more than 1 million men in Sweden. JAMA Psychiatry 2016; 73 (12): 1268-1275. |
[21] | Blom EH, Serlachius E, Chesney MA, Olsson EMG. Adolescent girls with emotional disorders have a lower end-tidal CO2 and increased respiratory rate compared with healthy controls. Psychophysiology 2014; 51 (5): 412-418. |
APA Style
Michael Raymond Binder. (2022). Neuronal Hyperexcitability: The Elusive But Modifiable Instigator of Disease. American Journal of Clinical and Experimental Medicine, 10(1), 1-7. https://doi.org/10.11648/j.ajcem.20221001.11
ACS Style
Michael Raymond Binder. Neuronal Hyperexcitability: The Elusive But Modifiable Instigator of Disease. Am. J. Clin. Exp. Med. 2022, 10(1), 1-7. doi: 10.11648/j.ajcem.20221001.11
AMA Style
Michael Raymond Binder. Neuronal Hyperexcitability: The Elusive But Modifiable Instigator of Disease. Am J Clin Exp Med. 2022;10(1):1-7. doi: 10.11648/j.ajcem.20221001.11
@article{10.11648/j.ajcem.20221001.11, author = {Michael Raymond Binder}, title = {Neuronal Hyperexcitability: The Elusive But Modifiable Instigator of Disease}, journal = {American Journal of Clinical and Experimental Medicine}, volume = {10}, number = {1}, pages = {1-7}, doi = {10.11648/j.ajcem.20221001.11}, url = {https://doi.org/10.11648/j.ajcem.20221001.11}, eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20221001.11}, abstract = {Despite enormous strides in medical diagnostics and the ability to analyze and track disease processes, the underlying cause of most psychiatric and medical disorders remains unclear. Consequently, the treatment of these disorders continues to be more palliative than preventive. However, an emerging hypothesis contends that severe and persistent stress is at the root of most psychiatric and general medical conditions. Although this idea is not new, what is new is the identification of a powerful but elusive endogenous driver of the stress. According to the Multi-Circuit Neuronal Hyperexcitability (MCNH) hypothesis, ordinary daily stressors are abnormally amplified by an inherent hyperexcitability of the neurological system. This pathophysiological trait, which appears to be inherited in an autosomal dominant distribution and expressed through the central and peripheral nervous systems, causes shockwaves to be repeatedly sent through the body, keeping it in fight-or-flight mode much or all of the time. The strain that this commonly-occurring trait places on various organs and systems of the body can cause repeated bouts of mental illness and a gradual progression of physical illnesses such as diabetes mellitus, high blood pressure, cardiovascular disease, autoimmune diseases, cancer, and dementia. Although the etiology of most illnesses is thought to be multifactorial, the genealogical distribution in which they occur and the relationship that they have to one another strongly suggests that among the various psychological, biological, and environmental factors that contribute to their development, the trait of neuronal hyperexcitability is the most important. This observation has enormous implications because neuronal hyperexcitability is a highly modifiable risk factor. Any psychological, behavioral, dietary, or medical intervention that quiets the nervous system can potentially prevent or delay the development of the various illnesses that are thought to be fueled by the neuronal hyperexcitability trait. In addition, there is emerging evidence that the trait can be detected through resting vital-sign measurements. The ease of this objective measurement and the power that it has to incentivize affected persons to take control of their health underscores the importance of recognizing the connection between neuronal hyperexcitability and the pathogenesis of disease.}, year = {2022} }
TY - JOUR T1 - Neuronal Hyperexcitability: The Elusive But Modifiable Instigator of Disease AU - Michael Raymond Binder Y1 - 2022/01/20 PY - 2022 N1 - https://doi.org/10.11648/j.ajcem.20221001.11 DO - 10.11648/j.ajcem.20221001.11 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 - 1 EP - 7 PB - Science Publishing Group SN - 2330-8133 UR - https://doi.org/10.11648/j.ajcem.20221001.11 AB - Despite enormous strides in medical diagnostics and the ability to analyze and track disease processes, the underlying cause of most psychiatric and medical disorders remains unclear. Consequently, the treatment of these disorders continues to be more palliative than preventive. However, an emerging hypothesis contends that severe and persistent stress is at the root of most psychiatric and general medical conditions. Although this idea is not new, what is new is the identification of a powerful but elusive endogenous driver of the stress. According to the Multi-Circuit Neuronal Hyperexcitability (MCNH) hypothesis, ordinary daily stressors are abnormally amplified by an inherent hyperexcitability of the neurological system. This pathophysiological trait, which appears to be inherited in an autosomal dominant distribution and expressed through the central and peripheral nervous systems, causes shockwaves to be repeatedly sent through the body, keeping it in fight-or-flight mode much or all of the time. The strain that this commonly-occurring trait places on various organs and systems of the body can cause repeated bouts of mental illness and a gradual progression of physical illnesses such as diabetes mellitus, high blood pressure, cardiovascular disease, autoimmune diseases, cancer, and dementia. Although the etiology of most illnesses is thought to be multifactorial, the genealogical distribution in which they occur and the relationship that they have to one another strongly suggests that among the various psychological, biological, and environmental factors that contribute to their development, the trait of neuronal hyperexcitability is the most important. This observation has enormous implications because neuronal hyperexcitability is a highly modifiable risk factor. Any psychological, behavioral, dietary, or medical intervention that quiets the nervous system can potentially prevent or delay the development of the various illnesses that are thought to be fueled by the neuronal hyperexcitability trait. In addition, there is emerging evidence that the trait can be detected through resting vital-sign measurements. The ease of this objective measurement and the power that it has to incentivize affected persons to take control of their health underscores the importance of recognizing the connection between neuronal hyperexcitability and the pathogenesis of disease. VL - 10 IS - 1 ER -