Although most human diseases are believed to be the consequence of chronic stress superimposed upon various risk genes, efforts to reduce stress are increasingly being thwarted by the ever-increasing pace of human society. However, there is mounting evidence that biopsychosocial stress is primarily dictated endogenously rather than environmentally. According to the multi-circuit neuronal hyperexcitability (MCNH) hypothesis of psychiatric disorders, pathological hyperactivity in specific brain circuits can cause the related thoughts, emotions, and physiological processes to become abnormally amplified. This, in turn, can cause the brain to become even more hyperactive because cognitive-emotional stress and the byproducts of the affected physiological processes have a stimulating effect on the brain. Consistent with this hypothesis, calming the brain, whether by natural or medical means, can be highly effective in reducing both psychiatric symptoms and the risk of developing any of a wide range of chronic medical conditions. However, calming the brain naturally requires consistent effort, and medical interventions can be costly, burdensome, and side-effect prone. That raises the question of whether there might be a more effective and efficient way to reduce the excitability of the neurological system. Although neuronal excitability has clearly been linked to specific risk genes, previous efforts to modify genes in plants and animals have met with limited success. However, the recent discovery of CRISPR/Cas9 technology has changed all that. Now, for the first time, there may be a way to readily replace abnormal DNA sequences with wild-type sequences. This has far-reaching implications for disease reduction and prevention both because neuronal hyperexcitability appears to be the underlying driver of most mental and physical illnesses and because the neuronal hyperexcitability trait has been linked primarily to a relatively small number of gene loci. This article will discuss the pervasive effects of the neuronal hyperexcitability trait and the extraordinary implications of using CRISPR/Cas9 to eliminate its genetic fingerprint from the human genome.
Published in | American Journal of Psychiatry and Neuroscience (Volume 11, Issue 1) |
DOI | 10.11648/j.ajpn.20231101.13 |
Page(s) | 22-29 |
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), 2023. Published by Science Publishing Group |
Neuronal Hyperexcitability, MCNH Hypothesis, CRISPR/Cas9 Technology, Genetic Engineering, Gene Editing, Genetic Scissors, Biomarkers of Disease, Preventive Medicine
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APA Style
Michael Raymond Binder. (2023). Exploring the Potential of Preventing Human Disease by Genetically Altering the Excitability of the Neurological System. American Journal of Psychiatry and Neuroscience, 11(1), 22-29. https://doi.org/10.11648/j.ajpn.20231101.13
ACS Style
Michael Raymond Binder. Exploring the Potential of Preventing Human Disease by Genetically Altering the Excitability of the Neurological System. Am. J. Psychiatry Neurosci. 2023, 11(1), 22-29. doi: 10.11648/j.ajpn.20231101.13
AMA Style
Michael Raymond Binder. Exploring the Potential of Preventing Human Disease by Genetically Altering the Excitability of the Neurological System. Am J Psychiatry Neurosci. 2023;11(1):22-29. doi: 10.11648/j.ajpn.20231101.13
@article{10.11648/j.ajpn.20231101.13, author = {Michael Raymond Binder}, title = {Exploring the Potential of Preventing Human Disease by Genetically Altering the Excitability of the Neurological System}, journal = {American Journal of Psychiatry and Neuroscience}, volume = {11}, number = {1}, pages = {22-29}, doi = {10.11648/j.ajpn.20231101.13}, url = {https://doi.org/10.11648/j.ajpn.20231101.13}, eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajpn.20231101.13}, abstract = {Although most human diseases are believed to be the consequence of chronic stress superimposed upon various risk genes, efforts to reduce stress are increasingly being thwarted by the ever-increasing pace of human society. However, there is mounting evidence that biopsychosocial stress is primarily dictated endogenously rather than environmentally. According to the multi-circuit neuronal hyperexcitability (MCNH) hypothesis of psychiatric disorders, pathological hyperactivity in specific brain circuits can cause the related thoughts, emotions, and physiological processes to become abnormally amplified. This, in turn, can cause the brain to become even more hyperactive because cognitive-emotional stress and the byproducts of the affected physiological processes have a stimulating effect on the brain. Consistent with this hypothesis, calming the brain, whether by natural or medical means, can be highly effective in reducing both psychiatric symptoms and the risk of developing any of a wide range of chronic medical conditions. However, calming the brain naturally requires consistent effort, and medical interventions can be costly, burdensome, and side-effect prone. That raises the question of whether there might be a more effective and efficient way to reduce the excitability of the neurological system. Although neuronal excitability has clearly been linked to specific risk genes, previous efforts to modify genes in plants and animals have met with limited success. However, the recent discovery of CRISPR/Cas9 technology has changed all that. Now, for the first time, there may be a way to readily replace abnormal DNA sequences with wild-type sequences. This has far-reaching implications for disease reduction and prevention both because neuronal hyperexcitability appears to be the underlying driver of most mental and physical illnesses and because the neuronal hyperexcitability trait has been linked primarily to a relatively small number of gene loci. This article will discuss the pervasive effects of the neuronal hyperexcitability trait and the extraordinary implications of using CRISPR/Cas9 to eliminate its genetic fingerprint from the human genome.}, year = {2023} }
TY - JOUR T1 - Exploring the Potential of Preventing Human Disease by Genetically Altering the Excitability of the Neurological System AU - Michael Raymond Binder Y1 - 2023/02/28 PY - 2023 N1 - https://doi.org/10.11648/j.ajpn.20231101.13 DO - 10.11648/j.ajpn.20231101.13 T2 - American Journal of Psychiatry and Neuroscience JF - American Journal of Psychiatry and Neuroscience JO - American Journal of Psychiatry and Neuroscience SP - 22 EP - 29 PB - Science Publishing Group SN - 2330-426X UR - https://doi.org/10.11648/j.ajpn.20231101.13 AB - Although most human diseases are believed to be the consequence of chronic stress superimposed upon various risk genes, efforts to reduce stress are increasingly being thwarted by the ever-increasing pace of human society. However, there is mounting evidence that biopsychosocial stress is primarily dictated endogenously rather than environmentally. According to the multi-circuit neuronal hyperexcitability (MCNH) hypothesis of psychiatric disorders, pathological hyperactivity in specific brain circuits can cause the related thoughts, emotions, and physiological processes to become abnormally amplified. This, in turn, can cause the brain to become even more hyperactive because cognitive-emotional stress and the byproducts of the affected physiological processes have a stimulating effect on the brain. Consistent with this hypothesis, calming the brain, whether by natural or medical means, can be highly effective in reducing both psychiatric symptoms and the risk of developing any of a wide range of chronic medical conditions. However, calming the brain naturally requires consistent effort, and medical interventions can be costly, burdensome, and side-effect prone. That raises the question of whether there might be a more effective and efficient way to reduce the excitability of the neurological system. Although neuronal excitability has clearly been linked to specific risk genes, previous efforts to modify genes in plants and animals have met with limited success. However, the recent discovery of CRISPR/Cas9 technology has changed all that. Now, for the first time, there may be a way to readily replace abnormal DNA sequences with wild-type sequences. This has far-reaching implications for disease reduction and prevention both because neuronal hyperexcitability appears to be the underlying driver of most mental and physical illnesses and because the neuronal hyperexcitability trait has been linked primarily to a relatively small number of gene loci. This article will discuss the pervasive effects of the neuronal hyperexcitability trait and the extraordinary implications of using CRISPR/Cas9 to eliminate its genetic fingerprint from the human genome. VL - 11 IS - 1 ER -