Please sign and circulate my petition to the WHO & APA to drop the scientifically challenged and highly stigmatizing term “schizophrenia”
Brian Koehler PhD, MS
New York University & Columbia University
Hi Greg,
Nice to see your comments. Our NIMH still funds research with DSM categories, although as you noted, under Thomas Insel, our former NIMH Director, stated our “patients deserve better” than DSM. The hope was RDoC would be more scientific. But the agenda is at root a reductionistic one-Insel saw “syndromes” like “schizophrenia” as being “caused” by inefficient/dysfunctional neural circuits and genes. No real emphasis was given on the biological embedding of adverse social experiences-including across generations-which there is now firm evidence for. Social and psychological factors are still sidelined. Brian
It is inconsistent with the research to not include the significance of social-psychological (socio-developmental) factors in the onset, course and outcomes of the heterogeneous group of people we diagnose with bipolar disorder. Expressed emotion, lack of social support, the presence of negative life events, personality factors,forms of interpretation of events, etc., all play a significant role in relapse and course of the disorder. There is a cohort effect not seen in all cultures since the mid-19th century. Even at the level of neurobiological alterations, one could make a reasonable case that hypercortisolemia (increased cortisol which can be neurotoxic) and other stress-related processes play a significant role. As in schizophrenia research, the atrophy of certain neural regions in bipolar disorder, e.g., the prefrontal cortex, insula, cerebellar vermis, corpus callosum, etc., are also observed in developmental traumatology research studies (exposure to traumatic and chronic stress from various events, sources, etc.). Gray and white matter (the information highway of the CNS) are affected. The hyperintensities seen in bipolar disorder are also observed in major depressive disorder. In fact as a stress researcher, I was the first to point out the significant overlap in the neuroscience of schizophrenia and bipolar disorder and the neuroscience of profound and chronic stress, formally at the ISPS London conference in 1997 and prior to that at meetings in the NYC , the states, and to Wayne Fenton, a colleague who was a deputy director at NIMH prior to his tragic death.
Some of the new biological research in bipolar disorder is centering on mitochondrial dysfunction and the role of oxidative stress in causing it. Again, severe life stress (SLS) invariably induces oxidative stress and thereby can play a significant role in the mitochodrial dysfunction. SLS can induce genomic and epigenomic alterations which may play important roles in the pathophysiology of schizophrenia, bipolar disorder and major depressive disorder. There is so much to say about the new research showing the relevant linkage. SLS shortens telomere length,alters neuronal morphology and gene expression through various epigenetic channels, reduces neurogenesis and synaptogesis, is associated with synaptic pathology, is also associated with the new findings in complementary C4 proteins recently identified in the New York Times as “scientists homing in on the genetic cause of schizophrenia’!
It is inconsistent with the research to not include the significance of social-psychological (socio-developmental) factors in the onset, course and outcomes of the heterogeneous group of people we diagnose with bipolar disorder. Expressed emotion, lack of social support, the presence of negative life events, personality factors,forms of interpretation of events, etc., all play a significant role in relapse and course of the disorder. There is a cohort effect not seen in all cultures since the mid-19th century. Even at the level of neurobiological alterations, one could make a reasonable case that hypercortisolemia (increased cortisol which can be neurotoxic) and other stress-related processes play a significant role. As in schizophrenia research, the atrophy of certain neural regions in bipolar disorder, e.g., the prefrontal cortex, insula, cerebellar vermis, corpus callosum, etc., are also observed in developmental traumatology research studies (exposure to traumatic and chronic stress from various events, sources, etc.). Gray and white matter (the information highway of the CNS) are affected. The hyperintensities seen in bipolar disorder are also observed in major depressive disorder. In fact as a stress researcher, I was the first to point out the significant overlap in the neuroscience of schizophrenia and bipolar disorder and the neuroscience of profound and chronic stress, formally at the ISPS London conference in 1997 and prior to that at meetings in the NYC , the states, and to Wayne Fenton, a colleague who was a deputy director at NIMH prior to his tragic death.
Some of the new biological research in bipolar disorder is centering on mitochondrial dysfunction and the role of oxidative stress in causing it. Again, severe life stress (SLS) invariably induces oxidative stress and thereby can play a significant role in the mitochodrial dysfunction. SLS can induce genomic and epigenomic alterations which may play important roles in the pathophysiology of schizophrenia, bipolar disorder and major depressive disorder. There is so much to say about the new research showing the relevant linkage. SLS shortens telomere length,alters neuronal morphology and gene expression through various epigenetic channels, reduces neurogenesis and synaptogesis, is associated with synaptic pathology, is also associated with the new findings in complementary C4 proteins recently identified in the New York Times as “scientists homing in on the genetic cause of schizophrenia’!
Please sign and circulate my petition to the WHO & APA to drop the scientifically challenged and highly stigmatizing term “schizophrenia”
Brian Koehler PhD, MS
New York University & Columbia University
https://www.madinamerica.com/2017/12/apa-drop-stigmatizing-term-schizophrenia/
https://www.change.org/p/american-psychiatric-association-apa-drop-the-stigmatizing-term-schizophrenia/nftexp/ex35/v4/644737274
Spanish translation thanks to Ana Sofia Rodriquez from Mexico:
https://discapacidades.nexos.com.mx/?p=65
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Hi Greg,
Nice to see your comments. Our NIMH still funds research with DSM categories, although as you noted, under Thomas Insel, our former NIMH Director, stated our “patients deserve better” than DSM. The hope was RDoC would be more scientific. But the agenda is at root a reductionistic one-Insel saw “syndromes” like “schizophrenia” as being “caused” by inefficient/dysfunctional neural circuits and genes. No real emphasis was given on the biological embedding of adverse social experiences-including across generations-which there is now firm evidence for. Social and psychological factors are still sidelined. Brian
Report comment
Please sign my petition to the WHO & APA to drop the scientifically challenged and highly stigmatizing term “schizophrenia”
Thanks,
Brian Koehler PhD
New York University & Columbia University
New York, NY
https://www.madinamerica.com/2017/12/apa-drop-stigmatizing-term-schizophrenia/
https://www.change.org/p/american-psychiatric-association-apa-drop-the-stigmatizing-term-schizophrenia
Spanish translation thanks to Ana Sofia Rodriquez from Mexico:
https://discapacidades.nexos.com.mx/?p=65
Report comment
It is inconsistent with the research to not include the significance of social-psychological (socio-developmental) factors in the onset, course and outcomes of the heterogeneous group of people we diagnose with bipolar disorder. Expressed emotion, lack of social support, the presence of negative life events, personality factors,forms of interpretation of events, etc., all play a significant role in relapse and course of the disorder. There is a cohort effect not seen in all cultures since the mid-19th century. Even at the level of neurobiological alterations, one could make a reasonable case that hypercortisolemia (increased cortisol which can be neurotoxic) and other stress-related processes play a significant role. As in schizophrenia research, the atrophy of certain neural regions in bipolar disorder, e.g., the prefrontal cortex, insula, cerebellar vermis, corpus callosum, etc., are also observed in developmental traumatology research studies (exposure to traumatic and chronic stress from various events, sources, etc.). Gray and white matter (the information highway of the CNS) are affected. The hyperintensities seen in bipolar disorder are also observed in major depressive disorder. In fact as a stress researcher, I was the first to point out the significant overlap in the neuroscience of schizophrenia and bipolar disorder and the neuroscience of profound and chronic stress, formally at the ISPS London conference in 1997 and prior to that at meetings in the NYC , the states, and to Wayne Fenton, a colleague who was a deputy director at NIMH prior to his tragic death.
Some of the new biological research in bipolar disorder is centering on mitochondrial dysfunction and the role of oxidative stress in causing it. Again, severe life stress (SLS) invariably induces oxidative stress and thereby can play a significant role in the mitochodrial dysfunction. SLS can induce genomic and epigenomic alterations which may play important roles in the pathophysiology of schizophrenia, bipolar disorder and major depressive disorder. There is so much to say about the new research showing the relevant linkage. SLS shortens telomere length,alters neuronal morphology and gene expression through various epigenetic channels, reduces neurogenesis and synaptogesis, is associated with synaptic pathology, is also associated with the new findings in complementary C4 proteins recently identified in the New York Times as “scientists homing in on the genetic cause of schizophrenia’!
Report comment
It is inconsistent with the research to not include the significance of social-psychological (socio-developmental) factors in the onset, course and outcomes of the heterogeneous group of people we diagnose with bipolar disorder. Expressed emotion, lack of social support, the presence of negative life events, personality factors,forms of interpretation of events, etc., all play a significant role in relapse and course of the disorder. There is a cohort effect not seen in all cultures since the mid-19th century. Even at the level of neurobiological alterations, one could make a reasonable case that hypercortisolemia (increased cortisol which can be neurotoxic) and other stress-related processes play a significant role. As in schizophrenia research, the atrophy of certain neural regions in bipolar disorder, e.g., the prefrontal cortex, insula, cerebellar vermis, corpus callosum, etc., are also observed in developmental traumatology research studies (exposure to traumatic and chronic stress from various events, sources, etc.). Gray and white matter (the information highway of the CNS) are affected. The hyperintensities seen in bipolar disorder are also observed in major depressive disorder. In fact as a stress researcher, I was the first to point out the significant overlap in the neuroscience of schizophrenia and bipolar disorder and the neuroscience of profound and chronic stress, formally at the ISPS London conference in 1997 and prior to that at meetings in the NYC , the states, and to Wayne Fenton, a colleague who was a deputy director at NIMH prior to his tragic death.
Some of the new biological research in bipolar disorder is centering on mitochondrial dysfunction and the role of oxidative stress in causing it. Again, severe life stress (SLS) invariably induces oxidative stress and thereby can play a significant role in the mitochodrial dysfunction. SLS can induce genomic and epigenomic alterations which may play important roles in the pathophysiology of schizophrenia, bipolar disorder and major depressive disorder. There is so much to say about the new research showing the relevant linkage. SLS shortens telomere length,alters neuronal morphology and gene expression through various epigenetic channels, reduces neurogenesis and synaptogesis, is associated with synaptic pathology, is also associated with the new findings in complementary C4 proteins recently identified in the New York Times as “scientists homing in on the genetic cause of schizophrenia’!
Report comment