G
Gerwyn
Guest
The Following is based on Gupta's own words in blue and mine in red.
Latest Update to Amygdala Hypothesis
by Ashok Gupta Fri Mar 27, 2009 11:17 am
Gupta, A (2009) - Updates to The Amygdala Conditioning Hypothesis for Chronic Fatigue Syndrome (ME/CFS) - A Short Report (DRAFT)
Summary of 2002 Paper
In my 2002 paper (1), it was HYPOTHESISED that ME/CFS is a neurobiological condition caused by a conditioned trauma in the amygdala following an acute viral, bacterial or physical insult, combined with psycho-social distress. Once the classical and operant conditioning has occurred, the amygdala becomes hyper-sensitive to signals .
Note CAUSED by in part psycho social distress
Classical and operant conditioning has never been observed in humans.Neither has conditioned trauma of the amygdala—what ever on earth that means..Conditioning is merely a theory outlined by behaviourists who claim that ALL behaviour is a a conditioned reponse to environmental stimuli
It could be hypothesised that certain genes may increase the intensity and length of both the initial illness and subsequent post-infective fatigue, thereby promoting the likelihood of conditioning effects in the amygdala and related brain structures involved in conditioning.
There are no brain structures related to conditioning
This is true of PTSD, another conditioning disorder
No PTSD is not a conditioning disorder it is a complex neurobiological disorder
n Gupta 2002 (1), in addition to chronic arousal of the HPA axis and sympathetic systems, it is hypothesised that during the trauma, a "stress signature" effect occurs where aspects of the immune system are also re-triggered chronically after onset. This refers to conditioning in the immune system, and recent
The HPA axis is depressed in patients with ME
In rats, the amygdala's involvement in conditioned immune responses has recently been confirmed, in association with the insular cortex and the hypothalamus (6).
6) Pacheco-Lpez G, Niemi MB, Kou W, Hrting M, Fandrey J, Schedlowski M. Neural substrates for behaviorally conditioned immunosuppression in the rat. J Neurosci. 2005 Mar 2;25(9):2330-7.
That is an interesting interpretation as the study actually says that the amgydala
Is NOT involved in the conditioned response
). In contrast, Am and VMH lesions did not affect conditioned taste aversion
This refers to conditioning in the immune system, and recent neurobiological research is showing that the rat model of immune system conditioning can also occur in humans(5)
(5) Marion U, Goebel et al. B
behaviourial Conditioning of Antihistamine Effects in Patients with Allergic Rhinitis. Psychotherapy and Psychosomatics, Vol 77, No.4, pages 227-234; May 2008
No it does not note the psychobabble.
It is likely that the hypothalamus carries out the instructions to stimulate the HPA axis directly from the amygdala (as has been demonstrated in animal experiments (7)), as well as aspects of the immune system. Furthermore, the amygdala also projects directly to the sympathetic nervous system.
(7) Ledoux, J. (1998), The Emotional Brain (Pheonix) chapters 6-9
That is unpublished data written in a book!
Finally some comments about the Medical hypothesis journal that contained Gupta,s original 2002 paper.
Medical Hypotheses was founded in 1975 by physiologist David Horrobin, who was the editor-in-chief of the journal until his death in 2003 as well as the head of the Schizophrenia Association in Britain.[4] Horrobin was a controversial figure, a scientist and entrepreneur best known for his promotion of evening primrose oil as a treatment for diseases, leading the British Medical Journal (BMJ) to predict that he "may prove to be the greatest snake oil salesman of his age."[
The most widely cited article[13] from Medical Hypotheses was published in 1991 by RS Smith in which he proposed the macrophage theory of depression as an alternative to the monoamine theory of depression.[14][15][16]
In 2007, journalist Roger Dobson published a book in which he collected and described 100 Medical Hypotheses articles called Death Can Be Cured.[17][18]
In what The Guardian columnist Ben Goldacre called an "almost surreally crass paper", two Medical Hypotheses authors posited "mongoloid" as an accurate term for people with Down syndrome because those with Down's share characteristics with people of Asian origin, including a reported interest in crafts, sitting with crossed legs and eating foods containing monosodium glutamate (MSG).[21]
In 2009, the journal's publisher, Elsevier, withdrew two articles written by AIDS denialists that had been accepted for publication. One of the articles, written by Peter Duesberg and David Rasnick, reportedly claimed that AIDS was not responsible for deaths in South Africa that another paper had attributed to it and misrepresented the results of medical research on antiretroviral drugs.[21]
A review panel convened by Elsevier recommended that Medical Hypotheses adopt some form of peer review to avoid publication of "baseless, speculative, non-testable and potentially harmful ideas". Editor Bruce Charlton said that peer review went against the journal's 30-year history and is not supported by either him or the journal's editorial board.[3]
So much for Gupta,s claim that his hypothesis was published in a peer reviewed medical journal!
Latest Update to Amygdala Hypothesis
by Ashok Gupta Fri Mar 27, 2009 11:17 am
Gupta, A (2009) - Updates to The Amygdala Conditioning Hypothesis for Chronic Fatigue Syndrome (ME/CFS) - A Short Report (DRAFT)
Summary of 2002 Paper
In my 2002 paper (1), it was HYPOTHESISED that ME/CFS is a neurobiological condition caused by a conditioned trauma in the amygdala following an acute viral, bacterial or physical insult, combined with psycho-social distress. Once the classical and operant conditioning has occurred, the amygdala becomes hyper-sensitive to signals .
Note CAUSED by in part psycho social distress
Classical and operant conditioning has never been observed in humans.Neither has conditioned trauma of the amygdala—what ever on earth that means..Conditioning is merely a theory outlined by behaviourists who claim that ALL behaviour is a a conditioned reponse to environmental stimuli
It could be hypothesised that certain genes may increase the intensity and length of both the initial illness and subsequent post-infective fatigue, thereby promoting the likelihood of conditioning effects in the amygdala and related brain structures involved in conditioning.
There are no brain structures related to conditioning
This is true of PTSD, another conditioning disorder
No PTSD is not a conditioning disorder it is a complex neurobiological disorder
n Gupta 2002 (1), in addition to chronic arousal of the HPA axis and sympathetic systems, it is hypothesised that during the trauma, a "stress signature" effect occurs where aspects of the immune system are also re-triggered chronically after onset. This refers to conditioning in the immune system, and recent
The HPA axis is depressed in patients with ME
In rats, the amygdala's involvement in conditioned immune responses has recently been confirmed, in association with the insular cortex and the hypothalamus (6).
6) Pacheco-Lpez G, Niemi MB, Kou W, Hrting M, Fandrey J, Schedlowski M. Neural substrates for behaviorally conditioned immunosuppression in the rat. J Neurosci. 2005 Mar 2;25(9):2330-7.
That is an interesting interpretation as the study actually says that the amgydala
Is NOT involved in the conditioned response
). In contrast, Am and VMH lesions did not affect conditioned taste aversion
This refers to conditioning in the immune system, and recent neurobiological research is showing that the rat model of immune system conditioning can also occur in humans(5)
(5) Marion U, Goebel et al. B
behaviourial Conditioning of Antihistamine Effects in Patients with Allergic Rhinitis. Psychotherapy and Psychosomatics, Vol 77, No.4, pages 227-234; May 2008
No it does not note the psychobabble.
It is likely that the hypothalamus carries out the instructions to stimulate the HPA axis directly from the amygdala (as has been demonstrated in animal experiments (7)), as well as aspects of the immune system. Furthermore, the amygdala also projects directly to the sympathetic nervous system.
(7) Ledoux, J. (1998), The Emotional Brain (Pheonix) chapters 6-9
That is unpublished data written in a book!
Finally some comments about the Medical hypothesis journal that contained Gupta,s original 2002 paper.
Medical Hypotheses was founded in 1975 by physiologist David Horrobin, who was the editor-in-chief of the journal until his death in 2003 as well as the head of the Schizophrenia Association in Britain.[4] Horrobin was a controversial figure, a scientist and entrepreneur best known for his promotion of evening primrose oil as a treatment for diseases, leading the British Medical Journal (BMJ) to predict that he "may prove to be the greatest snake oil salesman of his age."[
The most widely cited article[13] from Medical Hypotheses was published in 1991 by RS Smith in which he proposed the macrophage theory of depression as an alternative to the monoamine theory of depression.[14][15][16]
In 2007, journalist Roger Dobson published a book in which he collected and described 100 Medical Hypotheses articles called Death Can Be Cured.[17][18]
In what The Guardian columnist Ben Goldacre called an "almost surreally crass paper", two Medical Hypotheses authors posited "mongoloid" as an accurate term for people with Down syndrome because those with Down's share characteristics with people of Asian origin, including a reported interest in crafts, sitting with crossed legs and eating foods containing monosodium glutamate (MSG).[21]
In 2009, the journal's publisher, Elsevier, withdrew two articles written by AIDS denialists that had been accepted for publication. One of the articles, written by Peter Duesberg and David Rasnick, reportedly claimed that AIDS was not responsible for deaths in South Africa that another paper had attributed to it and misrepresented the results of medical research on antiretroviral drugs.[21]
A review panel convened by Elsevier recommended that Medical Hypotheses adopt some form of peer review to avoid publication of "baseless, speculative, non-testable and potentially harmful ideas". Editor Bruce Charlton said that peer review went against the journal's 30-year history and is not supported by either him or the journal's editorial board.[3]
So much for Gupta,s claim that his hypothesis was published in a peer reviewed medical journal!
