keehah
10th September 2011, 11:44 AM
I found the first two of his articles I have read (and linked here) very interesting and illuminating.
Interesting articles suggesting immune system overactivity being 'depression.' One more way vaccines may work on the human body.
The last is an evaluation and (self) treatment summary.
Self-management of psychiatric symptoms using over-the-counter (OTC) psychopharmacology: The S-DTM therapeutic model - self-diagnosis, self-treatment, self-monitoring. (http://www.hedweb.com/bgcharlton/sdtm.html)
The malaise theory of depression: Major depressive disorder
is sickness behavior and antidepressants are analgesic (http://www.hedweb.com/bgcharlton/depression.html)
Bruce G Charlton MD
The problem here is theoretical: since the psychological nature of depression is unclear (Charlton, 1995), the way in which antidepressants act upon depression is unclear, and the current rationale for drug treatment of MDD is also unclear (Charlton, 1998_). I propose a unifying theoretical framework for understanding depression and antidepressant action which has the potential to elucidate all these problems. As well as its primary virtue of making-sense in scientific and clinical terms, the malaise theory of depression also has the important advantage of being comprehensible and rational in 'lay' terms.
MDD is sickness behavior
Since major depressive disorder (MDD) is a recurrent pattern or signs and symptoms, it is reasonable to seek an adaptive function for this pattern which might explain why it occurs in a predictable form throughout populations and cross-culturally. Having established a plausible evolutionary function for the MDD syndrome, we can ask how the MDD syndrome is generated and ask what are the factors which mediate it. Finally, any clinically useful theory should be able to explain the ways in which pharmacological and other interventions have beneficial effects in patients suffering from MDD.
The evolutionary function of the behavioral pattern of major depressive disorder can be elucidated by a comparison with other animals. MDD turns out to be near-identical with the adaptive state termed sickness behavior (SB) in animals. Sickness behavior was first described by a veterinarian as a physiological and psychological adaptation to acute infective and inflammatory illness in many mammalian species (Hart, 1988_). The characteristic pattern of sickness behavior comprises pyrexia, fatigue, somnolence, psychomotor retardation, anhedonia (lack of ability to experience pleasures such as eating and sex) and impaired cognitive functioning (Kent et al, 1992). In other words the syndrome of SB is almost exactly the same as the standard diagnostic descriptions of MDD (Hickie & Lloyd, 1995; Yirmaya, 1997). The only apparent differences - somnolence and pyrexia - are explicable given that daytime somnolence typically leads to secondary insomnia with nocturnal sleep disruption, and that the presence of pyrexia has not yet been evaluated in MDD.
The evolved function of SB is to act as an energy-conserving, risk-minimizing, immune-enhancing state appropriate for a body mounting a short-term, all-out attack on an invading micro-organism (Hart, 1988; Kent et al, 1992). Major depressive disorder is therefore the behavioral response to a physical illness - it is a syndrome in which low mood is the product of malaise; where malaise describes the symptom of 'feeling ill'. By this account, the feeling of malaise should be regarded as the core emotion of depression (as suggested by Healy, 1990). Therefore major depressive disorder is not primarily an affective disorder: instead the primary pathology in major depressive disorder is somatic, and mood is a secondary and variable response to this disordered physical state.
Cytokines as mediating factors of sickness behavior
If major depressive disorder is sickness behavior - inappropriately-activated or excessively sustained, the next question concerns the 'proximate cause' of this behavioral pattern. Again the evidence appears clear. Mediating factors for the syndrome of MDD seem to involve hyper-activity of the immune system in response to 'non-self' antigenic challenge (for example, inflammation due to infection, carcinoma or 'autoimmune' disease). The chemical factors responsible for mediating sickness behavior appear to be the class of immune active agents known as cytokines (eg. interleukins and interferons (Hart, 1988; Kent et al, 1992; Hickie & Lloyd, 1995; Yirmaya, 1997). Indeed, SB is best considered as an integral and adaptive part of the pyrexial response; it is the behavioral change that assists in the generation and maintenance of raised body temperature produces a diminution of activity appropriate to immune activation.
http://www.hedweb.com/bgcharlton/subtypes-depression.pdf
Editorial
A model for self-treatment of four sub-types of symptomatic ‘depression’
using non-prescription agents: Neuroticism (anxiety and emotional instability);
malaise (fatigue and painful symptoms); demotivation (anhedonia)
and seasonal affective disorder ‘SAD’
summary
This article will present a model for how ‘depression’ (i.e. depressive symptoms) can be divided into four self-diagnosed sub-types or causes which might then be self-treated using agents available without prescription. (Another, much rarer, cause of depressed symptoms is the classical illness of ‘melancholia’, which when severe cannot be self-treated and typically requires hospitalization.) A self-management option and alternative is now needed due to an inappropriate emphasis of modern psychiatry on treatment of imprecise syndromal ‘disorders’ which may entail treating ‘depression’ at the cost of making the patient feel and function worse. By contrast, the basic theoretical stance of self-management is that depressed mood should be seen as a result of unpleasant symptoms – and it is the symptoms that require treatment, not the mood itself. Furthermore, drugs (or other interventions) need to be classified in terms of their potential therapeutic effects on these symptoms that may cause depressed mood. The four common causes of depressed mood considered here are the personality trait of Neuroticism; the state of malaise (fatigue, aching etc) which accompanies an illness with an activated immune system; demotivation due to lack of positive emotions (anhedonia); and the syndrome of seasonal affective disorder (SAD). Each of the four sub-types is then ‘matched’ with a first–line non-prescription agent. The ‘stabilizing’ agents such as St John’s Wort and the antihistamines chlorpheniramine and diphenhydramine are used for treatment of Neuroticism; analgesics/pain killers such as aspirin, ibuprofen, paracetamol/acetaminophen and the opiates are used to treat malaise; energizing agents such as caffeine and nicotine are used for the treatment of demotivation; and bright light used in the early morning to treat SAD. Self-treatments are intended to be used after research and experimentally, on a trial-and-error basis; with self-monitoring of beneficial and harmful effects, and a willingness to stop and switch treatments. The model of S-DTM (self-diagnosis, self-treatment and self–monitoring) is suggested as potentially applicable more widely within psychiatry and medicine.
2008 Published by Elsevier Ltd. [cont'd]
Here is a full list of links on the topic: http://www.hedweb.com/bgcharlton/
Interesting articles suggesting immune system overactivity being 'depression.' One more way vaccines may work on the human body.
The last is an evaluation and (self) treatment summary.
Self-management of psychiatric symptoms using over-the-counter (OTC) psychopharmacology: The S-DTM therapeutic model - self-diagnosis, self-treatment, self-monitoring. (http://www.hedweb.com/bgcharlton/sdtm.html)
The malaise theory of depression: Major depressive disorder
is sickness behavior and antidepressants are analgesic (http://www.hedweb.com/bgcharlton/depression.html)
Bruce G Charlton MD
The problem here is theoretical: since the psychological nature of depression is unclear (Charlton, 1995), the way in which antidepressants act upon depression is unclear, and the current rationale for drug treatment of MDD is also unclear (Charlton, 1998_). I propose a unifying theoretical framework for understanding depression and antidepressant action which has the potential to elucidate all these problems. As well as its primary virtue of making-sense in scientific and clinical terms, the malaise theory of depression also has the important advantage of being comprehensible and rational in 'lay' terms.
MDD is sickness behavior
Since major depressive disorder (MDD) is a recurrent pattern or signs and symptoms, it is reasonable to seek an adaptive function for this pattern which might explain why it occurs in a predictable form throughout populations and cross-culturally. Having established a plausible evolutionary function for the MDD syndrome, we can ask how the MDD syndrome is generated and ask what are the factors which mediate it. Finally, any clinically useful theory should be able to explain the ways in which pharmacological and other interventions have beneficial effects in patients suffering from MDD.
The evolutionary function of the behavioral pattern of major depressive disorder can be elucidated by a comparison with other animals. MDD turns out to be near-identical with the adaptive state termed sickness behavior (SB) in animals. Sickness behavior was first described by a veterinarian as a physiological and psychological adaptation to acute infective and inflammatory illness in many mammalian species (Hart, 1988_). The characteristic pattern of sickness behavior comprises pyrexia, fatigue, somnolence, psychomotor retardation, anhedonia (lack of ability to experience pleasures such as eating and sex) and impaired cognitive functioning (Kent et al, 1992). In other words the syndrome of SB is almost exactly the same as the standard diagnostic descriptions of MDD (Hickie & Lloyd, 1995; Yirmaya, 1997). The only apparent differences - somnolence and pyrexia - are explicable given that daytime somnolence typically leads to secondary insomnia with nocturnal sleep disruption, and that the presence of pyrexia has not yet been evaluated in MDD.
The evolved function of SB is to act as an energy-conserving, risk-minimizing, immune-enhancing state appropriate for a body mounting a short-term, all-out attack on an invading micro-organism (Hart, 1988; Kent et al, 1992). Major depressive disorder is therefore the behavioral response to a physical illness - it is a syndrome in which low mood is the product of malaise; where malaise describes the symptom of 'feeling ill'. By this account, the feeling of malaise should be regarded as the core emotion of depression (as suggested by Healy, 1990). Therefore major depressive disorder is not primarily an affective disorder: instead the primary pathology in major depressive disorder is somatic, and mood is a secondary and variable response to this disordered physical state.
Cytokines as mediating factors of sickness behavior
If major depressive disorder is sickness behavior - inappropriately-activated or excessively sustained, the next question concerns the 'proximate cause' of this behavioral pattern. Again the evidence appears clear. Mediating factors for the syndrome of MDD seem to involve hyper-activity of the immune system in response to 'non-self' antigenic challenge (for example, inflammation due to infection, carcinoma or 'autoimmune' disease). The chemical factors responsible for mediating sickness behavior appear to be the class of immune active agents known as cytokines (eg. interleukins and interferons (Hart, 1988; Kent et al, 1992; Hickie & Lloyd, 1995; Yirmaya, 1997). Indeed, SB is best considered as an integral and adaptive part of the pyrexial response; it is the behavioral change that assists in the generation and maintenance of raised body temperature produces a diminution of activity appropriate to immune activation.
http://www.hedweb.com/bgcharlton/subtypes-depression.pdf
Editorial
A model for self-treatment of four sub-types of symptomatic ‘depression’
using non-prescription agents: Neuroticism (anxiety and emotional instability);
malaise (fatigue and painful symptoms); demotivation (anhedonia)
and seasonal affective disorder ‘SAD’
summary
This article will present a model for how ‘depression’ (i.e. depressive symptoms) can be divided into four self-diagnosed sub-types or causes which might then be self-treated using agents available without prescription. (Another, much rarer, cause of depressed symptoms is the classical illness of ‘melancholia’, which when severe cannot be self-treated and typically requires hospitalization.) A self-management option and alternative is now needed due to an inappropriate emphasis of modern psychiatry on treatment of imprecise syndromal ‘disorders’ which may entail treating ‘depression’ at the cost of making the patient feel and function worse. By contrast, the basic theoretical stance of self-management is that depressed mood should be seen as a result of unpleasant symptoms – and it is the symptoms that require treatment, not the mood itself. Furthermore, drugs (or other interventions) need to be classified in terms of their potential therapeutic effects on these symptoms that may cause depressed mood. The four common causes of depressed mood considered here are the personality trait of Neuroticism; the state of malaise (fatigue, aching etc) which accompanies an illness with an activated immune system; demotivation due to lack of positive emotions (anhedonia); and the syndrome of seasonal affective disorder (SAD). Each of the four sub-types is then ‘matched’ with a first–line non-prescription agent. The ‘stabilizing’ agents such as St John’s Wort and the antihistamines chlorpheniramine and diphenhydramine are used for treatment of Neuroticism; analgesics/pain killers such as aspirin, ibuprofen, paracetamol/acetaminophen and the opiates are used to treat malaise; energizing agents such as caffeine and nicotine are used for the treatment of demotivation; and bright light used in the early morning to treat SAD. Self-treatments are intended to be used after research and experimentally, on a trial-and-error basis; with self-monitoring of beneficial and harmful effects, and a willingness to stop and switch treatments. The model of S-DTM (self-diagnosis, self-treatment and self–monitoring) is suggested as potentially applicable more widely within psychiatry and medicine.
2008 Published by Elsevier Ltd. [cont'd]
Here is a full list of links on the topic: http://www.hedweb.com/bgcharlton/