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This is a well-written review article on the harms of CBT/GET that I found it on THE NICEGUIDELINES BLOG: Doctor Speedy and ME in search of medical honesty.
A review on cognitive behavorial therapy (CBT) and graded exercise therapy (GET) in myalgic encephalomyelitis (ME) / chronic fatigue syndrome (CFS): CBT/GET is not only ineffective and not evidence-based, but also potentially harmful for many patients with ME/CFS
Frank N.M. Twisk and Michael Maes
A review on cognitive behavorial therapy (CBT) and graded exercise therapy (GET) in myalgic encephalomyelitis (ME) / chronic fatigue syndrome (CFS): CBT/GET is not only ineffective and not evidence-based, but also potentially harmful for many patients with ME/CFS
Frank N.M. Twisk and Michael Maes
ME/CFS is considered to be a rather harmless condition by most physicians, but patients with ME/CFS are often more functionally impaired than those suffering from type 2 diabetes, congestive heart failure, multiple sclerosis, and end-stage renal disease
a) the evidence-based success claim for CBT/GET is unjust, since the evidence base is lacking and CBT/GET is not significantly more effective than usual care; and
b) the exertion, and thus GET, can have numerous potential damaging physical effects on ME/CFS patients.
b) the exertion, and thus GET, can have numerous potential damaging physical effects on ME/CFS patients.
The (bio)psychosocial model (CBT/GET) has been invalidated by research
a) Two pillars of this model, i.e. decreased exercise capacity is caused by kinesiophobia (fear of movement) and physical deconditioning is a perpetuating factor in ME/CFS, have been invalidated by research results.
b) Another misconception is the central role of specific personality traits presumed by the (bio)psychosocial model. According to various studies psychological factors play no role at all, or at the least a very minor one...no differences between patients with ME/CFS and rheumatoid arthritis in measures of perfectionism, attitudes toward mental illness, defensiveness, social desirability, or sensitivity to punishment (a concept related to neuroticism) were found. The authors stated their study also invalidated the stereotype of CFS sufferers as perfectionists with negative attitudes toward psychiatry....psychosocial and environmental factors (including personality, coping style, mood, and psychiatric history) have no significant effect on illness outcomes. According to this study post viral ME/CFS is almost exclusively genetically determined.
a) Two pillars of this model, i.e. decreased exercise capacity is caused by kinesiophobia (fear of movement) and physical deconditioning is a perpetuating factor in ME/CFS, have been invalidated by research results.
b) Another misconception is the central role of specific personality traits presumed by the (bio)psychosocial model. According to various studies psychological factors play no role at all, or at the least a very minor one...no differences between patients with ME/CFS and rheumatoid arthritis in measures of perfectionism, attitudes toward mental illness, defensiveness, social desirability, or sensitivity to punishment (a concept related to neuroticism) were found. The authors stated their study also invalidated the stereotype of CFS sufferers as perfectionists with negative attitudes toward psychiatry....psychosocial and environmental factors (including personality, coping style, mood, and psychiatric history) have no significant effect on illness outcomes. According to this study post viral ME/CFS is almost exclusively genetically determined.
The evidence-based success claim for CBT/GET is unjust.
a) The evidence base for the success claim is almost non-existent
b) The effectiveness of CBT/GET is negligible
c) In clinical practice CBT/GET has proven to be counterproductive
a) The evidence base for the success claim is almost non-existent
b) The effectiveness of CBT/GET is negligible
c) In clinical practice CBT/GET has proven to be counterproductive
CBT/GET is most likely to be harmful for many ME/CFS patients
a) Reduced exercise capacity and post-exertional malaise in ME/CFS. This slow rate of recovery is most likely to be the reason why ME/CFS patients are not able to increase their physical activities for a long time...The results suggest that a daily activity limit may exist in this patient population.
b) Neurocognitive abnormalities and the negative effects of exertion. The effects of exercise are not limited to psychical complaints, exercise also seem to have important consequences for the neurocognitive performance...Neurocognitive impairment have been demonstrated by various researchers over time. e.g. quantitative and qualitative differences in activation of the working memory network, significant decreases in motor speed and impairment in working memory, and greater efforts, i.e. the use of more extensive regions of the verbal working memory system network, to process auditory information...Hypoperfusion and reduced energy levels are plausible explanations for the brain fog often reported by ME/
CFS patients...Exertion has an negative impact on perfusion of the left prefrontal lobe and cerebral oxygenation, which very well could explain the sustained negative effect of exercise on neurocognitive performance
c) Inflammation, immune dysfunction and immune system impairment and the additional negative consequences of exertion...intracellular inflammation is strongly correlated to aches and pain, muscular tension, fatigue, and the subjective feeling of infection; and that oxidative and nitrosative damage to fatty acids and proteins is related to aches and pain, muscular tension and fatigue. The reduced exercise capacity seems also to be correlated with (intracellular) immune system abnormalities...abnormal immune activity in the pathology of exercise intolerance in ME/CFS and are consistent with a channelopathy involving oxidative stress and nitric oxide-related toxicity...exercise has important negative consequences
for the immune system of many ME/CFS patients, which is already impaired and activated at rest. In addition to these general extra negative effects of exercise on immune dysfunction and inflammation, the negative impact of exertion by ME/CFS patients on specific immunological components have also been established.
d) Oxidative and nitrosative stress and the additional negative impact of exercise. There is sufficient evidence that the induction of oxidative and nitrosative stress are important phenomena in the pathophysiology of ME/CFS...Since levels are very likely to be increased in ME/CFS already, the oxidative and nitrosative stress as a
result of exercise has an additional negative impact on the patients condition.
e) Muscle abnormalities in ME/CFS and the negative consequences of exertion. Metabolic dysfunction and structural damage to mitochondria in muscle cells has been demonstrated by various researchers...
f) The (muscoskeletal) pain in ME/CFS patients and the negative impact of exercise A hypersensitive central nervous system and cardiovascular abnormalities also seem to be play a role in the pathophysiological explanation for pain...This increase of (muscle) pain after exercise can be explained by various mechanisms: impaired oxygenation due to disturbed vasodilatation/ vasoconstriction homeostasis, accentuated oxidative and nitrosative
stress, additional induction of inflammatory pathways, altered muscle membrane excitability, reduced aerobic metabolism, hypoperfusion, and dysfunction of central anti-nociceptive mechanisms.
g) Impairment of the ion channel function in ME/CFS and potential effects of exertion. Channelopathy, i.e. abnormal ion channel function, also seems to play a central role in the pathogenesis of CFS...Several authors have suggested that channelopathy may account for fluctuating fatigue, exercise intolerance and other symptoms...Channelopathy seems to increase as a result of exertion.
h) Stress response disturbances in ME/CFS and negative effects of exercise Various studies have established hypothalamic-pituitary-adrenal (HPA) axis anomalies in ME/CFS, including an insufficient stress response...The ability to respond adequately to physical or emotional stress also seems to be impaired in ME/CFS
patients...solely based upon established HPA axis stress response aberrations, it seems very likely that the endocrine disturbances are caused or amplified by physical exertion.
i) GET can physically harm patients with ME/CFS Based upon the abovementioned observations and various other studies, it can be alleged that in ME/CFS exertion and, by inference, GET, have an negative impact on pre-existing abnormalities, e.g. physical limitations, neurocognitive impairment, immune dysfunction, inflammation, oxidative and nitrosative stress, channelopathy, (muscle) pain, muscle weakness and defective stress responses.
a) Reduced exercise capacity and post-exertional malaise in ME/CFS. This slow rate of recovery is most likely to be the reason why ME/CFS patients are not able to increase their physical activities for a long time...The results suggest that a daily activity limit may exist in this patient population.
b) Neurocognitive abnormalities and the negative effects of exertion. The effects of exercise are not limited to psychical complaints, exercise also seem to have important consequences for the neurocognitive performance...Neurocognitive impairment have been demonstrated by various researchers over time. e.g. quantitative and qualitative differences in activation of the working memory network, significant decreases in motor speed and impairment in working memory, and greater efforts, i.e. the use of more extensive regions of the verbal working memory system network, to process auditory information...Hypoperfusion and reduced energy levels are plausible explanations for the brain fog often reported by ME/
CFS patients...Exertion has an negative impact on perfusion of the left prefrontal lobe and cerebral oxygenation, which very well could explain the sustained negative effect of exercise on neurocognitive performance
c) Inflammation, immune dysfunction and immune system impairment and the additional negative consequences of exertion...intracellular inflammation is strongly correlated to aches and pain, muscular tension, fatigue, and the subjective feeling of infection; and that oxidative and nitrosative damage to fatty acids and proteins is related to aches and pain, muscular tension and fatigue. The reduced exercise capacity seems also to be correlated with (intracellular) immune system abnormalities...abnormal immune activity in the pathology of exercise intolerance in ME/CFS and are consistent with a channelopathy involving oxidative stress and nitric oxide-related toxicity...exercise has important negative consequences
for the immune system of many ME/CFS patients, which is already impaired and activated at rest. In addition to these general extra negative effects of exercise on immune dysfunction and inflammation, the negative impact of exertion by ME/CFS patients on specific immunological components have also been established.
d) Oxidative and nitrosative stress and the additional negative impact of exercise. There is sufficient evidence that the induction of oxidative and nitrosative stress are important phenomena in the pathophysiology of ME/CFS...Since levels are very likely to be increased in ME/CFS already, the oxidative and nitrosative stress as a
result of exercise has an additional negative impact on the patients condition.
e) Muscle abnormalities in ME/CFS and the negative consequences of exertion. Metabolic dysfunction and structural damage to mitochondria in muscle cells has been demonstrated by various researchers...
f) The (muscoskeletal) pain in ME/CFS patients and the negative impact of exercise A hypersensitive central nervous system and cardiovascular abnormalities also seem to be play a role in the pathophysiological explanation for pain...This increase of (muscle) pain after exercise can be explained by various mechanisms: impaired oxygenation due to disturbed vasodilatation/ vasoconstriction homeostasis, accentuated oxidative and nitrosative
stress, additional induction of inflammatory pathways, altered muscle membrane excitability, reduced aerobic metabolism, hypoperfusion, and dysfunction of central anti-nociceptive mechanisms.
g) Impairment of the ion channel function in ME/CFS and potential effects of exertion. Channelopathy, i.e. abnormal ion channel function, also seems to play a central role in the pathogenesis of CFS...Several authors have suggested that channelopathy may account for fluctuating fatigue, exercise intolerance and other symptoms...Channelopathy seems to increase as a result of exertion.
h) Stress response disturbances in ME/CFS and negative effects of exercise Various studies have established hypothalamic-pituitary-adrenal (HPA) axis anomalies in ME/CFS, including an insufficient stress response...The ability to respond adequately to physical or emotional stress also seems to be impaired in ME/CFS
patients...solely based upon established HPA axis stress response aberrations, it seems very likely that the endocrine disturbances are caused or amplified by physical exertion.
i) GET can physically harm patients with ME/CFS Based upon the abovementioned observations and various other studies, it can be alleged that in ME/CFS exertion and, by inference, GET, have an negative impact on pre-existing abnormalities, e.g. physical limitations, neurocognitive impairment, immune dysfunction, inflammation, oxidative and nitrosative stress, channelopathy, (muscle) pain, muscle weakness and defective stress responses.
Not only is the evidence-based claim for CBT/GET unjust, there is compelling evidence that CBT/GET is potentially harmful for many ME/CFS patients. Numerous studies support the assertion that exercise and, consequently, GET, can aggravate several characteristic ME/CFS symptoms, e.g. neurocognitive complaints, reduced exercise capacity and widespread muscoskeletal pain, and amplifies pre-existing pathophysiological abnormalities in ME/CFS, e.g. immune dysfunction, induction of the IO&NS pathways, channelopathy and an impaired stress response. Large-scaled patient surveys and clinical practice show that CBT/GET often induces a deterioration of the clinical status of ME/CFS patients and is harmful for many patients. Therefore, it is medically unethical to subject ME/CFS patients to CBT/GET programs or variants, like GET with limits, without assessing biological abnormalities, monitoring functional impairment objectively and measuring the effect of exercise e.g. on the physical and neurocognitive performance