Frank Twisk

Frank N.M. Twisk, MBA, MBI, BEd, BEc, is a Dutch myalgic encephalomyelitis (ME) advocate and writer. Prior to becoming ill with ME in 1996, he was a project manager, business administrator, information scientist, mathematician, higher education teacher, and avid footballer. He encourages those of different talents to work together in the goal for scientific answers to ME and advocates for a clear distinction between ME and chronic fatigue syndrome (CFS).

Twisk is associated with a Dutch non-profit, ME-de-patiënten Foundation, in a voluntary (non-paid) capacity.

Interviews & Talks

 * 2015 - ME and my life: past, present and future (video - Dutch w/ English Closed Captions)

Published Articles, Commentary and Letters

 * 2016, Myalgic Encephalomyelitis, chronic fatigue syndrome or systemic exercise intolerance disease: What’s in a name?
 * 2016, Correspondence to The [[Lancet Psychiatry] on the PACE trial - "PACE: CBT and GET are not rehabilitative therapies".]
 * 7 Nov 2015, Deviant cellular and physiological responses to exercise in Myalgic Encephalomyelitis and chronic fatigue syndrome. "'Abstract: Post-exertional “malaise” is a hallmark symptom of Myalgic Encephalomyelitis (ME) and Chronic Fatigue Syndrome (CFS). Various abnormalities, including abnormal physiological responses to exertion, can account for post-exertional “malaise” and “exercise avoidance”. Since these abnormalities are not observed in sedentary healthy controls, the abnormalities and deviant responses cannot be explained by “exercise avoidance” and subsequent deconditioning, nor by psychogenic factors.'"
 * 26 Jun 2015, Accurate diagnosis of myalgic encephalomyelitis and chronic fatigue syndrome based upon objective test methods for characteristic symptoms (FULL TEXT) Abstract - Although myalgic encephalomyelitis (ME) and chronic fatigue syndrome (CFS) are considered to be synonymous, the definitional criteria for ME and CFS define two distinct, partially overlapping, clinical entities. ME, whether defined by the original criteria or by the recently proposed criteria, is not equivalent to CFS, let alone a severe variant of incapacitating chronic fatigue. Distinctive features of ME are: muscle weakness and easy muscle fatigability, cognitive impairment, circulatory deficits, a marked variability of the symptoms in presence and severity, but above all, post-exertional “malaise”: a (delayed) prolonged aggravation of symptoms after a minor exertion. In contrast, CFS is primarily defined by (unexplained) chronic fatigue, which should be accompanied by four out of a list of 8 symptoms, e.g., headaches. Due to the subjective nature of several symptoms of ME and CFS, researchers and clinicians have questioned the physiological origin of these symptoms and qualified ME and CFS as functional somatic syndromes. However, various characteristic symptoms, e.g., post-exertional “malaise” and muscle weakness, can be assessed objectively using well-accepted methods, e.g., cardiopulmonary exercise tests and cognitive tests. The objective measures acquired by these methods should be used to accurately diagnose patients, to evaluate the severity and impact of the illness objectively and to assess the positive and negative effects of proposed therapies impartially.
 * 2015, Letter to the Editor, by Frank Twisk in Fatigue: Biomedicine, Health & Behavior
 * 2015, Commentary on Jason et al. (2015): towards separate empirical case definitions of Myalgic Encephalomyelitis and chronic fatigue syndrome
 * 2014, Review Article: Deviant Cellular and Physiological Responses to Exercise in Myalgic Encephalomyelitis and Chronic Fatigue Syndrome
 * 2013, Rebuttal to Ickmans et al. Association between cognitive performance, physical fitness, and physical activity level in women with chronic fatigue syndrome.
 * 2011, Increased IgA responses to the LPS of commensal bacteria is associated with inflammation and activation of cell-mediated immunity in chronic fatigue syndrome.
 * 2010, Chronic fatigue syndrome: Harvey and Wessely's (bio)psychosocial model versus a bio(psychosocial) model based on inflammatory and oxidative and nitrosative stress pathways"'Abstract - Background: In a recently published paper, Harvey and Wessely put forward a 'biopsychosocial' explanatory model for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), which is proposed to be applicable to (chronic) fatigue even when apparent medical causes are present. Methods: Here, we review the model proposed by Harvey and Wessely, which is the rationale for behaviourally oriented interventions, such as cognitive behaviour therapy (CBT ) and graded exercise therapy (GET ), and compare this model with a biological model, in which inflammatory, immune, oxidative and nitrosative (IO&NS) pathways are key elements. Discussion: Although human and animal studies have established that the pathophysiology of ME/CFS includes IO&NS pathways, these abnormalities are not included in the model proposed by Harvey and Wessely. Activation of IO&NS pathways is known to induce fatigue and somatic (F&S) symptoms and can be induced or maintained by viral and bacterial infections, physical and psychosocial stressors, or organic disorders such as (auto)immune disorders. Studies have shown that ME/CFS and major depression are both clinical manifestations of shared IO&NS pathways, and that both disorders can be discriminated by specific symptoms and unshared or differentiating pathways. Interventions with CBT/GET are potentially harmful for many patients with ME/CFS, since the underlying pathophysiological abnormalities may be intensified by physical stressors. Conclusions: In contrast to Harvey and Wessely's (bio)psychosocial model for ME/CFS a bio(psychosocial) model based upon IO&NS abnormalities is likely more appropriate to this complex disorder. In clinical practice, we suggest physicians should also explore the IO&NS pathophysiology by applying laboratory tests that examine the pathways involved.'"
 * 2009, 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."'Abstract: Benign Myalgic Encephalomyelitis (ME) / Chronic Fatigue Syndrome (CFS) is a debilitating disease which, despite numerous biological abnormalities has remained highly controversial. Notwithstanding the medical pathogenesis of ME/CFS, the (bio)psychosocial model is adopted by many governmental organizations and medical professionals to legitimize the combination of Cognitive Behavioral Therapy (CBT) and Graded Exercise Therapy (GET) for ME/CFS. Justified by this model CBT and GET aim at eliminating presumed psychogenic and socially induced maintaining factors and reversing deconditioning, respectively. In this review we invalidate the (bio)psychosocial model for ME/CFS and demonstrate that the success claim for CBT/GET to treat ME/CFS is unjust. CBT/GET is not only hardly more effective than non-interventions or standard medical care, but many patients report that the therapy had affected them adversely, the majority of them even reporting substantial deterioration. Moreover, this review shows that exertion and thus GET most likely have a negative impact on many ME/CFS patients. Exertion induces post-exertional malaise with a decreased physical performance/aerobic capacity, increased muscoskeletal pain, neurocognitive impairment, 'fatigue', and weakness, and a long lasting 'recovery' time. This can be explained by findings that exertion may amplify pre-existing pathophysiological abnormalities underpinning ME/CFS, such as inflammation, immune dysfunction, oxidative and nitrosative stress, channelopathy, defective stress response mechanisms and a hypoactive hypothalamic-pituitary-adrenal axis. We conclude that it is unethical to treat patients with ME/CFS with ineffective, non-evidence-based and potentially harmful 'rehabilitation therapies', such as CBT/GET."

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