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".]
 * 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."

Online Presence

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