Chronic Fatigue Syndrome: A Quantum Mechanical Perspective
Authors: Simeoni Ricardo 
Published: May 2022

Chronic fatigue syndrome (CFS), also known as myalgic encephalomyelitis (ME) or systemic exertional intolerance disease (SEID), is an illness dominated by long-term fatigue persisting for more than six months, incapacitating to the point of sufferers being bedridden or housebound in some cases, and unexplained by some other underlying medical condition. CFS is also often characterised by unrefreshing sleep, post-exertional discomfort ranging from malaise to extreme exhaustion, orthostatic (upright posture) intolerance, muscle pain, cognitive impairment (including the commonly described symptom of "brain fog"), and deterioration in cellular bioenergetics [1-3]. Scientific estimates of the world-wide population percentage that suffer from CFS naturally vary, but a conservative estimate based on several studies is at least 0.4%, thereby equating to millions world-wide [1-4]. Thankfully, after decades of dismissal by some quarters, leading to despair and exasperation of sufferers, CFS is now widely accepted as a legitimate illness. However, while depreciating labels such as "yuppy flu" have subsequently been banished to recent history, this new-found acceptance provides comfort for sufferers only up to a certain point. Viz., CFS is still far from fully understood and is often described as a complex, multisystem illness with no clear pathological mechanisms or diagnostic biomarkers [1-3], from which treatment uncertainty ensues [1,2]. Sadly, due in no small part to this uncertainty and the illness characteristics of the opening paragraph, the suicide rate of CFS sufferers has been reported as approximately seven times that of their healthy counterparts [1,5]. The economic and other social impacts of CFS are difficult to determine because of the arbitrariness of case definitions, lack of evidence including prevalence data, diagnostic inability of some physicians due to factors such as disbelief and lack of understanding (one major survey [4] reveals that 62% of sufferers are not confident in their general physician’s understanding), and difficulty many sufferers have in explaining the symptoms of their illness (another survey [2] shows that a majority or substantial proportion, depending on factors such as country of origin, have difficulty explaining their illness to not only physicians but also family and friends). Societal impacts of CFS have nonetheless been assessed by various committees (e.g., associated with the United States’ Institute of Medicine) and working/action groups (e.g., associated with the European Union). As expected, the economic impact of CFS is formally declared to be significant, with the net income of a CFS household in Europe being substantially lower than general population households (i.e., individual productivity effect), and the total annual cost burden being tens of billions of dollars in the United States alone [1-4]. The World Health Organization generally classifies CFS as a neurological illness involving the central nervous system. Some notable and more specific examples of proposed CFS aetiology components are summarised below, with these examples reflecting the complex multisystem nature of CFS and not necessarily being mutually exclusive: • Recent studies suggest that CFS arises from functional changes in the brain, with spectroscopic and inflammatory brain changes (e.g., following repeated exercise) also demonstrated. However, uncertainty over the character, location and propensity of such changes remains and the need for further functional neuroimaging studies is recognised [2,3,6,7]. • A significant increase in red blood cell (RBC) stiffness is reported in CFS, suggesting that compromised RBC transport through microcapillaries may contribute to CFS aetiology and that this diminished deformability could form the basis of a first-pass diagnostic test [8]. Further to this point, the previously identified CFS characteristic of orthostatic intolerance (estimated to occur in up to 97% of cases) is linked to under-oxygenatation of the brain to which diminished RBC deformability is thought to be a contributing factor [9]. • Unusual RBC shape, leading to reduced blood flow and changes in molecular docking on the RBC surface, is reported in CFS [10]. The subsequent increase in the number of stomatocytes (RBCs that have lost their typical concave shape, due for example to membrane defect), adds to the previous point of diminished RBC deformability to support poor microcirculation as contributing to CFS aetiology. • Dysfunction of mitochondria (subcellular organelles within the cytoplasm of aerobic cells) is found in CFS, with the interference of adenosine triphosphate (ATP) production being one of several consequences within the explanatory pathological pathway [11] (ATP is fundamentally essential for cellular-level metabolic energy requirements as outlined in Section 3). • CFS is largely resolved as not being attributable to some ongoing infection, endocrine disorder, or psychiatric condition [3,6]. While some similarly do not assign an immunological disorder attribution, more often over-stimulation or over-reaction of the immune system (hyperimmune response), impaired immune system response, immuno-inflammatory, and oxidative damage to the immune system, are all utilised expressions associated with CFS [3,6,8,1113], which in several research circles is described as a neuroimmune disease [1,11,14]. This immunological quandary again highlights the complexity of the ongoing medical challenge at hand. One clear aspect of CFS is that underlying pathophysiology implicates a range of different acute infections as onset triggers in a significant minority of cases (i.e., infections like Epstein-Barr, Ross River and the 2003 outbreak variant of Severe Acute Respiratory Syndrome, or SARS, viruses). No other medical or psychological factors are definitively implicated in CFS [7]. For many observers such triggerings are mindful of, if not directly related to, the crippling fatigue that is widely reported within contemporary media and recent studies as a lasting symptom of COVID-19. Such COVID-19-triggred CFS has led to the coined phrases of COVID-19 "long-haulers" or "long COVID", and has returned CFS to the public awareness spotlight [12]. However, too familiarly the lack of definitive CFS biomarkers is again confirmed by long COVID research, and sadly the dismissive attitudes of some in the medical profession is also a point of exasperation for long COVID sufferers [12], contributing for example to the in-desperation-establishment of a "long COVID kids" Facebook site in the United Kingdom. Established treatments, such as cognitive behaviour therapy (CBT) and graded exercise therapy (GET), primarily aim to manage the symptoms and improve the overall function of sufferers. The confounding nature of CFS extends to these treatments, since there is wide ongoing debate over their effectiveness [1,15]. For example, while GET is shown to benefit some, for others it is essentially considered just "cruel". A host of alternative treatments, some of which may be described as holistic or naturopathic or similar, naturally also exist, such as cryogenic, floatation and oxygen therapies, to name just a few. It is not the intention or place of the present article to compare, critique or scientifically review such treatments. It will simply be stated that, at least anecdotally, some such treatments seem to bring relief to some individuals (which is a positive outcome for those lucky enough to find any relief), but certainly most do not consider these treatments to be CFS cures or long-term major alleviators for the majority. Contemporary scientific scrutiny into how COVID-19 can damage the brain [13,16,17], and suggesting that the virus’ fatigue and adverse neurological effects (such as loss of smell and taste, altered mental states that can lead to the development of psychoses, and brain shrinkage in regions essential for processing memory, cognition and emotion) are indeed due to some hyperimmune response with neuroinflammation, does however offer many CFS sufferers new hope. Viz., hope that as a result of such scrutiny highly effective treatments (e.g., neural rewiring therapies [16]) and eventual cure await, even with the caveat of caution around some uncertain degree of overlap between COVID and non-COVID CFS. The present article’s title with cartoon of a fatigued physicist upon first glance likely appears incongruous. However, while some delight was taken in choosing this "humorous-to-a-physicist" title, the article is journalistically serious and does not make light of CFS. Rather, in addition to the above CFS overview, the article reflects upon a presented clinical Case Study of a seemingly recovering CFS sufferer, to form a justified CFS hypothesis for future testing. The to-be-formed hypothesis follows from the unique neuro-perspectives of [18], which explore central nervous system impulse encoding revelations via a new approach to high-order electroencephalogram (EEG) phase analysis. Given that CFS has a neurological component, can these new perspectives be applied to the area of CFS, and in particular to the to-be-presented Case Study of recovery? While this tangent might seem a long bow to draw, perhaps a fresh CFS perspective is just what is currently needed. Despite the quantum mechanical aspects to come and references [18] and [19], the latter on a discrete oscillator phase noise effect applied within phase-shift keying radiofrequency (RF) digital signal modulation, being recommended prior readings for those with a biomedical engineering or similar background, no such specialist backgrounds are assumed for readers. In brief, the present article represents academic (science and medicine) journalism that is hopefully considered high-interest, and shares via Case Study the clinical/medical results, collated over several years, for a scientifically dependent individual. The eventually formed hypothesis is intended for testing within a future formalised study, and so presently may be countered by alternative explanatory hypotheses, such as placebo and simple recovery coincidence, which are also identified.