Addressing the Long COVID Crisis: Integrative Health and Long COVID

Abstract:

While COVID-19 has killed millions of people globally, its lasting effects on the health and well-being of entire populations are just becoming clear. As many as 30% of those diagnosed with COVID-19 report continuing health-related problems, regardless of the severity of the initial infection. Given the infection rate in the world, that translates to between 5.4 and 17.9 million globally; about 700 000 in the US. The syndrome goes by many names; here we call it “long COVID.” Patients experience a wide range of symptoms, including serious organ system effects such as pulmonary fibrosis, myocarditis, new diabetes diagnoses, stroke, and other cerebrovascular events. They also experience ongoing pain, fatigue, and cognitive dysfunction. We suggest here that these patients require an integrative health approach, one that combines traditional medical management, non-pharmacological approaches, and behavior and lifestyle changes. Such an approach has been shown to be beneficial in other chronic illnesses such as fibromyalgia, chronic fatigue syndrome, and post-Lyme disease.

Source: Roth A, Chan PS, Jonas W. Addressing the Long COVID Crisis: Integrative Health and Long COVID. Glob Adv Health Med. 2021 Nov 16;10:21649561211056597. doi: 10.1177/21649561211056597. PMID: 34820152; PMCID: PMC8606968. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8606968/  (Full text)

No Signs of Neuroinflammation in Women With Chronic Fatigue Syndrome or Q Fever Fatigue Syndrome Using the TSPO Ligand [ 11 C]-PK11195

Abstract:

Background and objectives: The pathophysiology of chronic fatigue syndrome (CFS) and Q fever fatigue syndrome (QFS) remains elusive. Recent data suggest a role for neuroinflammation as defined by increased expression of translocator protein (TSPO). In the present study, we investigated whether there are signs of neuroinflammation in female patients with CFS and QFS compared with healthy women, using PET with the TSPO ligand 11C-(R)-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinoline-carbox-amide ([11C]-PK11195).

Methods: The study population consisted of patients with CFS (n = 9), patients with QFS (n = 10), and healthy subjects (HSs) (n = 9). All subjects were women, matched for age (±5 years) and neighborhood, aged between 18 and 59 years, who did not use any medication other than paracetamol or oral contraceptives, and were not vaccinated in the last 6 months. None of the subjects reported substance abuse in the past 3 months or reported signs of underlying psychiatric disease on the Mini-International Neuropsychiatric Interview. All subjects underwent a [11C]-PK11195 PET scan, and the [11C]-PK11195 binding potential (BPND) was calculated.

Results: No statistically significant differences in BPND were found for patients with CFS or patients with QFS compared with HSs. BPND of [11C]-PK11195 correlated with symptom severity scores in patients with QFS, but a negative correlation was found in patients with CFS.

Discussion: In contrast to what was previously reported for CFS, we found no significant difference in BPND of [11C]-PK11195 when comparing patients with CFS or QFS with healthy neighborhood controls. In this small series, we were unable to find signs of neuroinflammation in patients with CFS and QFS.

Source: Raijmakers R, Roerink M, Keijmel S, Joosten L, Netea M, van der Meer J, Knoop H, Klein H, Bleeker-Rovers C, Doorduin J. No Signs of Neuroinflammation in Women With Chronic Fatigue Syndrome or Q Fever Fatigue Syndrome Using the TSPO Ligand [11C]-PK11195. Neurol Neuroimmunol Neuroinflamm. 2021 Nov 23;9(1):e1113. doi: 10.1212/NXI.0000000000001113. PMID: 34815320. https://pubmed.ncbi.nlm.nih.gov/34815320/

Missteps in Creating a Long Haul COVID Case Definition

Excerpt:

Millions of individuals who have not recovered from the COVID virus are now dealing with a host of symptoms that are challenging our health care system. Many are experiencing significant problems in being recognized by health care workers as a real disorder, as for many of them, there are no biological markers of persistent illness. Just as with ME/CFS, we need to be sure that long haul COVID patients are not victimized first by the pandemic and then by the health care skepticism of their significant symptoms. We have the conceptual and theoretical grounding to develop clinical and research case definitions for those with persisting COVID symptoms. Patients must be instrumentally involved in all such efforts as failure to do so will only further delegitimize their condition.

Read the rest of this article HERE.

Source: Leonard Jason, Ph.D. and Vernita Perkins, PhD. Missteps in Creating a Long Haul COVID Case Definition. Psychology Today. Posted November 22, 2021

An attempt to explain the neurological symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Abstract:

There is accumulating evidence of endothelial dysfunction, muscle and cerebral hypoperfusion in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). In this paper we deduce the pathomechanisms resulting in central nervous pathology and the myriad of neurocognitive symptoms. We outline tentative mechanisms of impaired cerebral blood flow, increase in intracranial pressure and central adrenergic hyperactivity and how they can well explain the key symptoms of cognitive impairment, brain fog, headache, hypersensitivity, sleep disturbances and dysautonomia.

Source: Wirth KJ, Scheibenbogen C, Paul F. An attempt to explain the neurological symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. J Transl Med. 2021 Nov 22;19(1):471. doi: 10.1186/s12967-021-03143-3. PMID: 34809664. https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-021-03143-3  (Full text)

Moxibustion for Chronic Fatigue Syndrome: A Systematic Review and Meta-Analysis

Abstract:

Objective: This review aimed at systematically evaluating the efficacy and safety of moxibustion for chronic fatigue syndrome (CFS).

Methods: Relevant trials were searched in seven digital databases up to January 2021. After literature screening, data extraction, and literature quality evaluation, the included studies were meta-analyzed using RevMan 5.4 software. The evidence level was assessed using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE).

Results: Fifteen studies involving 1030 CFS participants were included. Meta-analyses showed a favorable effect of moxibustion on the total effective rate compared with acupuncture (OR = 4.58, 95%CI = [2.85, 7.35], P < 0.00001) and drugs (OR = 6.36, 95%CI = [3.48, 11.59], P < 0.00001). Moxibustion also appeared to significantly reduce fatigue severity measured by fatigue scale-14 (FS-14) (WMD = -2.20, 95% CI = [-3.16, -1.24], P < 0.00001) and fatigue assessment instrument (FAI) (WMD = -16.36, 95% CI = [-26.58, -6.14], P=0.002) compared with the control group. In addition, among the 15 included studies, only two studies reported adverse events related to moxibustion, and the symptoms were relatively mild. The quality of evidence based on the 15 included trials was assessed as moderate to very low.

Conclusions: Based on limited evidence, moxibustion might be an effective and safe complementary therapy for CFS, which can be recommended to manage CFS. Because of the limited level of evidence in this review, further high-quality trials are still needed to confirm these findings.

Source: You J, Ye J, Li H, Ye W, Hong E. Moxibustion for Chronic Fatigue Syndrome: A Systematic Review and Meta-Analysis. Evid Based Complement Alternat Med. 2021 Nov 11;2021:6418217. doi: 10.1155/2021/6418217. PMID: 34804182; PMCID: PMC8601810. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8601810/ (Full text)

Tryptophan Metabolites, Cytokines, and Fatty Acid Binding Protein 2 in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Abstract:

Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) differ for triggers, mode of start, associated symptoms, evolution, and biochemical traits. Therefore, serious attempts are underway to partition them into subgroups useful for a personalized medicine approach to the disease. Here, we investigated clinical and biochemical traits in 40 ME/CFS patients and 40 sex- and age-matched healthy controls. Particularly, we analyzed serum levels of some cytokines, Fatty Acid Binding Protein 2 (FAPB-2), tryptophan, and some of its metabolites via serotonin and kynurenine.
ME/CFS patients were heterogeneous for genetic background, trigger, start mode, symptoms, and evolution. ME/CFS patients had higher levels of IL-17A (p = 0.018), FABP-2 (p = 0.002), and 3-hydroxykynurenine (p = 0.037) and lower levels of kynurenine (p = 0.012) and serotonin (p = 0.045) than controls. Changes in kynurenine and 3-hydroxykynurenine were associated with increased kynurenic acid/kynurenine and 3-hydroxykynurenine/kynurenine ratios, indirect measures of kynurenine aminotransferases and kynurenine 3-monooxygenase enzymatic activities, respectively. No correlation was found among cytokines, FABP-2, and tryptophan metabolites, suggesting that inflammation, anomalies of the intestinal barrier, and changes of tryptophan metabolism may be independently associated with the pathogenesis of the disease.
Interestingly, patients with the start of the disease after infection showed lower levels of kynurenine (p = 0.034) than those not starting after an infection. Changes in tryptophan metabolites and increased IL-17A levels in ME/CFS could both be compatible with anomalies in the sphere of energy metabolism. Overall, clinical traits together with serum biomarkers related to inflammation, intestine function, and tryptophan metabolism deserve to be further considered for the development of personalized medicine strategies for ME/CFS.
Source: Manuela Simonato, Stefano Dall’Acqua, Caterina Zilli, Stefania Sut, Romano Tenconi, Nicoletta Gallo, Paolo Sfriso, Leonardo Sartori, Francesco Cavallin, Ugo Fiocco, Paola Cogo, Paolo Agostinis, Anna Aldovini, Daniela Bruttomesso, Renzo Marcolongo, Stefano Comai, and Aldo Baritussio. Tryptophan Metabolites, Cytokines, and Fatty Acid Binding Protein 2 in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Biomedicines 2021, 9(11), 1724; https://doi.org/10.3390/biomedicines9111724 (registering DOI) https://www.mdpi.com/2227-9059/9/11/1724/htm (Full text)

Factors related to educational adaptations and social life at school experienced by young people with CFS/ME: a qualitative study

Abstract:

Objectives: To explore factors perceived as positive or negative among young people with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) in relation to school and everyday life.

Design: A qualitative study with semistructured individual interviews performed at the local hospital or at the informants’ homes between September 2017 and January 2018, with an additional telephone interview to collect data on experiences from the COVID-19 pandemic, conducted in September 2020. Data were analysed using a grounded theory approach.

Setting: The informants were recruited from two university hospitals that offer interdisciplinary assessments of young people with CFS/ME from various parts of Norway.

Participants: Five males and 13 females aged 13-21 years with CFS/ME diagnosed 3-56 months prior to the interviews participated.

Results: The informants were concerned about a lack of educational adaptations and missed social life at school. Educational and social adaptations could improve schooling and health among young people with CFS/ME. Negative experiences were related to a lack of knowledge about CFS/ME among school personnel and young people’s difficulties to limit activities. Online teaching as experienced during the COVID-19 pandemic was described as positive both for education and social life.

Conclusions: Young people with CFS/ME can benefit from better educational adaptations and increased social interaction with peers. From the participants’ view, factors that limit learning and socialisation include a lack of knowledge about CFS/ME among teachers and school personnel, expectations from teachers of doing more than they could manage at school, feeling alone coping with the disease and not recognising their own limitations regarding what they are able to do. Suggested factors perceived to enhance learning and socialisation were a better understanding of the disease among school personnel and peers, suitable educational adaptations and being able to socialise with peers.

Source: Similä WA, Nøst TH, Helland IB, Rø TB. Factors related to educational adaptations and social life at school experienced by young people with CFS/ME: a qualitative study. BMJ Open. 2021 Nov 18;11(11):e051094. doi: 10.1136/bmjopen-2021-051094. PMID: 34794992. https://pubmed.ncbi.nlm.nih.gov/34794992/

Post-COVID syndrome: the aftershock of SARS-CoV-2

Introduction:

Significant time has passed since the coronavirus disease of 2019 (COVID-19) pandemic outbreak, which led to severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection in hundreds of millions of individuals all around the globe. Accumulation evidence along the pandemic raised an association between the SARS-CoV-2 and autoimmunity (1). SARS-CoV-2 infected patients have a high presence of various autoantibodies (1). Moreover, numerous cases of new-onset of autoimmune-related disorders had been documented following the infection, including both organ-specific and systemic autoimmune diseases (1).

Recent studies focused on analyzing recovered COVID-19 patients demonstrate a broad spectrum of persistent and systemic symptoms, which had got the novel terms of “post-COVID syndrome”, “long COVID” and “chronic COVID-19” (2). This new disorder had led to the understanding that the absence of SARS-CoV-2 following COVID-19 does not necessarily mean full recovery (2).

Studies conducted follow-ups on COVID-19 patients indicate that 50-80% of symptomatic COVID-19 patients who recovered report non-specific symptoms, most commonly fatigue, headache, dyspnea, anosmia, and memory complaint (3–5). An Italian study that examined patients after a mean of 60 days from the first COVID-19 symptom on-set had found only 12.6% of the patients completely recovered; 55% had three or more symptoms, and worsened quality of life was observed among 44% of patients (3). Intriguingly, a systematic review and meta-analysis reported more than 50 possible long-term effects of the SAR-CoV-2 infection (6). The chronic phase of COVID-19 is also presented in objective findings; for example, a study conducted in Germany had found that 78% of recently recovered symptomatic COVID-19 patients had at least one chronic symptom; the most common abnormality was myocardial inflammation (60%) (4).

In this issue of the journal, Bertin D et al. documented a case of post-COVID syndrome with a one-year follow-up. This case describes persistent anti-cardiolipin IgG autoantibodies and eosinopenia with ongoing neurologic symptoms, demonstrating the long-term disease course of COVID-19 in many patients. Anti-cardiolipin autoantibodies and eosinopenia were defined as independent factors associated with COVID-19 severity, indicating their active involvement in the progression of the disease (7,8). Additional studies that included follow-up on recovered COVID-19 patients describe similar findings: patients report respiratory, neurologic, and non-specific symptoms, accompanied by the presents of autoantibodies (6). Interestingly, in a one-year prospective cohort study, neurocognitive symptoms frequency were found significantly higher in patients with ANA titer of ≥1:160 in comparison to <1:160 at 12 months post–COVID-19 symptom onset (9). It should be emphasized that the development of autoantibodies, which appears to be common following symptomatic SARS-CoV-2 infection, could act as the preclinical stage of many autoimmune diseases. Thus, the long-term autoimmune implications of SARS-CoV-2 could be severe.

Involvement of the autonomic nervous system dysfunction in post-COVID syndrome

Many viruses are well known to contribute to autoimmunity in genetically pre dispositioned individuals, such as those with human leukocyte antigen B27 (10). SARS-CoV-2 had been associated with numerous autoantibodies (1); some are believed to be the basis of the severe forms of COVID-19 (11). Furthermore, these autoantibodies, along with others, could lead to the multi-organ involvement of post-COVID syndrome, which manifests as broad and unspecific symptoms (6). Autoantibodies against the autonomic nervous system compounds are believed to be an incremental part of the post-COVID syndrome etiology. A study that included post-COVID syndrome patients had unidentified in all the subjects between 2 and 7 different functionally active autoantibodies that acted as receptor agonists, such as β2-adrenoceptor, α1-adrenoceptor, and angiotensin II receptor type 1 receptor (12). Functionally active autoantibodies such as those were present in several neurological and cardiac disorders, which might clarify the onset of neurological and cardiovascular symptoms of the post-COVID syndrome (12).

Post-COVID patients commonly have a clinical presentation similar to the encephalomyelitis/chronic fatigue syndrome (ME/CFS): severe fatigue, sleep disorders, cognition impairments, and different manifestations of autonomic dysfunction exacerbated in physical exercise (6,13–15). ME/CFS has an autoimmune etiology, which can be demonstrated by high titers of autoantibodies against autonomic receptors, such as beta-adrenergic and muscarinic receptors (16,17). These autoantibodies, similar to those found in patients with post-COVID symptoms, lead to unspecific symptoms due to autonomic nervous system dysregulation. In addition to ME/CFS, many features of the post-COVID syndrome are shared with fibromyalgia patients. It had been shown that 189/616 (30.7%) of COVID-19 recovered patients satisfied the American College of Rheumatology criteria for fibromyalgia, 43.4% of which were men (18).

Therapeutic options and vaccination

ME/CFS and fibromyalgia have solid evidence of dysregulated immune involvement (16,17,19). Moreover, current studies suggest that immunosuppression, such as monoclonal anti-CD20 antibody and cyclophosphamide, may benefit patients suffering from ME/CFS (20,21). Such immunosuppressive therapeutic options can assist in the depletion of B cells, thus reducing the functionally active autoantibodies linked to autonomic dysfunction. Beneficial effects had also been demonstrated by the use of anti-ß2 adrenergic receptor-binding immunoadsorption (22). It should be emphasized that such treatment can diminish other pathogenic antibodies that the medical community had not yet recognized. Due to the possible involvement of autoantibodies against the autonomic nervous system in the post-COVID syndrome, similar immunosuppressive options in these patients may be effective, thereby should be investigated.

Most individuals infected by SARS-CoV-2 are asymptomatic or experience mild symptoms (23,24). While the frequency of post-COVID syndrome in such individuals is still uncertain, it seems to be much lower than in symptomatic patients (9). Thus, avoiding COVID-19 with SARS-CoV-2 vaccination could prominently assist in preventing long-term symptoms of COVID-19, lower the prevalence of post-COVID syndrome and help overcome the pandemic. Nonetheless, even with the ongoing heist mass vaccination programs, the COVID-19 pandemic will leave its mark.

Conclusion

Due to the accumulating evidence of persistent post-infectious symptoms reported by numerous recovered patients, the focus of the medical and research communities might need to start shifting focus from the acute phase of COVID-19 to the chronic manifestations of the SARS-CoV-2 infection, referred to as by “post-COVID syndrome”. Post-COVID syndrome presents as non-specific symptoms, most commonly fatigue, headache, dyspnea, anosmia, and memory complaint, which is suspiciously similar to the infection-induced myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and fibromyalgia (15,18). As current studies suggest an involvement of immune-related dysfunction in the development of post-COVID syndrome, immunosuppressive therapeutic options could be beneficial in parallel to heist SARS-CoV-2 vaccination of the population (15,20,21).

References

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Article Info

Publication History

Accepted: November 9, 2021
Received: November 9, 2021

Publication stage

In Press Journal Pre-Proof

Identification

DOI: https://doi.org/10.1016/j.ijid.2021.11.020

Copyright

© 2021 The Author(s). Published by Elsevier Ltd on behalf of International Society for Infectious Diseases.

The Emerging Role of Gut Microbiota in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Current Evidence and Potential Therapeutic Applications

Abstract:

The well-known symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) are chronic pain, cognitive dysfunction, post-exertional malaise and severe fatigue. Another class of symptoms commonly reported in the context of ME/CFS are gastrointestinal (GI) problems. These may occur due to comorbidities such as Crohn’s disease or irritable bowel syndrome (IBS), or as a symptom of ME/CFS itself due to an interruption of the complex interplay between the gut microbiota (GM) and the host GI tract. An altered composition and overall decrease in diversity of GM has been observed in ME/CFS cases compared to controls. In this review, we reflect on genetics, infections, and other influences that may factor into the alterations seen in the GM of ME/CFS individuals, we discuss consequences arising from these changes, and we contemplate the therapeutic potential of treating the gut to alleviate ME/CFS symptoms holistically.

Source: Varesi A, Deumer US, Ananth S, Ricevuti G. The Emerging Role of Gut Microbiota in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Current Evidence and Potential Therapeutic Applications. J Clin Med. 2021 Oct 29;10(21):5077. doi: 10.3390/jcm10215077. PMID: 34768601. https://pubmed.ncbi.nlm.nih.gov/34768601/

mapMECFS: a portal to enhance data discovery across biological disciplines and collaborative sites

Abstract:

Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disease which involves multiple body systems (e.g., immune, nervous, digestive, circulatory) and research domains (e.g., immunology, metabolomics, the gut microbiome, genomics, neurology). Despite several decades of research, there are no established ME/CFS biomarkers available to diagnose and treat ME/CFS. Sharing data and integrating findings across these domains is essential to advance understanding of this complex disease by revealing diagnostic biomarkers and facilitating discovery of novel effective therapies.

Methods: The National Institutes of Health funded the development of a data sharing portal to support collaborative efforts among an initial group of three funded research centers. This was subsequently expanded to include the global ME/CFS research community. Using the open-source comprehensive knowledge archive network (CKAN) framework as the base, the ME/CFS Data Management and Coordinating Center developed an online portal with metadata collection, smart search capabilities, and domain-agnostic data integration to support data findability and reusability while reducing the barriers to sustainable data sharing.

Results: We designed the mapMECFS data portal to facilitate data sharing and integration by allowing ME/CFS researchers to browse, share, compare, and download molecular datasets from within one data repository. At the time of publication, mapMECFS contains data curated from public data repositories, peer-reviewed publications, and current ME/CFS Research Network members.

Conclusions: mapMECFS is a disease-specific data portal to improve data sharing and collaboration among ME/CFS researchers around the world. mapMECFS is accessible to the broader research community with registration. Further development is ongoing to include novel systems biology and data integration methods.

Source: Mathur R, Carnes MU, Harding A, Moore A, Thomas I, Giarrocco A, Long M, Underwood M, Townsend C, Ruiz-Esparza R, Barnette Q, Brown LM, Schu M. mapMECFS: a portal to enhance data discovery across biological disciplines and collaborative sites. J Transl Med. 2021 Nov 8;19(1):461. doi: 10.1186/s12967-021-03127-3. PMID: 34749736. https://pubmed.ncbi.nlm.nih.gov/34749736/