Off label use of Aripiprazole shows promise as a treatment for ME/CFS

Posted on 02/09/2021 by wames

Off label use of Aripiprazole shows promise as a treatment for Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS): a retrospective study of 101 patients treated with a low dose of Aripiprazole, by LD Crosby, S Kalanidhi, A Bonilla, A Subramanian, JS Ballon & H Bonilla in Journal of Translational Medicine vol 19, Article number: 50 (2021)

 

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a chronic, debilitating illness of unknown etiology. An ME/CFS diagnosis is based solely on symptoms with case definitions made by expert consensus, including the Fukuda (1994), Canadian Consensus Criteria (CCC, 2003), International Consensus Criteria (ICC, 2011), and the Institute of Medicine (IOM, 2015) case criteria. According to the most recent IOM case definition, the core symptoms of ME/CFS include debilitating fatigue, unrefreshing sleep, post-exertional malaise, and either cognitive dysfunction or orthostatic intolerance [1].

Although the cause of the illness is unknown, a growing body of evidence suggests that ME/CFS involves inflammation of the brain. Up to 85% of patients with ME/CFS report symptoms of cognitive impairment also referred to as “brain fog,” which includes difficulty with memory, attention, and information processing. Additional evidence includes changes in inflammatory cytokines in both plasma and cerebrospinal fluid correlated with the severity of symptoms [2]. Other studies using positron emission tomography (PET) show evidence of activated microglia or astrocytes in various regions of the brain in patients with ME/CFS [3].

Dopamine D2 receptor agonists have been shown to mediate neuroinflammation, microglial activation, and cell death in animal models and humans [4,5,6]. This suggests that dopamine-modulating drugs like aripiprazole may lead to clinical improvement in fatigue and cognitive symptoms in ME/CFS. Given the lack of approved drugs for treating this condition, we were interested in exploring the potential benefit of low doses of aripiprazole in our Stanford University ME/CFS clinical practice.

…In summary, the number of positive responders in a group of 101 patients taking aripiprazole was significantly greater than the number of patients who did not respond or had negative experiences. Also, the magnitude of perceived improvement was significant. Some patients failed to observe any benefit, and a small subset of patients experienced side effects that required the medication to be discontinued. Overall, these results suggest that aripiprazole may effectively reduce symptoms of ME/CFS and warrants further investigation in a randomized clinical trial. Exploring the mechanism of action for aripiprazole in neuroinflammatory conditions may also provide new insight into the pathogenesis of ME/CFS.

 

Health rising blog: Abilify shows promise in retrospective Chronic Fatigue Syndrome (ME/CFS) study, by Cort Johnson

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Lived experiences in daily life with ME (Denmark)

Posted on 02/09/2021 by wames

Lived experiences in daily life with myalgic encephalomyelitis, by Reeti KK Sandhu, Maj Sundby, Sidsel Ørneborg, Svetlana Solgaard Nielsen, Jeanette Reffstrup Christensen, Anette Enemark Larsen in British Journal of Occupational Therapy, November 2020 [doi.org/10.1177/0308022620966254]

 

Research abstract:

Introduction
Myalgic encephalomyelitis is a complex systemic condition, causing severe symptoms that limit the quality of life of the people living with it. This study examined changes in life, coping strategies, and the ability to obtain a successful occupational adaptation in people with myalgic encephalomyelitis in Denmark, viewed from the perspective of the model of human occupation.

Method
In-depth qualitative interviews with seven persons with myalgic encephalomyelitis aged 31–61 years were analysed with qualitative content analysis.

Results
The participants experienced severe changes in their lives leading to impaired occupational competences which affected their occupational identity and made them lonely. Pacing and environmental changes were the preferred coping strategies in their attempt to adapt to the new circumstances.

Conclusion
The participants experienced major changes in everyday life with the onset of myalgic encephalomyelitis. Pacing and environmental changes were not sufficient strategies to secure a successful occupational adaptation. Thus, people living with myalgic encephalomyelitis need assistance to enable a successful occupational adaptation and preserve hope. Access to occupational therapy within the Danish programme for people living with myalgic encephalomyelitis may support more effective occupational adaptation in the population.

Read full paper

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ME/CFS: Where will the drugs come from?

Posted on 02/08/2021 by wames

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Where will the drugs come from?, by Peter L Toogood, Daniel J Clau, Sameer Phadke, DavidHoffman in Pharmacological Research [doi.org/10.1016/j.phrs.2021.105465] 30 January 2021

 

Review abstract:

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic debilitating disease characterized by severe and disabling fatigue that fails to improve with rest; it is commonly accompanied by multifocal pain, as well as sleep disruption, and cognitive dysfunction. Even mild exertion can exacerbate symptoms.

The prevalence of ME/CFS in the U.S. is estimated to be 0.5-1.5% and is higher among females. Viral infection is an established trigger for the onset of ME/CFS symptoms, raising the possibility of an increase in ME/CFS prevalence resulting from the ongoing COVID-19 pandemic.

Current treatments are largely palliative and limited to alleviating symptoms and addressing the psychological sequelae associated with long-term disability. While ME/CFS is characterized by broad heterogeneity, common features include immune dysregulation and mitochondrial dysfunction. However, the underlying mechanistic basis of the disease remains poorly understood.

Herein, we review the current understanding, diagnosis and treatment of ME/CFS and summarize past clinical studies aimed at identifying effective therapies. We describe the current status of mechanistic studies, including the identification of multiple targets for potential pharmacological intervention, and ongoing efforts towards the discovery of new medicines for ME/CFS treatment.

6. Conclusion

While ME/CFS remains a poorly understood disease, there is a growing understanding of its mechanistic roots. New research directions are emerging with the potential to generate better diagnostic tools, biomarkers and pharmacological treatments. Approaches to therapy under investigation are directed at specific molecular or cellular irregularities associated with ME/CFS such as autoantibodies, immune dysregulation (e.g. NK cell function) or mitochondrial dysfunction. Recent discoveries suggest the possibility of target-based drug discovery programs directed against specific proteins implicated in either the initiation or propagation of ME/CFS symptoms (e.g. PDHK).

These developments are occurring at the same time as advances in the diagnosis and detection of ME/CFS. Investments in patient profiling and tool generation are starting to yield fruit, and we anticipate the availability of reliable clinical diagnostic tools in the near future.

Despite its significant human cost and economic impact, ME/CFS research has yet to attract major financial support.

Recognizing this deficiency, the U.S. National Institutes of Health (NIH) have established a Trans-NIH ME/CFS working group to coordinate a multi-institute effort to learn about and treat this disease. Nonetheless with an overall budget of ∼$42Bn, NIH’s spend on ME/CFS research in 2019 amounted to only ∼$15 M compared to $111 M on multiple sclerosis and $94 M on rheumatoid arthritis, both conditions for which there are multiple drugs already on the market.

Various private foundations and patient groups have been established to help support research and to advocate for increased government support, and these continue to play an essential role in increasing awareness and funding for the ME/CFS field (see for example Solve M.E. and ME Action).

However, at the current time, interest among pharmaceutical companies and biotech/venture investors appears to be almost non-existent. It is to be hoped that increased awareness of the basis and impact of ME/CFS will stimulate the investment in research that will be necessary for development of effective new therapies.

ME Association: What drugs are being developed for the treatment of ME/CFS?, by Dr Charles Shepherd, 2 Feb 2021

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Modulatory effects of cognitive exertion on regional functional connectivity of the salience network in women with ME/CFS

Posted on 02/05/2021 by wames

Modulatory effects of cognitive exertion on regional functional connectivity of the salience network in women with ME/CFS: A pilot study, by Riccardo Manca, Katija Khan, Micaela Mitolo, Matteo De Marco, Lynsey Grieveson, Rosemary Varley, Iain D Wilkinson, Annalena Venneri in Journal of the Neurological Sciences, January 2021 [doi.org/10.1016/j.jns.2021.117326]

 

Highlights

  • Cognitive effort can induce PEM and worsening of ME/CFS symptoms.
  • PEM is associated with changes in functional connectivity of the salience network.
  • Increased right insular FC with frontal areas is associated with symptom worsening.

Research abstract:

Background

A common symptom of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is post-exertional malaise (PEM). Various brain abnormalities have been observed in patients with ME/CFS, especially in insular and limbic system, but their link with ME/CFS symptoms is still unclear. This pilot study aimed at investigating the association between PEM in ME/CFS and changes in functional connectivity (FC) of two main networks: the salience network (SN) and the default-mode network (DMN).

Methods

A total of 16 women, 6 with and 10 without ME/CFS, underwent clinical and MRI assessment before and after cognitive exertion. Resting-state FC maps of 7 seeds (3 for the SN and 4 for the DMN) and clinical measures of fatigue, pain and cognition were analysed with repeated-measure models. FC-symptom change associations were also investigated

Results

Exertion induced increases in fatigue and pain in patients with ME/CFS, compared to the control group, while no changes were found in cognitive performance. At baseline, patients showed altered FC between some DMN seeds and frontal areas and stronger FC between all SN seeds and left temporal areas and the medulla. Significantly higher FC increases in patients than in controls were found only between the right insular seed and frontal and subcortical areas; these increases correlated with worsening of symptoms.

Conclusions

Cognitive exertion can induce worsening of ME/CFS-related symptoms.

These changes were here associated with strengthening of FC of the right insula with areas involved in reward processing and cognitive control.

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Numeric rating scales show prolonged post-exertional symptoms after orthostatic testing of adults with ME/CFS

Posted on 02/03/2021 by wames

Numeric rating scales show prolonged post-exertional symptoms after orthostatic testing of adults with Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome, by C (Linda) M C van Campen, Peter C Rowe, Freek WA Verheugt, Frans C Visser in Frontiers in Medicine Vol 7, p 602894, January 27 2021 [doi.org/10.3389/fmed.2020.602894]

 

Research abstract:

Introduction:

Muscle pain, fatigue, and concentration problems are common among individuals with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). These symptoms are commonly increased as part of the phenomenon of postexertional malaise (PEM). An increase in the severity of these symptoms is described following physical or mental exercise in ME/CFS patients.

Another important symptom of ME/CFS is orthostatic intolerance, which can be detected by head-up tilt testing (HUT). The effect of HUT on PEM has not been studied extensively. For this purpose, we assessed numeric rating scales (NRS) for pain, fatigue, and concentration pre- and post-HUT. As pain is a core symptom in fibromyalgia (FM), we subgrouped ME/CFS patients by the presence or absence of FM.

Methods and Results

In eligible ME/CFS patients who underwent HUT, NRS of pain, fatigue, and concentration were obtained pre-HUT, immediately after HUT, at 24 and 48 h, and at 7 days post test. We studied 174 ME/CFS patients with FM, 104 without FM, and 30 healthy controls (HC). Values for all symptoms were unchanged for HC pre- and post-HUT. Compared with pre-HUT, the three NRS post-HUT were significantly elevated in both ME/CFS patient groups even after 7 days. NRS pain was significantly higher at all time points measured in the ME/CFS patients with FM compared with those without FM.

In ME/CFS patients, the maximum fatigue and concentration scores occurred directly post-HUT, whereas pain perception reached the maximum 24 h post-HUT.

Conclusion

NRS scores of pain, fatigue, and concentration were significantly increased even at 7 days post-HUT compared with pre-HUT in ME/CFS patients with and without FM, suggesting that orthostatic stress is an important determinant of PEM.

 

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ME/CFS: the human herpesviruses are back!

Posted on 02/03/2021 by wames

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: the human herpesviruses are back! by  Maria Eugenia Ariza in Biomolecules 2021, 11(2), 185; 29 January 2021 [doi.org/10.3390/biom11020185]  (This article belongs to the Special Issue Epstein-Barr Virus Disease Mechanisms and Stress Responses)

 

Review abstract:

Figure 1. Model depicting how the combined effect of environmental insults, and stress in genetically susceptible individuals can trigger neurological, immune and metabolic dysfunction, which together could contribute to the symptomology observed in ME/CFS

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) or Systemic Exertion Intolerance Disease (SEID) is a chronic multisystem illness of unconfirmed etiology. There are currently no biomarkers and/or signatures available to assist in the diagnosis of the syndrome and while numerous mechanisms have been hypothesized to explain the pathology of ME/CFS, the triggers and/or drivers remain unknown.

Initial studies suggested a potential role of the human herpesviruses especially Epstein-Barr virus (EBV) in the disease process but inconsistent and conflicting data led to the erroneous suggestion that these viruses had no role in the syndrome.

New studies using more advanced approaches have now demonstrated that specific proteins encoded by EBV could contribute to the immune and neurological abnormalities exhibited by a subgroup of patients with ME/CFS. Elucidating the role of these herpesvirus proteins in ME/CFS may lead to the identification of specific biomarkers and the development of novel therapeutics.

5. Conclusions and Future Directions

It is clear that the lack of a universally accepted clinical criteria has led to multiple discrepancies, problems and confusion as to how to accurately diagnose and stratify patients with ME/CFS. This has severely hampered the pursue of studies to clearly define the environmental and genetic factors that act as triggers or the downstream mechanisms responsible for the development/progression of ME/CFS. Furthermore, numerous studies using small size patient cohorts, which lack the statistical power to achieve reproducible and rigorous results, have further complicated the task of identifying biomarkers/signatures that would be useful for diagnosing patients.

The role of some herpesviruses in the development and evolution of ME/CFS in a subset of patients has also been hampered because of the use of classical serological approaches focused primarily on viral proteins expressed during latency or late in the replicative cycle of these viruses or viral load as indicators for the involvement of herpesviruses in the pathobiology of ME/CFS. Recent studies using more advanced serological approaches as well as mechanistic studies have demonstrated the possible role of the EBV BRRF1 and BLLF3 gene products in ME/CFS pathophysiology.

Future directions should focus on exploring the use of these gene products for the development of novel therapeutics and/or as biomarkers with diagnostic application or disease progression. Additionally, additional studies need to be performed in light of the new evidence showing high level of abortive lytic replication of these viruses to determine whether other early herpesvirus proteins could contribute to the disease process.

Finally, since there is evidence suggesting simultaneous reactivation of multiple herpesviruses in a large percentage of ME/CFS patients, studies should examine whether or not there is cooperative effects between these viruses as well as other viruses within the virome that could contribute to human disease.

 

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Exercise modifies glutamate & other metabolic biomarkers in cerebrospinal fluid from Gulf War Illness & ME/CFS

Posted on 02/01/2021 by wames

Exercise modifies glutamate and other metabolic biomarkers in cerebrospinal fluid from Gulf War Illness and Myalgic encephalomyelitis / Chronic Fatigue Syndrome, by James N Baraniuk, Grant Kern, Vaishnavi Narayan, Amrita Cheema in PLoS ONE 16(1): e0244116,  January 13, 2021 [doi.org/10.1371/journal.pone.0244116]

 

 

Research abstract:

Myalgic encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS) and Gulf War Illness (GWI) share many symptoms of fatigue, pain, and cognitive dysfunction that are not relieved by rest. Patterns of serum metabolites in ME/CFS and GWI are different from control groups and suggest potential dysfunction of energy and lipid metabolism. The metabolomics of cerebrospinal fluid was contrasted between ME/CFS, GWI and sedentary controls in 2 sets of subjects who had lumbar punctures after either (a) rest or (b) submaximal exercise stress tests.

Postexercise GWI and control subjects were subdivided according to acquired transient postexertional postural tachycardia. Banked cerebrospinal fluid specimens were assayed using Biocrates AbsoluteIDQ® p180 kits for quantitative targeted metabolomics studies of amino acids, amines, acylcarnitines, sphingolipids, lysophospholipids, alkyl and ether phosphocholines. Glutamate was significantly higher in the subgroup of postexercise GWI subjects who did not develop postural tachycardia after exercise compared to nonexercise and other postexercise groups. The only difference between nonexercise groups was higher lysoPC a C28:0 in GWI than ME/CFS suggesting this biochemical or phospholipase activities may have potential as a biomarker to distinguish between the 2 diseases.

Exercise effects were suggested by elevation of short chain acylcarnitine C5-OH (C3-DC-M) in postexercise controls compared to nonexercise ME/CFS. Limitations include small subgroup sample sizes and absence of postexercise ME/CFS specimens. Mechanisms of glutamate neuroexcitotoxicity may contribute to neuropathology and “neuroinflammation” in the GWI subset who did not develop postural tachycardia after exercise. Dysfunctional lipid metabolism may distinguish the predominantly female ME/CFS group from predominantly male GWI subjects.

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Beyond bones: the relevance of variants of connective tissue (hypermobility) to FM, ME/CFS & controversies surrounding diagnostic classification

Posted on 01/29/2021 by wames

Beyond bones: The relevance of variants of connective tissue (hypermobility) to fibromyalgia, ME/CFS and controversies surrounding diagnostic classification: an observational study, by Jessica A Eccles, Beth Thompson, Kristy Themelis, Marisa L Amato, Robyn Stocks, Amy Pound, Anna-Marie Jones, Zdenka Cipinova, Lorraine Shah-Goodwin, Jean Timeyin, Charlotte R Thompson, Thomas Batty, Neil A Harrison, Hugo D Critchley and Kevin A Davies in Clin Med, January 2021 [doi.org/10.7861/clinmed.2020-0743]

 

Research abstract:

Background 

Hypermobile fingers by Matthew Thomas

Fibromyalgia and myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) are poorly understood conditions with overlapping symptoms, fuelling debate as to whether they are manifestations of the same spectrum or separate entities. Both are associated with hypermobility, but this remains significantly undiagnosed, despite impact on quality of life.

Objective 

We planned to understand the relevance of hypermobility to symptoms in fibromyalgia and ME/CFS.

Method 

Sixty-three patient participants presented with a confirmed diagnosis of fibromyalgia and/or ME/CFS; 24 participants were healthy controls. Patients were assessed for symptomatic hypermobility.

Results 

Evaluations showed exceptional overlap in patients between fibromyalgia and ME/CFS, plus 81% met Brighton criteria for hypermobility syndrome (odds ratio 7.08) and 18% met 2017 hypermobile Ehlers–Danlos syndrome (hEDS) criteria. Hypermobility scores significantly predicted symptom levels.

Conclusion

Symptomatic hypermobility is particularly relevant to fibromyalgia and ME/CFS, and our findings highlight high rates of mis-/underdiagnosis. These poorly understood conditions have a considerable impact on quality of life and our observations have implications for diagnosis and treatment targets.

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Why we need a study like DecodeME

Posted on 01/27/2021 by wames

Why we need a study like DecodeME – scientific paper published, by the ME/CFS Biomedical Partnership, 26 Jan 2021

Today, we know almost nothing for sure about what causes ME/CFS. We do know that the illness can be triggered by certain infectious diseases, such as glandular fever. But we don’t know why most people recover from those infections but a minority instead develop ME/CFS.

There are many competing hypotheses about what causes the illness, all with some evidence to support them. But nothing has yet been nailed down.

A scientific paper reviewed the available evidence about ME/CFS genetics and explained how big new DNA studies can help find causes of the disease.

The paper was written by Joshua Dibble, the PhD student of DecodeME’s lead scientist Professor Chris Ponting. He was funded by Action for ME and Scotland’s Chief Scientist Office. The other authors were Chris himself and Simon McGrath, who has ME/CFS and is also on the DecodeME team. In this blog post, we summarise our review.

Genetic studies offer a way forward because if genes are linked to ME/CFS, they must be a cause of the illness and not simply an effect of it. This is because diseases don’t change our DNA. In contrast, for studies looking at other molecules, any differences between patients and controls might simply be a consequence of the illness rather than a cause that drives it.

A very large genetic study can identify causes that have not previously been considered. In Alzheimer’s disease, for example, researchers were initially focusing on nerve cells in the brain. But big genetic studies drew researchers’ attention to other brain cells called glia that support the normal functioning of nerve cells.

In rheumatoid arthritis, genetic studies have helped to identify what goes wrong at the molecular level to set off the disease.

Comparing findings between different autoimmune diseases found that some of them shared a disease mechanism. As a result, drugs already used successfully in some autoimmune diseases are now used to treat patients with other autoimmune diseases that share a common mechanism.

Progress in all these diseases came from a type of genetic research called genome-wide association studies (GWAS).

GWAS shed light on many diseases that are caused not by a single gene but by many. In simple genetic diseases, such as cystic fibrosis, the illness is caused by a fault in a single gene. However, the role of genetics in most diseases is weaker, and usually the result of many different genetic differences, each having a small effect. Non-genetic factors, such as environmental influences and infections, also play a big role in most illnesses.

To reliably find the small genetic differences that occur in most diseases, we need very large studies: typically with at least 10,000 participants.

Evidence of a role for genetics in ME/CFS

Although usually just one person in a family gets ME/CFS, quite often more than one person is affected. This indicates that an increased risk of becoming ill with ME/CFS can run in families. Several studies have now provided evidence of an inherited, genetic role in ME/CFS, though the studies don’t agree on how big the role is.

ME/CFS genetics studies so far

Several studies of the genetics of ME/CFS have linked the disease to particular genes. However, none of these specific genetic links have yet been independently confirmed. Our paper critically reviews these studies.

The strongest genetic evidence to date

Human leucocyte antigens (HLA) proteins allow the immune system to target cancerous cells and cells infected by viruses and other bugs.

The situation with HLA genes (and proteins) is unusually complex. There are many genes for HLA proteins and often many versions of each gene.

The upshot of this is that we each have a set of HLA genes and while we will share individual HLA gene versions with other people, we are unlikely to have exactly the same set as anyone else.

(HLA genes also determine whether or not an organ transplant will be rejected. For an organ to be accepted, there must be a good match between the organ donor’s set of HLA genes and those of the person receiving the transplant.)

Certain versions of HLA genes increase the risk of autoimmune disease. Recently, two versions of HLA genes were linked to ME/CFS and each roughly doubled the risk of having ME/CFS. The study was large (458 patients, 4,500 controls) and done well, though the finding will need replication.

Other studies

The largest genetic studies to date used data from the UK Biobank of over half a million individuals. Nearly 2,000 of these individuals said they had a CFS diagnosis from a doctor (but it is not clear if they would meet specific ME/CFS criteria).

One analysis of these people with CFS found a link to a protein that transports an amino acid into mitochondria, the mini-power-stations of the cell. There is some evidence to support this finding. However, other slightly different analyses of the same data didn’t confirm this finding.

Our review also examines several other ME/CFS genetic studies. Most of them are rather small and some also appear to have technical shortcomings that we cover in the paper. For our review, we looked to see if the gene versions linked to ME/CFS in these studies were also linked to CFS using data from the UK Biobank. But disappointingly, they did not.

Benefits expected from ME/CFS Genome Wide Association Studies (GWAS)

Our review of available genetic studies and findings provides limited evidence that particular genes play a role in ME/CFS. It also highlights the need for larger and more rigorous studies that give more robust results. ME/CFS GWAS can do that.

GWAS have already helped to improve our understanding of the causes of many diseases and have helped to develop new treatments. GWAS for ME/CFS are long overdue. DecodeME will be the first study of this kind, and a Norwegian group is planning a separate ME/CFS GWAS. Replicated results from such studies would have four important benefits:

1. Finding causes

Positive results would help provide much needed insight into the biological causes of ME/CFS. In combination with other technologies, GWAS can pinpoint variations in DNA that change the activity of genes and as a result alter the risk of ME/CFS.

It is likely that many genes will be involved in increasing the risk of ME/CFS, each in a small way. If the genes turn out to have an activity in common (such as a particular immune function or the functioning of a certain type of brain cell), then that effectively flags up possible cellular or molecular causes of the disease. This would provide strong leads for further research.

2. Learning from other diseases

Researchers could investigate if the genetics of ME/CFS is shared with any other disease, indicating possible shared disease mechanisms. This provides the potential for reusing existing treatments to treat ME/CFS.

3. Subtypes and targeted treatments

GWAS findings could help split ME/CFS into different groups. This could eventually lead to identifying distinct subtypes of ME/CFS, each with a different cause and potentially a different treatment.

4. Respect

Lastly, discovering genetic factors that play a role in causing ME/CFS might improve how the disease is seen by both health professionals and society at large.

Find out more about the DecodeME GWAS and register for updates here on the DecodeME website.

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Risks for developing ME/CFS in college students following infectious mononucleosis

Posted on 01/27/2021 by wames

Risks for developing ME/CFS in college students following infectious mononucleosis: a prospective cohort study, Leonard A Jason, PhD, Joseph Cotler, PhD, Mohammed F Islam, PhD, Madison Sunnquist, PhD, Ben Z Katz, MD in Clinical Infectious Diseases, [doi.org/10.1093/cid/ciaa1886] 25 Dec 2020

 

Research abstract:

Background

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) involves severe fatigue, unrefreshing sleep, and cognitive impairment, leading to functional difficulties; prior studies have not evaluated risk factors with behavioral and immune data collected prior to developing ME/CFS. Up to 5% of university students develop infectious mononucleosis (IM) annually, and 9-12% meet criteria for ME/CFS six months later. We sought to determine predictors of ME/CFS.

Methods
We enrolled college students at the start of the school year (Time 1), identified those who developed IM (Time 2) and followed them for 6 months (Time 3), identifying three groups: those who developed ME/CFS, those who developed severe ME/CFS (meeting >1 set of criteria) and those who were asymptomatic. We conducted 8 behavioral and psychological surveys and analyzed cytokines at three time points.

Results
238 of the 4501 students (5.3%) developed IM; 6 months later, 55 of the 238 (23%) met criteria for ME/CFS and 157 (66%) were asymptomatic. 67 of the 157 asymptomatic students served as controls. Students with severe-ME/CFS were compared to students who were asymptomatic at three time points. The former group was not different from the latter group at Time 1 (prior to developing IM) in stress, coping, anxiety or depression, but were different in several behavioral measures and had significantly lower levels of IL-6 and IL-13. At Time 2 (when they developed IM), the two ME/CFS groups tended to have more autonomic complaints and behavioral symptoms while the severe- ME/CFS group had higher levels of IL-12 and lower levels of IL-13 than the recovered group.

Conclusion
At baseline, those who developed ME/CFS had more physical symptoms and immune irregularities, but not more psychological symptoms, than those who recovered.

DePaul University Newsroom press release: NIH-funded study examines mono, chronic fatigue syndrome in college students 22 January 2021

“Some people who are attacked by a virus stay sick. What we’ve found is that their emotional functioning and psychological states are not statistically different from those who get attacked by the same virus and recover. This becomes important validating information for those people who have this illness,” said Jason.

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