Category: Uncategorized

Remembering the Severely Ill and Appreciating ALL That You Do

Today we remember the severely ill in our community – those who have suffered the ravages of ME/CFS and borne the brunt of the disease with “grace and grit.” Some, like Sophia Mirza, whose birthday falls on August 8th, have not survived. Others must simply bear it year after year. And still others manage to improve, despite the odds. We honor all of the severely ill on this day, and we treasure their lives.

For the severely ill, simply surviving can absorb every ounce of strength they have. It’s difficult enough coping with the disease, but having to weather it alone is devastating. Not only do severely ill patients who have nobody to turn to experience extreme isolation, but the financial hardship can be devastating.

AMMES’ financial crisis fund is meant to assist severely ill patients with bills they cannot pay. On this day, my mind turns to them. I think of a woman who did not own a pair of shoes, and was sitting in the dark, alone, after her power had been cut off when her electricity bill hadn’t been paid. I think of a man who had been evicted on December 31st in the heart of the midwest, and who had nowhere to go on that frigid night. I think of a mother with ME, trying to raise her young son, who also has ME, the two of them attempting to get medical care that their insurance would not cover, because health insurance rarely covers visits to specialists. I think of all of the people who have received help from the financial crisis fund. Their stories ring in my ears.

And I think of the good people who have donated to the fund, because without their contributions, we couldn’t help anyone. I think of people who have included AMMES in their wills, and who I only know through a lawyer’s letter containing news of their demise along with a bequest. I am deeply saddened that I never got to meet these compassionate souls. Their hearts are kind. I think of the steady monthly donations of $3, $5, or $10 from people who surely can’t spare the money, but who still want to reach out and help. Their hearts are beautiful. I think of those in our community who have had the good fortune to remain financially stable, and who share their wealth. Their hearts are generous.

On this day, I remember and honor all who have suffered, and all who have joined hands to help them financially, medically, emotionally, and spiritually. Looking out for one another is what makes us a community. May those bonds remain strong and enduring.

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You can read more about the AMMES financial crisis fund here. We are always looking for more people to assist. Send them to us!

(Image from left to right: Sophia Mirza, Jamison Hill, Karina Hansen, Whitney Dafoe.)

IN MEMORIAM: DR. PAUL CHENEY

I was deeply saddened to learn that Dr. Paul Cheney had passed away on June 10th. Along with Dr. Dan Peterson, Dr. Cheney  practiced in Incline Village, Nevada during the outbreak of what appeared to be a new disease. It had the hallmarks of a viral infection, but their patients were not recovering. That disease would later be called “Chronic Fatigue Syndrome.”

Dr. Cheney’s passing has personal significance for me, because he was the doctor who diagnosed me in 1993. I had heard about him through the leader of our support group in Austin, Texas, who generously allowed me to listen to a tape she had made of her consult with him. I was impressed with Dr. Cheney’s wealth of knowledge, which stemmed not just from his clinical practice, but from his research background in immunology. He not only had an MD, but held a PhD in physics and had been a research associate in the Division of Immunology at the CDC. He had also served as Chief of Medicine at the USAF Hospital in Mt. Home, Idaho for three years before going into private practice.

On the wall of Dr. Cheney’s office was a map with pushpins indicating where his patients came from. There were pushpins in every state and all over the world. Over the course of his practice he saw thousands of patients, whom he tested extensively for immune and metabolic dysfunctions, cardiac function, co-infections (including Lyme disease), indicators of viral reactivation, antigen sensitivity, and autoimmune activity, among others. I don’t think anyone understood ME/CFS as well as he did. Dr. Cheney was our “resident genius.”

Dr. Cheney spent four hours with me during our initial consult. He was not just thorough, he was kind. When he pronounced me “severely ill” there was genuine concern in his eyes. He gave me a piece of advice that I never forgot. “You are in a leaky boat,” he said. “How much can you throw overboard?” Throwing things overboard has saved me on many occasions.

The last time I saw Dr. Cheney was at the IACFS/ME Conference in San Francisco in 2014. I gave him a big hug and introduced myself as a former patient. “I remember you,” he said. It had been 21 years.

RIP Dr. Cheney. The world is poorer without you in it.

More information

Dr Cheney on heart function – from Dr. Myhill’s site: “Dr Paul Cheney has been working with the CFS patients clinically and experimentally for decades and this page is based on many of his ideas. This pulls together many clinical issues which hitherto were inexplicable to me and provides the basis for new therapies for CFS.”

Phoenix Rising Dr. Cheney page – Contains many links to protocols, treatment plans, etc. Some links are dead, but most are still active.

The Cheney Chronicles #2: His Protocol For Chronic Fatigue Syndrome – Cort Johnson’s blog, Health Rising, has two articles detailing one patient’s consult with Dr. Cheney.

ProHealth has a number of articles about Dr. Cheney’s treatment approach.

A Colossus in the ME/CFS Field Passes: Remembering Paul Cheney MD, Ph.D. – Cort Johnson talks about the treatments Dr. Cheney used, as well as his theories about the pathophysiology of ME/CFS.

 

Potential role of microbiome in Chronic Fatigue Syndrome/Myalgic Encephalomyelits

Abstract:

Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is a severe multisystemic disease characterized by immunological abnormalities and dysfunction of energy metabolism. Recent evidences suggest strong correlations between dysbiosis and pathological condition. The present research explored the composition of the intestinal and oral microbiota in CFS/ME patients as compared to healthy controls. The fecal metabolomic profile of a subgroup of CFS/ME patients was also compared with the one of healthy controls. The fecal and salivary bacterial composition in CFS/ME patients was investigated by Illumina sequencing of 16S rRNA gene amplicons. The metabolomic analysis was performed by an UHPLC-MS.

The fecal microbiota of CFS/ME patients showed a reduction of Lachnospiraceae, particularly Anaerostipes, and an increased abundance of genera Bacteroides and Phascolarctobacterium compared to the non-CFS/ME groups. The oral microbiota of CFS/ME patients showed an increase of Rothia dentocariosa. The fecal metabolomic profile of CFS/ME patients revealed high levels of glutamic acid and argininosuccinic acid, together with a decrease of alpha-tocopherol. Our results reveal microbial signatures of dysbiosis in the intestinal microbiota of CFS/ME patients. Further studies are needed to better understand if the microbial composition changes are cause or consequence of the onset of CFS/ME and if they are related to any of the several secondary symptoms.

Source: Lupo, G.F.D., Rocchetti, G., Lucini, L. et al. Potential role of microbiome in Chronic Fatigue Syndrome/Myalgic Encephalomyelits (CFS/ME). Sci Rep 11, 7043 (2021). https://doi.org/10.1038/s41598-021-86425-6 https://www.nature.com/articles/s41598-021-86425-6 (Full text)

The SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2) in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: analysis of high-throughput genetic, epigenetic, and gene expression studies

Abstract:

Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) show specific epigenetic and gene expression signatures of the disease. However, it is unknown whether these signatures in ME/CFS include abnormal levels of the human angiotensin-converting enzyme ACE and ACE2, the latter being the main receptor described for host-cell invasion by SARS-CoV-2. To investigate that, we first reviewed published case-control genome-wide association studies based on single nucleotide polymorphism data, case-control epigenome-wide association studies based on DNA methylation data, and case-control gene expression studies based on microarray data.

From these published studies, we did not find any evidence for a difference between patients with ME/CFS and healthy controls in terms of genetic variation, DNA methylation, and gene expression levels of ACE and ACE2 . In line with this evidence, the analysis of a new data set on the ACE/ACE2 gene expression in peripheral blood mononuclear cells did not find any differences between a female cohort of 37 patients and 34 age-matched healthy controls. Future studies should be conducted to extend this investigation to other potential receptors used by SARS-CoV-2. These studies will help researchers and clinicians to better assess the health risk imposed by this virus when infecting patients with this debilitating disease.

Source: Malato J, Sotzny F, Bauer S, Freitag H, Fonseca A, Grabowska AD, Graça L, Cordeiro C, Nacul L, Lacerda EM, Castro-Marrero J, Scheibenbogen C, Westermeier F, Sepúlveda N. The SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2) in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: analysis of high-throughput genetic, epigenetic, and gene expression studies. medRxiv [Preprint]. 2021 Mar 24:2021.03.23.21254175. doi: 10.1101/2021.03.23.21254175. PMID: 33791744; PMCID: PMC8010776. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8010776/ (Full text)

RIP Dr. Jay A. Goldstein

I was deeply saddened to learn that Dr. Jay Goldstein had passed away on March 4, 2021. Dr. Goldstein was a pioneer among ME/CFS researchers and clinicians. He rose to prominence in the 1990s through his clinical practice, and through the publication of several seminal works, chief among them: Betrayal by the Brain : The Neurologic Basis of Chronic Fatigue Syndrome, Fibromyalgia Syndrome, and Related Neural Network Disorders, Tuning the Brain : Principles and Practice of Neurosomatic Medicine, and Chronic Fatigue Syndromes : The Limbic Hypothesis. In addition to his books, Dr. Goldstein was also one of the editors, along with Dr. Byron Hyde, of The Clinical and Scientific Basis of Myalgic Encephalomyelitis–Chronic Fatigue Syndrome, a collection of papers on clinical practice and research that remains unsurpassed in both depth and scope.

Dr. Goldstein believed that ME/CFS was the result of an insult to the limbic system, located deep within the brain. The limbic system is involved with memory, emotion, and regulation of the autonomic nervous system. This last function is of critical importance to maintaining homeostasis in the body, as the autonomic nervous system regulates appetite, body temperature, blood pressure, blood sugar, sleep, wakefulness, heart rate, digestion – in short, nearly every physiological function necessary for maintaining life.

Dr. Goldstein’s theory, as laid out in his book, Betrayal by the Brain, was that ME/CFS is essentially a communication problem between the limbic system and the rest of the nervous system. His “limbic hypothesis” essentially states that no matter what the underlying cause of ME/CFS, the result is an injury to the limbic system, which subsequently causes widespread neuroimmune dysfunction. He identified ME/CFS as a “neurosomatic” illness, that is, a disorder of central nervous system processing. Dr. Goldstein based his theory on what he knew of the brain, which was substantial, as well as what he had observed of his patients’ reactions to various psychotropic medications. Recent studies have shown that in his approach Dr. Goldstein was  far ahead of his time.

Dr. Goldstein will be sorely missed, not just for his tremendous insights but for his compassion and commitment to his patients. There will never be another like him. RIP Dr. Jay A. Goldstein.

Metabolic Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Not Due to Anti-mitochondrial Antibodies

Abstract:

Metabolic profiling studies have recently indicated dysfunctional mitochondria in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). This includes an impaired function of pyruvate dehydrogenase complex (PDC), possibly driven by serum factor(s), which leads to inadequate adenosine triphosphate generation and excessive lactate accumulation. A reminiscent energy blockade is likely to occur in primary biliary cholangitis (PBC), caused by anti-PDC autoantibodies, as recently proposed. PBC is associated with fatigue and post-exertional malaise, also signifying ME/CFS. We herein have investigated whether ME/CFS patients have autoreactive antibodies that could interfere with mitochondrial function.

We found that only 1 of 161 examined ME/CFS patients was positive for anti-PDC, while all PBC patients (15/15) presented significant IgM, IgG, and IgA anti-PDC reactivity, as previously shown. None of fibromyalgia patients (0/14), multiple sclerosis patients (0/29), and healthy blood donors (0/44) controls showed reactivities. Anti-mitochondrial autoantibodies (inner and outer membrane) were negative in ME/CFS cohort. Anti-cardiolipin antibody levels in patients did not differ significantly from healthy blood donors.

In conclusion, the impaired mitochondrial/metabolic dysfunction, observed in ME/CFS, cannot be explained by presence of circulating autoantibodies against the tested mitochondrial epitopes.

Copyright © 2020 Nilsson, Palmer, Apostolou, Gottfries, Rizwan, Dahle and Rosén.

Source: Nilsson I, Palmer J, Apostolou E, Gottfries CG, Rizwan M, Dahle C, Rosén A. Metabolic Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Not Due to Anti-mitochondrial Antibodies. Front Med (Lausanne). 2020 Mar 31;7:108. doi: 10.3389/fmed.2020.00108. eCollection 2020. https://www.frontiersin.org/articles/10.3389/fmed.2020.00108/full (Full text)

ANNOUNCING AMMES CONNECT!

 

AMMES Connect is the American ME and CFS Society’s brand new service. It is modeled after Craigslist, a popular classified advertisements website with sections devoted to jobs, housing , items wanted, services, community events, rides and free stuff, among others. AMMES Connect is similar in structure, but offers services tailored specifically to the ME/CFS community.

Like Craigslist, AMMES Connect allows people to post when a service or item is OFFERED and when it is WANTED. All services and items must be offered free of charge. People coming to AMMES Connect can search by locale and category. The following categories are included:

Housing – For patients looking for housing, or people offering housing to patients

Events – ME/CFS events, talks, meetings

Volunteers Needed – If you need volunteers for an ME/CFS event or project, place your ad here

Childcare – For people offering free childcare for patients with children, and patients looking for free childcare

Ride Board – For patients looking for rides to doctors’ appointments, shopping and other tasks, and for people offering rides

Free Services – For people volunteering free services such as help filling out disability forms, light housekeeping

Free Stuff – If you are giving something away, post it here

Jobs – If you are patient looking for employment, place your WANTED ad here. If you want to hire an ME/CFS patient, place your OFFERED ad here.

Fundraising – All fundraising events and activities should go here

Currently, AMMES is looking for beta testers to work out the bugs! We need people to post ads, and then give us feedback by filling out a short survey. If there are any kinks in the process, let us know!

You can find AMMES Connect here: https://ammes.org/ammes-connect/  You will have to register to use the AMMES website, but registration is free.

To place an ad go to the right side bar and click on “Place Ad.” That will take you to a form to fill out.

You can also click on Browse ads to see ads that have been placed, or you can search by category. (There won’t be many at this point.)

After you have placed your ad, please go to the right hand bar to Send Us Your Feedback!

Let us know what you think!

A nanoelectronics-blood-based diagnostic biomarker for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)

Abstract:

There is not currently a well-established, if any, biological test to diagnose myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). The molecular aberrations observed in numerous studies of ME/CFS blood cells offer the opportunity to develop a diagnostic assay from blood samples. Here we developed a nanoelectronics assay designed as an ultrasensitive assay capable of directly measuring biomolecular interactions in real time, at low cost, and in a multiplex format.

To pursue the goal of developing a reliable biomarker for ME/CFS and to demonstrate the utility of our platform for point-of-care diagnostics, we validated the array by testing patients with moderate to severe ME/CFS patients and healthy controls. The ME/CFS samples’ response to the hyperosmotic stressor observed as a unique characteristic of the impedance pattern and dramatically different from the response observed among the control samples. We believe the observed robust impedance modulation difference of the samples in response to hyperosmotic stress can potentially provide us with a unique indicator of ME/CFS. Moreover, using supervised machine learning algorithms, we developed a classifier for ME/CFS patients capable of identifying new patients, required for a robust diagnostic tool.

Source: R. Esfandyarpour, A. Kashi, M. Nemat-Gorgani, J. Wilhelmy, and R. W. Davis. A nanoelectronics-blood-based diagnostic biomarker for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). PNAS first published April 29, 2019 https://doi.org/10.1073/pnas.1901274116

Pharmaceutical Interventions in Chronic Fatigue Syndrome: A Literature-based Commentary

Abstract:

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disorder characterized by prolonged periods of fatigue, chronic pain, depression, and a complex constellation of other symptoms. Currently, ME/CFS has no known cause, nor are the mechanisms of illness well understood. Therefore, with few exceptions, attempts to treat ME/CFS have been directed mainly toward symptom management.

These treatments include antivirals, pain relievers, antidepressants, and oncologic agents as well as other single-intervention treatments. Results of these trials have been largely inconclusive and, in some cases, contradictory. Contributing factors include a lack of well-designed and -executed studies and the highly heterogeneous nature of ME/CFS, which has made a single etiology difficult to define.

Because the majority of single-intervention treatments have shown little efficacy, it may instead be beneficial to explore broader-acting combination therapies in which a more focused precision-medicine approach is supported by a systems-level analysis of endocrine and immune co-regulation.

Copyright © 2019. Published by Elsevier Inc.

Source: Richman S, Morris MC, Broderick G, Craddock TJA, Klimas NG, Fletcher MA. Pharmaceutical Interventions in Chronic Fatigue Syndrome: A Literature-based Commentary. Clin Ther. 2019 Mar 11. pii: S0149-2918(19)30071-2. doi: 10.1016/j.clinthera.2019.02.011. [Epub ahead of print]

Mitochondrial complex activity in permeabilised cells of chronic fatigue syndrome patients using two cell types

Abstract:

Abnormalities in mitochondrial function have previously been shown in chronic fatigue syndrome (CFS) patients, implying that mitochondrial dysfunction may contribute to the pathogenesis of disease. This study builds on previous work showing that mitochondrial respiratory parameters are impaired in whole cells from CFS patients by investigating the activity of individual mitochondrial respiratory chain complexes.

Two different cell types were used in these studies in order to assess individual complex activity locally in the skeletal muscle (myotubes) (n = 6) and systemically (peripheral blood mononuclear cells (PBMCs)) (control n = 6; CFS n = 13). Complex I, II and IV activity and respiratory activitysupported by fatty acid oxidation and glutaminolysis were measured usingextracellular flux analysis. Cells were permeabilised and combinations of substrates and inhibitors were added throughout the assays to allow states of mitochondrial respiration to be calculated and the activity of specific aspects of respiratory activity to be measured.

Results showed there to be no significant differences in individual mitochondrial complex activity or respiratory activity supported by fatty acid oxidation or glutaminolysis between healthy control and CFS cohorts in either skeletal muscle (p ≥ 0.190) or PBMCs (p ≥ 0.065).

This is the first study to use extracellular flux analysisto investigate individual mitochondrial complex activity in permeabilised cells in the context of CFS. The lack of difference in complex activity in CFS PBMCs suggests that the previously observed mitochondrial dysfunction in whole PBMCs is due to causes upstream of the mitochondrial respiratory chain.

Source: Tomas C, Brown AE, Newton JL, Elson JL. Mitochondrial complex activity in permeabilised cells of chronic fatigue syndrome patients using two cell types. PeerJ. 2019 Mar 1;7:e6500. doi: 10.7717/peerj.6500. eCollection 2019. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6398432/ (Full article)