Patients with CFS do not score higher on the autism-spectrum quotient than healthy controls

Patients with chronic fatigue syndrome do not score higher on the autism-spectrum quotient than healthy controls: Comparison with autism spectrum disorder, by Indre Bileviciute‐Ljungar, Daniel Maroti, Susanne Bejerot in Scandanavian Journal of Psychology 2018 May 8

 

Research abstract:

Clinically, there is an overlap of several symptoms of chronic fatigue syndrome (CFS) and autism spectrum disorder (ASD), including fatigue; brain “fog”; cognitive impairments; increased sensitivity to sound, light, and odour; increased pain and tenderness; and impaired emotional contact.

Adults with CFS (n = 59) or ASD (n = 50) and healthy controls (HC; n = 53) were assessed with the Autism-Spectrum Quotient (AQ) in a cross-sectional study. Non-parametric analysis was used to compare AQ scores among the groups. Univariate analysis of variance (ANCOVA) was used to identify if age, sex, or diagnostic group influenced the differences in scores.

Patients with ASD scored significantly higher on the AQ than the CFS group and the HC group. No differences in AQ scores were found between the CFS and HC groups. AQ results were influenced by the diagnostic group but not by age or sex, according to ANCOVA.

Despite clinical observations of symptom overlap between ASD and CFS, adult patients with CFS report few autistic traits in the self-report instrument, the AQ. The choice of instrument to assess autistic traits may influence the results.

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ME Awareness week 7-13 May 2018 – campaign season!

ME Awareness week 7-13 May 2018 – campaign season!

 

International ME Awareness day

began in 1993. American Tom Hennessey chose the birthdate of Florence Nightingale, as she was stricken by an ME-type illness in her 30s and was often bed-ridden during the rest of her life.

blue ribbon photoBlue Ribbon for ME

Awareness raising got a focus in the UK in 1995 with the start of BRAME (Blue Ribbon Awareness for the awareness of Myalgic Encephalomyelitis).

The colour Blue continued to feature as once a year people died their hair blue, wore blue clothes or lit up public buildings with blue lights.

Letter writing & the media

In the early days  a small number of people were interviewed by the media for news features on May 12th and campaign organisers invited patients and carers to write letters to politician, health professionals and the media.

Social media

With the increasing popularity of social media many more people, including those who were housebound with ME were able to add blue ribbons, or twibbons to their social media pages. Thunderclaps became popular as a way for a single message to be mass-shared, flash mob-style. Some wrote blog posts (short for weblog) about their experiences of ME to be published on their own and other people’s blogs and Facebook pages.

Hashtag campaigns

No campaign takes place these days without a hashtag. A # is a strategy for linking posts and conversations on twitter on the same theme, wherever in the world they originate from.

Photo campaigns

As more and more people began to own mobile phones it became possible to join awareness raising campaigns by sharing photos of themselves and their friends e.g. Wear blue for ME

 

Millions missing

The biggest global campaign for ME to date encourages more people to get involved by inviting them to share photos, not of themselves, but of their shoes as a symbol of the Millions Missing out on normal lives through illness.

Combined with demonstrations, letter writing, petitions, etc. #MillionsMissing aims to raise the profile of the need for health equality.

Join an event near you on May 12th e.g. Cardiff, Bristol, Gloucester, Shrewsbury, Liverpool

Cardiff event: Cardiff City Centre, in front of the central Library, top end of the Hayes between 12 and 4pm. This is situated next to John Lewis and St David’s Shopping Centre.

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Childhood sleep & adolescent CFS/ME

Research abstract:

Childhood sleep and adolescent chronic fatigue syndrome (CFS/ME): evidence of associations in a UK birth cohort, by SM Collin, T Norris, P Gringras, PS Blair, K Tilling, E Crawley in Sleep Med. 2018 Jun;46:26-36.

OBJECTIVE/BACKGROUND: Sleep abnormalities are characteristic of chronic fatigue syndrome (CFS, also known as ‘ME’), however it is unknown whether sleep might be a causal risk factor for CFS/ME.

PATIENTS/METHODS: We analysed data from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort. We describe sleep patterns of children aged 6 months to 11 years, who were subsequently classified as having (or not having) ‘chronic disabling fatigue’ (CDF, a proxy for CFS/ME) between the ages 13 and 18 years, and we investigated the associations of sleep duration at age nine years with CDF at age 13 years, as well as sleep duration at age 11 years with CDF at age 16 years.

RESULTS: Children who had CDF during adolescence had shorter night-time sleep duration from 6 months to 11 years of age, and there was strong evidence that difficulties in going to sleep were more common in children who subsequently developed CDF. The odds of CDF at age 13 years were 39% lower (odds ratio (OR) = 0.61, 95% CI = 0.43, 0.88) for each additional hour of night-time sleep at age nine years, and the odds of CDF at age 16 years were 51% lower (OR = 0.49, 95% CI = 0.34, 0.70) for each additional hour of night-time sleep at age 11 years. Mean night-time sleep duration at age nine years was 13.9 (95% CI = 3.75, 24.0) minutes shorter among children who developed CDF at age 13 years, and sleep duration at age 11 years was 18.7 (95% CI = 9.08, 28.4) minutes shorter among children who developed CDF at age 16 (compared with children who did not develop CDF at 13 and 16 years, respectively).

CONCLUSIONS: Children who develop chronic disabling fatigue in adolescence have shorter night-time sleep duration throughout early childhood, suggesting that sleep abnormalities may have a causal role in CFS/ME or that sleep abnormalities and CFS/ME are associated with a common pathophysiological cause.

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Are probiotic treatments useful on FM or CFS patients?

Review abstract:

Are probiotic treatments useful on fibromyalgia syndrome or chronic fatigue syndrome patients? A systematic review, by P. Roman, F. Carrillo-Trabalón, N. Sánchez-Labraca, AF Estévez, D. Cardona in Benef Microbes. 2018 Apr 26:1-10 [Epub ahead of print]

Evidence suggests that the gut microbiota might play an important role in fibromyalgia syndrome (FMS) and chronic fatigue syndrome (CFS). Our goal is to systematically review the reported effect of probiotic treatments in patients diagnosed with FMS or CFS. A systematic review was carried out using 14 databases (PubMed, Cochrane Library, Scopus, PsycINFO, and others) in February 2016 to search for randomised controlled trials (RCTs) and pilot studies of CFS or FMS patient, published in the last ten years (from 2006 to 2016). The Jadad scale was used to asseverate the quality of the clinical trials considered.

Two studies (n=83) met the inclusion criteria, which were performed in CFS patients and both studies were considered as a ‘High range of quality score’.

The administration of Lactobacillus casei strain Shirota in CFS patients, over the course of 8 weeks, reduced anxiety scores. Likewise, this probiotic changed the faecal composition following 8 weeks of treatment.

Additionally, the treatment with Bifidobacterium infantis 35624 in CFS patients, during the same period, reduced inflammatory biomarkers.

The evidence about the usefulness of probiotics in CFS and FMS patients remains limited. The studied strains of probiotics have demonstrated a significant effect on modulating the anxiety and inflammatory processes in CFS patients.

However, more experimental research, focusing mainly on the symptoms of the pathologies studied, is needed.

Read full article

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#TimeForUnrestWales – Join the campaign!

#TimeForUnrestWales

a campaign for health equality
and the recognition of the neurological condition of ME

Much work is needed to put ME & CFS on an equal basis with other neurological conditions!

WAMES is asking the Cabinet Secretary for Health:

to #HelpNHSbeMEaware and to provide, as a matter of urgency, support and finance for a national training and awareness programme.

You can join us:

Write to the  Cabinet Secretary, Vaughan Gething

Email: Correspondence.Vaughan.Gething@gov.wales
Address: National Assembly for Wales, Cardiff Bay, Cardiff  CF99 1NA

More info           WAMES’ letter to the Cabinet Secretary

Write to your AMs

asking them to support our campaign and also write to the Cabinet Secretary

Find their names & contact details

WAMES’ letter to the  AMs: #TimeForUnrestWales invitation

Share your experience

of your struggle to get an accurate diagnosis in your correspondence with the AMs and Cabinet Minister and with WAMES

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The Autoimmune Virus? Groundbreaking EBV finding could help explain ME/CFS

Simmaron Research blog post, by Cort Johnson, 30 April 2018: The Autoimmune Virus? Groundbreaking EBV Finding Could Help Explain ME/CFS

Viral Mystery 

“I’ve been a co-author in almost 500 papers. This one is more important than all of the rest put together. It is a capstone to a career in medical research,” Harley

I sensed some awe in Ron Davis’s voice as he pushed for more understanding of Epstein-Barr Virus’s effects in ME/CFS during a talk at the Brain Science conference.  Davis is not to my knowledge finding much evidence of EBV reactivation in the severe ME/CFS patient study – a surprise – but he is very interested in what happened during that initial EBV infection, which appears to have triggered chronic fatigue syndrome (ME/CFS) in so many people.

He’s not alone in his “admiration” for the virus. Simmaron’s Advisor, Dr. Daniel Peterson, whose clinical practice and research stemmed from an outbreak in the Lake Tahoe region of Chronic Fatigue Syndrome, has tracked EBV in patients for decades, noting very high titers to EBV and other herpes viruses in subsets of patients.

It’s not surprising that these two important figures have had their eyes on EBV. EBV, after all, is kind of in a league of its own.  An invader of B and epithelial cells, the 50th anniversary of its discovery was recently celebrated with numerous reviews.  Epstein-Barr was discovered in 1966 by Anthony Epstein and Yvonne Barr. It was the first human virus shown to cause cancer. The sequencing of its large genome in 1995 helped launch the genomic era.

One of the more massive and complicated viruses, it’s one of the very few viruses that’s able to avoid elimination: once EBV infects your B-cells, it’s in your body to stay. It’s able to effectively hide from the immune system and reactivate just enough so that when the infected B-cells die it can move on to other cells.

We’re well equipped to ward off EBV when we’re young – it usually produces only minor symptoms – but as our immune systems alter as we age, that changes.  Encountering EBV as an adolescent or adult (infectious mononucleosis, glandular fever)  – as increasingly happens in our germ phobic age – often means months of convalescence as our immune systems struggle to ward off this powerful virus.

The problems don’t stop there. We know that infectious mononucleosis (IM) is a common trigger of ME/CFS but coming down with IM/glandular fever in adolescence has also been shown to increase one’s risk of coming down with multiple sclerosis 2-4 fold and lupus by fifty percent.  Because of EBV’s ability to remain latent in the body, EBV reactivations are a huge problem for transplant patients with compromised immune systems.

The big question concerning EBV is how a virus which has essentially been latent for decades could contribute to serious diseases like MS and lupus. We now may have the answer. Last week, what will probably turn out to be a seminal paper in pathogen research directly showed for the first time how EBV appears to be able to trigger autoimmune diseases later in life and could conceivably play a role in ME/CFS.

The rather hum drum title of the paper “Transcription factors operate across disease loci with EBNA2 implicated in autoimmunity” in the Nature Genetics Journal hardly hinted at the possibilities the paper presents.

Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity John B. Harley, Xiaoting Chen, Mario Pujato, Daniel Miller, Avery Maddox, Carmy Forney, Albert F. Magnusen, Arthur Lynch, Kashish Chetal, Masashi Yukawa, Artem Barski, Nathan Salomonis, Kenneth M. Kaufman, Leah C. Kottyan & Matthew T. Weirauch. Nature Genetics (2018) doi:10.1038/s41588-018-0102-3

EBV  consists of several proteins of which EBNA-2 is one. EBNA-2 is EBV’s main viral transactivator; i.e. it’s a transcription factor that turns on genes in an infected cell that help EBV to survive. Essentially EBNA-2 allows EBV to hijack a cell’s genetics and put them to its own use.

The study – produced by researchers at Cinncinnati’s Children Hospital – demonstrated that once EBV infects B-cells, it turns on genes that have been identified as risk factors for a boatload of autoimmune diseases.

It turns out that even though the virus is, so to speak, latent; i.e. it’s not replicating – its transcription factor is still active  – altering the expression of our genes. The genes that it affects just happen to be the same genes that increase the risk of developing lupus, multiple sclerosis (MS), rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), inflammatory bowel disease (IBD), celiac disease, and type 1 diabetes.  Apparently decades of genetic assault from EBV’s transcription factor can set the stage or at least contribute to many autoimmune diseases.

Chronic diseases are usually caused by a variety of genetic and environmental factors. Because not everyone with these transcription factors comes down with a chronic illness, other factors must play a role. The authors believe, though, that the gene expression changes induced by the virus in the B cells could account for a large number of people with lupus and MS who fall ill.

“In lupus and MS, for example, the virus could account for a large percentage of those cases. We do not have a sense of the proportion in which the virus could be important in the other EBNA2-associated diseases,” Harley

Read more about the ME/CFS and research into the EBV virus

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#TimeForUnrestWales – the struggle to get an accurate diagnosis

#TimeForUnrestWales

 a campaign for recognition of ME and health equality

There is a Health and Social Care crisis for people with ME in Wales, starting with the struggle patients have to find an accurate diagnosis from doctors who understand ME.

The Welsh Government has had a plan to change that since 2014 – the Task & Finish Group Report and Recommendations – but NHS Wales has failed to take them seriously and  little has changed.

WAMES is therefore asking the Cabinet Secretary for Health:

to provide, as a matter of urgency, support and finance for a national training and awareness programme.

The Task & Finish Group Report describes the challenges:

For patients: achieving timely diagnosis for ME/CFS remains a significant challenge (5.1)

“Many patients still do not feel that GPs take them seriously and some continue to report experiencing hostility. Patients express concerns that GPs seem to have limited knowledge of their condition… 

Delayed and/or multiple referrals are common due to difficulty in identifying the condition and/or the most appropriate specialist, and diagnosis can sometimes take several years. Such significant delays in providing effective self-management support may result in considerably greater long term support needs.

Patient groups report that some GPs have a low understanding of the post-exertional nature of the condition, the sheer degree of physical debilitation which it can cause, sub-groups of patients and the range of severity that is seen. There are also difficulties with obtaining home visits where needed and with GPs understanding that, due to cognitive difficulties, patients may need a written summary of discussions.”

For GPs (5:1):

“GPs meanwhile face significant challenges in diagnosis and management because of multiple and complex symptoms and a historic lack of consensus on diagnosis and treatment. This is compounded by the lack of a clear referral pathway and the limited specialist interest in diagnosis or providing treatment once a diagnosis is reached…when they [Health Boards] provide training for GPs, sessions tend to be attended by those who already have an interest, without the knowledge spreading further.”

For Health Boards (5):

  • “limitations to the evidence base for appropriate interventions;
  • a shortage of professionals with specialist knowledge, interest or the confidence to diagnose 
  • few clinical champions within NHS Wales 
  • resource and financial constraints “

The Report recommends:

Recommendation 5: “Each Health Board should undertake work to raise awareness of ME/CFS and Fibromyalgia in primary care, to support timely diagnosis and effective management of both children and adults 

Health Boards should provide support to GPs to support people living with ME/CFS and Fibromyalgia to become experts in their own care and self-management, as well as providing clear pathways for referral for specialist support as appropriate. 

Recommendation 8: The All Wales Implementation Group to “provide advice on an All-Wales approach to the provision of training and support for GPs

WAMES has asked the Cabinet Secretary for Health & Social Services, Vaughan Gething, to #HelpNHSbeMEaware and:

to provide, as a matter of urgency, support and finance for a national training and awareness programme which takes into account:

  • The need to invite expert clinicians from outside Wales to take part – There are no medical experts in Wales available to share their knowledge, and if we wait for them to ‘miraculously appear’ there will be no training and awareness undertaken.
  • The controversy over aetiology, diagnostic criteria and management advice – It would be important to develop a strategy that accepts this current tension and informs staff about it.

Many NHS staff are happy to accept the current NICE guidelines (now being revised) whose treatment recommendations are based on a psycho-social understanding of CFS and partially based on research results that have been found to have been inaccurate).

On the other hand patients and some NHS staff know about the biomedical research revelations and understand ME to be a condition classified as neurological with neuro-immune-endocrine involvement.

Neither belief should be allowed to be a barrier to patients getting a diagnosis and accessing medical care and other support. e.g. A medical diagnosis is necessary to access social care, transport, educational adjustments, benefits etc.  Without social care severely affected patients can live in squalor and extreme distress.

Carers are collapsing under the strain of caring for their loved ones alone.  The right of patients, including children,  to choose the care they wish should be included as a theme running through the programme.

  • The need for a standard training / awareness programme for use across Wales – Experienced trainers need to develop a programme so that an even standard is achieved, in spite of the lack of local knowledge, the controversies surrounding the illness, and the limitations of outside experts with no knowledge of the NHS in Wales. This programme should also give staff the opportunity to hear the experiences of people with ME and CFS.
  • Funding for travel – The initiative could also fund clinicians to attend major conferences and workshops in England, where they can learn from international researchers and experienced clinicians.
  • Ongoing programme – There is a need for Health Boards to hold ongoing awareness sessions to ensure a wide range of staff are reached over a period of time.

Much work is needed to put ME & CFS on an equal basis with other neurological conditions!

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#TimeForUnrestWales – May 12th International ME Awareness Day 2018

It is #TimeForUnrestWales

Over the last few years a number of global campaigns have been launched to raise awareness of ME. Here in Wales they have struck a chord and we have been adding our voice to those around the world.

#TimeForUnrest
is a global campaign to grow and strengthen the global movement for equal recognition, education, research, and funding for ME.

For International ME Awareness Day and throughout the year WAMES is drawing attention to the pressing need for equal recognition, health and social care here in Wales.

It is #TimeForUnrestWales

NHS Wales has ignored the requests from past Health Ministers for Health, and the current Cabinet Minister, to implement the 2014 Task & Finish Group Report Recommendations, aimed at improving health care of people with ME and CFS.

NHS Wales has also ignored requests from patients, carers and WAMES during 2017 to introduce training and awareness sessions to #HelpNHSbeMEaware

NHS Wales is clearly unable to meet its legal and moral responsibility to care for people with ME and CFS so WAMES is writing to the Cabinet Minister for Health, Vaughan Gething, to challenge him to commit Government money and time to finding a solution.

All improvements in care begin with understanding the nature of ME, its impact on the lives of patients and their families, and how to accurately diagnose it.

It is Time for NHS Wales to be ME aware!

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Toxic brains, frozen spines & the Perrin Point: Ray Perrin, ME/CFS & FM

Health rising blog post, by Cort Johnson, 25 March 2018: Toxic brains, frozen spines and the Perrin Point: Ray Perrin, ME/CFS and Fibromyalgia

This is the second of three blogs examining the possibility that upper body/head issues play a role in chronic fatigue syndrome (ME/CFS) and/or fibromyalgia (FM). The first blog examined the possibility that high blood pressure in the brain was present in ME/CFS and FM.

In this blog, Health Rising examines Ray Perrin’s hypothesis that a toxic overload in the brain is causing ME/CFS and FM.

Ray Perrin PhD, D.O. a U. K. osteopath, has been digging into chronic fatigue syndrome (ME/CFS) and fibromyalgia (FM) for almost three decades.  His journey with ME/CFS began when a professional cyclist suffering from ME/CFS walked into his sports medicine clinic way back in 1989 and then walked out five treatments later healthy again.

Perrin wasn’t trying to treat the cyclist’s chronic fatigue syndrome; he was trying to fix his posture, but on the way to fixing his posture – which required using a variety of techniques – he ended up curing his ME/CFS. That cyclist provided Perrin with a clue that he’s been following up on for almost 30 years: the cyclist was experiencing a “mechanical strain” on his spine in the chest area. When Perrin improved the movement in his upper back, the cyclist was able to return to cycling.

“You’ve got to find out what you’ve done because you got me better and nobody else has.” I thought it was just a coincidence. But then I was a bit inquisitive. I’ve always been inquisitive and I wanted to find out what I had done. And that’s when I started looking at other patients who had the symptoms then and I noticed there were physical signs in all these patients, especially in the spine. That’s what set me on this long road and then I came up with my ideas and a hypothesis of what ME is and then the rest is history, as they say. 28 years on…Ray Perrin – the Ari Whitten interview.

Perrin comes from an osteopathic tradition in the U.K. which is very focused on reading physical signs and manipulating the body. He was the first medical professional I know of to propose that a unique physical structural problem is present in ME/CFS/FM. Perrin believes that the practice of reading the body is something of a lost art in the medical field. Perrin’s PhD thesis ended up being on ME/CFS.

They (doctors) look at what tests they can do and what their scan shows, but they don’t actually look at the person, feel the person. And I, as an osteopath, do. And this is what we do and I started looking for more and more signs that these patients all shared.  The Ari Whitten Interview

Personally, his general thesis doesn’t surprise me at all. My pain begins at the chest area and proceeds upwards. Trying to relieve my neck tightness with frequent stretching exercises resulted in nausea, flu-like symptoms and pain. After walking or exercising – it’s my chest and upper body which are in pain – not my legs. Touching virtually any part of my face will elicit pain. Whether or not Perrin’s hypothesis has found the or a cause of ME/CFS/FM, something is going on in my upper body.

A Toxic Brain
Perhaps only an osteopath – a doctor specializing in structural problems – could have come to Perrin’s conclusion. He believes that toxic overload in the brain, caused by a malfunctioning sympathetic nervous system, causes distinct physical signs in the upper bodies of ME/CFS/FM patients.

The Brain’s Lymphatic System
The lymphatic system in our body serves to collect and process large toxins, but no such system was believed to exist in the brain.  For hundreds of years, researchers have wondered how the brain effectively gets rid of its waste. The cerebral spinal fluid is one avenue but it seemed a poor second to the role the lymphatic system plays in the body.

The brain’s lymphatic system was rediscovered in 2017 by NIH researchers (two hundred years after an Italian anatomist reported that he’d spied lymphatic tissues in the brains of mice. Sometimes the medical system takes a long, long time to catch up :))  That finding is spurring new research into diseases like multiple sclerosis, Alzheimer’s and other neuroinflammatory disorders.  Perrin believes the buildup of amyloid proteins in Alzheimer’s could result from poor lymphatic drainage. (Avindra Nath, the lead investigator in the NIH’s intramural study believes ME/CFS may be an neuroinflammatory disorder.)

Interestingly, blocking that lymphatic drainage in mice results in a buildup of fluids in three areas of the brain associated with ME/CFS: the hypothalamus, the thalamus and the basal ganglia.

Decades ago, Perrin was on a similar trail. He believed lymphatic drainage from the brain was occurring but he didn’t know from where. He did know that the cerebral spinal fluid drains toxins from the brain through a bony plate (cribriform plate) situated above the nose. From there, the toxins drain into lymphatic vessels around the nasal sinuses and the optic, auditory and trigeminal nerves in the eye, ear and cheek and along the spine. From there they flow to the thoracic duct and finally into the blood, where they end up at the liver.

Perrin’s osteopathic training taught him that the main drainage point of the lymphatic system was found at the thoracic duct in the chest area. This thoracic duct has a pumping mechanism controlled by a system – the sympathetic nervous system – that researchers have long found to be dysregulated in ME/CFS and fibromyalgia.

Perrin hypothesized that blocked or congested lymphatic drainage pathways in ME/CFS and FM were causing toxins to build up in the central nervous system. That toxin buildup was disturbing the hypothalamus, which, in turn, was causing sympathetic nervous system problems.  The hypothalamus is the only part of the brain with direct access to the blood. It needs this access to regulate insulin levels in the blood but it comes at a cost  – less protection from toxins.

Those SNS problems were, in turn, blunting the pumping action of the key lymphatic drainage point – the thoracic duct. In fact it’s worse than that. Perrin believes the pump in ME/CFS/FM is working backwards – instead of pumping lymphatic fluid to the body, it’s actually pumping lymphatic fluids back towards the brain – and Perrin believes this can push toxins into the brain. (That retrograde pumping mechanism shows up in odd-looking varicose veins in the chest area.) Those toxins then destabilize the hypothalamus and sympathetic nervous system – which, in turn, whacks the pumping mechanism. In short, a vicious circle which maintains high toxin levels in the brain is present.

Perrin now believes that the entire brain is probably affected by increased toxin levels with the limbic system (hypothalamus, thalamus, basal ganglia) most affected. That’s enough of the brain to easily produce the movement, sleep, fatigue and cognitive problems found in ME/CFS/FM. Because the lymphatic drainage from the brain mostly occurs during the delta stages of sleep, it’s possible that the sleep problems in ME/CFS – which have been linked to autonomic nervous system dysfunction – are reducing drainage as well.

Physical Signs of ME/CFS and Fibromyalgia
Perrin is the first to postulate that direct physical evidence of ME/CFS and FM exists in the form of frozen or limited spinal mobility, particularly in the middle and upper back, swollen lymph vessels and specific tender points. He’s said he’s never seen an ME/CFS patient who doesn’t have a thoracic (upper and middle) spine problem.

The Perrin Point is a tender point about 2 to 3 cm to the left and 2 to 3 cm above your left nipple. It’s also generally found between in the third intercostal space between the third and fourth ribs (counting from the top).

Each of these physical findings, Perrin believes, relates to problems with fluid drainage from the brain. Each, Perrin also asserts, can be manipulated using cranial osteopathic techniques to stimulate renewed flow of cerebral spinal and lymphatic fluids, thus relieving the buildup of toxins in the brain and relieving the symptoms of ME/CFS/FM.

Once toxin levels drop and normal lymphatic drainage resumes, Perrin states the patient is free of chronic fatigue syndrome (ME/CFS). Throughout the book, Perrin refers to numerous recovery stories.

Success Story
One young ME/CFS patient who was virtually carried into his office had a strong curvature in her mid-upper back region, tender points in certain areas, lymphatic congestion and a very sluggish “cranial rhythm”. Perrin reported that an intensive course of soft tissue massage and spinal articulation improved her lymph drainage and the girl was able to successfully return to school, gain a degree and remained healthy at the time of the book’s printing.“.

Read more about the history of this hypothesis and the Perrin Treatment protocol

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Integration of DNA methylation & health scores identifies subtypes in ME/CFS

Research abstract:

Integration of DNA methylation & health scores identifies subtypes in myalgic encephalomyelitis/chronic fatigue syndrome, by Wilfred C de Vega, Lauren Erdman, Suzanne D Vernon, Anna Goldenberg & Patrick O McGowan in Epigenomics. 2018 Apr 25. doi: 10.2217/epi-2017-0150. [Epub ahead of print]

If your body cannot methylate properly, toxins build up in your bloodstream and will eventually cause disease. … In fact, methylation can turn genes on or off, which can be good or bad for our health, depending on the gene.  Read more

AIM:

To identify subtypes in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) based on DNA methylation profiles and health scores.

METHODS:

DNA methylome profiles in immune cells were integrated with symptomatology from 70 women with ME/CFS using similarity network fusion to identify subtypes.

RESULTS:

We discovered four ME/CFS subtypes associated with DNA methylation modifications in 1939 CpG sites, three RAND-36 categories and five DePaul Symptom Questionnaire measures. Methylation patterns of immune response genes and differences in physical functioning and postexertional malaise differentiated the subtypes.

CONCLUSION:

ME/CFS subtypes are associated with specific DNA methylation differences and health symptomatology and provide additional evidence of the potential relevance of metabolic and immune differences in ME/CFS with respect to specific symptoms.

Summary points

  • DNA methylation data and health score data using the RAND-36 survey and the DePaul Symptom Questionnaire were collected in 70 women diagnosed with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).
  • Potential clinical subtypes integrating DNA methylation differences in ME/CFS biomarkers (4699 sites in total) and health score data were identified using similarity network fusion, a clustering approach that preserves the data structures unique to each level of data.
  • Similarity network fusion analysis revealed the presence of four clinical subtypes among the ME/CFS patients based on methylation differences in 1939 sites, three RAND-36 categories and five DePaul measures (normalized mutual information [NMI] >0.2, Kruskal–Wallis FDR <0.05).
  • RAND-36 scores that significantly contributed to clustering corresponded to physical functioning (NMI = 0.26), social functioning (NMI = 0.23) and role limitations due to physical health (NMI = 0.23).
  • DePaul Symptom Questionnaire measures that were significantly different between ME/CFS clinical subtypes were associated with frequency of postexertional malaise, severity of pain/muscle weakness and severity of unrefreshing sleep.
  • Gene set enrichment analysis of the top 50 sites that contributed to differentiating the ME/CFS subtypes were mainly annotated to immune response.
  • The results are consistent with previous work that described immune and metabolic dysfunction in ME/CFS.
  • The described subtypes of our study are also generally consistent with previous ME/CFS work that identified immune gene and degree of symptom severity as highly relevant factors in differentiating ME/CFS subtypes.

Read full paper

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