ME/CFS: Myalgic Encephalomyelitis & Chronic Fatigue Syndrome

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Fibromyalgia Syndrome (FMS) &



 1 in 40 people are affected by FMS worldwide (80% of which are women) and is commonly characterized by widespread pain throughout the body, as well as fatigue (often referred to as 'fibro fog') and emotional distress.
 It most commonly develops between the ages of 25 and 55, although children can also get it.

ME/CFS -- ME(Myalgic Encephalomyelitis) &
Chronic Fatigue Syndrome (and Fibromyalgia )
    (Over one million Americans experience ME/CFS symptoms

Oct 2019: STUDIES

4. The opioid antagonist Naltrexone hydrochloride (NTX) .... may have potential for use as a treatment for ME/CFS.

5. Nasal drop vitamin B12 administration resulted in a significant increase in vitamin B12 serum levels and therefore may be effective. This pilot study suggest that the nasal drops may be used as an alternative to injections because two thirds of ME/CFS patients reported a positive effect, accompanied by an increased number of steps, improvement of the RAND-36 physical functioning scale and the CIS20r fatigue scale,

6. Promising results are obtained by treatment with Metformin, or possibly Momordica charantia extract, which will correct insulin resistance, with Meldonium improving the transportation of glucose into the mitochondria, with sodium dichloroacetate activating pyruvate dehydrogenase, and with nutraceutical support reducing oxidative and inflammatory impairment.

October 2018 - 2019 Clinical Trials ( source )

The IDO Metabolic Trap Hypothesis for the Etiology of ME/CFS.

Medically Documenting Disability in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)

Rethinking ME/CFS Diagnostic Reference Intervals via Machine Learning, and the Utility of Activin B for Defining Symptom Severity.

Current Research Provides Insight into the Biological Basis and Diagnostic Potential for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).

Post-Exertional Malaise Is Associated with Hypermetabolism, Hypoacetylation and Purine Metabolism Deregulation in ME/CFS Cases.

Healthcare Utilization in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Analysis of US Ambulatory Healthcare Data, 2000-2009.

Advances in ME/CFS: Past, Present, and Future.

Cellular Immune Function in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).

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

Meeting the Educational Needs of Young, ME/CFS Patients: Role of the Treating Physician.

Corrigendum: Neuroinflammation and Cytokines in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): A Critical Review of Research Methods.

Evidence of Clinical Pathology Abnormalities in People with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) from an Analytic Cross-Sectional Study.

Whole blood human transcriptome and virome analysis of ME/CFS patients experiencing post-exertional malaise following cardiopulmonary exercise testing.

Initiating Care of a Patient With Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).

Classification of ME/CFS in the United Kingdom.

The Importance of Accurate Diagnosis of ME/CFS in Children and Adolescents: A Commentary.

Neuroinflammation and Cytokines in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): A Critical Review of Research Methods.

Estimating Prevalence, Demographics, and Costs of ME/CFS Using Large Scale Medical Claims Data and Machine Learning.

Hope, disappointment and perseverance: Reflections of people with Myalgic encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Multiple Sclerosis participating in biomedical research. A qualitative focus group study.

The UK ME/CFS Biobank: A Disease-Specific Biobank for Advancing Clinical Research Into Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.

Blood Volume Status in ME/CFS Correlates With the Presence or Absence of Orthostatic Symptoms: Preliminary Results.

Hand Grip Strength as a Clinical Biomarker for ME/CFS and Disease Severity.

Low Sensitivity of Abbreviated Tilt Table Testing for Diagnosing Postural Tachycardia Syndrome in Adults With ME/CFS.

Can a Chronic BPPV With a History of Trauma be the Trigger of Symptoms in Vestibular Migraine, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), and Whiplash Associated Disorders (WAD)? A Retrospective Cohort Study.

Immunosignature Analysis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).

Chronic viral infections in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).

Why do some ME/CFS patients benefit from treatment with sodium dichloroacetate, but others do not?

Checking our blind spots: current status of research evidence summaries in ME/CFS.


April 2019: NIH Conference on ME/CFS
ME/CFS possible treatments
23rd minute:-

Case1: Treated with midorine for POTS , H1 & H2 Blockers incl. Zantac, Cromolyn Sodium, Monteleukast, Low dose Naltrexone (LDN), Rifaximin( for SIBO ),
Intravenous Gammaglobulin, Support Hose, High Sodium Diet

Anti-Herpes Virus drugs ?

53rd minute TREATMENTS:-

1. Intravenous Gamma Globulins ( for low levels of Mannose Binding Lectin)
2. Enbrel (Etanercept drug) ( for Cytokine Abnormalities)
3. Intravenous amino acids (for Amino Acid Deficiency)
4. ? (for Powassan Positive, Lyme disease)
5. Viside Infusions 5, (for Virus in Lymphoid Tissue)
6. Antiviral Therapy ( valcyte) ( for Virus in Spinal Fluid, herpesvirus 7)

68 minute -- IV Saline for temporary recovery

3hours 37min --- Very Severe Patients -- mutant gene ID02 ( but not significant and not yet measurable)
3hrs 59m  ----  100% diagnosis of ME/CFS ( suggested treatment: -- microcondrial repair drugs , possible contributors: too low selenium or high Mercury )
5hrs 10min  ---- OI (Orthostaical Intolerance) Standing Upright vs lying down -- so lie down as often as possible and readily treatable with various medications)
5hrs 26m ---- OI cont... fixing a spinal disk ( which constricted the spinal cord) cured ME/CFS

6hr 24m The part of the SUMMARY (which is available in slides) that might be semi-understood by a non-doctor. ( ends at 6hr 51m )

6hr 47 - Taking Butyrate as a possible treatment

Here's a STRETCH -- Note that ME/CFS got hyperbolically diagnosed around 1983 the same time that Ibuprofen got sold over-the-counter. How many of you started by taking Ibuprofen ?

2014 NIH Funding and Prevalence for Selected Diseases (Instead of $14m spent on ME/CFS it should be over $200m )

Disease area

Funding (Millions)

U.S. Prevalence

$ Spending per patient









Multiple sclerosis








VIDEO: Letter read by a UK MP from a severe ME/CFS sufferer ( share this with YOUR Representative) Get the $200+ million funding that ME/CFS deserves.

Dec 2018 Latest Studies and search for "chronic fatigue"  ( include the " 's ).

Dec 2018 "still few data to provide a promising hypothesis for the effective role of mineral and vitamin supplementation in the CFS " in the CONCLUSION

Nov 2018 Why do some ME/CFS patients benefit from treatment with sodium dichloroacetate, but others do not?

May 2018 Treating  with sodium dichloroacetate

March 2018:

Feb 21 2018 105 Studies found for: Recruiting, Not yet recruiting, Available Studies | fibromyalgia

The US CDC's ME/CFS webpage

The Solve ME/CFS Inititiative Webinars

MEAction #MEAction is an international network of patients

MassCFIDS The Massachusetts CFIDS/ME & FM Association

UK ME Association

Research Centers:


July 2021 Many of the symptoms in Fibromyalgia syndrome (FMS) are caused by antibodies that increase the activity of pain-sensing nerves throughout the body. (likely the result of autoimmune problems -- a disease of the immune system, rather than the currently held view that it originates in the brain.)
This finding strongly suggests that therapies which reduce antibody levels in patients are likely to be effective treatments. Such therapies are already available and are used to treat other disorders that are caused by autoantibodies.
The next step will be to identify what factors the symptom-inducing antibodies bind to. This will help us not only in terms of developing novel treatment strategies for FMS, but also of blood-based tests for diagnosis, which are missing today.

June 2021 Epstein-Barr virus (EBV) reactivation resulting from the inflammatory response to coronavirus infection may be the cause of previously unexplained long COVID symptoms—such as fatigue, brain fog, and rashes—

Epstein-Barr virus (EBV), also known as human herpesvirus 4, is a member of the herpes virus family. It is one of the most common human viruses. EBV is found all over the world.
Most people get infected with EBV at some point in their lives. EBV spreads most commonly through bodily fluids, primarily saliva.
EBV can cause infectious mononucleosis, also called mono, and other illnesses.
There is no vaccine to protect against EBV infection.
There is no specific treatment for EBV. :(

Mar 25th 2021 The National Institute for Allergy and Infectious Diseases has launched a comprehensive effort to define Long COVID (Post-Acute Sequelae of COVID, or PASC) — a four-year, $1.15-billion initiative that will establish patient registries along with central repositories for data and biological specimens.
Many Long COVID sufferers report relief from their symptoms after receiving one of the COVID-19 vaccines.

Feb 26th 2021 The silver lining to LONG HAUL COVID! That people who have been shouting about M.E. and CFS for the last 20 years are suddenly being heard. One of the studies that we’re planning is going to be directly comparing patients with Long Covid with patients with chronic fatigue syndrome because we think there are going to be some similarities.

The two main areas that we’re going to be looking at are in the mitochondria, effectively the battery that every single cell has that keeps it charged, that we know are affected by Long Covid, and then the other place that we’re interested in is the microcirculation, the smallest blood vessels – the ones that are responsible for delivering the oxygen, the nutrients and the hormones to your tissues.
DR David Strain clinical lead for COVID at the Royal Devon & Exeter Hospital.

Jan 20th 2021 ME/CFS, Chronic Fatigue Syndrome, compared to Long Haul COVID

Aug 2020 Doctors are finding striking similarities between chronic fatigue syndrome and long-term coronavirus symptoms

Sep 2019 Research: POTS, maybe an autoimmune disorder. If so then a simple blood test that could diagnose it. POTS is  large increases in heart rate and sometimes decreases in blood pressure when standing up. That can cause lightheadedness, heart palpitations and even loss of consciousness. Additional symptoms, including fatigue, pain, gastrointestinal issues, bleeding disorders, anxiety and brain fog.

AUG 2019 NYT on Netflix -- intense muscle pain triggered by exercise -- CPT2 How is carnitine palmitoyltransferase deficiency (CPT2) treated?
A change in
diet is the main treatment for CPT deficiency. This diet must avoid relying on fats for energy. It should provide a high amount of carbohydrates. It should contain a low amount of fats and protein. It’s also important to eat often. This can prevent low blood sugar. It can also prevent the body using fats for energy. And you should stay away from things that may trigger symptoms. These may include skipping meals, exposure to cold, stress, and a lot of exercise.

Jul 2019: Inside the brains of patients with ALS (amyotrophic lateral sclerosis), a debilitating neurodegenerative disease, is a telltale sign that marks almost every case: clumps of toxic proteins.
A key gene behind the formation of one type of these neuron-damaging aggregates has been identified. Inhibiting the gene's function curbs production of the harmful protein.
The dysfunctional gene similarly stunted erroneous protein production in cellular models of Huntington's disease and spinocerebellar ataxia, two neurodegenerative illnesses.

June 2019 Common antidepressants interact with opioid medication to lessen pain relief ( Don't take  Prozac(fluoxetine), Paxil(paroxetine) or Wellbutrin(bupropion) with Tramadol  --
 Zoloft(sertraline), Celexa(citalopram) or Lexapro(escitalopram),

2019 May: Metformin found to alleviate pain in people with fibromyalgia

2019, April accurately identify Chronic Fatigue Syndrome ... already found a candidate drug that seems to restore healthy function to immune cells .... hopeful that they can test their finding in a clinical trial in the future.( listen to the researcher in the NIH Conference video at  3hr 32m )

2019: Study Utilize CT38 to down-regulate CRF2 to restore a normal stress response, and potentially eliminate ME/CFS  symptoms."

2019: STUDY: Experimental blood test accurately spots fibromyalgia  "this work could lead to identification of a particular protein or acid—or combination of molecules—that is linked to fibromyalgia"

STUDY: 2018 August: Researchers Were Able to Predict ME/CFS With 84 Percent Accuracy

2018: July New Stem Cell Treatment for MS is a ‘Game-Changer’

2018, July: SLATE: " A 2009 article by two prominent mainstream Lyme experts noted that men and women are represented roughly equally among CDC-reported cases of Lyme disease but that patients with a chronic Lyme diagnosis are disproportionately female. They concluded, therefore, that chronic Lyme must be “unrelated to infection with B. burgdorferi” and instead consists of misdiagnoses of “illnesses with a female preponderance, such as fibromyalgia, chronic fatigue syndrome, or depression
"we know that women’s immune systems are substantially different than men’s, which may be rooted in the fact that women have to allow another creature, a baby, to grow inside them without immune attack. This is thought to be part of the reason that women are prone to autoimmune disease"

2018, June Study finds no strong evidence that cannabis reduces chronic pain

2018, June: Around $4 million funding for 5 years study of “Molecular and Single Cell Immunology of ME/CFS
Interesting listening to the video of Mark Davis -- T Cells either reacting to a pathogen
or to the body's own proteins( as in MS, Lupus, Rheumatoid Arthritis, Type 1 Diabetes....) .

 immunology and molecular biology

June 2018: no results found in COMPLETED trials WITH RESULTS advanced search of for " guaifenesin Fibromyalgia " or "guaifenesin ME/CFS".
But 98 results for "guaifenesin"  alone. (in search box "Intervention/treatment:").
 It appears that ADs promoting  guaifenesin  for Fibromyalgia is a scam ! (Guaifenesin is used to help clear mucus or phlegm from the chest when you have congestion from a cold or flu.)

May 2018 three main uses of lactate in the body:

  1. It's a major fuel source,
  2. it's the major material to support blood sugar level and
  3. it's a powerful signal for metabolic adaptation to stress.

Apr 2018: Epstein-Barr virus linked to seven serious diseases

Apr 2018: NY State creates website on Myalgic Encephalomyelitis ("Chronic Fatigue Syndrome")

a new grant of $2.1 million from the National Institutes of Health (NIH) in America. searching for disease biomarkers,

Objectively measuring ME/CFS ( avoid activity that creates an oxygen deficit. Not Aerobic activity but  Anaerobic activity instead. Where anaerobic means activity ( not high activity) lasting no longer than 2 minutes followed by at least 6 minutes of complete rest. )

Can CFS be cured by never exceeding your ENERGY THRESHOLD and DAILY LIMIT ?

Mast Cell Activation May Underlie 'Chronic Fatigue Syndrome' Mar 2018

Chronic Fatigue Syndrome -- A Roadmap for Testing and Treatment

Feb 2018 Lady Gaga cancels remainder of world tour due to 'severe pain' from fibromyalgia

Dec 27, 2016 Fuel Shortage: Norwegian Study Expands on Energy Problem in Chronic Fatigue Syndrome (ME/CFS)

Scientists reveal new avenue for drug treatment in neuropathic pain

  1. Lyrica, a medicine used to treat patients with seizures, pain from shingles, and nerve painfrom diabetesand spinal cord injuries, is offering new hope to those living with the pain of fibromyalgia.

  2. Duloxetine (Cymbalta) is used to treat depression and anxiety. In addition, duloxetine is used to help relieve nerve pain (peripheral neuropathy) in people with diabetes or ongoing pain due to medical conditions such as arthritis, chronic back pain, or fibromyalgia (a condition that causes widespread pain).

  3. Savella is the third medication approved to help manage fibromyalgia.

Feb 21 2018: 76 Studies found for: Completed Studies | Studies With Results | fibromyalgia
  • magnetic therapy -- Mean Change in 3-recording Average of the Subjects Daily Pain Rating on the 0-10 Numeric Pain Intensity Scale. Resonator A  -3.69 , Inactive Resonator -1.97
  • (Oral) Ketotifen  -- <placebo wins -- Change From Baseline in Weekly Average Pain Score-- Ketotifen  Placebo 
  • Eslicarbazepine Acetate -- placebo wins (mostly)

  • pregabalin (Lyrica)

     Proportion of Patient Global Impression Change (PGIC)
    at Week 15  
    [Units: Percentage of participants]
     Pregabalin   Placebo 
    Participants Analyzed  [Units: Participants]  49   44 
    Very much improved   16.3   2.3 
    Much improved   36.7   27.3 
    Minimally improved   22.4   27.3 
    No change   18.4   38.6 
    Minimally worse   6.1   2.3 
    Much worse   0   2.3 
    Very much worse   0   0 
  • Pregabalin  --placebo wins

  • Milnacipran  PARTICIPANTS (1) 30% reduction in pain (2)  "very much improved" and "much improved;" and (3) physical function improvement:--- Milnacipran  Placebo 56 ( out of 516 participants)

  • (Gabapentin ER)Fibromyalgia Impact: amounts to none

  • two AVACEN Widespread Pain After 4 Weeks = 8.9 [ 0 = Lowest pain score (Best Outcome)., 19 = Highest]

  • Duloxetine 60 mg -- placebo wins but Change From Baseline to 14-Week Endpoint in Fibromyalgia Impact Questionnaire :- Duloxetine 60 mg -18.41, Placebo 

  • Xyrem (Sodium Oxybate) 


The percentage of participants who met all 3 of the following criteria:

  • Reduction of >=20% from baseline to week 8 in both PVAS & FIQ total score and PGI-C response of "very much better" or "much better". (PGI-C is a 7 point likert scale measuring change in the participant's fibromyalgia symptoms that ranges from "very much worse" to "very much better" )

  • The PVAS ranges from 0 (no pain) to 100 (worst imaginable pain).

  • The FIQ ranges from 0 (best function) to 100 (worst function).

 Placebo   Xyrem
(Sodium Oxybate) 4.5g 
(Sodium Oxybate) 6.0g 
  Participants Analyzed  [Units: Participants]  66   62   67 
  The Primary Outcome Measure Was a Composite of Changes From Baseline in Three Co-primary Self Report Measures: Pain Visual Analog Scale (PVAS, Electronic Diaries), Fibromyalgia Impact Questionnaire (FIQ), and Patient Global Impression of Change (PGI-C).  [Units: Percentage of Participants]      
  Responders   12.9   29.8   28.1 
  Non - Responders (Reduction was not >=20%)  87.1   70.2   71.9 


Participants Analyzed   [Units: Participants]  106 
Number of Participants With Treatment-Emergent Adverse Events (AEs) and Serious Adverse Events (SAEs)    
All-causality adverse events (AEs)   102 
All-causality SAEs   3 

Change in Pain: -13.1 [0 (no pain) to 100 (worst possible pain)]

  • Duloxetine close to placebo. Duloxetine 2.79, Placebo   3.36 [ 7-point scale where a score of 1 indicates that the patient is “very much improved,” a  4  “no change,” and a 7 “very much worse.”]

  • Pregabalin  Daily pain Pregabalin -1.48, placebo -1.30 [ scores were assessed on an 11-point numerical rating scale  ranging from 0 (no pain) to 10 (worst possible pain).]
    % of Participants “Improved (Very Much Improved, Much Improved, or Minimally Improved)”: Pregabalin 70.0 , placebo 62.1

  • Saizen® (Somatropin) Growth hormone:
    of Participants With Less Than 11 Tender Points at Month 12 - Saizen® 53%, Placebo + Saizen®34%
    -- physical impairment, well-being, missed work, pain, fatigue, rest, stiffness, anxiety, and depression. Score ranges from 0 (best result - very well) to 100 (worst result - awful). Saizen® 52.5, Placebo + Saizen® 64.7

  • Xyrem Number of Participants Reporting Adverse Events   498  out of 560 ( 19 serious)

  • Xyrem

 Percentage of pain VAS responders. Subjects with a >= 30% reduction in pain VAS from baseline to endpoint (week 14) were considered responders; all other subjects were considered non-responders. The pain VAS ranges from 0 (no pain) to 100 (worst imaginable pain).  Placebo   Xyrem (Sodium Oxybate) 4.5g   Xyrem (Sodium Oxybate) 6.0g 
Participants Analyzed  [Units: Participants]  188   195   190 
 a Greater Than or Equal to 30% Reduction in Pain [Units: Percentage of Participants]      
Responder   20.2   35.4   35.3 
Non - Responder  ( no 30% reduction)  79.8   64.6   64.7 
  • Pregabalin   Change  Week 12 in Pain  -20.1  [0 “no pain” to 100 “worst possible pain]
  • Xyrem
   Placebo   Xyrem 4.5g   Xyrem 6.0g 
Participants Analyzed  [Units: Participants]  183   182   183 
% of Participants with a Greater Than or Equal to 30% Reduction in Pain      
Responder   27.3   46.2   39.3 
Non - Responder ( no 30% reduction)  72.7   53.8   60.7 
  • Pregabalin  ( the higher dose, 600mg, scored worse ! )

    Daily pain diary 0(no pain) to 10(worst possible

     Placebo   Pregabalin
    300 mg 
    450 mg 
    600 mg 
    Participants Analyzed  [Units: Participants]  184   184   181   186 
    Change in Pain Score at Endpoint (Up to Week 14)    -0.73     -1.06    -1.29  -0.96
  • Rotigotine  close to placebo
  • Lacosamide  not much better than placebo
  •  Tramadol Hydrochloride + Acetaminophen : Pain from 53.0 day14, to 44.9 day 56 [no pain 0 to "worst possible pain 100]
  • Drug Injectafer : Change in BPI, Pain Interference :- Injectafer  -4.1, Placebo -2.3 [Brief Pain Inventory (BPI) includes front and back body diagrams, 4 pain severity items and 7 pain interference items rated on 0–10 scales (with 0 being the best outcome and 10 being the worst outcome), and a question about percentage of pain relief by analgesics. The Pain Interference Score is calculated by adding the scores for the 7 pain interference questions and then dividing by 7 to give a score out of 10.]
  • Pregabalin  Pain Score for Fibromyalgia Population at Week 6: -3.37, baseline 6.69 [0 (no pain) to 10 (worst possible pain)]
Jan 2018: 13 Trials found for: cfs | Recruiting, Not yet recruiting, Available Studies | "Fatigue"
Jan 2018: 57 Trials found for: cfs | Available, Active, not recruiting, Completed Studies | "Fatigue"
  • RESULTS: Duloxetine po 60-120 mg/day for 12 weeks. Pain Severity Score: Duloxetine: -1.6,    Placebo: -0.8 ---
    Patient Global Impression of Improvement: Duloxetine: 3.2 , Placebo: 3.3
  • RESULTS: Viagra Change in Fatigue Impact Scale at 6 Weeks. Viagra: -32.6 Placebo: -1.5
  • RESULTS: Effect of Carnosine Supplementation on Chronic Fatigue Syndrome Severity. Carnosine -3.8, Placebo: -2.0
Jan 2018: 240 Studies found for: Recruiting, Not yet recruiting, Available Studies | "Fatigue"

Symposium highlights new chronic fatigue syndrome research

" a disease of things that are low" there's a metabolic problem going on.'s a hypometabolic disease ---molecules necessary for energy production... were "very, very low,"

The citric acid cycle is needed to burn glucose, which provides energy. These very low numbers suggest that a patient cannot generate energy or another key molecule used for energy, Adenosine triphosphate (ATP), very well.

"ATP is the gasoline of the body. The molecule allows energy to be consumed in your body," he said, noting it is necessary for movements such as muscle contractions.

Something in ME/CFS patients appears to shut down these necessary processes, he said. It appears that the pathway leading up to the citric acid cycle is somehow shut.

"Scientists have some theories about why the metabolic sequence in a ME/CFS patient might turn off. ....... the switch-off mechanism could be a "danger response." ME/CFS is a metabolic state designed to protect the body during a viral infection, for example, but for some reason it doesn't get turned back on after the infection has gone away.


Fibromyalgia and Male Physiology: Why It's Different A 2008 study published in Neuroimage showed that men have fewer serotonin receptors (brain cells that respond to it) than women. However, the process of reuptake—which is essentially "recycling" so the neurotransmitter can be used again—may be more efficient in men.
Drugs that slow reuptake are commonly prescribed for fibromyalgia. They're called SSRIs (selective serotonin reuptake inhibitors) or SNRIs (serotonin-norepinephrine reuptake inhibitors. Two of the three drugs approved for this condition are SNRIs: Cymbalta (duloxetine) and Savella (milnacipran).
the vagus nerve’s neurotransmitter, how it communicates with the body, is acetylcholine, which is inhibited by various meds regularly prescribed to many of us, including: Benadryl, Xanax and various other psych and stomach meds (Google acetylcholine inhibitors for a full list).
.If you're taking vitamin D, you're probably taking too much.   Two vitamin D capsules a day (at 2000 international units each) adds up to 4000 IU—the daily limit. If you’re taking in any vitamin D at all otherwise (and you almost certainly are), you’re already over the safe dosage.  There’s no solid evidence that taking multi- or any other kind of vitamin is beneficial to your health unless you’re vitamin-deficient.
t’s not uncommon to have a deficiency in it. Studies can’t agree on an exact number, but around 30-40 percent of U.S. adults don’t get enough of the D from their diet and sunlight. Only a few foods contain it at all and those that do, like fatty fish or egg yolks or cheese, may be hard to eat enough of to actually get the benefit. That’s why the U.S. dairy industry started fortifying milk with it. And the trouble with sunlight (which doesn't give you vitamin D, but does trigger your body's production of it) is that it’s harmful to get too much of it. It’s better to cover up and avoid skin cancer than it is to go unprotected in an effort to get enough vitamins. Plus, the darker your skin is, the fewer UVB rays get through to produce vitamin D in the first place.
High doses have the potential to cause nausea, vomiting, constipation, and weakness.  And since too much vitamin D can lead to too much calcium, you can also wind up with kidney stones and abnormal heart rhythms.
Unless you’re getting almost no vitamin D, you’re probably fine. 
Albrecht et al:- "excessive sensory nerve fibers around specialized blood vessel structures located in the palms of the hands,” . “This discovery provides concrete evidence of a fibromyalgia-specific pathology"

Are Peripheral Pain Generators Important in Fibromyalgia and Chronic Widespread Pain?

Fibromyalgia (FM) is a chronic widespread pain syndrome (CWPS) that is generally considered to be the result of a dysfunctional central pain modulating system. It is thought to importantly involve the descending pain inhibitory system.

FM is known to be associated with multimodal hypersensitivity: mechanical, thermal, visual, and auditory. It is associated with a variety of comorbid conditions including

  • irritable bowel syndrome,

  • painful bladder,

  • migraine headache, and

  • temporo-mandibular joint syndrome.

The relationship of the comorbid conditions to FM has not been clear. They can be considered to be the result of hyper-effective ascending central pain transmission resulting from deficient descending pain inhibition, or they can be considered as clinical entities in themselves, whose importance in FM lies in their acting as peripheral pain generators that enhance or initiate central sensitization, thereby contributing to chronic widespread pain.

There may, of course, be some truth in both of these concepts. The presence of peripheral pain generators that lead to central sensitization initiating or maintaining CWPS or FM remains controversial, however. This question is addressed in a masterful study by Albrecht et al. [1], published in this issue.

Albrecht et al. [1] investigated the innervation of arteriolevenule shunts (AVS) that are located deep in the dermis of hypothenar glabrous skin, an area that is often painful in FM patients. The function of these AVS, as the authors note, is to increase or decrease blood flow to glabrous skin as part of the body’s thermoregulatory mechanism.

Under thermal stress conditions, as much as 60% of the cardiac output is distributed to skin, and a high proportion of this is directed to glabrous skin. They hypothesized that FM patients may have a disorder involving the sensory and sympathetic innervation of the arterioles and AVS in glabrous skin, leading to or exacerbating the pain of FM.

They performed an immunofluorescent examination of arteriole and AVS innervation, using immunofluorescent labeling to identify unmyelinated peptidergic C fibers, lightly myelinated peptidergic Ad, and lightly myelinated non-peptidergic Ad fibers. The skin biopsies were double labeled to differentiate C fiber, Ad sensory fibers, and noradrenergic sympathetic fibers. Noradrenergic sympathetic fibers were identified by being positive for neuropeptide Y and negative for calcitonin-gene-related-peptide (CGRP). The relative proportions of sensory and sympathetic nerve innervation of arterioles and AVS and the density of innervation of arterioles and AVS were also measured.

AVS were significantly larger in the FM patients than in the controls. The increased size of the AVS correlated with increased tortuosity to some degree but more significantly to an increase in the innervation of the AVS. The overall innervation area was 4x greater in FM patient AVS than in control subjects AVS.

Peptidergic (CGRPcontaining) C-fiber sensory axons made up the largest component of the increased AVS innervation.

The CGRPcontaining vasodilatory sensory innervation was far greater in proportion to noradrenergic vasoconstrictive sympathetic innervation than the ratio of the two types of innervation was in control subjects.

In summary, the authors found that AVS in palmar glabrous skin of FM patients had increased sympathetic and sensory innervation compared to control subjects, whereas arteriole and venous innervation was normal.

This study suggests, as the authors point out that changes in blood flow and increased thermal sensitivity may each contribute to local palmar pain, a common complaint of FM patients. By so doing, they contribute to peripheral nerve sensitization which gives rise to local (peripheral) pain as well as contributing to central sensitization and central pain.

These findings contribute importantly to our concept of the nature of pain in CWPS or FM. Previous studies in this area showed that lidocaine injections into tender points in the trapezius muscle in FM patients result in decreased local tenderness, and also decreased heat hyperalgesia at points remote from the injection sites, showing that peripheral nociceptive input is important in maintaining central sensitization [2].

Myofascial trigger points were not specifically mentioned as the pain source in the trapezius muscles in that study, but subsequently, in other studies, myofascial trigger points were identified as sources of peripheral nociceptive pain that caused local tenderness [3–6].

The association and reproduction of pain in FM patients produced by stimulating peripheral nociceptive sites is suggestive, but not proof of a cause and effect relationship. It is the reduction in local and widespread pain in FM in response to treatment of the peripheral nociceptive sites that is most convincing in determining that peripheral nociceptive sites play an important role in initiating and maintaining pain [7,8]. It is unlikely that chronic changes in central pain modulation would produce the changes seen in innervation patterns of AVS.

Pain is not a simple sensation, and is rarely the result of a disorder in one system only. It is complex, involving multiple interactions. CWPS and FM cannot be considered to be solely a disorder of central pain modulation, and perhaps not even primarily so. Pain is the outcome of a complex interplay between the central modulation and peripheral pain input. That balance between inhibition and facilitation of incoming pain impulses determines the pain that we experience, as shown when descending pain modulation shifts from inhibition to facilitation following sustained isometric contraction sufficient to cause muscle nociception in FM patients [9]. The work of Albrecht et al. [1] advances our understanding of this interplay with their elegantly done study of AVS in FM patients that emphasizes the importance of peripheral pain generators in determining the clinical expression of pain. source

  • Magnesium: contributes towards normal muscle function, nervous system and the reduction of tiredness & fatigue.
  • L-Glutamine: anabolic support.?
  • Probiotic Max: improves digestive health.?
  • Omega 3 Fish Oil: helps combat inflammation.?
  • Ribose: helps to restore ATP the body’s natural energy source.?
  • Fultium D or Vit D: helps the body absorb calcium.?
  • Folic Acid: helps the body produce and maintain new cells. In particular, red blood cell formation.?
  • Turmeric ?

Multivitamins, vitamin D, calcium and vitamin C, — the most common supplements, — showed no advantage in the prevention of cardiovascular disease, heart attack, stroke or premature death.
The multivitamins included A, B1, B2, B3 (niacin), B6, B9 (folic acid), C, D and E; and ß-carotene; calcium; iron; zinc; magnesium; and selenium.
It's most beneficial to rely on a healthy diet to get your fill of vitamins and minerals," Dr. Jenkins said
From a systematic review of existing data and single randomized control trials published from 2012 to 2017.

Feb 1st 2018 Clinical Trials GcMAF  is a vitamin protein found naturally in the body. It activates the cells responsible for tissue repair and initiating an immune response against infection and inflammation. One Study COMPLETED on  Muscle Pain, Joint Pain  What is GcMAF?