Could new form of magnesium help brain fog in ME-CFS?

A new form of magnesium improves cognitive powers in old folks, will it also help the brain fog of FM and ME-CFS? asks Dr Richard Podell.

Might it also improve Fibromyalgia pain?

Cognitive function tends to declines as we age. For most people the decline is modest. This “semi-normal” decline is thought to be due in part to a decrease in the ability of cells to form communication contacts called synapses between one cell and another. A similar defect is seen with Alzheimer’s disease.

Animal studies show that one way to increase the number and function of synapses is to raise the brain’s level of the mineral magnesium. When scientists increase brain magnesium in lab rats, the rats become smarter—thinking more rapidly and accurately than they did before.

BUT, most forms of oral magnesium don’t pass easily from the blood into the brain. An exception is a new form of magnesium developed by a research team from MIT specifically for this purpose. This form is magnesium threonate, which is being developed by Neurocentria, Inc., a pharmaceutical company, under the brand name of MMFS-01.

Neurocentria’s team with collaborating researchers from both the U.S. and China
recently published a very important study. Their results strongly suggest that MMFS-01 can substantially improve cognitive function in aging humans.

Press release from Neurocentria Inc.

MMFS-01 is not yet commercially available. However, a “generic” magnesium threonate is available from the Life Extension Foundation under the brand name of Neuro-mag. Likely other “generics” are or will soon be available.

What is truly remarkable about the MMFS-01 study is that improvement in overall  cognitive function was seen within just six weeks. Improvement continued through 12 weeks, the full length of the study. Subjects treated with placebo did not improve much over-all.

More details for the study: The volunteers were age 50 to 70. All had test score evidence of mild cognitive impairment. Twenty five subjects took MMFS-01 and 26 took placebo. The treatment dose was between 1.5 and 2.0 grams per day in divided doses.

Four different cognitive tests were taken before treatment and again at six and twelve weeks. These tests measured executive function, working memory, attention and a concept called episodic memory.

  • With magnesium threonate executive function significantly improved compared to placebo at 6 and 12 weeks
  • Working memory improved significantly at six weeks but at 12 weeks the placebo group had improved also. So, the difference between the groups at 12 weeks was no longer statistically significant
  • Attention improved in the MMFS-01 group compared to baseline, but this improvement was not statistically better than for those taking placebo
  • Episodic memory improved with MMFS-01 by week 12, but was not significantly
    better than that seen with placebo.
  • When over-all cognitive ability was calculated by combining results from the four
    tests, subjects taking MMFS-01 scored significantly better than subjects taking
    placebo. This was true at week 6 (P=.017) and at week 12 (p=.003).
  • As important–subjects taking MMFS-01 who had the largest increase in red blood cell magnesium levels, were also the subjects most likely to show major cognitive improvement. There were no major side effects.

Separate research suggests that magnesium might also help treat fibromyalgia pain. This might be because magnesium tends to inhibit the activity of NMDA receptors. Activation of NMDA receptors is believed to be one mechanism that creates fibromyalgia pain. A recent open label clinical study from Mayo Clinic found that transdermal magnesium chloride spray taken twice daily for 3 weeks was followed by a reduction in fibromyalgia pain.

Key Questions: Should physicians treating FM or ME-CFS “brain fog” be offering  magnesium threonate as a potential treatment?

The arguments against:

  • We don’t know whether brain fog in fibromyalgia or ME-CFS has any relationship to the cognitive decline that is common with aging.
  • We have only one clinical study to support the beneficial effects of
    magnesium threonate.

The argument for:

  • Brain fog is a major problem for our patients
  • We have no proven treatments
  • For most (but not all patients), side effects from magnesium are minimal—
    mainly diarrhea if we get the dose up too high.

Should patients with FM or ME-CFS try magnesium threonate on their own?

I strongly recommend that all patients work with their doctor. Certain patients should not take extra magnesium, especially those with any degree of kidney dysfunction. Also, it would be useful to obtain a baseline red blood cell magnesium level and to monitor that level as treatment proceeds.

Since MMFS-01 is not available, using Life Extension’s or other generic equivalents
would be appropriate. Of course, ideally, some angel would fund a good controlled study.

But, as usual, that’s not likely to happen anytime soon.

Richard N. Podell, M.D., MPH
Clinical Professor, Department of Family Medicine
Rutgers-Robert Wood Johnson Medical School
Podell2@gmail.com

Rich’ Reviews: New form  of magnesium, from: ME Global Chronicle No. 17 June 2016 p48

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Video: Prof Warren Tate, researcher & parent of child with ME

Video: Life with ME/CFS: Professor Warren Tate Talks About ME/CFS

Prof Warren Tate

Professor Tate has a daughter who suffers from ME/CFS. As an award winning biomedical researcher, and close family member of a sufferer, Warren provides an invaluable perspective on the illness. 22 June 2016

 

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Prof Garth Nicolson’s research: ME & restoring mitochondrial functioning

Prof. Garth Nicolson introduces his research:

We have been involved in research on the role of mitochondrial function in ME/CFS for some time and have found that restoring inner mitochondrial membrane (IMM) trans-membrane potential is essential. When mitochondrial membrane lipids are damaged, the IMM becomes leaky and the membrane potential cannot be sustained, which results in loss of ATP production and increases in fatigue.

Since 2003 we have published several scientific papers that show that ME/CFS and other chronic illness conditions, including chronic infections like Lyme disease, chronic Mycoplasma and other complex infections, cause IMM dysfunction that can be repaired by Membrane Lipid Replacement (MLR) with NTFactor Lipids, resulting in improvements in fatigue, cognition, short-term memory and mood

Membrane Lipid Replacement: clinical studies using a natural medicine approach to restoring membrane function and improving health by GL Nicholson in International Journal of Clinical Medicine, 2016; 7: 133-143.

NTFactor Lipids is an all-natural membrane glycerolphospholipid product (for example, Patented Energy,). This has been reviewed recently in our article in Discoveries 2016

Clinical uses of Membrane Lipid Replacement supplements in restoring membrane function and reducing fatigue in chronic diseases and cancer, by GL Nicholson et al in  Discoveries 2016; 4(1): e54.

There are other potential useful benefits of MLR that we rarely discuss, such as the removal of excess, potentially toxic, cholesterol from cellular stores. (Presumedly similar mechanisms exist for removal of the damaged membrane glycerolphospholipids and their secretion and eventual excretion).

As quoted in an article just published in Lipid Insights by Thomas A. Lagace of the University of Ottawa Heart Institute,

“Phosphatidylcholine plays a critical role in cellular cholesterol sinks that buffer against cholesterol-induced ER stress and assist in the maintenance of cellular cholesterol gradients that drive interorganelle cholesterol transport.”

(Lagace, T.A. Phosphatidylcholine: greasing the cholesterol transport machinery. Lipid Insights 2015; 8(S1): 65-73. doi:10.4137/LPI.S31746).

Phosphatidylcholine is the most prevalent lipid in NTFactor Lipids, and it plays an
essential role in cholesterol transport and its removal at the cellular level and at the organ and systems levels. This may be due to a rather simple concentration gradient mechanism that sequesters cholesterol and oxidized glycerolphospholipids into Lipid Droplets for their eventual removal.

This could explain why our ME/CFS patients have better cholesterol, homocysteine and other blood tests after 6 months on MLR. (Blood homocysteine and fasting insulin levels are reduced and erythrocyte sedimentation rates are increased with a glycophospholipid-vitamin formulation: a retrospective study in older subjects, by Ellithorpe, R.R, Settineri R.,  Ellithorpe, T. and Nicolson, G.L. in Functional Foods in Health and Disease 2015; 5(4): 126-135.)

Eventually the use of MLR may enhance and hopefully replace costly cholesterol reducing
drugs (with side effects) that Big Pharma has been pushing for some time. For years ME/CFS patients have benefited from NTFactor lipid products without adverse reactions or events.

Prof. Emeritus Garth Nicolson, PhD, MD (H)
Department of Molecular Pathology, The Institute for Molecular Medicine

ME & mitochondrial functioning  from ME Global Chronicle No. 17 June 2016 p54

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Gut bacteria spotted eating brain chemicals for the first time

New Scientist article, by Andy Coghlan, 1 July 2016: Gut bacteria spotted eating brain chemicals for the first time:

Bacteria have been discovered in our guts that depend on one of our brain chemicals for survival. These bacteria consume GABA, a molecule crucial for calming the brain, and the fact that they gobble it up could help explain why the gut microbiome seems to affect mood.

Philip Strandwitz and his colleagues at Northeastern University in Boston discovered that they could only grow a species of recently discovered gut bacteria, called KLE1738, if they provide it with GABA molecules. “Nothing made it grow, except GABA,” Strandwitz said while announcing his findings at the annual meeting of the American Society for Microbiology in Boston last month.

GABA acts by inhibiting signals from nerve cells, calming down the activity of the brain, so it’s surprising to learn that a gut bacterium needs it to grow and reproduce. Having abnormally low levels of GABA is linked to depression and mood disorders, and this finding adds to growing evidence that our gut bacteria may affect our brains.

Treating depression

An experiment in 2011 showed that a different type of gut bacteria, called Lactobacillus rhamnosus, can dramatically alter GABA activity in the brains of mice, as well as influencing how they respond to stress. In this study, the researchers found that this effect vanished when they surgically removed the vagus nerve – which links the gut to the brain – suggesting it somehow plays a role in the influence gut bacteria can have on the brain.
Strandwitz is now looking for other gut bacteria that consume or even produce GABA, and he plans to test their effect on the brains and behaviour of animals. Such work may eventually lead to new treatments for mood disorders like depression or anxiety.

“Although research on microbial communities related to psychiatric disorders may never lead to a cure, it could have astonishing relevance to improving patients’ quality of life,” said Domenico Simone of George Washington University in Ashburn, Virginia.

Read more: Psychobiotics: How gut bacteria mess with your mind

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Dysfunctional low affinity antibodies leads to gut & immune problems in ME/CFS

Research abstract:

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a heterogeneous illness characterized by a number of comorbid conditions; gastrointestinal (GI) dysregulation make up one subgroup of this disease.

IgA is the most abundant antibody isotype found in mucosal secretions including the gut. In a process of class switch recombination (CSR), that relies on the interaction of plasmacytoid dendritic cells (pDCs) with B cells, in a T cell independent (TI) manner, low-affinity IgA are produced that limit the adhesion of commensal bacteria to intestinal epithelia without neutralizing them. These low-affinity antibodies also limit bacterial overgrowth and potential bacterial translocation thus maintaining gut homeostasis. This process is known as “immune exclusion”.

Two ligands on the surface of pDCs that are obligatory for the process; the membrane bound form of APRIL and BAFF. The upregulation of APRIL and BAFF on the surface of pDCs is dependent on low-level expression of type I interferon (IFN) which is produced by intestinal stromal cells in response to Toll-like receptor (TLR) engagement.

Previous studies suggest that peripheral pDCs are significantly lower in subjects with ME/CFS when compared to controls and studies conducted by us further suggest these cells likely redistribute from the periphery to the gut. We have observed that, in contrast to controls, gut-associated pDCs in subjects with ME/CFS lack APRIL and BAFF expression.

These data support a model of gut pathology in ME/CFS whereby dysregulated pDCs fail to promote the production of low-affinity IgA through the process of TI activation of B cells, thereby leading to bacterial overgrowth, dysbiosis, bacterial translocation and systemic immune activation.

Failure of gut-associated pDCs to express membrane bound APRIL and BAFF prevents their ability to promote low-affinity IgA expression in ME/CFS by Vincent C Lombardi, Svetlana F Khaiboullina, Kenny L De Meirleir, Tanja Mijatovic and Jan Hulstaert in The Journal of Immunology, May 1, 2016, vol.196 (1 Supplement) 137.4

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Nausea and sickness: non-drug options

MEA blog post, 29 June 2016: Dr Charles Shepherd reports on two non-drug options for nausea and sickness in ME/CFS

New guidance from the Royal College of Obstetricians and Gynaecologists adds further weight to the fact that two non-drug options – ginger and acupressure bands – can be helpful in relieving nausea.

BBC report: Ginger and acupressure ‘options for morning sickness’

These are non-drug options which are also worth considering when nausea occurs in ME/CFS.

However, whilst nausea and sickness can be a symptom of ME/CFS, it is important to exclude other possible medical explanations before doctors or patients conclude that this is ‘just another ME/CFS symptom’.

Medical information on acupressure bands: Sea-bands

More information on ginger (from Cancer Research UK):

Some people find ginger very helpful when feeling sick. People say it is particularly good for motion sickness. You can use ginger any way you like, for example as crystallised stem ginger. Or you can add freshly ground ginger to your favourite dishes, or to hot water or tea to make a soothing drink. You can try sipping ginger ale. Fizzy drinks sometimes help to reduce nausea too.

Researchers have been looking at using ginger alongside anti sickness medicines during chemotherapy. But the results so far have been mixed. So more research is needed.

Drug treatment options for nausea and vomiting. Source: patient information UK

* Cinnarizine, cyclizine, promethazine – these medicines belong to a group of medicines called antihistamines. The exact way that they work is not fully understood. It is thought that antihistamines block histamine 1 (H1) receptors in the area of the brain which creates nausea in response to chemicals in the body. They are thought to work well for nausea caused by a number of conditions including ear problems and motion (travel) sickness.

* Hyoscine – this medicine works by blocking a chemical in the brain called acetylcholine. It is a type of medicine called an antimuscarinic (or anticholinergic). It works well for nausea caused by ear problems and motion sickness.

* Chlorpromazine, haloperidol, perphenazine, prochlorperazine, levomepromazine– these medicines work by blocking a chemical in the brain called dopamine. They are useful for nausea that is caused by some cancers, radiation, and opiate medicines such as morphine and codeine. Prochlorperazine (or brand name Stemetil®) is one of the most used medicines for nausea. It works for many causes of nausea, including vertigo, ear problems and sickness in pregnancy.

* Metoclopramide – this medicine works directly on your gut. It eases the feelings of sickness by helping to empty the stomach and speed up how quickly food moves through the gut. It is often used for people with sickness due to gut problems or migraine. It is not usually used for more than a few days.

* Domperidone – this medicine works on the CTZ (an area of the brain known as the chemoreceptor trigger zone). It also speeds up the emptying of the gut. It is not usually used for more than a few days.

* Dexamethasone – this is a steroid medicine. It is a man-made version of a natural hormone produced by your own body. Dexamethasone has a wide range of actions on many parts of the body. The reason why it reduces nausea isn’t clear.

* Granisetron, ondansetron, and palonosetron – these medicines work by blocking a chemical called serotonin (5-HT) in the gut, and the brain. Serotonin (5-HT) has an action in the gut and the brain to cause nausea. These medicines are useful for controlling nausea and vomiting caused by chemotherapy.

* Aprepitant and fosaprepitant – these are newer medicines and work by blocking a chemical that acts on neurokinin receptors in the body to cause nausea. They are sometimes called neurokinin-1 receptor antagonists. They are usually given to people on a certain type of chemotherapy.

* Nabilone – it is still not clear how this medicine works to control nausea. It is normally prescribed for people who are having chemotherapy.

Medicines for nausea are available as tablets capsules, liquids, suppositories and skin patches. Some are given as injections into the muscle or directly into the vein.

Some of these medicines are also available as tablets that dissolve in the mouth against the gum. They are called buccal tablets. These medicines come in various different brand names.

Dr Charles Shepherd
Hon Medical Adviser, ME Association

 

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Dr Maureen Hanson radio interview about her gut research

Dr Maureen Hanson gives a radio interview about her recently published paper, “Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome“.

Maureen Hanson

It is an interview designed to explain the study to lay people.

WRFI Community Radio interview with Dr Maureen Hanson 28 June 2016

 

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Prof Ron Davis outlines key research needs for ME/CFS

OMF blog post, 1 July 2016: Open Medicine Ron Davis’ response to the NIH Request For Information (RFI): Input for New Research Strategies for ME/CFS.

We would like to share the information that Dr. Ron Davis sent in response to NIH’s Request for Input on new ME/CFS research strategies.

dr-ronald-davis-stanford

We are grateful for the opportunity to provide input to the Trans-National Institutes of Health (NIH) ME/CFS Working Group as they develop strategies to guide NIH’s research efforts and priority setting for research on ME/CFS. Our mission at the Stanford Chronic Fatigue Syndrome Research Center is to discover causes, a molecular diagnosis, and treatment options for ME/CFS. Through our research efforts, collaborations with the ME/CFS research and clinical community, and extensive engagement with patients, we have defined several elements of importance for future ME/CFS research programs.

Complex and multisystemic disease

A key consideration in ME/CFS research efforts is the complex and multisystemic nature of this disease, and we are happy to see the involvement of several NIH institutes in developing this plan. Because the causative factors driving the disease remain unknown, and because work from our team and others has indicated effects on neurology, metabolism, immunity, and more, it will be crucial that calls for proposals allow for open, unbiased, multifaceted, and systematic research.  Broadening the scope of ME/CFS research will create opportunities for engaging researchers in other disciplines.

Similarly, investigating numerous organ systems and biological pathways perturbed in ME/CFS may well reveal informative parallels to other diseases – for example, we and others have observed symptomatic, transcriptomic, and metabolic overlap between ME/CFS and neurodegenerative disorders like Parkinson’s Disease. It is important not to limit research to single organs like the brain, and to integrate results from many different organs and molecular processes so that they can be understood at the systems level. Big data approaches and high-throughput, large-scale molecular profiling should therefore be prioritized. Such efforts hold promise to identify key genes or pathways underlying ME/CFS. Similarly, large-scale in vitro drug screening efforts would help point to a variety of molecules and molecular processes as therapeutic targets.

Molecular etiology of ME/CFS

Understanding the molecular etiology of ME/CFS is another important opportunity. A long-standing belief in the field is that an infectious agent causes the disease, and that the pathogenicity of the as-yet-undiscovered organism is responsible for the severity of the illness.

An equally plausible explanation is that a stressor such as trauma, infection, or genotoxic stress may trigger a series of events that lead to a hypometabolic state. This model is observed in children with congenital mitochondrial disorders, where the phenotype does not present itself until after a serious viral infection. This shift in thinking opens up the possibility that ME/CFS has strong genetic and environmental associations, which may also explain the extensive heterogeneity in its presentation, progression, and recovery across patients.

The search for novel infectious agents should continue, but research efforts should also focus on understanding individual host susceptibility and response to infection. For example, it may not be a particular infectious agent that results in the disease, but rather a particular host state as a function of numerous biological and external factors that governs an individual’s susceptibility.

This perspective mirrors the NIGMS-funded Glue Grant on Inflammation and Host Response to Injury, which used an integrated omics approach to define variable responses to infection and trauma. Characterizing host responses to infection and understanding the mechanisms of the long-term sequelae may reveal insights into ME/CFS that are relevant to numerous other diseases of infectious origin, such as Chronic Lyme Disease and Post-Ebola Syndrome (Mattia et al., 2016). Moreover, such precision medicine approaches would build a more comprehensive understanding of ME/CFS and offer richer opportunities for therapeutic intervention.

Prevalence and landscape
Another major challenge is our lack of understanding of the prevalence and landscape of ME/CFS, which is largely due to the difficulty in diagnosing the disease. The search for precise molecular biomarkers is a great opportunity afforded by this research program, which would be accelerated through multi-omics approaches in large patient cohorts.

Current estimates of the prevalence of ME/CFS vary widely (800,000 to 2.5 million cases in the US) due to varying diagnostic and data collection methods. There is an opportunity here to improve these estimates based on modernized methods and community-defined standards, including criteria specified in the 2015 Institute of Medicine Report, and by considering questionnaire-based responses like the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort in the United Kingdom (Collin et al., 2016).

Novel methods & technologies

Because of these complex scientific challenges, ME/CFS research presents an excellent opportunity for developing and piloting novel methods and technologies in discovering biomarkers, elucidating disease mechanisms, and revealing therapeutic possiblities. The methods we need to understand this complex disease may very well not exist yet.

Engineering and technology development efforts towards highly sensitive, quantitative molecular profiling and/or measuring novel cellular properties, as well as novel computational analyses that integrate multiple datatypes to define disease mechanisms, should be encouraged. Again, it is highly likely that such efforts will prove useful in the study of other diseases, be they infectious, genetic, or complex in origin.

Long term studies
Beyond scientific considerations, we would like to note several programmatic considerations that we believe are key for rapid progress. Long-term studies of patients are absolutely essential. Such a mechanism has proven effective in the NIGMS Glue Grants described above. Moreover, maintaining an open structure in RFAs will allow scientists to develop and refine their hypotheses as research progresses, as appropriate for the unknown/uncertain nature of the field.

Collaboration & data sharing

As highlighted in several places above, the opportunities for collaborative efforts within and beyond the ME/CFS research community to understand and treat this disease are numerous. There are numerous experts spread across the world, each taking their own approaches based on their own expertise. We believe future funding programs should not only encourage, but establish frameworks for highly collaborative data sharing and strategizing that bring together researchers and clinicians.

All data should be made publicly available as early as possible (even before publication), in both raw and accessible formats. This will not only facilitate collaboration (for example by encouraging biocomputing experts to engage with the data) and integrative analyses, but also empower patients to understand more about their disease and what progress is being made. As we have all seen, the ME/CFS patient community is extremely active, engaged, and eager for actionable results.

We thank you once again for the opportunity to provide input on this matter, and look forward to the new strategies for ME/CFS research efforts put forth by this working group.

Yours sincerely,

Ronald W. Davis, Ph.D.
Professor of Biochemistry and Genetics, Stanford University Director, Stanford Chronic Fatigue Syndrome Research Center and Stanford Genome Technology Center Director, Scientific Advisory Board, Open Medicine Foundation[

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Eating difficulties in adolescents with CFS/ME

Research abstract:

BACKGROUND: An estimated 10% of children and adolescents with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) experience eating difficulties; however, little is known about why these difficulties develop, what the impact is or how to manage them.

METHODS: Semi-structured interviews were conducted with adolescents (aged 12-17 years) attending a specialist service who have a primary diagnosis of CFS/ME and experience nausea, abdominal pain and/or eating difficulties. A total of 11 adolescents were interviewed (eight female, mean age: 15 years). Transcripts were analysed thematically using techniques of constant comparison which commenced soon after data collection and informed further interview protocols.

RESULTS: Adolescents perceived their eating difficulties were caused by abdominal symptoms, being too fatigued to eat and changes to their senses of taste and smell. Some of the adolescents recognised how their eating difficulties were exacerbated and maintained by psychological factors of low mood and anxiety. The adolescents eating difficulties had a negative impact on their weight, fatigue, socialising and family life. They perceived helpful interventions to include modifying their diets, families adjusting and also medical interventions (e.g. medication). Adolescents identified that early education and support about diet and eating habits would have been helpful.

CONCLUSIONS: If adolescents diagnosed with CFS/ME develop eating difficulties, this has a significant impact on their quality of life, illness and on their families. Not eating increases fatigue, low mood and anxiety which further exacerbates the eating difficulties. Clinicians should screen for eating difficulties in those with symptoms of nausea and abdominal pain, warn adolescents and their families of the risk of developing eating difficulties and provide interventions and support as early as possible.

Source: Harris S, Gilbert M, Beasant L, Linney C, Broughton J, Crawley E. A qualitative investigation of eating difficulties in adolescents with chronic fatigue syndrome/myalgic encephalomyelitis, by Sarah Harris, Matthew Gilbert, Lucy Beasant, Catherine Linney, Jessica Broughton and Esther Crawley in Clin Child Psychol Psychiatry. 2016 May 23. [Epub ahead of print]

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The crucial role CoQ10 plays in FM & ME/CFS

Prohealth blog post by Karen Lee Richards, 27 June 2016: The crucial role CoQ10 plays in Fibromyalgia and ME/CFS

No two fibromyalgia or ME/CFS patients are exactly alike. Each has a unique set of symptoms with varying degrees of severity. There is, however, one common denominator for the vast majority – a serious, sometimes even profound, lack of energy.

What could possibly cause that kind of fatigue?

Multiple studies have suggested that mitochondrial dysfunction may play a significant role in both fibromyalgia and ME/CFS, which would explain much of the energy deficit experienced by patients.

Mitochondria are the engines – or energy producers – that power every cell in the body. It is the job of the mitochondria to take in nutrients, break them down and use them to create energy for the cells. The more energy a cell needs, the more mitochondria it contains. Cells that require a lot of energy – like the heart, brain and other vital organs – may have thousands of mitochondria.

How do the mitochondria produce energy? This is where CoQ10 (coenzyme Q10) comes in. CoQ10 is the catalyst that makes it possible for the mitochondria to produce ATP (adenosine triphosphate), the molecule upon which all cellular functions in the body depend. In fact, 95% of all cellular energy production depends on CoQ10.

Given that statistic, it’s not surprising to learn that, according to several different studies, people with FM and/or ME/CFS generally have very low levels of CoQ10. As we, therefore, might expect, many of the symptoms of a CoQ10 deficiency are remarkably similar to symptoms of FM and ME/CFS, such as:
• Fatigue
• Pain
• Headaches
• Exercise intolerance • Generalized weakness
• Memory loss
• Difficulty concentrating
• Depression
• Vision problems
• Seizures
• Heart failure

Because CoQ10 is essential to every cell in the body, a severe CoQ10 deficiency can cause mitochondrial dysfunction, which in turn has a serious negative impact on multiple organs and body systems.

Fibromyalgia and CoQ10

Since 2009, a team of Spanish researchers has led the way in conducting studies that link CoQ10, mitochondrial dysfunction and fibromyalgia. They have consistently found that FM patients are deficient in CoQ10 – often with a 40-50% reduction in CoQ10 levels compared to healthy controls.

Following are some of their significant findings:

  • The distribution of CoQ10 in the blood was altered in FM patients.(1)
  • A CoQ10 deficiency alters mitochondrial function, leading to increased oxidative stress in FM.(2)
  • FM patients tested had low CoQ10 levels; after supplementation, both CoQ10 levels and symptoms improved.(3)
  • Results suggest a role for mitochondrial dysfunction and oxidative stress in the headache symptoms associated with FM; oral CoQ10 supplementation restored biochemical parameters and induced a significant improvement in clinical and headache symptoms.(4)
  • This study suggests that mitochondrial dysfunction may be driving an inflammatory process in FM; oral supplementation restored biochemical parameters and induced a significant improvement in clinical symptoms.(5)
  • FM patients had a CoQ10 deficiency, mitochondrial dysfunction and increased expression of a particular inflammasome (an immune system sensor that can induce inflammation); oral supplementation reduced the inflammasome activation.(6)
  • FM patients had low levels of both CoQ10 and serotonin; following CoQ10 supplementation, CoQ10 and serotonin levels were restored and symptoms of depression were measurably improved.(7)

Many well-known FM/ME/CFS physicians, like Dr. Mark Pellegrino, Dr. Charles Lapp and Dr. Jacob Teitelbaum, have been recommending CoQ10 for their patients for years. In fact, CoQ10 is one nutritional supplement that is almost universally endorsed by traditional and alternative FM/ME/CFS practitioners alike.

ME/CFS and CoQ10

As with fibromyalgia, ME/CFS patients have also been found to be deficient in CoQ10. In a 2009 study, plasma CoQ10 was analyzed in 58 ME/CFS patients and 22 normal controls. Researchers found that CoQ10 levels were significantly lower in the ME/CFS patients than in the normal controls. Additionally, they demonstrated a relationship between low CoQ10 levels and increased fatigue, autonomic and neurocognitive symptoms. The researchers went on to note that low CoQ10 levels are a predictor of chronic heart failure and may explain the early mortality rates of ME/CFS patients due to heart failure.(8)

A 2016 article in the journal BioFactors reported on two studies using oral ubiquinol-10 (an advanced form of CoQ10) supplementation on ME/CFS patients. The first was an open label trial with 20 patients and the second a double-blinded, placebo controlled trial with 43 ME/CFS patients. Both trials found that ubiquinol-10 supplementation was effective in improving autonomic nervous function and cognitive function in ME/CFS.(9)

In her paper, “Chronic Fatigue Syndrome and Mitochondrial Dysfunction,” Dr. Sarah Myhill, MD, a UK-based ME/CFS researcher and clinician, makes the case that ME/CFS is actually a symptom of mitochondrial failure.(10) Dr. Myhill recommends that ME/CFS patients have their CoQ10 levels checked and begin taking CoQ10 supplements if they are low. She also notes that CoQ10 will work best in conjunction with acetyl L-carnitine, magnesium, D-ribose and Vitamin B3 (niacinamide).(11)

Medications That Deplete CoQ10

There are numerous prescription and over-the-counter medications that can deplete the body of CoQ10. Unfortunately several of them are frequently prescribed for FM and ME/CFS, including many antidepressants, anticonvulsants and analgesic/anti-inflammatory medications.

Statins, prescribed for lowering cholesterol, are particularly notorious for hindering the body’s production of CoQ10. More and more doctors are strongly recommending CoQ10 for their patients who are taking statins.

All CoQ10 Is Not Created Equal

The form of CoQ10 found in most supplements is called ubiquinone. In order to produce cellular energy, the body must convert the ubiquinone to ubiquinol. It is the ubiquinol that carries electrons through the mitochondria and produces energy.

Young healthy people (under 25) can easily convert CoQ10 to ubiquinol. But as we age or when we have a chronic illnesses, our ability to convert CoQ10 to ubiquinol diminishes. Therefore, it is particularly important for people with FM or ME/CFS to take the ubiquinol form of CoQ10 so they’re not expending precious energy converting ubiquinone to its usable form.

A 2007 study compared how well humans absorbed ubiquinone and ubiquinol. The results showed that it takes eight times as much ubiquinone to equal the blood plasma concentrations of ubiquinol. More specifically, 150 mg. of ubiquinol was equal to 1200 mg. of standard CoQ10.(12)

Additionally, in an unpublished study with aged rats, blood concentrations were sustained longer with ubiquinol. After eight hours, the concentration of ubiquinol CoQ10 was 3.75 times greater than standard CoQ10.(13)

How to Take Ubiquinol CoQ10

The suggested dosage of Ubiquinol CoQ10 for FM and ME/CFS patients varies, but most experts start at around 150-200 mg./day. One FM/ME/CFS physician told me that many of his patients take 600 mg. or more each day. Check with your physician to determine the best starting dosage for you.

It’s important to note that Ubiquinol CoQ10 is not a quick fix that will give you an immediate energy boost. Each individual is different, but it generally takes two to three weeks to restore optimal CoQ10 levels in blood plasma and tissues. You may, however, begin to notice a difference as your plasma levels start to increase around the fifth day. If you don’t notice any difference after three weeks, you may want to discuss increasing the dosage with your doctor.

References

More info: Ubiquinol-10 supplementation improves autonomic nervous function and cognitive function in chronic fatigue syndrome by S. Fukuda et al., 10 May 2016

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