Many people will experience extended periods of fatigue during the course of their lives. Myalgic Encephalomyelitis (ME) and Chronic Fatigue Syndrome (CFS), however, involve more than just chronic tiredness and can strike both children and adults. In order to be diagnosed, a patient must meet all seven strict criteria (fatigue, post-exertional malaise, fatigue or pain, sleep dysfunction, pain, neurological/cognitive problems and two of the following: autonomic manifestations, neuroendocrine manifestations and immune manifestations). It is estimated that 2.5 to 5 per cent of the world’s population is affected, though reporting methods can be inconsistent. Regardless of whether the actual number falls on the low or high end of estimates, it’s still a staggering number of people. The two conditions are often used interchangeably or abbreviated together (ME/CFS), however there are differences between ME and CFS. ME literally means “pain in the muscles and inflammation in the brain and the spinal cord.” For the purposes of this post, I will be exploring the latest research around CFS specifically.
While a 1997 study found no correlation between MTHFR polymorphisms and CFS, a 2012 examination of 88 patients by Dr. Paul Anderson of Anderson Medical Specialty Associates in Seattle found a higher prevalence of these mutations among a group of CFS and fibromyalgia patients than in the normal population, particularly homozygous C677T and compound heterozygous C677T/A1298C defects. Treating these patients with a methylation protocol that included methylfolate, methylcobalamin (B12), folinic acid and a vitamin B complex that contained the active forms resulted in significant increases in positive patient outcomes compared to the standard naturopathic treatment protocol. Thus, testing and evaluation of ME/CFS patients for MTHFR gene mutations is crucial to obtaining the healthiest outcomes. To understand how methylation comes into play in the treatment of ME/CFS, we must look more closely at the condition itself.
The World Health Organization (WHO) classifies ME/CFS as a disease of the central nervous system. It seems, however, to be more complicated than that. Its symptoms are not only neurological but also involve the immune and endocrine systems, and are often triggered by infections, toxin exposure or physical trauma. It is potentially an autoimmune and inflammatory disorder, with patients presenting with “oxidative and nitrosative stress (O&NS), activation of immune-inflammatory pathways and mitochondrial dysfunctions with depleted levels of adenosine triphosphate (ATP) synthesis” and “autoimmune responses” in up to 60 per cent of cases. Patients may have reduced natural killer (NK) cell function and chronic or recurrent infections. Mycotoxins are present in the urine of a very high percentage of patients and low cortisol is also often a feature of the illness. Dr. Anderson identifies the following as primary issues with CFS patients:
– immune dysfunction – chronic infections
– gastrointestinal malabsorption and dysbiosis (and infections)
– mitochondrial disorder/dysfunction leading to poor energy modulation
– detoxification deficits
– sleep disorders
– hormonal dysregulation
As he explains:
Overwhelmingly, CFS has been identified as a symptom of mitochondrial failure. In Dr. Sarah Myhill’s popular handout “CFS – The Central Cause: Mitochondrial Failure,” she explains how mitochondria are the “engines” that power our cells. A lack of adenosine triphosphate (ATP), which is produced by the mitochondria, slows the cells and thus the body’s functions. As the body struggles to make energy it compensates by switching to anaerobic metabolism and makes ATP from glucose by converting it to lactic acid. The lactic acid builds up and causes muscle pain and heaviness in the body, leaving the person glucose deficient. She recommends rest, dietary changes and supplementation, including D-Ribose, CoQ10, Acetyl L-Carnitine, NAD, magnesium and B12 shots. Replacing lost ATP and glutathione are critical.
Referring back to Dr. Anderson’s paper we can see how improving methylation will help reduce the symptoms and improve outcomes for ME/CFS patients. Methylation controls the body’s sulfur metabolism, which is critical for sufferers. Slow methylation prevents the body’s immune and detoxification systems to work adequately, which is important for combatting infections and eliminating toxins. Diminished methylation reduces the synthesis of choline, creatine, carnitine, CoQ10 and some components of myelin. Methylation also determines the rate of glutathione synthesis. Glutathione depletion is endemic in ME/CFS patients.
I have an entire post coming up devoted to glutathione, which is the body’s critical antioxidant. According to ME/CFS expert Richard Van Konynenburg Ph.D., depletion of this ubiquitous tripeptide leads to oxidative stress, mitochondrial dysfunction, toxin buildup, immune dysfunction, herpes virus reactivation, thyroid problems and other dysregulation. People with methylation defects are often deficient in glutathione, which can inflame or cause many different diseases. Improving glutathione levels is vital to the recovery of many chronic illness sufferers, not just those with ME/CFS.
Other nutrients that have been found to be effective in the treatment of ME/CFS are vitamin D, calcium, DHEA, lysine, fish oil and good quality multivitamins. Acupuncture may be helpful in the alleviation of symptoms. ME/CFS patients can find assistance and dialogue with other patients on the Phoenix Rising forums, which focus on the condition. Finding a competent doctor will be crucial in the treatment of ME/CFS, should you suffer from it. And if you cannot tolerate methylated vitamins, don’t despair. As Dr. Anderson explains:
-ASSESS Sn/Sx and SNP’s
-Start LOW and work up
-TREAT the patient not just the SNP’s
-Treat from the OUTSIDE in
-Monitor SIGNS AND SYMPTOMS etc to adjust therapy
To find out more about Dr. Anderson’s seminars for training health professionals, click here.
In addition to MTHFR, a number of other gene polymorphisms (SNPs) have been reported in ME/CFS patients (you may refer to page 13 of this presentation by Dr. Van Konynenburg). In fact, my explanations in this post have been quite simplistic in order to give you merely a general overview of this condition. If you want to learn more I highly recommend watching this ME/CFS presentation by Dr. Van Konynenburg and reading through the two accompanying handouts (the PDF files linked to below the videos) on the web page. Please note that while the website is written in Swedish, be assured that both the video and the handouts are presented in English. Even those with methylation defects who don’t have ME/CFS will learn a lot from this presentation.
As a final note, it is important to be aware that CFS may be the diagnosis, albeit incorrectly, when a doctor really doesn’t know what is wrong with you. In one study, only around 23 per cent of participants were found to have unambiguous CFS. As there are no “markers” for CFS, a thorough doctor will look for other possibilities before settling on this diagnosis. Something to watch out for is chronic Lyme disease masquerading (not so subtly) as CFS. Lyme disease is the subject of another post because it is so prevalent and under-diagnosed these days. As this master symptom list indicates, the symptoms for CFS, fibromyalgia, chronic myofascial pain and chronic Lyme disease are almost identical. As this patient explains, the misdiagnosis often applies to a variety of diseases such as multiple sclerosis (which actually has a lot in common with ME/CFS), lupus and Alzheimer’s. So be sure and do the proper testing and rule out Lyme before you suffer needlessly for longer than you should. An evaluation of spinal fluid can actually tell the difference between CFS and Lyme, demonstrating that the two conditions are actually separate. Whatever your eventual diagnosis, improving methylation will assist with your recovery from all of these illnesses.
Do you suffer from ME or CFS? What are your recommendations?