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FMS Scientific Studies & Latest Research

Treatment of Hypothalamic-Pituitary-Adrenal Axis Dysfunction in Patients with Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM)

Points addressed:

  • A review of the literature regarding evidence of significant hypothalamic-pituitary-adrenal axis (HPA) dysfunction in CFS andFM.
  • Indications and efficacy of treatment with physiological doses of cortisol
  • Expected risks and benefits of such treatment

Abstract:

There is clear evidence that adrenal axis dysfunction is present in patients with chronic fatigue syndrome (CFS) and fibromyalgia (FM) 1-21,23-28 and that treatment with low physiologic doses of cortisol have been shown to be safe, appropriate and effective.8,9,10,23,30 It should be considered the standard of care to treat patients with CFS and FM who have baseline cortisol levels under 12 ug/ml.8,9,10,31,32,33

COMMENTARY: DIFFERENTIAL DIAGNOSIS OFFIBROMYALGIA SYNDROME: PROPOSAL OF A MODEL AND ALGORITHM FOR PATIENTS PRESENTING WITH THEPRIMARY SYMPTOM OF CHRONIC WIDESPREAD PAIN

By: Michael J. Schneider, DC, PhD,a David M. Brady, ND, DC,b and Stephen M. Perle, DC, MSc


Fibromyalgia syndrome (FMS) remains an elusive condition of unknown etiology, in which patients report chronic widespread pain (allodynia or hyperalgesia) and a variety of other complaints including fatigue, sleep disorders, cognitive deficit, irritable bowel and bladder syndrome, headache, Raynaud’s syndrome, bruxism, atypical patterns of sensory dysethesia, and other symptoms. Despite the name of the condition, fibromyoalgia, there are no data to support the hypothesis that FMS is a distinct pathologic disorder of the soft tissues. More recent data tend to support the notion that FMS is a disorder of the central nervous system pain processing pathways and not some type of primary auto-immune disorder of the peripheral tissues. It is quite possible that the term FMS is a poor choice of words, for it implies that patients with a variable symptom complex all have the same singular disease or disorder. The diagnosis of FMS has been burdened by a controversial and problematic history since its inception in 1990, with a disturbing trend toward overdiagnosis in recent years. A recent study provided some evidence of the seriousness of improper FMS diagnosis, when a cohort of patients referred to a specialty rheumatology clinic with a tentative diagnosis of FMS were prospectively followed and the FMS diagnosis could only be confirmed in 34% of these patients.1

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Fibromyalgia syndrome (FMS) is a relatively new diagnostic entity that surfaced in the rheumatology literature in the late 20th century. Certain patients  experienced widespread aches and pains not confined to any specific muscle or joint. At first it was assumed that these patients had early signs of rheumatoid arthritis, lupus, ankylosing spondylitis, or some other systemic arthritic processes. However, for this particular type of patient, serum laboratory testing, such as sedimentation rate, HBLA, and rheumatoid factor, showed negative results. Rheumatologists began to talk among themselves about this interesting type of patient who appeared to have a musculoskeletal disorder but, at the same time, did not have any physical examination or laboratory findings suggestive of any specific diagnosis. The only positive physical finding was a characteristic lowered pain threshold over various soft tissues on digital pressure, which were termed tender points (TePs). There was also the curious finding that most of these patients also had an associated sleep disorder that seemed to correlate with the number of TePs.1,2 In 1989, a rheumatology consensus conference was held in Minneapolis, at which time this issue was discussed in great detail. This meeting resulted in publication the following year of what has become known as the 1990 American College of Rheumatology (ACR) criteria for the classification of fibromyalgia syndrome.3 Essentially, this was the birth of FMS as a new medical term. Although the 1990 ACR criteria were meant to be merely “classification criteria” for research purposes, they quickly filled the void and became used as “diagnostic criteria” by physicians eager to have some established criteria for making the diagnosis of FMS. Essentially, the ACR standard consists of just 2 criteria: (1) chronic, widespread pain (pain that is present on both sides of the body, above and below the waist, and in the axial skeleton) that has been present for more than 3 months, and (2) pain elicited by palpation of TePs. The presence of
“pain” was determined by use of an algometer during digital examination, when less than 4 kg of pressure over a TePevoked a painful response. For a diagnosis of FMS, the required finding was pain induced on palpation of a minimum of 11 of 18 predetermined TeP sites.

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By: Alan C. Logan, ND, FRSH

Fibromyalgia (FM) is a rheumatic disorder characterized by chronic widespread musculoskeletal pain and tenderness in the absence of well-defined  musculoskeletal or rheumatic disease. The finding of tenderness in 11 of 18 specified soft-tissue points on digital palpation confirms this diagnosis. In addition to  pain and tenderness, patients often present with fatigue, insomnia, cognitive difficulty, and gastrointestinal complaints (Goldenberg, 1999). FM patients present with a wide range of symptom fluctuations and high levels of comorbidity and are met clinically with an absence of curative interventions (Friedberg & Jason, 2001).
FM is a commonly diagnosed rheumatic condition that affects more women than men. The prevalence of FM is approximately 3,400 women and 500 men per  100,000; in women, the prevalence increases with age to more than 7% between the ages of 60 and 79 (Wolfe, Ross, Anderson, Russell, & Hebert, 1995). Although considerable international investigation has been devoted to understanding FM, no single etiologic factor has yet been identified.

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Bacterial overgrowth and yeast infections are thought to be one of the triggers that cause fibromyalgia and chronic fatigue syndrome.   As the standard American diets (SAD) have grown increasingly focused on processed foods, sugars and refined grains, and our environment is full of chemicals and pollution, this has led to a substantial increase in harmful bacteria in the intestinal tract for many of us. 

By: Alan H. Pressman, DC

Note: The information on this website is not a substitute for the advice of & treatment by a qualified professional.

Alan H. Pressman, MS, DC, DACBN, CCSP, is past president of the Council on Nutrition of the American Chiropractic Association; former chairman, department of nutrition, New York Chiropractic College, and, associate professor of biology, University of Bridgeport, Connecticut.  He is currently the director of research, Institute of Rehabilitative Nutrition, and maintains an active practice in New York City.

In a recent paper published in the journal Seminars in Arthritis and Rheumatism, rheumatologists Bland and Cooper reviewed the possible reversibility of degenerative joint disease.1 In this article they propose that the degeneration of hyaline cartilage occurs as a consequence of activation of monocytes, macrophages and neutrophils which re lease oxidants that in turn attack connective tissue and the joint lubricant substance hyaluronic acid. The activation of white cells that in turn release alarm substances and oxidants occurs as a consequence of an inflammatory cascade modulated through receptor sites on the surface of white cells which are stimulated by the presence of foreign molecules. These foreign molecules have been termed metabolic toxins and are from exogenous and endogenous sources.

Lifestyle Recommendations:

1. Avoid stress and extra obligations.

2. Work with your doctor on a balanced exercise program that includes wearing a pedometer to ensure that you collect steps and move more, putting in high intensity short bursts (20-60 seconds) of activity during the day to enhance growth hormone release and engaging in resistance training that works all major muscle groups (work each group at least 2 times a week).

3. Avoid corticosteroids and NSAIDS (if possible)

4. Avoid alcohol consumption and caffeine.

 

Studies show that poor cellular energy production due to poisoning of the energy-producing machinery of the cell (the mitochondria) is a common characteristic in both fibromyalgia and chronic fatigue syndrome.  In studies at the Abington Memorial Hospital in Pennsylvania, rheumatology researchers found that fibromyalgia patients suffer from a condition that could be described loosely as “muscle toxicity”, in which structures called mitochondria within muscle cells were inefficient in their production of energy.  In addition, fibromyalgia sufferers were found to have smaller than normal muscle fibers that exhibited misshapen mitochondria that were not found in normal subjects.

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