Our Philosophy

Our patients will occasionally tell us: “My primary care doctor doesn’t believe in fibromyalgia”. We encourage medical professionals who question the veracity of the complaints associated with FM & CFS to read the previously referenced articles documenting the physiological abnormalities associated with FM & CFS. It is impossible to fake HPA dysregulation, elevated muscle NF kappa B and glycation products, impaired brain blood flow, reduced mu-receptors and the genetic mutations that are being linked to these chronic conditions. The initial research with FM focused on psychological and insomnia related aspects of the condition, but this information was misinterpreted by some as proof that FM & CFS are purely psychological diseases. An illustrative point is that psychological stress can induce shingles, but stress is not the cause of shingles. Herpes zoster virus reactivation is the cause of shingles, and increased stress is one way to facilitate its reactivation. Immunosuppression is another way to produce viral reactivation. Stress can lead to compromises in immune function and that can allow opportunistic infections to flourish, but stress is not the underlying cause of the disease. This important distinction should be applied to FM & CFS. We agree with research that implicates infection as the driving force behind FM, CFS & most “autoimmune disease”. Fortunately, there are many ways to counteract the pathophysiology of FM, CFS & autoimmune disease. We will review some of our treatments in the next section. Before we do so, lets briefly discuss the conclusions of the aforementioned articles.

How does one contract FM & CFS?

There are many paths that lead to the tipping point, and once it is reached, it is difficult for most FM & CFS patients to find their way back to normal health. In general, this condition affects hardworking people, frequently the hardest working people. It is often initiated by a flu-like illness after which the person is never quite the same. But it is sometimes an automobile accident or other traumas that trigger the syndrome. A similar and likely related condition is called Reflex Sympathetic Dystrophy (RSD a.k.a. Complex Regional Pain Syndrome). RSD can be triggered by surgery, a fall, anesthesia and many other triggers. RSD thins the bone in the affected limb and it is often so painful that even the wind blowing across the limb is intolerable. FM & CFS patients share some of the features of RSD with an overactive sympathetic nervous system and dramatically increased pain sensitivity. Certainly, people would turn off this sympathetic overdrive if they could, but there is something that makes it persist. We find that it is usually infection driving the hyperactive sympathetic nervous system.

Lets review the research again:

FM appears to have a genetic component (Harris et. al. 2006) It may relate to the genes that code for methylation enzymes (Yasko 2005), and glutathione production (Van Konynenburg 2007), both of which impair immune function and predispose those people to new infections or reactivation of chronic infections. Infections with virus (EBV, CMV, HHV-6) and bacteria (Mycoplasma, Chlamydia pneumonia) have been associated with FM & CFS (Stratton 2000, Nicolson 2000 & 2003, Ablashi 2000). Chronic fungal sinusitis may be an overlooked source of chronic sinus disease (Ponikau et. al. 1999), and 70% of CFS & FM patients complain of chronic rhinosinusitis (Baranuik 1998). Low dose antifungal nasal spray can work wonders for some. When low serum gammaglobulin levels are associated with chronic sinus or respiratory illness, monthly gammaglobulin injections can be very effective (Toffel 2001). Toffel proposes that EBV infected B-cells can produce immunodeficiency that may predispose one to chronic respiratory infection.

Genetic mutations in methylation capacity, as Dr. Yasko suggests, may very well be a predisposing factor to chronic infections. Infections certainly trigger a systemic stress response and chronic stress can facilitate the growth of infections. All of this can create an endless cycle of chronic stress response and opportunistic infection. How does this lead to pain? The myriad of biochemical changes documented by FM & CFS researchers include the following:

1.) FM & CFS patients are in a state that reflects "relentless sympathetic hyperactivity" (Martinez-Lavin 2004),
2.) Elevated spinal CRF (McLean 2006)
3.) Elevated Substance P(Vaerøy 1988)
4.) Elevated inflammatory markers (Bazzichi 2007)
5.) Elevated serum norepinephrine (Torpy 2000)
6.) Reduced brain blood flow (Mountz 1995)
7.) Deranged neurotransmitter synthesis (Russell 1992),
8.) Reduced cognitive function (Glass 2001)
9.) Reduced mitochondrial membrane permeability (Begtsson 1989)
10.) Reduced growth hormone production (Bennett 1998)
11.) Dysregulation of the HPA axis (Demitrack 1998)
12.) Insufficient vitamin D levels are common in FM and lead to greater activation of anxiety and depression (Armstrong 2007)
13.) Mu-receptors are deficient leading to increased pain (Harris 2007)
14.) Abnormal nerve fibers are seen in skin biopsies from FM patients which may also contribute to enhanced pain sensitivity (Kim 2008).

Furthermore, chronic inflammation or infection will reduce the number of Vit D receptors, furthering the shift into hyperactivity in the sympathetic nervous system and deficiency of parasympathetic nervous system function. The above physiological abnormalities are clearly not consistent with a purely psychological condition.

Effective treatment should logically seek to oppose infection, restore mitochondrial function, restore vitamin D levels and other depleted nutrients in a manner that is cognizant of potential methylation problems, improve blood flow to the brain and other organs, lower substance P and normalize immune function. The next section will review treatment options available through the Fibromyalgia Treatment & Learning Center.