November 7, 2018

Fibromyalgia | Blog Series Part 1

by Nicola Schuler, CNTP, MNT and Dr. Miles Nichols, DAOM, MS, LAc

What is Fibromyalgia?

Fibromyalgia (or FM) is a neurological disorder of the central nervous system. It is a syndrome of chronic pain in the absence of an otherwise apparent disease or cause for the pain. Patients with FM experience pain differently than people without FM.

 

Primary symptoms associated with fibromyalgia:

• Widespread pain throughout the body
• Heightened and painful response to pressure resulting in exaggerated tenderness at specific points
• Debilitating exhaustion
• Joint stiffness
• Sleep Issues
• Unrefreshing sleep
• Cognitive decline (problems with brain fog, memory, concentration, etc.)

People with fibromyalgia (or FM) may also have depression or other psychological difficulties, headaches, and an inability to focus or concentrate. FM is only recently recognized as a disorder. It is considered a major health problem, which affects 1% to 5% of the general population (1). It is more common in women than men. Having FM can be challenging and in some cases can lead to a lower quality of life and high medical costs.

The condition is chronic. At this time, conventional medical treatment is focused on managing the condition and the associated pain. The cause or causes are not clear but fortunately significant advances have been made in understanding FM. Fortunately, functional medicine has some insights to offer for those suffering with FM.

What causes FM?

The precise cause of FM has not been identified at this time. Various factors can contribute to or trigger FM.
Currently, FM is considered to involve the interaction of several factors, including abnormalities in the central nervous system, genetic factors, psychological variables, and environmental factors (1).

It is thought that the symptom of pain in FM is related to central sensitization, which is an explanation for chronic pain of FM (2). Central sensitization refers to blunting of inhibitory pain pathways and alterations in neurotransmitter levels, leading to abnormal processing of sensory signals within the central nervous system, eventually lowering the threshold of pain and amplifying the sensations from normal signals, causing chronic pain (2). The details are not fully understood yet.

As the issue lies with the central processing of pain, we know that it is not in the peripheral body areas where FM patients experience the pain. The mechanisms thought to be involved include the central sensitization of pain, a suppression of the descending pathways that inhibit pain, excessive activity of glial cells, and abnormalities of neurotransmitter release or regulatory proteins or both (2). These mechanisms are probably not mutually exclusive.

In studies, FM patients show decreased connectivity between different parts of the brain. Findings suggest that abnormal connectivity patterns between pain-related regions and the remaining brain reflect an impaired central mechanism of pain modulation in FM (3). Weaker coupling between pain regions and other areas of the brain possibly indicate an inefficient control of pain circuits. The findings show that FM primarily is associated with decreased connectivity between regions of the brain, which could reflect a deficiency in pain regulation (3). Essentially the brain is overly sensitive to pain signals or misinterprets pain signals.

Unfortunately, these conventional understandings of the causes of FM leave a lot to be desired. There is not much that is actionable or straightforward in helping people struggling with FM to do something for themselves. Luckily, functional medicine has some strong links and connections with root causes that can be contributing to FM.

From a functional medicine perspective, inflammation is a key element when looking at most kinds of pain. FM pain is certainly one for which it is important to find root causes for inflammation and reverse them.

Functional Medicine Root Causes for FM:

• Gut issues (we will talk about that more in Part 2 of this article)
• Toxic Burden: mold toxin accumulation, toxic metals, and/or excessive chemical exposure
• Chronic Infections: Lyme disease, chronic bacterial or viral infections, or fungal / yeast overgrowths
• Insulin resistance: blood sugar and insulin issues can contribute to inflammation and pain
• Hormone and/or neurotransmitter imbalances

Finding a skilled functional medicine doctor familiar with these root causes can help to do some lab testing for HLA-DR genetics (associated with mold toxin accumulation), Lyme testing (find a Lyme-literate functional medicine doctor), gut testing like SIBO and comprehensive stool testing, comprehensive hormone blood panel, and a blood sugar panel that includes fasting glucose, HgA1c, and fasting insulin.

*NOTE: we DO NOT recommend urine-based neurotransmitter testing (however we do like urine testing for Organic Acids which can give a sense of neurotransmitter levels). It is not accurate in our opinion and research does not support this kind of testing. There are plasma neurotransmitter tests that are decent tests, but because of limitations in testing, we often use organic acids and/or a questionnaire and symptom picture to get a sense for neurotransmitter status.

Is FM genetic?

The other key factor believed to play a role in FM is genetics. There is an observed inherited component to FM. Studies have been conducted looking for family associations in FM and have found that anywhere from 26% to 52% of family members of a person diagnosed with FM also fit the criteria for a FM diagnosis (1).

Interestingly, the genetic aspect ties in with the issue of malfunctioning pain signaling. Researchers have identified pain-related genes and have found that pain-related genes affect the expression or function of specific proteins which influence the pain response (6). Currently, hundreds of pain-regulated genes related to pain perception or analgesia have been identified. These include the genes encoding voltage-gated sodium-channels (Nav), GTP cyclohydrolase 1 (GCH1), mu-opioid receptors, and catechol-O-methyl transferase (COMT); and various genes of the dopaminergic, glutamatergic, and GABAergic pathways (1).

However, we must keep in mind that genes are not destiny. Epigenetic, or environmental factors, affect how a particular gene or genes is expressed. Therefore, having these genes related to pain signaling is not a guarantee that fibromyalgia will follow. It is the genetic expression of these genes that is most relevant and this can be affected by epigenetic factors.

It is thought that hormone imbalances, particularly involving serotonin, dopamine and norepinephrine, can play a part in FM. Recent research has focused on how genes can trigger changes in gene expression in people with FM. Research has shown that genetic SNP’s, or genetic mutations of specific genes, result in an increased sensitivity to pain. These SNP’s are related to certain hormones which help to regulate pain. In fact, associations between FM and certain genetic mutations affecting the serotonergic, dopaminergic, and catecholaminergic pathways have been found (1). These mutations influence symptom severity as well as susceptibility to FM. However, the genetic factors identified to date do not fully explain the cause of FM (1). FM is considered to result from an interaction between genetic factors and environmental factors.

Please read on to Part 2 of this overview of FM. In Part 2 we cover the gut as a root cause, the triggers and risk factors for FM. Part 3 will cover the specific action steps to take if you have FM.

 

References

1. Park DJ, Lee SS. New insights into the genetics of fibromyalgia. Korean J Intern Med. 2017; 32:984-995.
2. Abeles AM, Pillinger MH, Solitar BM, Abeles M. Narrative Review: The Pathophysiology of Fibromyalgia. Ann Intern Med. 2007; 146:726-734.
3. Flodin P, Martinsen S, Löfgren M, Bileviciute-Ljungar I, Kosek E, Fransson P. Fibromyalgia is associated with decreased connectivity between pain- and sensorimotor brain areas. Brain Connect. 2014; 4:587-94.
4. Cook DB, Lange G, Ciccone DS, Liu WC, Steffener J, Natelson BH. Functional imaging of pain in patients with primary fibromyalgia. J Rheumatol. 2004; 31:364-78.
5. Kwiatek R, Barnden L, Tedman R, Jarrett R, Chew J, Rowe C, et al. Regional cerebral blood flow in fibromyalgia: single-photon-emission computed tomography evidence of reduction in the pontine tegmentum and thalami. Arthritis Rheum. 2000; 43:2823-33.
6. Mogil JS. Pain genetics: past, present and future. Trends Genet 2012; 28:258–266.
7. Wallace DJ, Hallegua DS. Fibromyalgia: the gastrointestinal link. Curr Pain Headache Rep. 2004; 8:364-8.
8. Goebel A, Buhner S, Schedel R, Lochs H, Sprotte G. Altered intestinal permeability in patients with primary fibromyalgia and in patients with complex regional pain syndrome. Rheumatology (Oxford). 2008; 47:1223-7.
9. Carranza-Lira S, Villalobos Hernandez IB. Prevalence of fibromyalgia in premenopausal and postmenopausal women and its relation to climacteric symptoms. Prz Menopauzalny. 2014; 13: 169–173.
10. Holton K. The role of diet in the treatment of fibromyalgia. Pain Management. 2016; 6.
11. Smith JD, Terpening CM, Schmidt SO, Gums JG. Relief of fibromyalgia symptoms following discontinuation of dietary excitotoxins. Ann Pharmacother. 2001; 35:702-6.
12. Lattanzio SM, Imbesi F. Fibromyalgia Syndrome: A Case Report on Controlled Remission of Symptoms by a Dietary Strategy. Front. Med. 2018 | https://doi.org/10.3389/fmed.2018.00094
13. Donaldson MS, Speight N, Loomis S. Fibromyalgia syndrome improved using a mostly raw vegetarian diet: An observational study. BMC Complement Altern Med. 2001; 1: 7.
14. Rodrigo L, Blanco I, Bobes J, and de Serres FJ. Clinical impact of a gluten-free diet on health-related quality of life in seven fibromyalgia syndrome patients with associated celiac disease. BMC Gastroenterol. 2013; 13: 157.
15. Curtis K, Osadchuk A, Katz J. An eight-week yoga intervention is associated with improvements in pain, psychological functioning and mindfulness, and changes in cortisol levels in women with fibromyalgia. J Pain Res. 2011 ;4:189-201.

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