Epigenetics and Fibro

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http://fibromyalgianewstoday.com/20...ic-widespread-joint-pain-fibromyalgia-symptom

“For too long, people with fibromyalgia have struggled to get a diagnosis for their painful symptoms. This research will help pave the way for better understanding, management and treatment of joint pain,” Simpson said.

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Int J Behav Med. 2016 Oct 18. [Epub ahead of print]
Classifying Fibromyalgia Syndrome as a Mental Disorder?-An Ambulatory Assessment Study.
Klaus K1, Fischer S2, Doerr JM2, Nater UM2, Mewes R3.
Author information

Abstract
PURPOSE:
Fibromyalgia syndrome (FMS) is associated with psychological distress. The recent revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) raises the question of whether FMS is classifiable as "somatic symptom disorder" (SSD) and consequently as a mental disorder. To address this, the present ambulatory assessment study focuses on the everyday life occurrence of SSD symptoms in FMS and their predictive value concerning severity indicators of widespread pain.

METHOD:
Ambulatory data were assessed six times daily on 14 consecutive days via iPod. Twenty-eight women suffering from FMS indicated symptoms associated with SSD (somatic illness beliefs, health anxiety, time/energy devoted to pain, or health concerns) and momentary pain levels. Questionnaires regarding potential covariates (such as somatization, depression, health status) were completed at two additional sessions in the research laboratory.

RESULTS:
On average, SSD symptoms occurred three to four times daily and were mild to moderate in severity. Furthermore, these symptoms were both concurrently and prospectively associated with momentary pain intensity and subjective impairment by pain. Twenty percent of the variance in pain intensity and 28 % of the variance in subjective impairment were explained by momentary variables (SSD symptoms and intake of pain medication). Eighty-two percent of persons with FMS fulfilled the psychological SSD criterion when considering everyday occurring symptoms with at least mild severity.

CONCLUSION:
FMS might be diagnosed as a mental disorder according to DSM-5 in many cases. SSD symptoms proved to have predictive value for FMS severity and may thus have clinical relevance for diagnostic, prognostic, and intervention purposes.
 
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We should start a poll.

Who thinks that Fibromyalgia is?

1. A central pain syndrome, to which one can be genetically predisposed.

2. A form of mental illness that can be prevented through intervention during early childhood.

3. Should be managed by Rheum/Psyche until we have a better understanding of the pathophys :laugh:.
 
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Before the poll starts prospective voters - this isn't a democracy:) - must read Andrew Scull's Hysteria: the disturbing history. As well
some information on pain catastrophizing and the Big 5 personality traits, specifically neuroticism. Once you do you will realize that
elevated pain catastrophizing explains the variation in 'Fibromyalgianess' better than any other construct. Once you accept that then
you have to ask yourself, what really is catastrophizing. Here you'll have to jump from the psychology literature to the sociology literature
on personality traits. Pain catastrophizing is simply an extreme form of the neurotic personality trait. Most of the literature on 'traits'
suggests that the genetic contribution is 40% and the environmental 60%. This strong environmental contribution explains the
strong familial clustering of FMS. It also explains the 'epidemic' of hysteria described by Scull, and the current 'epidemic' of pain in
the US. Chronic pain/neuroticism is a coping style that travels in FMS families like a contagion, very much like adolescent suicide.

Eventually, you come to the realization that the extreme forms of CNP are so hard to treat because they are a stable personality
trait that was formed early in life
. Viewing it from the lens of 'trait' explains the extreme difficulty in finding useful
treatments by the time they meet us. Being so hard to treat I think it's reasonable to suggest that the answer lies in prevention.
There's the rub, prevention of a 'trait', adding grit or resilience, needs to come early and from someone without the 'trait'
modeling the resilient behavior.

http://journals.lww.com/clinicalpai...n_Related_Catastrophizing__What_Is_It_.9.aspx
 
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Semin Arthritis Rheum. 2015 Oct;45(2):214-9. doi: 10.1016/j.semarthrit.2015.03.003. Epub 2015 Mar 19.
Small fiber neuropathy in women with fibromyalgia. An in vivo assessment using corneal confocal bio-microscopy.
Ramírez M1, Martínez-Martínez LA2, Hernández-Quintela E1, Velazco-Casapía J1, Vargas A2, Martínez-Lavín M3.
Author information

Abstract
OBJECTIVE:
A consistent line of investigation suggests that fibromyalgia is a neuropathic pain syndrome. This outlook has been recently reinforced by several controlled studies that describe decreased small nerve fiber density in skin biopsies of patients with fibromyalgia. The cornea receives the densest small fiber innervation of the body. Corneal confocal bio-microscopy is a new noninvasive method to evaluate small nerve fiber morphology. Our objective was to assess corneal small nerve fiber morphology in patients with fibromyalgia, and to associate corneal nerve microscopic features with neuropathic pain descriptors and other fibromyalgia symptoms.

METHODS:
We studied 17 female patients with fibromyalgia and 17 age-matched healthy control subjects. All the participants completed different questionnaires regarding the symptoms of fibromyalgia, including a neuropathic pain survey. A central corneal thickness scan was obtained with a confocal microscope. Nerve measurements were made by a single ophthalmologist without knowledge of the clinical diagnosis. Stromal nerve thickness was defined as the mean value between the widest and the narrowest portion of each analyzed stromal nerve. Corneal sub-basal plexus nerve density was also assessed.

RESULTS:
Patients with fibromyalgia had stromal nerve thickness of 5.0 ± 1.0 µm (mean ± standard deviation) significantly different from that of control's values (6.1 ± 1.3) p = 0.01. Patients also had decreased sub-basal plexus nerve density per square millimeter (85 ± 29) vs. 107 ± 26 of controls p = 0.02. When controls and patients were grouped together, there was an association between stromal nerve slenderness and neuropathic pain descriptors (Fisher's exact test p = 0.007).

CONCLUSION:
Women suffering from fibromyalgia have thinner corneal stromal nerves and diminished sub-basal plexus nerve density when compared to healthy controls. Nerve scarcity is associated with neuropathic pain descriptors. Small fiber neuropathy may play a role in the pathogenesis of fibromyalgia pain. Corneal confocal microscopy could become a useful test in the study of patients with fibromyalgia.
 
Reply
Letter To Editor:
Oaklander makes several points in her response to my commentary that deserve comment. About the only issue we seem to agree on is that reduced intraepidermal nerve fiber density (IENFD) is seen in many individuals with fibromyalgia. A large portion of my original commentary was congratulating Doppler et al. on their findings that the morphologic changes noted in the small nerves in individuals with fibromyalgia were quite different from those with classic small-fiber neuropathy (SFN).2 Their study suggested that there may be (at least) 2 subsets of small-fiber changes—one that may lead to pain in the classic distal distribution of neuropathic pain (and thus perhaps appropriately labeled SFN) and another set of changes that might be seen in many different conditions such as fibromyalgia.3 My commentary suggested that there is no evidence that these latter changes in small-fiber density and morphology are responsible for any of the symptoms seen in fibromyalgia—and that for now, these changes should be considered an epiphenomenon rather than causal. Finally, I noted that these changes have been found in many chronic pain conditions, and even more conditions not typically associated with pain. In fact, in the few months since I wrote the commentary, more abstracts and articles have been published noting these findings in even more disorders including Prurigo nodularis, Parkinson disease, and Charcot-Marie-Tooth disease—again pointing to the nonspecific nature of these findings.4,8,13 In contrast, Oaklander seems to believe that anytime reduced IENFDis seen in an individual,this is responsible for pain and other symptoms. This view is at odds with all of the nonpain conditions in which reduced IENFD has been noted, and this would be a nearly unprecedented finding in the pain field,because there is virtually no identifiable peripheral pathology that always causes pain. This is especially true for other types of neuropathies, in which many or most individuals experience decreased sensation and hypoesthesia—rather than pain and hyperalgesia.6 The biggest problem I have with the premise behind Oaklander’s letter is that she is dismissive of decades of work strongly pointing to a central nervous system (CNS) pathology in fibromyalgia. She refers to this as a “disruptive discovery,” and cites an article11 from Scientific American (SA) Mind to back up her claim that reduced IENFD is “the first pathology confirmed for FMS.” I would note that another article in SA published in the same year was entitled “Fibromyalgia: Maligned, Misunderstood and (Finally) Treatable—Research suggests it’s a disease of the central nervous system.”10 Rather than using SA news articles as evidence, I would prefer to use the hundreds of peer-reviewed data-driven articles in higher-impact journals that strongly suggest that the CNS plays a prominent role in the pathophysiology of fibromyalgia.1 There are now scores of evidence-based drug and nondrug treatments for fibromyalgia, nearly all of which are believed to work in the CNS.1 Furthermore, the mechanistic studies to date linking reduced IENFD to chronic pain states have all been cross-sectional and canonly demonstrate association.In contrast, there are many longitudinal studies on fibromyalgia identifying a variety of structural, functional, and chemical changes in the CNS in fibromyalgia that, when targeted by therapies acting on the CNS,show corresponding improvements in symptoms when these findings normalize with therapy.5,7,9,12 Only such longitudinal studies can establish causation. Oaklander ends with the statement: “Disease definitions require regular updates to incorporate new discoveries. This benefits not only the patients but also the clinicians and scientists.” So perhaps we have identified another point of agreement between us. The definition of SFN and the meaning of reduced IENFD need to beseriously rethought in light of emerging evidence that these are nonspecific findings noted in many disparate clinical settings. Science may eventually demonstrate that reduced IENFD is capable of leading to symptoms and should thus be considered an appropriate therapeutic target. But, we are not there yet. Until then, we all should be mindful that there have been many false promises of peripheral pathology in the pain field—and we owe it to our patients to exercise caution before overinterpreting the meaning of these findings.

Conflict of interest statement
The author has no conflicts of interest to declare.
References [1] Clauw DJ. Fibromyalgia: a clinical review. JAMA 2014;311:1547–55. [2] Clauw DJ. Whatisthe meaning of“small fiber neuropathy”in fibromyalgia? PAIN 2015;156:2115–6. [3] Doppler K, Rittner HL, Deckart M, Sommer C. Reduced dermal nerve fiber diameter in skin biopsies of patients with fibromyalgia. PAIN 2015;156: 2319–25. [4] Doppler K, Volkmann J, Sommer C. Skin biopsies in the differential diagnosis of parkinsonism: are we ready for simplified protocols? Brain 2016;139(pt 1):e5. [5] Foerster BR, Nascimento TD, DeBoer M, Bender MA, Rice IC, Truong DQ, Bikson M, Clauw DJ, Zubieta JK, Harris RE, DaSilva AF. Excitatory and inhibitory brain metabolites as targets of motor cortex transcranial direct current stimulation therapy and predictors of its efficacy in fibromyalgia. Arthritis Rheumatol 2015;67:576–81. [6] Gandhi RA, Selvarajah D. Understanding and treating painful diabetic neuropathy: time for a paradigm shift. Diabet Med 2015;32: 771–7. [7] Harris RE, Napadow V, Huggins JP, Pauer L, Kim J, Hampson J, Sundgren PC, Foerster B, Petrou M, Schmidt-Wilcke T, Clauw DJ. Pregabalin rectifies aberrant brain chemistry, connectivity, and functional response in chronic pain patients. Anesthesiology 2013; 119:1453–64. [8] Manganelli F, Nolano M, Pisciotta C, Provitera V, Fabrizi GM, Cavallaro T, Stancanelli A, Caporaso G, Shy ME, Santoro L. Charcot-Marie-Tooth disease: new insights from skin biopsy. Neurology 2015;85:1202–8. [9] Schmidt-Wilcke T, Ichesco E, Hampson JP, Kairys A, Peltier S, Harte S, Clauw DJ, Harris RE. Resting state connectivity correlates with drug and placebo response in fibromyalgia patients. Neuroimage Clin 2014;6: 252–61. [10] Stetka B. Fibromyalgia: maligned, misunderstood and (finally) treatable: research suggests it’s a disease of the central nervous system. Sci Am 2014.Availableat:http://www.scientificamerican.com/article/fibromyalgiamaligned-misunderstood-and-finally-treatable/. [11] Sutherland S. An unnerving enigma: new clues to fibromyalgia’s origins could crack the case of chronic pain. Sci Am Mind 2014;25: 54–9. [12] Tracey I. “Seeing” how our drugs work brings translational added value. Anesthesiology 2013;119:1247–8. [13] Zeidler C, Stander S. The pathogenesis of Prurigo nodularis—“SuperItch” in exploration. Eur J Pain 2016;20:37–40.
Daniel Clauw Department of Anesthesiology, University of Michigan, Ann Arbor, MI, USA E-mail address: [email protected] (D. Clauw) http://dx.doi.org/10.1097/j.pain.0000000000000525
 
Until then, we all should be mindful that there have been many false promises of peripheral pathology in the pain field—and we owe it to our patients to exercise caution before overinterpreting the meaning of these findings.

Historically, it is irrefutable that much, much more harm has been done to patients by misattributing real neurological disease as psychiatric in etiology. Science-based physicians should err on the side of biophysics/medical model of disease and not psuedo-science psychology.
 
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You might consider reading the actual papers and historical references, not just the abstracts prior to making pronouncements. Erring on the side of the biomedical model - the periphery - 'medicalizes' FMS for profit just as Charcot medicalized Hysteria for profit. Had Wolfe et al known about the history of hysteria > neurasthenia > neurosis in 1990 he likely would not have coined the term "Fibromyalgia" that he has since so very publicly distanced himself from.

There is an obvious financial bias at play when pain management opts to view FMS as a primarily biological event. Medicalizing subjective complaints is a great - albeit unethical and often mysogynistic - business model.

"Doppler and colleagues recently assessed dermal unmyelinated nerve fiber diameter of skin
biopsies of the distal and proximal leg and index finger in patients with fibromyalgia and patients with
non-diabetic small fiber neuropathy (SFN). They observed that nerve fiber diameterwas reduced in patients
with fibromyalgia, but not in patients with SFN. The authors
concluded that the pathological mechanism underlying small fiber damage might differ
between the two disorders, and that patients with fibromyalgia suffer from small fiber
pathologyrather than SFN. This difference in terminology is a matter of debate and
relates to the mechanism of disease; see for example the recent editorial on this topic
by Clauw and letter by Üçeyler and Sommer. Rather than considering small fiber
neuropathy as the cause of pain and other symptoms in fibromyalgia, these authors
contend that small fiber pathology in fibromyalgia should be treated as an adjunct find
ing since a cause-effect relationship between the small fiber abnormalities and disease
symptomatology has not been established. Our results are in agreement with this latter
statement, as we observed no correlation between CCM abnormalities and QST, patient
reported symptoms, WPI, SSS and disease duration.
Additionally, we observed signs of
centrally mediated pain in patients that presented with cornea small fiber pathology,
consistent with the idea that central and peripheral pathology coexist in fibromyalgia
(Fig. 3)."
 
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You might consider reading the actual papers and historical references, not just the abstracts prior to making pronouncements. Erring on the side of the biomedical model - the periphery - 'medicalizes' FMS for profit just as Charcot medicalized Hysteria for profit. Had Wolfe et al known about the history of hysteria > neurasthenia > neurosis in 1990 he likely would not have coined the term "Fibromyalgia" that he has since so very publicly distanced himself from.

There is an obvious financial bias at play when pain management opts to view FMS as a primarily biological event. Medicalizing subjective complaints is a great - albeit unethical and often mysogynistic - business model.

"Doppler and colleagues recently assessed dermal unmyelinated nerve fiber diameter of skin
biopsies of the distal and proximal leg and index finger in patients with fibromyalgia and patients with
non-diabetic small fiber neuropathy (SFN). They observed that nerve fiber diameterwas reduced in patients
with fibromyalgia, but not in patients with SFN. The authors
concluded that the pathological mechanism underlying small fiber damage might differ
between the two disorders, and that patients with fibromyalgia suffer from small fiber
pathologyrather than SFN. This difference in terminology is a matter of debate and
relates to the mechanism of disease; see for example the recent editorial on this topic
by Clauw and letter by Üçeyler and Sommer. Rather than considering small fiber
neuropathy as the cause of pain and other symptoms in fibromyalgia, these authors
contend that small fiber pathology in fibromyalgia should be treated as an adjunct find
ing since a cause-effect relationship between the small fiber abnormalities and disease
symptomatology has not been established. Our results are in agreement with this latter
statement, as we observed no correlation between CCM abnormalities and QST, patient
reported symptoms, WPI, SSS and disease duration.
Additionally, we observed signs of
centrally mediated pain in patients that presented with cornea small fiber pathology,
consistent with the idea that central and peripheral pathology coexist in fibromyalgia
(Fig. 3)."

Of course you didn't read far enough down and stopped at the part you liked:

"In conclusion, in a small cohort of fibromyalgia patients we observed signs of small fiber pathology in 51% of patients as measured by cornea confocal microscopy. Further profiling these patients shows that four distinct phenotypes were present: a group with normal cornea morphology with and without signs of central sensitization, and a group with abnormal cornea morphology parameters with and without signs of central sensitization. These phenotypes indicate possible differences in disease mechanisms and additionally may steer the clinician in his or her choice of treatment of this complex, multi-factorial disorder. Since this and other previous studies were relatively small, larger cohorts of patients with fibromyalgia are needed to come to definite conclusions regarding the existence of subgroups in sensory testing and involvement of smallfiber pathology in the mechanism of disease."

I content that instead of explaining away bonafide disease with GIGO-science-functional-MRI-phrenology, socio-psychobabble health services research, and retrospective touchy-feely human development studies, precious resources would be best appropriated for finding real molecular targets for pain treatment for these patients--either palliative or curative in nature.
 
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does it not bother you that many groups have been seeking that you ask for - "real molecular targets for pain treatment" - with not limited success, but essentially no success at all? NAIMS, Lilly, Pfizer, Forest Pharmaceuticals.....

additionally, in lieu of a definitive treatment at this point, utilizing risky treatment with no clear long term benefit such as opioids is not indicated, regardless of the opinions of the fibromyalgia community. so working on the touchy feely parts of medicine may be most appropriate, regardless of the fact that it is not concrete molecularly based...
 
does it not bother you that many groups have been seeking that you ask for - "real molecular targets for pain treatment" - with not limited success, but essentially no success at all? NAIMS, Lilly, Pfizer, Forest Pharmaceuticals.....

additionally, in lieu of a definitive treatment at this point, utilizing risky treatment with no clear long term benefit such as opioids is not indicated, regardless of the opinions of the fibromyalgia community. so working on the touchy feely parts of medicine may be most appropriate, regardless of the fact that it is not concrete molecularly based...

Did I assert that opioids are effective for FMS?
 
Joint Bone Spine. 2016 Jun 3. pii: S1297-319X(16)30059-8. doi: 10.1016/j.jbspin.2016.03.006. [Epub ahead of print]
Comparison of the Big Five personality traits in fibromyalgia and other rheumatic diseases.
Bucourt E1, Martaillé V2, Mulleman D2, Goupille P2, Joncker-Vannier I3, Huttenberger B4, Reveillere C1, Courtois R5.
Author information

Abstract
INTRODUCTION:
The personality of patients with fibromyalgia is still under debate. Some studies found high neuroticism associated with low extraversion, while others found that these traits do not differ from the normal population. Personality factors intervene in the emotional regulation and modulation of pain. The aim of the study was to determine the personality traits of patients with fibromyalgiacompared to other rheumatic diseases.

METHODS:
In a multicentric study, women with fibromyalgia, rheumatoid arthritis, spondyloarthritis or Sjögren's syndrome were asked to complete the Big Five Inventory, which encompasses five main personality dimensions, namely (1) extraversion vs. introversion, (2) agreeableness vs. antagonism, (3) conscientiousness vs. impulsivity, (4) neuroticism vs. emotional stability, and (5) openness vs. closed-mindedness. Variance analysis (Student's t-test and ANOVA with post-hoc comparisons or Bonferroni correction) was performed. We also conducted hierarchical and non-hierarchical cluster analyses.

RESULTS AND DISCUSSION:
Participants were 163 women with fibromyalgia (n=48), rheumatoid arthritis (n=46), spondyloarthritis (n=46) and Sjögren's syndrome (n=23). The mean age was 47.18years (±10.81years, range 21 to 65). Patients with fibromyalgia had higher scores on agreeableness (F(3, 159)=3.39, P<0.05), neuroticism (F(3, 159)=3.79, P<0.05) and openness (F(3, 159)=4.32, P<0.01) than those with other rheumatic diseases. This study highlights the specificity of personality in fibromyalgia. It also underlines the protective role of personality traits: in the fibromyalgia group, high neuroticism and low conscientiousness (high impulsivity) were associated with a high level of chronic pain.

Copyright © 2016 Société française de rhumatologie. Published by Elsevier SAS. All rights reserved.
 
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Treatment is exercise. Sprinkle Ultram, Lyrica, Cymbalta, Savella, Trazodone. No procedures, no opiates, no steroids, no NSAIDs, no BZD.
Where is the cost of this? And where is the benefit for my office of having to see these neuro-eroticist catastrophizers.
 
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Treatment is exercise. Sprinkle Ultram, Lyrica, Cymbalta, Savella, Trazodone. No procedures, no opiates, no steroids, no NSAIDs, no BZD.
Where is the cost of this? And where is the benefit for my office of having to see these neuro-eroticist catastrophizers.
only benefit is that you may reduce the likelihood that these patients will be enrolled in risky yet not beneficial interventions by well meaning but ill equipped PCPs...
 
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There is another benefit. Identifying this cohort also identifies their children who are at risk of acquiring the trait. Prevention is only possible if first identify the reservoir.
 
There is another benefit. Identifying this cohort also identifies their children who are at risk of acquiring the trait. Prevention is only possible if first identify the reservoir.

We all know that Chiropractic treatments as an infant would be the real solution
 
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It's called Pubmed, you might consider venturing there occasionally :)

Pain. 2015 Mar;156(3):514-20. doi: 10.1097/01.j.pain.0000460326.02891.fc.
Heritability of pain catastrophizing and associations with experimental pain outcomes: a twin study.
Trost Z1, Strachan E, Sullivan M, Vervoort T, Avery AR, Afari N.
Author information

Abstract
This study used a twin paradigm to examine genetic and environmental contributions to pain catastrophizing and the observed association between pain catastrophizing and cold-pressor task (CPT) outcomes. Male and female monozygotic (n = 206) and dizygotic twins (n = 194) from the University of Washington Twin Registry completed a measure of pain catastrophizing and performed a CPT challenge. As expected, pain catastrophizing emerged as a significant predictor of several CPT outcomes, including cold-pressor Immersion Tolerance, Pain Tolerance, and Delayed Pain Rating. The heritability estimate for pain catastrophizing was found to be 37% with the remaining 63% of variance attributable to unique environmental influence. Additionally, the observed associations between pain catastrophizing and CPT outcomes were not found attributable to shared genetics or environmental exposure, which suggests a direct relationship between catastrophizing and experimental pain outcomes. This study is the first to examine the heritability of pain catastrophizing and potential processes by which pain catastrophizing is related to experimental pain response.

Free PMC Article
 
It's called Pubmed, you might consider venturing there occasionally :)

Pain. 2015 Mar;156(3):514-20. doi: 10.1097/01.j.pain.0000460326.02891.fc.
Heritability of pain catastrophizing and associations with experimental pain outcomes: a twin study.
Trost Z1, Strachan E, Sullivan M, Vervoort T, Avery AR, Afari N.
Author information

Abstract
This study used a twin paradigm to examine genetic and environmental contributions to pain catastrophizing and the observed association between pain catastrophizing and cold-pressor task (CPT) outcomes. Male and female monozygotic (n = 206) and dizygotic twins (n = 194) from the University of Washington Twin Registry completed a measure of pain catastrophizing and performed a CPT challenge. As expected, pain catastrophizing emerged as a significant predictor of several CPT outcomes, including cold-pressor Immersion Tolerance, Pain Tolerance, and Delayed Pain Rating. The heritability estimate for pain catastrophizing was found to be 37% with the remaining 63% of variance attributable to unique environmental influence. Additionally, the observed associations between pain catastrophizing and CPT outcomes were not found attributable to shared genetics or environmental exposure, which suggests a direct relationship between catastrophizing and experimental pain outcomes. This study is the first to examine the heritability of pain catastrophizing and potential processes by which pain catastrophizing is related to experimental pain response.

Free PMC Article


a few twins took a survey? thats pretty flimsy.
 
to the orignial question...

Don't you think that would be nearly impossible to answer?

My fellowship director got mad at me one time when I was complaining about the L&I patient (workers comp in Washington) - saying what a load of crap it is they like free money and won't contribute. He really got after me saying...getting paid NOT to work changes a person, and you or I may act the exact same, if we found ourselves in that circumstance - in other words, hard to tell...don't judge.

I think the same reasoning applies. Maybe there is genetic disposition, and maybe having a messed up central nervous system changes the person fundamentally how they act, how they respond to things. How would you ever know or tell that?
 
"getting paid NOT to work changes a person" Perhaps, but the fact is that personality characteristics - conscientiousness and agreeableness - predict who will get injured at work, or end up on welfare, long before they ever do.
 
I'm so confused....

Heritability is a statistical concept with an inferred meaning. For example, if you applied the concept to UK's House of Lords, you could show that Peerage of the Nobility is 100% heritable. Still, no one in the House of Lords passes a genetic "Nobility Factor" to their progeny and plenty of bastards have inherited peerage that they don't deserve. Ditto for fibromyalgia.

https://en.wikipedia.org/wiki/Heritability
 
"getting paid NOT to work changes a person" Perhaps, but the fact is that personality characteristics - conscientiousness and agreeableness - predict who will get injured at work, or end up on welfare, long before they ever do.
I've always wanted to do a study on my population - I think it would be fascinating.

I would like to do a questionaire on anyone in the military requesting disability (under the age of 30) for low back pain. I want to know if the kid grew up in a household where one or both of the parents were on disability. i think the results would be fascinating.
 
Talk to Gene Carragee about that idea.
 
The most important thing for this group to understand is that the Heritability Index, as a statistical tool, method is GIGO science. Like meta-analysis, the Hertability Index was expropriated and extrapolated for applications far beyond its intended use (crop science). Its use in human polygenetic/phenotypic analysis is tenuous at best. The first thing everyone should do when ANYONE proposes that you base a real life medical decision for an actual individual patient upon a heritability study is to scorn and ridicule them for their ignorance.
 
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101N, I've never understood why you don't believe as fibromyalgia as a condition. You obviously believe in central sensitization and chronic widespread pain and you've read Daniel Clauw's work. Fibromyalgia seems like as good a name as any for a condition of the central nervous system causing pain symptoms that aren't related to any specific form of nociception and aren't likely to respond to opioids, surgery, injections, etc. If we got rid of the fibromyalgia concept and name, we'd have to invent another word for the same thing -- people who hurt all over for no damn reason.

There's a huge overlap between fibromyalgia and psychiatric conditions, but there's a huge overlap between all pain conditions and psych disorders, that doesn't mean that they are psych disorders. A quick Google search tells me that there's a high (60%+) comorbidity between arthritis and psychiatric conditions, but that doesn't mean that rheumatology should be considered a subspecialty of psychiatry.
 
Wrangler, you are a smart doc and I enjoy your posts. Read Wolfe's essay's on FMS wars

1.
2.

And Andrew Skull's Hysteria. I think that FMS - CS - is merely a reproduction of the hysteria/neurosis/neurasthenia
epidemics of last century by another name. But now there is a Pharma market that - while largely ineffective - is nevertheless
very lucrative. And their are a lot of researchers and academic depts that are beholding to Pharma.

Ask yourself - honestly - how do you prevent the development of chronic pain. As with lots of chronic diseases prevention
is much easier than cure. When you start looking at prevent you have to note that the most prevalent predictor of chronic
pain is negative affect or dispositional pessimism, ie, catastrophizing or neuroticism. When does neuroticism develop? What's the vector?

 
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When does neuroticism develop? What's the vector?




that seems like an easy problem to tackle. when you find the answer, let me know. i have a few in-laws that could use your advice.

all bluster, but no meat. we all agree with your overall concepts, but we actually like to try to solve problems, rather than incessantly bloviate about them.
 
They have a saying in AA, "you can't turn a pickle back into a cucumber."
 
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In academic sociology/economics circles - where they know the data on the Big Five Personality Traits - the saying is you can't add eggs to
a baked cake. Since chronic non-cancer pain in working-aged adults is so notoriously difficult to treat it's fair game to ask how to prevent it. That
becomes, how and when do you prevent the development of the neurotic personality trait. The graph below is from Heckman's research
- on conscientiousness & agreeableness - but it's equally germane to neuroticism because all 5 of the big 5 develop very early in life.

It's hard not to see parallels here with Case and Deaton's work, the recent election results, the despair in the red states, etc. Like addiction
treatment, early nurture is a bipartisan issue.
 

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http://fibromyalgianewstoday.com/20...ic-widespread-joint-pain-fibromyalgia-symptom

“For too long, people with fibromyalgia have struggled to get a diagnosis for their painful symptoms. This research will help pave the way for better understanding, management and treatment of joint pain,” Simpson said.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0165548

Abstract
Background
Chronic widespread musculoskeletal pain (CWP) is the cardinal symptom of fibromyalgia and affects about 12% of the general population. Familial aggregation of CWP has been repeatedly demonstrated with estimated heritabilities of around 50%, indicating a genetic susceptibility. The objective of the study was to explore genome-wide disease-differentially methylated positions (DMPs) for chronic widespread pain (CWP) in a sample of unrelated individuals and a subsample of discordant monozygotic (MZ) twins.

Methodology/Principle Findings
A total of N = 281 twin individuals from the TwinsUK registry, including N = 33 MZ twins discordant for self-reported CWP, were part of the discovery sample. The replication sample included 729 men and 756 women from a subsample of the KORA S4 survey–an independent population-based cohort from Southern Germany. Epigenome-wide analysis of DNA methylation was conducted using the Illumina Infinium HumanMethylation 450 DNA BeadChip in both the discovery and replication sample. Of our 40 main loci that were carried forward for replication, three CPGs reached significant p-values in the replication sample, including malate dehydrogenase 2 (MDH2; p-value 0.017), tetranectin (CLEC3B; p-value 0.039), and heat shock protein beta-6 (HSPB6; p-value 0.016). The associations between the collagen type I, alpha 2 chain (COL1A2) and monoamine oxidase B (MAOB) observed in the discovery sample–both of which have been previously reported to be biological candidates for pain–could not be replicated.

Conclusion/Significance
Our results may serve as a starting point to encourage further investigation in large and independent population-based cohorts of DNA methylation and other epigenetic changes as possible disease mechanisms in CWP. Ultimately, understanding the key mechanisms underlying CWP may lead to new treatments and inform clinical practice.
 
Am J Med Genet. 2000 Apr 3;96(2):202-16.
Association between the serotonin transporter promoter polymorphism and personality traits in a primarily female population sample.
Greenberg BD1, Li Q, Lucas FR, Hu S, Sirota LA, Benjamin J, Lesch KP, Hamer D, Murphy DL.
Author information

Abstract
The serotonin transporter (5-HTT) regulates serotonergic neurotransmission and is thought to influence emotion. A 5-HTT-linked polymorphic region (5-HTTLPR) has two common variants, short (s) and long (l). We previously found population and within-family associations between the lower-expressing s allele and neuroticism, a trait related to anxiety, hostility, and depression, on a standard measure (the NEO Personality Inventory, Revised [NEO-PI-R]) in a primarily male population (n=505), and that the s allele was dominant. We investigated this association in a new sample (n=397, 84% female, primarily sib-pairs). The results robustly replicated the 5-HTTLPR neuroticism association, and the dominance of the s allele. Combined data from the two studies (n=902) showed a highly significant association between the s allele and higher NEO Neuroticism both across individuals and within families. Association between genotype and a related measure, Anxiety on the 16PF inventory, was replicated in the new population and within families in the combined sample. Association to another trait, estimated TPQ Harm Avoidance, was not replicated in the new sample but found only within the combined sibship group. Another association found in our original study, between the s allele and lower scores on NEO-PI-R Agreeableness, was also replicated and was more robust in the current and the combined samples. Associations between the functional 5-HTTLPR polymorphism were similar in women and men. These results help to define specific personality features reproducibly associated with 5-HTTLPR genotype. Such associations were strongest for traits defined by the NEO, enhancing the attractiveness of the five-factor personality model in genetic research on complex behavioral dimensions. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:202-216, 2000. Published 2000 Wiley-Liss, Inc.

Br J Psychiatry. 2007 May;190:410-4.
Serotonergic function in children with attention-deficit hyperactivity disorder: relationship to later antisocial personality disorder.
Flory JD1, Newcorn JH, Miller C, Harty S, Halperin JM.
Author information

Abstract
BACKGROUND:
Impulsive aggression in adulthood is associated with disturbances in serotonergic function. In contrast, research examining this association in childhood has yielded inconsistent results.

AIMS:
The current study examined the prospective relationship between serotonergic function measured in childhood and the later emergence of antisocial personality disorder.

METHOD:
Hormonal response to fenfluramine, an index of serotonergic function, was assessed in 58 children with attention-deficit hyperactivity disorder between 1990 and 1997 when they were aged 7-11 years. Approximately 9 years later these individuals were evaluated for antisocial personality disorder.

RESULTS:
Lower serotonergic responsivity assessed in childhood predicted the development of antisocial personalitydisorder (t (56)=2.25, P=0.028).

CONCLUSIONS:
These results provide a critical link between the child and adult literature on the covariation of impulsive aggression and serotonergic function and suggest a potential explanation for inconsistencies in the childhood literature.

J Clin Psychiatry. 2008;69 Suppl 2:25-9.
Pharmacotherapy for patients with fibromyalgia.
Clauw DJ1.
Author information

Abstract
Fibromyalgia is a common and disabling syndrome. Despite research detailing the efficacy of a variety of medicinal treatments, most notably, tricyclic antidepressants, serotonin-norepinephrine re-uptake inhibitors, and alpha(2)delta ligands, there is still widespread, routine use of agents that are mostly ineffective in treating the central nature of fibromyalgic pain. This article discusses pharmacotherapeutic options for fibromyalgia, including those with high-level evidence for efficacy, moderate-level evidence, and little or no evidence for efficacy. The importance of an integrated treatment approach that includes pharmacotherapy and at least one, but preferably more, of the most effective nonmedicinal treatment options available (e.g., education, aerobic exercise, and cognitive-behavioral therapy) is also discussed.
 
The Association Between a History of Lifetime Traumatic Events and Pain Severity, Physical Function, and Affective Distress in Patients With Chronic Pain.
Nicol AL, et al. J Pain. 2016.
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Abstract
Evidence suggests that pain patients who report lifetime abuse experience greater psychological distress, have more severe pain and other physical symptoms, and greater functional disability. The aim of the present study was to determine the associations between a history of lifetime abuse and affective distress, fibromyalgianess (measured using the 2011 Fibromyalgia Survey), pain severity and interference, and physical functioning. A cross-sectional analysis of 3,081 individuals presenting with chronic pain was performed using validated measures and a history of abuse was assessed via patient self-report. Multivariate logistic regression showed that individuals with a history of abuse (n = 470; 15.25%) had greater depression, greater anxiety, worse physical functioning, greater pain severity, worse pain interference, higher catastrophizing, and higher scores on the Fibromyalgia Survey criteria (P < .001 for all comparisons). Mediation models showed that the Fibromyalgia Survey score and affective distress independently mediate the relationship between abuse and pain severity and physical functioning (Ps < .001). Our mediation models support a novel biopsychosocial paradigm wherein affective distress and fibromyalgianess interact to play significant roles in the association between abuse and pain. We posit that having a centralized pain phenotype underlies the mediation of increased pain morbidity in individuals with a history of abuse.

PERSPECTIVE: This article examines the associations between a history of lifetime abuse and affective distress, fibromyalgianess, pain severity and interference, and physical functioning in chronic pain patients. Our findings support a novel biopsychosocial paradigm in which affective distress and fibromyalgianess interact to play roles in the association between abuse and pain.



Psychosomatic Medicine:
November/December 1997 - Volume 59 - Issue 6 - pp 572-577
Special Issue: Consultation-Liaison C/L Psychiatry
Psychosocial Factors in Fibromyalgia Compared With Rheumatoid Arthritis: II. Sexual, Physical, and Emotional Abuse and Neglect
Walker, Edward A., MD; Keegan, David MD; Gardner, Gregory MD; Sullivan, Mark MD; Bernstein, David PhD; Katon, Wayne J. MD

Objective: Two recent reports have found associations between fibromyalgia and sexual victimization, but had methodologic characteristics that limited their interpretation.

Method: We compared 36 patients with fibromyalgia and 33 patients with rheumatoid arthritis by using structured interviews for sexual, physical, and emotional victimization histories, as well as dimensional self-report measures of victimization severity.

Results: Compared with the patients with rheumatoid arthritis, those with fibromyalgia had significantly higher lifetime prevalence rates of all forms of victimization, both adult and childhood, as well as combinations of adult and childhood trauma. Although childhood maltreatment was found to be a general risk factor for fibromyalgia, particular forms of maltreatment (eg, sexual abuse per se) did not have specific effects. Experiences of physical assault in adulthood, however, showed a strong and specific relationship with unexplained pain. Trauma severity was correlated significantly with measures of physical disability, psychiatric distress, illness adjustment, personality, and quality of sleep in patients with fibromyalgia but not in those with rheumatoid arthritis.

Conclusions: Fibromyalgia seems to be associated with increased risk of victimization, particularly adult physical abuse. Sexual, physical, and emotional trauma may be important factors in the development and maintenance of this disorder and its associated disability in many patients.

Trends Psychiatry Psychother. 2013;35(1):46-54.
Association between childhood trauma and loss of functionality in adult women with fibromyalgia.
Filippon AP1, Bassani DG2, Aguiar RW1, Ceitlin LH3.
Author information

Abstract
OBJECTIVE:
To investigate whether history of childhood trauma is associated with loss of functionality in adult women with fibromyalgia (FM). A secondary objective was to assess the presence of differences between depressed and non-depressed adult women with FM in a regression model for functionality.

METHODS:
A total of 114 adult women with FM according to the American College of Rheumatology diagnostic criteria answered the Childhood Trauma Questionnaire and the Fibromyalgia Impact Questionnaire. All subjects were interviewed by trained psychiatrists and evaluated for depression using the Mini International Neuropsychiatric Interview (MINI) - Brazilian version 5.0.0. Correlation and regression models were used to investigate associations between childhood trauma and loss of functionality among patients with FM. The sample was stratified by presence and absence of clinical depression.

RESULTS:
Overall, childhood trauma was associated with of loss of functionality in adult women with FM. When stratified by depression, the regression model significantly increased the association among non-depressed patients, even after adjustment for age and use of psychotropic medications.

CONCLUSIONS:
Childhood trauma showed a clinically important association with loss of functionality among adult women with FM. The associations were more pronounced among subjects without comorbid depression.

Arthritis Rheum. 1995 Feb;38(2):235-41.
Sexual and physical abuse in women with fibromyalgia syndrome.
Boisset-Pioro MH1, Esdaile JM, Fitzcharles MA.
Author information

Abstract
OBJECTIVE:
To determine the prevalence of sexual and physical abuse in female patients with fibromyalgia syndrome(FMS), as compared with rheumatic disease control patients.

METHODS:
Eighty-three female FMS patients and 161 consecutive female rheumatology (non-FMS) control patients answered a standardized confidential questionnaire recording previous sexual and physical abuse, drug and alcohol abuse, and eating disorders. Demographic information was collected on age, education, economic status, and cultural group.

RESULTS:
Overall abuse was greater in FMS patients than in control patients (53% versus 42%; P not significant). Significant differences were observed for lifetime sexual abuse (17% versus 6%), physical abuse (18% versus 4%), combined physical and sexual abuse (17% versus 5%), and drug abuse (16% versus 3%). There was a trend toward a higher incidence of childhood sexual abuse (37% versus 22%) and of eating disorders (10% versus 3%) in the FMS patient group.

CONCLUSION:
A high frequency of sexual abuse was identified both in control patients and in FMS patients. A statistical association was demonstrated between FMS and the frequency and severity of sexual abuse, and the frequency of physical abuse and drug abuse. These results raise the possibility that abuse may have an effect upon the expression and perpetuation of FMS in adult life.

Clin J Pain. 2005 Sep-Oct;21(5):378-86.
Sexual and physical abuse in women with fibromyalgia syndrome: a test of the trauma hypothesis.
Ciccone DS1, Elliott DK, Chandler HK, Nayak S, Raphael KG.
Author information

Abstract
OBJECTIVES:
According to the trauma hypothesis, women with fibromyalgia syndrome (FMS) are more likely to report a history of sexual and/or physical abuse than women without FMS. In this study, we rely on a community sample to test this hypothesis and the related prediction that women with FMS are more likely to have posttraumatic stress disorder than women without FMS.

METHODS:
Eligibility for the present study was limited to an existing community sample in which FMS and major depressive disorder were prevalent. The unique composition of the original sample allowed us to recruit women with and without FMS from the community. A total of 52 female participants were enrolled in the present FMS group and 53 in the control (no FMS) group. Sexual and physical abuse were assessed retrospectively using a standardized telephone interview.

RESULTS:
Except for rape, sexual and physical abuse were reported equally often by women in the FMS and control groups. Women who reported rape were 3.1 times more likely to have FMS than women who did not report rape (P<0.05). There was no evidence of increased childhood abuse in the FMS group. Women with FMS were more likely to have posttraumatic stress disorder symptoms (intrusive thoughts and arousal) as well as posttraumatic stress disorder diagnosis (P<0.01).

DISCUSSION:
With the exception of rape, no self-reported sexual or physical abuse event was associated with FMS in this community sample. In accord with the trauma hypothesis, however, posttraumatic stress disorder was more prevalent in the FMS group. Chronic stress in the form of posttraumatic stress disorder but not major depressive disorder may mediate the relationship between rape and FMS.

Eur J Pain. 2003;7(2):113-9.
Childhood adversities in patients with fibromyalgia and somatoform pain disorder.
Imbierowicz K1, Egle UT.
Author information

Abstract
Primary fibromyalgia is regarded as disorder with a complex symptomatology, and no morphological alterations. Findings increasingly point to a dysfunction of the central nervous pain processing. The study aims to discuss vulnerability for fibromyalgia from a developmental psychopathological perspective. We investigated the presence of psychosocial adversities affecting the childhood of adult fibromyalgia patients (FM) and compared them to those of patients with somatoform pain disorders (SOM) and a control group (CG) with medically explained chronic pain. Using the structured biographical interview for pain patients (SBI-P), 38 FM patients, 71 SOM patients, and 44 CG patients were compared on the basis of 14 childhood adversities verified as relevant regarding longterm effects for adult health by prospective studies. The FM patients show the highest score of childhood adversities. In addition to sexual and physical maltreatment, the FM patients more frequently reported a poor emotional relationship with both parents, a lack of physical affection, experiences of the parents' physical quarrels, as well as alcohol or other problems of addiction in the mother, separation, and a poor financial situation before the age of 7. These experiences were found to a similar extent in the SOM patients, but distinctly less frequently in the CG. The results point to early psychosocial adversities as holding a similar etiological meaning in fibromyalgia as well as in somatoform pain disorders. The potential role of these factors as increasing the vulnerability for fibromyalgia is discussed.
Arthritis Care Res. 1998 Apr;11(2):102-15.
Sexual and physical abuse in women with fibromyalgia: association with outpatient health care utilization and pain medication usage.
Alexander RW1, Bradley LA, Alarcón GS, Triana-Alexander M, Aaron LA, Alberts KR, Martin MY, Stewart KE.
Author information

Abstract
OBJECTIVE:
To evaluate the relationship between sexual and/or physical abuse and health care usage in patients with fibromyalgia (FM) and identify variables that may influence this relationship.

METHODS:
We assessed history of sexual/physical abuse, health care utilization, and medication usage, as well as related variables in 75 women with FM using standardized questionnaires, structured interviews, and laboratory pain perception tasks.

RESULTS:
Fifty-seven percent of FM patients reported a history of sexual/physical abuse. Compared to non-abused patients, abused patients reported significantly greater utilization of outpatient health care services for problems other than FM and greater use of medications for pain (P < or = 0.025). Consistent with our expectations, abused patients also were characterized by significantly greater pain, fatigue, functional disability, and stress, as well as by a tendency to label dolorimeter stimuli as painful regardless of their intensities (P < or = 0.05). Additional analyses suggested that the high frequency of sexual/physical abuse in our patients was associated primarily with seeking health care for chronic pain rather than the FM syndrome itself or genetic factors.

CONCLUSION:
There is an association in FM patients between sexual/physical abuse and increased use of outpatient health care services and medications for pain. This association may be influenced by clinical symptoms, functional disability, psychiatric disorders, stress, and abnormal pain perception. The relationships among these variables should be further tested in prospective, population-based studies.

Disabil Rehabil. 1999 Jan;21(1):23-30.
Relationship between traumatic events in childhood and chronic pain.
Goldberg RT1, Pachas WN, Keith D.
Author information

Abstract
PURPOSE:
The purpose was to examine the relationships between traumatic events in childhood, such as sexual and physical abuse, alcoholism, and drug addiction, and three types of chronic pain: facial pain, myofascial pain, and fibromyalgia. A fourth group, a heterogeneous group of other pain, was used as a comparison group.

METHOD:
Ninety one patients with chronic pain, age range 20-60, were consecutively recruited from the outpatient clinics of a rehabilitation hospital and a general hospital. Patients were given four measures for completion at evaluation: Childhood History Questionnaire; Childhood Traumatic Events Scale; McGill Melzack Pain Questionnaire; Pain Disability Index. Chi-square was used to test significant differences among four pain groups on sexual, physical, and verbal abuse; alcoholism; drug dependence; medications; major upheaval, childhood illness, death of a family member or friend, and separation or divorce of parents. Logistic regression was used to predict membership in the four pain groups.

RESULTS:
All pain groups had a history of abuse exceeding 48%: fibromyalgia, 64.7%; myofascial, 61.9%; facial, 50%; other pain, 48.3%. All groups had a history of family alcohol dependence exceeding 38%, and a history of drug dependence ranging from 5.8 to 19.1%. A combined history of pain, child physical abuse, and alcoholism was prevalent in 12.9 to 35.3%. Logistic regression showed patients who were female, with an alcoholic parent, using non-narcotic drugs were more likely to be members of the facial, myofascial, and fibromyalgia groups.

CONCLUSIONS:
Child traumatic events are significantly related to chronic pain. Since the problem of child abuse is broader than physical and sexual abuse, health and rehabilitation agencies must shift from individualized treatment to interdisciplinary treatment of the family and patient.
 
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Convince yourself that association is not causation and that retrospective, cross-sectional, or case-control methods are not designed to experimentally deduce conclusions about anything...

BTW, this thread is aggravating my "Fibromyalgianess" and affective distress. Thank God someone thought up a "new paradigm" to explain what's really happening to me.
 
Int J Behav Med. 2016 Oct 18. [Epub ahead of print]
Classifying Fibromyalgia Syndrome as a Mental Disorder?-An Ambulatory Assessment Study.
Klaus K1, Fischer S2, Doerr JM2, Nater UM2, Mewes R3.
Author information

Abstract
PURPOSE:
Fibromyalgia syndrome (FMS) is associated with psychological distress. The recent revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) raises the question of whether FMS is classifiable as "somatic symptom disorder" (SSD) and consequently as a mental disorder. To address this, the present ambulatory assessment study focuses on the everyday life occurrence of SSD symptoms in FMS and their predictive value concerning severity indicators of widespread pain.

METHOD:
Ambulatory data were assessed six times daily on 14 consecutive days via iPod. Twenty-eight women suffering from FMS indicated symptoms associated with SSD (somatic illness beliefs, health anxiety, time/energy devoted to pain, or health concerns) and momentary pain levels. Questionnaires regarding potential covariates (such as somatization, depression, health status) were completed at two additional sessions in the research laboratory.

RESULTS:
On average, SSD symptoms occurred three to four times daily and were mild to moderate in severity. Furthermore, these symptoms were both concurrently and prospectively associated with momentary pain intensity and subjective impairment by pain. Twenty percent of the variance in pain intensity and 28 % of the variance in subjective impairment were explained by momentary variables (SSD symptoms and intake of pain medication). Eighty-two percent of persons with FMS fulfilled the psychological SSD criterion when considering everyday occurring symptoms with at least mild severity.

CONCLUSION:
FMS might be diagnosed as a mental disorder according to DSM-5 in many cases. SSD symptoms proved to have predictive value for FMS severity and may thus have clinical relevance for diagnostic, prognostic, and intervention purposes.

I agree with 101N for ONCE!

Big Pharma has been pushing "fibro" to increase revenues by the BILLIONS! They pay off academic departments and prestigious "researchers" to push this Fibro narrative that can ONLY be treated with highly expensive pharma products that have many side effects.

Remember, Lyrica is the #1 selling Pfizer revenue generator at this time and used extensively for "fibro".
 
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