Fibromyalgia Support Group
You're not alone in your pain. Fibromyalgia is a condition that can be difficult to diagnose and manage. If you're trying to cope with pain throughout your body, sleep problems, general fatigue, or other common fibromyalgia symptoms, you're in the right place. The community is here for you to talk about therapies and share your challenges.
After the some of the distressing material that has been posted lately, I decided to post a listing of the physical differences found in fibro hoping that it would be helpful for those who are interested.
I came across this Medscape article a while ago, but see it was just updated. I also added some material about autoantibodies in fibromyalgia. I have deleted material from this to make it more readable without proper ellipses, and Im sorry to the writers (fibro fog). Following this part of the reference piece comes all the usual psychological BS. When I first read this I couldnt believe that all this could be in one place. It seemed to me when you placed the biology against the psychology it collapsed into absurdity. And scientists dont see this? Am I the only one?
From Medscape updated 2/14/2014
Fibromyalgia
Author: Chad S Boomershine, MD, PhD; Chief Editor: Herbert S Diamond, MD
Although the pathogenesis of fibromyalgia is not completely understood, research shows biochemical, metabolic, and immunoregulatory abnormalities. These substantiate the proposal that fibromyalgia can no longer be considered a subjective pain condition.
Serotonin
The most widely acknowledged biochemical abnormality associated with fibromyalgia is abnormally low serotonin levels. Many studies have linked serotonin, a neurotransmitter, to sleep, pain perception, headaches, and mood disorders. Lower-than-normal levels of serotonin have been observed in patients with fibromyalgia. A low platelet serotonin value is believed to be the cause of the low serum levels, which have been correlated with painful symptoms.
Substance P
Substance P is a neurotransmitter that is released when axons are stimulated. Elevated levels of substance P increase the sensitivity of nerves to pain or heighten awareness of pain. Four independent studies have found that levels of substance P are 2 to 3 times higher than normal in the CSF of patients with fibromyalgia.[36] These elevated levels cause fairly normal stimuli to result in exaggerated nociception.
Some authors believe that neither elevated substance P levels nor low serotonin levels alone can be the primary cause. Instead, the dual dysfunction may be responsible for fibromyalgia.
Adenosine triphosphate
Researchers have found low levels of adenosine triphosphate (ATP) in red blood cells of patients with fibromyalgia. Although the significance is unknown, it has been suggested that low platelet serotonin levels can be explained if platelet ATP levels are also low. ATP is necessary to move and then hold serotonin in platelets. More investigation into ATP and the link to serotonin is needed.
Dysfunction of the hypothalamic-pituitary-adrenal axis
Studies of the neuroendocrine aspects of fibromyalgia have found dysfunction of the HPA axis.[37] The HPA axis is a critical component of the stress-adaptation response. The sequence of HPA action is that corticotropin-releasing hormone (CRH) from the hypothalamus stimulates the anterior pituitary to release adrenocorticotropic hormone (ACTH). In turn, ACTH stimulates the adrenal cortex to produce glucocorticoids (eg, cortisol).
Some authors have noted that 5 main measurable neuroendocrine abnormalities are associated with dysfunction of the HPA axis.[38] These are as follows:
Low free cortisol levels in 24-hour urine samples
Loss of the normal circadian rhythm, with an elevated evening cortisol level (when it should be at its lowest level)
Insulin-induced hypoglycemia associated with an overproduction of ACTH
Low levels of growth hormone
Stimulated ACTH secretion leading to insufficient adrenal release of glucocorticoids
Circadian regulation and the stress-induced stimulation of the HPA axis are, in part, regulated by serotonin. Perturbations in serotonin metabolism (as well as premorbid abnormalities of the HPA axis) may explain the abnormalities of the HPA axis in fibromyalgia. Dysfunction of the HPA axis may exaggerate the effects of abnormal serotonin metabolism. Hypoactivity of the HPA axis may cause low central serotonin levels.
Growth hormone
Growth hormone, produced during delta sleep, is involved in tissue repair. Therefore, disrupted stage 4 (delta) sleep associated with fibromyalgia may account for low levels of growth hormone. Growth hormone stimulates the production of insulinlike growth factor I (IGF-I) in the liver. Some authors have found that most patients with fibromyalgia have low levels of IGF-I and that low levels are specific and sensitive for fibromyalgia.[39]
Nerve growth factor
In some studies, nerve growth factor was found to be 4 times higher in the CSF of patients with fibromyalgia than it was in the CSF of individuals without the condition. Nerve growth factor enhances the production of substance P in afferent neurons, increasing an individual's sensitivity to or awareness of pain. Nerve growth factor also may play a role in spreading or redistributing perceived pain signals.
Cognitive impairment
Fibromyalgia is associated with a decline in short-term, working, episodic, semantic (predominantly verbal), and procedural (skills) memory. Imaging modalities such as single-photon emission computed tomography (SPECT) scanning have helped to define some of the abnormalities linked to this cognitive dysfunction. SPECT shows decreased blood flow in the right and left caudate nuclei and thalami.
Functional magnetic resonance imaging (fMRI) can show brain activity by depicting increased blood flow to areas actively engaged in a task. Increased blood flow and, hence, increased oxygenation have different magnetic properties. These properties can be detected and measured using fMRI.
In a study of persons performing a task requiring memory (alphabetization), persons with fibromyalgia performed almost as well as controls, but fMRI showed that more brain areas were activated during the memory task in persons with fibromyalgia than in controls, because the task was harder for the patients to perform. In another study, working memory and episodic memory scores of patients with fibromyalgia were similar to those of healthy controls who were 20 years older.[40]
Another study measured neural activation during response inhibition using fMRI. Patients with fibromyalgia had lower activation in the inhibition and attention networks but increased activation in other areas. The study indicates that inhibition and pain perception may use overlapping networks, which may cause resources to be unavailable for other processes when they are taken up by pain processing.[41]
Cognitive dysfunction has been linked to CNS imbalances. Abnormal levels of such neurotransmitters as substance P, serotonin, dopamine, norepinephrine, and epinephrine may cause cognitive dysfunction. Neuroendocrine imbalance of the HPA axis may play a role. Another possible cause of cognitive dysfunction is the distracting quality of pain in fibromyalgia. Cognitive performance of patients with fibromyalgia is correlated with their reported level of pain.
Brain damage from the effects of stress hormones may be involved in the cognitive dysfunction in fibromyalgia. Researchers are exploring this possibility by measuring tissue volumes in the hippocampus. Others studies have implicated yeast overload, water retention, and glial cell abnormalities as causes of cognitive dysfunction in fibromyalgia.
Sleep disruption
Sleep dysfunction is considered an integral feature of fibromyalgia. About 70% of patients recognize a connection between poor sleep and increased pain, along with feeling unrefreshed, fatigued, and emotionally distressed.[42, 43] Several studies have linked abnormal sleep with these symptoms. Sleep studies have shown that patients with fibromyalgia have disordered sleep physiology.
Inheritance
The extremely important genetic contribution to fibromyalgia and related central sensitivity syndromes was first suggested by family studies.[45, 46] Subsequently, the application of sophisticated genotyping and statistical methodology has provided a detailed view of this relationship.[47, 48]
While considered unlikely to be sole triggers, infection may also contribute to exacerbation of symptoms via cytokinevagus nerve stimulation of the corticotropin-releasing hormone neuron/stress response system in bidirectional brainimmune system communication.[9]
Variables with an uncertain relationship to the development of fibromyalgia include the following:
Decreased collagen cross-linking
Hypermobility
Chiari malformation
Environmental chemicals
High-throughput genotyping is rapidly identifying a series of single-nucleotide polymorphism (SNP) haplotypes that influence neurotransmitter levels and receptor levels in the brain and thus contribute to the various abnormalities in pain processing.[32] Such SNP haplotypes constitute vulnerability elements in the development of fibromyalgia and other central sensitivity
Antipolymer antibodies are present in approximately 50% of patients with fibromyalgia. This biologic marker may provide conclusive evidence for a subgroup of people with fibromyalgia.
Note from Ann: For some reason, this doesnt include the now many studies on small fiber neuropathy, that I find so interesting.
From:
Arthritis and Research Therapy
Biology and therapy of fibromyalgia. Evidence-based biomarkers for fibromyalgia syndrome
Dina Dadabhoy1, Leslie J Crofford2, Michael Spaeth3, I Jon Russell4 and Daniel J Clauw5*
Antiserotonin antibody, antiganglioside antibody, and antiphospholipid antibody have been shown to be different in FM patients and control individuals, but the applicability of these findings is not yet clear [81] (Table 9). Antiserotonin antibody has been shown to be increased in FM in three cross-sectional studies by two different groups [81-83]. Antiganglioside antibody and antiphospholipid antibody have each been shown to be increased in FM in two cross-sectional studies by the same group [81,82]. A different group evaluating antiganglioside antibody in a third cross-sectional study was unable to reproduce the results [83]. Antithromboplastin antibody [83], antipolymer antibody [84], and anti-68/48 kDa and anti-45 kDa [85] have each been evaluated in one cross-sectional study and have shown increased levels in FM.
I know a lot of this is complicated stuff, but just scanning it gives you an idea.
We do not belong in mental hospitals. We need research with out preconceptions and bias!
.
I came across this Medscape article a while ago, but see it was just updated. I also added some material about autoantibodies in fibromyalgia. I have deleted material from this to make it more readable without proper ellipses, and Im sorry to the writers (fibro fog). Following this part of the reference piece comes all the usual psychological BS. When I first read this I couldnt believe that all this could be in one place. It seemed to me when you placed the biology against the psychology it collapsed into absurdity. And scientists dont see this? Am I the only one?
From Medscape updated 2/14/2014
Fibromyalgia
Author: Chad S Boomershine, MD, PhD; Chief Editor: Herbert S Diamond, MD
Although the pathogenesis of fibromyalgia is not completely understood, research shows biochemical, metabolic, and immunoregulatory abnormalities. These substantiate the proposal that fibromyalgia can no longer be considered a subjective pain condition.
Serotonin
The most widely acknowledged biochemical abnormality associated with fibromyalgia is abnormally low serotonin levels. Many studies have linked serotonin, a neurotransmitter, to sleep, pain perception, headaches, and mood disorders. Lower-than-normal levels of serotonin have been observed in patients with fibromyalgia. A low platelet serotonin value is believed to be the cause of the low serum levels, which have been correlated with painful symptoms.
Substance P
Substance P is a neurotransmitter that is released when axons are stimulated. Elevated levels of substance P increase the sensitivity of nerves to pain or heighten awareness of pain. Four independent studies have found that levels of substance P are 2 to 3 times higher than normal in the CSF of patients with fibromyalgia.[36] These elevated levels cause fairly normal stimuli to result in exaggerated nociception.
Some authors believe that neither elevated substance P levels nor low serotonin levels alone can be the primary cause. Instead, the dual dysfunction may be responsible for fibromyalgia.
Adenosine triphosphate
Researchers have found low levels of adenosine triphosphate (ATP) in red blood cells of patients with fibromyalgia. Although the significance is unknown, it has been suggested that low platelet serotonin levels can be explained if platelet ATP levels are also low. ATP is necessary to move and then hold serotonin in platelets. More investigation into ATP and the link to serotonin is needed.
Dysfunction of the hypothalamic-pituitary-adrenal axis
Studies of the neuroendocrine aspects of fibromyalgia have found dysfunction of the HPA axis.[37] The HPA axis is a critical component of the stress-adaptation response. The sequence of HPA action is that corticotropin-releasing hormone (CRH) from the hypothalamus stimulates the anterior pituitary to release adrenocorticotropic hormone (ACTH). In turn, ACTH stimulates the adrenal cortex to produce glucocorticoids (eg, cortisol).
Some authors have noted that 5 main measurable neuroendocrine abnormalities are associated with dysfunction of the HPA axis.[38] These are as follows:
Low free cortisol levels in 24-hour urine samples
Loss of the normal circadian rhythm, with an elevated evening cortisol level (when it should be at its lowest level)
Insulin-induced hypoglycemia associated with an overproduction of ACTH
Low levels of growth hormone
Stimulated ACTH secretion leading to insufficient adrenal release of glucocorticoids
Circadian regulation and the stress-induced stimulation of the HPA axis are, in part, regulated by serotonin. Perturbations in serotonin metabolism (as well as premorbid abnormalities of the HPA axis) may explain the abnormalities of the HPA axis in fibromyalgia. Dysfunction of the HPA axis may exaggerate the effects of abnormal serotonin metabolism. Hypoactivity of the HPA axis may cause low central serotonin levels.
Growth hormone
Growth hormone, produced during delta sleep, is involved in tissue repair. Therefore, disrupted stage 4 (delta) sleep associated with fibromyalgia may account for low levels of growth hormone. Growth hormone stimulates the production of insulinlike growth factor I (IGF-I) in the liver. Some authors have found that most patients with fibromyalgia have low levels of IGF-I and that low levels are specific and sensitive for fibromyalgia.[39]
Nerve growth factor
In some studies, nerve growth factor was found to be 4 times higher in the CSF of patients with fibromyalgia than it was in the CSF of individuals without the condition. Nerve growth factor enhances the production of substance P in afferent neurons, increasing an individual's sensitivity to or awareness of pain. Nerve growth factor also may play a role in spreading or redistributing perceived pain signals.
Cognitive impairment
Fibromyalgia is associated with a decline in short-term, working, episodic, semantic (predominantly verbal), and procedural (skills) memory. Imaging modalities such as single-photon emission computed tomography (SPECT) scanning have helped to define some of the abnormalities linked to this cognitive dysfunction. SPECT shows decreased blood flow in the right and left caudate nuclei and thalami.
Functional magnetic resonance imaging (fMRI) can show brain activity by depicting increased blood flow to areas actively engaged in a task. Increased blood flow and, hence, increased oxygenation have different magnetic properties. These properties can be detected and measured using fMRI.
In a study of persons performing a task requiring memory (alphabetization), persons with fibromyalgia performed almost as well as controls, but fMRI showed that more brain areas were activated during the memory task in persons with fibromyalgia than in controls, because the task was harder for the patients to perform. In another study, working memory and episodic memory scores of patients with fibromyalgia were similar to those of healthy controls who were 20 years older.[40]
Another study measured neural activation during response inhibition using fMRI. Patients with fibromyalgia had lower activation in the inhibition and attention networks but increased activation in other areas. The study indicates that inhibition and pain perception may use overlapping networks, which may cause resources to be unavailable for other processes when they are taken up by pain processing.[41]
Cognitive dysfunction has been linked to CNS imbalances. Abnormal levels of such neurotransmitters as substance P, serotonin, dopamine, norepinephrine, and epinephrine may cause cognitive dysfunction. Neuroendocrine imbalance of the HPA axis may play a role. Another possible cause of cognitive dysfunction is the distracting quality of pain in fibromyalgia. Cognitive performance of patients with fibromyalgia is correlated with their reported level of pain.
Brain damage from the effects of stress hormones may be involved in the cognitive dysfunction in fibromyalgia. Researchers are exploring this possibility by measuring tissue volumes in the hippocampus. Others studies have implicated yeast overload, water retention, and glial cell abnormalities as causes of cognitive dysfunction in fibromyalgia.
Sleep disruption
Sleep dysfunction is considered an integral feature of fibromyalgia. About 70% of patients recognize a connection between poor sleep and increased pain, along with feeling unrefreshed, fatigued, and emotionally distressed.[42, 43] Several studies have linked abnormal sleep with these symptoms. Sleep studies have shown that patients with fibromyalgia have disordered sleep physiology.
Inheritance
The extremely important genetic contribution to fibromyalgia and related central sensitivity syndromes was first suggested by family studies.[45, 46] Subsequently, the application of sophisticated genotyping and statistical methodology has provided a detailed view of this relationship.[47, 48]
While considered unlikely to be sole triggers, infection may also contribute to exacerbation of symptoms via cytokinevagus nerve stimulation of the corticotropin-releasing hormone neuron/stress response system in bidirectional brainimmune system communication.[9]
Variables with an uncertain relationship to the development of fibromyalgia include the following:
Decreased collagen cross-linking
Hypermobility
Chiari malformation
Environmental chemicals
High-throughput genotyping is rapidly identifying a series of single-nucleotide polymorphism (SNP) haplotypes that influence neurotransmitter levels and receptor levels in the brain and thus contribute to the various abnormalities in pain processing.[32] Such SNP haplotypes constitute vulnerability elements in the development of fibromyalgia and other central sensitivity
Antipolymer antibodies are present in approximately 50% of patients with fibromyalgia. This biologic marker may provide conclusive evidence for a subgroup of people with fibromyalgia.
Note from Ann: For some reason, this doesnt include the now many studies on small fiber neuropathy, that I find so interesting.
From:
Arthritis and Research Therapy
Biology and therapy of fibromyalgia. Evidence-based biomarkers for fibromyalgia syndrome
Dina Dadabhoy1, Leslie J Crofford2, Michael Spaeth3, I Jon Russell4 and Daniel J Clauw5*
Antiserotonin antibody, antiganglioside antibody, and antiphospholipid antibody have been shown to be different in FM patients and control individuals, but the applicability of these findings is not yet clear [81] (Table 9). Antiserotonin antibody has been shown to be increased in FM in three cross-sectional studies by two different groups [81-83]. Antiganglioside antibody and antiphospholipid antibody have each been shown to be increased in FM in two cross-sectional studies by the same group [81,82]. A different group evaluating antiganglioside antibody in a third cross-sectional study was unable to reproduce the results [83]. Antithromboplastin antibody [83], antipolymer antibody [84], and anti-68/48 kDa and anti-45 kDa [85] have each been evaluated in one cross-sectional study and have shown increased levels in FM.
I know a lot of this is complicated stuff, but just scanning it gives you an idea.
We do not belong in mental hospitals. We need research with out preconceptions and bias!
.
The recent reporting on fibro is upsetting. Any doc that has seen many fibro patients know the common factors that we have. Many of us suffer from illnesses of some kind. Many, like me have autoimmune issues. You just can't shrug the factors off.... These are all physical illnesses.
Docs have to stop labeling ppl they cannot understand.
Thanks for this, Ann.