Is Fibromyalgia a Mitochondrial Disorder?

mitochondria

Given my very limited knowledge of science and how the body works, I’ve been wondering for awhile if the mitochondria could be a part of what causes (or maybe fuels?) fibromyalgia. It looks like I’m not the only one wondering that and some researchers are starting to research this very thing. This article details several small studies done recently into whether FM is a mitochondrial disorder. I found this particularly interesting.

“Significant reductions in mitochondrial enzyme activity (in complexes I, II, III and IV) were found in the FM patients but not the healthy controls. That, in combination with reduced levels of mitochondrial proteins, indicated that mitochondrial functioning was indeed significantly reduced. So were CoQ10 and ATP levels and mitochondrial DNA levels. In fact, every aspect of mitochondrial functioning tested was found to have taken a significant hit in the FM patients.

“That suggested mitochondrial damage had occurred and that finding set the stage for the next test. Since damaged mitochondrial DNA are known to spark an inflammatory response, the researchers asserted they should also be able to find evidence of inflammation in the skin – and they did. Double the levels of the pro-inflammatory cytokine TNF-a were found in the skin of the FM patients.

“Not only were the increased cytokine levels strongly associated with reduced mtDNA – suggesting that the mitochondrial problems had indeed sparked the inflammation – but they were highly correlated with the pain levels in FM (p<.001) as well. That suggested the mitochondrial problems could be causing or contributing to the pain the FM patients were experiencing.

“A threefold increase in TNF-a levels in the saliva and the blood collected from the biopsy area relative to the healthy controls suggested that widespread or systemic inflammation and oxidative stress was present as well. The FM patients looked pretty much like a soup of mitochondrial dysfunction, oxidative stress and inflammation.”

And this bit makes me want to try adding CoQ10 back into my daily supplement routine. I did it years ago and didn’t notice much of a change, but maybe it’s worth trying again.

“CoQ10 is a particularly intriguing nutrient given its ability to both boost ATP production and reduce levels of oxidative stress. C0Q10 levels are reportedly low in many neurodegenerative disorders including Parkinson’s disease, diabetes, fibromyalgia and cancer.

“A fibromyalgia study by this Spanish research group found a 50% reduction in COQ10 levels in FM. With dozens of mostly small studies examining mitochondrial dysfunction and CoQ10 levels/supplementation in FM and other disorders under it’s belt, this Spanish research group has been leading the way in this area.”

Read the full article here.

Brain Abnormalities Discovered in Patients with Chronic Fatigue Syndrome

cfs brain

The red, blue, and green spheres correspond to size and locations of increased cortical thickness in the right occipital, precentral, and middle temporal regions, respectively. The green arrows also point to the middle temporal region of increased thickness. Credit: Radiological Society of North America

 

A new study by Michael Zeineh of the Stanford University School of Medicine now proves that chronic fatigue syndrome (CFS) is not hypochondria or our imagination, it is a real disease. Zeineh and his team discovered brain abnormalities in CFS patients that will hopefully help doctors to better treat this debilitating disease. There is a lot of cross over between CFS and fibromyalgia, as anyone who suffers from one or both of these devastating diseases will tell you. Patients with one of these diseases (or both) battle chronic disease, chronic pain, micro-inflammation, environmental sensitivities (such as light, smells, foods, weather, etc.) and much more every single day. So the next time you think that just because you can’t see our illness it isn’t real, think again. Thanks to researchers like Zeineh we are slowly but surely getting proof that our diseases are real and terrible.

The entire article about Zeineh’s research continues below.

Study finds brain abnormalities in chronic fatigue patients

An imaging study by Stanford University School of Medicine investigators has found distinct differences between the brains of patients with chronic fatigue syndrome and those of healthy people. he findings could lead to more definitive diagnoses of the syndrome and may also point to an underlying mechanism in the disease process.

It’s not uncommon for CFS patients to face several mischaracterizations of their condition, or even suspicions of hypochondria, before receiving a diagnosis of CFS. The abnormalities identified in the study, to be published Oct. 29 in Radiology, may help to resolve those ambiguities, said lead author Michael Zeineh, MD, PhD, assistant professor of radiology.

“Using a trio of sophisticated imaging methodologies, we found that CFS patients’ brains diverge from those of healthy subjects in at least three distinct ways,” Zeineh said.

CFS affects between 1 million and 4 million individuals in the United States and millions more worldwide. Coming up with a more precise number of cases is tough because it’s difficult to actually diagnose the disease. While all CFS patients share a common symptom—crushing, unremitting fatigue that persists for six months or longer—the additional symptoms can vary from one patient to the next, and they often overlap with those of other conditions.

Scientific Challenge

“CFS is one of the greatest scientific and medical challenges of our time,” said the study’s senior author, Jose Montoya, MD, professor of infectious diseases and geographic medicine. “Its symptoms often include not only overwhelming fatigue but also joint and muscle pain, incapacitating headaches, food intolerance, sore throat, enlargement of the lymph nodes, gastrointestinal problems, abnormal blood-pressure and heart-rate events, and hypersensitivity to light, noise or other sensations.”

The combination of symptoms can devastate a patient’s life for 10, 20 or even 30 years, said Montoya, who has been following 200 CFS patients for several years in an effort to identify the syndrome’s underlying mechanisms. He hopes to accelerate the development of more-effective treatments than now exist. (A new Stanford Medicine magazine story describes the study in more detail.)

“In addition to potentially providing the CFS-specific diagnostic biomarker we’ve been desperately seeking for decades, these findings hold the promise of identifying the area or areas of the brain where the disease has hijacked the central nervous system,” Montoya said.

“If you don’t understand the disease, you’re throwing darts blindfolded,” said Zeineh. “We asked ourselves whether brain imaging could turn up something concrete that differs between CFS patients’ and healthy people’s brains. And, interestingly, it did.”

The Stanford investigators compared brain images of 15 CFS patients chosen from the group Montoya has been following to those of 14 age- and sex-matched healthy volunteers with no history of fatigue or other conditions causing symptoms similar to those of CFS.

Three Key Findings

The analysis yielded three noteworthy results, the researchers said. First, an MRI showed that overall white-matter content of CFS patients’ brains, compared with that of healthy subjects’ brains, was reduced. The term “white matter” largely denotes the long, cablelike nerve tracts carrying signals among broadly dispersed concentrations of “gray matter.” The latter areas specialize in processing information, and the former in conveying the information from one part of the brain to another.

That finding wasn’t entirely unexpected, Zeineh said. CFS is thought to involve chronic inflammation, quite possibly as a protracted immunological response to an as-yet unspecified viral infection. Inflammation, meanwhile, is known to take a particular toll on white matter.

But a second finding was entirely unexpected. Using an advanced imaging technique—diffusion-tensor imaging, which is especially suited to assessing the integrity of white matter—Zeineh and his colleagues identified a consistent abnormality in a particular part of a nerve tract in the right hemisphere of CFS patients’ brains. This tract, which connects two parts of the brain called the frontal lobe and temporal lobe, is called the right arcuate fasciculus, and in CFS patients it assumed an abnormal appearance.

Furthermore, there was a fairly strong correlation between the degree of abnormality in a CFS patient’s right arcuate fasciculus and the severity of the patient’s condition, as assessed by performance on a standard psychometric test used to evaluate fatigue.

Right vs. Left

Although the right arcuate fasciculus’s function is still somewhat mysterious, its counterpart in the brain’s left hemisphere has been extensively explored. The left arcuate fasciculus connects two critical language areas of the left side of the brain termed Wernicke’s and Broca’s areas, which are gray-matter structures several centimeters apart. These two structures are important to understanding and generating speech, respectively. Right-handed people almost always have language organized in this fashion exclusively in the left side of the brain, but the precise side (left or right) and location of speech production and comprehension are not so clear-cut in left-handed people. (It’s sometimes said that every left-hander’s brain is a natural experiment.) So, pooling left- and right-handed people’s brain images can be misleading. And, sure enough, the finding of an abnormality in the right arcuate fasciculus, pronounced among right-handers, was murky until the two left-handed patients and four left-handed control subjects’ images were exempted from the analysis.

Bolstering these observations was the third finding: a thickening of the gray matter at the two areas of the brain connected by the right arcuate fasciculus in CFS patients, compared with controls. Its correspondence with the observed abnormality in the white matter joining them makes it unlikely that the two were chance findings, Zeineh said.

Although these results were quite robust, he said, they will need to be confirmed. “This study was a start,” he said. “It shows us where to look.” The Stanford scientists are in the planning stages of a substantially larger study.

More information: “Right Arcuate Fasciculus Abnormality in Chronic Fatigue Syndrome” Radiology, 2014.

Fibromyaglia Awareness Day – May 12

Fibromyalgia Awareness Day

Today is Fibromyalgia Awareness Day! In honor of this, I thought I’d repost one of my first posts discussing what fibromyalgia is. Wear your purple today and show everyone you are a fibromyalgia warrior! #FibromyalgiaAwarenessDay

 

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Originally posted 07/30/2012

What is Fibromyalgia?

For those of you who (unfortunately) aren’t already intimately aware of what fibromyalgia is, I thought I’d give a brief introduction to it.  Fibromyalgia is also know as Fibromyalgia Syndrome (FMS) and chronic pain disorder.  It actually has some links to PTSD, as far as the way the brain works — or rather the way it works but isn’t supposed to be working.  Here is the definition of fibromyalgia from the Mayo Clinic’s website.  I find that WebMD has some outdated information on fibromyalgia and prefer to reference sites like Mayo’s.

Fibromyalgia ribbon

Definition
Fibromyalgia is a disorder characterized by widespread musculoskeletal pain accompanied by fatigue, sleep, memory and mood issues. Researchers believe that fibromyalgia amplifies painful sensations by affecting the way your brain processes pain signals. Symptoms sometimes begin after a physical trauma, surgery, infection or significant psychological stress. In other cases, symptoms gradually accumulate over time with no single triggering event.

Women are much more likely to develop fibromyalgia than are men. Many people who have fibromyalgia also have tension headaches, temporomandibular joint (TMJ) disorders, irritable bowel syndrome, anxiety and depression.

While there is no cure for fibromyalgia, a variety of medications can help control symptoms. Exercise, relaxation and stress-reduction measures also may help.

Symptoms
The pain associated with fibromyalgia often is described as a constant dull ache, typically arising from muscles. To be considered widespread, the pain must occur on both sides of your body and above and below your waist.

Fibromyalgia is characterized by additional pain when firm pressure is applied to specific areas of your body, called tender points. Tender point locations include:

  • Back of the head
  • Between shoulder blades
  • Top of shoulders
  • Front sides of neck
  • Upper chest
  • Outer elbows
  • Upper hips
  • Sides of hips
  • Inner knees

Fatigue and sleep disturbances
People with fibromyalgia often awaken tired, even though they report sleeping for long periods of time. Sleep is frequently disrupted by pain, and many patients with fibromyalgia have other sleep disorders, such as restless legs syndrome and sleep apnea, that further worsen symptoms.

If you want to read more about fibromyalgia, here is the link to information it through the Mayo Clinic:  http://www.mayoclinic.com/health/fibromyalgia/DS00079/

My Fibromyalgia

For me, fibromyalgia at it’s best is the “dull ache” described in the information above.  I hurt everywhere, all the time.  I have trouble relating to people how much pain I’m in.  If you’ve never been in chronic pain, then you really have no clue what I’m going through.  The closest analogy I can come up with — and it’s a poor one — is having a migraine headache only the headache is your entire body.  It hurts to move, it sometimes hurts to breath, sometimes it even hurts to be awake.  I have every single “tender point” in the so-called diagnostic test where your doctor pokes you all over and if you yelp in pain to enough of his pokes, then you have fibromyalgia.  My rheumatologist did that to me once and it spiked my pain so badly, he hasn’t done it again.  He likes to do it at every check up to see how much his patients improve, but for me he doesn’t bother.  I can tell him if I’m improving or not and don’t need him spiking my pain by poking me.

I often use the scale of 1 to 10 (1 being no pain and 10 being the most pain you can imagine) to try to tell people, especially my husband and immediate family, how much pain I’m in on any given day.  An average to good day is a 5 or a 6 on that scale for me.  I always feel the worst right when I wake and as the evening progresses.  10am to 2pm is the best part of the day for me, and unfortunately I spend those hours at work.  After 4 solid years of non-stop, chronic pain, you get used to a certain amount of pain.  On the good days where I drop below a 5, it’s actually kind of startling to suddenly realize “Hey, I’m feeling pretty good right now.  My pain isn’t terrible.”  At those times, your inclination is to rush out and do something fun, or something you don’t normally have the energy to do, like go shopping.  That’s an urge you have to fight because if you overdo it any given day, you’ll pay for it the next day.  Living with fibro is all about balance.  Balance in everything.  You have to balance the amount of time you sit in one place (like at your desk) with the amount of time you stretch, walk around, and exercise.  You have to get a full 8 to 9 hours of sleep each night to balance out the toll the pain takes on you every day.  You have to balance out your depression with good emotions to try to stay in the “up beat” state of mind doctors have found leads to the least amount of pain on a daily basis for people with fibro.  You have to eat a balanced diet.  You have to balance the time you spend working with time you spend on yourself, meeting your needs and your pain’s needs.  You have to balance the time you spend with your husband and family with the time you want to spend in bed, exhausted, just giving in to the pain for awhile.

This blog is about my search for balance in life.  My path to making the best of my life in pain.  My search for the best path out of the mess fibro has made of my life.  I’m always trying to make myself feel better, be better.  I’m trying to learn to control my pain and improve my quality of life, and thereby improve the quality of life of my husband and those around me who are affected by my fibro.  I hope that writing about my experiences and my journey will help me but will also help anyone out there reading this as well.

 

Article on Fibromyalgia Research

I stumbled upon this article about a doctor who has spent practically his whole career studying fibromyalgia and working with fibromyalgia sufferers. It has a good synopsis of how far research has come on fibromyalgia since the diagnosis first started appearing in the 1980s. I know I get frustrated sometimes at the lack of research being done into this invisible disease, but this article is a good reminder that things are being discovered and that our knowledge of this disease has come a long way, even if we still don’t understand so much about it. I won’t post the whole article here but I recommend reading it. Below are the bits I found most interesting.

Fibromyalgia researcher reveals secrets of a painful mystery

(I loved the metaphors he uses to describe how fibromyalgia works, how our brains interpret pain signals. These are probably the best metaphors for fibromyalgia I have heard.

Russell used a metaphor of two radios: One has a volume knob that works, but the other blares even the subtlest sounds as painful screeches. What feels like a touch to most people feels like a poke to people with fibromyalgia.

Researchers found that in the brains of people with fibromyalgia, pain centers lit up if a thumbnail was pressed with relatively minor pressure. The person felt real pain.

Cerebral spinal fluid samples extracted from fibromyalgia sufferers hinted at the processes, Russell said.

Fibromyalgia sufferers typically have three times the normal level of substance P, a pain amplifier, he said. Blocking substance P reduced pain in hands, he said, but not widespread pain. Substance P was one piece of the puzzle.

Fibromyalgia sufferers also have diminished levels of two important brain signaling chemicals, serotonin and norepinephrine. Prozac, a common antidepressant, works by increasing brain serotonin.

About 40 percent of fibromyalgia patients also experience mood disorders, suggesting a connection, Russell said, but Prozac didn’t ease their pain.

Fibromyalgia sufferers were later found to have high levels of glutamate, the main chemical involved in experiencing pain, Russell said.

Also elevated was a chemical called nerve growth factor, which stimulates repair in brain circuitry. That begs the question, Russell said, “Repair from what?”

Brain scans have shown that people with fibromyalgia lose gray matter — home to thought and memory — more quickly than others.

Sufferers of other types of chronic pain experience similar losses in gray matter, he said. The connection between pain and nerve death isn’t clear.

Earlier this year, researchers discovered a gene highly associated with fibromyalgia. It may predispose some people to develop the disease.

Relieve Chronic Pain By De-Stressing, Study Says

Relieve Chronic Pain By De-Stressing, Study Says

Destress Pain Management
Living with chronic pain can be truly stressful, but a new study contributes to growing research that managing stress may help reduce discomfort as well. Doctors from the University of Montreal found an association between the intensity of the pain experienced by chronic pain patients and their reported stress levels.

In the small study of just 24 participants, 16 of whom had chronic pain and 18 of whom were healthy control subjects, researchers found that patients who had a smaller hippocampus were more likely to also have higher cortisol levels. And higher levels of the stress hormone, in turn, contribute to increased reported pain scores on a scale of intensity.

“Our study shows that a small hippocampal volume is associated with higher cortisol levels, which lead to increased vulnerability to pain and could increase the risk of developing pain chronicity,” lead author Étienne Vachon-Presseau said in a statement.

Vachon-Presseau and colleagues measured cortisol levels in saliva samples supplied by all study participants. They then asked them to report pain levels, measured hippocampus size using fMRI and tracked response to pain stimuli using another fMRI.

The fMRI tests revealed that subjects with the smallest hippocampus sizes by volume were also more likely to have a greater response to pain in an area of the brain that’s linked to anticipatory anxiety. Subsequently, analysis showed that those patients were also more likely to have higher levels of cortisol.

Previous research has also shown an association between stress response and chronic pain sufferers. Now, many chronic pain specialists recommend a de-stressing practice like meditation to help ease pain response. The researchers hope their study will help support that treatment.
that treatment.

Posted: 03/03/2013 on Huffingtonpost.com

Chronic Pain Costs US up to $635 Billion

A fascinating new study by John’s Hopkin’s University shows that the annual cost of people suffering from chronic pain is as high as $635 billion a year.  The study shows that someone who suffers from severe chronic pain (like we fibromyalgia sufferers) have annual health care costs on average $7,726 higher than a person with no pain.  Chronic pain sufferers cost the US more than people with cancer and other major diseases.

This study may be the first to show the impact on health care and labor sectors of people suffering from chronic pain.  Maybe now that there is study showing the economic fall out of chronic pain, more research will be funded to study WHY we are in pain, and hopefully find something to help treat us.  Wouldn’t that be wonderful!!!

Here’s the article:

Chronic Pain Costs U.S. Up to $635 Billion, Study Shows

ScienceDaily (Sep. 11, 2012) — Health economists from Johns Hopkins University writing in The Journal of Pain reported the annual cost of chronic pain is as high as $635 billion a year, which is more than the yearly costs for cancer, heart disease and diabetes.

Previous studies have not shown a comprehensive analysis of the impact on health care and labor markets associated with people with chronic pain. The Johns Hopkins researchers estimated the annual economic costs of chronic pain in the U.S. by assessing incremental costs of health care due to pain and the indirect costs of pain from lower productivity. They compared the costs of health care for persons with chronic pain with those who do not report chronic pain.

The authors defined persons with pain as those who have pain that limits their ability to work, are diagnosed with joint pain or arthritis, or have a disability that limits capacity for work. To measure indirect costs, they used a model to predict health care costs if someone has any type of pain and subtracted predicted health care costs of persons who do not have pain. The impact of incremental costs of selected pain conditions were calculated for various payers of health care services.

Results showed that mean health care expenditures for adults were $4,475. Prevalence estimates for pain conditions were 10 percent for moderate pain, 11 percent for severe pain, 33 percent for joint pain, 25 percent for arthritis, and 12 percent for functional disability. Persons with moderate pain had health care expenditures $4,516 higher than someone with no pain, and individuals with severe pain had costs $3,210 higher than those with moderate pain. Similar differences were found for other pain conditions: $4,048 higher for joint pain, $5,838 for arthritis, and $9,680 for functional disabilities.

Also, adults with pain reported missing more days from work than people without pain. Pain negatively impacted three components of productivity: work days missed, number of annual hours worked and hourly wages.

Based on their analysis of the data, the authors determined that that the total cost for pain in the United States ranged from $560 to $635 billion. Total incremental costs of health care due to pain ranged from $261 to $300 billion, and the value of lost productivity ranged from $299 to $334 billion. Compared with other major disease conditions, the per-person cost of pain is lower but the total cost is higher.

Read more

New way to treat chronic pain, suggested by study

Interesting article on new research on the genetics of chronic pain.  I’m glad to see research on systemic chronic pain is being done.  Maybe there is hope for a new drug one day to help sufferers of chronic pain, fibromyalgia, and other such diseases.

New way to treat chronic pain, suggested by study.

ScienceDaily (Mar. 26, 2012) — Nearly one in five people suffers from the insidious and often devastating problem of chronic pain.

That the problem persists, and is growing, is striking given the many breakthroughs in understanding the basic biology of pain over the past two decades. A major challenge for treating chronic pain is to understand why certain people develop pain while others, with apparently similar disorders or injuries, do not. An equally important challenge is to develop individualized therapies that will be effective in specific patient populations.

Research published online in Nature Medicine points to solutions to both challenges. A research team led by Prof. Jeffrey Mogil of McGill University in Montreal and Prof. Michael Salter of The Hospital for Sick Children (SickKids), affiliated with the University of Toronto, has identified a major gene affecting chronic pain sensitivity. The findings also suggest a new approach to individualizing treatment of chronic pain.

The gene that the researchers identified encodes the pain receptor known as P2X7. Specifically, the scientists discovered that a single amino-acid change in P2X7 controls sensitivity to the two main causes of chronic pain: inflammation and nerve damage.

The amino-acid change is known to affect only one function of P2X7 receptors — the forming of pores that permit large molecules to pass through — while leaving intact the other function, of allowing much tinier ions to flow through. Using a peptide that targets pore formation only, the researchers found that pain behaviours were dramatically reduced.

The scientists then examined genetic differences among human patients suffering from two distinct types of persistent pain: chronic post-mastectomy pain and osteoarthritis. In both cases, they found that individuals with genetically inherited low pore formation in P2X7 receptors experienced lower pain levels.

“Our findings indicate that it may be possible to develop drugs that block pores in this crucial receptor, while leaving its other function intact — thereby killing pain while minimizing side effects,” said Prof. Mogil, E.P. Taylor Professor of Pain Research in McGill’s Department of Psychology.

Read more here.