Discussion in 'Fibromyalgia Main Forum' started by LISALOO, Oct 8, 2008.


    LISALOO New Member

    I read the sports section and didn't see anyone post this:

    Many remain amazed that the Tampa Bay Rays are preparing for the American League Championship Series. That Rocco Baldelli is doing the same might be more miraculous.

    "It's tough to explain how I feel," Baldelli said Monday amid the champagne celebration after the Rays' first postseason series victory, vs. the Chicago White Sox. "I didn't know how this would feel. I couldn't be more happy."

    While the Rays' worst-to-first story casts them as the low-budget upstarts against the well-monied, defending champion Boston Red Sox, Baldelli's mere presence on their playoff roster signifies clearing far more daunting hurdles.

    Once among the game's most anticipated five-tool prospects, Baldelli's career was sidetracked by four years of injuries.

    'Scared to death'

    Team trainer Ron Porterfield recounts the day in the middle of last summer when he took a 4 p.m. phone call from the Rays' outfielder.

    "We hit rock bottom together," recalls Porterfield. "He was on rehab assignment with our A-ball team in Vero Beach (Fla.). He was crying. He said, 'Something's not right. My legs hurt so bad I can't even dig into the (batter's) box.'

    "At that point I got a little concerned — actually scared. The guy thought he was going to die. He was scared to death."

    Porterfield stayed on the phone with Baldelli for three hours, right up until game time. Assistant trainer Nick Paparesta drove Baldelli back to St. Petersburg. The next morning, Baldelli was in the office with Porterfield and an endocrinologist.

    There would be dozens of conversations with specialists and visits to some of the leading clinics in the nation. There would be multiple invasive biopsies. There would be frustration, pain and despair.

    After months of testing, Baldelli was eventually diagnosed with a mitochondrial disorder, which slows muscle recovery and causes fatigue. Mitochondria, present in all cells except red blood cells, create the energy needed to sustain life. In extreme cases, body parts, including the brain, heart, liver, and kidneys or the endocrine or respiratory systems fail.

    And even with treatment, rest and a host of vitamin supplements, Baldelli had doubts about ever playing again.

    "My first goal was to get on the field and try to take BP," said Baldelli.

    "I'm thinking that my career was probably over. I'm a pretty realistic person. If I couldn't hit in batting practice, how am I going to play major league baseball?"

    Baldelli's condition, rare for an athlete, might have generated more attention had his promising career not been placed in doubt already.

    "When I first got here, I thought for sure I was looking at a superstar, not just a good player," said Rays senior advisor Don Zimmer. "Then unfortunate things started happening. This is a very sad story with this kid."

    Baldelli made his major league debut at 21, hit .289 and .280 in his first two seasons and showed both power (27 homers) and speed (44 steals) for Tampa Bay teams that went a combined 133-190.

    Then came the injuries.

    He missed all of 2005 and part of 2006 due to a torn knee ligament, then Tommy John surgery. After hitting .302 with 16 homers in the second half of 2006, it was a hamstring injury that initially sent him to rehab in 2007. Then the fatigue set in.

    "Within a year I went from being a professional athlete to someone who didn't want to do anything athletic," Baldelli said. "I wanted to sit in the chair all day. It was painful."

    Like the Rays, most fans were supportive, although some were less than sympathetic. One blogger called him "worthless." Some suggested the Rays cut their losses by releasing him.

    Few, including Baldelli himself, fully understood what he was dealing with.

    "Everyone thinks I've got chronic fatigue syndrome," he said. "I've probably heard that 1,000 times. But they have no idea what I'm dealing with. It's literally muscle fatigue where I cramp up. My muscles stop working."

    Baldelli stuck with his recovery program, which consisted largely of rest. His teammates, on their way to the franchise's first winning season and playoff berth, provided positive therapy.

    "I would go to all the home games," he said. "We had never won here, and it spurred me to try to get my act together and do everything to get back as fast as possible."

    Porterfield's goal: Get Baldelli ready for a September call-up.

    "We beat that by about a month," Porterfield said.

    Limitations remain

    His Aug. 10 return was in the nick of time for the Rays, who had just lost third baseman Evan Longoria and outfielder Carl Crawford to the disabled list.

    Baldelli hit an RBI single in his second at-bat, and hit .351 with two homers in his first 37 at-bats.

    Baldelli aimed to pace himself since, hit .263 overall and played in three Division Series games.

    In Game 2, not only did he single home an eighth-inning insurance run, he scored from first on Dioner Navarro's bloop single off the Tropicana Field turf.

    "His bat speed looks the same to me," says manager Joe Maddon. "His approach at the plate is very good. When he's able to play on defense, it looks very familiar also. It's just that he can't play as often or with the same kind of sustained intensity."

    Baldelli and Porterfield understand his limitations.

    "Pre-August 2007, I used to crack the whip on him," Porterfield said. "I'd say, 'C'mon, man, we can get through this' just like I would any other athlete. Was I helping him? Probably not."

    Baldelli says he feels as strong as ever, just not for extended periods. It's his legs that bother first.

    "Sometimes I get on the field and try to do things I used to do pretty easily. Now I shouldn't be even trying them anymore," he said. "Before this year I ran virtually every ground ball out, reasonably as hard as I could go. Now the coaches and and Joe tell me to do what you have to do to stay out there."

    Baldelli's teammates are pulling for him.

    "He inspires me," said Carlos Pena. "This kid comes to the ballpark every day with a smile, even going through serious health issues. To not only put the uniform on, but do what he has done — contributing in a great way for us — to me that's a testament to his character and an example for all of us."

    In turn, he is grateful his teammates provided the platform for his most memorable season yet.

    "This is the most fun I've ever had," he says. "Going into this year, I never thought I'd have a chance of playing this year, never mind a chance to play in the playoffs."

    The article makes it sound like he had mitochondrial myopathy, which Greg Lemond had.
    [This Message was Edited on 10/08/2008]
  2. ladybugmandy

    ladybugmandy Member

    it looks like he thinks that CFS is nothing compared to what he has...if only he knew what WE go through!
  3. SpecialK82

    SpecialK82 New Member

    I don't think he understands (or maybe doesn't want to admit) that what he is going through is what alot of us feel. I hope that he keeps his story in the spotlight until he can get a diagnosis - it would be a shame if he has CFS but cannot admit to the name.
  4. simonedb

    simonedb Member

    well so much for baldelli being the poster child for cfs!
    how depressing, for us.
    this really bums me out.
    yea, with cfids/m.e. your muscles do cramp up.
    its so interesting, he is a prized athlete so the docs hunkered down and took him seriously and did what they could, if they would aggressively approach everyone with his symptoms we all might have different dx or better help too.
    very interesting.
  5. monicaz49

    monicaz49 New Member

    sounds like he truly doesnt think he has something with such a harmless name such as CFS. I remember when i first got real sick someone mentioned CFS to me and I thought...if they only knew how much my body is going's not just being tired. He probably is not educated on what CFS is, how much it effects and how severe it can be. Im wondering if he has other stuff going on or if its just fatigue and pain.

  6. Elisa

    Elisa Member

    I just wonder if he didn't have such an all star work-up and he was just a regular guy would he have been diagnosed with CFS?

    He now knows he has a mitochondrial disorder - maybe this is one of the many causes of CFS...

    God Bless,

  7. banya

    banya New Member

    I believe you are right, if he didn't have his all star work up he probably would have been diagnosed with CFS. It happens a lot.

    CFS has lost a spokesperson, but mitochondrial disease has gained one - so to the person who is feeling bad about losing your potential star spokesman, please know that those suffering from a mitochondrial disease are appreciative of the media coverage on this one. They are suffering the same as you, but their diagnosis gives them very little hope of recovery. Almost all cases of mitochondrial disease are progressive; some progressing faster than others.

    Although the disease is still being referred to as rare, the truth is - it's not. It's extremely underdiagnosed. In the last few years, estimates went from 1 in 4,000 to 1 in 200 and many believe it's more common than that.
  8. simonedb

    simonedb Member

    oh don't get me wrong, not dissing mitochondria disorders, but real cfids (not just vague fatigue of unknown origin) is very related to mitochondria dysfunction. I think I am going to start using that term when I talk to one of my docs who is less supportive, gets more respect than cfs or fm.
    I think we are so in the dark ages with all this stuff, many things are under same umbrella but they give them different names, he very well might have m.e.
    I have the exact same problem as him when I used to try to still work out gregariously, I still really miss it. Perhaps there is a sub-branch of a mitochondira disorder beyond m.e. that I have that they could do more for, but it looks like at the end of the day, all thse issues, m.e., als, ms etc do not have a magic bullet to complete normalcy.

    LISALOO New Member

    mitochondrial disfunction can be a piece of CFS, but not the whole picture.

    My hubby was reading the section later at night, and he took the like about chronic fatigue differently. He took it as Rocco said everyone said he had CFS, but he just had something different.

    Mitochondrial myapothy, if that's what he has is way beyond mitochondrial dysfunction, you can die from it. It is a different diagnosis from CFS.
    [This Message was Edited on 10/09/2008]
  10. banya

    banya New Member

    Tampa Bay Rays’ Baldelli’s Miraculous Comeback an Inspiration To Those Suffering from Mitochondrial Disease

    PITTSBURGH – The United Mitochondrial Disease Foundation (UMDF) is urging baseball fans everywhere to Root for Rocco, Tampa Bay Rays outfielder Rocco Baldelli, as Baldelli and the Rays get ready to face off against the Boston Red Sox in the American League Championship Series. Baldelli made a remarkable return to the Rays late this season after being diagnosed with a form of mitochondrial disease, which sometimes left his muscles so weak he couldn’t even walk.

    “The Rays have gone from last to first place in the American League East and Rocco personally has made one of the greatest comebacks in baseball history,” said UMDF CEO and Executive Director Chuck Mohan. “Rocco’s miraculous comeback from the devastating effects of mitochondrial disease is an inspiration to all those suffering from this heartbreaking and often debilitating illness.”

    After an incredible first season in 2003, during which he vied for the “Rookie of the Year” title, Baldelli was plagued by injuries including muscle strains and torn ligaments. In 2007, he missed most of the season after being sidelined with a torn hamstring and unexplained muscle weakness. It wasn’t until earlier this year that Baldelli was finally diagnosed with mitochondrial myopathy, a disease caused by malfunctioning mitochondria in the cells, which starve muscles of the energy needed to function.

    Every 30 minutes a child is born with a mitochondrial disease. Many do not survive beyond their teenage years. Because mitochondrial diseases can affect any organ or body system at any age, they are often misdiagnosed. Symptoms can include blindness, deafness, strokes, seizures, cardiac disease, liver disease, diabetes, the inability to digest food and susceptibility to infection.

    Researchers have linked mitochondrial dysfunction to a range of other well-known diseases, including autism, Alzheimer’s, Parkinson’s and even cancer.

    Rocco’s is a great story of perseverance; however, he really is one of the lucky ones. There are many families, who are dealing with much, much worse situations, including having their children die before their eyes without ever understanding why,” said Mohan. “We desperately need more money for research to find cure for this horrifying illness. "We root for Rocco for the incredible heart and determination that he has shown in the face of this terrible disease; but also so that others might learn from his struggle.”
  11. monicaz49

    monicaz49 New Member

    so, wait...if mitochandrial disease is different than do you distinguish between the two for diagnosis??? IS there a diagnostic marker/test for mitochandrial disease??!!!!
  12. victoria

    victoria New Member

    he had a mitochondrial biopsy to dx.

    I have a friend who had one done, she was found to have the same/similar condition, not sure there is a 'name' for it.

    The test cost $20K about 8 years ago, she had it done while still employed with good benefits. So it's not a test many of us could likely have for starters.

    They said in the article he had rest plus vitamin supplements... wonder what they were?

    I can say my friend was told there's no medical treatment available (altho she continues to research) ... she counts herself amongst those with CFIDS/FM despite the biopsy results. Supplements have not been of much benefit.

    For his sake, I hope he maintains his improvement, BUT, it will be interesting to see if he DOES maintain it -- just as many of us have cycled up and down over the years.

  13. Rafiki

    Rafiki New Member

    by Dr. David S. Bell, MD, FAAP


    Reproduced with generous permission from the April 2008 issue of Dr. Bell’s e-newsletter, Lyndonville News.

    ME/CFS is a disorder involving the cells’ energy-producing mitochondria – but it’s a mitochondrial disease like no other, Dr. Bell believes. He explains why it hasn’t been diagnosed, classified, and studied like other kinds of mitochondrial diseases - and why a change may be “just around the corner.”


    In the past week I have seen two patients who had an exercise lactate test which showed an elevation of blood lactate after mild exercise [considered a sign of mitochondrial damage]. They were told by their physician that they had “mitochondrial disease.” They were advised to take some vitamins, maybe some CoQ-10, and have a nice day. Like nearly everything else, the term mitochondrial disease left these patients feeling bewildered and somewhat lost.

    While I agree that ME/CFS is a mitochondrial disease, this term needs clarification because ME/CFS is a mitochondrial disease like no other.

    Until recently, when a child was diagnosed as having a mitochondrial disease, it was a disaster, even a death sentence, for it meant that there were major abnormalities in the mitochondrial or nuclear DNA that regulated energy production. Without energy (ATP) it is impossible to survive. These diseases are called MELAS, Kearns-Sayre, Leber hereditary optic neuropathy, and so on. Nearly three hundred mitochondrial illnesses have been identified from genetic mutations. It is a specialized area of pediatrics, where it is possible to measure severe abnormalities in the mitochondria on muscle biopsy testing.

    This is what most clinicians think of when the words "mitochondrial disease" are mentioned, but these illnesses do not, in general, apply to ME/CFS. Many patients with ME/CFS have had muscle biopsies, and most of the mitochondrial tests on these biopsies are relatively normal. We will return to why this is in a bit.

    What are Mitochondria?

    Think of mitochondria as the power factories of the cell.

    * Nearly every cell in the body has them, usually around 500 or so in every cell.

    * They take in oxygen and glucose (blood sugar) and put out carbon dioxide and energy (ATP).

    There are two hundred different steps in this process, and we will quiz you after this article. Actually, all you need to know is that:

    * ATP is the prime energy storage chemical (battery) of the body, and

    * Oxidative phosphorylation (ox-phos) is the complex of electron transport chains that do the major work of conversion.

    Because the mechanism of energy production is essential to nearly every cell, a defect will have symptoms in every organ system. Sound familiar? Oxidative metabolism, the ability to utilize oxygen to produce energy, is quite efficient, and it is fascinating to look at the theories of how it came to be part of our cells.

    However, when the energy demand is excessive, the cells revert to a more primitive, and less efficient, form of energy production - anaerobic metabolism (metabolism without oxygen). For an interesting study on the anaerobic threshold [point of reversion] in ME/CFS, see the literature review that follows.

    When to Suspect Mitochondrial Disease

    In a recent review article (Haas et al., 2007) there is a list of symptoms that suggest looking for mitochondrial disease. Among these symptoms are neurologic symptoms such as ataxia (coordination problems), myoclonus (twitching), and encephalopathy (brain injury), exercise intolerance, sensitivity to general anesthesia, and constipation.

    A score sheet has been developed to help in when to suspect mitochondrial disease - and most ME/CFS patients would fall into the positive range. For lots of information on mitochondria please go to But remember that they are talking about “conventional” mitochondrial disorders, not ME/CFS.

    A Mitochondrial Problem Can Be
    Secondary to Some Other Problem

    There is another form of mitochondrial disease, or “secondary mitochondrial disease.” In secondary mitochondrial disease the primary problem is not with the mitochondria, but some other problem that messes up mitochondrial function. There are many illnesses where the primary defect ends up causing problems with the generation of energy in mitochondria.

    For example, thyroid hormone is needed for successful oxidative phosphorylation. With hypothyroidism (low thyroid) energy production is impaired, and fatigue, weakness, temperature regulatory problems, and difficulty concentrating result. This is one of the reasons that when you start to describe fatigue to your primary care physician, he or she begins to write out a script to test for thyroid hormone.

    So What Is the Problem?

    Why has ME/CFS not been diagnosed, studied and classified like other mitochondrial diseases? There are several reasons:

    a. Mitochondrial disease is thought of by clinicians as a fatal disease of infancy, not one that occurs later in life.

    b. Mitochondrial disease is usually thought of as a fixed, structural disease, and ME/CFS is a relapsing, remitting illness with some persons even becoming entirely well.

    c. Mitochondrial diseases are hard to diagnose, requiring muscle biopsies and detailed ox-phos testing.

    d. Ox-phos testing is often normal in ME/CFS, and this has been the critical piece that has diverted attention from mitochondria.

    e. Physicians are used to thinking of organ-specific diseases (liver, kidney, etc), and mitochondria are in all cells.

    f. Few physicians have taken ME/CFS seriously until recently, and research in this area has been scant.

    Of the above reasons, only reason “d” is important to us here (ox-phos testing is often normal in ME/CFS). In 1990 I did a muscle biopsy study on 10 ME/CFS patients with Dr. June Aprille, PhD, an expert in cellular metabolism. All ten persons had relatively normal ox-phos studies. Although we did not publish this finding, it is consistent with the few published studies that have been done.

    How can you have mitochondrial disease when the mechanism tests normal? I think that the answer to this paradox is just around the corner.


    If you have a patient with emphysema who is sitting in an armchair, he or she is not out of breath. You can measure the damage in tests, but to make symptoms, you have to “stress” the system – make the patient run up and down stairs. If a person with G-6-PD deficiency [linked to fava bean allergy] is sitting quietly, the blood looks normal. But feed this person fava beans and abnormalities quickly become obvious.

    Persons with ME/CFS keep themselves at a balance point. They rest for two hours, then do a half hour of activity, then rest, then do more and so on. The worse the illness, the less overall activity is possible. If a ME/CFS patient does absolutely nothing for a few days, they usually feel pretty good. But go to the shopping mall for eight hours and the crash occurs.

    Here is the problem: In the patients studied for mitochondrial disease, they have been resting up (staying above the balance point), and a muscle biopsy done at that moment will probably not show much. But have a ME/CFS patient exercise, and then study mitochondrial function. My hunch is that the ox-phos reactions will be seriously impaired, but this has not been systematically and methodically done. For me, this hypothesis is generated by the VanNess, Snell, and Stevens “Two-day Exercise Test” study described in the next section.

    There are lots of studies that implicate mitochondrial problems; Dr. Hirohiko Kuratsune and carnitine; Dr. Suzanne Vernon and genomics; Dr. Kenny DeMeirleir, Dr. Martin Pall, Dr. Paul Cheney, and many others. But this problem cannot be studied in tiny fragments. It is time for a good study to look at the different steps of the body’s ability to generate energy. Let’s hope we get to see it within our lifetimes.

    Literature Review - the “Two-day Exercise Test”

    In the most recent Journal of Chronic Fatigue Syndrome (Vol 14, Number 2, 2007) there are two articles which may be the first to offer an objective proof of disability in ME/CFS. More importantly, if shown to be correct, they may give us an avenue to test and measure the biochemical abnormality which causes the symptom pattern. I would like to briefly review these two papers and present a case of pediatric ME/CFS which demonstrates the same abnormalities.

    In the first of these papers, Margaret Ciccolella, a lawyer, teams up with Staci Stevens, Chris Snell, and Mark Van Ness of the University of the Pacific to review the legal issues surrounding exercise testing and disability(1). As everyone familiar with ME/CFS well knows, insurance companies require proof of disability, which a standard exercise test may or may not demonstrate. However, even if disability is present, insurance companies have been quick to say that the patient was not trying hard enough, or that the patient is de-conditioned.

    The second paper of this series by VanNess, Snell and Stevens explains the two-day exercise test and presents results for six patients with ME/CFS(2).

    As clinicians have observed, the symptom of “post-exertional malaise” is one of the most distinguishing features of CFS. This symptom is listed as one of the eight in the criteria of the Centers for Disease Control(3), and is central to the diagnosis in the recent Canadian Case Definition(4) and the proposed pediatric case definition(5). It is beginning to look like the symptom of post-exertional malaise is at the root of disability, and may be central to the pathophysiology of this complex illness spectrum.

    A person with ME/CFS may be at home for several days doing little except basic activities of daily living. When this patient decides to go shopping, he or she will drive to the mall and shop for one or two hours. During this time, observers would say that the person looks entirely well, not appearing disabled. However, following this activity the patient will experience an exacerbation of pain and other symptoms of ME/CFS. This exacerbation may last one, two or three days, and, in my opinion, the more severe the illness, the longer and more severe the exacerbation.

    This phenomenon is known as post-exertional malaise. The symptoms of the illness (malaise) are exacerbated by mental, physical or emotional activities (post-exertional). In an employment environment, the patient may be able to do a job well for one or even several days. However, disability lies in the inability to sustain this normal level of activity. The two-day exercise test is the first to begin to explain this phenomenon.

    The exercise test is no different from what has been used for years. The patient exercises on a stationary bicycle (bicycle ergometry) and breathes through plastic tubing to measure the concentration of oxygen and carbon dioxide as well as the total amount of air. The six female patients and six sedentary matched control subjects of the study were all able to achieve maximal exertion. The ME/CFS patients had a slightly lower V02max (maximal oxygen utilization) than controls (28.4 ml/kg/min vs. 26.2 ml/kg/min) and lower VO2 at anaerobic threshold (15.01 ml/kg/min vs. 17.55 mg/kg/min) on the first day of exercise testing.

    These values are not dramatic, nor are they statistically significant.

    It is on the second day that interesting results are seen. The same test was repeated the following day for all 12 subjects. As is often the case, sedentary controls improved slightly in their ability to utilize oxygen, going from 28.4 to 28.9 ml/kg/min for VO2max and from 17.55 to 18.00 ml/kg/min for oxygen utilization at anaerobic threshold. The CFS patients however worsened in both categories: VO2max fell 22% from 26.23 to 20.47 ml/kg/min, and oxygen utilization at anaerobic threshold fell 27%, from 15.01 to 11.01 ml/kg/min.

    To put this into perspective, these values are in the “severe disability” range on the AMA guidelines, and the decline in function from day one to day two cannot be explained by inactivity.

    Sedentary or de-conditioned persons do not change their oxygen utilization because of an exercise test. Even patients with heart disease, cystic fibrosis or other diseases do not vary more than 7% from one day to the next. However, the patients with ME/CFS in this study had a significant drop; something occurred because of the test on the first day that interfered with their ability to utilize oxygen on the next day. And this is exactly what patients with ME/CFS have been describing with the symptom of post-exertional malaise.

    As the authors state, “The fall in oxygen consumption among the CFS patients on the second test appears to suggest metabolic dysfunction rather than a sedentary lifestyle as the cause of diminished exercise capacity in CFS.”


    The results of the two-day exercise testing are objective and not dependent upon subjective symptoms. Moreover, hypochondriasis, intentional falsification, and/or poor effort can be detected by the physiologic parameters. Therefore:

    * The two-day exercise test, if confirmed in a larger trial, could become a clinical trial end point.

    * More importantly, evaluations could be designed which would demonstrate the specific metabolic abnormality generated by the exercise of day one and demonstrated on the second day exercise test.

    It would be my hope that these findings be explored without delay.


    1. Ciccolella M, Stevens S, Snell C, VanNess J: "Legal and Scientific Considerations of the Exercise Stress Test". JCFS 2008, 14(2):61-75.
    2. VanNess JM, Snell CR, Stevens S: "Diminished Cardiopulmonary Capacity During Post-Exertional Malaise". JCFS 2008, 14(2):77-85.
    3. Fukuda K, Straus S, Hickie I, Sharpe M, Dobbins J, Komaroff A, Group ICS: "The chronic fatigue syndrome: a comprehensive approach to its definition and study." Ann Intern Med 1994, 121:953-959.
    4. Carruthers B, Jain A, DeMeirlier K, Peterson D, Klimas N, Lerner A, Bested A, Flor-Henry P, Joshi P, Powles ACP et al: "Myalgic encephalomyelitis/chronic fatigue syndrome: Clinical working case definition, diagnostic and treatment protocols." J Chronic Fatigue Syndrome 2003, 11(1):1-12.
    5. Jason L, Bell D, Rowe K, Van Hoof E, Jordan K, Lapp C, A G, Miike T, Torres-Harding S, DeMeirleir K. "A Pediatric Case Definition for Myalgic Encephalomyelitis and Chronic Fatigue Syndrome." J CFS 2006, 13:1-44

    Dr. Bell's Disclaimer: Any medical advice that is presented in the Lyndonville News is generic and for general informational purposes only. ME/CFS/FM is an extremely complex illness and specific advice may not be appropriate for an individual with this illness. Therefore, should you be interested or wish to pursue any of the ideas presented here, please discuss them with your personal physician.

    Note: This information has not been evaluated by the FDA. It is not meant to prevent, diagnose, treat or cure any illness, condition or disease. It is very important that you make no change in your healthcare plan or health support regimen without researching and discussing it in collaboration with your professional healthcare team.
  14. simonedb

    simonedb Member

    right on rafiki! thanks for an awesome article.
  15. Rafiki

    Rafiki New Member


  16. banya

    banya New Member

    You asked how you distinguish between the two for a diagnosis. The only way to tell is by being evaluated by a specialist in the field. At the risk of sounding like Joe Biden, I'm going to repeat... The ONLY way to tell is to be evaluated by a specialist! I wish I could tell you it was easy, but there's no one simple test. You're going to need to do a lot of research on your own for this one and I'd suggest the UMDF website or the mitoaction website to start, if you're interested.

    Diagnosis/testing. In some individuals, the clinical picture is characteristic of a specific mitochondrial disorder (e.g., LHON, NARP, or maternally inherited LS), and the diagnosis can be confirmed by molecular genetic testing of DNA extracted from a blood sample. In many individuals, such is not the case, and a more structured approach is needed, including family history, blood and/or CSF lactate concentration, neuroimaging, cardiac evaluation, and muscle biopsy for histologic or histochemical evidence of mitochondrial disease, and molecular genetic testing for a mtDNA mutation.

    IMO, getting a diagnosis for this disease is challenging and the expense of the procedure is only a small part of that challenge. But I wouldn't assume your insurance company wouldn't pay for it. I have very crummy insurance but they paid for my biopsy without much of a fight, four years ago. (I had a FMS diagnosis, with fatigue, muscle pain, migraines, and breathing difficulty being the symptoms).

    I happen to find Dr. Bell's article interesting, but I'm concerned it may be very misleading to those who know very little about mitochondrial disease. I just don't buy into the fact that he knows what is a mitochondrial disease and what is CFS. Research hasn't gotten there yet. I guess I'm biased, as I'm fairly well aquainted with many "mito" patients through networking. Most were misdiagnosed prior to getting a positive muscle biopsy and most of those misdiagnosis included CFS and or FMS, but often many other diseases like MS.

    So, how can it be that you can pull these patients out of the CFS pool and biopsy them and have them be positive, while Dr. Bell pulls ten patients out and biopsies them with normal results? I could hazard a few guesses here, but one thing I do know that is a negative biopsy (especially by someone who isn't a specialist in the field) doesn't rule out the kind of mitochondrial disease that will kill you. I've spoken to the mom who lost her daughter from the disease a few short months after getting a normal biopsy result. (The autopsy proved she had it). I've spoken to people who have had multiple biopsies before finding the defect. It's rather like looking for a needle in a haystack sometimes and most mito docs will tell you that a negative biopsy doesn't rule out the disease.

    When we've asked these specialists about the possibility of CFS patients possibly having a mitochondrial disease, we are told that it's believed we will find a portion of them do. No one knows what portion and no one knows where that leaves everyone else. Possibly other metabolic condition with a secondary mitochondrial dysfunction as Dr. Bell suggests. Either way, I think we need to keep our energy levels up until they figure this out. I'm doing much better since I focussed on that.
  17. simonedb

    simonedb Member

    what do you mean "keep our energy levels up", you mean figuratively or metaphorically? :)
  18. banya

    banya New Member

    I actually meant by supplementing with energy enhancing products.

    We need to learn to listen to our bodies and rest when we're exhausted, follow a good diet, make sure you stay hydrated and supplement with those products which enhance your energy levels. You can follow the same vitamin cocktail that is prescribed by the doctors who are treating patients with energy deficiencies.

    CoQ10, L-carnitine, a good multi vitamin, (B vitamins seem to help a lot) and there are some others that may be useful. The thing is that not everyone is dealing with the same exact deficiencies, so you'll need to experiment to see what works best for you. That includes your diet... some need to avoid fat, some do better with more protein, reducing carbs, etc.

    If you can possibly manage some exercise, do it. According to studies it will increase your good mitochondria and eventually you may see some improvement. Unfortunately not everyone is going to be able to do this, but for those who can - it's worth a try.

  19. Jeanette62

    Jeanette62 New Member

    Interesting articles !

    It would be nice if the 2 day exercise test was done for all of us presenting with these symptoms.

    What kind of doctor would you see - an exercise physiologist?
  20. SpecialK82

    SpecialK82 New Member

    thanks for the article - I think it make alot of sense to do a 2 day test for CFS.

    I just wish we could push this research - all the delay is frustrating!!!