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Mitochondrial dysfunction - mainstream view in CFS or not?

Discussion in 'Diagnostic Guidelines and Laboratory Testing' started by Sasha, Jun 2, 2011.

  1. JT1024

    JT1024 Senior Member

    A clinical trial coming up! http://clinicaltrials.gov/ct2/show/NCT01471652?recr=Open&intr=Ubiquinone&cntry1=NA:US

    Chronic Fatigue Syndrome: A Presumptive Mitochondrial Disorder (CFS:M)
    This study is not yet open for participant recruitment.
    Verified May 2012 by Columbia University

    First Received on November 9, 2011. Last Updated on May 31, 2012 History of Changes
    Sponsor: Alfred E. Slonim
    Information provided by (Responsible Party): Alfred E. Slonim, Columbia University
    ClinicalTrials.gov Identifier: NCT01471652
    [​IMG] Purpose
    The pathogenesis of chronic fatigue syndrome (CFS) is poorly understood and no effective therapy has been developed. Recent studies suggest that a preceding viral infection causes mitochondrial dysfunction of the brain and skeletal muscle of genetically susceptible individuals. There is no specific laboratory test to identify patients with CFS. However, certain clinical manifestations are similar to those seen in mitochondrial disorders. Both patients with mitochondrial disorders and CFS manifest elevated serum lactate levels after exercise, and demonstrate elevated brain cerebrospinal fluid levels and decreased brain glutathione levels on nuclear magnetic resonance (NMR) spectroscopy.
    Therapy consisting of daily conditioning exercise, dietary recommendations, and nutraceutical supplements (ENT) has been show to be beneficial in treating patients with mitochondrial disorders. Similar therapy has been instituted in individual patients with CFS and has been shown to also improve their clinical conditions.
    A placebo-controlled trial will be undertaken in 24 CFS patients aged 25-55. Patients fulfilling the CDC criteria for CFS will participate in this 6 month study. Other medical causes for fatigue will be excluded. Half the patients will receive treatment consisting of daily conditioning exercise plus nutraceutical supplements (ENT), that has been shown to be beneficial for patients with mitochondrial dysfunction, while the other half will receive daily conditioning exercise and placebo tablets. Response to ENT will be evaluated by maximum oxygen consumption (VO2max) and circulating lactate levels during & after treadmill exercise, a 6-minute walk test, and a fatigue questionnaire. In addition, whether ENT corrects the elevated brain cerebrospinal fluid levels and decreased brain glutathione levels will be measured. To ensure compliance to therapy patients will be monitored frequently. The objective of this study is to assess the safety and efficacy of ENT and whether ENT leads to sustained improvement of CFS patients compared to their baseline status, and compared to an exercised group of patients not receiving supplements.

    Chronic Fatigue Syndrome Drug: Nutraceutical supplements
    Drug: Placebo Phase 2

    Study Type: Interventional
    Study Design: Allocation: Randomized
    Endpoint Classification: Safety/Efficacy Study
    Intervention Model: Parallel Assignment
    Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor)
    Primary Purpose: Treatment
    Official Title: Chronic Fatigue Syndrome: Correction of Mitochondrial Dysfunction by Conditioning Exercise and Nutraceutical Therapy.

    Resource links provided by NLM:

    Genetics Home Reference related topics: ataxia neuropathy spectrum childhood myocerebrohepatopathy spectrum myoclonic epilepsy myopathy sensory ataxia
    MedlinePlus related topics: Chronic Fatigue Syndrome Dietary Supplements Exercise and Physical Fitness Fatigue
    Drug Information available for: Acetyl-L-carnitine
    U.S. FDA Resources

    Further study details as provided by Columbia University:

    Primary Outcome Measures:
    • Change in rate of fatigue status and other CFS symptoms [ Time Frame: 0, 3, and 6 months ] [ Designated as safety issue: No ]
      Rate of decrease in fatigue and other CFS symptoms, as measured by SF-36 and The Fatigue Assessment Instrument.
    Secondary Outcome Measures:
    • Change in brain lactate and glutathione levels [ Time Frame: 0 and 6 months ] [ Designated as safety issue: No ]
      Patients will undergo nuclear magnetic resonance spectroscopy of the brain prior to starting therapy (baseline) and repeat it after 6 months of therapy.
    Estimated Enrollment: 24
    Study Start Date: September 2012
    Estimated Study Completion Date: September 2014
    Estimated Primary Completion Date: September 2014 (Final data collection date for primary outcome measure)
    ArmsAssigned Interventions
    Active Comparator: Nutraceuticals
    Subjects will receive a combination of 4 nutraceuticals (CoEnzyme Q10, acetyl-L-carnitine, alpha-lipoic acid, docosahexaenoic acid (DHA)) and a multivitamin. Drug: Nutraceutical supplements
    1. CoEnzyme Q10: oral gel capsule bid
    2. Acetyl L-carnitine: oral capsule bid
    3. Alpha Lipoic Acid: oral tablet qd
    4. Docosahexaenoic acid: oral gel capsule bid
    Placebo Comparator: Placebo Drug: Placebo
    Capsule form to imitate the following nutraceuticals:
    1. Placebo 1: oral gel capsule bid
    2. Placebo 2: oral capsule bid
    3. Placebo 3: oral tablet qd
    4. Placebo 4: oral gel capsule bid

    Detailed Description:
    Chronic fatigue syndrome (CFS), also known as myalgic encephalitis (ME), is clinically characterized as a multisystem illness exhibiting debilitating fatigue, musculoskeletal pain, disturbed sleep, and impaired memory and concentration. Its diagnosis is non-specific and symptom based, with no real biomarkers yet identified. The etiology and pathophysiology of CFS remain obscure. There is a long-standing hypothesis that individuals with CFS have normal metabolism and their fatigue is psychological, with energy being wasted through the processes of anxiety, stress, and depression. The more CFS is investigated, however, the clearer it becomes that this is incorrect, and that it is probably a metabolic dysfunction resulting in insufficient energy production. A number of studies have suggested that there may be a genetic contribution to CFS. In addition, a severe viral illness frequently predisposes the onset of CFS, while a number of pathogens have been linked to CFS (2, 3, 6). Although some patients develop CFS after an acute infection such as mononucleosis, some investigators believe it arises from the reactivation of a latent virus in the host, both resulting in a chronic low-level activation of the immune system.
    As more data are acquired, we and others believe that CFS is actually a metabolic mitochondrial dysfunction resulting in insufficient energy production. Mounting evidence indicates that viral infections in genetically susceptible individuals can cause changes in mitochondrial function. Many features observed in CFS are similar to those seen in genetic mitochondrial disorders. Firstly, some muscle biopsies in patients with CFS have shown both abnormal mitochondrial degeneration and severe deletions of mitochondrial DNA genes. Mitochondrial dysfunction increases the production of free radicals and reactive oxygen species (ROS), which cause oxidative damage, believed to contribute to CFS pathogenesis. Carnitine is required for metabolic reactions including mitochondrial fatty acid oxidation. A deficiency of serum acylcarnitine has been observed in CFS patients, suggesting that there is increased utilization of carnitine in CFS, thereby decreasing energy production. In mitochondrial disorders, utilization of pyruvate is decreased, resulting in higher circulating and muscle levels of lactate, as well as decreased oxidative phosphorylation and energy production. Brain ventricular cerebrospinal lactate is elevated, and brain glutathione is decreased, in both mitochondrial disorders and CFS. In CFS patients cerebrospinal lactate is increased by approximately 300% compared to that found in generalized anxiety disorder and healthy individuals. Using brain NMR spectroscopy, the distinction between CFS and psychological disorders can be demonstrated.
    [​IMG] Eligibility

    Ages Eligible for Study: 25 Years to 55 Years
    Genders Eligible for Study: Both
    Accepts Healthy Volunteers: No
    Inclusion Criteria:
    Subjects must meet the criteria for CFS of the US Centers for Disease Control and Prevention (CDC), which requires persistent, unexplained fatigue for at least 6 months, concurrent with four of the following:
    • impaired memory/concentration
    • sore throat, new headaches
    • unrefreshing sleep, muscle pain
    • multi-joint pain
    • tender lymph nodes
    • post-exertional malaise
    As well, due to the frequency of visits subjects must currently reside in the greater New York area.
    Exclusion Criteria:
    • shortness of breath
    • heart disease
    • high blood pressure
    • other severe chronic illnesses
    • clinical depression
    • generalized anxiety disorder
    • insomnia
    • inflammatory arthritis
    • anemia
    • hypothyroidism
    • other conditions associated with significant fatigue
    • history of alcohol, tobacco, or drug abuse
    [​IMG] Contacts and Locations
    Please refer to this study by its ClinicalTrials.gov identifier: NCT01471652

    Contact: Alfred E Slonim, MD 212-305-5717 as2718@columbia.edu

    United States, New York
    Columbia University Department of Clinical Genetics Not yet recruiting
    New York, New York, United States, 10032
    Principal Investigator: Alfred E Slonim, MD
    Sponsors and Collaborators
    Alfred E. Slonim
    Principal Investigator: Alfred E Slonim, MD Columbia University
    [​IMG] More Information

    No publications provided

    Responsible Party: Alfred E. Slonim, Professor of Clinical Pediatrics, Columbia University
    ClinicalTrials.gov Identifier: NCT01471652 History of Changes
    Other Study ID Numbers: AAAJ0702
    Study First Received: November 9, 2011
    Last Updated: May 31, 2012
    Health Authority: United States: Food and Drug Administration
    United States: Institutional Review Board

    Keywords provided by Columbia University:
    myalgic encephalopathy
    chronic fatigue syndrome
    post viral infection
    muscle pain unrefreshing sleep
    fuzzy thought
    poor memory

    Additional relevant MeSH terms:
    Fatigue Syndrome, Chronic
    Mitochondrial Diseases
    Signs and Symptoms
    Virus Diseases
    Muscular Diseases
    Musculoskeletal Diseases
    Central Nervous System Diseases
    Nervous System Diseases
    Neuromuscular Diseases
    Metabolic Diseases
    Acetylcarnitine Thioctic Acid
    Nootropic Agents
    Central Nervous System Agents
    Therapeutic Uses
    Pharmacologic Actions
    Vitamin B Complex
    Growth Substances
    Physiological Effects of Drugs
    Molecular Mechanisms of Pharmacological Action
    Protective Agents

    ClinicalTrials.gov processed this record on August 13, 2012

    Back to top of Main Content
    peggy-sue likes this.
  2. JT1024

    JT1024 Senior Member

    This looks like a really good book... Too bad it costs $167.20. It specifically mentions CFS and Fibro in Chapters 7 and 8.

    Acquired Mitochondropathy – A New Paradigm in Western Medicine explaining Chronic Diseases
    By Enno Freye

    PUBLISHED: October 2011
    PUBLISHER: Springer
    PAGES: 392

    The book on Acquired Mitochondropathy offers a new perspective on the understanding and the treatment of chronic ailments. Addressing a new paradigm deemed necessary, since in one of every four adults in the western world chronic ailments are on the rise. Resulting from energy dysfunction of cellular organelles, the mitochondria, the most of the common symptoms the physician faces during medical consultation are presented. An increasing focus on chronic disabilities presents difficulties for the busy practitioner, since patients typically describe a complex pattern of discomfort, disability, and distress, with pain affecting physical, social, and psychological functioning, which have to be put in the proper perspective. Since clinicians must efficiently condense widely varied symptomatic descriptions into characteristic patterns to permit accurate diagnosis and implement effective treatment, this book serves as a useful educational resource for the healthcare provider.
  3. peggy-sue


    Wow, that sounds like the most amazing study!
    I can't wait for the outcome!!!!!!
    But I wish they were using EPA, not DHA - DHA is bad stuff.
    How are they going to be able to work out which nutraceutical is doing what?

    An Acetyl l-carnitine complex is one I find does a whole load of good; EPA does me good.
    Co-Q-10 as ubiquinol - (I think, it was the expensive, proper one) did me a great deal of harm - I lost 3 months of functioning while on it.
    I've never experimented with alpha lipoic acid.

    Whatever, I still think this is probably one of the best studies and the most hopeful, we have had to date.
    (I need to go and do a wee dance :balloons: )
  4. JT1024

    JT1024 Senior Member

    I think they already have ideas re what nutraceutical does what because of research already performed on mitchondrial diseases. I have not found any reference to the DHA yet but the others are mentioned below in an article I downloaded today (MITO 101 –Supplements and Nutrition) by Mark A. Tarnopolsky, Professor of Pediatrics and Medicine, Rm 2H26, Neuromuscular and Neurometabolic Disease Clinic, 1200 Main St. W., McMaster University Medical Center, Hamilton, Ontario, Canada.

    Coenzyme Q10 is a co-factor involved in electron transfer from complex I and II to complex III of the electron transport chain and can function as an anti-oxidant. There are many studies that have evaluated the potential efficacy of CoQ10 in mitochondrial disease, but the literature is not conclusive due to different formulations (some of which are poorly absorbed), small sample size, and variability in clinical features and outcome variables. The balance of data suggests that CoQ10 is likely to be of benefit in primary, and some secondary, mitochondrial disorders (review see 1, 2, 6).

    Alpha-lipoic acid is an anti-oxidant located in the mitochondria with high theoretical potential for use in mitochondrial disease 1, although to date it has been studied only as part of a combination 3.

    L-carnitine is required for the entry of long-chain fatty acids into the mitochondria for β-oxidation. Supplementation is recommended if plasma levels are low, or if patients are taking valproic acid or statins (both relatively contraindicated in mitochondrial disease).

    A randomized double-blind, cross-over study using a combination of α-lipoic acid + creatine monohydrate + CoQ10 in proven mitochondrial disease showed decreased levels of lactate and of a marker of oxidative stress 3, and another similar combination also found evidence for efficacy 5.

    Creatine is not something I had considered before but I it appears it may be of value to Mito patients as well. While there is mention of its benefit in some studies, others say it is of no value. Evaluating conflicting studies is not easy!

    Just found something on DHA:

    Curr Opin Clin Nutr Metab Care. 2012 Mar;15(2):122-6.
    Update on lipids and mitochondrial function: impact of dietary n-3 polyunsaturated fatty acids.

    Stanley WC, Khairallah RJ, Dabkowski ER.

    Division of Cardiology, Department of Medicine, University of Maryland, Baltimore, Maryland 21201, USA. wstanley@medicine.umaryland.edu



    Recent evidence has linked n-3 polyunsaturated fatty acid (PUFA) supplementation with dramatic alterations of mitochondrial phospholipid membranes and favorable changes in mitochondrial function. In the present review, we examine the novel effects of n-3 PUFA on mitochondria, with an emphasis on cardiac mitochondrial phospholipids.

    There is growing evidence that dietary n-3 PUFA, particularly docosahexaenoic acid (DHA), has profound effects on mitochondrial membrane phospholipid composition and mitochondrial function. Supplementation with n-3 PUFA increases membrane phospholipid DHA and depletes arachidonic acid, and can increase cardiolipin, a tetra-acyl phospholipid that is unique to mitochondrial and essential for optimal mitochondrial function. Recent studies show that supplementation with DHA decreases propensity for cardiac mitochondria to undergo permeability transition, a catastrophic event often leading to cell death. This finding provides a potential mechanism for the cardioprotective effect of DHA. Interestingly, other n-3 PUFAs that modify membrane composition to a lesser extent have substantially less of an effect on mitochondria and do not appear to directly protect the heart.

    Current data support a role for n-3 PUFA supplementation, particularly DHA, on mitochondria that are strongly associated with changes in mitochondrial phospholipid composition.
    anne_likes_red likes this.
  5. *GG*

    *GG* senior member

    Concord, NH
    Thanks for the Info MDL, I have done similar things, and have gained more health back. I made many changes at once (was tired of changing 1 thing at a time, and not having any better results). I take oxygen with my vPAP when I sleep at night. I do Cholestryamine with Chlorella. And I do get some exercise, so fresh air is something I have been doing also.


    PS Thanks for sharing.
  6. pamb

    pamb Senior Member

    Edmonton, AB, Canada
    This is not much help for a UK person but... my husband was tested by Myhill in 2009 and came up with quite poor mito function, and partial methylation block was just confirmed in testing through Dr. Genuis in Edmonton, Canada. Starting next week we're embarking upon Genuis' environmental medicine approach (the philosophy Myhill uses) and though I don't know any details yet he has said he wants to to a level before/deeper to rid toxins and add in what's missing, and then tackle the methylation. Which gave me a bit of peace of mind as John reacted quite badly to even a very gentle approach on the methylation protocol. I will report in a couple of months, once I know protocol and, just maybe, have some changes to report. Should be interesting, couldn't be any (ok, not MUCH) worse than life as it is at the moment.
    Little Bluestem likes this.
  7. Ian

    Ian Senior Member

    If mainstream medicine admitted CFS was caused by mitochondrial failure, they would have to address that issue, instead of just treating it like a mental disorder.
    Adamskitutu likes this.
  8. xchocoholic

    xchocoholic Senior Member

    Hi Marian,

    good to hear that your dd is feeling better. I was wondering what the changes she made had to do with H2S.
    I've made almost the same changes as your dd, I'm actually on the paleo / wahls now so no gluten, dairy, grains, legumes, etc ..

    I backed off eating so much protein / meat because I'm not digesting it. I was eating at least 3/4 of a lb a day tho. I suspect that I ended up with putrification dysbiosis which didn't help. I feel much better eating only 1/4 lb daily.

    I always have a stuffy nose and was looking for Dr. chester's nasal cleaning program. Do you happen to have the link ? thanks ...

    BTW. I'm doing a parasite cleanse now and these appear to be a problem for me. I saw cod worms already ... :alien: I'm mentioning this because I felt great about 1 year after getting the gluten, etc out of my diet but then it ended after going on a road trip. I may have picked up parasites and didn't realize the importaince of treating for those until now. I just wonder how many of us with food intolerances have these.

    tc ... x
  9. xchocoholic

    xchocoholic Senior Member

  10. Little Bluestem

    Little Bluestem All Good Things Must Come to an End

    I am less than enthusiastic about the up-coming Columbia University trial posted above. It says
    But the supplement (ENT) group is also going to be exercised. Treadmill exercise, which I assume will be aerobic. That is usually not good for people with CFS. The bad effects of the exercise may override any good effects of the supplements. For this trial to make any sense to me, it would need a supplement only group. And if it is aerobic exercise, the poor people in the exercise only group are pretty much guaranteed to get worse! To me, this trial sounds irresponsible. Whatever happened to “First do no harm”?
    Asklipia and Adamskitutu like this.
  11. August59

    August59 Daughters High School Graduation

    Upstate SC, USA
    I don't like it either because they assume right up front that anyone with CFS can excersise on a regular basis. I'm not convinced the supplement list will work the way they intend it to.

    I also thought that people with ME/CFS were suppose to use an Omega 3 Fish Oil that had a high ratio of EPA to DHA, but then I read the article above and definetly feel confuded. Cardolipin is something I would want more of, but is DHA the only way to increase the levels??
  12. richvank

    richvank Senior Member

    Hi, LB and August59.

    I emailed Dr. Slonim several months ago about the exercise sensitivity of PWMEs/PWCs, but he may not have grasped the seriousness of this issue. I've also cautioned him about infrequent dosing with ALA with regard to moving mercury around. Again, I don't know if he believes this to be an issue. I think his background is in genetic mitochondrial diseases, and he may not be very familiar with ME/CFS.

    Best regards,

  13. JT1024

    JT1024 Senior Member

    As far as the clinical trial/study goes, I think there has to be the consideration that many/most PWC cannot "exercise" in the traditional sense since becoming ill. Also, treating the patient with the nutraceuticals prior to attempting exercise might enable the patient to actually perform the exercise.

    Very recently, I increased my CoQ10 supplementation (from 100mg to 300mg/day). I've been astounded that I've woken up not feeling totally exhausted and having reduced pain and stiffness. This has been only three days so far. I'm hoping the improvement is real and not a placebo effect.

    I've had Fibro for over 20 years and have had horrific stiffness and pain in my hips and lower back.. I have tried many things over the past years (stretching, massage, myofascial release, cranio-sacral therapy, etc). Every morning every day, the stiffness and pain has been horrible....until the last few mornings.

    I've been able to walk better and actually do things I have not been able to do for quite a while. I'm continuing to learn details on mitochondrial function etc but I can only do it when I'm not tired. I've done much more than usual so it is time for bed for me.

    I definitely think mitchondrial treatments are worth investigating more fully.
    anne_likes_red and Hanna like this.
  14. Little Bluestem

    Little Bluestem All Good Things Must Come to an End

    Like! Like! Like! Like! Like! Like! Like! Like! Like! Like! Like! Like! Like! Like! Like! Like! Like! Like! Like! Like! Like! Like!

    Thank-you! Thank-you! Thank-you! Thank-you! Thank-you! Thank-you! Thank-you! Thank-you! Thank-you!

    The problem appears to me to be that they are assuming that since in CFS patients “certain clinical manifestations are similar to those seen in mitochondrial disorders”, the CFS patients will respond to treatment in exactly the same way as patients with mitochondrial disorders. Doesn’t someone review these research proposals? How does that kind of basic logical fallacy get overlooked?
    August59 and xchocoholic like this.
  15. xchocoholic

    xchocoholic Senior Member

    Overlooking logic seems to be an important part of the curriculum at med school. Lol. Tc .. X
    Bjorkish, August59 and NPDivi like this.
  16. August59

    August59 Daughters High School Graduation

    Upstate SC, USA
    Considering how old their reference material is and the fact that they probably still went by the CDC's old definition which just pretty much included anyone that had just been tired for about 6 months. We should tell these guys that we wish ME/CFS was researched and studied enough that such a clear understanding of the disease was known. We may know more in a year or two, but they should wait till updated references become available. Not use twenty year old information, when a significant amount of information from 2 to 3 years ago is not even substantial enough to base a study off of.
  17. JT1024

    JT1024 Senior Member

    Found this while re increasing cardiolipin:

    Dutch researchers found that linoleic acid, readily available from sunflower, hemp, grape seed and other oils, restores and even increases cardiolipin levels(Valianpour, 2003) Chronic over-consumption of omega-3 fats, such as those from fish oils, creates a deficit of omega-6 fats that interferes with the rate of oxygen use by mitochondria, with consequent decrease of cardiolipin (Yamaoka, 1999) (Hauff, 2006).

    Working with linoleic acid to bolster cardiolipin is phosphatidylcholine (PC), which assists protein reconstitution by its ability to transfer acyl groups(Xu, 2003) (Schlame, 1991) and enhance protein signaling. PC exists in every cell of the body, occupying the outer leaflet of the membrane. Throughout the course of life, PC levels become depleted and may drop as low as 10% of the membrane in elderly people. Being so, supplementation is warranted, not only to maintain cardiolipin levels and mitochondrial stability body-wide, but also to retard senescence and to improve brain function and memory capacity.

    Source: http://www.getwellslidell.com/?p=769
  18. Little Bluestem

    Little Bluestem All Good Things Must Come to an End

    You read so much about too much omega-6 fat being bad for you. It is interesting to see that you can also have too little.

    Does anyone know if it is possible to test your omega fat balance.
  19. August59

    August59 Daughters High School Graduation

    Upstate SC, USA
    Thanks JT - I'm like Little Bluestem above here asking about testing of Omega oils, but one thing I just thought of and I've made this mistake before. In my mind I want to keep associating EPA with Omega-3 and DHA with Omega-6, but they are both Omega-3 oils. The thing with Omega-6 is with our culture now using an over abundance of polyunsaturated vegetable oils we tend to get much more Omega-6 than Omega-3. However with the Omega-3 oil the ratio of EPA to DHA is not that important and probably should lean towards getting more DHA, but I know there was a thread on here awhile back that talked about either in general of people with ME/CFS should get more EPA than DHA, but I don't remeber why???

    So, cardiolipin can actually be raised by Omega-3 DHA only (this where these 2 articles differ), Omega-6 and linoleic acid plus some other oils.

    So, I see a descrepancy between the article above and the article at the top of the page. It may not be direct discrepancy, but may have more to do with the amount of cardiolipin produced?? Research time!
  20. peggy-sue


    It was originally a book by Prof. Basant Puri I read which said to use EPA, not DHA.
    It's an old book, he did have a theory about how a virus would impact on the body to cause ME, which has not panned out. His interest in ME was piqued when some of his patients reported improvement on taking this Vegepa product.
    I have been taking it since 2003, I really think it helps.
    I do have some anecdotal evidence for this - I ran out and used a commercial one from Boots, which had DHA in it as well, for a couple of months.
    My brain function went out the window. Less then two weeks back on the Vegepa, and my brain was a whole load better.
    I'm sticking with EPA, I'm avoiding DHA.
    Puri compared the two things to parts of a car. DHA is the metal that forms the body, EPA is the engine oil that keeps everything working.
    He's done some interesting work on ME, though.

    Michael likes this.

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