Guest guest Posted February 18, 1999 Report Share Posted February 18, 1999 Hi, I know what you mean, The only thing worse is doctors who won't follow up on latest findings. I actully was called wierd because signs and symptoms don't fit a pattern & was sent home. And if one is assertive(not aggressive or angry), then we are called difficult patients. At this point if this DD does kill me, it will be death by neglect! Christie >From: " Crane " <ccrane@...> > >Jim- >thank you for these studies! I never know if I'm glad to know about all >these awful things or not <grin>. > > in North Carolina > >> Re: Mitochondrial Disease >> >> >> From: Jim Toomey <jim_toomey@...> >> >> Some CFS mito studies or excerpts >> >> Rgds, >> Jim >> >> ----- >> >> 1)Chazotte, B and Pettengill, M. >> >> Using membrane potential to follow cytokine effects on >> mitochondria and possible dysfunction in chronic >> fatigue syndrome. (Meeting Abstract). Biophysical >> Journal 1999, 76, 1, A363. >> >> Short report of study focusing on cellular and >> mitochondrial energy metabolism in individual living >> cells using laser scanning confocal microscopy. The >> findings suggested " possible mitochondrial >> dysfunction. Interferon-a added to cultured human >> fibroblasts or leukocytes was found to decrease >> mitochondrial membrane potentials and areas at >> mitochondrial potentials. Interleukin-2 also affects >> mitochondrial potentials and may induce an unexplained >> photosensitivity. " >> >> 2)Cheney et al put out a " talking paper " in 1992? >> 1994? (can't find actual paper right now but working >> from some notes) that identified over a half a dozen >> metabolites that are not functioning properly. >> Essential chemicals are either not crossing cell >> membranes, or are not " piggy-backing " other needed >> chemicals into the cell if able to cross. >> Subsequently, the cellular mitochondria have a reduced >> amount of the essential elements necessary to combust >> fat and oxygen to release energy --> ATP. The >> dysfunction is not well understood at present ... >> >> 3)Acta Neuropathol (Berl) 1991;83(1):61-5 >> Mitochondrial abnormalities in the postviral fatigue >> syndrome. >> Behan WM, More IA, Behan PO >> Department of Pathology, University of Glasgow, >> Scotland. >> >> We have examined the muscle biopsies of 50 patients >> who had postviral fatigue syndrome (PFS) for from 1 to >> 17 years. We found mild to severe atrophy of type II >> fibres in 39 biopsies, with a mild to moderate excess >> of lipid. On ultrastructural examination, 35 of these >> specimens showed branching and fusion of mitochondrial >> cristae. Mitochondrial degeneration was obvious in 40 >> of the biopsies with swelling, vacuolation, myelin >> figures and secondary lysosomes. These abnormalities >> were in obvious contrast to control biopsies, where >> even mild changes were rarely detected. The findings >> described here provide the first evidence that PFS may >> be due to a mitochondrial disorder precipitated by a >> virus infection. >> >> 4)Ciba Found Symp 1993;173:146-54; discussion 154-9 >> Enteroviruses and postviral fatigue syndrome. >> Behan PO, Behan WM, Gow JW, Cavanagh H, Gillespie S >> Department of Neurology, University of Glasgow, UK. >> >> “An increase in the number and size of muscle >> mitochondria was found in 70% of PFS cases, suggesting >> an abnormality in metabolic function. Evidence of >> hypothalamic dysfunction was present, particularly >> involving 5-hydroxytryptamine metabolism.” >> >> 5)In vitro Study of Muscle Aerobic Metabolism in >> Chronic Fatigue Syndrome >> >> [ Journal of Chronic Fatigue Syndrome Vol. 5, No. 1, >> 1999 ] >> WIhelmina M. H. Behan, MD, FRCPath, FRCP >> Ian J. Holt, PhD >> H. Kay, MBChB >> Pamela Moonie, BSc >> >> Muscle aerobic metabolism in CFS…mitochondrial DNA >> (mtDNA) volume was measured and mtDNA rearrangements >> sought. The results showed that myoblasts >> from ten of 16 cases of CFS had defects in aerobic >> metabolism >> >> 6)TITLE: Reduced oxidative muscle metabolism in >> chronic fatigue syndrome >> AUTHORS: McCully KK; Natelson BH; Iotti S; Sisto S >> Leigh JS Jr >> >> In conclusion, oxidative metabolism is reduced in CFS >> patients compared to sedentary controls. >> NLM PUBMED CIT. ID: 8618560 >> SOURCE: Muscle Nerve 1996 May;19(5):621-5 >> >> 7)Neuromuscul Disord 1998 May;8(3-4):204-9 >> >> Heterogeneity in chronic fatigue syndrome: evidence >> from magnetic resonance spectroscopy of muscle. >> Lane RJ, Barrett MC, DJ, Kemp GJ, Lodi R >> >> “…but at the end of exercise, intracellular pH in the >> SATET +ve patients was significantly lower than in >> both the SATET -ve cases and controls (P < 0.03), and >> the SATET +ve patients also showed a significantly >> lower ATP synthesis rate during recovery (P < 0.01), >> indicating impaired mitochondrial oxidative >> phosphorylation…. >> >> This cannot be explained satisfactorily by the effects >> of 'inactivity' or 'deconditioning'.” >> >> >> __________________________________________________ >> Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 8, 2000 Report Share Posted January 8, 2000 A few years ago I had a baby that was born with gobal neurological impairment and he was tested for a Mitochondrial Disorder by having a muscle biopsy. The neurologist was the one involved with this diagnosis. In the end I was told that it was not a Mitochondrial Disorder, and all other tests (including every genentic test available) came up with no answers (the story of my life). He only lived a few months, which was a blessing with his impairments. I asked the neurologist about having myself tested for a Mitochondrial Disorder, and he assured me that that was not necessary because he felt sure that that was not my problem. Being that I am feeling much better than I did a few years ago, I have to believe that this is true. I am looking into getting the myco test done through IMM. My gut tells me that some kind of infection is at the root of my illness. --- >From: siouxie@... > >To whomever posted the info about mitochondrial disease: > >What specialty of doctors sees people with mitochondrial disease? What >type of health care professional should I look for if I want to be >evaluated for this? This looks as if it might be fruitful in my case. > >Thanks. > >Sue > > >--------------------------- Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 14, 2000 Report Share Posted January 14, 2000 Some CFS mito studies or excerpts Rgds, Jim ----- 1)Chazotte, B and Pettengill, M. Using membrane potential to follow cytokine effects on mitochondria and possible dysfunction in chronic fatigue syndrome. (Meeting Abstract). Biophysical Journal 1999, 76, 1, A363. Short report of study focusing on cellular and mitochondrial energy metabolism in individual living cells using laser scanning confocal microscopy. The findings suggested " possible mitochondrial dysfunction. Interferon-a added to cultured human fibroblasts or leukocytes was found to decrease mitochondrial membrane potentials and areas at mitochondrial potentials. Interleukin-2 also affects mitochondrial potentials and may induce an unexplained photosensitivity. " 2)Cheney et al put out a " talking paper " in 1992? 1994? (can't find actual paper right now but working from some notes) that identified over a half a dozen metabolites that are not functioning properly. Essential chemicals are either not crossing cell membranes, or are not " piggy-backing " other needed chemicals into the cell if able to cross. Subsequently, the cellular mitochondria have a reduced amount of the essential elements necessary to combust fat and oxygen to release energy --> ATP. The dysfunction is not well understood at present ... 3)Acta Neuropathol (Berl) 1991;83(1):61-5 Mitochondrial abnormalities in the postviral fatigue syndrome. Behan WM, More IA, Behan PO Department of Pathology, University of Glasgow, Scotland. We have examined the muscle biopsies of 50 patients who had postviral fatigue syndrome (PFS) for from 1 to 17 years. We found mild to severe atrophy of type II fibres in 39 biopsies, with a mild to moderate excess of lipid. On ultrastructural examination, 35 of these specimens showed branching and fusion of mitochondrial cristae. Mitochondrial degeneration was obvious in 40 of the biopsies with swelling, vacuolation, myelin figures and secondary lysosomes. These abnormalities were in obvious contrast to control biopsies, where even mild changes were rarely detected. The findings described here provide the first evidence that PFS may be due to a mitochondrial disorder precipitated by a virus infection. 4)Ciba Found Symp 1993;173:146-54; discussion 154-9 Enteroviruses and postviral fatigue syndrome. Behan PO, Behan WM, Gow JW, Cavanagh H, Gillespie S Department of Neurology, University of Glasgow, UK. “An increase in the number and size of muscle mitochondria was found in 70% of PFS cases, suggesting an abnormality in metabolic function. Evidence of hypothalamic dysfunction was present, particularly involving 5-hydroxytryptamine metabolism.” 5)In vitro Study of Muscle Aerobic Metabolism in Chronic Fatigue Syndrome [ Journal of Chronic Fatigue Syndrome Vol. 5, No. 1, 1999 ] WIhelmina M. H. Behan, MD, FRCPath, FRCP Ian J. Holt, PhD H. Kay, MBChB Pamela Moonie, BSc Muscle aerobic metabolism in CFS…mitochondrial DNA (mtDNA) volume was measured and mtDNA rearrangements sought. The results showed that myoblasts from ten of 16 cases of CFS had defects in aerobic metabolism 6)TITLE: Reduced oxidative muscle metabolism in chronic fatigue syndrome AUTHORS: McCully KK; Natelson BH; Iotti S; Sisto S Leigh JS Jr In conclusion, oxidative metabolism is reduced in CFS patients compared to sedentary controls. NLM PUBMED CIT. ID: 8618560 SOURCE: Muscle Nerve 1996 May;19(5):621-5 7)Neuromuscul Disord 1998 May;8(3-4):204-9 Heterogeneity in chronic fatigue syndrome: evidence from magnetic resonance spectroscopy of muscle. Lane RJ, Barrett MC, DJ, Kemp GJ, Lodi R “…but at the end of exercise, intracellular pH in the SATET +ve patients was significantly lower than in both the SATET -ve cases and controls (P < 0.03), and the SATET +ve patients also showed a significantly lower ATP synthesis rate during recovery (P < 0.01), indicating impaired mitochondrial oxidative phosphorylation…. This cannot be explained satisfactorily by the effects of 'inactivity' or 'deconditioning'.” __________________________________________________ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 14, 2000 Report Share Posted January 14, 2000 Jim- thank you for these studies! I never know if I'm glad to know about all these awful things or not <grin>. in North Carolina > Re: Mitochondrial Disease > > > From: Jim Toomey <jim_toomey@...> > > Some CFS mito studies or excerpts > > Rgds, > Jim > > ----- > > 1)Chazotte, B and Pettengill, M. > > Using membrane potential to follow cytokine effects on > mitochondria and possible dysfunction in chronic > fatigue syndrome. (Meeting Abstract). Biophysical > Journal 1999, 76, 1, A363. > > Short report of study focusing on cellular and > mitochondrial energy metabolism in individual living > cells using laser scanning confocal microscopy. The > findings suggested " possible mitochondrial > dysfunction. Interferon-a added to cultured human > fibroblasts or leukocytes was found to decrease > mitochondrial membrane potentials and areas at > mitochondrial potentials. Interleukin-2 also affects > mitochondrial potentials and may induce an unexplained > photosensitivity. " > > 2)Cheney et al put out a " talking paper " in 1992? > 1994? (can't find actual paper right now but working > from some notes) that identified over a half a dozen > metabolites that are not functioning properly. > Essential chemicals are either not crossing cell > membranes, or are not " piggy-backing " other needed > chemicals into the cell if able to cross. > Subsequently, the cellular mitochondria have a reduced > amount of the essential elements necessary to combust > fat and oxygen to release energy --> ATP. The > dysfunction is not well understood at present ... > > 3)Acta Neuropathol (Berl) 1991;83(1):61-5 > Mitochondrial abnormalities in the postviral fatigue > syndrome. > Behan WM, More IA, Behan PO > Department of Pathology, University of Glasgow, > Scotland. > > We have examined the muscle biopsies of 50 patients > who had postviral fatigue syndrome (PFS) for from 1 to > 17 years. We found mild to severe atrophy of type II > fibres in 39 biopsies, with a mild to moderate excess > of lipid. On ultrastructural examination, 35 of these > specimens showed branching and fusion of mitochondrial > cristae. Mitochondrial degeneration was obvious in 40 > of the biopsies with swelling, vacuolation, myelin > figures and secondary lysosomes. These abnormalities > were in obvious contrast to control biopsies, where > even mild changes were rarely detected. The findings > described here provide the first evidence that PFS may > be due to a mitochondrial disorder precipitated by a > virus infection. > > 4)Ciba Found Symp 1993;173:146-54; discussion 154-9 > Enteroviruses and postviral fatigue syndrome. > Behan PO, Behan WM, Gow JW, Cavanagh H, Gillespie S > Department of Neurology, University of Glasgow, UK. > > “An increase in the number and size of muscle > mitochondria was found in 70% of PFS cases, suggesting > an abnormality in metabolic function. Evidence of > hypothalamic dysfunction was present, particularly > involving 5-hydroxytryptamine metabolism.” > > 5)In vitro Study of Muscle Aerobic Metabolism in > Chronic Fatigue Syndrome > > [ Journal of Chronic Fatigue Syndrome Vol. 5, No. 1, > 1999 ] > WIhelmina M. H. Behan, MD, FRCPath, FRCP > Ian J. Holt, PhD > H. Kay, MBChB > Pamela Moonie, BSc > > Muscle aerobic metabolism in CFS…mitochondrial DNA > (mtDNA) volume was measured and mtDNA rearrangements > sought. The results showed that myoblasts > from ten of 16 cases of CFS had defects in aerobic > metabolism > > 6)TITLE: Reduced oxidative muscle metabolism in > chronic fatigue syndrome > AUTHORS: McCully KK; Natelson BH; Iotti S; Sisto S > Leigh JS Jr > > In conclusion, oxidative metabolism is reduced in CFS > patients compared to sedentary controls. > NLM PUBMED CIT. ID: 8618560 > SOURCE: Muscle Nerve 1996 May;19(5):621-5 > > 7)Neuromuscul Disord 1998 May;8(3-4):204-9 > > Heterogeneity in chronic fatigue syndrome: evidence > from magnetic resonance spectroscopy of muscle. > Lane RJ, Barrett MC, DJ, Kemp GJ, Lodi R > > “…but at the end of exercise, intracellular pH in the > SATET +ve patients was significantly lower than in > both the SATET -ve cases and controls (P < 0.03), and > the SATET +ve patients also showed a significantly > lower ATP synthesis rate during recovery (P < 0.01), > indicating impaired mitochondrial oxidative > phosphorylation…. > > This cannot be explained satisfactorily by the effects > of 'inactivity' or 'deconditioning'.” > > > __________________________________________________ > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 16, 2000 Report Share Posted January 16, 2000 Hi, Oh! I do hope you are right!! Mito diseases are inherited ONLY through the mother and if that was what your baby had, you were right to ask for testing!! And the fresh muscle tissue biospy is the definative dx! I can get you more info if you would like. If you are in Midwest, Cleveland CLinic does them, and rheumatologists and neurologists cover this disorder from what I have learned so far. This is scary stuff, but might very well be another factor in the CFS/FM mystery. Take care, CHristie At 08:09 PM 1/8/00 -0500, you wrote: >From: oliveira@... ( Oliveira) > >A few years ago I had a baby that was born with gobal neurological >impairment and he was tested for a Mitochondrial Disorder by having a muscle >biopsy. The neurologist was the one involved with this diagnosis. In the >end I was told that it was not a Mitochondrial Disorder, and all other tests >(including every genentic test available) came up with no answers (the story >of my life). He only lived a few months, which was a blessing with his >impairments. I asked the neurologist about having myself tested for a >Mitochondrial Disorder, and he assured me that that was not necessary >because he felt sure that that was not my problem. Being that I am feeling >much better than I did a few years ago, I have to believe that this is true. >I am looking into getting the myco test done through IMM. My gut tells me >that some kind of infection is at the root of my illness. >--- > >>From: siouxie@... >> >>To whomever posted the info about mitochondrial disease: >> >>What specialty of doctors sees people with mitochondrial disease? What >>type of health care professional should I look for if I want to be >>evaluated for this? This looks as if it might be fruitful in my case. >> >>Thanks. >> >>Sue >> >> >>--------------------------- Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 16, 2000 Report Share Posted January 16, 2000 >A few years ago I had a baby that was born with gobal neurological >impairment and he was tested for a Mitochondrial Disorder by having a muscle >biopsy. The neurologist was the one involved with this diagnosis. In the >end I was told that it was not a Mitochondrial Disorder, Hi, I'm sorry - he did NOT have a mito disease - that is a relief and please do not let previous post upset you! I'm upset about this stuff enough for everyone right now! PULM's partner who doesn't know meor my history, says my cardio-stress was normal even tho I couldn' do it!!! Same old stuff here.....! CHristie Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 17, 2000 Report Share Posted January 17, 2000 Hi, TNANK YOU so much - this is incredibly helpful!!! Also think mito's are interwoven with our mystery illness. Take care, Christie At 04:45 PM 1/14/00 -0800, you wrote: >From: Jim Toomey <jim_toomey@...> > >Some CFS mito studies or excerpts > >Rgds, >Jim > >----- > >1)Chazotte, B and Pettengill, M. > >Using membrane potential to follow cytokine effects on >mitochondria and possible dysfunction in chronic >fatigue syndrome. (Meeting Abstract). Biophysical >Journal 1999, 76, 1, A363. > >Short report of study focusing on cellular and >mitochondrial energy metabolism in individual living >cells using laser scanning confocal microscopy. The >findings suggested " possible mitochondrial >dysfunction. Interferon-a added to cultured human >fibroblasts or leukocytes was found to decrease >mitochondrial membrane potentials and areas at >mitochondrial potentials. Interleukin-2 also affects >mitochondrial potentials and may induce an unexplained >photosensitivity. " > >2)Cheney et al put out a " talking paper " in 1992? >1994? (can't find actual paper right now but working >from some notes) that identified over a half a dozen >metabolites that are not functioning properly. >Essential chemicals are either not crossing cell >membranes, or are not " piggy-backing " other needed >chemicals into the cell if able to cross. >Subsequently, the cellular mitochondria have a reduced >amount of the essential elements necessary to combust >fat and oxygen to release energy --> ATP. The >dysfunction is not well understood at present ... > >3)Acta Neuropathol (Berl) 1991;83(1):61-5 >Mitochondrial abnormalities in the postviral fatigue >syndrome. >Behan WM, More IA, Behan PO >Department of Pathology, University of Glasgow, >Scotland. > >We have examined the muscle biopsies of 50 patients >who had postviral fatigue syndrome (PFS) for from 1 to >17 years. We found mild to severe atrophy of type II >fibres in 39 biopsies, with a mild to moderate excess >of lipid. On ultrastructural examination, 35 of these >specimens showed branching and fusion of mitochondrial >cristae. Mitochondrial degeneration was obvious in 40 >of the biopsies with swelling, vacuolation, myelin >figures and secondary lysosomes. These abnormalities >were in obvious contrast to control biopsies, where >even mild changes were rarely detected. The findings >described here provide the first evidence that PFS may >be due to a mitochondrial disorder precipitated by a >virus infection. > >4)Ciba Found Symp 1993;173:146-54; discussion 154-9 >Enteroviruses and postviral fatigue syndrome. >Behan PO, Behan WM, Gow JW, Cavanagh H, Gillespie S >Department of Neurology, University of Glasgow, UK. > >“An increase in the number and size of muscle >mitochondria was found in 70% of PFS cases, suggesting >an abnormality in metabolic function. Evidence of >hypothalamic dysfunction was present, particularly >involving 5-hydroxytryptamine metabolism.” > >5)In vitro Study of Muscle Aerobic Metabolism in >Chronic Fatigue Syndrome > >[ Journal of Chronic Fatigue Syndrome Vol. 5, No. 1, >1999 ] >WIhelmina M. H. Behan, MD, FRCPath, FRCP >Ian J. Holt, PhD > H. Kay, MBChB >Pamela Moonie, BSc > >Muscle aerobic metabolism in CFS…mitochondrial DNA >(mtDNA) volume was measured and mtDNA rearrangements >sought. The results showed that myoblasts >from ten of 16 cases of CFS had defects in aerobic >metabolism > >6)TITLE: Reduced oxidative muscle metabolism in >chronic fatigue syndrome >AUTHORS: McCully KK; Natelson BH; Iotti S; Sisto S >Leigh JS Jr > >In conclusion, oxidative metabolism is reduced in CFS >patients compared to sedentary controls. >NLM PUBMED CIT. ID: 8618560 >SOURCE: Muscle Nerve 1996 May;19(5):621-5 > >7)Neuromuscul Disord 1998 May;8(3-4):204-9 > >Heterogeneity in chronic fatigue syndrome: evidence >from magnetic resonance spectroscopy of muscle. >Lane RJ, Barrett MC, DJ, Kemp GJ, Lodi R > >“…but at the end of exercise, intracellular pH in the >SATET +ve patients was significantly lower than in >both the SATET -ve cases and controls (P < 0.03), and >the SATET +ve patients also showed a significantly >lower ATP synthesis rate during recovery (P < 0.01), >indicating impaired mitochondrial oxidative >phosphorylation…. > >This cannot be explained satisfactorily by the effects >of 'inactivity' or 'deconditioning'.” > > >__________________________________________________ > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 17, 2000 Report Share Posted January 17, 2000 >Interferon-a added to cultured human >fibroblasts or leukocytes was found to decrease >mitochondrial membrane potentials and areas at >mitochondrial potentials. Hi, I need a better mind than mine. How does anyone read this - that decreasing mito membrane potentials is a positive or a negative? >From: Jim Toomey <jim_toomey@...> > >Some CFS mito studies or excerpts > >----- > >1)Chazotte, B and Pettengill, M. > >Using membrane potential to follow cytokine effects on >mitochondria and possible dysfunction in chronic >fatigue syndrome. (Meeting Abstract). Biophysical >Journal 1999, 76, 1, A363. > >Short report of study focusing on cellular and >mitochondrial energy metabolism in individual living >cells using laser scanning confocal microscopy. The >findings suggested " possible mitochondrial >dysfunction. Interferon-a added to cultured human >fibroblasts or leukocytes was found to decrease >mitochondrial membrane potentials and areas at >mitochondrial potentials. Interleukin-2 also affects >mitochondrial potentials and may induce an unexplained >photosensitivity. " Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 5, 2000 Report Share Posted July 5, 2000 In a message dated 7/5/00 5:44:08 AM Pacific Daylight Time, esp@... writes: << What was important to me about going through the mito testing was that now I have a doctor who 1) knows specificaly wants wrong in the metabolic pathways and can treat accordingly (instead of the russian roulette of trying things) 2) can tell me what to NOT take (Xanax and Klonopin made me very very very severely sick and bedridden, standard CFS drugs for sleep). Many drugs are very contraindicated with mito problems and now I have someone who knows exactly which ones. 3) I can follow the specific research in my metabolic situation which again is more specific than some of the CFS treatments. >> I can't take Klonopin or Xanax either. I feel so very much WORSE on them. Why is this? Also, what other things are bad and should I avoid with Mito problems? karen Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 5, 2000 Report Share Posted July 5, 2000 Beth, please give name and phone number of your doctor. Thanks >From: ES <esp@...> >Reply-egroups >egroups >Subject: mitochondrial disease >Date: Wed, 05 Jul 2000 08:38:21 -0400 > >Jim, > >Thanks for responding to my mito diagnosis. Since I'll be leaving the >list in about a week please feel free to e-mail me directly. I'd like to >keep in touch with other CFS/mito people. > >Are you taking perscription Carnitine/Carnitor? Did it help??? I am >about to start it. > >I consider myself as having both diagnosises: CFS & mito. My case of CFS >obviously involves metabolic problems in the mitochondria. It doesn't >fit into one of the well-known Mito disease classifications though so my >guess is for now I have CFS with a mito involvement which, down the >road, will be a new named mito disease....though of course that assumes >there is no active virus going on...if there is then it would eventually >be named for the virus and mito involvement would be secondary. It's >still all a great mystery. > >What was important to me about going through the mito testing was that >now I have a doctor who 1) knows specificaly wants wrong in the >metabolic pathways and can treat accordingly (instead of the russian >roulette of trying things) 2) can tell me what to NOT take (Xanax and >Klonopin made me very very very severely sick and bedridden, standard >CFS drugs for sleep). Many drugs are very contraindicated with mito >problems and now I have someone who knows exactly which ones. 3) I can >follow the specific research in my metabolic situation which again is >more specific than some of the CFS treatments. > >Also research on Mito is about to increase dramatically....for instance >your muscle biopsy of 10 years ago would now have told them much much >much more if it was redone now. They are using incredibily high-tech >procedures now to look at each part of the metabolic process. In about a >year there is supposed to be a blood test available for diagnosis and >then it should get really interesting as many more people will be able >to get tested....the more mito diagnosis that start happening the more >research will increase. > >When I get a full written diagnosis treatment plan I will post that. It >may be another month or so before I have this. best, Beth > > ________________________________________________________________________ Get Your Private, Free E-mail from MSN Hotmail at http://www.hotmail.com Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 26, 2003 Report Share Posted January 26, 2003 What would you like to know concerning the mitochondria and oxygen? Lane Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 26, 2003 Report Share Posted January 26, 2003 , When I was taking my son for Hyperbaric Oxygen treatments last fall at Ocean Hyperbarics, http://www.oceanhbo.com/ There was a family there who's little girl was doing absolutly wonderful after receiveing quite a number of treatments. She suffers from mitochondrial disease. She is 4 years old and very adorable. I won't release their name but as her mother told me their story, I would have found it hard to believe without seeing that little girl in person. If you have medical questions about treatment for mitochondrial disease, Doctor Neubauer who runs Ocean Hyperbarics, http://www.drneubauerhbo.com/ knows and can help. Dave Snow At 10:46 PM 1/25/03 -0600, you wrote: >Does anyone have any information about mitochondrial disease and HBOT? > >Thanks, > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 26, 2003 Report Share Posted January 26, 2003 Hi , The little I know is that the PO2 level at the mitochondria is approx 1-2%. Many believe that due to this low perfusion, HBOT to be toxic. However, others have shown that the very opposite is true: HBOT is ideal because it increases the O2 perfusion at the basic cellular levels. From my personal experience with HBOT and my recently identified " heteroplasmic nucleotide change in the ND1 subunit of the mitochondrially encoded complex I chain " , I agree wholeheartedly with Dr. Harch, et al. Sorry I can't be more helpful. I am currently actively pressuring, oops, I mean enthusiastically encouraging a mitochondria specialist to begin researching this area. Joanne ________________________________________________________________ Sign Up for Juno Platinum Internet Access Today Only $9.95 per month! Visit www.juno.com Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 26, 2003 Report Share Posted January 26, 2003 Dr. Neubauer from Florida has had a wonderful case with mitochondrial disease the little girls name is Grace and her mothers name is you can call there office at 954-771-4000 and ask for to give you a call back and she will. It was amazeing I watched this girl go from not walking eating by g-tube and so much more to almost a complete recovery. They did a Television special on this child. She made so much progress. IM not to sure of the protocol they used to treat her but the results were amazing. Hope I was able to give you something to go on. Darin 972-427-8825 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 28, 2003 Report Share Posted January 28, 2003 Hi Dr. , Re: pO2 level at the mitochondria being 1 -2 mm HG, Did I misunderstand and/ or misapply? Sorry. Doesn't the partial pressure effect the hemoglobin's ability to bond with the oxygen, i.e. the greater the pO2, the stronger the bond/ the more oxygen can be transported/ exchanged increasing the SAO2? If this is true, and HDOT increases the pO2 level, doesn't it facilitate its ability to bind with the hemoglobin -- enabling the cell's " power pack " to work more efficiently? Please, will you clarify? I recently share this with someone else besides and I need to go back and correct my mistake. Thanks! I appreciate your help! Joanne Brindley ________________________________________________________________ Sign Up for Juno Platinum Internet Access Today Only $9.95 per month! Visit www.juno.com Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 28, 2005 Report Share Posted January 28, 2005 Keep encouraging your friend to get her daughter treated with HBOT. Having personally visited with Gracie's mom and having observed Gracie's improvements I sincerely believe it would be worthwhile for your friend to try HBOT with her daughter. Virginia Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 29, 2005 Report Share Posted January 29, 2005 Hi ! My name is Joanne and I have dystonia and mitochondrial dysfunction. I have done awesome with HBOT, especially in combination with physical therapy. The pO2 levels at the mitochondrial level, if I remember correctly, is 2. Therefore any additional O2 can't help but be beneficial. Of course, there are concerns about free radicals, but that is why various vitamins are recommended during treatment. Feel free to contact me. Joanne Brindley auntie_j@... 508 580-4554 ___________________________________________________________________ Speed up your surfing with Juno SpeedBand. Now includes pop-up blocker! Only $14.95/month -visit http://www.juno.com/surf to sign up today! Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 31, 2005 Report Share Posted January 31, 2005 Dear Mrs. Brindley, and friends, human mitochondrial disease is helped by hyperbaric oxygen. Mitochondria are cellular organelles derived from protobacteria that seeked shelter from oxygen in the depths of higher animals'cells. An oxygen cascade limits pO2 at mitochondrial levels to very low figures. Any tissue with an impaired protective system may develop toxicity. Free radicals are not only produced by higer levels of oxygen (oxidative stress), but paradoxically the more by hypoxia. As for supplementation with vitamins being useful to limit the damage, specific data remains inconclusive. Hyperbaric oxygen, on the contrary, seems to help both directly and indirectly, by stabilizing cell membranes and by upregulating the production of catalase, superoxide dismutase and peroxidase, the cell's enzimatic protective array. It is a challenge to the tissues, so it must be done at the proper dosage. If brain or pulmonary tissues were affected, higher pressures and concentration, or longish -or too frequent- sessions may prove deleterious. Physical therapy or exercise will augment the rate of oxygen provision and consumption at selected organs and structures, so it should not be done while receiving oxygen, but only inbetween sessions, after some rest, unless the pressures were ultra-low or mild, and only after its harmlessness had been established for the individual patient. Nonetheless, hyperbaric oxygen has ben shown to be helpful in these otherwise incurable conditions, as you have experienced. Best regards, Ignacio Fojgel, M.D. Maimonides University Buenos Aires, Argentina auntie_j@... wrote: >Hi ! >My name is Joanne and I have dystonia and mitochondrial dysfunction. I have done awesome with HBOT, especially in combination with physical therapy. The pO2 levels at the mitochondrial level, if I remember correctly, is 2. Therefore any additional O2 can't help but be beneficial. Of course, there are concerns about free radicals, but that is why various vitamins are recommended during treatment. > >Feel free to contact me. >Joanne Brindley >auntie_j@... >508 580-4554 > >___________________________________________________________________ > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 30, 2007 Report Share Posted June 30, 2007 Hi, idarchetype2000. Dr. Myhill and I have just finished writing a paper on mitochondrial dysfunction in CFS, and are in the process of trying to get it published in a journal. While we can't totally rule out inherited genetic issues involving either the mitochondrial genome or the parts of the cell's nuclear genome that code for most of the proteins in the mitochondria, it appears that in most cases of CFS we are dealing with mitochondrial dysfunction as a secondary effect, rather than a primary mitochondrial disease. My own view is that glutathione depletion, associated with a methylation cycle block, is what initially causes the mito dysfunction, and then other things happen to compound the problem, as a result of the lack of enough glutathione to protect the mitochondria, including buildup of toxins, buildup of viral infections, and damage by reactive oxygen species, and depltion of intracellular magnesium. If you look at the results of mito testing from Biolab in London, which people have reported on these lists, those are the kinds of things you see. But in my opinion, they are downstream of the root cause, which we are going after with the treatment to lift the methylation cycle block. Over 50 people are now trying the simplified treatment approach, and the reports coming back are really fun to read. The symptoms of CFS are falling away one at a time as this treatment takes hold. If you want to track the progress, join the ImmuneSupport CFS discussion board and read the threads that have " methylation " in their titles. Rich > > I have been doing research trying to understand more about the results > of my genova detox panel test and came across mitochondrial diseases > and wondered if having problems with one's phase 11 of detox could > indicate mitochondrial disease. > Reading about mitochondrial related problems it seems to me that half > the people who have fms/cfs could just have undiagonsed mitochondrial > disorders, seems like something physicians may not look into because > can be invasive testing and may be trained to only think of it in > extreme cases like with deafness etc. > any knowledge on this ? > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 30, 2007 Report Share Posted June 30, 2007 For Dr Myhil's mitochondrial dysfunction information, see http://www.ei-resource.org/Articles/cfs-art20.asp Her web site is here: http://www.drmyhill.co.uk/ Sue rvankonynen wrote: > Dr. Myhill and I have just finished writing a paper on mitochondrial > dysfunction in CFS, and are in the process of trying to get it > published in a journal. While we can't totally rule out inherited > genetic issues involving either the mitochondrial genome or the parts > of the cell's nuclear genome that code for most of the proteins in the > mitochondria, it appears that in most cases of CFS we are dealing with > mitochondrial dysfunction as a secondary effect, rather than a primary > mitochondrial disease. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 30, 2007 Report Share Posted June 30, 2007 Um, what is " phase 11 " ? What scale is this on? As always, TIA, Marcia on in Salem, Massachusetts > > I have been doing research trying to understand more about the results > of my genova detox panel test and came across mitochondrial diseases > and wondered if having problems with one's phase 11 of detox could > indicate mitochondrial disease. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 30, 2007 Report Share Posted June 30, 2007 I have been trying to look into this also. I think it makes sense, while trying different CFS " protocols " (that can take months or years to yield benefit), to also investigate the possibility of a Mito DISEASE (not just a Mito DYSFUNCTION secondary to the CFS disease). You've probably found www.umdf.org That site indicates the different levels of testing involved in investigating these diseases. Also the " Mitoldies " group is for adults with Mito DISEASE. Someone posted this link a few days ago: http://www.fodsupport.org/medical_info.htm#fodlabs This lists labs that do skin fibroblast testing, which can show evidence of metabolic or mitochondrial disease. It is quite difficult to find doctors who deal with adult onset mito disease. Also the most informative testing is muscle biopsy, invasive as you note, and difficult to get done correctly (the issue of " frozen " versus " fresh " muscle biopsy apparently becomes important). My current thinking is that getting skin fibroblasts tested might be a next step, before trying to find a mito doctor and getting a muscle biopsy done. I think this would involve contacting one of the labs, getting a kit or instructions, and taking them to an agreeable dermatologist. He/she takes the skin biopsies (not very invasive little skin punch samples), sends them to the lab, and receives the results. If they indicate a problem, then the next step in investigative testing/doctor finding can be taken. The frustrating thing is that even if you do have a Mito DISEASE, extensive testing (including genetic blood tests, muscle biopsy, etc.) with even the most knowledgeable doctors may not result in a specific diagnosis. As an aside, and an example of the many possibilities, this woman talks about Lyme and a mitochondrial disease involving vitamin B1 metabolism: www.lymeinfo.net/thiamin.html Good luck; please share what you learn. > > I have been doing research trying to understand more about the results > of my genova detox panel test and came across mitochondrial diseases > and wondered if having problems with one's phase 11 of detox could > indicate mitochondrial disease. > Reading about mitochondrial related problems it seems to me that half > the people who have fms/cfs could just have undiagonsed mitochondrial > disorders, seems like something physicians may not look into because > can be invasive testing and may be trained to only think of it in > extreme cases like with deafness etc. > any knowledge on this ? > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 30, 2007 Report Share Posted June 30, 2007 thanks for the input, its helpful, there are so many layers to all this that I can use all the help I can get. to the person who asked what phase 11 is, I am not the best person to explain as I just have a laymens understanding, but perhaps if you google genova diagnostics and read the info about their detoxification profile, comprehensive, there would be some info there. The gist of it is when we detox chemicals, nutrients, there are different phases we go through from the time we ingest it until the time its out of us and the profile looks at how we are functioning in that process to help make determinations on individual treatment approach. > > > > I have been doing research trying to understand more about the results > > of my genova detox panel test and came across mitochondrial diseases > > and wondered if having problems with one's phase 11 of detox could > > indicate mitochondrial disease. > > Reading about mitochondrial related problems it seems to me that half > > the people who have fms/cfs could just have undiagonsed mitochondrial > > disorders, seems like something physicians may not look into because > > can be invasive testing and may be trained to only think of it in > > extreme cases like with deafness etc. > > any knowledge on this ? > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 30, 2007 Report Share Posted June 30, 2007 Ah, thanks for directing me to Genova's web site. I was thinking your reference was to the Yasko protocol's " Step 1 " and " Step 2 " , but it looks like you were referring to Genova's " Phase I " and " Phase II " . Alas, too much brain fog today to read through it all and understand it, but I bookmarked it to come back and try again later. Marcia on in Salem, Massachusetts > > to the person who asked what phase 11 is, I am not the best person to > explain as I just have a laymens understanding, but perhaps if you > google genova diagnostics and read the info about their > detoxification profile, comprehensive, there would be some info > there. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 30, 2007 Report Share Posted June 30, 2007 miss id, You're on the right path because CFS Specialists have been saying we have malfunction of the Mitochondria since the earliest days of CFS. I also recall some patients suspected of full on Mito disorders and getting tested at s Hopkins and the NIH. Actual Mito disease must be difficult to isolate, becasue they were receiving mixed reports even at those institutions.(then I lost track of them). I also thought a blood test was coming, a less invasive tool. For some reason, in recent years, I've had difficulty getting a discussion going on Mitochondria on this list, so I'm glad it's being brought up. If anyone wants to do a search of the archives of this list, you will probably find some interesting (Mito) posts, going back to the beginning (1999). It might also be interesting to do a google search on Mito + CFS...perhaps our Researchers thinking might be found there...specific to CFS. Mitochondria dysfunction is definitely still alive in Dr. Cheney's thinking. That is precisely the difference he says in the Diastolic Heart Failure that we have as opposed to more standard (DD is a newer field, period, in Cardiology). AS he explained it to me, CFS DD is a problem of energy, rather than structure of the heart. Patients who are horizontal are actually protecting their heart. ( I'd think probably muscles, brain, also) Mitochondria also has always been suspected as part of our muscle " weakness/fatigue " . The results of those PWCs tested by an MRS brain scan (including me) show small lactate peaks in sections of the brain. These peaks are found much higher in those born with full Mitochondria disease. They indicate a problem metabolising sugar, meaning there's a metabolic waste product in brain that should not be there.. Proper metabolising requires functioning Mitochondria. I remember long ago, Dr. Cheney, saying we have Glutathione depletion, which means we do not detox properly. He spent alot of the 90s trying to find ways to raise it. This was before some of the products we have now, which he is using, which are more efficient methods. His trial of Immunocal/Immunopro are why I began IP in 2000? But he also told me in 2005 that Glutathione and other enzymes are need for the Mitochondria to function properly. It's been said that technically aging and dying are Mitochondria failure. Glutathione also began to be focused on in many chronic diseases some years ago. So hopefully, both of these will be featured more in Medicine in general, and will help us with CFS. These advances may, (I hope!), make it easier to bring the topics up with our doctors too, even tho our own experts are constantly turned down for funding of areas they have been onto for many years! There is a transcript from Carol S's appointment with Dr. Cheney with some discussion of the CFS MRS findings. It is on immunesupport.com. It's possible that one might find PWCs on Mito patient forums. I found this to be the case many years ago on patient forums of severe Dysautonomia. Since our own Researchers are not properly funded or recognised, other fields which are, or at least more so, can give us insights. Even if the whole overview of ME/CFS is not covered there. TC, Katrina > > I have been doing research trying to understand more about the results > of my genova detox panel test and came across mitochondrial diseases > and wondered if having problems with one's phase 11 of detox could > indicate mitochondrial disease. > Reading about mitochondrial related problems it seems to me that half > the people who have fms/cfs could just have undiagonsed mitochondrial > disorders, seems like something physicians may not look into because > can be invasive testing and may be trained to only think of it in > extreme cases like with deafness etc. > any knowledge on this ? > Quote Link to comment Share on other sites More sharing options...
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