martiz

An excerpt from a paper Rich Van Konynenberg wrote about how he connected the dots between ME/CFIDS and Autism: http://aboutmecfs.org.violet.arvixe.com/Trt/TrtMethylTheory.aspx A Simplified Treatment Approach Based on the Glutathione Depletion-Methylation Cycle Block Pathogenesis Hypothesis for Chronic Fatigue Syndrome (CFS) by Rich Van Konynenburg, Ph.D. . . . Autism, CFS and the Methylation Cycle. After I read the paper by S. Jill James and her coworkers (referred to above), I began to suspect that the genetic factors and biochemical mechanism they had found in autism are the same or similar to those important in CFS. A block earlier than glutathione in the sulfur metabolism, at the methylation cycle, could explain the persistent glutathione depletion in CFS. It began to dawn on me that other aspects of CFS that did not appear to be explained by glutathione depletion per se could be explained by a methylation cycle block. It was difficult for me initially to believe that there was a connection between autism and CFS, given the profoundly different symptoms and different affected population groups (primarily boys in autism, compared to primarily adult women in CFS). However, I knew of others who had publicly suggested such a connection in the past. (Dr. Michael Goldberg in the U.S. and Prof. Malcolm Hooper in the UK), and this new study seemed to provide more detailed evidence of this connection at the genetic and biochemical levels. I began to look into autism in more detail, and I attended the Long Beach conference of the Defeat Autism Now! (DAN!) project in October of 2005. The more I learned about autism, the more I became convinced that are dealing in CFS with many of the same issues at the genetic and biochemical levels. The book by Drs. Jon Pangborn and Sidney Baker entitled "Autism: Effective Biomedical Treatments" (Autism Research Institute, September, 2005) provides excellent explanations of the biochemistry of autism, and the parallels with CFS can be seen there. I want to emphasize that I did not develop the Glutathione Depletion--Methylation Cycle Block Hypothesis out of thin air. The autism researchers had already provided a convincing basis for this model in that disorder. S. Jill James and coworkers did much of the clinical work that underlies it. Richard Deth and his coworkers had worked out much of the theory of the methylation cycle block and had applied it to autism. Professors James and Deth had been presenting talks on their work at autism conferences. The physicians in the DAN! project (as well as Dr. Amy Yasko, though I had not yet learned of her work when I began to understand the importance of the methylation cycle block) had already been treating autism cases by measures intended to lift the methylation cycle block. What I did was to apply the results of their work to CFS, and to present a detailed biochemical and symptomological case to support the proposition that this model also applies to CFS. What is the Essence of the Glutathione Depletion-Methylation Cycle Block Hypothesis for the Pathogenesis of CFS? This hypothesis proposes first that in order to develop CFS, a person must have inherited genetic variations (also called SNPs or single-nucleotide polymorphisms) in a combination of certain genes that code for enzymes and other proteins associated with the methylation cycle and related pathways. The hypothesis further proposes that the person must also be subjected to some combination of a variety of long-term physical, chemical, biological or psychological/emotional stressors that lowers glutathione levels to the point that a block occurs in the enzyme methionine synthase in the methylation cycle, in response to the oxidative stress that is inherent in glutathione depletion. The formation of this block is aided by the presence of the inherited genetic polymorphisms. This lowering of glutathione levels also simultaneously removes the normal protection that glutathione provides to vitamin B12 and allows the accumulation in the body of toxins that can interfere with the utilization of vitamin B12, mercury perhaps being the dominant one. This hypothesis further proposes that the result of the above is that the level of methylcobalamin is held too low to support the methionine synthase reaction, and it therefore becomes chronically blocked. This produces a vicious circle mechanism that causes CFS to become a chronic condition. Finally, this hypothesis proposes that all the features of CFS can be shown to originate from this root cause. While I have not yet demonstrated this for every feature of CFS, the first paper cited in this article explains a large number of them in detail on this basis. Previous treatments for CFS have dealt with downstream issues in the pathogenesis, but they have not completely addressed this root cause, and, in my opinion, that is we have not seen many completely cured CFS cases up to now. Note that when I refer to cured cases, I do not mean that the genetic predisposition has been removed, but that that the PWCs are healthy from the symptomatic point of view. As I became more convinced of the parallels between autism and CFS, I began to point out this connection to some clinicians directly and to others via the internet, as well as to PWCs in internet groups, and I began encouraging them to consider the treatments that were being used by the Defeat Autism Now! project to treat autism, focusing on unblocking the methylation cycle. A small number of PWCs tried this approach, and while some initial benefits were observed from this, it did not seem to be an effective approach over the long term, at least in the way I was suggesting that it be applied. Dr. Amy Yasko I then learned of the work of Dr. Amy Yasko, N.D., Ph.D. in autism. I studied her materials, including the book written by her and Dr. Garry Gordon entitled "The Puzzle of Autism," joined her discussion forum at http://www.ch3nutrigenomics.com and eventually attended her teaching seminar in Boston in October of 2006. After considering all of this, I concluded that it was likely that her treatment approach could help many PWCs, so I decided to emphasize it. An important feature of her work is her effort to tie the genetics of individuals to the biochemistry and to do tailored treatment based on genetics, again directed toward correcting the methylation cycle block, but also incorporating support for a variety of body systems and organs. I also learned that Dr. Yasko had had some experience in using her approach in cases of CFS as well as a variety of adult neurological disorders, but that she was currently focusing primarily on autism. . . ."

I thought I would start a new thread rather than hijack Rich's post about GABA As others have noted, ME/CFIDS and POTS have a similar symptom list and are thought to be related. I thought I would point out that for several years now, ME/CFIDS and Autism are thought to be related. In 2005, a prominent ME/CFIDS researcher made the connection between ME/CFIDS and autism. I have attached some links to those who like to do research and a couple of excerpts for ease of reading. Happy to discuss and throw ideas around. Marti Initial post from RichGotsPots thread about GABA: Quote Marti Said: (ME/CFIDS population being much like the autistic population - I have gotten a lot of help from this type of doctor). RAMA Said: In what way? Increased sensitivity to light and sound are probably the only things I can see as similar. My wife works in Autism and we've talked about this at length. Marti Said: The methylation pathway defects are exactly the same, the glutathione deficiency. The difference in manifestation is thought to be the age of the brain at the time of insult/assault - the older the brain, then females are affected. A young brain, males are affected. Dr. Amy Yasko from Maine and some DAN! doctors have been working in this area for some years. Rich Van Konynenberg, an ME/CFIDS researcher was the first to make the connection some years ago and is bridging the two populations. I can provide some of his papers or Dr. Yasko's if you want more info.... I have two autistic children in my Sunday School class and have similar genetic defects/methylation defects (I have compared their genetic tests and bloodwork to my own. I have several autistic relatives but I have never had access to their bloodwork. My SS kids and I share the same doc and I have tried to help their parents understand the tests. MTHFR C677T/A1298C is a major one. CBS COMT MTR MTTR Here is a link of some of Rich's papers. The first one is from 2004 where he has made the jump from ME/CFIDS to Autism. http://aboutmecfs.or...rtGSHIntro.aspx Dr Yasko - she has allowed ME/CFIDS adults to participate in her forum for parents of autistic kids since the populations are similar. She is now accepting ME/CFIDS adults as "patients" - not full blown patients as her focus is the children. But she will review bloodwork and genetics. http://www.dramyyasko.com/ Let me know if you want more info. Marti

I have sensitivity to light and sound that began after my last relapse when the POTS took front and center and the ME/CFIDS and Fibro took a back seat. My house is very dark which my son hates so I remove the dark blinds when he is home from college. I CANNOT have him talking to me when a movie is playing - we watch a lot of movies we have already seen and so he tries to start a conversation - it drives me beserk! One of my autistic SS kids must make noises with a toy on the table and the constant rapping makes me crazy! But I also see other behaviors in myself and my son that are similar - shyness in social settings, exaggerated and prolonged response to hurt, physical or emotional, increased level of anxiety, some OCD tendencies. One of the kids who is autistic has a sister who is hyper mobile which I now find interesting. But there is more shared biochemically than social traits but that's just my opinion. I don't know any severely autistic children just the two high functioning ones. And my relatives who are affected are also high functioning. Marti

Hi Issie, Isn't that the way things go.... you hear or learn something then all of a sudden, references to that subject are everywhere! I have gotten the most help for my ME/CFIDS from following all of the dietary restrictions that autistic kids follow. My son and I take the same vitamins that they take - with bioavailable versions of most B vitamins, no iron, no copper. We are gluten free, casein free and like you, I am finding that I feel better with a grain free diet. My son displayed autistic tendencies when he was young but it wasn't severe enough to see a doctor so he was never diagnosed. He was very OCD as I was when I was young. But he is very bright and that has to do with the glutamate issue as well. The brain need glutamate to learn and lay down memories. The autistic population have an imbalance in the GABA/Glutamate system so they have excess glutamate in their brains which is why most of the population are so bright almost savant. Unfortunately, too much glutamate causes early cell death due to the excitatory effect which doesn't show until they are older. Luckily, we learned about this before my son became an adult so he also is off glutamates. It was so hard getting off glutamates but now when I ingest some in a restaurant -most likely MSG in flavorings or just plain MSG, I have a severe reaction - urticaria (hives) from neck to waist. So, we rarely eat out because one meal out has such high levels of glutamates. I have found that taking an extra GABA helps resolve that faster - so I have taken 1000mg in one day! But not at the same time as the extra GABA was after dinner or in the middle of the night when the hives started. And no, I can report that I never had the reaction you speak of - in fact, it has been the opposite. I would wake up after a meal out, wired and unable to sleep, itching and skin crawlies. It would only be after taking another GABA and a Benadryl that I would be able to go to sleep (it was probably the benadryl that helped me sleep but I feel that there surely was a time that I just took one extra gaba). Not sure as that was some years ago - now we just don't eat out. Our brains need glutamates - it's the excess from processed foods that gets us into trouble. Right now, I seem to be doing well on a paleo type diet. Marti

In what way? Increased sensitivity to light and sound are probably the only things I can see as similar. My wife works in Autism and we've talked about this at length. The methylation pathway defects are exactly the same, the glutathione deficiency. The difference in manifestation is thought to be the age of the brain at the time of insult/assault - the older the brain, then females are affected. A young brain, males are affected. Dr. Amy Yasko from Maine and some DAN! doctors have been working in this area for some years. Rich Van Konynenberg, an ME/CFIDS researcher was the first to make the connection some years ago and is bridging the two populations. I can provide some of his papers or Dr. Yasko's if you want more info.... I have two autistic children in my Sunday School class and have similar genetic defects/methylation defects (I have compared their genetic tests and bloodwork to my own. I have several autistic relatives but I have never had access to their bloodwork. My SS kids and I share the same doc and I have tried to help their parents understand the tests. MTHFR C677T/A1298C is a major one. CBS COMT MTR MTTR Here is a link of some of Rich's papers. The first one is from 2004 where he has made the jump from ME/CFIDS to Autism. http://aboutmecfs.org.violet.arvixe.com/Trt/TrtGSHIntro.aspx Dr Yasko - she has allowed ME/CFIDS adults to participate in her forum for parents of autistic kids since the populations are similar. She is now accepting ME/CFIDS adults as "patients" - not full blown patients as her focus is the children. But she will review bloodwork and genetics. http://www.dramyyasko.com/ Let me know if you want more info. Marti

Hi LInda, What is myalgic encephalomyolitis? I googled it and cannot find it. Do you mean ME - Myalgic encephalomyelitis? as in Chronic Fatigue Sydnrome? Marti

Thanks Marti, so they get GABA levels through plasma and spinal fluid. I wonder if for POTS it matters what position we are in when they are taken. Was it taken by an autonomic lab? No, none of these tests were done by an autonomic lab. I have only recently been focusing on the autonomic issues. Actually, I have had them tested by urine, plasma and spinal fluid. Urine was part of the Genova Diagnostics ONE test through an autism doctor (ME/CFIDS population being much like the autistic population - I have gotten a lot of help from this type of doctor). The plasma and the CSF was part of a research study that I participated in at Georgetown University by an ME/CFIDS doctor. He is finding increased CSF pressure and elevated proteins in the CSF. I doubt that CSF is a common way to check these amino acid levels - it was part of the workup for the study. I think the most common way is urine or plasma. I found it interesting that the plasma showed 4 amino acids that were abnormal but normal in CSF. Both tests were done while supine (blood draw on the first day and spinal tap the next day). I am not getting the feeling that position has a bearing. I have never read much connecting GABA/Glutamate to adrenaline or cortisol. But I suppose there might be a connection. Hmmm. interesting thought. I would not have thought so but perhaps posture would make a difference. Marti Marti

Rich, To answer your initial question: I have had my organic acids/amino acids tested - both plasma and Cerebral Spinal Fluid. My glutamate (several versions) and my gaba levels were all normal. Let me know if you want numbers and ranges. Marti

Hi Issie, I found something right away. I disagree with a couple of points but the article seems pretty accurate. I pasted it here so you can read about the tingling that sounds like the reaction that you had. I bolded some points that we have already discussed. _______________________________________________ http://www.denvernaturopathic.com/news/GABA.html Side Effects: Although the newer studies with body builders report using high doses of GABA with little side effect, these results may not reflect the experience of a more sedentary person. Carl Pfeiffer devotes a full page in his book to describing an unpleasant experience he had after taking a 10 gram dose of GABA: “About ten minutes after taking the GABA, I started to wheeze and my breath rate increased to 45 a minute. Five minutes later, my heart rate peaked at 140 and my blood pressure at 180/100. I was choking, fidgeting and could not sit still. I had a massive anxiety attack, thinking I was going to die…….I vomited into the waste basket. Over the next half hour, this anxiety attack let up, but I continued to be nauseous for the next two hours. “This dose of GABA also caused a constant flush sensation, like that of niacin, although my skin was not red. I had a tingling in my hands and over my entire body. This effect occurred even at the lesser dose of 3 g of GABA and is likely neuralgic, unlike the effect of niacin which is primarily vascular……” [20] Home Experimentation: Probably the only way you will figure out if GABA works for you is to try it. GABA is nontoxic and appears generally safe to take. There is nothing stopping you from testing these contradictory claims for yourself. Below are suggested doses for treating various conditions. I personally had never taken GABA before reviewing this research and then stalled experimenting on it until I wrote this article. Once done with the preliminary drafts I experimented using 750 mg. capsules of GABA. I began taking them at 12 hour intervals. After the second dose I began to experience the tingling sensations reported by Pfeifer. I too thought them reminiscent of a niacin flush without the surface heat from vasodilatation. It was very noticeable for about five minutes and then only slightly noticeable if I paid attention and looked for it. I did not feel particularly calm during my normal activity but did wonder if something was different while driving, especially while merging onto the freeway, an experience where I typically notice some agitation. Interesting to note, it was just after getting on the highway while driving that I noticed the tingling. Suggested Dosages: I would consider suggesting GABA to patients who are over anxious or who complain of insomnia due to “too many thoughts which I can't shut off.” Again I like the coffee analogy: If they look or feel like they drank too much coffee, GABA may help. Research no longer supports using GABA for depression, bipolar disease or PMS: if it looks like they need a cup of coffee, don't use GABA For increasing Human Growth Hormone production the studies used between 3 and 18 grams. Keep in mind that at these doses expect tingling. CAUTIONS GABA may cause sleepiness, that is if it works: Do not operate or drive heavy machinery while taking GABA, at least until you know what effect it has on you. Do not take GABA if you have been diagnosed with bipolar or unipolar depressive disorders. If taking doses greater than 3-4 grams do not be surprised if you experience a flushed tingling sensation; this appears to be a common experience. Caution should also be taken in combining GABA with any drug which affects GABA pathways in the brain. These drugs include but are not limited to barbiturates, benzodiazepines, and alcohol. GABA has not been tested in pregnant or breast-feeding women, children, or people with liver or kidney disease. G . . . Other ways to skin the cat: other ways to increase GABA effect Another approach is to look at substances which change GABA action in the brain. There seems to be more and better clinical research on the use of many of these substances in humans than there is on GABA. There are numerous natural substances which affect GABA. In fact understanding GABA helps explain the action of many commonly used herbs, vitamins and minerals. Valerian root has a long history of use as a tranquilizer and works by increasing the effect of GABA on its receptors [30] American Ginseng also acts on the GABA receptors. [31] So does Kava Kava. [32] All sorts of other unexpected things change GABA activity; the chemicals formed by aging whiskey in oak barrels increase GABA effect. Aging really does make whiskey mellower literally based on what it does to brain neurotransmitters. [33] These chemicals are released from the alcohol as a fragrance and appear to reach the brain by inhalation. [34] The fragrance of Oolong tea has a similar effect, increasing GABA action. [35] Extracts of green tea, black tea and oolong tea elicit a GABA response in test models. [36] Epigallocatechin gallate extracts from tea had the opposite effect, inhibiting the GABA response. Coffee extracts also inhibit GABA response. [37] Magnesium binds to GABA sites and increases effect. [38] Taurine protects against glutamate overstimulation. [39] [40] Its inhibitory effect may act as anxiolytic. [41] Serotonin is another neurotransmitter and it enhances GABA. Therefore, as precursors to serotonin, Tryptophan and 5-HTP increase GABA action. Theanine is an amino acid found in large amounts in tea. It is why a cup of tea can be calming despite the fact it contains caffeine. Theanine may increase glutamate transport [42] and increase GABA levels. The vitamin B6 derivative pyridoxal phosphate is a cofactor in the synthesis of GABA. Some people have trouble converting Vitamin B-6 to pyridoxal phosphate and for those people taking this active B-6 may increase GABA levels. While these other supplements alter or potentiate the GABA receptor, they do not add any GABA to the system. Many companies add one or more of these other materials to capsules containing GABA. The idea may be to amplify the effect of any GABA that crosses the Blood Brain Barrier into the brain. These other ingredients may work independently and be the active ingredient in the product. _____________ Marti here: I have never taken more than 500 mg per day. Carl Pfeiffer and the author of the article were taking higher doses. What dose causes this effect in you? Do you take B6, 5HTP, theanine, taurine, high dose of magnesium, benzo's, or other substances that can increase the effect of GABA? Another article mentions that some people get wired but that it is rare. Let me know if you want me to keep researching. HTH, Marti

Hi Issie, I am not sure. I will research this. Like you, I am very sensitive to glutamates but can take 500mg of GABA a day. I have never tried taking more - I will try that and see if I get ramped up. Is it possible that the gaba formula was not 100% gaba - sometimes B vitamins and the like are added. B6 can cause that wired feeling. I get skin crawling sensations from B6. But we are all a little different so there may be something in your genetics or enzymes that can't process gaba, perhaps. I am planting a few flowers so I will look this up when the sun goes down and see if I can find anything about your reaction. Just came inside to rest. Marti

Wanted to add that I would get carsick very easily and had very low blood pressure when I was young. My bp was low even when I was well.

Hi Rich, There are no specific GABA nerves that can be tested - there are cells in the CNS that have GABA and Glutamate receptors. If you want to test for your levels, then ask for an Organic Acids & Amino Acids Urine test or tell them to order CPT 82131. RAMA: I believe your friends have it backwards. Glutamate is the precursor to GABA but not the other way around. http://themedicalbiochemistrypage.org/nerves.html Transmitter Molecule Derived From Site of Synthesis Acetylcholine Choline CNS, parasympathetic nerves Serotonin 5-Hydroxytryptamine (5-HT) Tryptophan CNS, chromaffin cells of the gut, enteric cells GABA Glutamate CNS Glutamate CNS and here: http://en.wikipedia.org/wiki/Glutamic_acid GABA precursor Glutamate also serves as the precursor for the synthesis of the inhibitory GABA in GABA-ergic neurons. This reaction is catalyzed by glutamate decarboxylase (GAD), which is most abundant in the cerebellum and pancreas. Stiff-man syndrome is a neurologic disorder caused by anti-GAD antibodies, leading to a decrease in GABA synthesis and, therefore, impaired motor function such as muscle stiffness and spasm. Since the pancreas is also abundant for the enzyme GAD, a direct immunological destruction occurs in the pancreas and the patients will have diabetes mellitus. HTH, Marti

Hi there, Caveat: my condition is not as bad as yours. I never go anymore. They don't know what to do for me so it is too much effort, too much expense. I probably wouldn't even get saline which would be the only reason I would want to go. You have a port so that changes things. It can get frightening but it makes me worse to go (having to wait hours, the anxiety of the doc I might get, the resistance, etc) Marti

what area of the country? I have not found someone to help me. Any info would be great.

Should I delete my vote since it was not lying? I don't want to skew your poll. If so, I would switch my vote. let me know. Or since it is sitting, not vote at all. Sorry! Marti

I voted but my test was done while sitting. 1131 I also have the same dopamine results - not sure what that means. Marti

What a great video! I watched it twice. Question: @ 26:10 - Dr. Thompson says that there is no diagnosis code. Is that true? I found orthostatic hypotension and several with tachychardia but not POTS specifically. 2012 ICD-10-CM Code I95.1 Orthostatic hypotension Applicable To Hypotension, postural Type 1 Excludes neurogenic orthostatic hypotension [shy-Drager] (G90.3) orthostatic hypotension due to drugs (I95.2) Mortality Data Between 1999-2007 there were 190 deaths in the United States where ICD-10 I95.1 was indicated as the underlying cause of death [source: cdc.gov ] ICD-10 I95.1 as underlying cause of death data broken down

I am curious why the assumption is that any letter would be negative, subjective, over-the-top, defensive, accusatory, etc. Perhaps that has happened often in that past with this population? Personally, it feels wrong to stand by and let young people be bullied in this way by people in authority over them. I would certainly be watching the program for long term mental and physical damage. It reminds me of the way that my sister was treated in the 50's and 60's. She was born with cerebral palsy and if she had been born a decade earlier would have be institutionalized. My parents were instructed to raise her a certain way (as a child who was mentally handicapped, which she was not). She went on to college but never reached her full potential due to the damaging emotional and mental effects of being trapped in a body with limits and no one listening to her that her mind was fine. As far as Levine's grinch thing - a nice, respectful letter is certainly possible asking him to respectfully refrain from using that terminology. Perhaps he doesn't know how many people find it offensive? (I know some people don't care- that's okay. Some people do care). Just my opinion. No one has to act on it. Marti

Several things have upset me since I have started to focus on POTS rather then ME. The ME/CFIDS population has the same problem - people are too fatigued to start a grass roots effort. BUT - it is not difficult to create a letter signed by different people protesting the behavioral aspect of the Mayo Pain program. Not to make it all negative - focus on the good but make sure they drop the psychological punishment which is barbaric. Also, I am willing to send a letter to Dr. Levine - hate to harp but that Grinch thing is insulting and should be stopped. Seems these groups (Levine and his cohorts and Mayo) are selecting tabloid style headlines that are catchy even if they are not accurate. I am willing to try - would need some team members. Marti

chronic constipation, difficulty standing up too fast - almost fainting (normal for normal people but it seemed worse for me - happened even if I got up slowly), nausea. The main one - I just felt better horizontally. Thought I was lazy but I was very type A. Getting horizontal or getting my feet up felt so good that I would sigh in relief. Preferred to sit on the floor (still do) than in a chair. During activity, would/will look at the floor lovingly, aching to lay down. This is all before I actually had full blown POTS which included a whole other realm of symptoms. Each relapse has been worse than the previous one, so symptoms continue to escalate. Marti

Futurehope: I have been on and off (mostly off) the protocol for about a year. I was never able to do Month 1 - 3. I had to start with Pre-Month 1 & 2. The furthest I was ever able to get was the end of Pre-Month 2 and just the very beginning of Month 1. Usually, a couple of weeks of Month 1 and I have to drop back down to Pre-Month 2 again. (this is different for each person). This is not a cure. As soon as you stop the protocol, the symptoms come back. If it works for you, you have to regard it as medication - it must be done regularly. My endo feels I should do less but do it every day as opposed to 3 x per week as is normally written. Someone posted a link that showed that the bad effects of deconditioning can occur after 20 hours of inactivity. - Dr. from Mayo - Dr. Raj?) so every day or twice a day is a the modification that I have made to his protocol. Also, I try to keep my HR to the base pace and have not gotten to the higher levels. Once you complete the Levine program, you either continue at the final level indefinitely or you can increase the length of time or increase the level of exertion. You just can never stop (I'm fine with that if I got some relief). Potluck: The first part of the program is exercising while sitting down using a rower or recumbent bike then as time goes on, progressing to treadmill and other upright exercises. Currently, I am exercising while laying down as I have been very symptomatic lately. I mounted my cheap tabletop cycle to the wall and I lay on my back on my bed and cycle while watching a movie. I find that if I am not standing, I can exercise for longer with less symptoms which is better for me in the long run. I do not know if Dr. Levine means for it to be for all types of POTS patients. Personally, I believe he is only looking at one subset - those with POTS that was caused by deconditioning. I think it will work well for these patients. For everyone else, I think the program would be useful but still just one small piece of the puzzle. Lately, I started (again!) with 5 minutes twice a day and I am up to 20 minutes daily (some days doing it twice a day but not consistently enough to say 20min twice a day.) Marti

I had it in Houston Texas - Dr. Aziz Shabani.

I take 500mg daily. I have been on this dose for 2 years. I also reduce my glutamates (no MSG, synthetic sweeteners, etc) Glutamates are excitotoxins while GABA is a calming. I do not take it with niacin. It is part of most of the autism protocols - DAN!, Yasko. I read something recently about POTS and glutamic receptors. I will try to find the link. Marti

This is an important point. It reminds me of cancer - patients are not considered cancer-free until 7 years have passed of no re-occurrence. Claiming that he is cured as he leaves Mayo seems premature. Having been through several cycles of remission and relapse, I would remain cautious about claiming myself to be free of the disorder. And while I would attempt to live life at it's fullest, I would be ever mindful of creating a situation where I could relapse. Yes, that would mean I would not participate in some activities so I would not be living life to the fullest compared to other people but could certainly live MY life to the fullest within MY parameters. For example, during a remission, my son and I bought a catamaran and learned how to sail. It was great fun and those are great memories but I would not attempt to do so if I were in a remission again. The heat, the amount of time spent upright, the dangers of being in the ocean if I had an episode, etc. I would choose other activities that would not trigger a relapse. This seems especially true for viral onset as viruses do not go away, they can be reactivated with the proper triggers. Having said all of that - I also agree that miracles can happen. The body is an amazing thing.

Mine was an informal diagnois. No tests confirming or disproving. It was diagnosed with I was diagnosed with ME/CFIDS and had minor OI at that time. Well, I thought it was minor but looking back, it wasn't minor at all. I just attributed the symptoms to ME/CFIDS. The Sjogrens' doesn't seem to have progressed much, thankfully. Several autoimmune issues going on. Marti