Julie Rehmeyer's 'Through the Shadowlands'
Writer Never Give Up talks about Julie Rehmeyer's new book "Through the Shadowlands: A Science Writer's Odyssey into an Illness Science Doesn't Understand" and shares an interview with Julie ...
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MEGLATHERY MD: RCCX MODULE MAY EXPLAIN OVERLAPPING SYNDROMES

Discussion in 'General ME/CFS News' started by JaimeS, May 2, 2016.

  1. Jenny TipsforME

    Jenny TipsforME Senior Member

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    @Snowdrop I stand corrected on the Eysenck one. This is the only one I remember results pre and early ME. Just redone it: I am now emotionally stable and moderately introvert. Before ME I was high on neuroticism and a bit introvert. Early ME I was very introvert and a little neurotic.

    I doubt this is directly to do with ME though. Could be indirect such as getting life in perspective, meditation.
     
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  2. Snowdrop

    Snowdrop Rebel without a biscuit

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    I tend to think 'perspective' whatever that may mean - happen's naturally with age.
    Thus the expression youth is wasted on the young. That is--they lack experience and that accumulation of experience is what gives perspective.
    Admittedly this is not a monolithic construct either--as with all things--some people find perspective in more areas or to a greater degree in an area than others will.
     
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  3. stripey14

    stripey14

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    Just wanted to say that I met with the accountant/admin for the Non-profit, RCCX Project, Inc. and she explained to me that what I said above about returning the money if we were unable to fund a viable RCCX investigation (not enough funds to do what Karen and I plan and not able to find another investigator interested in the RCCX) is not legal. In that case, the funds would go to another non-profit providing help/support for people with chronic illness which is what the attorney who set up the entity wrote into the bylaws. I want to be 100% transparent about what we are doing. I am not an expert in this setting up nonprofits and funding research so I have hired the best to set it up right. Now they are getting me up to speed so that I can be cost-effective.
     
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  4. stripey14

    stripey14

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    Just a few brief statement to address some questions above:
    Most CYP21A2 mutations are uncharacterized and many are not picked up even as variances of unknown significance on testing (see above).

    Also CYP21A2 heterozygosity is known to be associated with an exaggerated stress response and low baseline arousal in the literature which is really one of the prominent features of CAPS. The rest of the features can be seen as stemming from that-sensory sensitivities, hyperfocus alternating with low concentration/arousal, easily traumatized (stimuli in the setting of high catecholamines is associated a stronger traumatic association), appreciation for detail, perfectionism, special abilities, a tendency to want to control sensory input (some are thrill seekers and some are quite timid. Not all are introverts.

    I became an introvert after getting sick.) etc. I believe that in many ways this is a brain wired to detect and respond to danger or changes in the environment as a result of these hormonal influences when the brain is forming in infancy. Hypermobiles are recognized now in the literature to have a larger than normal amygdala (high cortisol and androgens in infancy can do this), autistic features/autism in some (sensory issues being prominent), high empathy. This is before getting chronic illness. In my experience, other people who have developed similar chronic illness without hypermobility have these features, too.

    I'm not saying that it explains everyone but it does provide a switch for deterioration after exposure to prolonged or very high stress. Stress being physical, emotional, infectious, even perceived (!). If the stress hormone demand increases above normal with each stress response and the person doesn't have 100% capacity to make 21 hydroxylase, CRH will increase (telling the body to make more cortisol) and stimulate mast cells to degranulate (most potent stimulator of mast cells in the body according to Dr. Theo, mast cells dump mediators causing a cytokine storm) while ramping up catecholamine and cytokine production.

    This theory could describe the mind-body link to stress-produced and exacerbated illness. This vulnerability would be in about 20% of the population (according to the prevalence of HSP which is similar) and would be variably associated with hypermobility and other serious immune system abnormalities via co-segregation of TNXB and C4, respectively.

    Finally, my CV is on the website and I don't usually go around flashing my credentials, but I am ivy league educated, went to the 2nd best primary care medical school in the country when I was there (was selected for a very competitive MD PhD program, but chose to do 2 residencies instead), completed residencies and attained board certification in both internal medicine (2000-2010) and psychiatry (2003-present).

    With the onset of my illness in 2009, I made the decision to let my internal medicine certification lapse as I much prefer psychiatry. I have set up a small, local (and very full, so I am not advertising!) holistic practice. By "holistic", I mean that I do a very extensive evaluation aimed at assessing how each person views him/herself, him/her past, life's challenges, coping skills, emotional range, level of arousal, stress response, etc. I look for signs of dysautonomia. I do a Beighton scale. I do extensive family histories looking for special abilities, chronic illness, psychiatric disorders, autoimmune diseases, etc. Then I do a psychiatric exam focused on symptoms which respond to medications.

    Most of my patients don't want medications. I see my patients either every week or every other week and we work hard during sessions. I am trained in CBT (don't use much as I find it invalidating if not done carefully or for some people in general, plus it doesn't go deep. I was shocked above to see someone summarizing my theory and saying that I recommended CBT as a top recommendation!), DBT (emotional dysregulation), EMDR (trauma processing, with additional training in use of this with dissociation) , psychodynamic/insight therapy, Acceptance and Commitment Therapy (mindfulness is a big component).

    As most of my patients have trouble with exaggerated acute stress response, I have developed a program of teaching, trauma processing and real life application of skills which results in everyone being able to graduate from my practice and get on with their lives eventually, most of them light on the medication. That's what I do. I know CAPS when I see it and in people with it, I see MCAS breaking though when the stress increases and I have seen some develop chronic illness right in front of me, hypermobile and not hypermobile.

    I feel ethically bound to share these observations and what I learned about how the RCCX module could explain them. I have EDS, MCAS, CFS and I had raised ICP. I am not a professional science writer. I did the best I could.
     
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  5. Jenny TipsforME

    Jenny TipsforME Senior Member

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    @stripey14 I think people here seem supervigilant as gate keepers but you know there's been lots of false hope and what resources there are channelled into actively unhelpful research (rather than just benignly useless). On the other hand, it is important not to dismiss ideas too readily. I have to say I'm finding your ideas confusing but that's probably at least 50% brain fog. There might be something in it.

    Could you boil it down to a 1 or 2 sentence hypothesis? Eg are you saying that you expect significantly higher CYP21A2 heterozygosity in pwme compared to healthy controls? Are you saying pwme usually have EDS?
     
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  6. stripey14

    stripey14

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    Hi Jenny, not so easy to boil it down into a couple sentences, but I will try. The RCCX module is the only place in the genome where genes can travel together and people can inherit two "rare" diseases at once at a much higher rate then would happen by chance. In fact, these genes have been shown to travel together often.

    The genes of the RCCX are: RP1 (function unknown), CYP 21A2 (congenital adrenal hyperplasia if two copies, exaggerated acute stress response if one copy, probably 20% of the population carry this if it is the cause of psych profile CAPS), TNXB (hypermobility of varying degrees, from none to severe, meeting criteria for EDS), C4 (MS, CVID, other autoimmune diseases, schizophrenia).

    These genes can mix and match, traveling together and mutating often, likely creating family histories filled with the conditions associated with these genes. This is exactly the pattern i've been finding in my patients and their families for years. This is also what I've seen in the forums I have been following.

    I am assuming that CYP 21A2 mutations are responsible for the CAPS psych profile due to hormone derangements during brain development in infancy and the development of chronic illness in the setting of prolonged or severe acute stress via overwhelming 21 hydroxylase, resulting in more severe hormone derangements and mast cell activation/cytokine storm due to high CRH.

    According to my theory, hypermobility is common in the chronic illness population because of the high prevalence of TNXB mutations running with CYP21A2 mutations (a known fact that the frequently are inherited together). Some meet criteria for EDS, but not all.

    It is highly likely that some TNXB mutations create only slight hypermobility or people who are not hypermobile at all, and I think some may actually be stiff. We don't actually know how the different mutations present, other than the haploinsufficient one causing Hypermobility severe enough to be called EDS and the less severe ones causing some degree of hypermobility with calcific aortic valves or vesicoureteral reflux.

    According to my theory, if you are CYP21A2 homo or hetero you will have caps, and exaggerated acute stress response and a vulnerability for chronic illness. If you also have TNXB mutation then you probably will have some degree of hypermobility, possibly meeting criteria for EDS along with chronic illness vulnerability and caps.

    Right now, there is no way to test for the vast majority of these mutations as the RCCX is riddled with pseudogenes and retrotransposons. We need a very sophisticated genetics lab to characterize these mutations. We also need to do quite a few provocative tests to demonstrate the underlying hormonal problems.

    It is likely that the different mutations will have quite a bit of variability clinically. I also believe that the caps profile is attractive to other people who have it ( frequently marry each other) and that some of us are actually homozygotes for uncharacterized mutations of this gene. These homozygotes would be more severely ill and this may be the genetic loading that men require to become ill (as men are less frequently affected, especially in the hypermobile population and anecdotally seem to be more likely to be very ill when they are affected). The expected CYP21A2 hormonal aberrations would be expected to affect women more than men with the same degree of genetic loading.

    That is an oversimplified explanation. I hope that's helpful. It is very late and my brain is not working so well, so I hope this is coherent. I'm also trying to use Siri to do this, so please excuse any odd capitalizations etc. Any one reading this post as the first introduction to my theory may find it easier to go to the website and look at the pathophysiology diagrams and read about the possible clinical implications in the Theory for Patients section.www.rccxandillness.com.
     
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  7. Jenny TipsforME

    Jenny TipsforME Senior Member

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    @stripey14
    This observation would be accepted by many:

    "A person, usually female with a genetic vulnerability (familial) is exposed to chronic stress or a strong stressor which results in a cascade of physiological events causing characteristic chronic illness involving multiple overlapping, co-morbid syndromes/symptoms/diseases" (for us strong stressor would be something like glandular fever?)

    There is a lot of co-morbidity you just have to glance through people's twitter bios. It could be there's a common root cause or vulnerability. Although perhaps the diagnosis is ill-defined. Rather than ME/CFS, fibromyalgia and POTS perhaps I should have one diagnosis with a better case definition or using biomarkers rather than syndromes.

    Also, don't most families have people with the conditions you list and the psychological profile you describe? It seems so big that it would be hard to refute. It feels to me like it needs to start smaller. What results would convince you that this theory is incorrect?

    Having just looked at my dna results I could accept that there might be mutations which are broad vulnerability like the ones for autoimmune vulnerability (SNPs which if expressed are associated with a number of conditions such as rheumatoid arthritis, lupus etc) but in this case it is a different cluster involving Dysautonomia, autism, EDS etc.

    I struggle to see how you get from these mutations and multisystemic conditions to using a variety of talking therapies as the treatment of choice for patients though. Am I reading that right? I can see the logic that it's useful to have techniques to cope with stress but is that adequate treatment for these conditions?

    In terms of fundraising for research. It would be good to have more clarity about the study you will do. Is this a GWAS study? How much do you need to raise? How will you recruit participants and controls? Seeing as there's a personality aspect to this, a snowball sample or getting participants to come forward online would bias the results. Kickstarter would only take money from people if you raise enough. That might be a way around your fundraising dilemma. Otherwise it would be important to say where the money will go ahead of time if you don't raise enough (eg another research charity).

    Do you know that Nancy Klimas is doing a genetic ME study by crowdsourcing the dna data instead of raising money? If you're saying that 23andme.com doesn't provide enough information that wouldn't work for you though.
     
    Last edited: May 20, 2016
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  8. stripey14

    stripey14

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    Yes, for example glandular fever, Lyme, mold for some, surgery, physical trauma, catastrophic event (9/11), etc.

    I agree 100%, but no one is ready for that, yet. This theory unites groups of people who aren't ready to be united for several reasons: it seemingly goes against firmly held ideas (for example, "TNXB is a rare cause of hypermobility"-true if you talk about haploinsufficient TNXB mutations but I'm not talking about EDS and I'm not talking about halpoinsufficient mutations, I am talking about ALL mutations; "CFS/ME is misdiagnosed in people with EDS, all the problems are due to EDS" I disagree, why are all the symptoms, even the bizarre ones, the same and EDS people seem to need a trigger to get sick. I was at the top of my game (better than the game of 90% of people) when I got sick despite EDS. An adrenal fatigue group member told me they didn't like terms medical terms like POTS. What I attempted to do with that website was speak to a HUGE audience in language every one could understand about medical conditions with very confusing and overlapping symptoms.



    Yes, this psych profile is very common-20%. The trick is correlating it with family histories, symptom histories, hormonal abnormalities with very extensive testing and correlating that with specific CYP21A2 mutations. Any study doing this will have a huge number of patients, controls (not sick, not CAPS), sick , not sick (CAPS alone). We have not finished writing the protocol. We are also making sure our lab can sequence and characterize RCCX module. Many can't. Ronald Davis, PhD has a copy of the theory and perhaps he will be interested in our samples. He contacted me after I wrote to him. If people have CAPS or are sick and clearly have known non mutated CYP21A2 variances (although there are rare ways to develop the hormonal issues without this mutation). If there are no patterns in the sophisticated hormone challenges we will do.

    Absolutely NOT adequate. You didn't understand what I said. Another person on the forum read my theory and said that's what I said. As mentioned in my refute to her analysis (you can scroll back and see the whole thing), hormone/enzyme support would be first line (if this theory is correct and I cannot make treatment recommendations anyway) before one is too sick, maybe CRH blockers/something to decrease progesterone when illness starts, then treating the anything maintaining the need for cortisol, i.e. contributing the stress response, including cytokine dumping, MCAS, volume issues, mental health issues. People with CAPS have an exaggerated stress response, so grounding, mindfulness, other therapies may even prevent illness, but are VERY important to decreasing this stress load. As an aside, I was discusing my credentials for someone who didn't understand them.


    No, too complicated for that. The RCCX is very complex.


    see below.

    We have 3 clinics here, then we will expand. Online would not be terrible initially because first we want to show the link between CAPS, CYP21A2 mutations, illness and family history. Then we can look at what percentage of chronically ill people have this going on (that will need samples without selection bias).

    I didn't come on here to fund-raise. I came on because someone was talking about my theory and I wanted to answer questions. I was told that I shouldn't be fund-raising as we are not qualified to do research. Please see my response above. I put out my theory with no intention to do research, I just wanted it out there for someone to see and follow up (this was after writing to many experts and either getting no response or a positive response).

    Then Karen Herbst, international cutaneous adipose tissue expert contacted me right away saying that she sees a high rate of hypermobility and all of the comorbidities including CFS in a high number of her patients and most from what she can see have CAPS. She knew I was right and wrote an IRB protocol right then and there that we are fine tuning. She suggested a non profit, so I hired an attorney and set it up. He said that we needed a website BEFORE we could apply. I did that. I set it up for ALL research looking at RCCX Module in Chronic Illness, not just for Karen and I.

    In this thread in defense of my actions in terms of fund-raising I said we would return unused money if our study doesn't have enough funding and if no one is interested in the RCCX. Yesterday after finally getting an appointment with the admin/accountant person, I now know that that is illegal and that the lawyer wrote into the bylaws that the money would go to another charity to help people with chronic illness. I corrected that statement on this thread.

    We are set up to collect money and have received a few donations, but we are not actively fund-raising as I am the only person doing everything right now (I have a few volunteers but we haven't moved forward because they are sick and not ready to start). I posted on one site about fund raising to generate interest in the theory. I made it clear on that thread where we are in the process. We are not ready to submit the IRB until we figure out if we can use our lab or if we need to hire a better one.

    Karen has been travelling internationally presenting at conferences, I believe. We won't have numbers for a while. When we do, we will be very transparent about where the money goes. I am working for free and so is Karen (she is paid by the university), I am a volunteer.



    Yes, I tried to contact her before I realized that very few people are qualified to look at the RCCX and we will need to be much more manual about our analysis especially in the beginning.
     
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  9. Jenny TipsforME

    Jenny TipsforME Senior Member

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    @stripey14 I've got no idea if you are right but
    Does sound a more appropriate response if this is the issue. I also happen to think meditation and talking therapy are a good idea, just not by themselves. I've found meditation helpful but it pales into insignificance compared to taking cardio meds for POTS.

    You mention progesterone. Would you have any predictions from your theory on how relevant patients would respond to the mini-pill? Are you expecting high cortisol? Pwme tend towards low cortisol usually.

    I think your theory is interesting. I'll keep an eye on how it goes.
     
    Last edited: May 21, 2016
  10. stripey14

    stripey14

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    You mention progesterone. Would you have any predictions from your theory on how relevant patients would respond to the mini-pill? Are you expecting high cortisol? Pwme tend towards low cortisol usually.

    The hormone testing and recommendations/predictions are difficult because of the dynamic nature of the process. We know heteros for the known mutations of CYP21A2 who are NOT SICK overreact in terms of cortisol to acute stress and have slightly low basal cortisol . As 21 hydroxylase becomes overwhelmed (people get sick according to the theory), I would expect basal cortisol to drop lower and the stress response to remain till close to the bitter end, but not high enough for the stress. This is just speculation. We don't know.

    Also, the stress of having low basal cortisol becomes a driver for the acute stress response. It's very complicated and we need to do multiple samples and we need to have challenges which reveal this dynamic process. The key point is to show that the sick and well people with CAPS vary from normals and each-other. Then we have to match these responses with genotypes.

    Progesterone is also dynamic and complicated. I expect it to be low (due to the exaggerated stress response) in those with CAPS who are hetero (or homo for mild mutations) CYP21A2 mutations and are not sick. When 21 hydroxylase is overwhelmed, 17 hydroxylase progesterone would build up and high 17 hydroxyprogesterone has been found in a small CFS years ago. My theory is the only explanation for that finding!

    Exogenous progesterone could theoretically build up in this population , especially if the stress response is high and 21 hydroxylase is stressed and there are many reports of people becoming sick on exogenous progesterone being used when perimenopausal. This is a common occurrence in the EDS population, HMSA recommends against ANY exogenous progesterone (not just for laxity reasons) and on the website. I discuss my severe symptoms of presumed progesterone excess which responded to treatment to decrease it. Karen was partially drawn to my theory because her adipose disorder patients get very sick on progesterone (many have chronic fatigue, CAPS, some with hypermobility).

    That said, many do fine on the pill when they are young and not so stressed.

    I am well aware of the abnormalities in CFS. The mystery of CFS, FM, psych disorders led me to become board certified in internal medicine and psychiatry. It also led me to the NIH where I did research on bipolar disorder after college. When I learned about the RCCX and especially CY21A2 being co-inherited with C4 and TNXB, I realized that highly suggested by the hormonal data collected thus far. I review the literature regarding these hormonal aberrations in these populations on the website (in the Journal Article).

    Thank you for your interest!
     
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  11. Valentijn

    Valentijn Senior Member

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    Could you describe your understanding of ME/CFS? I'm a bit put off by it continually being called "CFS" or "CFS/ME", which psych researchers also constantly do, as an objection to ME sounding too medical.

    Which symptoms do you feel are essential in identifying ME patients? Which criteria do you think are most accurate?
     
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  12. stripey14

    stripey14

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    I left out the word "hormonal" abnormalities. I review my understanding of hormonal abnormalities in the journal article (literature review).

    I am leaving this thread as I feel I have explained everything that I have been asked to explain which is reasonable. If anyone has any further questions, please contact me via the above methods. I am approachable and will try to help with any questions but I don't have time to justify my credentials over and over.
     
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  13. JaimeS

    JaimeS Senior Member

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    It's okay if @stripey14 doesn't want to respond anymore; I'm laying out my thoughts for the rest of you.

    Phrases like "mind-body link" make this community nervous. IMO, it isn't that people don't believe such a thing exists, we are just very used to the 'mind' part being examined at the expense of the 'body'.

    I can't think that any frame of mind could have gotten me into this very physical mess, or that better emotional coping could've prevented it.

    The number one best question for broad-based theories.

    Few people talk about hormonal dysregulation in ME/CFS, but because my onset was slower, I was tested endocrinologically like mad. I don't have low cortisol, but I have a poor cortisol response -- not the same thing. GH response was zilch. I actually really wanted a CRH-blocker after a bit of research on some of this... I tend to feel better when my cortisol is lower.

    Additionally, by a process described at length a few times on this forum, one of the things that helped me with my POTS more than any other was Vitex agnus-castus, generally used for progesterone-regulation.

    You don't have to justify your medical credentials to anyone. When people here ask you what you understand about ME/CFS, they aren't asking about your degree or the school from which you earned it. There are lots of people who went to very hightly-rated institutions who wouldn't recognize a patient with ME if she began to vividly describe an episode of PEM during an appointment. Since medical education about ME/CFS is notoriously poor, most people's schooling did not include it, or else included a good dose of wild supposition in place of facts.

    Moreover, even in the community, the definition seems to vary person to person. I've heard people say, "if you didn't have a distinct, infectious onset, it's not ME." "If you don't have overt PEM, it's not ME" etc. @Valentijn was asking you about the framework in which you understand / define the illness, which is extraordinarily important.

    In general, ME is considered the most 'medical' term (and honestly the more accurate symptom / pathology descriptor.) However, lots of us in the US were actually diagnosed with 'CFS', so some people say 'ME/CFS'. If you just call it 'CFS', it's a little demeaning. I have Google Alerts for ME, ME/CFS, and CFS, and pieces that only mention CFS are almost without exception non-scholarly and insultingly plastered with psychogenic explanations of the illness. Finally, there's CFS/ME... that little afterthought of ME. That's like, people tacked on the more serious name at the end to appease people, but they really still mean 'CFS', and all that implies. :thumbdown:

    The paragraph above was not intended to be humorous. Imagine if you had the choice between your illness being defined as 'myalgic encephalomyelitis' or 'sleepytime flu'. Whether people say 'ME' or 'CFS' is (often) a weirdly accurate indicator of the quality and nature of the research to follow... and that's why it's important what you choose to call it.

    -Jaime
     
  14. Snowdrop

    Snowdrop Rebel without a biscuit

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    @JaimeS

    Thank you for that post above. It pretty clearly explains some legitimate concerns.

    The mind-body thing is a red flag. The body part is easily understood but the mind part requires some defining. I find that mind and brain can be used interchangeably even by people who have education that should allow them to be more precise. Mind and brain are not the same and the term mind is the one generally used because it lacks any precision any ability to measure, probe or otherwise quantify and observe--therefore anything can be claimed about it there is no 'proof' to discredit anything when the term mind is used.

    Scientists are better to stick with researching the brain and it's components, processes and activities. If that effort is made there are clues enough to follow for understanding all sorts of important things that could lead to useful knowledge that can be applied to health.

    Psychiatry has sometimes helped people who are desperately in need to a better level of functioning. That doesn't negate the fact that it has quite some ways to go before declaring the discipline a huge success.

    I think what we know of the 'mind' is likely to look somewhat like a single star in a galaxy of stars. There is far too much certainty in concepts of mind and it would seem that the struggle for supremacy of concept can at times find justification in the use of force.

    Although, that would be taking this now off topic but it is always a menacing presence behind any talk of mind treatments.
     
  15. JaimeS

    JaimeS Senior Member

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    Absolutely.
     
  16. Jenny TipsforME

    Jenny TipsforME Senior Member

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    In the term mind-body I would put brain in the body section, in that it's a physical entity that's part of the body. Mind would be more the content of thoughts. Even mental illness isn't necessarily a problem in the mind. The problem is often a brain chemistry issue although it can maybe be hacked through the mind.

    A treatment that treats neurotransmitters or hormones is a body treatment.
    A treatment that attempts to change how you think is a mind treatment.
     
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  17. Jenny TipsforME

    Jenny TipsforME Senior Member

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    In the context of this thread, what @stripey14 is describing seems to be more accurately mind AND body treatment. This is different from the associations I have with mind-body approaches which tend to take the view that you change your mind to change your body. I don't think mind-body in this sense is adequate for ME which is why I was querying it. I can see the validity of including mind stuff within a jigsaw of biomedical treatment, to be genuinely holistic. But as @JaimeS says there can be an unfortunate tendency towards treatment being all-mind as soon as mind-body is accepted.
     
  18. ElderberrySmellingFather

    ElderberrySmellingFather

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    @stripey14 Hi there!

    I find this very interesting. I´ve done a 23andme test, and ran the raw data through the Enlis genome explorer and found that I am heterozygous for a mutation in the gene that codes for 21-hydroxylase. I don´t really understand if this means I am a carrier or directly affected, as I believe one would need to be a "compound heterozygote" to be directly affected with the disorder. In either case, I´ve included a couple of screen captures from the report the Enlis Genome explorer created showing some information in general, and more specifically the mutation that was discovered.

    I am waiting for my primary physician to hear back from the specialists about looking further into this, as I have had some issues for a while. Just thought it could be interesting getting some feedback on this from someone who´s obviously a lot more knowledgable about this particular disorder than anyone I´ve run into thus far.


    Skjermbilde 2016-11-14 kl. 23.37.29.png Skjermbilde 2016-11-14 kl. 23.37.44.png
     
  19. barbc56

    barbc56 Senior Member

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    Any updates about this?
     
  20. wastwater

    wastwater Senior Member

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    Think I probably inherited a tendency towards a leaky brain,is that called vasculitis,maybe,I think
     

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