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Dr Trevor Marshall
Research Team
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Posted: Mon Feb 18th, 2008 05:51 |
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Yes, 30 Lux illumination seems to be a value tolerable to everybody. Out-of-doors it is typically 100 times greater than that.
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healingjason
Member in Phase 3
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Posted: Thu Feb 21st, 2008 03:58 |
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Following Trevor’s recent postings, I have been trying to understand the information on sun/light exposure on the MP site and need some help in relating this to Jason’s specific pathology and clinical symptoms, both pre-MP and since he has been on his ‘diluted’ MP.
I do note Trevor’s urgings to keep Jason out of the sun and to monitor his 25-D level as the best way to bring about improvement and recovery. However, as the Board is aware, the impediments to me doing this are quite substantial. This leaves me with the difficult matter of trying to work out whether to push for greater MP compliance (D-testing and sun restrictions) or continue on as I have, that is, doing what I can to limit contraventions of the MP and accepting that I cannot readily overcome these but not to lose heart that some improvement is possible.
From what we can tell, Jason does not seem to manifest any photosensitivity, unless one considers his cognitive malfunctioning as a form of photosensitivity. He does not suffer skin rashes or dermatological changes, fatigue or breathing difficulties but I suppose he could be considered to suffer from brain fog, mood swings etc which are included as photosensitivity symptoms on the site. Of course, these symptoms are also collectively labelled as ‘autistic’ symptoms. There is no obvious waxing and waning of his symptoms that varies with the seasons and exposure to sunlight so I am inclined to think that he has not displayed photosensitivity thus far.
Could it be said that Jason does or does not suffer from photosensitivity?
I gather photosensivity occurs for many folk prior to going on the MP. I understand their clinical symptoms include photosensitivity or hypervitaminosis D caused by L‑forms pushing the person’s 1-25 level to a point where sunlight causes them to feel ill because this leads to still more or excessive 1-25D. Put simply, the living Th1 bacteria produce excessive 1-25D.
Correct me if I am wrong but I have this concept that the body likes a certain 1-25 D level and any amount over this shows up as ill-health or, more specifically, as photosensitivity. The photosensitivity is the body’s way of saying that no more 1-25 can be tolerated and for the person to go inside. For my explanatory purposes, I will call this category of sick Th1 diseased people as belonging to ‘category 1’.
For my purpose, I think this category of ill persons can be distinguished from others with Th1 disease.
I gather that most folk who are suffering a Th1 illness have a large L-form pathogen load and will become photosensitive once they are on the MP if they have not already exhibited this. I gather this is because the killing of the pathogens by the immune system also causes 1-25D levels to rise acutely and any added sun will cause too much 1-25 D to be produced and the same photosensitive reaction ensues as for category 1 folk. Put simply, the killing of the bacteria leads to too much 1-25D. I will put these Th1 diseased people into a separate category – ‘category 2’ folk.
I get the idea that, for category 2 folks, the onset of photosensitivity should be welcomed because it indicates that bacteria are being killed and these folk can expect the photosensitivity to be temporary. I gather that an increase in 1-25D produced in this way can only occur if the vitamin 25-D level is brought down by restricting vitamin D exposure. As I understand it, sunlight and dietary restrictions permit the body to accommodate rising 1-25D levels caused by the killing of bacteria (called a herx or immunopathology effect). If 25-D is brought down then 1-25D from this source is also brought down thus providing scope for more bugs to be killed – the ‘well’ of 1-25 that the Th1 diseased body can live with consists of that arising from 25-D, that produced by living pathogens and that produced by the immune system killing the pathogens. If 25-D is not brought down then the 1-25 D that the body can live with gets taken up by that produced by 25-D and the living pathogens leaving less room for the immune system to function.
Thus, if 25-D is kept up by sun exposure then the immune reaction is dampened and this is why the sun appears to be palliative. However, in the longer term, the Th1 illness gets worse since the bugs continue unhindered.
Have I got this right or is this understanding way too simplistic?
Since being on the MP, to the extent that he has, Jason has had no photosensitivity if autistic behaviours are not viewed as photosensitivity reactions This could mean that he has not got his 25-D levels down enough to accommodate the killing. He will remain a sick Th1 person who is not healing. This is a separate category of Th1 sick people and I will call this ‘category 3’ people.
I note, however, that the site contemplates people with a relatively low bacteria load not having nor getting photosensitive but who can recover on the MP. I take this to mean that they are able to kill bugs by Benicar acting pretty much alone to enable the immune system to function along with the abxs. I will call this category of sick Th1 people ‘category 4’ people.
If one assumes Jason has not been photosensitive (as is likely in my opinion) then he would be in either category 3 or 4 but not category 1 or 2.
Meg has hypothesised that Jason’s severe autism suggests he has a high bacteria load, meaning he would be in category 3 where the sun is acting to palliate him now but were D levels brought down then he would start to become photosensitive.
Could Benicar be used in greater quantities or given more often to assist him, that is, offset the sunlight factor to bring on the herxing and photosensitivity?
On the other hand, Jason is relatively young and he may not have acquired a large enough bacteria load to bring on photosensitivity nor might his load be expected to lead to any photosensitivity on the MP. That is, he could in category 4 and this suggests nothing needs to be changed for his protocol and I just need to be patient.
Assuming the Board finds these categories useful, could the Board proffer a view as which category of Th1 diseased folk Jason might most likely belong to? Would such a view have implications for his treatment?
John
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Father of Jason, 11 year old autistic boy. Chronic infection evident from urinary amino acids (see bioscreenmedical.com). Benicar 40 mg QW8H from 7 Apr 07. Phase 3 from 28 June 08. Covered up, sunscreen.
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Jeannine R.N.
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Posted: Thu Feb 21st, 2008 04:45 |
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John,
Photosensitivity can cause all kinds of symptoms. For me it is pain,fatigue,mood swings etc....it mimics the symptoms I already have. They increase when I get too much light to the eyes or when out in the sun to long... even when I am covered up MP style. It would be hard for someone who cannot communicate these things to convey that they are light sensitive. It took me awhile to figure it out myself
Jeannine
Last edited on Thu Feb 21st, 2008 04:47 by Jeannine R.N.
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CFS FM Lyme Morgellon's 125D49 Ph1Aug06 25D <4(april 08)Prozac Valium Aleve ModPh2May07 Ph2Apr08 NoIRs limited outings covered lo lux home
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Jimbbb
Member
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Posted: Thu Feb 21st, 2008 12:31 |
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Jeanine/John,
I recall a thread where Joyce W. was able to do some sun sensitivity studies of various skin creams by going out in to the sun and then monitoring the rise in pulse rate soon after exposure if the cream was ineffective. She found that to be a good quick indicator. I would also think that perhaps monitoring pulse rate (not blood pressure) and watching for a rise above the resting rate might also be a good indication of immunopathology which might be extremely useful for someone like Jason who cannot express the perhaps subtle symptoms. I know first hand that a day or so before I come down with a cold or flu bug my pulse rate would go up by 20-40+ from normal. That is even before temperature starts or symptoms start or you in any way 'feel' sick -- your body is already busy at work. The higher pulse rate also explains fatigue when you are sick -- your heart is working hard even when you are laid out flat, so it would be not unlike jogging all day long and feeling winded/tired. A nice simple way to get a reading of something affecting your immune system. Anyone else have comments on pulse rate and immuno? If not you could give it a try and report back. No need for fancy equipment .. just your finger (not thumb!) on your wrist. (you could also spring for one of those Polar chest straps and a watch that shows/records reading throughout the day -- kind of expensive tho).
J
Last edited on Thu Feb 21st, 2008 12:32 by Jimbbb
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Interested (healthy) bystander with distant cousin who has Chronic Lyme.
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Dr Trevor Marshall
Research Team
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Posted: Thu Feb 21st, 2008 13:43 |
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I never found that my pulse was a good indicator of anything. I found that the symptoms of a sun exposure began 4-8 hours after exposure, peaked in the second day and then persisted for at least another day. If you look back through the early posts at SarcInfo (from 2002/2003) you will find this reported again and again.
We have been there, done that...
It is foolish to assume that any Th1 patient is not sensitive to sun exposure. I cannot change the way the body works, I can only report upon it. Those who have fully recovered with the MP have all had some degree of photosensitivity, and most photosensitivity has been severe.
John, it is time to snap out of denial. Jason is sick. Very sick. Of course the solar exposure will exacerbate cognitive dysfunction. All the disease symptoms are exacerbated by changes in the D metabolism, and by immunopathology. If Jason is to lead a long and fruitful life he needs help, and he needs it now.
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Dr Trevor Marshall
Research Team
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Posted: Fri Feb 22nd, 2008 00:26 |
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A new study is out: "Some cases of autism may be traced to the immune system of mothers during pregnancy"
http://www.eurekalert.org/pub_releases/2008-02/uoc--sco021108.php"Future studies should consider the immune system interactions between mother and child as a focal point in creating greater understanding of, and eventually finding effective preventions for, this complex neurodevelopmental disorder."
Understanding this study result is difficult, as we don't yet know exactly why the Th1 pathogens in the mother cause antibodies to be formed, nor have these authors differentiated whether, for example, Th1 pathogen-caused 'autoantibodies', such as Ds-DNA (Lupus) or RF (R.A.) are involved in this behavior.
Based on the diagnoses other than autism in our cohort, I would remark that we do know that innate immune failure due to the Th1 pathogens sometimes causes antibodies, leading to a diagnosis of an autoimmune syndrome. Therefore the existence of antibodies in some Th1-affected mothers is not so remarkable to me. In fact, I would suspect it is probable.
The issue is whether the damage done by the antibodies is reversible, and the few children in our cohort have shown that it certainly seems to be reversible, as the Th1 pathogen load in the child is reduced (by the MP).
..Trevor..
Last edited on Fri Feb 22nd, 2008 15:47 by Dr Trevor Marshall
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healingjason
Member in Phase 3
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Posted: Tue Apr 15th, 2008 01:33 |
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Why are autistics mostly male?
I am moved to again raise the question of why autistics are mostly male (3:1 ratio) in the light of Amy’s recent piece on her bacteriality website about cognitive dysfunction in CFS sufferers being mostly female.
I raised this issue a while back but I got only one response from MarkN (on August 29) as follows:
I'll take a stab at the MP perspective on this part:
The reason for the striking 4:1 sex difference is totally unknown. However, there is a clue or two. Estrogen and testosterone have very different effects on vitamin D metabolism. In mid‑pregnancy, when brains are rapidly developing, boy brains bathe in testosterone and girl brains bathe in estrogen. The majority of studies have found estrogen has multiple enhancing effects on vitamin D metabolism while testosterone does not .... If estrogen potentiates activated vitamin D, but testosterone does not, the differences in sex steroids during brain development may mean that estrogen protects developing female brains from vitamin D deficiencies, while testosterone exposes male brains to those same deficiencies.
Assuming this is true .....The female baby has higher metabolism of 25-D to 1,25-D, which is not healthy, but maybe less disabling to the immune system. The male has higher 25-D and lower 1,25-D, more disabling to the immune system.
I have to say that i did not understand Mark's commentary.
I think the gist of Amy’s piece is that, of CFS sufferers, child-bearing females have more scope to get Th1 pathogens and hence are more likely to get pathogens in the brain than men because men don’t have an endometrium.
Trevor has stated that
“The dysfunction caused by the Th2 pathogens affects women disproportionately".
Amy’s piece also speaks of gradual or chronic declines in cognitive dysfunction. In contrast, for most autistics, the disease emerges before the person is 4 years old, as well as most sufferers being male. I therefore suggest that the decline or chronicity of ASD is much quicker than for CFS sufferers. Why?
Could it be that girls carry similar burdens of pathogens but they can survive longer without expressing cognitive disease? Indeed, do they need to reach a child-bearing age before the pathogens begin to express themselves in the form of cognitive disease? Perhaps girls actually have stronger immunity than boys whereas women have weaker immunity than men.
Perhaps there are some cognitive disorders other than ASD that only young females get which balance the numbers of cognitively ill infants. I note there is at least one other cognitive disorder that affects young girls disproportionately and that is Rett’s syndrome. However, I understand this is a known genetic disorder. Could this condition be ruled out as a Th1 disease? Interestingly, Wikipedia states that boys do get Rett's in the womb but do not survive.
What I am getting at is that there may be other Th1 cognitive illnesses that girls get more than boys that would balance the greater ASD number in boys but I doubt it. In other words, I think the question still remains as to how to explain more boys getting Th1 autism/cognitive dysfunction compared to girls.
Do men disproportionately suffer other Th1 disease manifestations, for example, sarcoidosis, Lyme? I note these are illnesses that require time to become manifest, unlike autism which hits very hard and very soon and mostly in males.
I think ASD sufferers and CFS sufferers can be considered similar in terms of the diversity of symptom expression. I understand the point about the unpredictability and diversity of symptom expression in CFS women being explained by variability in bacterial flora (pea soup).
ASD sufferers also have very diverse symptoms in terms of cognitive, affective and sensory dysfunction. My Jason is not hyper-sensitive but hypo-sensitive, unlike many ASDs who are hyper-sensitive. However, Jason is very cognitively challenged compared to his ASD school peers but I understand there are other ASD sufferers that cannot be schooled. Jason is also able to show affection, although this could be a result of therapy, including the MP.
Any views?
John
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Father of Jason, 11 year old autistic boy. Chronic infection evident from urinary amino acids (see bioscreenmedical.com). Benicar 40 mg QW8H from 7 Apr 07. Phase 3 from 28 June 08. Covered up, sunscreen.
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jcwat101
Research Professional
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Posted: Tue Apr 15th, 2008 03:07 |
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I think it may be that it is a different mix of pathogens in the "pea soup" that causes autism vs. CFS. CFS cognitive dysfunction and is pretty different from autism, I think. Most women do not suffer from the same sort of effect on relating to people. It may be that hormonal differences affect the particular autism pathogens differently, making men more prone to them.
Another option is it could be more a matter of what area of the brain gets the worst level of infection and the amount of backup capacity in relational abilities that is available. From this point of view, since men are already prone to be less relational/social/expressive on average, I think it easier to be pushed over into that area of "deficiency" (there is less backup social capacity promoted by estrogen available). I haven't researched it much, just sharing my speculations.
Personally, I think it will just be a matter of further research and I don't think it probably worth worrying too much about.
Joyce Waterhouse
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20 yrs with CFS/FM/Lyme/IBS, food sensitivities; 1,25D/25D 8/04:64/11 1/05:22/6 9/05:1,25D=12 10/06:22/8, 4/07:25/<4 chewed Ben. 40mg q8h; Mod. P2: 2/23/05, P2: 4/06; P3: 1/1/07
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healingjason
Member in Phase 3
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Posted: Tue Apr 15th, 2008 04:20 |
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Joyce
As I have posted earlier (my post of 4 June 2007), Prof Tim Roberts of the University of Newcastle in Australia did research on both CFS and ASD subjects and he observed similar abnormalities in various laboratory markers - urinary acids, stool flora etc - which he thought was suggestive of a similar infectious cause. He was looking for a single organism/germ which he could not find (culture).
I can see how the pea soup pathogen concept can explain how these disparate groups could share laboratory abnormalities but show different cognitive dysfunctionality
John
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Father of Jason, 11 year old autistic boy. Chronic infection evident from urinary amino acids (see bioscreenmedical.com). Benicar 40 mg QW8H from 7 Apr 07. Phase 3 from 28 June 08. Covered up, sunscreen.
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healingjason
Member in Phase 3
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Posted: Thu May 1st, 2008 23:20 |
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John,
At the Karolinska conference last week there was a presentation about genes in Autism. The researchers were really flummoxed. Too many gene mutations, they said - no idea where they all came from, they said...
Amy asked them if they had contemplated bacterial pathogens causing the expression changes and mutations, and the researchers "couldn't rule out that possibility" LOL 
Trevor
Thank you for this advice. I have read Amy’s recent piece on the Conference and this led me to re-read her earlier piece on successive infection.
As Jason improves, ever so slowly but inexorably I hope, so my mind opens up more and slowly grasps the concepts you are espousing.
I think you are saying that the failure of geneticists to identify common genetic defects in autistics, despite years of looking and (too) many dollars spent, is because each autistic’s genetic material has been more or less uniquely mutated by his/her idiosyncratic population of pathogens. Hence, the very failure to find common mutations across autistic individuals provides still further evidence that autism is a 'pea soup' chronic Th1 infection, like all the other Th1 diseases. That is, each autistic has been overwhelmed by his/her own relatively unique set of pathogens.
The other concept which has struck me is the idea that an environmental factor can cause autism even before a person is born.
The autism world has got bogged down in the debate over whether autism is in‑born genetic or caused after birth due to some environmental insult. Now, the popular idea is to have an each way bet and suppose that autistics have a genetic predisposition that causes them to succumb to an environmental insult, notably, some toxic metal exposure.
As I understand it, the MP view cuts through all of this and states that autism can be in-born or after-born yet still be environmentally caused. Whether the autism is before or after birth depends on when the pathogen load (ie the environmental cause) reaches a threshold of effect when disease starts to show which can occur before, soon after or even much after birth.
I gather that it is not a genetic pre-disposition that is relevant but the pathogen load that the foetus has within it as it enters the world. This load can derive from the father’s sperm and/or from the mother’s womb.
When and whether a child becomes overwhelmed with pathogens and starts expressing ASD disease symptoms will depend on their subsequent L-form exposure and the load it has inherited from within the womb.
Garth Nicolson's work suggests an ASD child could inherit a pathogen load from the Gulf War vet's sperm and/or from the mother's womb if the mother has 'caught' the pathogens via exposure from the Gulf War veteran. Thereafter, the child could pick up more pathogens from exposure to the father and/or the mother, especially in the neo-natal period soon after birth before acquired immunity and if vitamin D-laced formula is fed to the infant. Thereafter, L-form contaminated vaccines and too many beta-lactam antibiotics adds further to the pathogen load.
Thus, children can begin to express autistic symptoms at birth or later in early infancy. I imagine a child who does not succumb to full blown autism could develop ADHD at a later age. I suppose the broad spectrum of child behavioural dysfunction reflects the 'pea soupness' or variability in the number and types of pathogens that can afflict child development in different ways.
My own child did not fit into an apparent vaccine triggered cohort as his autism emerged some months after his vaccines. He also did not seem autistic from birth. However, he was probably showing subtle signs of ASD (failure to point) before his obvious collapse into near catatonia at about 20 months. The MP can explain this history of disease expression.
I thank you Trevor for giving me the intellectual hope that I can heal my son. Is it possible that the only unknown seems to be when not if?
John
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Father of Jason, 11 year old autistic boy. Chronic infection evident from urinary amino acids (see bioscreenmedical.com). Benicar 40 mg QW8H from 7 Apr 07. Phase 3 from 28 June 08. Covered up, sunscreen.
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Dr Trevor Marshall
Research Team
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Posted: Thu May 1st, 2008 23:41 |
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because each autistic’s genetic material has been more or less uniquely mutated by his/her idiosyncratic population of pathogens
That is correct.
The rest of your understanding is correct, except that the child/adult may drift toward a different Th1 syndrome (eg arthritis) as they grow older, depending on pathogen colonization. They need not progress to full-blown ASD or ADHD, those tendencies may be overwhelmed by drift towards more apparent failure of a different part of the body.
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healingjason
Member in Phase 3
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Posted: Wed May 7th, 2008 01:16 |
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Vitamin D and brain function study
An autism news service I subscribe to (Schafer Report) referred to new research on vitamin D and brain function – see:
http://tiny.cc/WMJfx
http://www.fasebj.org/cgi/content/abstract/22/4/982
This may be known to MPers.
Does anybody have access to the full text of this study? I would like to read it.
My posting is not an implicit endorsement of this study - far from it! I post merely to alert Trevor and MPers of this research. Any need to rebut this?
John
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Father of Jason, 11 year old autistic boy. Chronic infection evident from urinary amino acids (see bioscreenmedical.com). Benicar 40 mg QW8H from 7 Apr 07. Phase 3 from 28 June 08. Covered up, sunscreen.
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jrfoutin
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Posted: Wed May 7th, 2008 02:25 |
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John,
From just reading the abstract, it appears their take is that low 25D is seen, so best to provide more D to at risk groups. This is likely why you said you didn't endorse the study.
Your question on whether it needs to be refuted is multi-layered. Like similar studies of other Th1 conditions, with similar recommendations to blanket at-risk groups with more supplemental D, refuting might get to be a full time job right now. They did note low 25D without checking on that "other" D or a pathogenesis. In a very odd kind of way, they actually confirm the Marshall Pathogenesis for each disease with telltale low 25D. It's their current recommended action that can create problems for suffering patients.
I like Dr Marshall's recent publication:
Marshall TG: Vitamin D discovery outpaces FDA decision making. BioEssays. 2008 Feb;30(2):173-82 Online ISSN: 1521-1878 Print ISSN: 0265-9247
Preprint of FullText available from URL http://TrevorMarshall.com/BioEssays-Feb08-Marshall-Preprint.pdf
See inset on Meg Mangin's Karolinska poster (handout preprint):
http://autoimmunityresearch.org/dmm2008/DMM2008_Meg_Handout.pdf
Best to you John--Janet
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Sarcoidosis 125D61, MP10/05 ModP2 12/05 Ph2 6/06 Ph3 10/06, NoIRs limited outings covered, 2/08 25D6.2
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Dr Trevor Marshall
Research Team
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Posted: Wed May 7th, 2008 02:31 |
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I put out my position clearly in my BioEssays response, just published this month:
http://www.ncbi.nlm.nih.gov/pubmed/18404718
http://AutoimmunityResearch.org/Bioessays_reply_may08_preprint.pdf
in answer to the letters:
http://AutoimmunityResearch.org/BioEssays_May08_letters.pdf
"Dr Boucher has highlighted many of the difficulties confronting clinical medicine as it expands its knowledge-base from the level of tissues, as seen under the microscope, to that of individual genes and proteins, interacting at the sub-microscopic scale of the molecule. Even though there are decades of clinical studies attempting to delineate the association between health, disease, and the Vitamin D metabolites, any study conducted without reference to genes, or transcription, must necessarily lead to an incomplete characterization."
..Trevor..
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healingjason
Member in Phase 3
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Posted: Fri May 23rd, 2008 04:34 |
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Study re ASD children having Th1 sick mothers
I am posting to comment on Amy’s piece on her bacteriality site on the tendency for ASD children to have Th1 sick mothers – see at http://bacteriality.com/news/#autism.
BTW, the full text of the study that she refers to can be found at
http://pediatrics.aappublications.org/cgi/reprint/121/5/e1357
I note that the study authors make reference to other studies that purport to show that parents of ASD kids have similar but milder autistic-like behaviours and dysfunctions, belonging to a broader autism phenotype (BAP) - the parents are ‘virtual’ autistics.
In this study, the authors conclude that the BAP mothers, not the BAP fathers, are more likely to be the carriers of defective genes, although a Dad with a more severe psychiatric disorder is more likely to have an ASD off spring than other BAP Dads.
I also note that the authors think the offspring of BAP parents suffer greater deficits. Thus, other environmental factors or genes need to come into the picture to explain this.
The authors may overstate the relative severity of the children's mental disabilities. I note that Asbergers Syndrome children are in the Autism category and these children are fairly high functioning. Their BAP parents could well have a degree of (high functioning) Asbergers Syndrome, as well as other BAP conditions identified by the authors.
I note also that more than 30 per cent of the children diagnosed with Autism were diagnosed after age 6 years. I suspect many, if not all, of these children have language. Otherwise, they would have been diagnosed with Autism at a younger age. In other words, the Autism found by the authors in these children may not be that much more severe than the BAP adult disorders of their parents.
This is not to understate the severity of Asbergers Syndrome but I doubt the Syndrome is especially more severe than the BAP disorders identified.
I am interested in the observation that the fathers of children with autism were older than control fathers. I was a relatively old Dad at 42 years with respect to Jason. However, I was not suffering a BAP disorder, as defined by the study. Jason’s mother was not suffering a BAP disorder either. The study does not rule out ‘normal’ parents (as defined by the study) having autistic children and my wife and I would appear to fall into this category.
I expect the ‘Marshall pathogenesis’ view of autism can explain the age of the father as a risk factor for autism in terms of an older father acquiring more potentially disease causing L-forms over time.
Garth Nicolson found that Gulf Veterans were at greater risk of having ASD children because they passed on infectious agents to their children (perhaps also via a mother infected by the father) and he inferred that these agents cause the autism.
I am also interested in why the girls of BAP mothers are not as badly affected as boys, in terms of acquiring autism.
From a genetic perspective, the authors need to explain why defective genes that predispose a child to autism are passed onto boys rather than girls. They are silent on this gender imbalance.
Can the ‘Marshall pathogenesis’ explain why BAP mothers pass on pathogens to boys that cause them to be autistic but not girls? Would girls get another Th1 disease some time later rather than autism as an infant (say, teenage CFS)? Do male infants have more receptors vulnerable to innate immunity dysregulation in the brain than girls? I think this is the explanation on Amy's site as to why women are more prone to cognitive illness later in life.
Is the gender imbalance due to something we just do not know yet?
John
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Father of Jason, 11 year old autistic boy. Chronic infection evident from urinary amino acids (see bioscreenmedical.com). Benicar 40 mg QW8H from 7 Apr 07. Phase 3 from 28 June 08. Covered up, sunscreen.
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jrfoutin
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Posted: Fri May 23rd, 2008 15:09 |
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Would the one disease/successive infection/pea soup definition apply to differences in disease expression in the male/female instance also? (Hormone variety in the recipe for soup... back to Dr Marshall's early infertility research.)
Also interesting is implications of pathogens using the family/generational/time process (evolution outcomes?). It might seem to be a place to look for further research. Definining pathogen advantages from these 2nd/3rd/4th generation iterations of disease might be quite interesting.
I appreciate Amy's statement:
"...circumstances enforce the reality that often, an entire family must make the effort to rid themselves of Th1 disease and successfully conquer their illnesses together."
Also, this might be interesting for implications when considering study cohort subgroups. Studies of this kind that would by definition require generalist family practice physicians (and they might also find renewed validity for their focus and incentive to participate with intact -- but ill families).
Best to all--Janet
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Sarcoidosis 125D61, MP10/05 ModP2 12/05 Ph2 6/06 Ph3 10/06, NoIRs limited outings covered, 2/08 25D6.2
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Dr Trevor Marshall
Research Team
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Posted: Fri May 23rd, 2008 18:50 |
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1. The gender imbalance comes from the same root cause as the disease imblance. The progress of mutations and junk protein (etc) from the pathogens is dependent on the peasoup contents and the individual's ability to fight the pathogens (which depends on their sex). Everybody carries the Th1 pathogens. Some get daignosably sick while young, others don't get diagnosably sick until older.
2. Pathogens spread within families, most easily passed down the maternal line.
3. The majority of "Defective Genes" are not herited. Science is dead wrong in failing to understand that the pathogens not only have direct access to Homo sapiens' DNA translational machinery, they also have direct access to Homo sapiens' DNA repair machinery, and they mess up both. Most 'Defective genes' are simply pathogenic effects which can be observed, albeit at a very low rate, requiring powerful statistical analysis to distinguish from background noise.
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jrfoutin
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Posted: Fri May 23rd, 2008 19:04 |
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Yes, I'm certainly not looking for more than pathogens in DNA mutations. (I really enjoyed Paul's vimeo mini clip of the genealogy circle when you pointed to another presenter's poster at Karolinska DMM2008, showing something other than DNA was clearly at play in disease.)
But I'm asking more about what would be the advantages that pathogens might have in parent to child generational transitions (beyond mere survival of their species), that they could not obtain across human to human infection processes? (And remembering that little dead neonatal prepped mouse in Nobel Laureate Rolf Z example.)
Do they have a generational advantage beyond opportunisitic, already alive unrelated people-to-people transfer, especially since there is an obvious mother to (yet born, or newly born) child pattern?
Thank you--Janet
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Sarcoidosis 125D61, MP10/05 ModP2 12/05 Ph2 6/06 Ph3 10/06, NoIRs limited outings covered, 2/08 25D6.2
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Freddie Ash
Member in Phase 3
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Posted: Wed May 28th, 2008 23:17 |
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HI ALL
This is Fred in WV. Just a note from our local news this morning, some one has done a study on children and they found out the Autism is caused when the childs T cells are suppressed. Now if they can just find out what suppresse the T cells we will all know the cause of Autism. It is funny how the rest of the medical world are just finding that out. Score another one for Dr Marshall and his staff here. Thank you Dr Marshall for all the great work you and the staff have done here. I do not know who did that study but if we can find out maybe we should direct them to this web site.
Remember, we are all in this together and I am pulling for us.
Your friend in Sarcoidosis
Freddie
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Freddie: dx-sarc 2/82 lymph; skin, eyes, joints, esophagus, intestines, spleen, heart,lungs-meds digitek, L-thyroxine, nexium, furosemide, nattokinase36mg,eat cinnamon w/meals,25D-7; 125-D43
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healingjason
Member in Phase 3
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Posted: Thu Jun 19th, 2008 01:22 |
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Hi Freddie
I would also like to know the study you refer to.
Your post got me looking at this and I have a few things to report that Trevor and other MPers may be interested in.
T cell abnormalities were looked at by Dr Reed Warren in the 1980s and 1990s (he died in 1998) and the idea got about that autistics had defective immune systems and their autism might be related to a failure to clear pathogens of some kind. I think viruses were seen as more probable culprits and L-forms were not on the radar at that time (to my knowledge).
With respect to the purported underperforming immune systems of autistics, a range of abnormalities were found in T cell subset counts and other blood measures. I think the idea was that ASD kids have an immunological genetic weakness which predisposes the child to succumbing to some pathogen which could cause the cognitive defects associated with autism. There was also an interest, and there still is, in the idea that autism is an autoimmune process. Indeed, I got Jason’s blood tested by a MS research lab when he was 3 to see if he had antibodies in his blood to myelin and this proved negative.
I don’t really have much of a clue about this work on immune defects and the reported abnormalities but I think it lost a bit of impetus after Dr Warren died.
I have read an article published in 2002 which summarises the research – see http://www.ncbi.nlm.nih.gov/pubmed/12199139?dopt=Abstract. I have a full text copy of this if folk are interested.
Of particular interest to me is that Jason’s T cells were studied when he was only 3 years of age, and results were reported as follows:
Total T lymphocytes: 65 %
Helper T Lymphocytes: 43 %
Suppressor T Lymphocytes: 17 %
T helper/suppressor ratio: 2.5 (ref range 1.0 – 2.4)
The T helper/suppressor ratio was abnormally high. I presume this is the CD4+/CD8+ ratio which is discussed in the autism/immunology literature. Warren found depressed ratios and I recall not looking at this issue further years ago because Jason’s abnormal finding was inconsistent with Warren’s.
Since Freddie’ post, I got to looking at this further and have now found that an abnormally high CD4/CD8 ratio was found by another researcher to be present in (older than Jason) ASD subjects, as well as depressed ratios.
This study is at Lymphocyte function in autism and Rett syndrome.
I really don't have much of a clue about T cells and what an abnormally high CD4/CD8 ratio might mean.
I have searched through the MP site and note that Trevor has stated
“Until we see data to show otherwise or until we more precisely understand the role of infected Lymphocytes, CD expression is of little interest concerning the pathogenesis of Th1 inflammation." ..Trevor..
I am not sure when Trevor stated this but I was wondering if Trevor might like to comment, at this juncture, about the research on T cells and autism and whether Jason’s abnormal ratio might signify something relevant to the Th1 disease within him.
John
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Father of Jason, 11 year old autistic boy. Chronic infection evident from urinary amino acids (see bioscreenmedical.com). Benicar 40 mg QW8H from 7 Apr 07. Phase 3 from 28 June 08. Covered up, sunscreen.
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