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healingjason
Member in Phase 3
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Posted: Sun Jun 3rd, 2007 23:31 |
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Interested MPers
This is another post which goes to the topic of Th1 origins of autism.
Below is an extract from a post from Trevor in another forum:
" ...we have a molecular-biology-based model for chronic inflammatory disease which is well developed and well tested. The only variable is whether ASD (Autism Spectrum Disorders) is a chronic inflammatory disease described by the model. When a patient responds according to the model's predictions then we can be pretty certain that the progress of that patient will be along the same trajectory as others who have gone before.
So as long as Jason follows the expected symptomatic and healing trajectory then we can have confidence in the outcome. There is no black-magic, no experimental drugs, just a model based on how the body actually works "
Is ASD is a chronic inflammatory disease?
I obtained laboratory data from researchers at University of Newcastle some 7 years ago that goes directly to Trevor's statement "The only variable is whether ASD is a chronic inflammatory disease described by the model." This lab data is relevant to autistics in general and my Jason in particular.
University of Newcastle research
I had a urine specimen examined in 2000 by Prof Tim Roberts and Dr Hugh Dunstan of the University of Newcastle, Australia. These researchers had done a lot of work with adult CFS patients and they applied a urine screen they had developed for such adults to 36 autistic children. The children examined were patients of a Sydney doctor specialising in treating ASD children and children with other learning disorders. The Newcastle researchers performed a raft of tests on the stool (for gut flora) and on blood as well.
The Newcastle results were presented at the World Autism Congress in 2002 in Melbourne. One finding was that the children were believed by the researchers to be suffering from an ‘occult infection’. However, many other findings were reported (such as unbalanced bowel flora and low essential fatty acids) and the ‘occult infection’ finding was not especially highlighted.
I looked further into the urine test results and, in particular, an ‘unidentified metabolite’ found in the urine which the researchers labelled ‘UM 27’. In my boy, this metabolite was very highly elevated relative to normal adult and normal child controls and even compared to average ASD children. Indeed, for my boy, UM 27 represented 22 per cent of his urinary amino acids where a normal healthy adult exhibited an average of 0.27 per cent, a normal child 2.1 per cent and an ASD average child 11.4 per cent. There were also several other metabolites which were elevated, also believed to be reflective of a body suffering a chronic infection.
I have since learned from Prof Roberts directly that he believes this metabolite to be the end product of a chronic disease process:
"The molecule looks to be a breakdown product of the body rather than a molecule produced by an infective organism but why there is so much of it seen in the urine of autistic children we do not know. My guess is that the bug involved causes the release of this molecule from human cells. An understanding of this will lead to us finding the bug is my hypothesis. " [e-mail to me dated 22 February 2007]
I have had a close look at the documents Prof Roberts sent me and there are some very interesting statements that go to a view that is very similar to those of the MP. Below is a sprinkling to stimulate people's interest.
On the matter of our research into Chronic Fatigue Syndrome, Fibromyalgia, Rheumatoid Arthritis, and Autism, it has been our finding that we have a situation where there is a switching of the metabolism of the body into a catabolic state. Such a catabolic state is usually a short term acute response to an activation of the immune system in response to an infection or a trauma. In the case of the syndromes mentioned above, it seems that this catabolic state is maintained for a very long time. Our interpretation of this is that these groups of people are carrying a chronic infection which their immune systems are unable to completely clear up. We believe these infections are of the intra-cellular type probably due to rickettsia, ehrlichia, and mycoplasma families of bacteria or possibly also viruses.
If one is unlucky enough to get a particularly aggressive organism then the immune system is chronically activated, a catabolic state chronically persists,
Our interpretation of this is that the symptoms such as tiredness, memory fog, chronic pain, headache, gut dysfunction etc are the result of the ongoing chronic immune response the body is making in an attempt to rid itself of the chronic infection. As a side-result of this massive production of defensive proteins such as cytokines, interleukins, and antibodies there is collateral damage to other systems of the body itself.
There is often also a sensitivity to light and a difficulty experienced in reading.
In a project that is currently underway we are comparing the changes seen in molecules measured by gas chromatography in the urine and blood of children with autism. Our studies to date have revealed a change in the metabolic profile of blood lipids, faecal lipids and bacteria and urinary organic and amino acids in children with autism.
The changes we see in these apparently unrelated disorders are very similar and reflect the catabolic state seen when the body’s immune system is fighting chronic infection.
Our preliminary studies found that there was an ongoing catabolic response and that there was also a marked disturbance in the gut bacteria.
We conclude from our studies that there is an underlying primary external infective agent which induces ongoing activation of the immune system, with subsequent marked alteration of the faecal microbial flora. This multisystem disturbance in homeostasis results in the expression of symptoms in patients with autism.
Evolution of disease
Finally, it is important to consider the process of natural selection in chronic disease. Our work has consistently shown that in the chronic states mentioned above there is evidence of activation of the immune system. Others have found that there is usually a switch in the immune system to the antibody arm of the immune system (Thelper 2 type cytokines). We hypothesise that there exist in each of these disease states one or more micro-organisms which are the primary infective agents for that disorder. The process of evolution is natural selection of that individual in the population who is able to grow to sexual maturity and to reproduce. Thus after each generation there are more and more of that type of individual in the species. The important point to remember is that evolution applies to both humans and to the micro-organisms. Why then have scientists not found the causative microbes yet? The answer lies in the difficulty of culturing these organisms using conventional agar plates, and in the tendency of clinicians to believe that there are no new disease causing organisms to be discovered. The finding of Helicobacter pylori in the stomach of individuals with gastric ulcers occurred in 1982 but it was not until 1997 that the Royal Australian College of General Practice accepted this bacteria as the causative agent of stomach ulcers.
In our laboratory we have been seeking these underlying infective agents by looking in the blood, urine and faeces of affected individuals for unusual molecules that may be flags of hidden infective agents. We are also using modern DNA detection methods to look for the presence of organisms without having to culture them on agar plates. I will conclude with one example of our success in finding a new organism and a new explanation of a disease that was previously thought to be an auto-immune disease. As a result of our findings treatment now is with tetracycline antibiotics rather than with immunosuppressive drugs. Apart from the Newcastle findings, Prof Garth Nicolson has provided me with his research showing that the bloods of ASD children are replete with mycoplasma species. However, he does not know if these are opportunistic co-infections or the primary underlying cause of a child’s autism.
Given the Newcastle research, I am fairly confident that my boy has a chronic Th1 infection and that his autism is the product of an inflammatory disease process described by the MP model.
Expected symptomatic and healing trajectory?
What remains of course is whether Jason will follow a healing trajectory path as others with different symptoms have. Two months into the MP, Jason's herxing does not seem much like the extreme herxing that I am led to believe occurs for many on the MP on Benicar alone or while on phase 1.
I am hoping the most interesting phase is to come in phase 2 when I understand the phase 2/3 abxs will impact the brain where most of Jason's inflammation seems to be.
John
Dad of Jason
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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: Mon Jun 4th, 2007 00:25 |
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The model demonstrates why it is important to get Jason's 25-hydroxyvitamin-D level measured. This is a common metabolite, and pretty easy to do. 25-D is immunosuppressive, and a delayed start of immunopathology must always be checked out by first measuring to see whether the 25-D has already fallen into the therapeutic range (30nmol/L and below).
(added later)
I understand that there are problems drawing blood in Jason's current situation, and you have not been able to track this data.
Last edited on Mon Jun 4th, 2007 05:26 by Dr Trevor Marshall
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healingjason
Member in Phase 3
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Posted: Thu Jun 21st, 2007 01:36 |
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Autism and neo-natal brain pathogens
I am interested in better understanding how Trevor thinks neo-natal brain pathogens cause brain dysfunction or disease and whether this thinking can be applied to explain the emergence of autism after some period of apparently normal development.
I am struggling to understand Trevor’s concept and would appreciate being educated on this.
I think Trevor is suggesting that, in many people with Th1 disease, it is feasible that pathogenic microbes colonised the brain in the neo-natal period (when the immune system is undeveloped) and these survive producing sub-clinical symptoms until a more pervasive Th1 illness takes hold in an adult where there are, typically, other sites of microbial infection other than in the brain. Once a Th1 illness is established through excessive levels of 1-25D, the brain also begins to go haywire.
Was Trevor attracted to this idea because people with Th1 illnesses originating from sites other then the brain also showed signs of brain dysfunction?
I note Trevor’s slide showing how Rolf Zinkernagle has shown that a virus that is re-injected into an adult mouse that received the virus as a neonate will die whereas those injected with the virus but not infected as a neo-nate will survive. Is Trevor using this finding to suggest that folk with Th1 illness were likely exposed to neonatal brain pathogens while those unaffected by Th1 illness were not? Is it that we are all exposed to similar pathogens but those with adult Th1 illness can be differentiated from those who are not on the basis of the population of occult bacteria that have been living in the brain since being neo-nates?
For children that come down with learning disorders, including autism, is it plausible to suggest that the neo-natal brain pathogens have more quickly emerged from an occult sub-clinical status to an active clinical status compared to adults suffering Th1 diseases? The sources of microbial colonisation would seem to be multiple and go beyond the neonatal-natal period to include contaminated multiple vaccines given before the autism seems to hit many families by age 2 or 3 years.
The potential connection of neo-natal pathogens to autism is of particular interest me.
People would be aware of the controversy over excessive numbers of vaccines causing autism. There have been posts on this thread that discuss how small microbes in vaccines are not screened out and it could be this, rather then the mercury preservative in vaccines, that contribute to causing autism. Numbers of ASD kids are still rising notwithstanding the removal of the mercury preservative from vaccines suggesting microbial contamination of vaccines could be the more likely cause.
Another factor that may explain the unchecked rise in ASD numbers is that the hepatitis B vaccine has now been virtually mandated for neonates in recent years. It has become almost mandatory in Australia since 2000. I am exploring whether my boy was so exposed as a neo-nate. I don’t think he was but I will need to check this out.
Have I got my thinking right on this matter of neo-natal brain pathogens?
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 Jun 21st, 2007 02:28 |
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John, I am sorry, I have a paper to finish by tomorrow night. Can you please remind me of these questions at the weekend?
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tickbite
Member
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Posted: Thu Jun 21st, 2007 11:22 |
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Definitely remind Trevor over the weekend, John.
It is not hard to see the unmistakable recognition between the two; Rolf's experiment and the autism function as you report. I would say that the reference is very illuminating. Also very insightful are the number of people i've spoken to who after receiving vaccines or booster shots within several months display heavy signs of inflammation. Another story comes from Alan Cantwell's book "The Cancer Microbe." The story about the origination of HIV coming about from contaminated vaccines of which were being tested on U.S. gay male populations and an African population that the W.H.O. were involved in. That book was interesting to say the least. It may all sound like conspiracy, but therein lies the truth.
As far as Trevor's initial interest in the "neo natal pathogens persist in the brain" thoughts, we'll leave that up to him to say. However, pulling down the myth of autoimmunity must be one of them. Molecular mimicry my ....
I think you've got your thinking correct, John.
It is interesting how viruses work....
“Insulator” Helps Silence Genes in Dormant Herpes Virus
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"Lyme","CFS", Meningitis
Phase3 8-2-07, MP on hold 11/2007
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healingjason
Member in Phase 3
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Posted: Sun Jun 24th, 2007 20:37 |
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From my last post
Another factor that may explain the unchecked rise in ASD numbers is that the hepatitis B vaccine has now been virtually mandated for neonates in recent years. It has become almost mandatory in Australia since 2000. I am exploring whether my boy was so exposed as a neo-nate. I don’t think he was but I will need to check this out.
Jason was not given a hep B shot as a neo-nate but he did get a vitamin K shot, as did my normal 13 year old. This is routine for births in my State's hospitals and I gatrher in the US too.
I did a quick Google of this and note, as with all vaccines, this intra-muscular shot is not free of controversy and it has been linked to childhood cancer. I know nothing as to whether microbial contamination could be possible with this. I gather it is supplied by major vaccine makes so contamination would seem plausible. However, I wonder if an intramuscular injection would readily deliver pathogens to the brain.
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: Mon Jun 25th, 2007 04:03 |
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The really important thing to be drawn from Rolf's work is the reminder that the infant is unprotected in the days and weeks following birth, until it starts producing antibodies. The innate immune system is all it has got, although many think that antibody transfer from the mother may be present in the breast milk. I am not sure that would be much help, but I just don't know. Nobody does.
Dave Relman's lab has, however, done a study where they found that a baby picks up all of the mother's, and most of the family's, flora within a couple of weeks of birth.
For children that come down with learning disorders, including autism, is it plausible to suggest that the neo-natal brain pathogens have more quickly emerged from an occult sub-clinical status to an active clinical status compared to adults suffering Th1 diseases?
In a word, Yes.
I would also de-emphasize vaccines at this point. I am sure they contribute to the mix of pathogens, but as we start to hone in on the key pathogens, it is almost certain the key pathogens are passed from mother to child, probably during gestation, and then the infant collects more key nasties from its environment.
I know it is tempting to look for somebody to blame, but these diseases go back centuries, and are caused by processes more ancient than immunization.
Once the immune system becomes weakened it is unable to clear mercury, and so the heavy metals build up in the body. I doubt they reach toxic levels though. And certainly we have seen that the neurological diseases are caused by the plethora of metagenomic pathogens, not by something simple like heavy metals. Folk recover on the MP while their mouths are still full of mercury amalgam
..Trevor..
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Claudia
Member in Phase 3
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Posted: Mon Jun 25th, 2007 12:43 |
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Breastfeeding is important in two ways - first, it passes on important immunity from mother to child until the baby's own system is mature. Secondly, if you breastfeed the baby, it will NOT be given formula laced with "Vitamin D"!
I've just read a list (on a hospital website) which says breastfed babies have reduced risk of Autism as well as other conditions including:
Reduced chance of having childhood cancers
Lower incidence of juvenile diabetes
Reduced risk of Hodgkin's Disease
Less risk of Crohn's Disease
Lower incidence of asthma
Less risk of infantile autism
Less chance of having eczema
Decreased chance of SIDS Plus, interestingly, they are likely to have better vision and a higher IQ 
Regardless of where the child gets their pathogens from, there is no point in aggravating the situation by not breastfeeding our infants. Oh, and I also have read about the 12yo child in the recent case in US courts - trying to prove the autism/murcury link - that she suffers a host of other medical problems. Does this sound suspiciously like Th1 disease? From a news report: Today, Michelle suffers from a litany of health problems, including severe autism, inflammatory bowel disease, glaucoma and epilepsy.
- Claudia
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MP Phase1 23Mar_06; Phase2 July 10_06; Phase3 Nov 4_06. Dx Thyroiditis (Thyroxine); arthritis; glaucoma; CFS (1988-92);Kidney & bladder probs. Feb06 1,25D=43.3; Aug07 1,25D=27.5; Feb06 25D=44; Aug07 25D=28; Nov07 25D=36; Mar08 25D=16.4
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Dr Trevor Marshall
Research Team
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Posted: Mon Jun 25th, 2007 15:29 |
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Claudia,
I have seen no proof that immunity passes from mother to child in the breast milk. It may, or it may not. I am not arguing against breast feeding - it is the only way infants should be nurtured. However, I am pointing out that, to the best of my knowledge, specific science does not support the so often stated pragma that antibodies from mum are useful for the child when passed in breast milk.
Dave Relman's work shows that the children very quickly pick up their mother's flora (within days). If antibodies to those species were being passed to the kid, and if the kid could assimilate those antibodies from its diet, the child would not be susceptible to the flora. So this data argues against the antibody transfer, if any, being of any benefit to the child.
Of course, all this is moot anyway, because the same folk talking about antibody transfer also say that adaptive immunity is active in the GI tract, whereas it is innate immunity which is more important there. So we gotta learn to crawl before we can walk...Last edited on Mon Jun 25th, 2007 21:03 by Dr Trevor Marshall
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healingjason
Member in Phase 3
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Posted: Mon Jun 25th, 2007 21:02 |
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Trevor wrote
"I would also de-emphasise vaccines at this point. I am sure they contribute to the mix of pathogens, but as we start to hone in on the key pathogens, it is almost certain the key pathogens are passed from mother to child, probably during gestation, and then the infant collects more key nasties from its environment.
I know it is tempting to look for somebody to blame, but these diseases go back centuries, and are caused by processes more ancient than immunization."
I understand your caution about jumping on the anti-vaccine bandwagon, but I'm not sure I understand your comment that 'these diseases go back centuries etc.'
Autism, defined as a specific set of behaviours and 'deficits', goes back only to 1943. Also, is not CFS a relatively new disease, to the extent it is recognised as a disease?
Are you referring to a process of pathogens evolving over time and developing into pathogens capable of causing new diseases? That is, the diseases might be new in terms of symptoms but the process of pathogenic development and evolution is old. What is also new is the environment into which these pathogens grow and develop, such as more vitamin D in the food chain?
Can you explain further Trevor?
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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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patrickburke
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Posted: Mon Jun 25th, 2007 21:15 |
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John,
IMHO its probably just the words "Autism" and "CFS" that are relatively new.
Sincerely,
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Sarcoidosis/lungs; Ph1 May05; Ph2 Jun05; Ph3 Dec05; No ABX 2/08; No D tests; still covered since 6/04; Noirs ended 6/07; Minimal light avoidance.
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Dr Trevor Marshall
Research Team
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Posted: Mon Jun 25th, 2007 21:19 |
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I am talking about the illness we understand as the Th1 disease portfolio, caused by symbiotic metagenomic intraphagocytic communities of bacteria which accumulate continually during a lifetime.
What name you give illness doesn't really matter. The fact that some conditions are not currently diagnosed as illness doesn't matter either, for in a decade we will be using tests which pick up the impending bacterial load before it causes overt illness that is far more difficult to manage.
Only a decade? Yes, because we already know the exact cause (well, pretty exact )
The pathogens have been around for centuries. Shakespeare and Beethoven both apparently suffered from them. Three factors have worked to tip the symbiotic balance towards the pathogens during the 20th century
1. The inappropriate use of beta-lactam antibiotics which generated more chronic bacteria (L-forms) at the same time they got rid of the acute infection
2. The addition of Vitamin D to our diets, from pre-natal vitamins right through life
3. The attitude that any amount of sunshine is always good for you. Sun-loving is a 20th century phenomena, although IMO this is of lower importance than 1 or 2.
There also are the factors that Medicine has clung too long to the postulates of Koch, and has for too long revered an evidence-base over true science. These are only secondary issues, for example describing why Emmy Kleinberger-Nobel, or Emil Wirostko, or Alan Cantwell, or Lida Mattman, were not able to effect change one or more decades ago.
..Trevor...
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healingjason
Member in Phase 3
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Posted: Mon Jun 25th, 2007 21:41 |
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Patrick said
'IMHO its probably just the words "Autism" and "CFS" that are relatively new.'
Good point Patrick. Perhaps my boy's 'autism' would have been called something else years ago, especially as he does not now exhibit some of the supposed classic signs of autism – he is very affectionate, sensitive to criticism and has lost most of his classic repetitive behaviours – lining up objects etc.
This said, the psychologists are pretty convinced autism defines a relatively new set of behavioural symptoms.
Also, I think Trevor would agree that the jury is still out on whether autism is a Th1 disease. If Jason comes through the MP with a cure, or is very much better, then we can be more certain that it is.
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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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patrickburke
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Posted: Mon Jun 25th, 2007 21:47 |
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John,
How old is psychology really and have they ever proved anything?
Sincerely,
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Sarcoidosis/lungs; Ph1 May05; Ph2 Jun05; Ph3 Dec05; No ABX 2/08; No D tests; still covered since 6/04; Noirs ended 6/07; Minimal light avoidance.
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Dr Trevor Marshall
Research Team
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Posted: Mon Jun 25th, 2007 21:54 |
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I am certain that ASD, the whole spectrum of disorders, is due to Th1 disease processes.
It is not possible to have seen the number of case histories that I have, or to have met the folk I have, without coming to the understanding that these Th1 pathogens are pervasive, throughout all chronic disease processes.
John, you too are falling into the mistake of being swayed by consensus, by an evidence base. This has not helped other kids who are suffering, and it will not help yours. We all need to keep our minds open.
There is a lot happening over the next few months, and most of it I am not at liberty to share publicly. Let's review the evidence base again in December, for it will have shifted.
..Trevor..
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Russ
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Posted: Tue Jun 26th, 2007 00:12 |
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Dr. Marshall,
I get excited every time I read your posts. Sounds like there is a lot happening now and all the hard work by you and the rest of the staff will soon reach a wider audience. Congrats.
About the 3 factors that tipped the symbiotic balance, what role do you think that #3 (sun-loving culture) has played in these diseases? My understanding was that sun exposure was not immunosuppressive like ingested vitamin D and only negatively affected those who are already ill (and even then not in an immunosuppressive way). Maybe when sun exposure is excessive it does start to have an immunosuppressive effect?
Thanks as always!
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Lyme/Borrelia, Connective Tissue Disease | May '06: 1-25D=59 25D=30 | Jul '06: Phase 1 | Aug '06 25D=16 | Oct '06 25D=6 | Nov '06: Phase 2 | Jul '07: Phase 3 | covering up & wearing NOIRs | no other meds or supplements
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Dr Trevor Marshall
Research Team
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Posted: Tue Jun 26th, 2007 00:26 |
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Russ,
Sun is only a problem when people get sick with Th1, I think. There was a recent study linking phototherapy for psoriasis with an increase in atherosclerosis.
But we do know that 19th century (and earlier) buildings were (generally) not made with glass walls, and certainly bikinis and sunbathing were 20th century inventions.
The experience from the tuberculosis sanitoria shows quite clearly that folk without chronic disease (but with active TB) do have their recovery helped by sunlight. Scadding confirmed this in his 1948 lecture to the Royal Society. Scadding also agonized over his inability to treat sarcoidosis in the same way, with Vitamin D and sunlight
On the other hand, latent TB is having a resurgence in the US now, it is at about 4-10% of recovered TB cases, about the same as the chronic phase of Lyme (PTLDS). I think that both are caused by the Th1-weakened immune system being unable to clear the pathogens.
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Moxie
Member in Phase 3
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Posted: Tue Jun 26th, 2007 03:31 |
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I guess post-polio syndrome fits into that category as well?? (latent TB resurgence)
By the way, when you read Florence Nightingale's biographies, it seems very obvious she had Th1 inflammatory disease along with Elizabeth Barret-Browning. Of course, they didn't have labels for their illness at that time.
Generally a long sea cruise was recommended, and hopefully the patient would have fully recovered on their return!!
Moxie
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CFS 25 years - FMS. Benicar 3 daily - Ph 2 16/5/05 - Ph 3 10/5/06 Metformin 500mg 1/2 bd. Vit D 45nmol/L (18ng/ml) 1,25 D 92pmol/L (38.3pg/ml)
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Dr Trevor Marshall
Research Team
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Posted: Tue Jun 26th, 2007 12:48 |
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There is data available on how children collect bacteria from their families, it is being studied extensively by Dave Relman's group at Stanford.
Last edited on Thu Jun 28th, 2007 04:07 by Dr Trevor Marshall
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eClaire
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Posted: Wed Jun 27th, 2007 07:46 |
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Dr. Marshall,
Last night something occurred to me that I wanted to throw out regarding the explosion of Th1 illness to see what you think. From what I've read, the average age of women when they have children in both the US and Europe has been going up. It would seem that if co-infections increase with age, then giving birth later in life would result in one passing on more CWD. (And would this also apply to men and perhaps account for schizophrenia born to couples where the men are over 40 something?) Before the explosion of TH1 illness, I can see where this might not have mattered so much, but since then I can see where it might have a much bigger impact. We may not have seen its impact just yet, but I was thinking that this would contribute to the exponential growth of Th1 illness in the future (unless of course we do learn to identify significant load before illness onset).
Just a thought...thanks, Claire
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CFS FMS MCS COPD hypermobility IBS/GERD osteoporosis 125D48 25D8 Ph1Dec06 ModPh2Jun07 NoIRs limited outings covered up low lux home abx brk 3/2/08 to 5/25/08
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