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Russ
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Posted: Thu Jul 26th, 2012 10:05 |
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If I remember correctly, I think that Dr. Marshall now places much less importance on 1,25D levels. I don't think that high 1,25D levels are a requirement of "Th1 disease" diagnosis anymore.
Another thought, in sick individuals I believe that 25D is convertd to 1,25D locally in the infected cells. So maybe with autism the high 1,25D levels are primarily in the brain and this does not show up as easily on blood tests.
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*** I recently moved to Connecticut so if anyone knows of MP docs in this state or nearby, please send me a PM. ***
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Dr Trevor Marshall
Foundation Staff
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Posted: Thu Jul 26th, 2012 10:22 |
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The problem is that we are measuring 1,25-D transported through the bloodstream by the D-Binding protein (DBP), aka GcMAF. Pathogens which affect DBP, most notably HIV, depress the measured values of 1,25-D even though the levels inside the cells are still the same. Other viruses are also suspected to down-regulate circulating DBP.
So 1,25-D it is not a very reliable marker, it is primarily useful when it is high.
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cbay
Member*
| Joined: | Tue Sep 21st, 2010 |
| Location: | Austin, Texas USA |
| Posts: | 178 |
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Offline
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Posted: Thu Jul 26th, 2012 13:54 |
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| Is it possible the 1,25-D samples were not handled correctly for accurate testing? I haven't looked over the study or their methods.
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MP July'10 | OCD`94, GERD`03, IBS`04, ADHD`05, Depression`07, Anxiety `10 | 125D45 June10 | 25D19 June12 | My Progress
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healingjason
Member
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Posted: Thu Jul 26th, 2012 23:09 |
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The samples were refrigerated at -20 degrees C which I imagine is cold enough to be considered frozen.
If there was mishandling the mishandling could affect the controls results as well.
Perhaps the "low" ASD results are not really much lower than the controls. We don't know the results for the 13 ASD kids whose parents were related. These may have biased the ASD results to some extent. It would be useful to know the results if these had been excluded.
The issue is to explain the low 25D, 1,25D and calcium. Low 25D can be due to Th1 disease and it looks like "low" 1,25D is not inconsistent with Th1 disease. Not sure if low serum Ca can be explained as part of a Th1 disease process.
The view that all these are caused by ASD kids being kept indoors moreso than other kids to the point of being D deprived in a sun drenched country like Egypt seems a long stretch of the imagination, especially as only a small amount of sun exposure is needed for D sufficiency.
I have not heard of ASD kids being especially kept indoors in any other country.
I think a better explanation than this is needed.
I am aware of the idea of dark skinned Somali ASD kids being supposedly D deficient in Sweden but Egypt is nothing like Sweden from a sun point of view and both the ASD and the control groups in the (Egypt ) study would be similar in terms of skin tone I expect.
John
Last edited on Fri Jul 27th, 2012 02:52 by healingjason
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Dad of Jason 16 yrs ASD. Chronic infection evident from testing by the Uni Newcastle, Aust. MP meds from 7 Apr 07. Benicar 40 mg QW6H. Phase 3 from 28 June 08. Mostly covered, sunscreen. 25D - 10 (08/09), 22 (02/10), 17 (02/11)
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seanlane
Member
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Posted: Sat Aug 4th, 2012 03:01 |
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Although there are a lot of theories in this one....I found some of it to be relevant in what to avoid.
The build up of glutamate and it's possible relation to glucose levels....I found interesting as well
http://www.dramyyasko.com/wp-content/uploads/2011/08/The-Role-of-Excitotoxins-in-Autistic-Type-Behavior.pdf
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bipolar CFS neuropathy arrhythmia food sensitivities psoriasis MCS guillain-barre tinnitus 125D58 Ph1Jul/08 Ph2Oct/08 25D=17.8 Sept/08 25D=11.8 Jul/09 Ph3 Sept/09
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healingjason
Member
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Posted: Thu Sep 13th, 2012 02:43 |
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Trevor and MPers
There has been much fanfare in my home town about a recent study that purports to presage a blood test that will infallibly predict ASD occurring before symptoms emerge by identifying particular genes in the blood of young infants see - http://www.nature.com/mp/journal/vaop/ncurrent/pdf/mp2012126a.pdf and http://au.news.yahoo.com/local/vic/a/-/local/14836535/researchers-develop-genetic-test-for-autism-risk/.
The presumed benefit of this is that parents will find that they are doomed to have an autistic child 6 months or so before the usual behavioural assessment can be made. Thus, steps can be taken to “intervene” with behaviour therapy earlier. For the life of me, I can’t see how behaviour therapy can do much good at age 6 months but then I am a cynic because this therapy has so spectacularly failed for us over many years.
This said, there is the suggestion that drugs can be developed to turn off “autism genes” or turn on newly discovered (by this study) autism protective genes.
I would be really interested if Trevor or anyone can have a look at this and comment whether there is anything new here.
For example, is the discovery of autism genes really a discovery of gene expression gone wrong by environment (epigenetics?) factors? Are the particular genes identified related in anyway to a dysfunctional VDR up-regulating “autism” genes or downregulating ”autism protective” genes?
Are these genes any of the 615(?) genes that are known to be affected by vitamin D metabolism? Could any of the autism genes be mal-expressed because of the activities of the metagenome, implying corrective action by the MP would eliminate this gene expression, effectively eliminating so-called “autism genes”?
Is there cause for concern that my Jason is doomed by his genes and no amount of MP or immune-stimulatory therapy will rid him of his autism genes or give him “autism protective” genes?
John
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Dad of Jason 16 yrs ASD. Chronic infection evident from testing by the Uni Newcastle, Aust. MP meds from 7 Apr 07. Benicar 40 mg QW6H. Phase 3 from 28 June 08. Mostly covered, sunscreen. 25D - 10 (08/09), 22 (02/10), 17 (02/11)
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Paisleykilt
Member*
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Posted: Thu Sep 13th, 2012 02:49 |
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| As someone who has a brother with autism, this is of great interest to me, too!
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MP start May'11 (no breaks) | Lyme Disease/CFS/Fibromyalgia (depending which specialist to believe) | muscle/joint pain, severe fatigue, neurological symptoms | last 25D= 11.2 ng/mL Jan.'13
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Dr Trevor Marshall
Foundation Staff
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Posted: Thu Sep 13th, 2012 04:55 |
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Is there cause for concern that my Jason is doomed by his genes and no amount of MP or immune-stimulatory therapy will rid him of his autism genes or give him “autism protective” genes
John, I really can't give this subject my full attention right now, I am rushing to finish off some FDA paperwork before I leave for the Moscow conference.
But if you go to my St Petersburg conference on YouTube:
http://www.youtube.com/watch?v=_rFmAMDdbjs
you will find at the 29:20 mark I put on a slide which shows why the current concept of genetic SNP's is faulty, at best, and totally misleading, at worst. By ignoring the microbes when doing gene scans these researchers have been not only looking for needles in a haystack, but chasing phantoms as well. As a result there are between 3 and 20 million needles (SNPs) found so far, depending who you talk to. Not one of these 'discoveries' has ever lead to a cure (lasting beyond a couple of years, the first bubble boys ended up with leukemia, and the the second attempt is still too early to tell).
However, Science will get it right one day  I would not be surprised if you find that the genes, far from 'dooming' Jason are actually the 'doom' of these scientists who keep trying to drum up more money by promising what they know they can't deliver - solid, useful clinical results
I will write more when I get to Moscow at the end of the month, and the pressure lifts a little.
..Trevor..
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healingjason
Member
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Posted: Fri Feb 22nd, 2013 01:28 |
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On “Jason’s Progress” and this “AUTISM” thread, there has been a brief discussion of 2 studies which found low 25D in the circulating blood of ASD sufferers – see http://www.jneuroinflammation.com/content/pdf/1742-2094-9-201.pdf and http://www.ncbi.nlm.nih.gov/pubmed/20569030. The latter study also reported low 1,25D levels.
I raised a concern on the “AUTISM” thread that the low 1,25D result was not consistent with ‘classic’ Th1 disease. Trevor responded that a low 1,25D result might reflect low levels of vitamin D binding protein (VDBP), especially as viruses (eg HIV) can disable VDBP which carries vitamin D metabolites in the blood to target organs.
I am also aware that low blood levels of 1,25D may not reflect 1,25D levels in Th1 diseased tissue, such as the brain where 1,25D levels could be high due to a Th1 disease process there.
In exploring VDBP further, I have found that it is likely that VDBP is depressed in ASD sufferers. For HIV sufferers, I understand VDBP is destroyed by the HI virus excreting a metabolite called nagalase – the work of Yamamoto et al is cited in the MPKB in regard to this. Bradstreet has reported that ASD children also have high levels of nagalase – see http://www.la-press.com/initial-observations-of-elevated-alpha-n-acetylgalactosaminidase-activ-article-a3450-abstract.
While Bradstreet did not test VDBP, I imagine it can be inferred that VDBP would be depressed as it is by negalase for HIV sufferers. Bradstreet’s interest is not VDBP (and its effect on circulating vitamin D metabolites) but macrophage activating factor (MAF) which is reduced if its substrate, VDBP, is reduced. His concern is that reduced MAF is immunosuppressive and that unspecified viruses have ultimately caused this (and ASD symptoms) and that this can be redressed by injections of GcMAF, as pioneered by Yamamoto et al for HIV and also cancer sufferers.
Bradstreet has had a long interest in medical causes of ASD and claims to have cured his own son some years ago (I can’t recall how). Now, his interest is GcMAF injections – see http://www.la-press.com/initial-observations-of-elevated-alpha-n-acetylgalactosaminidase-activ-article-a3450-abstract.
Interestingly, this site has a page that is lifted straight from the MPKB I think – see http://www.gcmaf.eu/info/index.php?option=com_content&view=article&id=142&Itemid=76. Does this outfit have the Foundations impramater?
Bradstreet is alert to the literature that low levels of vitamin D have been observed in ASD blood and his paper infers (I think) that this can be attributed to low VDBP. He seems to have no awareness of how low levels of 25D in particular could otherwise be explained (ie by the Marshall pathogenesis). He supports supplementing with vitamin D for his ASD patients who receive GCMAF injections in an effort to raise VDBP
It seems plausible to me that low VDBP – caused by viruses producing nagalase - could explain low levels of circulating 25D and 1,25D since it is VDBP that largely carries these metabolites from the liver and kidney respectively. However, I underand that bacteria also cause perturbations it vitamin D metabolites in Th1 affected sites of the body (i.e. outside the liver and kidney), as discovered by Trevor.
In the case of ASD, it seems to me that we cannot know to what extent vitamin D metabolite changes are caused by viral infections affecting VDBP or, alternatively, by microbiota infections in sites beyond the liver and kidney. Most likely, I suspect both disease processes are in play. I recall Garth Nicolson found evidence of viral infections, as well as mycoplasmas in ASD sufferers.
The important question for me is whether GcMAF injections are warranted to assist Jason to recover. I appreciate that the MP also works to address viral infections, as well as microbiota damage to the VDR. I ask whether GcMAF injections might complement the MP, given that ASD sufferers have almost universally been found to have high levels of nagalase (by Bradstreet) and hence are immunosuppressed by low levels of endogenous MAF, perhaps more so than other Th1 disease sufferers. The nagalase levels of ASD subjects were even higher than those of HIV and HCV sufferers. Perhaps the severity of nagalase-based illness may explain why Jason is relatively slow to respond to the MP.
This said, I would be wary of experimenting with GcMAF injections because of concerns about purity and introducing other bugs into Jason’s fragile immune system. I certainly would not go with vitamin D supplementation as part of any therapy.
I was wondering if Trevor sees a potential role for GcMAF in concert with the MP, without vitamin D supplementation of course? Perhaps he and others might care to comment on the above.
John
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Dad of Jason 16 yrs ASD. Chronic infection evident from testing by the Uni Newcastle, Aust. MP meds from 7 Apr 07. Benicar 40 mg QW6H. Phase 3 from 28 June 08. Mostly covered, sunscreen. 25D - 10 (08/09), 22 (02/10), 17 (02/11)
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Dr Trevor Marshall
Foundation Staff
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Posted: Fri Feb 22nd, 2013 16:21 |
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My colleague in Norway, Dr Flatabo, tells me he has tried that therapy with one of his kids (patients) with autism, and he has not benefited. I am keeping a watchful eye on this new therapy, but it really does seem to be mostly marketing hype at this point. I will let you know if that changes.
An ILADS doc, whom I respect, says it didn't work for his patient with Lyme, either.
..Trevor..
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healingjason
Member
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Posted: Fri Feb 22nd, 2013 23:51 |
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Thanks Trevor for your views on the GcMAF therapy.
Do you have a view on how those suffering viral infections, such as those with HIV and now it seems those with ASD, need to be treated on the MP? If these folk have low levels of VDBP does this not impact endogenously produced vitaminD? Would not there be less circulating vitamin D? And if so, do these folk need to be less concerned about ingesting vitamin D or about exposing themselves to sun and light? In other words, does the MP need to be varied for these folk in the light of the impact of viral illness on VDBP and less vitamin D being transported attached to less VDBP?
John
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Dad of Jason 16 yrs ASD. Chronic infection evident from testing by the Uni Newcastle, Aust. MP meds from 7 Apr 07. Benicar 40 mg QW6H. Phase 3 from 28 June 08. Mostly covered, sunscreen. 25D - 10 (08/09), 22 (02/10), 17 (02/11)
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Dr Trevor Marshall
Foundation Staff
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Posted: Sat Feb 23rd, 2013 02:21 |
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The required Vitamin D metabolites are produced in individual nucleated cells. There doesn't need to be any carried around the body, as we have proven with our members gaining bone strength despite lowered circulating 25-D levels.
GcMAF/DBP is a macrophage activating factor. But I suspect that whatever is added to the blood (once removed from a patient) to make the GcMAF levels increase, is having effects beyond GcMAF. I haven't seen any science to indicate either 25-D or 1,25-D are necessary to GcMAF's MAF activity.
One reason scientists have been so misled over the VDR is that they have been experimenting with mice, whose VDR is very different in function from our own. Last week's key announcement should start to put an end to that.
http://www.nytimes.com/2013/02/12/science/testing-of-some-deadly-diseases-on-mice-mislead-report-says.html
..Trevor..
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