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sunflower
Guest
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Posted: Wed Aug 6th, 2008 06:08 |
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| i don't know if this is the right place to post this, but i found this article very interesting: http://advanceindiana.blogspot.com/2008/08/have-health-experts-been-wrong-about.html sun
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lyme,fibro,candida,allergies,gerd,osteopenia/ pain,fatigue,dizzy,memoryloss20+yrs/ celexa,vicodin,cal-mag/beni 40mg q6h 11-05/phase 3,8-06/1,25d=34 25d=36,18,17,10,13,5,7
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Dr Trevor Marshall
Research Team
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Posted: Wed Aug 6th, 2008 06:46 |
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Sun,
This is not really a good place to discuss this topic. It is a complex one, which we explored at our LAX 2006 conference with Dr Alan Cantwell, one of the most controversial figures in the AIDS debate.
It is not a good time to discuss this as Science is right in the middle of a number of discoveries which will change the way that all infectious diseases are seen in isolation, assumed to be caused by one pathogen, and nothing else. This concept dates back to the Postulates of Koch, and is 19th century thinking.
What I will say is that even the conspiracy theorists don't understand the complexities of what they are playing with. I want to direct you to one paper. Knowing what you all know about the VDR, you can understand what would happen if somehow the VDRs that Benicar is activating were to be co-opted by a virus, and no longer be available to drive your immune function. That is exactly what the HIV virus does.
http://jme.endocrinology-journals.org/cgi/content/full/38/6/587"Our data show VDR-dependent activation of the HIV-1 LTR in this cell type, supporting a possible role for this receptor in HIV-LTR-mediated transactivation and therefore on the progress of AIDS."
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"In conclusion, our data point to the importance of VDR signaling in HIV transactivation, which can occur through ‘classical’ and ‘non-classical’ mechanisms."
It turns out that the active phase of HIV infection co-opts the VDR,without the need for 1,25-D activation, as part of its own replication, obviously leaving the patient immuno-compromized. From that point on, IMO, everything just slides slowly downhill through all the Th1 diseases which occur during the chronic phase of AIDS.
As we get the word out about our own work, at that point we can start to help the HIV researchers. At this point even the researchers who did that study I cited, apparently have no idea of the implications of what they have found...
My own wild guess is that the surge in AIDS incidence might well be found to coincide with the surge in Th1 disease, as Th1 weakened innate immune systems would be unable to deal with the assault of HIV...
Trevor
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migsies
Member in Phase 3
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Posted: Thu Aug 7th, 2008 00:59 |
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Interesting post Sun! I am not too surprised by these researacher's findings and I am pleased to see them focus on the role of the VDR in HIV. Perhaps Dr. Marshall's work on the role of innate immunity in disease is finally having some impact on research priorities. I certainly hope so.
Maybe with time we will discover that some aspects of their model of VDR dependent viral reactivation extends to a number of other viral entities, including the plethora of herpes viruses. Such a model would be consistent with the experience that some people have with herpes reactivation in response to immune activity and/or solar exposure (once immunosuppression from the initial D25 surge declines and the D1,25 is able to work on the VDR). I suppose one would expect strong positive selection for the expression and survival of any virus that can dissable innate immunity (hence apoptosis), by linking itself to the VDR or associated genes or other yet undetermined mechanism. It seems to me that this type of infection would put the host in the pardoxical situation of having to "decide" between a downregulated immune state that predisposes to an assortment of secondary/opportunistic intracellular infections, and an innate immune activation that might offer short term protection but is linked to the expression of a viral antigen hence the ravages of chronic inflammation. In the long term, as the body struggles to find balance, one might predict ongoing cellular damage (including mitochondrial damage) and a decline in innate immune function. At some point, this process might manifest as an increased Th1 response reflecting a compensatory attempt by the host to control the levels of intracellular infection in the face of declining innate immune function. Sound familiar? Of course, as we all know from Dr. Marshalls work, a hyperactvie Th1 response is fraught with problems too.
Maybe the factors that determine whether one gets over an initial viral infection or progresses to chronic illnesses such as CFS include not only familial clustering and exposure to pathogens (epidemiological factors) but also the chance event that viral insertion and/or reactivation (inherited viral gene components) occurs in association with genes involved in innate immunity and apoptosis. As they say on HGTV...location, location, location. This mixture of stochasticity and epidemiological pattern, not to mention our modern day "genetics" based medical paradigm, might explain why researchers have been so befuddled, looking for elusive pattern and endlessly debating whether these chronic illnesses are of genetic or infectious origin. Ignorance of L-forms is probably another factor. IMO, pattern can usually only be teased appart from randomness if one has a good hypothesis that includes at least key components of the underlying mechanism.
In all fairness, I do not mean to favor a viral hypothesis of chronic illness and underestimate the role of L-forms in initiating or perpetuating the kind of inflammation and cellular damage that could ultimately lead to innate immune system decline and viral reactivations. This would be overly simplistic and besides, I am personally not attached to any particular dogma, I am only interested in explanations that adequately explain the phenomena in question or provide good clinical outcomes. IMO, we are dealing with a very complex set of factors and it seems to me that once cellular infection is set into motion it becomes almost impossible and counterproductive to assess blame. For the record, I strongly support Dr. Marshall's attempts to get at the problem of innate immunity from the angle of the VDR as this is the most expeditious approach. I just hope that this HIV study doesn't add a new wrinkle, a new and potentially frustrating layer of complexity. The implications are certainly troubling.
Anyway, it is the interplay between these viral pathogens and the L-forms, and the way they jointly modulate innate immunity, that raises all the interesting and relevant questions for me. How I wish that the relationship between infection and innate immunity were a primary focus of NIH funding, as I am certain that therein lies not only a better understanding of chronic illness but perhaps also the prevention of innate immune related diseases prevously thought to be inevitable, such as cancer. I am glad that Dr. Marshall has been hot on this trail, offering up some answers, treatment, and drawing attention to the importance of the intracellular microbial millieu to innate immunity and disease in general.
Thank you Sun for the interesting link!
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Sarcoidosis FM Lyme babesia 25D>7(Feb07) Ph1Aug05 Ph2Oct05 Ph3 Jun06 Valium Lyrica Ambien NoIRs limited outings covered Phase I 8/05, II 10/05, III 6/06.
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eClaire
Member in Phase 2
| Joined: | Mon Sep 25th, 2006 |
| Location: | Virginia USA |
| Posts: | 566 |
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Online
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Posted: Fri Aug 8th, 2008 05:53 |
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When my brother was diagnosed with AIDS, he recovered from the brink of death from pneumonia and was put on AZT and given two years to live. As those two years drew to a close, he appeared to be just weeks from death. Then the AIDS cocktail was approved for wide-scale use, and he went on to live another 8.5 years. I have no doubt that the AZT contributed to his declining health, and who knows the affect of the other drugs? I did see the side affects, however, and they were horrendous, causing him at times to give up the drugs until his doctor would switch the combination (essentially he would go on a medicine strike).
Except for pneumonia one other time, my brother continued to be someone who rarely caught a virus and never had a cold (much like me) although that is what was predicted by his doctors (he eventually stopped taking precautions around sick people because he seemed impervious to other viruses). Eventually, he suffered from congestive heart failure. (This is the fate I believe I was headed toward if not for the MP.)
One thing that my brother said when he was first diagnosed that has always stuck in my mind is that he now understood what I had been going through (this was before my CFS diagnosis but not before I had nearly all of the symptoms attributed to that label), as our illnesses seemed nearly idential to him. Indeed, in the couple years before being diagnosed with AIDS he had started to become sensitive to formaldehyde.
I am hopeful that AIDS will one day be better understood and that the work of Dr. Marshall will one day help people with an AIDS diagnosis just like it is helping so many other people.
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 3/2-5/25/08; Temazepam 9/26/08; Ph2Oct29
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