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Meg Mangin R.N.
Research Team
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Posted: Tue Oct 4th, 2005 23:13 |
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AIDS/HIV
I have indeed given a lot of thought to the pathogenesis of AIDS, assisted by a group of colleagues centered on Dr Alan Cantwell. For example
http://tinyurl.com/922q7
and these: (very, very slow to load)
http://tinyurl.com/bh7qh
http://tinyurl.com/9duvr
..Trevor..
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Meg Mangin R.N.
Research Team
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Posted: Wed Oct 12th, 2005 10:27 |
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(filelink)
AIDS and 1,25-D
Severe Deficiency of 1,25-Dihydroxyvitamin D3 in Human Immunodeficiency Virus Infection: Association with Immunological Hyperactivity and Only Minor Changes in Calcium Homeostasis]
Charlotte J. Haug, Pål Aukrust, Egil Haug, Lars Mørkrid, Fredrik Müller and Stig S. Frøland The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 11 3832-3838 Copyright © 1998 by The Endocrine Society
Hypercalcaemia and elevated 1,25(OH)(2)D(3) levels associated with disseminated Mycobacterium avium infection in AIDS.
Author: Playford EG , Bansal AS , Looke DF , Whitby M , Hogan PG
Source: J Infect, 42(2): 157-8 2001
==============================
What effect would concurrent viral and CWD bacterial infections have on 1,25-D?
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Meg Mangin R.N.
Research Team
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Posted: Sat Oct 15th, 2005 01:46 |
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(filelink)
Do you think using antiretroviral therapy (ART) in sick patients with low 1,25 D as a preliminary intervention is worthwhile prior to starting MP?
I would deprecate ART as these are moderately toxic drugs. The issue with AIDS is that the HIV does not kill the patients - the Th1 bacteria do. HIV merely conditions the immune system to allow the Th1 bacteria to rampage. That is why so many folks harbor HIV but never develop AIDS, and why the activists have kept themselves alive with Doxycycline. That is also why patients recover from HAART to TB or Sarc. I am sure it is best to go after the Th1 bacteria (eg with mino) as quickly as possible.
..Trevor..
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Meg Mangin R.N.
Research Team
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Posted: Sat Oct 15th, 2005 02:25 |
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(filelink)
Dr. Marshall's papers on AIDS
I have written quite a bit about AIDS, for example, the second half of this letter to the Editor at CHEST from early 2003.
http://www.chestjournal.org/cgi/eletters/124/1/6
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Aussie Barb
Research Team
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Posted: Mon Apr 10th, 2006 18:33 |
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| The answer to your question about 1,25-D affecting maturation of monocytes in AIDS is contained in the paper "The effect of 1,25-vitamin D3 on maturation of monocytes from HIV-infected patients varies with degree of immunodeficiency" http://tinyurl.com/nzoxr
____________________
Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| 24+ years not Dx| ABCofMP
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Aussie Barb
Research Team
| Joined: | Thu Jul 22nd, 2004 |
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Posted: Mon Aug 21st, 2006 21:51 |
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Dr Marshall Private Discussion Forum
The AIDS presentation I gave at our recent conference, to introduce Alan Cantwell's presentation on AIDS, basically explained how the HIV virus disables innate immunity by disabling generation of 1,25-dihydroxyvitamin-D. When innate immuny has been suppressed, the intraphagocytic bacterial infection, which we address so well with the MP, can start to take over the immune system. This in turn suppresses the immune systems ability to kill HIV, so the virus count starts to increase, and it is a slippery slope from there to the Th1 diseases which typically kill AIDS patients.
In other words, I said that, based on what we have found in Th1 disease, that AIDS is a two-stage disease - you have the HIV infection ad the intraphagocytic infection. You have commented that the post-HIV illnesses do appear to be related to Th1 disease, and indeed they are. Alan then went on to explain how even Kaposi's Sarcoma is also related to the Th1 pathogens.
The DVDs of the conference transcript won't be ready for another month (I am guessing) but I think your friend will be very interested not only to hear my presentation, but also to listen to the symptoms being explained by folks who have recovered from their Th1 disease. A therapeutic probe will reveal the extent of the intra-phagocytic bacterial load...
We have no clinical experience with AIDS patients yet. But the understanding is in place, and, IMO, it is just a matter of time until 'post-HIV wasting disease', and many of the other post-HIV disease are found to be Th1 in pathogenesis.
The key is that HIV, uniquely among the pathogenic viruses, totally suppresses the body's generation of 1,25-dihydroxyvitamin-D and makes it easy for the chronic Th1 pathogens to proliferate.
..Trevor..
The really key breakthrough we made was bringing together bio and clinical medicine to describe how the Vitamins D predispose the innate immune system to L-form parasitization. The action of HIV on 1,25-D is just an extension of that understanding.
Yes, exactly the same phase 1 MP, being very careful about runaway herx. The pathogen load in this case is probably not that excessive if her CD4+ are still around 400ish, though.
Watch what happens to the disease markers. Remember that there will be some white cell apoptosis... so the white blood cell count may even fall a little once the antibiotics really take hold. Watch the SED rate, too.
ps: Oh - and remember that there will be relatively little killing of the L-forms until her 25-D falls below about 50nmol/L
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Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| 24+ years not Dx| ABCofMP
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Meg Mangin R.N.
Research Team
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Posted: Fri Jul 27th, 2007 16:03 |
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Dr Trevor Marshall
"The HIV virus replicates with the help of the Vitamin D receptor. There are very close ties between the VDR, which is at the heart of innate immunity, and the HIV Virus itself, and even closer ties between the VDR and the chronic phase of the illness; it's a circular process. This chronic phase is dominated by increasing severity of chronic immune dysfunction."
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Please see the DVD presentations on AIDS by Dr. Marshall and Dr Alan Cantwell at the ARF 2006 conference in Los Angeles.
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