HIV Views, News and Reviews
HIV and Complimentary Medicine.
1. Dementia.
For obvious reasons HIV dementia is a subject not many people want to discuss. It may however not be all gloom and doom. The available research suggests that infection of the Central Nervous System (CNS) occurs soon after primary infection of the body. Although a number of different mechanisms have been proposed for HIV Dementia, it has been shown that there is an increase in inflammatory immune system substances in the brain and that the higher the amount of these substances the worse is the Dementia. A number of plant derived compounds, which are able to suppress these substances and reduce the level of HIV replication are available. These compounds are able to enter the brain and based on the available scientific evidence, should be of benefit for people living with HIV. We have a product available but due to the highly specialised nature of the brain, it is beyond our resources to adequately test the material for efficacy. In the technical information below we have issued a challenge to an expert in the field to research this material. Based on our research, this material is essentially nontoxic and is derived, like all our products from herb and spice extracts that have been used as foods for centuries. This material is available at a small charge on compassionate grounds (however we can offer no guarantee of efficacy or comment on side effects.) E-mail if you require assistance.
For people living with HIV and at risk of dementia we strongly recommend folinic acid supplementation along with B group vitamins.(See Brain)
e-mail peak@phrenesis.com.au
Technical Information
The mechanism of CNS infection with HIV is not fully understood however it is known that brain macrophages and microglia are selectively infected and produce a range of cytokines and Arachadonic acid (AA) metabolites in response to infection. A number of mechanisms have been proposed for the damage caused in the brain (1) and a reoccuring theme is the production of toxic, cytokines and AA metabolites. A similar mechanism as has been proposed for damage elsewhere in the body. In research published in the Journal of Experimental Medicine (2) it was found that the cytokines, Tumour Necrosis Factor (TNF) and Interleukin 1 (IL-1) are increased in interactions between infected brain cells and that these two cytokines produce damage to brain cells consistent with damage seen in HIV dementia. Further more it was found that a significant increases in Cyclo-oxygenase and Lipoxygenase AA metabolites occurred. Prostaglandin E2 (PGE2) and Leukatriene B4 (LTB4) have been associated in other research with neural toxicity and suppression of immunity (3 and References quoted in 3). PGE2 has been shown to suppress both T and B Lymphocyte function and Natural Killer cell function (4-8). Of interest is the fact that suppression of AA metabolites reduces the production of TNF and IL-1.
Research has shown that suppression of TNF, IL-1, PGE2 and LTB4 suppresses the replication of HIV by blocking Nuclear Regulation Factor Kappa B. There are a number of plant compounds that alter the production of these compounds and are of sufficiently small molecular size to cross the blood brain barrier. They can be administered directly to the brain by transdermal application along the carotid artery. We have a suitable, essentially nontoxic product that in invitro testing alters at a cellular level, HIV replication and the production of neurotoxic cytokines and AA metabolites and based on the available scientific knowledge should be of assistance to people living with HIV Dementia.
The challenge is to have this product adequately tested for efficacy by experts in the field. Dementia is a very specialised field well beyond the expertise of a small food/biotechnology company.
The statistics for AIDS dementia are horrifying, the material is available, is any researcher or expert in dementia prepared to take up the challenge?
References
1.Ann. N. Y. Acad. Sci. 747, 205-224 (1994)
2. J. Exp. Med. 176 , 1703-1718 (1992)
3. Virology 208, 590-600 (1995)
4.Prog. Lipid Res.20, 649-654 (1981)
5.Adv. Prostaglandin, Thromboxane, Leukatriennes Res. 9, 331-339 (1982)
6.J. Clin. Invest. 50, 442-448. (1971)
7.Infect. Immun. 26, 311-315 (1979)
8. Cell. Immonol. 61, 52-61 (1981)
9. Biochem. Biophys. Res. Commun. 147, 86-93 (1987)
2.Kaposi's Sarcoma.
We are currently researching a gel product for applying to Kaposi's Sarcoma of the skin. Results of this research will be published as soon as they are available. We can supply this product on compassionate grounds at a small charge to cover costs. We are unable to offer any guarantees regarding efficacy or side effects at this stage but from previous research we do know that the material is essentially non-toxic and that the side effects should be minimal. E-mail if you require assistance. (See below)
Technical Details
HIV induces a variety of cellular responses, which promote the replication of the virus. One of the most important responses is to up regulate the production of Nuclear Factor Kappa B (NF kB). NF kB controls the expression of a variety of gene associated responses to inflammation, infection and stress. Unfortunately increases in NF kB enhance HIV replication. A number of specialized anti-oxidants have been shown to inhibit NF kB and Vascular Cell Adhesion Molecule (VCAM 1) and thus the replication rate of HIV and malignant Tumours (1). Research has indicated that inhibition of inflammatory response genes in Kaposi's Sarcoma cells infected with Herpes 8 may play an important role in the pathogenesis of Kaposi's Sarcoma (2). Our research has shown that both PNP 7 and PNP 4 have activity in reducing inflammatory cytokines and prostaglandins and there is good evidence that PNP 7 inhibits NF kB. We believe that a combination product should benefit Kaposis sarcoma suffers.
References:
(1) Arteriosclerosis, Thrombosis and Vascular Biology. Vol16, No. 12 (Dec. 1996)
(2) J. Acquired Immune Deficiency Syndromes and Human Retrovirology 13:1-11 (1996)