Radiesse provides a correction that has been proven to last one year without surgery.

Radiesse is not permanent and therefore avoids the risks associated with permanent materials. (you mean the risk of not having to fork out a couple of thousand dollars all over again?  Risk to whom, the plastic surgeon?)

and if that's not bad enough (again, their own words...)

Its unclear where this  material should be injected (dermally or sub dermally) to achieve correction of
facial defects.

and

It tends to be unforgiving if not applied properly.

Exercise: The Antidote for a High-Fat Meal

By Kathleen Doheny
HealthDay Reporter 45 minutes ago

THURSDAY, Aug. 31 (HealthDay News) -- So, you've just polished off a meal high
in fat, and now you're feeling guilty? Wait an hour or two, then get a little
exercise, and you can reverse the potential damage to your arteries, a new study
suggests.

And you don't even have to head to the gym for that exercise. "We're talking
about a walk, we're not talking about changing your clothes and sweating," said
Janet P. Wallace, a professor of kinesiology at Indiana University, and lead
investigator for the study.

The study, coincidentally, follows another study published earlier this month in
the Journal of the American College of Cardiology in which researchers found
that eating just one piece of carrot cake high in saturated fat and drinking a
milkshake can reduce the body's ability to protect itself against heart disease.

The fat in the cake and shake, it seems, reduces the ability of the body's
"good" cholesterol -- the high-density lipoprotein, or HDL -- to do its job
--protecting the inner lining of the arteries from inflammatory substances that
promote vessel-clogging plaque.

According to Wallace, after a fatty meal, arteries lose their ability to expand
in response to an increase in blood flow. The effect peaks four to six hours
after eating -- usually just in time for your next meal. So, four hours after a
fatty meal, your arteries look like those of a person with heart disease, she
said.

"That post-meal period is a hot topic among all the researchers in heart
disease, diabetes and obesity," Wallace said. "That period sets up the
environment for the artery to be unhealthy. And when the artery is unhealthy,
that is when it leads to heart disease, insulin resistance and other problems."

To see if exercise could make a difference, Wallace and her colleagues studied
eight healthy 25-year-olds, looking at three scenarios. Each of the participants
-- five men and three women -- completed all three scenarios. They ate a low-fat
breakfast. They ate a high-fat breakfast. And they ate a high-fat breakfast
followed two hours later by a 45-minute walk on a treadmill at a moderate pace.
The high-fat meal contained about 48 grams of fat and the low-fat one actually
had no fat; each consisted of about 940 calories.

The researchers used a blood pressure cuff to measure blood flow in the brachial
artery, located in the arm, before and after each scenario. "The brachial artery
represents what is going on in the arteries of the heart," Wallace said.

After the high-fat meal alone, the brachial artery dilation dropped from 6
percent to 4 percent, Wallace said. "The ideal range is about 6 to 10," she
said. "A range of 3 to 5 is not good."

After the low-fat meal, dilation went from 6 percent to 6.5 percent, a slight
improvement.

But, "after the high-fat meal and exercise, it went from 6 percent (before the
meal) to 8 and a half percent," she said.

"Exercise does great things, and this obviously shows exercise is very effective
in counteracting that high-fat meal," Wallace added.

The study results were published in the September issue of the European Journal
of Applied Physiology.

Next, Wallace hopes to study the effect of exercise before a high-fat meal. "I
think we will find it works as well." She emphasized that her research isn't
meant to encourage people to indulge in high-fat fare. But she's realistic:
"There are people who are going to eat high-fat meals," she said.

If you're a fatty-food fan, Wallace suggests some exercise -- after getting your
doctor's OK.

But Jeannie Moloo, a Sacramento, Calif., registered dietitian and a spokeswoman
for the American Dietetic Association, offered a caveat about the study: "We
need to keep in mind the results apply only to the population investigated and
that was young, healthy and physically active adults. The small number of
subjects, only eight, makes it difficult to tell if there are differences in
responses between men and women."

And Moloo, like Wallace, cautioned that the research isn't an excuse to indulge
in fatty foods.

More information

To learn more about a healthy diet, visit the American Dietetic Association.

http://news.yahoo.com/s/hsn/20060831/hl_hsn/exercisetheantidoteforahighfatmeal

Are you referring to the unfolded protein response (UPR) studies in mouse macrophages? Its interesting if they can show an increase in SREBP's in human macrophages. What's more important is the mechanism behind increased levels of SREBP's if this actually occurs.

C-Reactive Protein creates foam cells when it accumulates in macrophage-rich regions of developing atherosclerotic lesions and mediates uptake of native low-density lipoprotein (LDL) by macrophages, thereby potentially contributing to foam cell formation. So normalizing C-Reactive Protein is important regardless of the cause.

Many have observed an increase in blood pressure, with long-term use of protease inhibitors, and an associated rise in C-Reactive Protein. Others suggest that this is a normal aging effect unrelated to protease inhibitor use. This is why studies like Don Kotler's comparing lipodystrophy in normally aging HIV negative people with lipodytrophy in aging people with HIV. Unless you have the comparison, you can't be sure what you're really observing.

--- In PozHealth@yahoogroups.com, Butch Kara <longjohnmaniac@...> wrote:
>
> Norm, I was unaware that any protease inhibitors had been implicated in increasing C-reactive protein, which, as many of us know, is a marker for inflammation. My CRP tests always came back very low while I was on ritonovir, sequinavir, and lopinavir. Chronic HIV does cause elevated CRP as it's an inflammatory disease, which fact was mentioned in the first article I cited. However, the second mechanism of atherogenesis (forming arterial plaque) referred to in both articles has nothing to do with inflammation or elevated C reactive protein - they are talking about up-regulation of particular genetic expressions by the PI class of drugs, including atazanvir, which may increase arterial plaque by turning macrophages into foam cells (as well as by other routes at the cellular level). If so, despite either a good lipid and/or good inflammation profile, PI's may still pose a unique risk for developing heart disease.
> Tom in MO
>
> Original message:
> Re: Reyataz does not affect lipid metabolism, even with Norvir boost
> Posted by: "Norm Stuart" nspop2@... norm_w_stuart
> Date: Wed Aug 30, 2006 6:41 am (PDT)
>
> The episodic or chronic increase in C-Reactive Protein, associated with
> protease inhibitors, appears to be directly mediated by an increase in
> blood pressure, which in turn many believe is caused by increased body
> mass.
> There is no reliable evidence to associate this with Reyataz. Others
> have noted this same rise in blood pressure and C-Reactive Protein in
> people with HIV who have not been treated with protease inhibitors, and
> relate this to normal aging.
> Regardless of the cause, C-Reactive Protein can be normalized with
> either of two Angiotensin-2 Receptor Blockers, Micardis (telmisartan)
> and Benicar (olmesartan).
> Both of these ARBs virtually eliminate inflammation in the
> cardiovascular system, and also greatly reduce any existing
> inflammation
> in the liver and kidneys regardless of the cause. I agree with those
> who
> believe that arterial plaquing is a response to cardiovascular
> inflammation. Eliminate the inflammation and you have probably
> eliminated the arterial plaquing.
> Micardis provides the additional benefit that it can reduce elevated
> blood sugar. Micardis is structurally similar to the diabetic drug
> Actos
> (pioglitazone) being tested in people with HIV for lipodystrophy.
> Having taken both, I can say they both normalize blood pressure and
> C-Reactive Protein equally well, and Micardis does reduce HBA1C,
> essentially a hemoglobin measure of peak blood sugar levels.
> Micardis is slightly less convenient in that each tablet comes in a
> foil
> bubble pack in a box, whereas Benicar tablets are dispensed in a small
> bottle. The equivalent dose (not yet published) is 40 mg of Benicar
> equals 80 mg of Micardis.
>
>
> . Re: Reyataz does not affect lipid metabolism, even with Norvir
> boost
> Posted by: "Butch Kara" longjohnmaniac@... longjohnmaniac
> Date: Tue Aug 29, 2006 10:42 pm (PDT)
> Although it's good that even boosted atazanavir doesn't mess with
> your lipid levels, there may be more to PI's and atherosclerosis than
> lipid levels - it's been suspected for several years that PI's promote
> atherosclerosis through another mechanism. Apparently (see second citation
> below) this also includes atazanavir (Reyataz).
> Tom in MO
>
> J. Clin. Invest. 111:317-318 (2003). doi:10.1172/JCI200317746.
> Copyright ©2003 by the American Society for Clinical Investigation
> Commentary
> HIV protease inhibitors and atherosclerosis
> David Y. Hui
> Department of Pathology, University of Cincinnati College of
> Medicine, Cincinnati, Ohio, USA
> Address correspondence to: David Y. Hui, Department of Pathology,
> University of Cincinnati College of Medicine, 231 Albert Sabin Way,
> Cincinnati, Ohio 45267-0529, USA. Phone: (513) 558-9152; Fax: (513) 558-2141;
> E-mail: huidy@...
> The advent of highly active antiretroviral therapy (HAART), including
> the use of HIV protease inhibitors (PIs) has significantly reduced the
> morbidity and mortality of AIDS in HIV infected patients.
> Unfortunately, the adverse effects of PIs, including dyslipidemia, lipodystrophy,
> insulin resistance, and premature atherosclerosis, are cause for concern
> for their use in chronic management of HIV infection (1, 2). At
> present, the relationship between HAART and premature atherosclerosis in
> HIV-infected patients is unclear. Lipid abnormalities and insulin resistance
> induced by PIs can certainly increase the risk of premature
> atherosclerosis. Chronic inflammation associated with HIV infection, particularly
> the increased level of C reactive protein (3), may also contribute to
> accelerated atherosclerosis in these patients. Whether the treatment
> regimen alone directly contributes to accelerated atherosclerosis,
> however, has not been scrutinized vigorously.
> In this issue of the JCI, Dressman et al. showed that HIV PIs
> directly promote atherosclerosis in mice (4). Importantly, the authors
> demonstrated that PIs at a dosage that did not induce hyperlipidemia are
> potent promoters of atherosclerosis, thus providing the first evidence for a
> direct effect of PIs in atherosclerosis. Although the in vivo studies
> were performed in genetically-engineered mouse models of
> atherosclerosis, their in vitro results that PIs also induced foam cell formation in a
> human macrophage cell line are of significance.
> The study by Dressman et al. (4) also suggested that PIs directly
> promote atherosclerosis by inducing CD36 gene expression in macrophages.
> This observation is consistent with the documented role of macrophage
> CD36 in atherosclerosis (5). However, the results were in direct contrast
> to another study, which reported that PIs decreased monocyte CD36
> levels in healthy volunteers and HIV-infected individuals (6). The
> discrepancy between the two studies may be due to differences in experimental
> design. Whereas Dressman et al. examined CD36 mRNA and protein expression
> in mouse macrophages and differentiated human THP-1 cells, Serghides
> and colleagues focused on CD36 expression in human monocytes and
> undifferentiated THP-1 cells. Thus, it is possible that PIs have opposite
> effects on CD36 expression in monocytes and macrophages. If this turns out
> to be the case, PI-induced down regulation of CD36 expression in
> monocytes and other cell types may be responsible for impaired glucose
> tolerance, insulin resistance, and hyperlipidemia (6), whereas their
> up-regulation of macrophage CD36 may promote foam cell formation and
> atherosclerosis (4). CD36 is a major fatty acid transporter in tissues
> with high metabolic capacity (5). Its down-regulation in tissues such as
> the heart, adipose, and skeletal muscle would impair fatty acid
> utilization and decrease insulin responsiveness in these tissues, thus
> resulting in glucose intolerance, insulin resistance, and hyperlipidemia. These
> two effects may act synergistically in promoting premature
> atherosclerosis.
> Dressman et al. (4) also found that PI-induced macrophage CD36
> expression is related to the activation of PPAR in a protein kinase C
> dependent manner. How compounds designed to inhibit protease activity
> influence protein kinase C activity and activate PPAR gene transcription
> remains unclear. However, it is now established that PIs, particularly
> ritonavir, are also inhibitors of proteasome-mediated protein degradation
> pathways (7, 8). These include their inhibition of activated SREBP
> degradation, resulting in constitutive activation of SREBP-1 and SREBP-2
> responsive genes (8). Since activated SREBPs are also promoters of PPAR
> expression (9), the PI-induced PPAR and CD36 expression may be mediated via
> PI-induced activated SREBP accumulation in the macrophage nucleus. This
> hypothesis would predict that PIs promote atherosclerosis through two
> mechanisms, both involving increased SREBP activity (Figure 1). One
> mechanism is through PI-induced metabolic complications that
> increased the risk of atherosclerosis; the other mechanism is a direct
> effect of PIs on macro-phage foam cell formation. If this hypothesis is
> proven correct, then novel compounds that inactivate SREBP activity may
> be designed and used to alleviate both metabolic and cellular
> complications that pro-mote cardiovascular events associated with HAART.
>
> ***************
> Molecular Pharmacology Fast Forward
> First published on June 23, 2005; DOI: 10.1124/mol.105.012898
>
> HIV Protease Inhibitors Activate the Unfolded Protein Response in
> Macrophages: Implication for Atherosclerosis and Cardiovascular Disease
> Huiping Zhou, William M. Pandak, Jr., Vijay Lyall, Ramesh Natarajan,
> and Phillip B. Hylemon
> Department of Microbiology & Immunology (H.Z., P.B.H.), Division of
> Gastroenterology, Department of Internal Medicine and McGuire Veterans
> Affairs Medical Center (W.M.P.), Department of Physiology (V.L.), and
> Division of Pulmonary and Critical Care Medicine, Department of Internal
> Medicine (R.N.), Virginia Commonwealth University, Richmond, Virginia
>
> Human immunodeficiency virus (HIV) protease inhibitors have been
> successfully used in highly active antiretroviral therapy for HIV-1
> infection. Treatment of patients infected with HIV with HIV protease
> inhibitors is unfortunately associated with a number of clinically significant
> metabolic abnormalities and an increased risk of premature
> atherosclerosis and myocardial infarction. However, the cellular/molecular
> mechanisms of the HIV protease inhibitor-induced lipid dysregulation and
> atherosclerosis remain elusive. Macrophages are the most prominent cell type
> present in athe rosclerotic lesions and play essential roles in both
> early lesion development and late lesion complications. In this study, we
> demonstrate that three different HIV protease inhibitors (ritonavir,
> indinavir, and atazanavir) induce endoplasmic reticulum stress and
> activate the unfolded protein response in mouse macrophages. Furthermore, at
> therapeutic concentrations (5-15 µM), these HIV protease
> inhibitors were found to increase the levels of transcriptionally
> active sterol regulatory element binding proteins, decrease endogenous
> cholesterol esterification, cause the accumulation of free cholesterol in
> intracellular membranes, deplete endoplasmic reticulum calcium stores,
> activate caspase-12, and increase apoptosis in macrophages. These
> findings provide possible cellular mechanisms by which HIV protease
> inhibitors promote atherosclerosis and cardiovascular disease in HIV-1 infected
> patients treated with HIV protease inhibitors.
> Received March 16, 2005; accepted June 23, 2005
> Address correspondence to: Dr. Phillip B. Hylemon, Department of
> Microbiology and Immunology, Virginia Commonwealth University, P.O. Box
> 980678, Richmond, VA 23298-0678. E-mail: hylemon@...
>
>
> Original message:
> Reyataz does not affect lipid metabolism - even with Norvir boost
> Posted by: "Norm Stuart" nspop2@... norm_w_stuart
> Date: Tue Aug 29, 2006 6:36 am (PDT)
>
> Impact of Boosted vs Unboosted Atazanavir-based Regimens on the Lipid
> Profiles of HIV Positive Patients
> Conclusion
> The authors concluded, "There does not appear to be a difference
> between
> atazanavir and atazanavir/ritonavir [in their effect] on total
> cholesterol and triglycerides over the first 3 months
>
>
> ---------------------------------
> Do you Yahoo!?
> Everyone is raving about the all-new Yahoo! Mail.
>

The other more effective drug for ITP was probably Rituxan, a monoclonal antibody to CD20. This attaches to "B cells" and marks them for destruction. Removing the current population of B cells often stops ITP. Rituxan is also a super treatment for B cell lymphoma. Apart from the occassional allergic reaction, Rituxan is remarkably side-effect free.

As for Carnitine. Once d4T has killed off 85% of your mitochondria, you will probably experience metabolic problems from this for the rest of your life, even though you stopped taking d4T thirty years ago. If there is re-popualtion of mitochondria, it appears to be very slow.

Carnitine is like a train of boxcars, available to bring raw materials to the mitochindria. If 85% of your Mitochondria are gone, then adding boxcars to keep the remaining mitochondrial factories well supplied will help the remaining mitochondria operate at full capacity. So taking Carnitor / Carnitine will help.

But boxcars won't protect the mitochondrial factories from bombing raids by d4T or AZT. If the factory machinery is damaged, more raw material won't help. There will already lots of raw material waiting on the shipping dock to be processed, which can't be processed because the machinery is damaged.

People taking protease inhibitors have eleated lipids due to a problem with the PPAR-alpha nuclear structures being inhibited. Since this doesn't have anything to do with Mitochondria, Carnitine won't help solve this problem - but Tricor can. 

--- In PozHealth@yahoogroups.com, "Bill Gaul" <wgaul1@...> wrote:
>
> Norm -
>
> The thrombocytopenia was determined to be ITP - an immune reaction to the Crixivan. It was sudden in onset (only caught it because I was in the second week of a Phase 1 study) and repeated on re-challenge. It's rare, but is established as a side effect now. There was an article published in the journal "Blood" on my case. The hematologist I saw after the second onset (the first was treated with Immune-globulin) said I was producing very healthy platelets, even though reduced in number, so I had no symptoms. Apparently thrombocytopenia causes lower counts - and - less healthy platelets usually. They did say they were surprised I didn't even bruise from blood draws. That 11,000 is very low and dangerous. The ER physician that did my intake looked under my watch band and said "hmm..." after he got the test results. He was expecting purple markings. I cleared the second bout with prednisone. The more effective treatment wasn't approved by Merk, and also supposedly isn't as effective with repeated use.
>
> What doesn't make sense about your statement about Carnitor is: What about new and undamaged fat cells? Wouldn't improved function help to prevent the kind of changes mitochondrial damage causes, and maybe even further DNA damage? It's certainly worth a try - and cheaper than liposuction. I don't think Zerit is the only problem med in this area. I haven't taken it for four years now, and still have a lot of metabolic repercussions. I wouldn't disagree on the facial wasting issue re: Zerit, since it usually doesn't reverse and I've had it for about five years, or more.
>
> BG
> ----- Original Message -----
> From: Norm Stuart
> To: PozHealth@yahoogroups.com
> Sent: Tuesday, August 29, 2006 4:33 PM
> Subject: [PozHealth] Re: new member / Zerit vs new meds & Sculptra
>
>
> Taking L-Carnitine can help improve the production of remaining mitochondria in people who have depleted mitochondria populations.
>
> While I have no idea what drugs you were being given for low platelet counts, I am not aware of any treatments which make the remaining platelets more effective. All treatments for thrombocytopenia I know of are designed to reduce the destruction of platelets or increase production of platelets.
>
> With a platelet count of 11,000 (compared with a more normal range of 140,000 to 250,000) it would be safe to say that these tretaments were not working well, regardless of what they were.
>
> Your lack of symptoms, such as bruising, is not unusual. Often, low platelet levels do not lead to clinical problems; rather, they are picked up on a routine full blood count. Occasionally, there may be bruising, nosebleeds and/or bleeding gums - but this is not typical in thrombocytopenia. But if you received an injury, only a blood transfusion would have saved your life.
>

As much as I would wish the fellow would participate,,, he is not a
lab rat and has free will.  We are not a fascist country (despite a
lot of what is going on lately) and coercing someone legally "for
the greater good" seems dispicable and morally wrong...

Just becuase he is mentally ill, unemployed, and on disability does
not dimish his rights!

--- In PozHealth@yahoogroups.com, PoWeRTX@... wrote:
>
> Dr Susan Diamond from Dallas is looking for an attorney who  may
want to do
> some research on legal ways to convince someone to cooperate with
researchers
> for the greater good. I would appreciate if anyone can refer me
to  any legal
> groups that could help on this case.
>
>
> ******************************
> I am a physician in private practice in Dallas, Texas and have
been taking
> care of AIDS patients for almost 20 years.
>
> Last year I came  across a patient in my practice who had
detectable HIV in
> his system and was  treated with 3 drugs including Crixivan for a
number of
> years.  He then  stopped his medications when he lost his job and
yet remained
> undetectable for  over 2 years.
>
> In collaboration with Dr. Roger Bedimo, head of Infectious
Disease at the
> VAH in Dallas his blood was sent to Dr. Richard Koup's group at
the NIH.  Dr.
> Joe Casazza, a senior investigator at the NIH analyzed the
samples and found
> that the patient had developed an immune tolerance.   Although Dr.
Casazza had
> seem this before he had never seen a patient with such  a strong
and robust
> response that was so easy to study.
>
> Unfortunately,  the patient decided that he did not want to
participate any
> further.  He  has a long history of severe mental illness and is
unemployed and
> on  disability.
>
> It is a shame he can choose not to participate further and  that
he unique
> response to HIV cannot be studied further to help elucidate the
immune system's
> reaction to control  HIV.
>
> *********************************************
>
>
>
>
> Regards,
>
> Nelson Vergel
> powerusa dot  org
>

Norm -- you consistently assume the worst and those negative assumptions
have consistently been untrue. Please try to stick with the facts and take
at face value what is presented. None of us here are liars or deceptive or
mean or among the evil in this world  -- you can take that seriously. We all
pretty much want the best for each other.

I didn't put any words in Jon's Kaiser's mouth. I repeated the assertion you
made about him (basically being an idiot) and why he had "his patients" on
D4t, and he responded that the patients in the study were not his patients.
They were derived from several different places independent of his practice.
What they were taking was not something that he controlled. I made no
comments and did not editorialize. I simply cut and pasted Jon's answer
verbatim.

It stood on its own - as does his work.

All this negativity and personal attacks on Jon (and me) -- is a red herring
- no it's a huge red ORCA - beyond being a ridiculous waste of time when we
could all be doing something else that is positive and uplifting. Like Jon
is doing!

Jon showed that a comprehensive progressive nutrient program improved immune
response --- an increase in CD4 count of 25% overall among those receiving
the intervention over a loss among placebo recipients -this was a
statistically significant finding (p=0.01) - in a quality study. That in
itself is wonderful and all of us should be grateful that he did it and that
he continues to work diligently to answer each question that comes up as he
tries to help people with what should be the simplest and most accesible of
information. That superior nutrition can measurably benefit people with HIV.

END OF STORY.

Have a great day, filled with Marianne Williamson's words and thoughts!

Michael Mooney
www.michaelmooney.net
www.medibolics.com


Re: Jon Kaiser is a true champion
Posted by: "Norm Stuart" nspop2@...   norm_w_stuart
Wed Aug 30, 2006 4:33 pm (PST)

Michael Mooney - When you put words into Jon Kaiser's mouth claiming he
said "there weren't alternatives to d4T in 2003", that's twisted. It
made Jon Kaiser sound like a barking nutcase, which didn't sound at all
like the Jon Kaiser I have met. I knew your comments had to be wildly
incorrect.


--- In PozHealth@yahoogroups.com, "Michael Mooney" <mmooney@...> wrote:
>
> To hear people on this list tear about what Jon Kaiser did first by
assuming
> that the patients in the study were his --- which they were not ---
then by
> pursuing other means of detraction that were simply conjecture and
taking
> the most negative side of a possibility and pursuing it as if it were
true,
> I am quite simply dumbfounded and tremendously disappointed.
>
> Attacking someone through his work is notorious enough, but to attack
one of
> our own fighters, someone who is going against the mainstream to
validate
> options that he has seen work in his patients the same way Joan
Priestley
> saw them work before Kaiser did is so twisted, I wonder whether it's
worth
> it to exchange in this group at all.
>
> The negativity here is pathological.
>
> To say that he is a liar, after he answered the hardest question posed
to
> him by one of the toughest interviewers is just strange. His answers
were
> quite clear and he answered each of them with answers that showed he
had
> been working out every consideration that could come up.
>
> Thank God, we have people like Jon who devote themselves to helping
people
> regardless of what the mainstream thinks.
>
> Michael Mooney
>
>
> Tue Aug 29, 2006 1:08 pm (PST)
>

d4T is more likely to sell for $50 a year, not $50 a month. The additional cost
of tenofovir puts this way out of reach for most poeple. Even the additional $50
or so a year to change form d4T to AZT is often prohibitive for people who have
neuropathy and know they are permanently damaging their nerves.

Simon

On Thursday, August 31, 2006, at 00:36AM, Norm Stuart <nspop2@...>
wrote:

>
><<Original Attached>>

I think Susan Diamond should talk with Dr Jay Levy at UCSF. She will learn that her patient, while a very small percentage is not that unique.

People who have a high percentage of T Regulatory Cells and CNAR CD8+ cells are able to control HIV without any additional therapy. If your levels of these cells are even higher, you don't even get infected with HIV. Interleukin-2 raises the level of these cells.

So very bright researchers are aware of this and publishing papers on their research. I don't think one more patient in this situation is even useful - although every researcher wants several of their very own to try things on.

I have a friend in Sweden who is a high T-Reg producer. His T4 count initially declined to 450 or so. Then over the next six years, his T4 count and percent returned to normal and his viral load became undetectable. The person he was infected by now has AIDS and is quite sick really. Labs tests show they still have the same viral types.

I'm not sure what is meant by immune tolerance. Immune tolerance is where the immune system does not respond to one or more antigens. An immune tolerance to HIV would result in a very elevated viral load. I'm sure what he has is a strong cellular non-cytolitic suppressive response - and that is T-Regs and CNAR cells.

--- In PozHealth@yahoogroups.com, PoWeRTX@... wrote:
>
> Dr Susan Diamond from Dallas is looking for an attorney who may want to do
> some research on legal ways to convince someone to cooperate with researchers
> for the greater good. I would appreciate if anyone can refer me to any legal
> groups that could help on this case.
>
>
> ******************************
> I am a physician in private practice in Dallas, Texas and have been taking
> care of AIDS patients for almost 20 years.
>
> Last year I came across a patient in my practice who had detectable HIV in
> his system and was treated with 3 drugs including Crixivan for a number of
> years. He then stopped his medications when he lost his job and yet remained
> undetectable for over 2 years.
>
> In collaboration with Dr. Roger Bedimo, head of Infectious Disease at the
> VAH in Dallas his blood was sent to Dr. Richard Koup's group at the NIH. Dr.
> Joe Casazza, a senior investigator at the NIH analyzed the samples and found
> that the patient had developed an immune tolerance. Although Dr. Casazza had
> seem this before he had never seen a patient with such a strong and robust
> response that was so easy to study.
>
> Unfortunately, the patient decided that he did not want to participate any
> further. He has a long history of severe mental illness and is unemployed and
> on disability.
>
> It is a shame he can choose not to participate further and that he unique
> response to HIV cannot be studied further to help elucidate the immune system's
> reaction to control HIV.
>
> *********************************************
>
>
>
>
> Regards,
>
> Nelson Vergel
> powerusa dot org
>

All of these drug names can be very confusing when you're not familiar with them.

The name of the drug you mention in your other post sounds like Fuzeon. This is an injectible drug which is most often used by people whose virus has become resistant to other antiviral drugs.

If your friend's virus has not become resistant to most other drugs, Fuzeon is an odd treatment to be using, simply because of the inconvenience of twice daily injections. Perhaps there is some reason he is trying to avoid using protease inhibitors like Reyataz (atazanavir). If that's true, the twice daily injections will have them seeing the benefits of a protease inhibitor like Reyataz in a new light.

Zidovudine, Retrovir and AZT are all name for the same drug.

Truvada is a combination of Viread and Emtriva. Emtriva is an newer version of Epivir which is less likely to cause the fairly unusual side-effect of Epivir which would explain your friend's symptoms - if Epivir was the cause.

If they are taking Truvada, I can think of no good reason to also take AZT.

I think AZT (Retrovir) along with d4T (Zerit) should be removed from the market as they provide minimal viral control while over the long term causing long term damage to the energy producing structures in human cells known as the Mitochondria.

--- In PozHealth@yahoogroups.com, "wantsome_24" <wantsome_24@...> wrote:
>
> I just got better info of what my friend is going to start on.
> Zidovudine, Retrovir, and Trevada. Does this sound like a good
> combination? He was on Viread, Kalatra, And Epivir. The Epivir failed
> and they gave him something else that put him in ICU with a VERY high
> fever and Very low blood pressure. Any info would greatly be accepted.
>

You need to go back again and get better information. Zidovudine and
Retrovir are the same drug (also known as AZT).



On 8/30/06 4:18 PM, "wantsome_24" <wantsome_24@...> wrote:

>   I just got better info of what my friend is going to start on.
> Zidovudine, Retrovir, and Trevada. Does this sound like a good
> combination? He was on Viread, Kalatra, And Epivir. The Epivir failed
> and they gave him something else that put him in ICU with a VERY high
> fever and Very low blood pressure. Any info would greatly be accepted.
>
>