Fish Oil Boosts Exercise Benefit, Trims Pounds

Antiretroviral Therapy Is Associated with Increased Cholesterol and Apolipoprotein Levels in HIV Positive Women

Dyslipidemia, or elevated blood fat levels, is a common problem in people with HIV, especially those taking combination antiretroviral therapy. However, there is less data on blood lipid abnormalities in women, since most studies have included a majority of men.

Researchers conducted a cross-sectional study to assess the prevalence of abnormal plasma lipid and lipoprotein levels, as well as other biomarkers for cardiovascular disease. The study included 184 HIV positive women seen at two HIV clinics in Atlanta during 2002.

Results

Most of the women (89%) were African American, with median age of 41 years (range 21-72).

6% of the women were diabetic, 44% smoked cigarettes, and 67% were overweight -- all known to be cardiovascular risk factors.

41% of the women were taking protease inhibitors (PIs) for at least three months, 20% were taking non-nucleoside reverse transcriptase inhibitors (NNRTIs), and 38% had not been on antiretroviral therapy for the past three months.

Women being treated with PI- or NNRTI-based regimens had higher total cholesterol and triglyceride levels than patients not on antiretroviral therapy (P < 0.05 for each).

Women treated with either PIs or NNRTIs had significantly higher apolipoprotein B and apolipoprotein C-III levels than patients not taking therapy (P < 0.01 for each).

Conclusion

"In this cross-sectional study of HIV-infected women, either PI or NNRTI therapy elevated levels of total cholesterol and specific apolipoproteins," the researchers concluded. "These findings, on a background of an older population with additional risk factors of smoking, obesity, and diabetes, may lead to future atherosclerotic events in these patients."

08/01/06

Reference
D Rimland, J L Guest, I Hernandez-Ramos, and others. Antiretroviral Therapy in HIV-Positive Women is Associated With Increased Apolipoproteins and Total Cholesterol. Journal of Acquired Immune Deficiency Syndromes 42(3): 307-313. July 2006.

#17889

From: PoWeRTX@...
Date: Mon Jul 31, 2006 10:24 pm
Subject: Enfuvirtide in HIV-1-infected individuals changing therapy to a nucleoside rever

nelsonvergel

Offline

Antivir Ther. 2006;11(4):409-19.

Related Articles, Links

Enfuvirtide in HIV-1-infected individuals changing therapy to a nucleoside reverse transcriptase inhibitor sparing regimen: the ALLIANCE Study.

Dwyer DE, Workman C, Hales G, Amin J, Cooper D, Miller J; Alliance Study Group.

Centre for Infectious Diseases and Microbiology Laboratory Services, Institute of Clinical Pathology and Medical Research, Westmead Hospital, Westmead, Australia. dominic_dwyer@...

The role of the fusion inhibitor enfuvirtide in nucleoside reverse transcriptase inhibitor (NRTI)-sparing regimens was assessed in an open-label study of fifty-nine highly antiretroviral drug exposed HIV-1-infected individuals. There was a reduction in plasma HIV-1 RNA of 1.43 (95% confidence interval [Cl]: -2.06, -1.22) log10 copies/ml plasma over 96 weeks, and 44% (95% CI: 31, 58) of individuals had a viral load less than 400 copies/ml. A viral load below detection at 96 weeks was predicted by a baseline genotypic sensitivity score greater than 1. There was an average increase of 67 cells/microl (95% Cl: 15, 120) from baseline CD4+ T-cell count to week 96, and the percentage of patients with CD4+ T-cell counts above 100 and 200 cells/microl increased over the trial. Injection site reactions (ISRs) were less common in people with CD4+ T-cell counts >250 cells/microl at any time during follow-up, and were more severe in patients with lower baseline peripheral fat. Adherence over 48 weeks to enfuvirtide injections ranged from 96.3-99.5%. During the 96 week trial there were two discontinuations due to ISRs and two discontinuations following hypersensitivity reactions. Over the 96 weeks of study lean body mass increased by an average 2.7 kg (95% Cl; 1.7, 3.6 kg). Mean peripheral fat increased by 0.2 kg (95% Cl; -0.2, 0.6 kg). Baseline NRTI-associated toxicities resolved in 17% of participants during follow-up. Enfuvirtide is an important component of antiretroviral therapy in highly treatment-experienced individuals where NRTI sparing may be desirable.

Regards,

Nelson Vergel
powerusa dot org

#17888

From: Nelson Vergel <nelsonvergel@...>
Date: Tue Aug 1, 2006 2:44 am
Subject: Merck Integrase + Prezista

nelsonvergel

Offline

I am very excited about the integrase family of drugs. I started the Merck BENCHMRK study two months ago with Prezista (plus Viread and Combivir as backbone, but I had resistance to all nukes). I am assuming I am not getting the placebo.

My viral load is undetectable for the first time in 23 years (baseline was 69,000.)

My Cd4 cells have gone up from 180 to 414 cells/ml

I certainly think there is hope.

TMC 125, a non nuke that does not excite me much for salvage, should be available in expanded access in a few weeks. The Merck integrase inhibitor may be available in expanded access in a few months also. Also, Maraviroc, Pfizer's CCR5 entry inhibitor, may be available in expanded access late this year.

The Gilead integrase and TANOX's TNX 355 IV drug should come out in phase III studies also by the end of the year.

So Jeff..hang in there....there is hope coming!

Regards,

Nelson Vergel
powerusa dot org

----- Original Message ----
From: Kelly Scott <kscott@...>
To: Jeffrey Young <jyoung681@...>; pozhealth@yahoogroups.com
Sent: Monday, July 31, 2006 12:08:00 AM
Subject: RE: [PozHealth] Update 1 - On The Road To Wellness & Restoration

Uh, you may want to be damn careful about adding that integrase inhibitor. Just adding one efficacious new drug is like being on a single drug regime: and you’re liable then to ‘waste’ the new drug, quickly breeding resistance.

I’m resistant to most nukes, non-nukes and protease myself, though my counts are going south yet, nor my clinical condition. So I’m waiting for an integrase, a receptor inhibitor (both new classes) AND maybe then adding T20 or a newer one of that type. I ended up being resistant by adding drugs serially through the early 90s,: don’t want to do that again.

As for Houston …. hoo boy. They thought it out: they HAVE no zoning, quite deliberately they are stuck with ‘spot zoning’ which is batshit crazy for communities..

Kelly Scott

Seattle

From: PozHealth@yahoogroups.com [mailto:PozHealth@yahoogroups.com] On Behalf Of Jeffrey Young
Sent: Sunday, July 30, 2006 6:23 PM
To: pozhealth@yahoogroups.com
Subject: [PozHealth] Update 1 - On The Road To Wellness & Restoration

I want to catch everyone up to the current events here in Houston . The main issue was the lab results of my first 30 days on the new drugs. Sadly, my labs were unchanged. These results were a bit of a shock because most patients that go on a new drug regimen experience a boost in CD4 T-cells and a drop in viral load. They at least experience a drop in viral load. My labs indicate that neither of these two factors occurred. Dr. Schrader has two theories. First, it is just taking more time for my new meds to kick in and kick ass. Due to the fact that I have an extremely high viral load, this could be what is slowing the new drugs down. Dr. Schrader is very optimistic that the next blood draw will be better. The other theory is that my two new drugs are from two classes of HIV drugs to which I am already resistant. I mean that my virus is already resistant to all the other drugs in that same class of HIV drug so I may already be resistant to the new drugs. That would really suck. Not to worry, there is a Plan B already in the works. A new drug from a new class called “Integrase Inhibitors” is just months away from the FDA’s Expanded Access Program. When approved, I will be able to add this drug into my cocktail and from all the talk about this new drug; it has great potential for multi-resistant drug patients. My next blood draw is Monday – July 31, 2006. I should get the results a week later. These results will give us a better idea about what is happening and what is not happening inside my body. I am very optimistic about the results because I have had more energy lately and I’ve been working out in the small gym within the condo complex where we currently reside. My appetite is very good and I am certain that I have added a few more pounds to my frame. One positive result in the last three months has been a slow but steady weight gain. I look forward to breaking the 160 pound barrier that has been the roadrunner to my Wylie Coyote for so long. The damn bird has slipped out of my grasp for far too long. Using the “ACME Workout Routine”, I hope to tip the scale during my next weigh in on Monday.

I’ve had sometime to explore Houston . Here are a few things that I have discovered that interest me.

1. James Coney Island – They make chili cheese dogs that are close to the World Famous Skyline Coney from Cincinnati that I love so much.

Happy Tails Dog Spa – I had Lucky and Nellie groomed there and it is quite the experience. I hope to take advantage of the doggie day care once a month so the puppies can interact with other dogs. Plus, they have web cams so you can go online a watch your dogs play.

3. Ziggy’s Healthy Grill – They serve Buffalo burgers and Ostrich burgers.

4. Sarpino’s Pizza – Good Pizza and I get AAdvantage Dining Miles!

Houston’s communities are not well thought out like in Dallas . There do not appear to be any zoning laws so you find residential mixed right in with commercial establishments. There is not a Cedar Springs where all the gay owned and operated bars, restaurants, & retail are conveniently located next to each other. The treasures are a harder to discover but they are definitely worth finding. I hope to try a restaurant called “Barnaby’s Café” soon. The exterior of the restaurant says “run down shack” but the people say that the food and ambiance inside is fantastic. I look forward to this culinary adventure.

Jeff Young

#17887

From: JuLev@...
Date: Mon Jul 31, 2006 2:30 pm
Subject: NATAP: Lymphoma & HIV

jules72orange

Offline

HIV-related Lymphoma Survival IncreasingRESULTS: There were no statistically significant differences in terms of either lymphoma or HIV-related characteristics in the two time periods. ...
www.natap.org/2005/HIV/122805_01.htm

Incidence of Non-AIDS defining Malignancies in the HIV Outpatient ...--Non-Hodgkin's Lymphoma (NHL) --cervical cancer And to describe incidence rates of non-AIDS defining malignancies in HIV-infected persons. ...
www.natap.org/2004/CROI/croi_25.htm

#17886

From: "Norm Stuart" <nspop2@...>
Date: Mon Jul 31, 2006 10:38 pm
Subject: Blue Cross of California Mail Order Meds scheme quashed

norm_w_stuart

Offline

BLUE CROSS OF CALIFORNIA FORCED TO BACK DOWN ON AIDS MEDS

Activists Demand Public Correction

Last week Blue Cross of California began notifying its members they would no longer be permitted to receive HIV medications from local retail pharmacies but instead were required to utilize an out of state mail order pharmacy. The notification dated July 18 indicated the new requirement was being retroactively implemented effective June 15.

"This would have done enormous harm to people living with HIV/AIDS in California," said Terry Leftgoff, an HIV/AIDS community activist who lives in West Hollywood. "In addition to violating state noticing requirements, this new requirement would have threatened to disrupt treatment regimens and make many AIDS drugs unobtainable by violating the state ADAP program that requires the use of an in-state pharmacy."

In the face of mounting criticism from AIDS activists, government regulators and independent pharmacies throughout California, Blue Cross did a quick reversal today, indicating the notices were sent 'in error' and that HIV/AIDS medications listed on the state ADAP formulary would be exempted from such requirements.

Late last week local pharmacies began reporting that Blue Cross had begun rejecting ordinary refill requests raising the possibility that life saving treatments might be interrupted. "We worked together to educate Blue Cross and are pleased the giant insurer came to understand how such an onerous requirement would endanger their members with HIV/AIDS," said Leftgoff. "We call on Blue Cross to send out correction notices that fully explain the promised exemption to everyone who received the original notices to ensure no treatment is needlessly interrupted."

Those in the HIV/AIDS community became particularly concerned since such a drastic mandated change at the large insurer would sever a crucial part of the local medical support team upon which those living with HIV/AIDS depend to remain compliant with multiple complicated prescriptions. "It is crucial that patients be allowed to utilize a pharmacist they trust to watch for contraindications and side effects," said Leftgoff . "Forcing people to use a faceless pharmacy located 2,000 miles away in Ohio is utterly foolhardy."

In separate but related news the parent of Blue Cross of California, Wellpoint Inc., the nation's largest health insurer, reported last week that second quarter profit grew 34% to $751.2 million and revenue grew 27% to $14.2 billion.

#17885

From: "Joe Fiore" <joe_d_o@...>
Date: Mon Jul 31, 2006 5:56 pm
Subject: hi blood pressure

joe_d_o2000

Offline

Hi everyone,

My doc says i've been "borderline" high blood pressure (130/85) and he thinks its the testosterone/deca shots. I do one shot of 100 testo and 100 deca every two weeks. I have been doing androgel in the second week, but not all the time. Is this a common side effect of the shots? SHould i take a break and come back or stop it. I've gotten a lot of benefit. ANy feedback? Please respond privately to joe_d_o@...

Thanks,

Joe

#17884

From: JuLev@...
Date: Mon Jul 31, 2006 2:18 pm
Subject: Re: Re: NATAP: lymphoma & HIV

jules72orange

Offline

I'm not very familiar with these cancers.

In a message dated 7/31/06 2:15:08 PM, nspop2@... writes:

Jules, It surprises me that Hodgkin's lymphoma is so prevalent among HIV+ smokers. Very interesting.
In the general (HIV negative) population, there does not appears to be any link between Hodgkin disease and lifestyle factors such as smoking, diet, exercise, use of alcohol.
*** My summary of your HOPs report ***
Studies have shown a decline in AIDS-defining malignancies since the advent of highly active antiretroviral therapy.
-- Kaposi's sarcoma (KS)
-- Non-Hodgkin's Lymphoma (NHL)
-- cervical cancer
However, the incidence of five non-AIDS defining malignancies are significantly higher in HIV-infected persons than in the general population. The incidence of these five non-AIDS defining malignancies occur disproportionately among HIV+ smokers.
The five non-AIDS defining malignancies more prevalent among those with HIV, and the percentage of these HIV+ persons who were smokers:
-- lung: 100% were smokers
-- head/neck: 92%
-- Hodgkin's: 87%
-- anorectal: 79%
-- melanoma: 85%
Smokers were defined as current or former smokers who had quit within the past 10 years or the 10 years prior to cancer diagnosis.
--- In PozHealth@yahoogroups.com, JuLev@... wrote:
>
> Here is a link to study reported at CROI 2004.
>
> Incidence of Non-AIDS defining Malignancies in the HIV Outpatient ...However,
> the incidence of non-AIDS defining cancers among HIV-infected individuals
> seem to be increasing. We determined the incidence of 5 cancers among HIV ...
> www.natap.org/2004/CROI/croi_25.htm
>

#17883

From: "g7_hope" <g7_hope@...>
Date: Tue Aug 1, 2006 1:26 am
Subject: HIV Meds and the "Grapefuit Effect"

g7_hope

Offline

Hi all,

I tested Poz in 1986.  I did get very sick there for about a two year
period.  My T-cell count went all the way down to the 40's.  I also
developed Ulcerative Colitis, which eventually ended with me having
Pull Through Surgery.  I am fine now as far as that is concerned.
Once my doctor put me on the Three Drug Therapy ( 3-TC ? ) I improved
very well.  My health has been great ever since, though I have
developed some drug resistance and had to switch drugs a few times.
My fault, due to inconsistancy in taking my drugs.  Also my previous
drug put my cholesterol at a very high level.

I currently have been on Reyataz and Truvada for the last two months
and have not seen any side effects.  Since then my cholesterol has
become better.

I am planning to improve my nutrition and I want to start by doing a
body detox.  I have purchased a product called GSE which is a
grapefruit seed extract to take internally as part of the detox.  Then
I found out about the study on drugs and grapefruit juice.  Does
anyone know anything about the "Grapefruit Effect" in regards to the
HIV meds, specifically the two I am taking???? For those of you who
are unaware of this effect note the following:


What about the "grapefruit juice effect"? - There is a phenomenon
known as the "grapefruit juice effect". Two components found in
grapefruit juice, naringin and naringenin**, inhibit production of an
enzyme in the intestinal tract, thus increasing the rate of absorption
for certain classes of drugs (including some antihistamines, birth
control pills, anti-epilepsy medications and some antibiotics.)


Also, on the studies in regards to the fish oil.  Is there a set daily
amount reccommended??  I didn't see any amounts in the study reports.

Thanks,

Tom

#17882

From: JuLev@...
Date: Mon Jul 31, 2006 2:19 pm
Subject: NATAP: Non-Hodgkin Lymphoma & HIV

jules72orange

Offline

Systemic non-Hodgkin lymphoma in individuals with known dates of HIV seroconversion: incidence and predictors

AIDS: Volume 18(4) 5 March 2004 pp 673-681

Abstract
Objectives: To investigate temporal changes in the risk of non-Hodgkin lymphoma (NHL) and estimate NHL incidence in risk groups and the prognostic role of these risks and current, nadir and time-weighted average CD4 cell count.

Methods: Secular trends in time from HIV seroconversion to an NHL diagnosis was estimated using Cox models from data pooled from the 22 seroconverter cohorts in the CASCADE collaboration for three periods (pre-1997, 1997-1998, 1999-2002), adjusting for age at seroconversion, exposure category and sex.

Results: Of 7103 seroconverters, 129 developed NHL. Compared with pre-1997, there was little reduction in NHL risk in 1997-1998 [relative risk (RR), 0.66; 95% confidence interval (CI), 0.37-1.17] then a substantial reduction in 1999-2002 (RR, 0.25, 95% CI, 0.12-0.53). Compared with individuals with CD4 cell count > 350 × 106 cells/l, the RR of NHL increased to 1.9 (95% CI, 1.0-3.6), 1.4 (95% CI, 0.6-3.5) and 11.2 (95% CI, 6.3-20.0) at CD4 cell counts 200-349, 100-199 and < 100 × 106 cells/l, respectively. There was no evidence that nadir (P = 0.41) or time-weighted average CD4 cell count (P = 0.38) contributed further to predicting NHL risk or were better predictors than current CD4 cell count. For individuals with CD4 cell count > 350 × 106 cells/l pre-HAART, an NHL incidence of 1.8 and 0.4/1000 person-years was estimated for those at highest and lowest risk, respectively, when classified by age and exposure category.

Conclusion: There appears to be no justification for initiating HAART at CD4 cell counts > 100 × 106 cells/l based specifically on concerns over NHL. The risk of NHL is, however, greatly increased at lower CD4 cell counts.

Introduction
Reliable information on the incidence and predictors of non-Hodgkin lymphoma (NHL) and other AIDS-related infections and tumours in HIV-infected individuals is important in informing decisions on whether to initiate anti-HIV therapy.

Immune suppression has long been established as an important risk factor for NHL as its incidence in organ recipients treated with immunosuppressive drugs is estimated to be 10-50 times that of the general population [1-3]. It has been reported that the risk is higher still in HIV-infected individuals, at 50-200 times that of the general population [4,5]. A number of factors are likely to determine the risk of developing NHL in an HIV-infected person, particularly the extent of immune suppression, as measured by CD4 cell counts, and incidence rates are, therefore, unlikely to be uniform across the infected population. It has also been reported that the risk of NHL is strongly influenced by the CD4 cell count nadir [6], suggesting that, regardless of current CD4 cell count level and therapeutic management, a person's risk of NHL may have already been determined by previous HIV history including exposure to suboptimal anti-HIV therapy.

Although the risk of the majority of AIDS-defining diseases has fallen substantially, in most studies the incidence of NHL did not appear to drop as dramatically as other diseases following the introduction of highly active antiretroviral therapy (HAART) [7,8]. While it has been proposed that HAART should be initiated earlier in individuals at higher risk of NHL, benefit would only be obtained from this approach if HAART has a strong effect in delaying the onset of NHL.

The present study assesses the changes in the risk of NHL over time from 1987 to 2002 in order to estimate the risks before and after the introduction of HAART. The role of sex, age at seroconversion and exposure category as predictors of this risk are also examined. Aspects of immune suppression thought to lead to a higher risk of NHL are explored, including the role of current, nadir and time-weighted average CD4 cell count since HIV seroconversion. The nadir and time-weighted average CD4 cell count may be important predictors if prior immune system damage increases the risk of NHL even after subsequent improvement. Finally, absolute incidence rates are estimated based on the important factors identified in the analyses in order to compare these with those in the general population.

Methods
Data from the 22 cohorts from Europe, Australia, and Canada in CASCADE pooled in July 2002 were analysed. Details of the CASCADE Collaboration appear elsewhere [9]; briefly, all the cohorts consist of HIV-1-infected individuals for whom the date of seroconversion can be reliably estimated, the most common method (84%) being the mid-point between the first positive and last negative antibody test dates with a maximum of 3 years between test dates (90% having an interval of < 2 years). Individuals under 16 years of age at seroconversion were excluded because both the progression and the treatment of HIV disease differ in children from that in adults. Systemic NHL was considered and Burkitt's, immunoblastic, or equivalent were not distinguished, but primary cerebral lymphoma was excluded as it may be difficult to distinguish from cerebral infections.

Cox models [10] stratified by cohort were used to analyse the time from estimated HIV seroconversion to a diagnosis of NHL, allowing for late entry [11] of individuals at the time of enrolment into the original cohort. Individuals were still considered at risk of NHL even if they had one or more other AIDS events diagnosed first. Such individuals were censored at the date of their last clinical assessment. Individuals with no recorded AIDS diagnoses were censored incorporating a reporting lag to either the appropriate national AIDS registry or the clinical database [12]. Calendar period was grouped as pre-1997 (before HAART became widely available), 1997-1998 (the period marking the initial introduction of HAART), or 1999-2002 (when over 50% of person-time at risk was spent on HAART in our cohorts); it was fitted as a time-dependent covariate in order to investigate temporal changes in the risk of NHL. Various measures of immunodeficiency mediated through CD4 cell counts were investigated as predictors of the risk of NHL. Initially, fractional polynomial models [13] were fitted to explore the relationship between CD4 cell count predictors and risk of NHL and to suggest appropriate CD4 cell count categories for subsequent models.

In addition to current CD4 cell count, both the nadir CD4 cell count and a time-weighted average CD4 cell count since seroconversion were considered as time-dependent predictors of NHL risk. The nadir CD4 cell count may be important if having a low CD4 cell count, even for a brief period, causes a long-term increase in the risk of NHL despite potential subsequent immune system improvement. The time-weighted average CD4 cell count takes into account all previous CD4 cell counts and the time spent at each level, thus providing a summary measure of the cumulative immunodeficiency as measured by the CD4 cell count profile prior to a given point in time. Finally, the proportion of time an individual had spent at CD4 cell counts < 100 × 106 cells/l was examined as a predictor of NHL risk. Non-nested models were compared using the Akaike's information criterion. All models were adjusted for sex, exposure category and age at seroconversion, and the prognostic importance of these factors was assessed using Wald tests. A model using a fractional polynomial for age at seroconversion showed that a non-linear age effect with a lower risk only at lower age was a better fit than linearity, as expected [4]. Considering age groups based on quartiles, there was no evidence that the risk differed between the upper three groups, and so two age groups (< 25 and ≥ 25 years) were used subsequently. The most important cofactors were used in a Poisson regression to estimate absolute incidence rates of NHL among different subgroups.

The data were left-censored on 1 June 1987 to exclude a period in which CD4 cell counts may not have been comparable because of a lack of standardization. CD4 cell counts were considered to be current in our analyses for up to 6 months or until the next count, whichever came first. If another CD4 cell count was not available within 6 months, the individual would leave the risk set until the time of the next available CD4 cell count. As individuals regularly attending clinic will, therefore, contribute proportionately more time at risk, a sensitivity analysis with no CD4 cell count expiry was used to confirm the results.

Results

Of 7591 seroconverters aged 16 years or more at seroconversion, 109 were excluded because their exposure category was not known. A further 379 were excluded as they had no CD4 cell count data available, leaving 7103 individuals, among whom 129 developed NHL. However, 36 were diagnosed without a CD4 cell count available within the last 6 months [median time from diagnosis to last prior CD4 cell count 15 months (range, 6-89); Table 1]. In order to assess the effect of CD4 cell count parameters, these events were not included subsequently, although the individuals were included up until 6 months after their last CD4 cell count prior to NHL.

Overall, the proportion of person-time spent with CD4 cell count < 100 × 106 cells/l decreased from 10% pre-1997 to 5% and 3% in 1997-1998 and 1999-2002, respectively. Correspondingly, the proportion of person-time spent with CD4 cell count > 350 × 106 cells/l increased from 57% to 61% and 66%, respectively. Of the 93 subjects with NHL with a CD4 cell count measurement within the prior 6 months, 45 (48%) were diagnosed with their last CD4 cell count at < 100 × 106 cells/l, while seven (8%), 19 (20%), and 22 (24%) were diagnosed at CD4 cell counts of 100-149, 200-349 and ≥ 350 × 106 cells/l, respectively. Of the 22 individuals with NHL diagnosed when their last CD4 cell count was ≥ 350 × 106 cells/l, 18 had never had a CD4 cell count of < 200 × 106 cells/l recorded. Of the individuals with NHL, 70 (75%) subsequently died, 38 of whom had CD4 cell counts of < 100 × 106 cells/l at the time of NHL diagnosis (median of 12 weeks from NHL diagnosis to death for those with diagnosis at CD4 cell count < 100 × 106 cells/l and a median 19 weeks for those with CD4 cell count > 100 × 106 cells/l (Kaplan-Meier).

Overall, compared with pre-1997, the relative risk (RR) of a NHL diagnosis was 0.66 [95% confidence interval (CI), 0.37-1.17] in 1997-1998 and 0.25 (95% CI, 0.12-0.53) in 1999-2002. After adjusting for calendar period, the risk of NHL was elevated at CD4 cell counts 100-350 × 106 cells/l compared with > 350 × 106 cells/l, but there was a very marked increase in risk at CD4 cell counts < 100 × 106 cells/l (Fig. 1). Similar results were obtained for the non-linear effects of nadir and time-weighted average CD4 cell counts. Therefore, in subsequent models, these CD4 cell count measures were categorized into 0-99, 100-199, 200-349 and > 350 × 106 cells/l.

Comparison of models based on four different CD4 cell count measures (Table 2) showed that the current CD4 cell count was a better predictor of the risk of NHL than the nadir CD4 cell count, the time-weighted average CD4 cell count or the proportion of time spent at CD4 cell count < 100 × 106 cells/l. Nevertheless, all four measures were extremely strong predictors of the risk of NHL. For example, compared with individuals with current CD4 cell counts of > 350 × 106 cells/l, the RR of NHL was 1.93 (95% CI, 1.03-3.63), 1.44 (95% CI, 0.60-3.48), and 11.18 (95% CI, 6.26-19.98) for those with CD4 cell counts of 200-349, 100-199 and < 100 × 106 cells/l, respectively. There was no evidence that the nadir CD4 cell count, the time-weighted average CD4 cell count or the proportion of time with CD4 cell counts < 100 × 106 cells/l provided important additional information after adjusting for the current CD4 cell count (P = 0.41, 0.38, 0.66, respectively). In each case, there was no trend in risk and all RR values were small compared with the effect of current CD4 cell count (Table 3). Similarly, after adjusting for current CD4 cell count, individuals whose nadir CD4 cell count was more than 200 × 106 cells/l lower than their current CD4 cell count had a similar risk of NHL to those whose CD4 cell count had never been more than 100 × 106 cells/l lower than their current count (RR, 1.33; 95% CI, 0.57-3.06; P = 0.80) and this effect did not appear to vary between the three calendar periods considered (interaction P = 0.56). There was also no evidence to suggest that the effect of current CD4 cell count varied according to the nadir CD4 cell count group (interaction P = 0.89), or even according to whether or not the nadir was < 100 × 106 cells/l (interaction P = 0.71).

Similar effects of demographic factors were observed across all CD4 cell count models (Table 2). In the best fitting model (current CD4 cell count only), there was evidence that exposure category was predictive of the risk of NHL (P = 0.02). Those in the 'other' exposure category, the majority of whom were haemophiliacs, appeared to be at higher risk than gay men (RR, 3.47; 95% CI, 1.27-9.51), although the number of patients in this category was small and hence the CI values are wide. Those infected through sex between men and women or injecting drug use appeared to be at lower risk of NHL compared with gay men (combined RR, 0.66; 95% CI, 0.33-1.32; P = 0.23). Individuals aged < 25 years at seroconversion appeared to be at a slightly lower risk of NHL compared with those aged ≥ 25 years (RR, 0.63; 95% CI, 0.37-1.08; P = 0.09), as did women compared with men (RR, 0.55; 95% CI, 0.24-1.29; P = 0.17). Although these effects were not significant at conventional levels, relatively few NHL diagnoses meant the power of the statistical tests to detect differences was low.

If some subgroups of HIV-infected individuals had substantially higher rates of NHL at higher CD4 cell counts, this could provide a rationale for earlier initiation of HAART in these subgroups. In order to examine this, an analysis of population effectiveness [14] was used to assess the effect of HAART on the incidence of NHL in low- and high-risk individuals, by considering the calendar period up to 1996, when HAART was not available, and 1999-2002, when 51% person-time in CASCADE was spent on HAART. Individuals exposed through 'other' routes were excluded from estimation of incidence rates as numbers were small and people are now rarely exposed to HIV through these routes in our cohorts. As expected, the estimated absolute incidence rates of NHL in both the pre-1997 and the 1999-2002 periods were higher in the highest risk group emerging from the previous analysis (i.e., those aged ≥ 25 years at seroconversion and infected through sex between men) compared with those aged < 25 years and infected through injecting drug use or sex between men and women. However, even in the highest risk group, there appeared to be little gradient in the incidence of NHL by CD4 cell count category at intermediate CD4 cell counts > 100 × 106 cells/l (Table 4).

Discussion

The risk of NHL has fallen since the introduction of HAART, albeit not as immediately as the decrease observed in other AIDS-defining conditions. Compared with pre-1997, the relative risk of NHL in 1997-1998 was 0.66 (95% CI, 0.37-1.17), similar to the estimate from the Swiss cohort study [15] of 0.61 (95% CI, 0.30-1.29). However, we estimated that in 1999-2002, the risk of NHL occurring as either the first AIDS-defining event or subsequently had fallen significantly to 0.25 times that of pre-1997 (95% CI, 0.12-0.53).

A number of reasons may account for such a delay. First, it may be that the incubation of Epstein-Barr virus, reported to be associated with NHL, is relatively long and more time is needed to observe the impact of therapy. Even excluding the possible effects of a viral cofactor, the development of NHL may occur over a longer period of time than some opportunistic infections, and some people diagnosed in 1997-1998 may, therefore, have actually developed NHL pre-1997 (i.e. pretherapy). Second, it may be that a slow improvement in immune function still leaves people at a relatively high risk of developing NHL for a period after starting HAART. The fact that we found current CD4 cell count to be, by far, the strongest predictor of immediate NHL risk, and that risks were only substantially increased at very low CD4 cell counts suggests that this is unlikely to account for the delay in risk reduction. Third, it may be that anti-HIV therapies available more recently are more effective against NHL. Clearly a large amount of the effect of HAART on NHL risk, as captured by the effect of calendar period at risk in our model, is mediated through the effects of HAART on the CD4 cell count. However, even after adjusting for current CD4 cell count, calendar year at risk remains a marginal predictor of NHL diagnosis, suggesting that HAART is having other beneficial effects not strongly mediated through CD4 cell counts.

The incidence of NHL, as expected, varies significantly with CD4 cell count. However, in contrast to a previous finding from a prevalent cohort [6], after adjusting for the duration of HIV infection, the nadir CD4 cell count is not as important a predictor as the current CD4 cell count. In a prevalent cohort, there may be confounding between duration of HIV infection and nadir CD4 cell count, as the longer a person is infected the lower will be their nadir count. As the risk of all AIDS-defining events increases with duration of HIV infection, this may explain why nadir CD4 cell count was found to be a stronger predictor of NHL than is current CD4 cell count in this prevalent cohort. Alternatively, the relatively low power of our study, because of the small number of individuals developing NHL, may have masked a genuine effect of nadir CD4 cell count in addition to CD4 cell count. However, the risk estimates showed little variation in the risk of NHL according to nadir CD4 cell count, in contrast to a large variation in risk according to the current CD4 cell count.

CD4 cell count history is likely to be poorly estimated in prevalent cohorts compared with seroincident cohorts, where patients are generally under follow-up well before their cell count falls to lower levels. Similarly, prevalent cohorts are likely to suffer from overascertainment of NHL diagnoses at high CD4 cell counts, because of illness prompting individuals to present to clinical care who may not otherwise have had regular follow-up. This may also partly explain increasing median CD4 cell count at NHL diagnosis over time, reported in several studies [6,16,17].

The risk of NHL appears to be higher in haemophiliacs, in men and in older individuals, in agreement with previous findings [4], implicating viral cofactors in the development of lymphomas [18]. The lower risk in injecting drug users also appears to be in line with a recent finding from an American study [19] suggesting that the use of illicit drugs may suppress B cells, the overexpression of which leads to the development of lymphomas.

We estimate that NHL incidence in HIV-infected individuals varies between 0.3 and 3.4 events per 1000 person-years at CD4 cell count ≥ 100 × 106 cells/l. This is in agreement with findings from other cohorts of 3 [16] and 3-7 [6] events per 1000 person-years. Given that the incidence of NHL in the general population is estimated to be 0.2 per 1000 person-years [20], it would appear that previous estimates of a 50-200-fold increase in risk for infected individuals are high and correspond more to the risk for those with severe immunosuppression (< 100 × 106 cells/l). This may be because such studies typically link AIDS and tumour registries and derived incidence rates are, therefore, related to the risk of NHL around the time of AIDS diagnosis.

In assessing the role of CD4 cell count, seroconverter studies are essential to control adequately for the entire history of immune suppression in an HIV-infected person. As a number of HIV-infected individuals present for clinical care at relatively late stages of HIV infection, it is reassuring that, regardless of duration of relatively severe immune suppression, those who respond to HAART and increase their CD4 cell count do not appear to remain at higher risk of NHL. For those individuals presenting earlier in their disease course, there appears to be no CD4 cell count level > 100 × 106 cells/l at which initiation of HAART based specifically on concerns over NHL would be justified. The risk of NHL is, however, greatly increased at CD4 cell count < 100 × 106 cells/l.

Sponsorship: CASCADE is funded through a grant from the European Union (QLK2-2000-01431) and has received additional funding from GlaxoSmithKline.

#17881

From: JuLev@...
Date: Mon Jul 31, 2006 1:14 pm
Subject: NATAP: non-Hodgkin lymphoma & HIV

jules72orange

Offline

#17880

From: PoWeRTX@...
Date: Mon Jul 31, 2006 1:01 pm
Subject: Stress From Exercise Does Not Threaten The Heart, Hopkins Study Shows

nelsonvergel

Offline

Stress From Exercise Does Not Threaten The Heart, Hopkins Study Shows

30 Jul 2006

A Johns Hopkins study should ease the concerns held by many older adults with mild high blood pressure about the strain or harm exercise could cause their hearts. Results of the research on 104 men and women age 55 to 75 showed that a moderate program of physical exertion had no ill effects on the heart's ability to pump blood nor does it produce a harmful increase in heart size.

In this study, "moderate" translated to sustained exercise for about an hour, three times a week. Researchers say that people's concerns stem from the fact that during each workout, blood pressure can on average rise from 40 millimeters to 60 millimeters of mercury. The Hopkins study is believed to be the first to evaluate the effects of exercise on the heart's ability to function, to pump and to fill up with blood.

"While having high blood pressure at rest is a well-established risk factor for heart problems, older people should not fear the effects of moderate exercise on the heart, despite short-term bump-ups in blood pressure during their workout," says lead study investigator and exercise physiologist Kerry Stewart, Ed.D., a professor of medicine and director of clinical and research exercise physiology at The Johns Hopkins University School of Medicine and its Heart Institute. "Exercise is a highly effective means of increasing the heart's efficiency and reducing body fat, factors that may ward off future health problems, such as heart disease and diabetes."

A report on the Hopkins study, published in the July issue of the journal Heart, showed that after six months of aerobic exercise on a treadmill, bicycle or stepper, plus weightlifting, participants showed no overall ill effects in 11 measures of diastolic heart function, when the organ's main chamber fills with blood between beats. They also found that exercise produced no increase in eight measures of heart size, including left ventricular mass and wall thickness. In contrast, a long-term effect of hypertension, even when the body is relaxed, is hypertrophy, an enlargement of the heart that eventually stiffens and weakens the muscle.

Not only were there no ill effects sustained, despite periodic increases in blood pressure during the workout, Stewart and his team reported, but results also suggest that the exercise producing these effects benefited the hearts of those who made the most gains in physical fitness and for those who lost the most abdominal fat.

Researchers found, for example, that each single point gain in aerobic fitness (of 1 milliliter per kilogram per minute), as measured by peak oxygen uptake by the blood during exercise, translated to a 1.5 percent improvement in one key measure (the E/A ratio), used to measure diastolic heart function. In addition, every 10-point decrease in abdominal fat (of 1 square centimeter) translated to a 1.2 percent gain in a second key measure (the Em/Am ratio).

And, researchers say, unlike the increased heart size that results from high blood pressure, any increase in heart size observed in the active group was similar to what athletes experience when their hearts get bigger and stronger, not stiff.

They describe the activity-related form as physiological hypertrophy as opposed to the former kind, which they call pathological hypertrophy.

For a six-month period, the Hopkins team assessed the benefits of a supervised program of exercise training in a group of 104 older men and women, measuring heart function, and body fitness and fat levels at the start and end of the study. All of the participants were in general good health except for untreated, mild hypertension. Half were randomly placed in a widely recommended moderate exercise program while the rest maintained their usual physical routine and diet.

The active group participated in a supervised series of exercises for 60 minutes, three times per week. The combination of exercises was designed to work all major muscle groups, including the heart, with substantial improvements observed in active participants' body fat, and muscle and fitness levels.

Aerobic fitness, as measured by peak oxygen uptake on a treadmill, increased by 17 percent (from 24.4 milliliters per kilogram per minute to 28.4 milliliters per kilogram per minute), as did average strength (from an estimated ability to lift a total of 383 kilograms from 328 kilograms, using seven different weight machines). The average weight loss in this group was only four pounds, because much of the loss of fat was offset by increased muscle mass. The fat in the abdominal region, measured by magnetic resonance imaging, was reduced by 20 percent among exercisers. The group that was not exercising had either no or significantly less improvement than the exercising group. Special scans, using an X-ray machine, were used to assess total body fat.

"Making gains in body fitness and losing abdominal fat are truly important to the long-term health of the heart," says study co-author and cardiologist Edward Shapiro, M.D., a professor at Hopkins. "Our results confirm that moderate-intensity exercise can have many health benefits - including gains in heart function that are linked to increased fitness and reduced fatness.

"Our study also shows that the vast majority of older people with mildly elevated blood pressure can benefit from moderate exercise, and they should talk about it with their physician to determine an appropriate exercise and any other options for treatment."

The Hopkins study's exercise program followed current guidelines from the American College of Sports Medicine. The study was part of a larger, ongoing trial, called the Senior Hypertension and Physical Exercise study (or SHAPE, for short). It is believed to be the first detailed examination of the guidelines' effectiveness and the separate effects of exercise on blood pressure, heart structure and cardiovascular function, with nearly an equal number of men and women enrolled.

A study published last year by the Hopkins scientists showed that exercise reduced by more than 20 percent the number of people who develop metabolic syndrome, a clustering of three or more risk factors for developing heart disease, diabetes and stroke. Risk factors include high blood pressure, elevated blood glucose levels, excess abdominal fat and abnormal cholesterol.

###

Funding for the study was provided by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health (NIH), with additional assistance from the Johns Hopkins Bayview General Clinical Research Center, also funded by the NIH. Besides Stewart and Shapiro, other Hopkins researchers who took part in this study were Pamela Ouyang, M.D.; Anita Bacher, M.S.N., M.P.H.; and Sandra Lima.

On the Web: http://heart.bmjjournals.com/cgi/content/full/92/7/893

Contact: David March
Johns Hopkins Medical Institutions

Article URL: http://www.medicalnewstoday.com/medicalnews.php?newsid=48293

Regards,

Nelson Vergel
salvagetherapies dot org

#17879

From: "Norm Stuart" <nspop2@...>
Date: Mon Jul 31, 2006 5:10 pm
Subject: Re: NATAP: lymphoma & HIV

norm_w_stuart

Offline

Jules, It surprises me that Hodgkin's lymphoma is so prevalent among HIV+ smokers. Very interesting.

In the general (HIV negative) population, there does not appears to be any link between Hodgkin disease and lifestyle factors such as smoking, diet, exercise, use of alcohol.

*** My summary of your HOPs report ***

Studies have shown a decline in AIDS-defining malignancies since the advent of highly active antiretroviral therapy.

-- Kaposi's sarcoma (KS)
-- Non-Hodgkin's Lymphoma (NHL)
-- cervical cancer

However, the incidence of five non-AIDS defining malignancies are significantly higher in HIV-infected persons than in the general population. The incidence of these five non-AIDS defining malignancies occur disproportionately among HIV+ smokers.

The five non-AIDS defining malignancies more prevalent among those with HIV, and the percentage of these HIV+ persons who were smokers:

-- lung: 100% were smokers
-- head/neck: 92%
-- Hodgkin's: 87%
-- anorectal: 79%
-- melanoma: 85%

Smokers were defined as current or former smokers who had quit within the past 10 years or the 10 years prior to cancer diagnosis.

--- In PozHealth@yahoogroups.com, JuLev@... wrote:
>
> Here is a link to study reported at CROI 2004.
>
> Incidence of Non-AIDS defining Malignancies in the HIV Outpatient ...However,
> the incidence of non-AIDS defining cancers among HIV-infected individuals
> seem to be increasing. We determined the incidence of 5 cancers among HIV ...
> www.natap.org/2004/CROI/croi_25.htm
>

#17878

From: "Dave Vowell" <dvowell@...>
Date: Mon Jul 31, 2006 5:25 pm
Subject: Bio Alcamid in Montreal

gdvowell

Offline

Hi Everyone:

After much soul-searching and knashing of teeth, I have decided to
have the Bio-Alcamid treatment done by Dr. Yves Hebert at the Clinique
Esthetique in Montreal, Canada. Has anyone in the group heard anything
about Dr. Hebert? If so, could you post to me either privately or to
the group. Since I have not posted very often, I hope I am going about
this in the proper way. Thanks in advance for any info you can provide.
Dave Vowell

#17877

From: "Norm Stuart" <nspop2@...>
Date: Mon Jul 31, 2006 6:48 am
Subject: Re: Fish Oil Boosts Exercise Benefit, Trims Pounds

norm_w_stuart

Offline

http://www.unisa.edu.au/researcher/issue/2005March/obesity.asp

That's a really interesting study. Here is a mention of the study on a University of Southern Australia at Adelaide website where Professors Peter Howe and Jon Buckley did this research study.

--- In PozHealth@yahoogroups.com, PoWeRTX@... wrote:
>
>
> Fish Oil Boosts Exercise Benefit, Trims Pounds
>
> (http://health.dailynewscentral.com/index2.php?option=content&task=view&id=0002358&pop=1&page=0#)
> _http://health.dailynewscentral.com/content/view/0002358/31/_ (http://health.dailynewscentral.com/content/view/0002358/31/) Wri
> tten by Rita Jenkins| 30 July, 2006 18:26 GMT
>
>
> Fish oil containing Omega 3 fatty acids plus moderate exercise can help
> overweight people shed pounds, even if their diet remains the same, scientists
> have found. A regimen of daily fish oil and moderate exercise is enough to
> spur weight loss without other dietary changes, according to research conducted
> at the University of South Australia.
> The Omega-3 fatty acids in oily fish are already known to slow aging in the
> human brain. The latest study shows they can contribute to significant weight
> loss by increasing the elasticity of blood vessel walls and improving the
> flow of blood to muscles during exercise.
> Exercise equivalent to aking a 45-minute walk three times a week appears
> sufficient to produce the weight loss benefit.
> Risk of Diabetes, Heart Disease
> Professor Peter Howe led a study involving 68 overweight-to-obese adults.
> PhD candidate Alison Hill monitored the participants during the 12-week trial.
> All of the volunteers had risk factors for metabolic syndrome -- a cluster
> of symptoms, such as hypertension, that are associated with obesity and can
> lead to Type 2 diabetes or cardiovascular disease.
> Some had high blood triglycerides, a type of fat that indicates future heart
> and arterial disease. Some had insulin resistance or heightened insulin
> levels, both of which are precursors to diabetes.
> The researchers assigned each volunteer to one of four groups: those who
> took fish oil and walked or ran for 45 minutes three times a week; those who
> took fish oil without exercise; those who took sunflower oil and walked or ran
> for 45 minutes three times a week; and those who took sunflower oil without
> exercise.
> No Change in Eating Habits
> All of the volunteers ate whatever they wanted. The first group -- those who
> combined fish oil with exercise -- lost weight, while none of the other
> groups did.
> Those who took the daily doses of fish oil and exercised lost an average of
> 4.5 pounds over a three-month period.
> "If you take the Omega-3 each day and exercise moderately, our studies show
> your weight will drop," said Hill.
> Howe called the impact on body shape and body composition of the
> participants "the most exciting outcome of the research."
>
>
> Regards,
>
> Nelson Vergel
> salvagetherapies dot org
>

#17876

From: "guyinsouthala@..." <guyinsouthala@...>
Date: Mon Jul 31, 2006 6:03 am
Subject: Re: Mail Order, was: Phoenix - Reyataz Needed

guyinsouthala

Offline

what mail order company do you use? When I google mail order pharmacies a bunch of cheezy looking ads pop up - makes me uneasy which ones are reputable? Thanks,

Sam

How low will we go? Check out Yahoo! Messenger�s low PC-to-Phone call rates.

Reply | Forward | Messages in this Topic (5)

#17875

From: JuLev@...
Date: Mon Jul 31, 2006 9:54 am
Subject: NATAP: lymphoma & HIV

jules72orange

Offline

Here is a link to study reported at CROI 2004.

Incidence of Non-AIDS defining Malignancies in the HIV Outpatient ...However, the incidence of non-AIDS defining cancers among HIV-infected individuals seem to be increasing. We determined the incidence of 5 cancers among HIV ...
www.natap.org/2004/CROI/croi_25.htm

#17874

From: "Kelly Scott" <kscott@...>
Date: Mon Jul 31, 2006 5:08 am
Subject: RE: Update 1 - On The Road To Wellness & Restoration

kscott@...

Uh, you may want to be damn careful about adding that integrase inhibitor.� Just adding one efficacious new drug is like being on a single drug regime: and you’re liable then to ‘waste’ the new drug, quickly breeding resistance.

I’m resistant to most nukes, non-nukes and protease myself, though my counts are going south yet, nor my clinical condition. So I’m waiting for an integrase, a receptor inhibitor (both new classes) AND maybe then adding T20 or a newer one of that type.� I ended up being resistant by adding drugs serially through the early 90s,: don’t want to do that again.

As for Houston…. hoo boy.� They thought it out: they HAVE no zoning, quite deliberately they are stuck with ‘spot zoning’ which is batshit crazy for communities..

Kelly Scott

Seattle

I want to catch everyone up to the current events here in Houston. The main issue was the lab results of my first 30 days on the new drugs. Sadly, my labs were unchanged. These results were a bit of a shock because most patients that go on a new drug regimen experience a boost in CD4 T-cells and a drop in viral load. They at least experience a drop in viral load. My labs indicate that neither of these two factors occurred. Dr. Schrader has two theories. First, it is just taking more time for my new meds to kick in and kick ass. Due to the fact that I have an extremely high viral load, this could be what is slowing the new drugs down. Dr. Schrader is very optimistic that the next blood draw will be better. The other theory is that my two new drugs are from two classes of HIV drugs to which I am already resistant. I mean that my virus is already resistant to all the other drugs in that same class of HIV drug so I may already be resistant to the new drugs. That would really suck. Not to worry, there is a Plan B already in the works. A new drug from a new class called “Integrase Inhibitors” is just months away from the FDA’s Expanded Access Program. When approved, I will be able to add this drug into my cocktail and from all the talk about this new drug; it has great potential for multi-resistant drug patients. My next blood draw is Monday – July 31, 2006. I should get the results a week later. These results will give us a better idea about what is happening and what is not happening inside my body. I am very optimistic about the results because I have had more energy lately and I’ve been working out in the small gym within the condo complex where we currently reside. My appetite is very good and I am certain that I have added a few more pounds to my frame. One positive result in the last three months has been a slow but steady weight gain. I look forward to breaking the 160 pound barrier that has been the roadrunner to my Wylie Coyote for so long. The damn bird has slipped out of my grasp for far too long. Using the “ACME Workout Routine”, I hope to tip the scale during my next weigh in on Monday.

I’ve had sometime to explore Houston. Here are a few things that I have discovered that interest me.

1. James Coney Island – They make chili cheese dogs that are close to the World Famous Skyline Coney from Cincinnati that I love so much.

Happy Tails Dog Spa – I had Lucky and Nellie groomed there and it is quite the experience. I hope to take advantage of the doggie day care once a month so the puppies can interact with other dogs. Plus, they have web cams so you can go online a watch your dogs play.

3. Ziggy’s Healthy Grill – They serve Buffalo burgers and Ostrich burgers.

4. Sarpino’s Pizza – Good Pizza and I get AAdvantage Dining Miles!

Houston’s communities are not well thought out like in Dallas. There do not appear to be any zoning laws so you find residential mixed right in with commercial establishments. There is not a Cedar Springs where all the gay owned and operated bars, restaurants, & retail are conveniently located next to each other. The treasures are a harder to discover but they are definitely worth finding. I hope to try a restaurant called “Barnaby’s Caf�” soon. The exterior of the restaurant says “run down shack” but the people say that the food and ambiance inside is fantastic. I look forward to this culinary adventure.

Jeff Young

#17873

From: PoWeRTX@...
Date: Sun Jul 30, 2006 11:58 pm
Subject: Fish Oil Boosts Exercise Benefit, Trims Pounds

nelsonvergel

Offline

http://health.dailynewscentral.com/content/view/0002358/31/

Fish Oil Boosts Exercise Benefit, Trims Pounds

Written by Rita Jenkins| 30 July, 2006 18:26 GMT

fish oil omega fatty acids weight loss

Fish oil containing Omega 3 fatty acids plus moderate exercise can help overweight people shed pounds, even if their diet remains the same, scientists have found. A regimen of daily fish oil and moderate exercise is enough to spur weight loss without other dietary changes, according to research conducted at the University of South Australia.

The Omega-3 fatty acids in oily fish are already known to slow aging in the human brain. The latest study shows they can contribute to significant weight loss by increasing the elasticity of blood vessel walls and improving the flow of blood to muscles during exercise.

Exercise equivalent to aking a 45-minute walk three times a week appears sufficient to produce the weight loss benefit.

Risk of Diabetes, Heart Disease

Professor Peter Howe led a study involving 68 overweight-to-obese adults. PhD candidate Alison Hill monitored the participants during the 12-week trial.

All of the volunteers had risk factors for metabolic syndrome -- a cluster of symptoms, such as hypertension, that are associated with obesity and can lead to Type 2 diabetes or cardiovascular disease.

Some had high blood triglycerides, a type of fat that indicates future heart and arterial disease. Some had insulin resistance or heightened insulin levels, both of which are precursors to diabetes.

The researchers assigned each volunteer to one of four groups: those who took fish oil and walked or ran for 45 minutes three times a week; those who took fish oil without exercise; those who took sunflower oil and walked or ran for 45 minutes three times a week; and those who took sunflower oil without exercise.

No Change in Eating Habits

All of the volunteers ate whatever they wanted. The first group -- those who combined fish oil with exercise -- lost weight, while none of the other groups did.

Those who took the daily doses of fish oil and exercised lost an average of 4.5 pounds over a three-month period.

"If you take the Omega-3 each day and exercise moderately, our studies show your weight will drop," said Hill.

Howe called the impact on body shape and body composition of the participants "the most exciting outcome of the research."

Regards,

Nelson Vergel
salvagetherapies dot org

#17872

From: PoWeRTX@...
Date: Mon Jul 31, 2006 12:01 am
Subject: Imbalance of insulin is the killer factor

nelsonvergel

Offline

Alternative Medicine: Imbalance of insulin is the killer factor

30 Jul 2006
Rajen M

WE LIVE in strange times — at least nutritionally. Just following the “rules” that everyone takes for granted and advises, does not necessarily mean success.

In fact, it could even be a prescription for failure.

For example, modern nutritional wisdom would predict that the diet of the ancient Egyptians — high in complex carbohydrates, low in fat, no refined sugar and almost no red meat — should have conferred health and longevity. It didn’t.

Translations of the ancient Egyptian papyrus writings and detailed modern investigations of their mummies tell us a completely different story.

The evidence speaks of people plagued with obesity, severe atherosclerosis, elevated blood fats and dying in their thirties with heart attacks — some 5,000 years ago! It appears that their low fat and high carbohydrate diet did not serve them well.

New rules

ARE you struggling with your blood cholesterol, pressure, weight or blood sugar on a diet of fruits, vegetables, brown rice, wholemeal bread and whole grains, living the low-fat and fat-free way and still failing?

Don’t despair. Stop blaming yourself! You have not failed. You are just following the wrong diet.

If you have been feeling discouraged because your nutritionist said, “Cut your fat to 25 grams a day or less and your weight will come down,” and you did but it didn’t, don’t despair.

There is a better and, yes, easier way. If your suffer form high cholesterol, you have probably forgotten what it is like to eat a steak. It must seem like a long time since you ate an egg. Still, your cholesterol remains stubbornly elevated. Take heart. There is a better way.

Metabolic chaos

CHANGING your diet can and will help you regain control over these metabolic disorders. You can literally melt away the fat, reduce blood cholesterol, lower your blood pressure and normalise blood sugar by simply changing the way you eat.

In fact, you can maintain these benefits for a lifetime. Good health is within your grasp. It can be fun and, yes, easy. All you need is the right information.

The major modern lifestyle diseases — obesity, hypertension, heart disease, elevated body fats (including cholesterol) and diabetes — have a common link.

In fact, these “diseases” are not really diseases at all. They are symptoms of a more basic but deeper disorder: hyperinsulinemia (high blood insulin).

Prolonged hyperinsulinemia leads to insulin resistance. That means that it would take your body more and more insulin to get the same effects.

It is a little bit like if somebody knocked you on the head every day. After a while, you get used to it and probably feel no pain. In order to feel pain, that person has to hit you harder.

Hyper insulinemia

LET us take a look at how high blood insulin develops. When you eat food, your body identifies it as its basic components — carbohydrate, protein and fat. These are broken down and absorbed into the blood stream causing a rise in your blood sugar.

Years of dietary and lifestyle abuse in susceptible people can lead to a malfunction of the body’s balance.

As a result, the blood insulin tends to rise. This means even more circulating insulin.

Thus, food that you eat (even if a little) would provoke a rapid rise in insulin. The sluggish system would favour the storage of eaten sugars and fats.

This leads to excessive body fat and obesity. Thus, insulin makes you fat!

Effects of abuse

CONTINUED dietary abuse (excess carbohydrates) results in further elevation of insulin levels. This makes the receptors even more sluggish. This leads to even more insulin resistance. At one point, all the insulin your pancreas can make will not be enough to keep the system going.

The combined forces of rising blood sugar and high blood insulin damage the pancreas. The blood glucose skyrockets. This leads to Type II diabetes.

High blood insulin has many effects:

• Kidneys are prompted to hold water and salt.

• Promotes growth of arterial walls (makes them thicker and less pliable).

• Increases circulating levels of norepinephrine (adrenaline-like substances that cause the heart to beat faster and blood vessels to constrict).

• Favours the lying down of circulating cholesterol below the arterial lining (causing thickening and thus, blockage).

• Any circulating fat or glucose is quickly stored as body fat.

Fatal quartet

THE bad news: All these disorders are related — you might be suffering from more than one — obesity, hypertension and diabetes. Over time, there may be more — high cholesterol and coronary artery disease.

The good news: You can treat them all the same way: by reducing your levels of circulating insulin.

So hypercholesterolnamia, hyperinsulinemia, hypertension, ateriosclerosis and obesity can be corrected by dietary manipulation. When the insulin comes down, they go away.

Some of these problems took years to develop and would thus take a while to reverse.

More importantly, by simply manipulating your food, you could prevent the progression of disease.

The beauty of this programme is that food is powerful. In fact, as Barry Sears puts it, “food is a drug”.

It can hurt or heal. It is up to you and how you use it.

Ultimately, it boils down to this: your body is an awesome self-healing mechanism. With the right nutritional tools it well heal itself.

The trick is to keep the insulin levels low. That is rather simple. Just cut back on your refined carbohydrates — the starches and sugars.

That is quite a bit — rice, bread, noodles, pasta, pizza, roti canai. I hear you asking, “What do you eat, then?” Let us talk again next Sunday.

The writer is a pharmacist with a doctorate in Holistic Medicine. He is a director of the Malaysian Herbal Corporation and a CEO of a group of companies in alternative healthcare.

Regards,

Nelson Vergel
salvagetherapies dot org

#17871

From: PoWeRTX@...
Date: Sun Jul 30, 2006 11:55 pm
Subject: 'Graying' of HIV takes mental toll, too

nelsonvergel

Offline

'Graying' of HIV takes mental toll, too

Posted 7/30/2006 8:30 PM ET

By Mary Brophy Marcus, Special for USA TODAY

As the number of HIV-positive Americans over 50 grows, a study shows that this group is likely to have high rates of depression, and many of them have numerous age-related medical conditions that are complicated by their already compromised health.

The comprehensive study, Research on Older Adults with HIV, reports on the complex health and personal problems juggled by aging HIV-positive Americans. The results will be presented at the 16th International AIDS Conference in Toronto, which begins Aug. 13.

More than 1 million people in America are living with HIV/AIDS, the Centers for Disease Control and Prevention recently reported. The number of people over 50 with HIV/AIDS is growing significantly despite the fact that new HIV/AIDS diagnoses are not increasing in that age group.

It's the "graying" of HIV/AIDS, says Stephen Karpiak, research director of the AIDS Community Research Initiative of America, lead study author and a former research scientist at Columbia University Medical School. He credits anti-retroviral drugs introduced in the mid-'90s with the fact that people with HIV/AIDS are living longer.

The study was done last year in New York City. (Of 100,000 New Yorkers living with HIV/AIDS, 31% are over 50, according to the New York City Department of Health and Mental Hygiene.) Researchers asked 1,000 HIV-positive adults over 50 about their sexual behavior, health status and numerous other key issues, such as support networks and mental well-being.

Almost 67% of study subjects said they were heterosexual. Seventy percent lived alone, and 82% were not working. More than half were on disability. Many had age-related conditions such as arthritis, high blood pressure, vision loss and diabetes.

Brenda Lee Curry, 61, a great-grandmother from New York who has been HIV-positive since 1985, takes as many as 10 medications a day for HIV, high blood pressure and hepatitis, among other conditions. Curry says she developed neuropathy — trembling in her hands — from mixing so many medicines. She also has had depression and has had trouble finding resources for older women with HIV. "But at this point, I do not let this disease define me," says Curry, who founded Copasetic Women, a support group for HIV-positive women over 50.

Understanding how an HIV-compromised immune system is affected by normal age-related conditions could improve the quality of life for many HIV-positive seniors, Karpiak says.

Another significant finding: HIV-positive adults experience high levels of depression, almost 13 times higher than the general New York City population. The stigma of HIV is pervasive, which probably plays a major role in the higher rates of depression, Karpiak says. Fewer than half of the study subjects have shared their diagnosis with their families; only 35% have told friends. They keep their diagnoses to themselves "possibly out of guilt or fear of rejection," he says.

Karpiak and his colleagues say the study reveals a fragile health care system that is under-serving older people with HIV/AIDS. They're concerned that conditions will only get worse. But, Karpiak says, "it's also the beginning of learning how to best sustain the health and quality of life for the aging HIV-infected population."

Find this article at:
http://www.usatoday.com/news/health/2006-07-30-hiv-toll_x.htm

Regards,

Nelson Vergel
salvagetherapies dot org

#17870

From: "John R." <johnrsf94114@...>
Date: Mon Jul 31, 2006 12:35 am
Subject: Re: lymphoma

johnrsf94114

Offline

Lymphoma has been classified as an AIDS-defining opportunistic infection since the CDC first defined AIDS in the early 1980s. Here's a link to what I believe is still the operative definition of AIDS. http://wonder.cdc.gov/wonder/help/AIDS/MMWR-12-18-1992.html

trippreed <trippreed@...> wrote:

Has lymphoma been classified as an opportunistic illness?

Thanks,
Tripp

#17869

From: lsmyle@...
Date: Mon Jul 31, 2006 2:53 am
Subject: Re: increase in lymphoma for long term HIV+

larrysmyle

Offline

Tripp,

Before protease, people like myself, with no OI's, but zero t-cells were expected to either die from wasting (which I was), or get non-Hodgekins lymphoma or die of a a heart attack within 1 1/2 to 2 years. My observation has been that there has been a decrease in lymphoma, but again this is anecdotal. I'm sure someone out there has the stats. Jules? Nelson?

Larry

-------------- Original message --------------
From: "trippreed" <trippreed@...>

I have witnessed an increase in lymphoma in long term HIV+ survivors.
I've heard that statistics don't support that there is an increase in
lymphoma w/ long term survivors vs other HIV+ persons. My anecdotal
observations conflict w/ that statisic.
Also are the lymphomas generally non-hodgkins in nature?
If anyone knew Don P. from this group...he died from his 3rd bout w/
lymphoma this weekend.
Thanks,
Tripp

#17868

From: "Jeffrey Young" <jyoung681@...>
Date: Mon Jul 31, 2006 1:22 am
Subject: Update 1 - On The Road To Wellness & Restoration

cd4rocketman

Offline

I want to catch everyone up to the current events here in Houston.� The main issue was the lab results of my first 30 days on the new drugs.� Sadly, my labs were unchanged.� These results were a bit of a shock because most patients that go on a new drug regimen experience a boost in CD4 T-cells and a drop in viral load. �They at least experience a drop in viral load.� My labs indicate that neither of these two factors occurred.�� Dr. Schrader has two theories.� First, it is just taking more time for my new meds to kick in and kick ass.� Due to the fact that I have an extremely high viral load, this could be what is slowing the new drugs down.� Dr. Schrader is very optimistic that the next blood draw will be better.� The other theory is that my two new drugs are from two classes of HIV drugs to which I am already resistant.� I mean that my virus is already resistant to all the other drugs in that same class of HIV drug so I may already be resistant to the new drugs.� That would really suck.� Not to worry, there is a Plan B already in the works.� A new drug from a new class called “Integrase Inhibitors” is just months away from the FDA’s Expanded Access Program.� When approved, I will be able to add this drug into my cocktail and from all the talk about this new drug; it has great potential for multi-resistant drug patients.� My next blood draw is Monday – July 31, 2006.� I should get the results a week later.� These results will give us a better idea about what is happening and what is not happening inside my body.� I am very optimistic about the results because I have had more energy lately and I’ve been working out in the small gym within the condo complex where we currently reside.� My appetite is very good and I am certain that I have added a few more pounds to my frame.�� One positive result in the last three months has been a slow but steady weight gain.� I look forward to breaking the 160 pound barrier that has been the roadrunner to my Wylie Coyote for so long.� The damn bird has slipped out of my grasp for far too long.� Using the “ACME Workout Routine”, I hope to tip the scale during my next weigh in on Monday.� �

I’ve had sometime to explore Houston.� Here are a few things that I have discovered that interest me.

1.� James Coney Island – They make chili cheese dogs that are close to the World Famous Skyline Coney from Cincinnati that I love so much.

Happy Tails Dog Spa – I had Lucky and Nellie groomed there and it is quite the experience.� I hope to take advantage of the doggie day care once a month so the puppies can interact with other dogs.� Plus, they have web cams so you can go online a watch your dogs play.

3.� Ziggy’s Healthy Grill – They serve Buffalo burgers and Ostrich burgers.

4.� Sarpino’s Pizza – Good Pizza and I get AAdvantage Dining Miles! �

Houston’s communities are not well thought out like in Dallas.� There do not appear to be any zoning laws so you find residential mixed right in with commercial establishments.� There is not a Cedar Springs where all the gay owned and operated bars, restaurants, & retail are conveniently located next to each other.� The treasures are a harder to discover but they are definitely worth finding.� I hope to try a restaurant called “Barnaby’s Caf�” soon.� The exterior of the restaurant says “run down shack” but the people say that the food and ambiance inside is fantastic.� I look forward to this culinary adventure.

Jeff Young

#17867

From: "John R." <johnrsf94114@...>
Date: Sun Jul 30, 2006 11:50 pm
Subject: Re: Re: The salmon scam

johnrsf94114

Offline

Frozen wild salmon is available year round, if you happen to have a Trader Joe's near you. I also really like the frozen Alaskan Salmon burgers I buy at Costco. They're made by Trident, and probably available elsewhere. They make a very easy, tasty, quick dinner -- just saute them or broil them straight from the freezer, and put them on a bun with some tarter sauce and sliced tomatoes. Yum! Not too high in sodium, and plenty of the healthy and tasty fish fat.

Butch Kara <longjohnmaniac@...> wrote:

Relatively cheap is an understatement - most Alaskan canned salmon I"ve seen is regularly on sale (at least here in Missouri) for under $1.50 a can. I stock up all the time. A very cheap source of high quality protein and omega 3s . If you avoid adding salt to anything else in your diet, the extra sodium in the canned salmon shouldn't be excessive. The reason canned wild salmon is so cheap is that during the salmon runs they can only sell so much fresh wild salmon - the rest has to be preserved -either frozen or canned.

Original message:

Your surest bet for a salmon fix,
especially in winter, may be canned Alaska salmon. It�s fairly cheap,
is sold year
round, and generally has "Alaska" stamped on its lid.

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#17866

From: "John R." <johnrsf94114@...>
Date: Sun Jul 30, 2006 11:07 pm
Subject: Re: Fl

johnrsf94114

Offline

I did read all of the cautions, including my Doctors caution to take Niaspan at night. But I took one 500 mg tablet as soon as I picked it up at the pharmacy. Nothing happened until six hours later when I got the tingling, itching Niacin flush in my face and neck for about 30 minutes.

Just to throw caution to the wind, I took another two 500 mg tablets at bedtime. No effects that I can recall, so maybe my Doctor is correct. Take the Niaspan at night and you won't know if you had side-effects.

I take 2000 mg. Slo Niacin from Costco, divided into morning and evening doses, and rarely have flushing. I've noticed that the flushing is worse if I drink alcohol, and can be aleviated somewhat if I take aspirin with the niacin. I take 81 mg aspirin every evening with my niacin, so that probably helps eliminate the effect of wine or beer with dinner. If I stop the niacin for a while and restart, I tend to experience a bit of flushing again.

I take 20 mg Lipitor and 145 mg Tricor, as well as 4000 mg. fish oil capsules and 2000 mg. acetyl l-carnitine. Lipid numbers have been good, but liver enzymes somewhat elevated. I'm going to go over everything I'm taking with my doctor at my next visit to see whether I should consider reducing or eliminating anything I'm taking.

#17865

From: "Norm Stuart" <nspop2@...>
Date: Sun Jul 30, 2006 9:44 pm
Subject: Re: increase in lymphoma for long term HIV+

norm_w_stuart

Offline

http://www.lymphoma-net.org/causes-and-factors.cfm

Lymphoma is strongly associated with immune suppression. It is also associated with Epstein-Barr virus and those co-infected with either HTLV-1 or HIV.

While the risk of lymphoma remains constant for those with immune supression, remaining immune suppressed for longer periods of time gives you additional opportunity to develop lymphoma.

http://www.aegis.com/topics/oi/

I had a friend who first developed lymphoma 14 years ago and died from lymphoma 9 years ago. His history is instructive. He first developed High-Grade Lymphoma which was put into complete remission in less than a month with Rituxan, a monoclonal antibody which targets lymphoma cells for immune destruction. The side-effects of Rituxan are so minimal that my friend went to the gym to work out after each infusion.

http://www.lymphomainfo.net/therapy/immunotherapy/mab.html

Although Rituxan has now been an approved drug for lymphoma for a number of years, it is still greatly under-used by oncologists, who are suspicious of the immune system and still favor their four drug CHOP therapy which can kill people with HIV, even if they don't have lymphoma. Newer forms of Rituxan are Zevalin and Bexxar which combine Rituxan with a short-lived radioactive molecule.

Another therapy uses Interleukin-2, either in the body or on glass plates outside the body, to grow up specific T cells which target Lymphoma.

http://www.lymphomainfo.net/therapy/immunotherapy/t-cell.html

Several years later he developed Low-Grade lymphoma, which at the time was not believed to respond to Rituxan. He was treated with radiation which eventually failed to control the lymphoma. The newer types of Rituxan antibody Zevalin and Bexxar combine radiation with the antibody and are more effective in treating Low-Grade lymphoma.

If I were to ever develop non-Hodgkins lymphoma I would use Interleukin-2 with either Rituxan, Zevalin or Bexxar. I would never use CHOP as this therapy destroys the immune system and prevent therapy with Interleukin-2, Rituxan, Zevalin or Bexxar from working - since these assist the immune system in destroying lymphoma. You cannot successfully assist the immune system and destroy it at the same time.

As a note: Hodgkins lymphoma is an entirely different beast. Hodgkins is strongly associated with people who hold in anger and stress. Chemotherapy is often couple with meetings with a psychologist to help people prone to Hodgkins express their emotions.

--- In PozHealth@yahoogroups.com, "trippreed" <trippreed@...> wrote:
>
> I have witnessed an increase in lymphoma in long term HIV+ survivors.
> I've heard that statistics don't support that there is an increase in
> lymphoma w/ long term survivors vs other HIV+ persons. My anecdotal
> observations conflict w/ that statisic.
> Also are the lymphomas generally non-hodgkins in nature?
> If anyone knew Don P. from this group...he died from his 3rd bout w/
> lymphoma this weekend.
> Thanks,
> Tripp
>

#17864

From: Butch Kara <longjohnmaniac@...>
Date: Sun Jul 30, 2006 8:20 pm
Subject: Re: Lexapro

longjohnmaniac

Offline

http://www.dr-bob.org/babble/

Did your doctor prescribe it for depression or for anxiety/panic disorder? It's used for both although it's basically an antidepressant. It's good it works for many. It didn't work for me however, and there must be reasons for the high rate of "recidivism" noted by Will (altho I wouldn't compare stopping an intolerable drug to a reversion to criminal behavior....). I was given Lexapro for anxiety following a heart attack and did not like it, stopped after a month. One immediate sexual effect can be anorgasmia - even if you can get aroused (and some don't get that far) you can't climax. A real bummer! Having had a heart attack it wasn't pleasant to be "on the verge" indefinitely with a racing heart. I might have enjoyed that in my younger days, though I still think eventually one wants to complete the cycle - the eternal return etc. The anorgasmic effect lasted for a month or two after I stopped it.

Also, I felt slightly drugged on the stuff, and it produced a constant low level hum in my head, very annoying. I decided instead if I had a panic attack, I'd take a small dose of Xanax, which relieves the panic and can be taken as needed, not every day. Doctors fear their patients will become addicted to Xanax but taking Lexapro every day isn't considered addictive. I've never had cravings for Xanax and always take the least amount needed to quell any symptoms. Since I wasn't depressed to begin with, it may be that Lexapro didn't work for me because I didn't need my serotonin reuptake inhibited. It might work well for you though.

There's a great website overseen by a psychiatrist at the U of Chicago named "Dr Bob" which has lots of info as well as a very active patient forum appropriately called "PsychoBabble". Many posts about all kinds of drugs, and you can use the search feature to search the site. I wish you well.

http://www.dr-bob.org/

Butch

Original message:

11a. Lexapro
    Posted by: "safford@..." safford@... passiondc20009
    Date: Sat Jul 29, 2006 5:10 pm (PDT)

hi-

my dr just prescribed this for me. anyone have any information about
it too share?

many thanks.

________________________________________________________________________
_______________________________________________________________________

11b. Re: Lexapro
    Posted by: "Will Wilson" wilthomson@... weewill53
    Date: Sat Jul 29, 2006 10:15 pm (PDT)

It's a really great anti-depressant. Takes about 2 weeks to take
effect, then once it does things will even out for you. You'll notice an
increase in your energy level and you'll find it easier to deal with the
day-to-day activities. Don't plan on stopping it for at least one year
(recidivism rate before 12 months is very high); I took it for almost 20
months before I stopped. For me it was a very easy and gentle drug, I
experienced no side effects (other than feeling like I could face life
again). I do hope your doc has suggested "talk therapy" or a support
group in conjunction with this medication. Good luck, in a couple of weeks
you'll be awfully glad you started this.

Will

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Reply | Forward | Messages in this Topic (7)

#17863

From: "trippreed" <trippreed@...>
Date: Sun Jul 30, 2006 4:52 pm
Subject: lymphoma

trippreed

Offline

Has lymphoma been classified as an opportunistic illness?

Thanks,
Tripp

#17862

From: "trippreed" <trippreed@...>
Date: Sun Jul 30, 2006 4:39 pm
Subject: increase in lymphoma for long term HIV+

trippreed

Offline

I have witnessed an increase in lymphoma in long term HIV+ survivors.
I've heard that statistics don't support that there is an increase in
lymphoma w/ long term survivors vs other HIV+ persons.  My anecdotal
observations conflict w/ that statisic.
Also are the lymphomas generally non-hodgkins in nature?
If anyone knew Don P. from this group...he died from his 3rd bout w/
lymphoma this weekend.
Thanks,
Tripp

#17861

From: "Norm Stuart" <nspop2@...>
Date: Sun Jul 30, 2006 6:07 am
Subject: Re: Lexapro

norm_w_stuart

Offline