Sunday, November 30, 2014

World AIDS Day December 1, 2014

World AIDS Day December 1, 2014


As I sit here thinking about another year coming close to an end with World AIDS DAY knocking on our door, I can help but think how blessed I have been the past 6 years of my life.

I know my journey has not been as long and tiresome as the many who have endured the AIDS epidemic now for 30 plus years. I have so much respect for those who have endured PROMISE after PROMISE, HOPE after HOPE of a CURE for this HORRIFIC DIESEASE. I know that for so many of the wonderful people I have met online through social media (Dab Garner, Shelby Welchel, Maria Mejia, Jeremy Scott Hobbs, Timothy Ray Brown, Bob Bowers, Kevin Maloney) and the list goes on, the journey living with HIV/AIDS has not been a pleasant experience. These wonderful people along with so many others have fought for years not only to live, but they have fought for our rights to have the medical care that we receive here in AMERICA. Without people like these individuals fighting government, making statements and teaching others about the medical needs of those affected by HIV/AIDS we could not continue to enjoy getting the medical care needed to fight.

I have learned in the past 6 years being Positive that you can NOT make it on YOUR own. WE all need each other. We all need someone who “HAS BEEN THERE”, to help us understand the why’s and how’s when it comes to dealing with a DISEASE like HIV/AIDS. I have been so blessed and honored to get to know the people who “HAVE BEEN THERE”… Those people are LOVING and CARING and WANT to SHARE!! Those people want others to LISTEN and take NOTE so they DO NOT HAVE TO GO THROUGH THE SAME THINGS.

If I would have LISTENED and HEEDED the WORDS of the GREAT PEOPLE I have met in the last 6 years ~ BEFORE I BECAME HIV+ ~ I WOULD NOT BE HIV+!!!!!!

The message

 ~ AS SIMPLE AS IT CAN BE ~

~~
IF YOU RESPECT YOURSELF

PROTECT YOURSELF

PRACTICE SAFER SEX!!!
~~

It can be told in many languages but it all boils down to those simple words. If you care enough about yourself, you will protect yourself from the spread of HIV/AIDS.

~YES~

 ~ SEX is NATURAL~

 ~ SEX is FUN~

~ Unprotected SEX CAN = HIV/AIDS ~

HARSH BUT TRUE!!!
HIV/AIDS is NOT FUN!!!

Popping pills everyday that make you sick, that are highly toxic, and can have adverse side effects on your body is NO WAY to spend the rest of your life. ASK ME ~ I KNOW!! ASK ANYONE who is HIV+ and they will tell you the same. The PILL LOAD only increases the LONGER you live with HIV/AIDS. They do NOT tell you that in the “CUTE” little T.V. Commercials!! ASK A SURVIVOR ~ THEY WILL TELL YOU THE TRUTH!!

HIV/AIDS SUCKS!!!!

~ SO my point this “WORLD AIDS DAY” ~

RESPECT YOURSELF
~~
PROTECT YOURSELF
~~
PRACTICE SAFER SEX

We can put an END to HIV/AIDS – IT will take everyone doing their part to PRACTICE SAFER SEX until this DISEASE is wiped out!!!

God Bless you all,
David A. Moorman




Thursday, November 27, 2014

Dab Garner


Posted on November 20, 2013 by  in Features

Real-Life Teddy Bear
Diagnosed with AIDS at a time when it was still called GRID, cuddly advocate and long-time survivor Dab Garner is still going strong in the fight against HIV/AIDS
Text & Photos by Sean Black
Dab_MG_7832
Dab Garner, founder and CEO of Dab the AIDS Bear Project, and an aggressive ally for the rights and health of others, points to the right cheek of his ruggedly handsome face; a face that bares no apparent signs of his many years living with HIV and the struggles and losses he has endured.
“Her little mouth was on the side of her face, her ear was over here,” he begins, describing Candace, a crack-addicted infant born with HIV along with a number of heartbreaking physical deformities and challenges as a result of fetal alcohol syndrome.
“She couldn’t hear out of it. She was constantly sick and small for her size.” His voice breaks and tears begin to trickle from the corners of his piercing eyes. Remembering the baby girl who helped bring him into his lifelong fight against AIDS, back in 1985, he notes that Candace was one of the earliest known cases of mother-to-child transmission. The daughter of a troubled woman who died shortly after her birth, Candace entered as her mother exited a world that had already been forever changed.
Navigating mountains of red tape and unable to legally adopt, Dab and his second partner, Brad, both living with HIV and unsure of there own precarious health conditions, were finally able to bring Candace home from the hospital. With a life expectancy of only several months and round-the-clock needs, life wasn’t easy for the ailing child nor was it for her new “godparents.” But, the loving and non-conventional family endured. Dab, a full-time college student and professional model, whose work opportunities were waning after he was publicly named in the press as being infected with HIV (more than a decade before the HIPAA Privacy Rule), and Brad, a San Francisco police officer, received an enormous amount of help from friends; mostly those belonging to a community he still holds sacred to this day.
“My leather group was the only group that really didn’t treat me any differently.” Recognizing the individuals who stepped up to help him and his lover through this difficult time, Dab recalls many by name. “There was Vicky, Vivian, Marilyn, Liz, Terri, Allison, Carol, Ben, Alex, Randy, Marshall, Andy, Bill, James, Jack, Sandra, and Tina. Oh, and Olivia and Sheila who were lesbian leather lovers,” Dab smiles as we acknowledge the playful sounds and alliteration of his words.
Looking back to the cold month before his twentieth birthday, in the winter of 1982, when he had just been diagnosed with PCP and GRID, a familiar nightmare began to repeat itself. “I don’t think I had ever been so scared in my entire life. I just watched two people, who I loved, die alone in those rooms.” Losing loved ones at such an early age was new for Dab and many others at this troubling time. His losses were that of his best-friend Michael, and his first boyfriend Derek, a successful fashion photographer and the reason for his move to San Francisco, just days after graduating from high school. The “Motherland” he sought after leaving his rigid Pensacola roots was slowly sinking around him. After three weeks of his terrifying ordeal, Dab started getting better and was eventually released with the intervention and aid of legal action. “Friends had to get a lawyer to get me out of that room.”
Having to watch Derek and Michael suffer and die alone in isolation upset and angered Dab. “It broke my heart that I could not go into the room to show them love and to comfort them.” Dab took action. “I pondered what I could do to make them feel love since the doctors and nurses wore protective garments restricting any form of human touch. So being a hairy, gay man [i.e., a bear], I decided to give them a teddy bear with a note saying how much I wished I could be in there with them, to hold them, and to let them know they were very much loved.”
While he was in quarantine, Dab made friends with a nurse named Vicky. Taking a large risk by disclosing patient information, she would let him know when someone with AIDS came into the hospital and was placed in similar scary confines. “Even though I might not personally know them, I would go get them a bear so that I could at least let that person know that someone cared about them.”
Edit_MG_7720
Dab started helping others and talking about HIV on a broader spectrum at that time, beginning with one of the first international conferences on HIV/AIDS, held in Paris, and attended by over 2,800 people. Dab remembers that French virologist Dr. Luc Montagnier, who won the 2008 Nobel Prize for his co-discovery of HIV was presenting. Dab also attended the first AIDS candlelight vigil held in San Francisco while a similar one was being conducted in tandem in New York City. Extending his voice as more opportunities availed themselves through early fundraising venues such as the AIDS Walks, bicycle rides, LGBT Pride festivals, health fairs, men’s and women’s events, high schools, conferences, he continued speaking openly about his disease.
Dab also got involved in organizations like the AIDS Coalition to Unleash Power (ACT UP) and began making trips to our nation’s capital, which he still does, on a regular basis. Further continuing his legacy of love today, Dab estimates that he presents at more than 150 events each year. “Pretty much anywhere they will put a microphone in my hand,” he attests proudly. In addition, Dab has amassed an army of caring soldiers, 509 to be exact, over the last thirty-two years. Called Ambassadors of Hope, these individuals, who reside in twenty-three countries, spread messages of hope, compassion, and love for people living with HIV while taking pictures with their bears. “Dab the AIDS Bear isn’t just one individual, it’s a collective team of people—activists, community leaders, members of organizations, students, celebrities and every day citizens,” he humbly shares.
Pausing to take a reflective breath, he concludes with how he got his nickname. “Candace had a really bad lisp when she would talk. So when she tried to say the word ‘Dad,’ it came out ‘Dab.’ When my friends heard this, they all thought it was so adorable, so from then on I became ‘Dab.’” After a way too short life, Candace lost her battle to AIDS on August 14, 1989, at the age of four. As this little angel was dying, her “Dab” made a certain promise to her, to which he has held true, to this day—making other children like her feel special and loved.
For more information about how to help the Dab the AIDS Bear Project this holiday season and all year long, link to Dab’s entry in our Holiday Gift Guide or log on to www.dabtheaidsbearproject.com.

Sean Black is an Editor at Large for A&U.

Sunday, November 23, 2014

Matters of the HEART {Part 2}


Prevention and Management of HIV-Associated Cardiovascular Disease

November 17, 2014
 
"Our understanding of mechanisms of HIV-associated cardiovascular disease (CVD) has not yet translated into tailored clinical interventions," says Virginia Triant, M.D., M.P.H., of Massachusetts General Hospital. Triant provided a state-of-the-art presentation on cardiovascular complications in people living with HIV at IDWeek 2014.
The first article in this series covered the context and causes of HIV-related CVD. This second article focuses on how healthcare providers can integrate the prevention and management of CVD into HIV chronic care -- addressing both the traditional risk factors of CVD, and other risk factors that are HIV-specific.

Estimating Risk

Part of the challenge for clinicians is that it is unclear to what extent general population guidelines can be applied in the management of CVD in people living with HIV.
It isn't clear that any of the available tools to predict CVD risk in the general population underestimate risk in HIV. For instance, the Framingham risk score (FRS) was found to underestimate risk of AMI (acute mydocardial infarction) and stroke in people living with HIV on antiretroviral therapy in the D.A.D study and stroke in the Multicenter AIDS Cohort study.
However, new cardiovascular risk guidelines from the 2013 American College of Cardiology/American Heart Association (ACC/AHA) have added some complexity to HIV-specific risk prediction. These guidelines employ new CVD risk prediction equations -- the pooled cohorts equations (PCE). There have been reports that they may overestimate risk in the general population but they also appear to underestimate risk in people living with HIV.
Furthermore, the Framingham risk score and ACC/AHA guidelines do not seem to be in complete agreement about which people living with HIV are at low or high risk of CVD -- with discordant results in about 17% of cases.
Triant suggested that clinicians should consider calculating both the Framingham risk score and the ACC/AHA risk score.
Patients who are in a high-risk category by at least one score (greater than 10% for FRS and greater than 7.5% for ACC/AHA) merit:
  • Suppressive antiretroviral therapy, if not already treated
  • Strong consideration of statins
  • Aggressive CVD risk-factor reduction

Management of Dyslipidemia in HIV

Some questions about the ACC/AHA guidelines remain. Rates of dyslipidemia are much higher in people living with HIV than in control patients, with a distinctive pattern of low high-density lipoprotein (HDL) and high triglycerides. Although statins are the main treatment, dyslipidemia may be more difficult to treat in people living with HIV, and the effects as well as drug interactions with antiretroviral drugs need to be considered.
In patients living with HIV, the use of statins has been shown to effectively lower low-density lipoprotein (LDL). Data presented at CROI 2014 also suggested that statin use may also decrease immune activation, and contribute to immune reconstitution independently of antiretroviral therapy. In addition, in at least one observational cohort, statin use was associated with significantly decreased mortality in people living with HIV who were on suppressive antiretroviral therapy.
There are controversies, however, regarding the approach to treating cholesterol recommended by the 2013 ACC/AHA cholesterol treatment guidelines. These recommend statin initiation in four major benefit groups:
  • Those with clinical atherosclerotic cardiovascular disease (ASCVD)
  • LDL ≥ 190 mg/dL
  • Diabetes age 40-75
  • Estimated 10-year ASCVD risk ≥ 7.5%
In contrast to the past, the guidelines set no LDL treatment targets and recommend no non-statin therapies. Using the new risk calculator (the PCEs) to estimate 10-year ASCVD risk, the guidelines recommend substantially increased statin treatment in general population -- with 12.8 million additional adults eligible for statin therapy (mostly among older patients without cardiovascular disease).
They also recommend significantly increased statin use in people living with HIV without traditional risk factors for CVD -- despite the fact that people living with HIV have a different typical cholesterol profile and for whom the mechanism of CVD is different. At present, there is not much evidence of efficacy and safety from randomized clinical trials for treating people living with HIV at risk as determined by the new ACC/AHA risk calculator and the guidelines statin intensity definition is not directly applicable in this population.
Nevertheless, Triant believes it is likely that that statins will be effective in the risk groups outlined by guidelines. The question might rather be, "Do they go far enough?" Even using both Framingham and PCE risk calculation, the risk of CVD appears to be underestimated in HIV, and there is a chance that a larger segment of the population living with HIV may benefit from statins. Future research will address some of these gaps.
In the meantime, on the basis of the available guidelines and published data on the use of statins in people living with HIV to date, Triant recommended the following clinical strategy for the management of dyslipidemia in HIV:
  • Check fasting lipids
    • At HIV diagnosis
    • Prior to and within 1-3 months after starting or changing antiretroviral therapy
    • Every 6-12 months
  • Consider starting statins based on ACC/AHA cholesterol guidelines
  • Consider therapy with:
    • Statins, if LDL is above ATP-III (adult treatment panel) goal, or TG (triglyceride) is between 200-500 with elevated non-HDL
    • Fibrates, if TG > 500
  • 2013 HIV primary care guidelines include detailed statin-antiretroviral interaction chart

Management of HIV-specific CVD Risk Factors

In addition, CVD risk in HIV disease may be reduced by targeting HIV-associated inflammation and immune activation using established anti-inflammatory therapies (such as aspirin), antiretroviral therapy or novel immunomodulatory agents, according to Triant.
Aspirin, which is commonly used to reduce CVD from traditional risk, may also have potential reducing CVD in HIV disease, but studies suggest that aspirin is dramatically underused by people living with HIV who meet the traditional CVD-risk criteria. One paper reported that 31% of people living with HIV met the criteria for using aspirin to reduce CVD risk, but only 1.6% were receiving it. A reasonable clinical strategy, however, is that anyone with low bleeding risk who has known CVD or a high predicted CVD risk, should be taking aspirin.
There are also data to show that aspirin can decrease immune activation and platelet activation in people with HIV but whether it should be used more widely to prevent AMI or stroke in people living with HIV who don't meet the usual criteria for CVD is unclear.
"Interventions targeted at HIV-specific inflammation and immune activation may better reflect pathogenesis and reduce CVD," said Triant.Antiretroviral therapy, may help since the most direct intervention would be treating the virus itself. Although the START trial will be the first randomized clinical trial to look at the rates of comorbidities including CVD in patients started on early versus deferred antiretroviral therapy, there has already been a paradigm shift in the role of treatment in relation to CVD risk in HIV.
"The CVD-related benefit from virologic suppression and immune reconstitution achieved by treating HIV are thought to outweigh possible proatherogenic effects of individual medications," said Triant.
This change has been reflected in current HIV treatment guidelines. For instance, in 2010, the IAS-USA HIV treatment guidelines, recommended the initiation of antiretroviral therapy specifically for patients with high cardiovascular risk regardless of CD4 count; and the current DHHS HIV treatment guidelines, recommend antiretroviral therapy for all people living with HIV based upon the "growing awareness that untreated HIV infection or uncontrolled viremia may be associated with the development of many non-AIDS defining diseases, including cardiovascular disease (CVD), kidney disease, liver disease, neurologic complications, and malignancy."
So the clinical strategy is now to treat HIV to reduce inflammation, immune activation, and associated cardiovascular risk, but to consider underlying CVD risk when selecting specific antiretroviral medications that may have varying risk.
However, there appears to be a limit to this strategy as treatment intensification seems to have little or no effect in patients who already have suppressed viral loads. For instance, recent studies have found that when raltegravir (Isentress) was added to suppressive treatment, there was no effect on either flow mediated dilatation (FMD) or markers of viral replication.
Novel interventions, immune-modulators, such as using maraviroc (Selzentry, Celsentri) may be an exception to this rule, by virtue of its activity as a CCR5 antagonist, rather than as an antiretroviral. Recent papers in the literature explore its theoretical role in preventing/delaying atherosclerosis, andone study in mice found that maraviroc reduced the atherosclerotic progression by interfering with inflammatory cell recruitment into plaques suggesting that it could have a potential cardioprotective effect in HIV.
Similarly, Triant believes a number of older immune-modulators may have potential for reducing CVD risk in people living with HIV. These include methotrexate, which has been reported to decrease CVD risk in the general population. A randomized controlled trial is currently underway to assess the effect of low-dose methotrexate on inflammatory markers and endothelial function in HIV-positive patients on suppressive antiretroviral therapy. Meanwhile, current data on other immune modulators has been mixed.

Managing Traditional Risk Factors

The other key strategy for fighting CVD in people living with HIV is to manage traditional CVD risk factors (e.g. smoking, diabetes and hypertension) aggressively.
People living with HIV on suppressive ART may lose more years of life due to smoking than HIV.
Triant's recommended clinical strategy for smoking cessation:
  • Apply guidelines for general population to all HIV smokers:
    • Routine screening integrated into HIV primary care
    • Strong, brief, intensive repeated counseling
    • Pharmacologic interventions (varenicline is safe and effective in HIV)
  • Consider systematic approaches to identify HIV smokers and ensure smoking cessation interventions are applied

Diabetes and Hypertension Management

Additionally, Triant suggests using the follow strategy to monitor and manage diabetes and hypertension:
  • Check fasting glucose or HbA1C (glycated hemoglobin) at HIV diagnosis, 1-3 months after starting or changing treatment regimen, and every 6-12 months thereafter
  • Check HbA1C every 6 months in patients with diabetes
  • Diet and exercise intervention recommended:
    • Shown to decrease HbA1C for HIV patients
  • Check blood pressure annually
  • Follow existing 2014 Hypertension Guidelines for general population
    • No HIV-specific guidelines
  • Consider drug-drug interactions
    • Use of some calcium-channel blockers contraindicated with protease inhibitors

  • Discussion

    Many questions remain regarding the optimal management of CVD risk in people living with HIV, such as whether to use statins more broadly, whether immune-modulators will work and whether CVD prevention strategies should be the same in HIV-infected women and patients in resource-limited settings?
    However, it is clear that clinicians should build CVD risk assessment into their clinical practice, start statins in those who qualify, have a low threshold for diagnostic work-ups in their patients living with HIV, treat HIV and manage traditional CVD risk factors.
    "The intensity and consistency of HIV care provide opportunities to prevent and manage chronic disease complications," Triant concluded.
    Read Part 1 to review the context and pathophysiology of cardiovascular disease in people living with HIV.
    Theo Smart is an HIV activist and medical writer with more than 20 years of experience. You can follow him on Twitter @theosmart.

    Copyright © 2014 Remedy Health Media, LLC. All rights reserved.

    Matters of the HEART {Part One}


    Cardiovascular Complications in Patients Living With HIV


    November 17, 2014
    With the rise of heart disease as one of the leading causes of death globally, clinicians should anticipate a significant impact of cardiovascular disease (CVD) in people living with HIV. However, in the case of HIV disease, "the pathophysiology of CVD is driven in large part by HIV-related immunologic and inflammatory changes, and current CVD prevention paradigms do not reflect this pathophysiology," according to Virginia Triant, M.D., M.P.H., of Massachusetts General Hospital.
    Triant gave a state-of-the-art presentation on cardiovascular complications in people living with HIV at IDWeek 2014 in Philadelphia. This article focuses on what is now known about the context and pathophysiology of cardiovascular disease in people living with HIV -- as the understanding of these complications has evolved considerably in recent years.
    The second article in the series will focus on how healthcare providers can integrate the prevention and management of CVD into HIV chronic care -- addressing both the traditional risk factors of CVD, and other risk factors that might be HIV-specific.

    Context of HIV and CVD

    Aging-associated non-communicable comorbidities such as hypertension, myocardial infarction, peripheral arterial disease and impaired renal function are significantly more prevalent among people living with HIV than HIV-negative people.
    Several large cohort studies have found an increased risk of acute myocardial infarctions (MI) and coronary heart disease (CHD) in people living with HIV. A study that Triant presented at CROI 2014 found an elevated relative risk of major adverse cardiac events (MACE), which included myocardial infarction, stroke, angina and coronary revascularization, in people living with HIV than in HIV-negative people, across gender and age groups. The risk was increased even among those who traditionally would have been considered to be at low risk for heart disease -- which may reflect "the different distribution of CVD risk factors in HIV, with important contributions from non-traditional risk factors reflecting HIV-related immune dysregulation."
    Since the advent of antiretroviral therapy, CVD has become a major cause of mortality in HIV disease --although management practices in recent years may have lowered CVD-related mortality in the D.A.D cohort. Still, it remains the third most frequent non-AIDS-related cause of death amonth HIV-positive women.

    Pathophysiology of HIV and CVD

    Ever since the heightened risk of CVD began to be recognized in people living with HIV, the understanding of its causes has been evolving. A number of the traditional risk factors, such as smoking, which is far more common in people living with HIV than in HIV-negative individuals, played a role. However, these were found to only account for around 10%-25% of the heightened risk in large cohort studies.
    Then much of the blame was placed on antiretroviral therapy, in particular, certain drugs, includingselect protease inhibitors and possibly abacavir (Ziagen). For instance, in the D.A.D. study, which was a prospective cohort study with 33,347 subjects, the relative risk of acute MI was 1.16 per year -- but the increased risk was seen on protease inhibitor-based regimens and not non-nucleoside reverse transcriptase inhibitor-containing regimens.
    But, again, there is a 40%-80% increased risk of acute MI that persists despite accounting for both established CVD risk factors and antiretroviral therapy use.
    Today, "the persistently increased risk is thought to be driven by HIV-specific inflammation and immune activation," said Triant, "and this is supported by extensive data."
    For instance, in the SMART study (comparing continuous antiretroviral therapy versus episodic treatment) there was an increased CVD event rate in the arm given episodic antiretroviral therapy vs. the arm given continuous treatment (P = .05). A subsequent analyses of the SMART study found that, at baseline, markers of inflammation, including high-sensitivity C-reactive protein, IL-6, and d-dimer, all strongly correlated to overall mortality; and that after one month of treatment interruption, and viral replication continued, both IL-6 and d-dimer levels increased.
    In addition, the increased immune activation in people living with HIV appears to be linked with a number of markers of CVD. In the Women's Interagency HIV Study, there was increased immune activation in women living with HIV vs. controls without HIV. Among those living with HIV, having a higher frequency of activated T cells was associated with an increased prevalence of carotid artery lesions -- regardless of age, antiretroviral medications, or viral load.
    One possible mechanism for the chronic immune activation (despite suppressed viral loads) is believed to be the mass bacterial translocation from the gut that occurs over the course of HIV infection. Lipopolysaccharides (LPS) released by these bacteria activate monocytes and macrophages, which, in turn, are associated with increased levels of soluble CD14 -- a biomarker of monocyte activation.
    Recently, an analysis of ACTG 5078, documented that both LPS and sCD14 were elevated in people living with HIV and were associated with the development of subclinical atherosclerosis. This effect was independent of traditional CVD risk factors.
    Another study has found that another monocyte/macrophage activation marker, sCD163, was elevated in men living with chronic HIV infection and low or undetectable viremia when compared to HIV-negative controls -- and was associated with non-calcified coronary plaques and arterial inflammation.
    subsequent study found that relatively young people living with HIV had an increased prevalence of plaque features that are highly vulnerable to acute rupture compared to HIV-negative individuals, which could be the reason for the heightened rates of MI's and sudden cardiac death.
    People living with more advanced HIV disease -- as evidenced by low CD4 cell counts and high viral loads appear to be at higher risk. For instance, an analysis of the HIV Outpatient Study found that people living with HIV with CD4 counts below 500 were at an increased risk of CVD events independently of whether they had other known CVD risk factors or were on antiretroviral therapy. Similarly, another analysis of the Partners HealthCare System cohort, found that having a CD4 count below 200 was independently associated with AMI (acute myocardial infarction). In fact, having a low CD4 count was a more important factor than any individual antiretroviral medication with respect to increased risk of AMI or viral load.
    But even though viral load was not an independent risk factor in the Partner's HealthCare System Cohort, an increased viral load was a predictor of AMI risk. Other studies have found that an increased viral load was linked to ischemic stroke events, and that a detectable viral load (viral load above 50 copies/ml) was associated with increased risk of myocardial infarction.
    Similarly, an analysis of the 82,459 people living with HIV in the Veterans Aging Cohort Study Virtual Cohort from April 1, 2003, through December 31, 2009 found an increased AMI risk in participants with both detectable viral loads and CD4 counts below 200. But even in patients achieving virologic suppression, there was an increased risk of AMI in contrast to people who did not have HIV.
    There seems to be some elevated risk of CVD in people living with HIV regardless of treatment, viral load or immunodeficiency. This has been shown in a study of cardiovascular risk in elite controllers -- people living with HIV who have low viral loads and are immunologically stable without treatment. Despite their status as non-progressors, they have increased carotid intima-media thickness -- a surrogate marker of atherosclerosis -- compared to HIV-negative individuals.
    Therefore, HIV infection, regardless of treatment, CD4 count or viral load, is associated with some degree of immune activation and an increased risk of cardiovascular disease.
    In conclusion, for people living with HIV, the increased risk of cardiovascular disease is multifactorial due to traditional risk factors, HIV-related immune activation and immunodeficiency, and antiretroviral therapy may increase the risk in some ways and decrease it in others. But this complexity is not yet accounted for in how the disease is being prevented or managed.
    Read Part 2 to see how providers can integrate the prevention and management of cardiovascular disease into HIV care.
    Theo Smart is an HIV activist and medical writer with more than 20 years of experience. You can follow him on Twitter @theosmart.

    Copyright © 2014 Remedy Health Media, LLC. All rights reserved.

    Tired of misleading hyperbole!?!



    The End of AIDS Is a Cynical Lie


    November 15, 2014
    We hope to have a vaccine ready for testing in about two years. Yet another terrible disease is about to yield to patience, persistence and outright genius.
    — Margaret Heckler, then secretary of HHS,
    announcing the discovery of HIV on April 23, 1984
    I am not going to be here for the cure. I am not going to see the end of AIDS. And neither will you.
    This isn't news to me. HIV has frustrated researchers for the last 30 years. Countless potential remedies have come along, some snake oil and some not, and my weariness over finding the magic bullet isn't just the result of feeling burned so many times before. I am just practical about science, human behavior and the fact that important HIV treatment and prevention tools are beyond the reach of much of the world's population.

    "What bothers me quite a lot, though, is using the cure for HIV as a carrot at the end of a very long stick."
    What bothers me quite a lot, though, is using the cure for HIV as a carrot at the end of a very long stick. The seemingly imminent "end of AIDS" has become a rallying cry for everything from AIDS Walk pledges to research dollars. And however well-meaning these contentions might be, I find it to be a sad and cynical ploy for donations and engagement.
    In an excellent piece for POZ Magazine ("Selling the End of AIDS"), Benjamin Ryan examines the current infatuation with the end of the epidemic and how various HIV/AIDS community groups and government officials are using cure-scented language as a way to attract donors and bolster public interest. Everyone from New York City officials to the American Foundation for AIDS Research (amfAR) to our national leaders are riding the bandwagon, and it feels shortsighted at best, if not outright manipulative.
    Cure research advocates will be the first to tell you that we are many years away from a practical cure that can be applied to everyone who needs it, much less an effective vaccine. But that isn't stopping those trumpeting "an end to AIDS" from playing fast and loose with epidemiological trends -- or from being deliberately coy about what they really mean.

    When you read the fine print of these claims, ending AIDS doesn't resemble what you're probably imagining. When the Obama administration confidently shares its vision for an "AIDS-free generation" by the year 2020, it's actually envisioning a day when no child is born with HIV. That's an entirely different proposition altogether, and is of little solace to the over two million people worldwide who are infected with HIV each year. Likewise, the ongoing fundraising appeals by amfAR to "be here for the cure" might rake in cash from hopeful donors, but as noted by Ryan in his POZ piece, even its own leadership acknowledges that we don't presently have the tools to achieve a cure.

    The fact that the state of New York has adopted a plan to reverse the trend of new HIV infections is exciting, especially since it includes a renewed push for testing, treatment and the adoption of pre-exposure prophylaxis (PrEP) among those at risk. What an excellent strategy. Too bad officials undercut their own trustworthiness by saying they will "end the AIDS epidemic in New York state." Upon closer inspection, their goal is to reduce the number of new HIV infections below the number of HIV-related deaths. Oh, so that's what the end of AIDS looks like.

    Our public credibility as HIV advocates is constantly at stake. We must tell the truth, whether about modes of transmission, sexual risk behaviors or the importance of treatment. We don't make claims we can't back up. We don't play with the emotions of people who, like me, have labored in the HIV trenches for the last 30 years and want nothing more than for this nightmare to finally come to an end.
    It's a shame that the truth isn't good enough. In the last few years, we have determined that those living with HIV who achieve viral suppression are not transmitting HIV to their partners (known as treatment as prevention, or TasP). We have celebrated the arrival of PrEP and its astounding ability to prevent new infections. But any cleareyed advocate will acknowledge that, as exciting as these developments are, they have a finite audience and their worldwide application is not, for the foreseeable future, practical or even possible.

    Politicians understand the value of making claims of impending victory and its effect on their approval ratings and war chest. We will free Iraq from dictatorship and spread democracy. We will conquer terrorist groups wherever they hide. We will pass legislation on immigration reform and gun control. Until we don't. But hey, it was a great message while it lasted. It should come as no surprise, then, that some of the cavalier promises about an end to HIV are being made by President Obama and New York Governor Andrew M. Cuomo.

    Politics has always been shameless. But you would think that public health officials, not to mention community-based service agencies and research organizations, would show a little more restraint when it comes to misleading hyperbole.

    Once you have announced an impending end to AIDS, it doesn't really leave you anywhere to go, except to backtrack. Shall we wipe World AIDS Day from our calendars in five years? Ten?
    Worse still, the casual observer at risk for HIV, who may only absorb the most prominent messages in the public sphere, might just take "the end of AIDS" to heart -- and behave as if it were true. It was hard enough to modify risk behaviors when HIV was nearly always fatal. Imagine trying that when people think the crisis is over.

    Nothing will prevent dedicated HIV advocates from continuing to work to prevent new infections and help those living with the virus. We have soldiered on through many years of false hopes, setbacks and triumphs. I am committed to a day when there are fewer infections, not more, and people with HIV have access to treatment and live free of stigma.
    Just don't play me for a fool.

    Copyright © 2014 Remedy Health Media, LLC. All rights reserved.

    Tuesday, November 18, 2014

    When Your HIV Regimen Makes You Sick, Speak Up

    Looking back on the last 5 years of my life on HIV Regimen, I wish  I would have spoke up much sooner. I have finally changed my HIV Regimen and I am NO LONGER having the horrible side effects I PUT UP WITH for 5 years, because the DOCTORS kept telling me HOW AWESOME I WAS DOING ON THE MEDICATION I WAS ON AT THE TIME> If the medication you are on is making you sick, causing unpleasant side effects and wrecking your life SPEAK UP AND LET YOUR DOCTOR KNOW!!!! You DO NOT HAVE TO SUFFER to feel better!!!

    I feel so much better since I have changed my HIV Regimen and I HAVE NO SIDE EFFECTS - PRAISE THE LORD!!!!!

    David Moorman


    When Your HIV Regimen Makes You Sick, Speak Up


    November 17, 2014
    David Duran
    David Duran
    When I first began taking antiretroviral medication after being diagnosed, my body just didn't want to cooperate. Unfortunately, what I remember from my first year of being HIV positive was a lot of trial and error, which involved me being sick a lot. I was even hospitalized from one combination that, apparently, I was allergic to.

    My first thoughts were that this was just how my life would be. I was more than disillusioned, and could not imagine taking a pill and not having it negatively affect me. I remember begging my doctor to let me try a one-a-day pill and when he agreed, I sentenced myself to another year of awful side effects because I was too timid to question my doctor. The doctor knew best, right? I just assumed that waking up nauseous each morning and having occasional stomach troubles were side effects I would have to learn to deal with, so I did.

    Being newly diagnosed, I chose not to immerse myself in all the information that was readily available to me. Instead, I became reclusive and almost subservient to my primary care physician when it came to anything related to my diagnosis. If he told me to take a pill while standing on one leg and drinking pineapple juice, I was going to do it. Obviously, such a ridiculous request was never asked of me, but if it had been, I don't doubt I would have run to the store to buy some juice. Instead, what I got were a lot of doctor's orders that were most likely in my best interest, but didn't necessarily guarantee success for me personally. But since I hadn't taken control of my personal health decisions in tandem with my doctor, I allowed myself to live in a state of discomfort.

    Each day that I woke up and ran to the bathroom, I was reminded of how much my HIV diagnosis was taking over my life. It was always on my mind, and each week that went by, I continued to convince myself that this was normal and that I was just going to have to live with it. I mean, at least I wasn't going to die, and if having that statement be true required me to be a little sick each morning, so be it.

    It sounds completely insane to me now, but I, not unlike others who are newly diagnosed, was completely vulnerable and naive. After each doctor's visit, my blood work came back with improvements -- the medication was working, just like the doctor said it would. When I finally mustered up the courage to discuss my morning nausea and diarrhea, the doctor prescribed another medication to help. At that time, this sounded rational, but what wasn't rational was that this additional medication was given to me eight months after starting that new regimen of antiretroviral meds.
    What I know now that I didn't know then was that HIV medication should not keep the patient suffering in silence. Side effects are common, but should subside after the first few months of taking the medication. Long lasting and ever present side effects should be a red flag to stop using that particular medication. That being said, any decision regarding medications should be made with a medical doctor, but unless you know your options, it's very easy to just let others make the decisions for you.

    Nothing is more empowering than knowing everything there is to know about something. When I took the time to learn the science behind what antiretroviral medications were and how they worked once I took them, I felt a lot better about popping a pill into my mouth each day. But I was also very aware that these chemicals might be to blame for my morning sickness. It was then that I really took the time to learn about all the available medications that were out there. Each medication has risks and side effects, and I was perfectly OK with knowing that. I was also ready to decide for myself which medication I wanted to give the opportunity not to make me sick each morning.

    "For almost a year, I woke up each day, sick to my stomach, because I refused to consider for a moment that something just might not be right."

    I remember walking in to see my doctor with the utmost confidence because that was the day that I was going to consult with him about changing things up. I was knowledgeable, I was prepared and I was anxious to get the conversation started. The moment I presented my doctor with the idea of switching, I was immediately questioned as to why. He made his case showing me the lab work and how healthy I was. I almost had a moment of weakness where, again, I felt like the doctor knew best. But luckily, after I explained my long-term side effects and how the additional medication he prescribed wasn't really helping, he agreed and together we made a decision to make the switch.
    My personal experience reflects a pure lack of confidence, as well as knowledge, and a genuine fear to contradict a medical professional. For almost a year, I woke up each day, sick to my stomach, because I refused to consider for a moment that something just might not be right. I didn't want to bother with learning about my options, and I failed to tell my doctor exactly what was happening. In retrospect, being the outspoken person I now am, I can't believe how I caused myself to live the way I did, for such a long period of time in my life. Today, I always walk in to see my doctor with pure confidence and absolutely no fear, and I probably divulge more information than needed, but at least now I feel great each time I walk out of there, knowing that I'm in charge of my body.

    David Duran is a freelance journalist and writer based in Brooklyn, N.Y. You can follow him on Twitter at@theemuki.

    Copyright © 2014 Remedy Health Media, LLC. All rights reserved.