You can definitely gain weight on HIV meds, but it’s not a side effect; it’s simply what we call “return to health.” When you have untreated HIV infection, especially with a high viral load, you’re likely to have trouble gaining or maintaining weight. You could say that when you’re eating, you’re “feeding the virus,” and the ongoing, uncontrolled viral infection results in chronic inflammation, also contributing to weight loss.
When you start meds, you suppress viral replication and shut off the inflammation. You’re now feeding yourself rather than virus, and your weight returns to what it would have been if you were HIV-negative. Some people may not like that, but chronic illness is a lousy way to lose weight.
I’d have to know what you mean by workout supplements—there are so many. Protein and creatine are generally fine.
It means you’re negative. An HIV-negative person has an “undetectable” viral load, because there’s no HIV to detect.
You scared me for a moment, because on my first reading of your question, I thought your boyfriend was 14 years old. I’ve recovered now, having finally noticed and interpreted the “+” sign.
With his undetectable viral load and your being on PrEP, the chances of transmission are infinitesimally small—frankly, it would make medical headlines. You’ve already got both belt and suspenders holding up your pants; you don’t have to glue them to your skin.
(I know it’s politically incorrect of me to talk about sex without condoms. When I say things like this in front of a microphone, there are invariably people in the audience who gasp and then write nasty comments on their evaluation forms.)
Of course, this presumes monogamy…something no one can ever be completely confident of, since it involves trusting your partner. Without condoms, he could bring something else home to you. You also have to trust that he continues to take his medications and maintains an undetectable viral load. But at some point, relationships are about trust. If you trust your partner, you can consider condomless sex. And let’s not call it “unprotected,” because you’re already protected in two very good ways.
It’s probably true that kidney issues are more common in the “real world” than in clinical trials, because real world patients are more likely to be older and to have more comorbidities (other medical conditions) than clinical trial participants, which puts them at greater risk for toxicity. In addition, while kidney problems happen both to people who take tenofovir and people who don’t, you can bet that in the real world, if you’re on tenofovir your kidney problems will be blamed on the drug, whether it’s the cause or not. Kidney toxicity from tenofovir is “uncommon” but it’s certainly not “extremely rare,” which is the reason for the development of tenofovir alafenamide (TAF).
A small decline in bone density occurs when you initiate any new regimen that includes nucleoside analogs. It tends to occur in the first 6 months and then levels off. In a young, healthy person this would be of no clinical consequence, but in an older person who already has osteopenia or osteoporosis, it could be important. The decline in bone density is somewhat more pronounced with tenofovir than with other drugs.
So why is tenofovir preferred? The nice thing about tenofovir is that we can predict and measure toxicity fairly well. Specifically, we can predict what will happen to bone density and we can measure what happens to kidney function, allowing us to change therapy if we see a problem. In contrast, there’s still the question of whether abacavir (a part of Triumeq) increases the risk of heart attack. If it does, there’s no way to measure or predict the effect, other than to avoid the drug in people at the highest risk. In addition, abacavir was less effective than tenofovir in a large randomized trial. Fortunately, that doesn’t appear to be an issue when it’s used with dolutegavir (i.e. Triumeq).
I discussed Triumeq in greater detail on this site a week or two ago.
1. None of the currently recommended regimens, including the singlet-tablet regimen, will cause lipodystrophy.
2. None of the single-table regimens are likely to cause diarrhea. If it does occur, it should be very temporary. You’re unlikely to experience mood swings with any of them except Atripla.
You should not need to take time off to adjust to treatment. A weekend should be sufficient.
I’m agnostic on this question. While I believe that almost everyone with HIV should be on treatment, I’m not sure what to do with elite controllers—people who maintain undetectable viral loads off therapy—provided their CD4 counts are high and stable. You’re almost an elite controller.
The argument in favor of treating is that elite controllers still have measurably higher levels of inflammation and immune activation than HIV-positive people whose viral loads are suppressed on antiretroviral therapy. Reducing those levels is presumably good for you over the long term.
However, I can think of two arguments against treating: First, because you’re at such low risk of developing complications in the short-term, it would be almost impossible to demonstrate that treatment has a clinically meaningful benefit, even in a very large study. Second, there’s the possibility that further suppressing your viral load would cause your immune system to “forget” about HIV, potentially taking away whatever characteristic it is that allows your immune system to keep HIV under such good control. Whether that matters, since you’d be on treatment for the rest of your life anyway, is unclear.
If you decide not to start treatment, you might want to consider joining a study. I understand that an ACTG study is being planned to look at the effects of treating (vs. not treating) elite controllers on immune activation and inflammation.
Yes, you should be shocked. We should all be shocked and dismayed. Treatment is prevention, and could have a major impact on the HIV epidemic, but not if only 28% are suppressed.
In fact, it has not been well established that HIV accelerates the aging process or reduces life expectancy even with treatment. In fact this is a subject of enormous controversy. There are a number of problems with studies that suggest this acceleration in aging. One is the use of inappropriate comparisons. For example, many studies compare data from inner city HIV clinics—which may includes poor minorities, HCV-coinfected people, and injection drug users—with the general population. If the HIV-positive people die earlier, is it really because HIV is making them age faster, or is it because of other factors that have nothing to do with HIV?
An interesting study that does not suffer from this bias is a recent Kaiser study looking at the difference in risk of heart attack between HIV-positive an HIV-negative patients over time (see figure). They found that while historically there had been an increased risk of heart attack in HIV-positive people, that difference has been shrinking over time and has now disappeared. The assumption is that we are using more “heart friendly” drugs to treat HIV infection and that we’re being more aggressive at treating other conditions that could increase the risk. The fact that this study comes from Kaiser means that there’s greater homogeneity than in some of the other comparison studies. In other words, the HIV-positive people are fairly similar to the HIV-negative people from a socioeconomic standpoint—they all have jobs that allow them to enroll in Kaiser for insurance. This homogeneity makes the comparison much more meaningful
There’s no question that people with well controlled HIV infection have somewhat higher levels of inflammation and immune activation than HIV-negative people, but their levels are still just a small fraction of what they would be if their viral loads weren’t suppressed. There’s a lot of discussion and debate about how much this ongoing inflammation and immune activation will affect longevity and quality of life during the aging process, but there’s no evidence at all that it will reduce life expectancy by 10-20 years. In fact, there have been a number of studies from various countries that estimate that the life expectancy of an HIV-positive person with an undetectable viral load and a CD4 count above 500 is approximately the same as that of the general population.
A properly used, intact condom that doesn’t break is virtually 100% effective at preventing HIV transmission.
See continuation below.