HIV & the whole body — every system, every visit, monitored.

Here is the single most important fact in this entire article, and it belongs at the top rather than buried at the bottom: if you start antiretroviral therapy with a reasonably intact immune system and stay on it, your life expectancy is now close to that of someone without HIV. In the largest analysis of its kind — 206,891 people across Europe and North America — a 40-year-old woman starting modern treatment after 2015 could expect another 39.0 years of life, and a 40-year-old man another 37.0 years, approaching general-population figures.1 That is the headline. Everything below is the fine print.

The fine print is real, though, and nobody is served by pretending otherwise. The same research that documented near-normal lifespans also documented something else: people living with HIV spend more of those years managing at least one additional chronic condition. Federal treatment guidelines put it at roughly fifteen additional years of life with a major comorbidity compared with people who do not have HIV — narrowing to about ten years for people who started treatment with a CD4 count above 500.2 The lifespan is normal. The healthspan starts asking questions sooner.

This article is the map of those questions. It is organized by body system, because that is how your care actually gets delivered — a lipid panel here, a kidney number there, a bone density scan that somebody forgets to order. Read it once to understand the terrain, then use the monitoring schedule as the thing you print and bring to your next appointment.

Why "system burden" is the right frame — and why it is not a doom frame

For the first fifteen years of the epidemic, HIV medicine was about opportunistic infections. Everything was acute. Then combination therapy arrived, deaths from AIDS-defining illnesses collapsed, and the field discovered a second story underneath the first one: HIV is an inflammatory condition that keeps working on the body even when the virus is undetectable in blood.

The clearest proof came from a trial that was designed to test the opposite idea. The SMART study enrolled 5,472 people across 318 sites in 33 countries to test whether taking breaks from treatment — guided by CD4 count — could reduce the side effects of long-term therapy. Enrollment was halted early in January 2006 because the interruption strategy roughly doubled the risk of disease progression or death, and it increased the hazard of cardiovascular events by about 70%. It also failed at its own goal: stopping and starting did not reduce treatment-associated adverse events.12 The lesson was not just "keep taking your pills." It was that uncontrolled HIV damages the cardiovascular system, and that continuous suppression is itself a whole-body intervention.

Two decades of research since have filled in the mechanism: persistent immune activation and chronic low-grade inflammation, driven partly by damage to the gut immune system that never fully repairs, partly by residual viral products, and partly by co-infections such as cytomegalovirus. Current federal guidelines now devote an entire chapter to immune activation, inflammation, and their cardiovascular and metabolic consequences.2

The curve shifts left — it does not shoot up

The useful mental model is a shift along the x-axis rather than a spike on the y-axis. Take heart disease: guidelines describe roughly a two-fold higher risk of atherosclerotic cardiovascular disease in people living with HIV, with onset approximately ten years younger than in the general population.2 The condition is the same condition. The screening should simply start earlier. Same with bone loss, same with some cancers, same with the cluster of things clinicians file under "frailty."

Where this becomes a genuine problem is when nobody adjusts the schedule. General-population screening guidelines are built around general-population risk curves, and standard cardiovascular risk calculators are known to underestimate risk in people living with HIV.2 If your care follows the default calendar, you can be technically well-monitored and still be looked at ten years too late. Knowing which items on the list move earlier is the practical skill this article is trying to hand you.

Heart and blood vessels — the biggest single opportunity

Cardiovascular disease is now among the leading causes of death among older people living with HIV in the United States, alongside cancer.2 The reasons stack: traditional risk factors are common (smoking rates in particular have historically run higher in this population), chronic inflammation and immune activation accelerate plaque formation, some older antiretrovirals worsened lipids, and — critically — risk calculators built on general populations tend to underestimate what is actually happening in the arteries.2

Then came REPRIEVE, which changed the conversation more than any HIV cardiovascular study before it.

The number-needed-to-treat figures are worth knowing because they are unusually good for a prevention drug: approximately 106 people treated to prevent one major event overall, and about 53 in the low-to-moderate risk group.3 An imaging substudy helped explain why: pitavastatin reduced noncalcified coronary plaque volume by about 7% and reduced plaque progression by roughly a third, suggesting effects beyond LDL-lowering alone.3

How the guidance has moved — and where it sits now

Guidelines followed the evidence quickly. In February 2024, federal HIV guideline panels working with cardiology bodies issued recommendations that for people with HIV aged 40–75 with a 10-year atherosclerotic cardiovascular risk between 5% and under 20%, a moderate-or-higher-intensity statin should be initiated — pitavastatin 4 mg, atorvastatin 20 mg, or rosuvastatin 10 mg. For people below 5% estimated risk the panel expressed a favorable view rather than a firm recommendation, and for people under 40 the data were considered insufficient.4

One currency note, because it matters if you or your clinician go looking: as of the May 2026 update, the federal adult and adolescent antiretroviral guidelines retired their standalone statin section and now defer to the March 2026 multisociety dyslipidemia guideline, which contains its own recommendations specific to people with HIV.2 The substance did not reverse; the document you cite changed. If a clinician tells you "there's no HIV-specific statin guidance," that is out of date.

What to actually ask

• "What is my 10-year cardiovascular risk estimate, and do you adjust it for HIV?" The honest answer is that calculators underestimate in this population.2
• "Given REPRIEVE, should I be on a statin?" If you are 40 or older, this is a legitimate question regardless of your LDL.4
• "Does my statin interact with my antiretrovirals?" This is not a small detail — some statin–antiretroviral combinations require dose limits. Pitavastatin was chosen for REPRIEVE partly for its interaction profile.4
• "Can we address blood pressure and smoking with the same seriousness?" Statins do not replace either.

For a deeper walk through blood pressure targets, lipids, and cardiac symptoms, see HIV & Heart Health.

Kidneys — quiet, measurable, and worth watching closely

Kidney disease in HIV used to mean HIV-associated nephropathy, a distinctive and aggressive condition that mostly affected Black people with advanced, untreated HIV. Effective antiretroviral therapy dramatically reduced it. It has not vanished, but for most people on treatment today the kidney story is quieter and more cumulative: a combination of aging, blood pressure, diabetes, and — for some — medication exposure.

Because kidney decline is silent until it is substantial, the entire strategy is routine numbers. Infectious disease guidance for chronic kidney disease in HIV recommends monitoring creatinine-based estimated glomerular filtration rate (eGFR) at treatment initiation or any regimen change, and at least twice yearly in stable individuals, plus urinalysis or quantitative albuminuria/proteinuria testing at baseline.6 The urine test matters as much as the blood test: albumin in the urine often shows up before eGFR moves.

Tenofovir: which one, and what it does

Tenofovir disoproxil fumarate (TDF) has been one of the workhorses of HIV treatment for two decades, and it carries a small but genuine kidney signal. Typical exposure is associated with a modest decrease in filtration rate, and a minority of people develop proximal tubulopathy — a defect in how the kidney's tubules reabsorb phosphate, glucose, and protein. Tubular problems most often appear within the first three to six months but can emerge after years of use. Cohort analyses have estimated that each additional year of TDF exposure is associated with increased risks of chronic kidney disease, proteinuria, and rapid eGFR decline.6

Tenofovir alafenamide (TAF), the newer prodrug, delivers far lower plasma tenofovir concentrations and has a considerably more favorable kidney and bone profile — which is a large part of why most modern regimens use it. If you have been on TDF for many years and have any kidney or bone concern, "should I switch?" is a fair and specific question.

Practical kidney protection

• Know your two numbers: eGFR and urine albumin-to-creatinine ratio. Ask for both, at least annually, and more often if you are on TDF, a boosted regimen, or have diabetes or hypertension.6
• Blood pressure is kidney treatment. ACE inhibitors and ARBs are the standard first choice when there is protein in the urine, because they protect the kidney beyond their blood-pressure effect.5
• Be careful with NSAIDs. Regular ibuprofen or naproxen on top of an at-risk kidney is a common, avoidable hit.
• Creatinine changes are not always kidney damage. Some antiretrovirals (dolutegravir, bictegravir, cobicistat, rilpivirine) block creatinine secretion in the tubule, nudging the number up without changing true filtration. Your clinician should distinguish the two rather than panic — or dismiss.5

More detail, including what different eGFR ranges mean in practice, is in HIV & Kidney Health.

Bone — the system most often forgotten entirely

Bone is where the "curve shifts left" pattern is most stark and most under-managed. Federal guidelines describe roughly a 1.5-fold higher risk of fragility fracture among people living with HIV and approximately a four-fold higher risk of hip fracture, and note that tenofovir disoproxil fumarate and boosted protease inhibitors are associated with greater bone mineral density loss.2 The drivers are the familiar stack again: inflammation, low vitamin D, low body weight, smoking, alcohol, hypogonadism, corticosteroid use, and specific antiretroviral exposures.

An international expert panel — 34 HIV specialists from 16 countries — laid out the screening approach that most HIV clinicians now work from. Their recommendations were deliberately tiered rather than "scan everybody":

Vitamin D, calcium, and when medication enters the picture

Vitamin D insufficiency is extremely common and easily checked. Adequate vitamin D and calcium intake — through diet where possible — is the foundation, and correcting a documented deficiency is standard before or alongside any bone-specific treatment.7 Weight-bearing and resistance exercise genuinely matters here; it is one of the few interventions that acts on bone, muscle, balance, and cardiovascular risk simultaneously.

When bone density crosses into osteoporosis, or when fracture risk is high enough on assessment, bisphosphonates are the usual first-line pharmacologic treatment and have been studied in people living with HIV. The important practical point is sequencing: get the vitamin D corrected, get the modifiable risks addressed, get the DXA on the calendar at the right age — and if you are a cisgender man who turned 50 and has never had a bone density scan, that is the single most common gap in the list.7

Brain and cognition — real, common, mostly mild, and frequently something else

This section requires unusual care, because the research language here is genuinely contested and has caused real distress to people who read it out of context.

The framework most often quoted comes from a 2007 working group convened by the National Institute of Mental Health and the National Institute of Neurological Disorders and Stroke, published in Neurology and universally known as the Frascati criteria. It defined three research categories under the umbrella term HIV-associated neurocognitive disorders (HAND): asymptomatic neurocognitive impairment (ANI), mild neurocognitive disorder (MND), and HIV-associated dementia (HAD). Classification requires formal neuropsychological testing across at least five cognitive domains, an assessment of daily functioning, and exclusion of other explanations.8

Two things follow from that definition, and both get lost in translation. First, these are research categories, and federal guidelines explicitly note they have not been validated for routine clinical use.2 Second, "asymptomatic neurocognitive impairment" means exactly what it says — a test result, not a symptom. That is why you will see the striking figure that up to about 30% of people on suppressive therapy meet research criteria for HAND, mostly in the asymptomatic category.2 The criteria have been substantively criticized for exactly this reason: applied to people without HIV, the same statistical thresholds can misclassify more than 20% of cognitively healthy individuals as impaired.8

The differential is the whole game

Before anything gets attributed to HIV, guidelines direct clinicians to look for reversible causes — hypothyroidism, low vitamin B12, syphilis, obstructive sleep apnea, and cerebrovascular disease among them.2 Add to that list depression, chronic poor sleep, alcohol, and the sedating medications that accumulate on a long medication list, and you have covered most of what actually produces brain fog in a person whose viral load is undetectable.

Screening tools matter too. The Mini-Mental State Examination, still widely used in general practice, is poorly suited here because it misses the executive dysfunction pattern typical of HIV-associated changes; the Montreal Cognitive Assessment (MoCA) is more sensitive, and guidelines suggest a threshold below the standard cutoff of 26 is likely more appropriate.2 Referral to a neurologist or neuropsychologist is recommended when findings are significant or progressive.2

The practical takeaway: if your thinking feels different, say so out loud at your appointment and ask for the reversible-cause workup by name — thyroid, B12, syphilis serology, a sleep apnea screen, a depression screen, and a medication review. Do not accept "that's just HIV" as the first answer, and do not accept "that's just aging" either. For the fuller version, see Fatigue & Brain Fog.

Liver — fatty liver is now the main event

For twenty years, liver care in HIV meant hepatitis C. That changed twice: first because direct-acting antivirals made hepatitis C curable in eight to twelve weeks for the great majority of people, and second because as coinfection got treated, metabolic liver disease emerged as the dominant remaining problem.

Metabolic dysfunction-associated steatotic liver disease (MASLD — the current name for what was called NAFLD) is substantially more common in people living with HIV than in the general population. A 2025 review in The Lancet HIV summarized the field as MASLD affecting roughly 26–40% of people living with HIV, progressing more rapidly than in people without HIV, with clinically significant fibrosis in about 10–15%.13 Meta-analyses of HIV monoinfection have landed in the same range, pooling fatty liver prevalence around 38% and significant fibrosis around 13%.13

Why higher? The same inflammation story, plus insulin resistance, plus weight gain associated with some modern regimens (see hormones and metabolism), plus a history of older antiretrovirals that were directly toxic to mitochondria, plus alcohol in some cases. The name change to MASLD reflects that this is a metabolic condition, not a moral one.

What monitoring looks like

• Liver enzymes on your regular labs. Federal guidelines include liver enzyme monitoring in routine follow-up, with the interval individualized.2 Normal enzymes do not rule out fibrosis, which is why the next item exists.
• Non-invasive fibrosis scoring. Simple calculated scores such as FIB-4 use routine blood values and age to flag who needs more. Elastography ("FibroScan") is the common next step, and imaging or specialist referral follows from there.13
• Hepatitis screening and vaccination. Hepatitis A and B vaccination, hepatitis B and C screening, and repeat hepatitis C testing where there is ongoing exposure risk are all part of standard primary care guidance for people with HIV.5
• Hepatitis C is curable — including after reinfection. If you have ever tested positive and never been treated, or were treated in the interferon era and told it failed, this is worth reopening. See HIV & Hepatitis C Coinfection.

There is no approved medication specific to MASLD in people living with HIV, and this is an active research area rather than a settled one.13 What has evidence is unglamorous and real: weight reduction where appropriate, physical activity, treating diabetes and lipids, and reducing alcohol.

Gut — where a lot of the inflammation actually starts

The gut is not usually on anybody's HIV monitoring list, and yet it may be the most mechanistically important system in this entire article. In the earliest weeks of HIV infection, the virus massively depletes CD4 cells in gut-associated lymphoid tissue — the largest immune organ in the body. Antiretroviral therapy restores CD4 counts in blood far more completely than it restores the gut immune barrier.

The consequence is a leaky barrier: bacterial products cross from the intestine into circulation in greater quantities than they should, a process called microbial translocation, and the immune system responds with the chronic low-grade activation that shows up downstream as cardiovascular, metabolic, bone, and cognitive risk. Research in people on suppressive therapy has documented intestinal dysbiosis alongside increased microbial translocation and systemic inflammation,15 and studies have found that increased intestinal permeability can persist despite durable viral suppression.15

What this does and does not justify

This is the section where the honest answer is "we know the mechanism better than we know the fix," and where it is easy to be sold something. So, plainly:

• Established: gut immune damage occurs early, is incompletely reversed by treatment, and contributes to persistent inflammation.15
• Established: starting treatment earlier limits the initial damage — one more reason the "treat immediately" standard exists.2
• Under investigation: probiotics, prebiotics, synbiotics, dietary fiber patterns, and fecal microbiota approaches as ways to reduce translocation and inflammation. These are legitimate research directions, not established therapies, and no probiotic product currently has the evidence to be recommended as an anti-inflammatory intervention in HIV.
• Reasonable regardless: a fiber-rich diet, adequate protein, and limiting ultra-processed food and alcohol. These are recommended for cardiovascular and metabolic reasons that stand on their own, whatever the microbiome turns out to explain.

If a supplement is marketed to you specifically as repairing HIV-related gut damage or "lowering inflammation markers," ask what randomized evidence exists in people living with HIV. Right now, the answer is: preliminary.

Lungs — more than pneumonia history

Lung health in HIV has a long shadow — Pneumocystis pneumonia defined the early epidemic, and people who survived severe episodes sometimes carry lasting structural damage. But the current concern is chronic obstructive pulmonary disease (COPD) and emphysema, which occur more often in people living with HIV than would be expected from smoking alone.

Reported COPD prevalence among people living with HIV in high-income countries has ranged from roughly 3% to 38% across studies, with a narrower range in lower- and middle-income settings, and the association with HIV persists after adjusting for smoking.14 Earlier cohort work found that roughly 16–20% of people living with HIV had asthma or COPD, and that poorly controlled HIV was associated with an accelerated rate of lung function decline on the order of 55–75 mL per year.14 The wide prevalence range reflects genuinely different populations and diagnostic methods — the direction of the signal, not a precise number, is the point.

The lung checklist

• Smoking cessation is the highest-value intervention in this entire article. It acts on lung disease, cardiovascular risk, and lung cancer risk at once. Ask specifically about medication support (varenicline, bupropion, nicotine replacement) plus counseling — the combination outperforms willpower.5
• Spirometry if you have symptoms. Chronic cough, sputum, wheeze, or breathlessness on stairs deserves a breathing test, not a shrug. Attributing exertional breathlessness to "deconditioning" is a common miss.14
• Vaccination. Pneumococcal vaccination, annual influenza vaccination, and staying current on COVID-19 vaccination are standard elements of primary care guidance for people with HIV.5
• Lung cancer screening. Low-dose CT screening applies to people living with HIV who meet age and smoking-history criteria — and lung cancer occurs in excess in this population (see below).16
• Post-viral recovery. If breathlessness or exercise intolerance persisted after a COVID-19 illness, say so; it changes the workup and it should not be folded silently into "HIV fatigue."

Cancer — different cancers, earlier screening

AIDS-defining cancers — Kaposi sarcoma, certain non-Hodgkin lymphomas, invasive cervical cancer — fell sharply with effective treatment. What remains, and what now dominates, is a set of non-AIDS-defining cancers that occur in excess. A systematic review and meta-analysis found all twenty infection-related non-AIDS-defining cancers examined, and half of the twenty non-infection-related ones, in excess among people living with HIV. Standardized mortality ratios were highest for anal cancer (124.07), Hodgkin lymphoma (41.03), liver cancer (8.36), and lung cancer and melanoma (each 3.95).16

Those ratios look frightening in isolation and need context: anal cancer remains an uncommon cancer in absolute terms, and the very large ratio reflects how rare it is in the general population. The correct response is not fear — it is screening that is actually offered.

Anal cancer: the ANCHOR trial settled a twenty-year argument

Human papillomavirus (HPV) causes the overwhelming majority of anal cancers, and anal HPV is markedly more common among people living with HIV. A landmark meta-analysis found pooled anal HPV-16 prevalence of 35.4% (95% CI 32.9–37.9) among HIV-positive men who have sex with men versus 12.5% (9.8–15.4) among HIV-negative men who have sex with men, with high-grade anal intraepithelial neoplasia in 29.1% versus 21.5% and substantially higher annual incidence of high-grade lesions.10

For years, clinicians knew how to find high-grade squamous intraepithelial lesions (HSIL) — the precancerous change — but had no randomized proof that treating them prevented cancer. So screening was inconsistent, and in many places nonexistent. ANCHOR answered the question directly.

Consensus screening guidance followed. The International Anal Neoplasia Society's 2024 consensus recommends initiating screening at age 35 for men who have sex with men and transgender women living with HIV, with annual cytology and an extended 12–24-month interval where capacity is limited.10 Federal opportunistic infection guidelines recommend screening for and treating anal HSIL, and some state guidance extends screening to all people with HIV aged 35 and older, with cisgender women screened from age 45.10 The real-world barrier is capacity: high-resolution anoscopy requires trained clinicians and there are not enough of them, which is exactly why asking early and asking for a referral matters.

The rest of the cancer checklist

• HPV vaccination. Recommended per age-based national guidance; it prevents the infections that cause anal, cervical, and oropharyngeal cancers. Vaccination does not replace screening if you have already been exposed.5
• Cervical cancer screening follows HIV-specific schedules that are more frequent than general-population intervals — confirm which schedule you are on.5
• Liver cancer surveillance if you have cirrhosis or chronic hepatitis B — typically ultrasound-based, at defined intervals.5
• Colorectal, breast, and prostate screening follow general-population guidance; the point is simply that they happen. Specialty HIV care sometimes crowds out ordinary primary care.5
• Skin checks. Melanoma appears in the excess list; in Florida, with year-round sun exposure, this is a low-effort addition to an annual visit.16

Hormones and metabolism — including the weight conversation

Metabolic health in HIV has a complicated history, and it helps to separate the eras. The late 1990s and 2000s brought lipodystrophy: lipoatrophy (fat loss in face, limbs, and buttocks) driven largely by older nucleoside analogues, and lipohypertrophy (fat accumulation in the abdomen, upper back, and breasts). Those specific drugs are gone from first-line regimens, but people who took them may still be living with body changes and with the stigma attached to a body that visibly announced a diagnosis.

Today's conversation is different: weight gain associated with modern, otherwise excellent regimens. The clearest evidence came from ADVANCE, a randomized trial of 1,053 treatment-naive adults in South Africa comparing dolutegravir with tenofovir alafenamide, dolutegravir with tenofovir disoproxil fumarate, and a standard efavirenz-based regimen.11

Gains were greater in women, and at 48 weeks had not plateaued; by the four-year analysis the trajectory had slowed after roughly week 96, and no dolutegravir resistance emerged.11 Federal guidelines now address weight gain on treated HIV as its own topic.2

Two things need saying about this at once. First, it is real, and if you gained substantial weight after a regimen switch, you were not imagining it and you were not simply eating more. Second, the regimens in question are among the most effective and best-tolerated ever developed, and integrase inhibitors remain first-line for good reasons. The honest framing is a tradeoff to monitor and discuss — weight, waist, blood pressure, lipids, and glucose tracked deliberately after any switch — not a reason to abandon an effective regimen on your own.

Glucose, thyroid, and sex hormones

• Diabetes and insulin resistance. Glucose and metabolic panel monitoring are part of routine follow-up in federal guidelines, with intervals individualized, and diabetes screening is included in HIV primary care guidance.25 Given the weight and lipid picture above, this is one to ask about specifically after a regimen change.
• Thyroid. Worth testing when there is unexplained fatigue, weight change, or cognitive fog — hypothyroidism is on the guideline list of reversible causes of cognitive symptoms.2
• Testosterone and estradiol. Low libido, fatigue, mood change, erectile difficulty, and bone loss can all connect to hormone levels, and hypogonadism is a recognized contributor to low bone density.7 Bring symptoms up rather than waiting to be asked.
• Gender-affirming hormone therapy. If you are taking it, it belongs in the same interaction review as everything else — and it is fully compatible with HIV treatment when checked properly.17
• Menopause. Overlapping symptoms — sleep disruption, mood change, cognitive fog, bone loss — make this a place where "it's the HIV" gets said too easily. Ask for the menopause conversation on its own terms.5

Mental health — not a separate department

Depression is roughly two to three times more common among people living with HIV than in the general population, and the treatment cascade is poor: less than half of cases are recognized, a minority are treated, and a small fraction receive adequate treatment and reach remission.18 The CDC's Medical Monitoring Project found that 27% of US adults receiving HIV care had diagnosed depression.18 Federal guidelines project that by 2030 roughly 64% of people with HIV in the US will have at least one mental health comorbidity.2

This is not a soft add-on to a physical-health article. Untreated depression tracks with worse outcomes across the systems described above, and a meta-analysis found that people without depression were significantly more likely to be virally suppressed (odds ratio 1.30; 95% CI 1.15–1.48).18 Sticking with daily medication for decades is a psychological task as much as a pharmacological one, and it gets harder when you are depressed, isolated, unhoused, or carrying trauma.

There is also a shared biology worth naming, because it dismantles the "just mental" framing. The same chronic inflammation implicated in cardiovascular, metabolic, and cognitive changes is increasingly understood as relevant to depression. Guidelines now treat immune activation and inflammation as a cross-cutting feature of treated HIV rather than a cardiology footnote.2

What integrated care should look like

• Routine screening, not crisis response. Brief depression and anxiety screening at regular intervals is part of HIV primary care guidance — and it should be repeated, not done once at diagnosis.5
• Trauma-informed care. Rates of post-traumatic stress and of lifetime violence exposure are elevated in this population; a clinician who asks about it gently and without judgment is doing medicine, not overreach.5
• Interaction-checked prescribing. Several antidepressants and antipsychotics interact with antiretrovirals through shared liver enzymes. This is manageable and routine — but it must be checked.17
• Substance use as health care. Alcohol and stimulant use affect liver, heart, cognition, and sleep. Naming it accurately gets you help; hiding it removes options.5
• Isolation is a clinical problem. Peer support and long-term survivor groups are not decoration; for many people they are the intervention that makes the rest of it sustainable.22

Our fuller treatment of this is at Mental Health & HIV.

Polypharmacy — the risk that grows out of good care

Here is the paradox of everything above: follow the guidance faithfully and you may end up on eight or more medications. Antiretrovirals, a statin, a blood pressure agent, something for diabetes, an antidepressant, a proton pump inhibitor, a PDE-5 inhibitor, hormone therapy, vitamin D, calcium, and whatever supplements were recommended by someone who is not your prescriber. Each was reasonable on its own. The list as a whole is now its own risk factor.

The numbers are consistent across cohorts. In the POPPY study, polypharmacy was present in 65.8% of people living with HIV aged 50 and older, versus 48.1% of those under 50 and 13.2% of HIV-negative controls aged 50 and older; at least one potential drug–drug interaction involving non-antiretroviral medications was found in 36.1%, 20.3%, and 16.4% respectively.19 In the Swiss HIV Cohort Study, polypharmacy defined as five or more non-HIV medications was present in 44% of people aged 65 and older versus 12% of younger participants, with potentially inappropriate medications identified in 31% of older participants.19 Federal guidelines cite Swiss data in which, among people aged 75 and older, 66% had polypharmacy and 67% had at least one potentially inappropriate prescription.2

The deprescribing conversation

Ask once a year: "Can we review everything I take and see whether anything can come off?" Good candidates for review include acid-suppressing medications started years ago for a reason nobody remembers (some genuinely interfere with antiretroviral absorption), sedatives and sleep aids, anticholinergic medications that worsen cognition and falls, duplicate therapies from different specialists, and supplements — calcium, magnesium, iron, and multivitamins containing polyvalent cations can bind certain integrase inhibitors and reduce their absorption if taken at the same time.17

Two practical habits: keep one written list — paper or phone — that includes over-the-counter products, supplements, and anything prescribed by a specialist, and use one pharmacy where possible so somebody besides you can see the whole picture.5

The monitoring schedule — print this and bring it

Questions to bring to your next appointment

Appointments are short. These are ordered so that if you only get through the first five, you have covered the highest-value ground.

1. "Which items on the standard monitoring list am I currently behind on?" This one question does more than any other. It reframes the visit from symptoms to systems.
2. "Given REPRIEVE, should I be on a statin — and does it interact with my regimen?" Ask if you are 40 or older, whatever your cholesterol says.34
3. "What are my eGFR and urine albumin-to-creatinine ratio, and are they trending?" A single value tells you much less than a direction.6
4. "Have I ever had a bone density scan, and should I have one now?" Especially if you are a man over 50, postmenopausal, or have been on TDF long-term.7
5. "Can we review every medication and supplement I take for interactions and for anything that could come off?" Bring the written list.17
6. "Is anal cancer screening available here, and if not, who can you refer me to?" Ask from age 35.10
7. "My thinking feels different — can we rule out thyroid, B12, syphilis, sleep apnea, depression, and my medications?" Name the workup so it happens.2
8. "Should I be screened for fatty liver, and what is my FIB-4?" Particularly with weight gain, diabetes, or a hepatitis history.13
9. "I've gained weight since switching regimens — what are the options?" This is a legitimate clinical issue with real data behind it.11
10. "Am I current on every vaccine recommended for people living with HIV?" Ask for the full list, not just the flu shot.5
11. "Who is my primary care clinician, and who is coordinating between specialists?" With a growing list of systems, the coordination question becomes the most important one.5
12. "What would you monitor differently if I were ten years older?" A useful way to surface the earlier-onset pattern without a debate about it.2

Florida — an aging epidemic and the system built to carry it

Florida is one of the clearest places in the country to see why this article exists. At the end of 2023, there were 128,387 adults living with HIV in Florida — and 72,873 of them, roughly 56%, were aged 50 or older. Another 18% were aged 40–49. Twenty percent of the 4,719 new adult HIV diagnoses in Florida that year were in people aged 50 and above.20

Read those numbers next to everything above and the implication is direct: the majority of Floridians living with HIV are in exactly the age band where cardiovascular screening, bone density, anal cancer screening, cognitive workups, and medication review stop being optional. And a fifth of new diagnoses arrive in people who need the whole comorbidity conversation from day one, not in a decade.

Nationally, the Ryan White HIV/AIDS Program — the safety net that serves a large share of people in HIV care in Florida — reports the same demographic shift. In its 2024 client-level data, 47.4% of clients were aged 50 or older and 13.4% were 65 or older, up from 9.5% in 2020. Among clients aged 50 and above, retention in care was 81.1% and viral suppression 92.9%, and 59.2% were living at or below the federal poverty level.21

One Florida-specific practicality worth naming: seasonal and interstate movement. If you split the year between Florida and another state, ask explicitly how your labs, imaging, and screening records travel — a bone scan or an anoscopy that happened in another state's system is easy to lose, and repeating it is a waste of your time and someone's money.

Where to start — this week, this year

Nothing in this article requires you to become your own physician. It asks something smaller: that you know which systems are on the list, and that you ask about them out loud.

This week

• Write your full medication list. Everything, including over-the-counter products and supplements. Put it in your phone.
• Print the monitoring table. Mark the rows you know you have done in the past year.
• Run your list through the Liverpool Interaction Checker. Bring anything it flags to your clinician rather than acting on it alone.17
• Ask for your last lab results in writing. Your eGFR, urine protein, lipids, liver enzymes, and A1c belong to you.

This year

• Have the statin conversation if you are 40 or older.4
• Get the bone question answered — fracture risk assessment or a DXA scan, whichever fits your age and risk.7
• Ask about anal cancer screening if you are 35 or older, and ask for a referral if it is not offered locally.10
• Book the ordinary screenings — colorectal, cervical, breast, prostate, skin, dental, eyes. Living long means using general-population medicine too.5
• Take the mental health item as seriously as the lipid panel. It affects every other outcome here.18
• Do one deprescribing review. Ask what could come off, not only what should go on.19