Do Steroids Increase Cholesterol Levels?

Steroids reliably alter cholesterol levels, but the direction of the change depends on which steroid you’re talking about. Anabolic steroids, the kind used for muscle building, push your lipid profile in a distinctly dangerous direction: they crush HDL (the “good” cholesterol) and raise LDL (the “bad” cholesterol). Corticosteroids like prednisone, prescribed for inflammation and autoimmune conditions, shift cholesterol too, but in a pattern that surprises most people. The details matter far more than the yes-or-no answer, because the type of steroid, how it’s taken, and how long you use it all determine how much your cardiovascular risk actually changes.

How Anabolic Steroids Wreck the Lipid Profile

If you use anabolic-androgenic steroids (AAS), the effect on your cholesterol is not subtle. A literature review covering multiple studies found that anabolic steroids lowered HDL levels by a weighted average of about 52%, while raising LDL levels by an average of roughly 36%.¹ Those are large swings. For context, a 52% drop in HDL would take most people from a normal, protective range to a level associated with significantly elevated heart disease risk.

A review of cardiac and metabolic effects in athletes found that AAS abuse could increase LDL by more than 20% and decrease HDL anywhere from 20% to 70%, with these abnormalities appearing within as little as nine weeks of use. The same review estimated that the resulting lipoprotein distortions could raise coronary artery disease risk by three to six times.² The mechanism involves increased activity of hepatic triglyceride lipase, an enzyme in the liver that breaks down HDL particles. When anabolic steroids ramp up this enzyme’s activity, HDL gets cleared from the blood faster than the body can replace it.³

A study looking at bodybuilders who self-administered AAS found that HDL dropped from about 1.08 to 0.43 mmol/L, while apolipoprotein B (a marker carried by LDL particles) rose significantly. Interestingly, total cholesterol and triglycerides didn’t always change much in that particular study, meaning the real damage was hidden inside the ratio between good and bad cholesterol rather than in the headline number your doctor reads off a basic panel.⁴

Not All Anabolic Steroids Are Equal

One of the biggest factors determining how badly an anabolic steroid hits your cholesterol is whether it’s taken orally or injected. Oral steroids that belong to the 17-alpha-alkylated class, like stanozolol (Winstrol), are far more damaging to the lipid profile than injectable testosterone. A study directly comparing the two found that stanozolol reduced HDL by 33% and the HDL2 subfraction by 71%, while raising LDL by 29%. Testosterone injections, by contrast, only lowered HDL by 9% and actually decreased LDL by 16%.⁵

The difference comes down to how the liver handles each compound. Oral 17-alpha-alkylated steroids pass through the liver on first absorption and powerfully stimulate hepatic lipase activity, which accelerates HDL breakdown. Stanozolol boosted hepatic lipase activity by 123% in that same study, while testosterone’s effect was not statistically significant. Injectable testosterone also converts partly to estradiol through aromatization, which helps maintain HDL (more on that below). This is why researchers have noted that injectable testosterone may be preferable in clinical settings where androgen therapy is needed.⁵

Similarly, nandrolone decanoate (Deca-Durabolin), another injectable, showed no significant changes to HDL, total cholesterol, or triglycerides after four and eight weeks of use in one study, reinforcing that the route of administration and specific compound make a real difference.⁴

Corticosteroids Tell a Different Story

When most people hear “steroids and cholesterol,” they picture anabolic steroids. But corticosteroids, the anti-inflammatory drugs like prednisone, prednisolone, and hydrocortisone, affect cholesterol too, and the pattern looks quite different. Where anabolic steroids reliably crush HDL, corticosteroids often raise it.

A study of healthy men given prednisone for two weeks found significant increases in HDL cholesterol (from about 39 to 50 mg/dL) and also in VLDL cholesterol and triglycerides. LDL didn’t change significantly. All values returned to baseline within two weeks of stopping.⁶ Another short-term study found that HDL rose by up to 27% within five days of starting prednisone, with no significant changes to VLDL or LDL.⁷ The HDL increase appears to involve downregulation of cholesteryl ester transfer protein (CETP), a molecule that normally shuttles cholesterol out of HDL particles. When glucocorticoids suppress CETP activity, HDL particles keep their cholesterol and grow larger.⁸

But the short-term picture is misleading if you’re on corticosteroids for months or years. Glucocorticoids also increase fat breakdown in fat tissue and boost the liver’s production of new fats, which contributes to higher triglycerides and VLDL over time.⁹ And the specific corticosteroid matters. Patients with adrenal insufficiency taking prednisolone had significantly higher total cholesterol and LDL than matched patients taking hydrocortisone (total cholesterol roughly 6.0 vs. 5.3 mmol/L, LDL roughly 3.8 vs. 3.1 mmol/L).¹⁰

In rheumatoid arthritis patients, the relationship gets even more tangled. Corticosteroid use was associated with higher lipid levels, but reducing the prednisone dose was associated with drops in both total cholesterol and HDL cholesterol simultaneously, suggesting that the anti-inflammatory benefit of prednisone (which itself lowers cardiovascular risk) may partly offset the drug’s direct lipid effects.¹¹

Why Estrogen Conversion Matters

One underappreciated piece of this puzzle is estrogen. Testosterone naturally converts to estradiol through an enzyme called aromatase, and that estradiol plays a real role in maintaining HDL levels, even in men. When researchers blocked estrogen production in men while keeping testosterone at normal levels, HDL dropped significantly, especially the HDL2 subfraction. Once the blockade was removed, everything returned to baseline within four weeks.¹²

This matters for steroid users because many anabolic steroids, particularly the oral 17-alpha-alkylated ones, don’t convert to estrogen efficiently. That means they suppress HDL both by activating hepatic lipase and by failing to provide the estrogen that would normally help maintain it. Meanwhile, injectable testosterone does aromatize, which partly explains why its HDL-lowering effect is so much milder. The relationship between testosterone, estradiol, and lipids is not straightforward, though. In a study of healthy middle-aged men, free testosterone was a stronger predictor of HDL levels than estradiol in multivariate analysis, while estradiol was the more important predictor of apolipoprotein E levels.¹³ The takeaway is that the balance between these hormones matters more than either one alone.

Do the Cholesterol Changes Reverse When You Stop?

Mostly yes, but not overnight. A case study of a bodybuilder found that HDL and LDL normalized roughly two and a half to four months after stopping anabolic steroids.¹⁴ A larger study tracking former AAS users found that cholesterol profiles generally normalized within six months, though some individuals still had suppressed reproductive hormones for up to a year.¹⁵

However, how long you used steroids affects recovery speed. In a study comparing eight-week and fourteen-week AAS cycles, the fourteen-week users had notably slower recovery of their HDL, apolipoprotein A-I, and apolipoprotein B levels. Six weeks after stopping, neither group had fully returned to baseline.¹⁶ For people cycling on and off anabolic steroids repeatedly, this raises a concern: if you restart before your lipids have fully recovered, you may be spending the majority of your time with a dangerously unfavorable cholesterol profile.

Does the Cholesterol Shift Actually Cause Heart Disease?

Abnormal lipid numbers are a risk factor, not a guarantee, so people sometimes dismiss steroid-related cholesterol changes as temporary and harmless. The evidence suggests otherwise. A study of young male anabolic steroid users used intravascular ultrasound to look directly at their coronary arteries. A quarter of the AAS users had coronary artery plaques in at least two segments, including fibro-lipid and calcium-containing plaques. None of the non-users or sedentary controls had any detectable coronary artery disease.¹⁷ These were young men who should have been decades away from plaque buildup. The HDL dysfunction caused by AAS appears to reduce the body’s ability to pull cholesterol out of artery walls, a process called cholesterol efflux, which may explain why damage accrues faster than the lipid numbers alone would predict.

For corticosteroid users, the cardiovascular picture is murkier. Chronic corticosteroid use raises blood pressure, blood sugar, and body fat in addition to affecting lipids, so untangling which component drives heart disease is difficult. But the lipid changes are part of a larger metabolic package that clearly increases cardiovascular risk with long-term use.

What About Inhaled or Topical Steroids?

If you use an inhaled corticosteroid for asthma or a topical steroid for eczema, the cholesterol effects are minimal to nonexistent. A study of asthmatic patients given high-dose inhaled budesonide (1600 micrograms daily for four weeks) found a slight decrease in total cholesterol and a small increase in HDL. The changes were statistically detectable but clinically minor, and triglycerides didn’t budge.¹⁸ The reason is simply that very little of the drug makes it into systemic circulation. The steroid stays mostly in the lungs or on the skin, so the liver and lipid metabolism see negligible exposure.

Sex Differences in Steroid-Lipid Interactions

Men and women don’t respond identically to steroid hormones when it comes to cholesterol. A genetic analysis using Mendelian randomization found that in men, higher levels of DHEAS (a steroid precursor) correlated with lower total cholesterol, LDL, and apolipoprotein B, and higher progesterone correlated with lower total cholesterol and LDL. In women, the associations were different: higher DHEAS correlated with lower total cholesterol, but higher androstenedione correlated with lower triglycerides and apolipoprotein A. Neither progesterone nor estradiol showed significant lipid associations in women in that particular analysis.¹⁹

Research on transgender hormone therapy also provides a window into these differences. Transgender women receiving estrogen plus antiandrogen therapy saw HDL rise and LDL fall, which looks beneficial on paper, but their triglycerides, blood pressure, and visceral fat also increased, and LDL particle size decreased (smaller, denser LDL particles are more harmful). Transgender men receiving testosterone saw HDL drop and triglycerides rise, mirroring what happens with anabolic steroid use, though total and LDL cholesterol were largely unaffected.²⁰ The picture with sex hormones and lipids is rarely one of pure benefit or pure harm; each hormone reshuffles the deck in its own way.

Stress Hormones and Your Cholesterol

Your body produces its own glucocorticoids, primarily cortisol, and these endogenous steroids influence cholesterol too. A study of undergraduate students found that during exam periods, when cortisol levels were elevated, total cholesterol, HDL, and LDL all rose significantly compared to non-exam periods. There was also a positive correlation between cortisol levels and the total cholesterol-to-HDL ratio, a common cardiac risk marker.²¹ In older adults, endogenous cortisol levels have also been found to correlate with HDL cholesterol, suggesting that glucocorticoids play a role in the normal regulation of lipid levels across the lifespan.²²

This is worth knowing because it means chronic psychological stress could be a stealth contributor to unfavorable cholesterol shifts, operating through the same cortisol pathway that corticosteroid medications exploit at higher doses.

Can Exercise Offset Steroid-Related Lipid Changes?

There’s encouraging evidence on this front, at least for corticosteroids. An animal study found that chronic glucocorticoid administration caused the full dyslipidemia package: higher total cholesterol, LDL, VLDL, and triglycerides, along with lower HDL. Exercise training was effective at preventing the increases in total cholesterol, LDL, VLDL, and triglycerides induced by the glucocorticoid.²³ While animal data doesn’t translate perfectly to humans, it fits with the broader understanding that aerobic exercise improves HDL and lowers triglycerides through mechanisms that work partly independently of whatever else is happening hormonally.

For anabolic steroid users, the irony is that many of them exercise intensely, yet the lipid damage still occurs. Resistance training alone doesn’t seem to protect against the HDL-crushing effects of oral anabolic steroids. The cardiovascular study that found plaques in young steroid users was specifically looking at athletes, people who exercised regularly and still developed early coronary artery disease. Exercise is not a free pass to ignore what anabolic steroids do to your blood lipids.

Newer Selective Androgen Receptor Modulators

SARMs (selective androgen receptor modulators) were developed partly in hopes of getting the muscle-building benefits of anabolic steroids without the side effects. On the cholesterol front, the data so far is not reassuring. A clinical trial of the SARM OPK-88004 found dose-related suppression of apolipoprotein A-I, which is the main protein component of HDL. That suppression tracked closely with HDL declines.²⁴ Apolipoprotein B, the LDL-associated protein, didn’t change significantly, so the pattern may be somewhat milder than traditional oral anabolic steroids. But the HDL-lowering effect suggests that SARMs haven’t fully escaped the lipid problem that has plagued androgens generally. Anyone taking SARMs under the assumption that they’re “safe” alternatives to steroids should know that the cholesterol trade-off appears to persist, at least in the compounds tested so far.

Children on Corticosteroids After Organ Transplant

Pediatric patients offer another angle on how steroids interact with cholesterol. Children who receive kidney transplants are commonly put on corticosteroids as part of their immunosuppression regimen. In a comparison of children on maintenance steroids versus a steroid-minimization protocol, those receiving steroids had higher total cholesterol and LDL early after transplant. But the steroid-minimization group had substantially lower HDL that persisted throughout the first year.²⁵ That’s a counterintuitive finding: reducing steroids didn’t simply improve the lipid profile. It moved some numbers in the right direction and others in the wrong direction, likely because the other immunosuppressive drugs used in place of steroids have their own lipid effects. The lesson for parents and clinicians is that switching away from corticosteroids doesn’t automatically clean up a child’s cholesterol panel; the whole medication package has to be considered together.

A Single Dose Can Move the Needle

Even a single injection of testosterone can affect cholesterol, though briefly. A study found that one dose of testosterone increased total cholesterol by about 15% within two days. The effect was gone by day fifteen. HDL, LDL, and VLDL individually didn’t change significantly at that time point. The mechanism appeared to involve upregulation of the enzyme that helps the liver produce cholesterol.²⁶ This study is a reminder that steroid-lipid interactions begin almost immediately, well before most users would think to get their bloodwork checked. For someone getting a therapeutic testosterone injection and having a cholesterol panel drawn the next morning, the timing alone could give a misleadingly high result.