Can Steroids Cause High Cholesterol?

Both major classes of drugs commonly called “steroids” can shift your cholesterol in unfavorable directions, but they do it differently and to very different degrees. Corticosteroids like prednisone, prescribed for inflammation and autoimmune conditions, tend to push total cholesterol and LDL upward. Anabolic androgenic steroids, used for muscle building or hormone therapy, hit cholesterol harder, often slashing HDL (the protective kind) by more than half while driving LDL sharply higher. The size of the effect, the speed at which it develops, and whether it reverses all depend on which steroid, what dose, and how long you take it.

What Corticosteroids Do to Your Lipid Profile

Corticosteroids like prednisone, prednisolone, hydrocortisone, and dexamethasone are prescribed for a wide range of conditions, from asthma flares to organ transplant maintenance. One of their less-discussed side effects is a measurable change in blood lipids. In one study, even a short course of low-dose corticosteroids raised total cholesterol from about 195 to 219 mg/dL in just one month, along with a jump in HDL cholesterol from 52 to 70 mg/dL.¹ That HDL increase might sound like a good thing, but the total cholesterol rise was closely linked to increases in LDL, and individual responses varied widely. Some people saw dramatic swings; others barely budged.

The type of corticosteroid matters too. A matched comparison of patients with adrenal insufficiency found that those taking prednisolone had significantly higher total cholesterol and LDL cholesterol than those on hydrocortisone, even though triglycerides and HDL did not differ much between the two groups.² This suggests that not all corticosteroids are interchangeable when it comes to cardiovascular side effects. If you are on long-term steroid replacement, the specific drug your doctor chooses can make a meaningful difference to your lipid numbers.

When high doses are used over prolonged periods, the cardiovascular stakes get more serious. Glucocorticoid treatment has been associated with both dyslipidemia and hypertension, a combination that may predispose patients to coronary artery disease.³ This is one reason doctors try to taper corticosteroid doses as quickly as a condition allows, rather than keeping patients on high doses indefinitely.

Why Corticosteroids Raise Cholesterol

Glucocorticoids have complex effects on how your body handles fats. They ramp up the liver’s production of triglyceride-rich particles, but the bigger problem may be on the removal side. Animal research has shown that glucocorticoid treatment impairs the activity of lipoprotein lipase in fat tissue, an enzyme responsible for clearing those triglyceride particles from the bloodstream. The resulting buildup is less about overproduction and more about the body’s inability to clear fats efficiently.⁴ At the same time, glucocorticoids influence the expression of genes tied to fat synthesis, export, and metabolism in the liver, contributing to fat accumulation there.⁵

In conditions like Cushing’s disease, where the body produces too much cortisol on its own, you can see what chronic glucocorticoid excess does to lipids without any pills involved. Patients with active Cushing’s disease frequently develop elevated triglycerides and total cholesterol, and both the severity of their cortisol excess and whether they have impaired blood sugar regulation independently contribute to how bad their lipid profiles get.⁶ The mechanisms are similar to what happens with prescribed glucocorticoids: cortisol drives fat breakdown, floods the liver with free fatty acids, and boosts the production of VLDL particles that eventually become LDL.⁷ Cushing’s syndrome essentially serves as a natural experiment that confirms what the drug studies show.

Anabolic Steroids Hit Cholesterol Much Harder

If corticosteroids nudge cholesterol in a bad direction, anabolic androgenic steroids shove it. The hallmark pattern is a dramatic drop in HDL and a steep rise in LDL. In a study of bodybuilders and powerlifters using androgens, HDL cholesterol fell by about 55% while LDL jumped roughly 61%, and the LDL-to-HDL ratio — a key marker of cardiovascular risk — shot up by around 280%.⁸

Those are group averages. Individual cases can be far more extreme. One well-documented case involved a bodybuilder who used anabolic steroids repeatedly over five years. His HDL cholesterol dropped as low as 0.1–0.2 mmol/L (roughly 4–8 mg/dL, when a healthy level is above 40), while his LDL climbed to 5.8–6.5 mmol/L (about 224–251 mg/dL). That represents a roughly 90% reduction in HDL and a 100% increase in LDL.⁹ A study comparing young male anabolic steroid users to nonusers found median HDL levels of just 19 mg/dL in users versus 44 mg/dL in nonusers, while LDL was 144 mg/dL versus 96 mg/dL.¹⁰

These are not subtle, borderline shifts. An HDL of 19 mg/dL in a young man who is otherwise physically fit is profoundly abnormal. And the damage goes beyond just the numbers on a lab report: that same study found that the cholesterol-clearing ability of HDL particles was significantly diminished in steroid users, and coronary artery disease was already present in some of these young men.

The Enzyme Behind the Anabolic Steroid Effect

The mechanism is quite different from corticosteroids. Anabolic steroids powerfully stimulate an enzyme in the liver called hepatic triglyceride lipase (HTGL). This enzyme breaks down HDL particles, which is why HDL levels plummet so quickly during use.¹¹ It also shifts the production of the protein building blocks that HDL and LDL particles are made from.

The speed of this process is striking. In a study tracking stanozolol (a commonly used oral anabolic steroid), HTGL activity jumped 62% after just the first day of use, climbed to 161% by day two, and reached 230% above baseline by day three. HDL cholesterol, meanwhile, stayed stable for the first two days but then dropped 14% by day three and 39% by day seven.¹² The enzyme revs up first, and HDL follows it downward within days. Testosterone itself has the same effect: in a three-week study of testosterone administration, hepatic lipase activity rose more than 60% above baseline, and HDL dropped significantly across all its subtypes.¹³ Testosterone also made LDL particles smaller and denser, a shift associated with higher cardiovascular risk even when the total LDL number does not change much.

Do Cholesterol Levels Recover After Stopping?

For anabolic steroids, the good news is that cholesterol usually bounces back faster than other hormone-related effects. In one study of former anabolic steroid users, cholesterol profiles normalized within about six months of stopping, even while reproductive hormones like LH and FSH remained suppressed for up to a year in some individuals.¹⁴ The bodybuilder case mentioned earlier also showed recovery: after ten weeks off anabolic steroids, his HDL roughly tripled (from 0.4 to 1.0 mmol/L) and his LDL fell back into the normal range.⁹ The catch is that every time he went back on, his levels cratered again, even worse than before. People who cycle on and off repeatedly are subjecting their arteries to repeated insults, and recovery between cycles does not necessarily undo the cumulative damage to blood vessel walls.

For corticosteroids, the picture is similar in direction but less dramatic in scale. In liver transplant recipients, withdrawing prednisone led to a meaningful drop in average serum cholesterol, from about 223 to 188 mg/dL, and the number of patients with cholesterol above 220 mg/dL dropped from 13 to 4. Meanwhile, a matched control group that stayed on prednisone saw no improvement.¹⁵ Stopping the drug helped, but the underlying condition that requires the drug may not allow stopping, which creates a frustrating clinical trade-off.

Inhaled Versus Oral Corticosteroids

If you use an inhaled corticosteroid for asthma, you might wonder whether the same cholesterol concerns apply. The evidence here is reassuring. Oral corticosteroids have a clear association with elevated total cholesterol and reduced HDL, but for inhaled corticosteroids there are no conclusive studies showing the same cholesterol effects, even at high doses.¹⁶ The reason is straightforward: inhaled steroids deliver the drug directly to the lungs, with relatively little reaching the bloodstream. High-dose inhaled steroids can affect body weight, and weight gain itself can shift cholesterol, but the direct steroid-driven lipid effect seen with oral forms is largely avoided.

This distinction matters practically. If your doctor switches you from an oral burst of prednisone to a daily inhaled steroid for asthma control, the cholesterol trade-off improves substantially. The same logic applies to topical corticosteroid creams and steroid injections into joints: the systemic absorption is much lower than with daily pills, so the lipid effects are negligible in most cases.

How Sex Hormones Shape the Cholesterol Response

Your sex plays a role in how steroid hormones interact with cholesterol, even apart from anabolic steroid misuse. A large genetic analysis found that naturally occurring steroid hormones like DHEAS and progesterone have different relationships with cholesterol in men and women. In men, higher DHEAS was linked to lower total cholesterol, lower LDL, and lower apolipoprotein B. In women, DHEAS was linked to lower total cholesterol as well, but the pattern for other hormones diverged: androstenedione in women was associated with lower triglycerides and lower apolipoprotein A.¹⁷

These sex differences have practical implications for hormone therapy. In transgender and gender-diverse youth, estradiol treatment raised HDL by about 11 mg/dL over six months, while testosterone treatment lowered HDL by about 7 mg/dL over the same period.¹⁸ The testosterone-treated group’s HDL fell to nearly the same baseline level as the estradiol group had started at, which mirrors the general observation that men carry lower HDL than women throughout adult life. This is not a reason to avoid medically supervised hormone therapy, but it does mean lipid monitoring is a reasonable part of follow-up care, especially for people starting testosterone.

Can Diet Help While You Are on Steroids?

For people who need corticosteroids and cannot simply stop them, diet offers some degree of counterbalance. A study of patients on corticosteroid therapy found that following the DASH eating pattern (rich in fruits, vegetables, whole grains, and low-fat dairy, and low in saturated fat and sodium) significantly reduced total cholesterol and fasting blood sugar compared to those who continued eating their usual diet.¹⁹ Diet alone will not fully override the cholesterol-raising effect of a potent steroid, but it can blunt the impact. For someone on long-term prednisone who faces the added insult of steroid-driven appetite increases and weight gain, paying attention to diet becomes doubly important.

For anabolic steroid users, diet modifications are unlikely to make a meaningful dent in the severe HDL suppression those drugs cause. The enzyme-driven destruction of HDL particles is so aggressive that no amount of oatmeal or olive oil will compensate while the drug is active. The most effective intervention there is reducing or stopping the drug.

Steroid Hormones, the Liver, and Long-Term Metabolic Risk

Beyond their direct effects on circulating cholesterol, steroid hormones also reshape how the liver handles fat. Research into prenatal steroid exposure has shown that glucocorticoid signaling can activate a molecular pathway in the liver that ramps up the production of new fatty acids, potentially increasing the risk of fatty liver disease later in life when combined with a high-fat diet.²⁰ While this research is still being extended to clinical populations, it fits with the broader pattern: glucocorticoids make the liver a more efficient fat factory, and that extra fat production feeds into the elevated cholesterol and triglyceride levels seen in patients on these drugs.

Immunosuppressant regimens that include corticosteroids, common after organ transplants, contribute to a cluster of cardiovascular risk factors including dyslipidemia, hypertension, elevated blood sugar, and accelerated atherosclerosis.²¹ For transplant recipients, managing cholesterol is not optional but part of the ongoing care plan. Statins are commonly co-prescribed in this population, and minimizing the corticosteroid dose, or withdrawing it entirely when safe, remains one of the most effective ways to improve the lipid profile.

The situation is a useful reminder that “steroids” is not a single thing. Corticosteroids, anabolic steroids, sex hormones used in transition-related care, and the body’s own steroid hormones all interact with cholesterol, but through different enzymes, different tissues, and with different clinical consequences. Lumping them together leads to confusion that can cause patients to worry about the wrong risks or miss the real ones. A short course of prednisone for a poison ivy rash is not in the same universe as years of underground-lab testosterone at bodybuilding doses, even though both involve “steroids” and both touch cholesterol.