Do Steroids Raise Cholesterol? 7 Critical Facts on HDL

Data in brief

Three measured numbers set the scale of this question. All three come from men, and two of them come from weight lifters.

What this guide covers

Do steroids raise cholesterol? The direct answer

Yes, but the word cholesterol hides what actually happens. Anabolic androgenic steroids raise LDL cholesterol modestly and lower HDL cholesterol severely, and in the studies where both were tracked the HDL side of the panel moved several times further than the LDL side. In 19 strength athletes who self administered for eight or 14 weeks, HDL fell from 1.08 to 0.43 mmol/L and apolipoprotein B rose from 0.96 to 1.32 g/L, while total cholesterol and triglycerides did not change significantly (PMID 15155420).

That last detail is why the question gets answered badly so often. A man looks at his total cholesterol, sees a normal figure, and concludes that nothing happened. The review of 49 studies covering 1,467 athletes describes the same signature: elevated LDL cholesterol and low HDL cholesterol in otherwise healthy young athletes (PMID 20816133).

Three variables decide the size of it: the route the compound takes, whether the dose is replacement or supraphysiological, and how long it runs. The rest of this page takes them one at a time.

Route and dose: the same hormone, three different panels

The table below is every setting in which this has been measured properly, ordered by how hard the panel was hit. Read the second and sixth rows together: the same molecule at two different doses produced a 9 per cent fall and a 4 mg/dL fall.

None of these studies is a recommendation, and the doses in them are not targets. They are the only controlled numbers that exist for this question.

The ladder, from a replacement dose to a stack

Put the studies on one axis and the pattern is not subtle. The further a protocol sits from replacement, and the more of it arrives by mouth, the less HDL cholesterol survives it.

The two injectable bars come from different laboratories and different men, which is why they disagree by seven points. Both are far from the oral bar above them, and both are far from the 60 per cent seen when athletes chose their own compounds and stacked them.

Why an oral does it: hepatic lipase, measured in order

The enzyme in the middle of this is hepatic lipase, which strips lipid from HDL particles and prefers the large HDL2 particles. Oral stanozolol raised post-heparin hepatic triglyceride lipase activity by 123 per cent in the crossover trial; the injectable arm raised it 25 per cent, which was not significant (PMID 2915439).

A 1987 study settled the order of events. Hepatic triglyceride lipase activity rose before HDL cholesterol fell, which is the signature of cause rather than coincidence (PMID 3657514). The 17-alpha-alkyl group that lets an oral compound survive first pass through the liver is the same feature that puts it in front of that enzyme at a high concentration.

The oestrogen question has also been tested directly, and the answer surprises most people. Fourteen weight lifters received injectable testosterone, an aromatase inhibitor, or both. Testosterone alone cut HDL cholesterol by 16 per cent. Adding the inhibitor made it 20 per cent, took HDL2 down 30 per cent instead of 23, and pushed hepatic lipase up 38 per cent instead of 21 (PMID 8487666). Oestradiol was holding part of the HDL value up, and removing it removed a brake.

TRT and cholesterol is a different question

Men searching for TRT and cholesterol are usually reading numbers collected from cycles, and the two situations do not belong in the same sentence. The pooled analysis of 19 studies in 272 hypogonadal men on intramuscular testosterone esters found post treatment minus pre treatment differences of 14 mg/dL [17 to 11] for total cholesterol, 5 mg/dL [8 to 1] for LDL cholesterol, 4 mg/dL [5 to 2] for HDL cholesterol and 1 mg/dL [6 down to 4 up] for triglycerides (PMID 11566455). Total and LDL cholesterol fell; HDL fell a little as well.

One finding in that analysis runs against intuition: the falls in HDL cholesterol were larger at lower doses of testosterone ester, and they were not explained by dosing frequency, treatment duration, the rise in total testosterone, or aromatisation to oestradiol. The authors say plainly that the aggregate effect of these changes on cardiovascular risk remains unknown.

Since then the largest trial has reported. TRAVERSE randomised 5,246 men aged 45 to 80 with existing or high cardiovascular risk and symptomatic hypogonadism to testosterone gel or placebo for a mean of 21.7 months. A primary cardiovascular event occurred in 7.0 per cent on testosterone and 7.3 per cent on placebo, hazard ratio 0.96 [0.78 to 1.17], meeting the noninferiority criterion (PMID 37326322). That is a statement about replacement doses in that population, and it is not transferable to supraphysiological use.

What comes back, and what the evidence says helps

The honest version of this section is short, because most of what gets recommended has never been tested in this population. The last two rows are there precisely because they are so often stated as fact.

The number is not the whole injury: HDL also stopped working

Everything above measures how much HDL cholesterol is present. A 2019 study measured what the remaining particles could still do. Twenty strength trained steroid users, 20 age matched strength trained non-users and 10 sedentary controls had cholesterol efflux capacity tested with radiolabelled cholesterol, and had their coronary arteries imaged.

This matters for how a result gets read. A man whose HDL cholesterol has partly recovered after a break is not necessarily back to where he started, because the concentration and the function are separate measurements and only one of them appears on a standard report.

Imaging in a larger group points the same way. Among 86 weight lifters, steroid users showed a left ventricular ejection fraction of 52 per cent against 63 in non-users, and higher coronary plaque volume, with lifetime dose tracking plaque burden (PMID 28533317).

Six claims about steroids and cholesterol that do not survive

Each of these is repeated constantly. Each is contradicted by a study named on this page.

Where people go wrong reading this

• Comparing a cycle study to a TRT study. The two literatures use different doses, different routes and different populations, and the numbers are an order of magnitude apart.
• Treating one draw as a trend. Between-draw variation for HDL cholesterol alone is about 11 per cent in people whose health has not changed (PMID 23648634).
• Waiting for symptoms. None of the changes on this page produce symptoms. They are visible only on a panel, which is the argument for having a baseline before anything starts, covered in the baseline guide.
• Reading lipids alone. Pressure and red cell counts move in the same direction in this population, and the combination is what a clinician reads. See the blood pressure page and the red cell markers.
• Assuming SARMs are exempt. An ascending dose trial of LGD-4033 in healthy men recorded dose dependent suppression of HDL cholesterol and triglycerides alongside testosterone suppression (PMID 22459616).

What none of this establishes is an individual risk figure. The pooled analysis of replacement doses says outright that the aggregate effect of the lipid changes on cardiovascular risk remains unknown (PMID 11566455), and that honesty applies with more force to doses nobody has run a trial on.