Atorvastatin, sold as Lipitor and as many generics, is a statin: a prescription drug that lowers LDL cholesterol (low-density lipoprotein, the main cholesterol-carrying particle linked to clogged arteries) by blocking the liver enzyme HMG-CoA reductase. The FDA first approved it in December 1996, and the first generic atorvastatin approval followed in November 2011 (Drugs@FDA).

It is one of the most studied drugs in cardiology. Large randomized trials showed that atorvastatin lowers the risk of heart attack and stroke, and that 80 mg/day prevents more events than 10 mg/day in people with heart disease. People who use testosterone or anabolic steroids often ask about it because these drugs can lower HDL (“good”) cholesterol and, with oral steroids especially, raise LDL. No trial has tested atorvastatin, or any statin, specifically in anabolic steroid users.

This page summarizes what the FDA label, the major outcome trials and the published research report. It is for education only and is not medical advice.

Property	Detail
Drug class	HMG-CoA reductase inhibitor (statin)
Brands and approval	Lipitor (FDA approval December 1996); generic atorvastatin since November 2011
Route	Oral tablet, once daily, with or without food
Strengths	10, 20, 40 and 80 mg
Labeled adult dose	Start 10–20 mg once daily; range 10–80 mg; 40 mg start if an LDL-C drop over 45% is needed
LDL-C lowering (label)	About 39% at 10 mg to 60% at 80 mg after 6 weeks
Half-life (label)	About 14 h for the parent drug; 20–30 h for total HMG-CoA reductase inhibitory activity
Main metabolism	CYP3A4, plus liver uptake transporters OATP1B1/1B3
US status	Prescription only; not a controlled substance
WADA status	Not listed on the 2026 Prohibited List

What it is

Atorvastatin is a small-molecule drug given as atorvastatin calcium trihydrate. The label lists the formula of the salt as (C₃₃H₃₄FN₂O₅)₂Ca·3H₂O, with a molecular weight of 1209.42. Each tablet is labeled by its content of atorvastatin base: 10, 20, 40 or 80 mg (FDA label).

HMG-CoA reductase is the rate-limiting enzyme of cholesterol synthesis: it converts HMG-CoA to mevalonate, an early building block of cholesterol. When atorvastatin blocks it, liver cells make less cholesterol and respond by putting more LDL receptors on their surface. Those receptors pull LDL particles out of the blood. The label also notes that atorvastatin reduces LDL production and LDL particle number (FDA label).

The liver is both the main site of action and the main site of cholesterol synthesis. According to the label, the dose correlates with LDL lowering better than blood levels of the drug do.

Pharmacokinetics

From the current Lipitor label (FDA label):

Parameter	Value
Time to peak level	1–2 h
Absolute oral bioavailability	About 14% (parent drug); about 30% for total HMG-CoA reductase inhibitory activity
Effect of food	Lowers peak by about 25% and exposure by about 9%; LDL lowering is the same
Evening vs morning dosing	Blood levels about 30% lower in the evening; LDL lowering is the same
Protein binding	98% or more
Volume of distribution	About 381 L
Metabolism	Mainly CYP3A4, to ortho- and para-hydroxylated active metabolites
Share of activity from metabolites	About 70% of circulating inhibitory activity
Elimination half-life	About 14 h (parent); 20–30 h (inhibitory activity)
Excretion	Mainly in bile; under 2% of a dose in urine

The active metabolites keep working longer than the parent drug, and the label allows dosing at any time of day.

Several groups have different exposure:

Older adults (65 and over): peak levels about 40% higher and total exposure about 30% higher than in young adults.
Liver disease: in chronic alcoholic liver disease, peak level and exposure were 4-fold higher with Child-Pugh A disease, and about 16-fold and 11-fold higher with Child-Pugh B disease.
Kidney disease: kidney function does not change blood levels or LDL lowering, so no dose change is needed. Kidney impairment is still a risk factor for muscle injury.

Approved medical use

The label approves atorvastatin for the following uses (FDA label):

To reduce cardiovascular risk in adults with several risk factors for coronary heart disease (CHD) but no CHD yet, in adults with type 2 diabetes and other risk factors, and in adults with established CHD.
To lower LDL-C, together with diet, in adults with primary hyperlipidemia (high blood cholesterol) and in adults and children aged 10 and older with heterozygous familial hypercholesterolemia (HeFH, an inherited cause of very high LDL).
Homozygous familial hypercholesterolemia (HoFH) in adults and children aged 10 and older, with other LDL-lowering treatments.
Primary dysbetalipoproteinemia and hypertriglyceridemia in adults, together with diet.

Population	Labeled dose
Adults	Start 10 or 20 mg once daily; range 10–80 mg once daily
Adults needing an LDL-C reduction over 45%	May start at 40 mg once daily
Children 10 and older with HeFH	Start 10 mg once daily; range 10–20 mg
Children 10 and older with HoFH	Start 10–20 mg once daily; range 10–80 mg

The label advises checking LDL-C as early as 4 weeks after starting and adjusting the dose if needed. A missed dose should be skipped, not doubled.

What the research shows

LDL lowering by dose

In two placebo-controlled dose-response trials in people with high cholesterol, atorvastatin was given once daily for 6 weeks. Pooled results, as adjusted mean percent change from baseline (FDA label):

Dose	n	LDL-C	Total cholesterol	Apo B	Triglycerides	HDL-C
Placebo	21	+4%	+4%	+3%	+10%	−3%
10 mg	22	−39%	−29%	−32%	−19%	+6%
20 mg	20	−43%	−33%	−35%	−26%	+9%
40 mg	21	−50%	−37%	−42%	−29%	+6%
80 mg	23	−60%	−45%	−50%	−37%	+5%

The label says a response appears within 2 weeks, and the maximum response is usually reached within 4 weeks. HDL rose only modestly (5–9%) at any dose.

In three 16-week head-to-head trials, atorvastatin 10 mg lowered LDL-C by 35–37%. That was more than lovastatin 20 mg (−27%), pravastatin 20 mg (−23%) and simvastatin 10 mg (−30%). The label notes that these trials did not compare higher doses of the other statins.

Cardiovascular outcomes

Atorvastatin has been tested in several large outcome trials, both against placebo and as high dose vs lower dose.

Trial	Population (n)	Comparison	Median follow-up	Main result
ASCOT-LLA	Hypertension, at least 3 other risk factors, total cholesterol 6.5 mmol/L or lower (10,305)	10 mg vs placebo	3.3 years	Nonfatal MI or fatal CHD: HR 0.64 (95% CI 0.50–0.83)
CARDS	Type 2 diabetes, no prior cardiovascular disease, LDL-C 4.14 mmol/L or lower (2,838)	10 mg vs placebo	3.9 years	Major cardiovascular events: −37% (95% CI −52 to −17)
PROVE IT-TIMI 22	Recent acute coronary syndrome (4,162)	80 mg vs pravastatin 40 mg	Mean 2 years	Composite endpoint at 2 years: 22.4% vs 26.3%; 16% lower hazard (95% CI 5–26)
TNT	Stable CHD (10,001)	80 mg vs 10 mg	4.9 years	Major cardiovascular events: 8.7% vs 10.9%; HR 0.78 (95% CI 0.69–0.89)
SPARCL	Recent stroke or TIA, no known CHD (4,731)	80 mg vs placebo	4.9 years	Stroke: 11.2% vs 13.1%; adjusted HR 0.84 (95% CI 0.71–0.99)

Sources: Sever et al., Lancet 2003; Colhoun et al., Lancet 2004; Cannon et al., NEJM 2004; LaRosa et al., NEJM 2005; Amarenco et al., NEJM 2006.

Key details:

ASCOT-LLA was stopped after a median 3.3 years instead of the planned 5. Stroke was also reduced (HR 0.73, 95% CI 0.56–0.96). Total deaths were not significantly different (185 vs 212; HR 0.87, 95% CI 0.71–1.06).
CARDS was stopped 2 years early for benefit. Stroke fell by 48%. The 27% fall in deaths just missed statistical significance (p = 0.059). The investigators reported no excess of adverse events with atorvastatin.
PROVE IT-TIMI 22 reached a median LDL-C of 62 mg/dL on atorvastatin 80 mg vs 95 mg/dL on pravastatin 40 mg.
TNT reached a mean LDL-C of 77 mg/dL on 80 mg vs 101 mg/dL on 10 mg. All-cause mortality was not different. Persistent liver enzyme rises were more common on 80 mg (1.2% vs 0.2%).
SPARCL reduced overall stroke and major cardiovascular events, but hemorrhagic strokes were more common on atorvastatin (55 vs 33). Total deaths were similar (216 vs 211). See the hemorrhagic stroke warning below.

The Cholesterol Treatment Trialists’ (CTT) Collaboration pooled 26 statin trials with about 170,000 participants. Each 1.0 mmol/L (about 39 mg/dL) reduction in LDL-C lowered major vascular events by about a fifth (rate ratio 0.78, 95% CI 0.76–0.80) and all-cause mortality by 10% (RR 0.90, 95% CI 0.87–0.93). More intensive regimens gave a further 15% reduction in major vascular events compared with less intensive ones. The analysis found no effect on cancer incidence (RR 1.00) (CTT, Lancet 2010).

Lipid changes with testosterone and anabolic steroids

Atorvastatin is not approved for, and has not been tested in, people taking anabolic-androgenic steroids (AAS). The studies below describe what these hormones do to blood lipids. They are background for why the question comes up, not evidence that a statin helps in this setting.

Study	Design	Androgen exposure	Lipid findings
Whitsel et al., Am J Med 2001	Meta-analysis of 19 studies, 272 hypogonadal men	Testosterone ester injections at replacement doses, about 6 months	Total cholesterol −14 mg/dL, LDL-C −5 mg/dL, HDL-C −4 mg/dL; triglycerides unchanged
Bhasin et al., Am J Physiol 2001	Randomized, 61 young men, natural testosterone suppressed	Testosterone enanthate 25–600 mg/week for 20 weeks	HDL-C change negatively correlated with testosterone level (higher dose, lower HDL)
Kouri et al., Clin J Sport Med 1996	Placebo-controlled crossover, 16 men	Testosterone cypionate 150 → 300 → 600 mg/week over 6 weeks	HDL-C fell 21% after the first 300 mg dose; LDL-C and total cholesterol unchanged
Hartgens et al., Br J Sports Med 2004	Non-blinded study of 19 self-administering athletes; separate randomized trial in 16 bodybuilders	Self-chosen AAS combinations for 8 or 14 weeks; nandrolone decanoate 200 mg/week for 8 weeks in the trial	Self-administered AAS: HDL-C 1.08 to 0.43 mmol/L (≈42 to 17 mg/dL); apo B 0.96 to 1.32 g/L; Lp(a) fell. Nandrolone alone: no change except a fall in Lp(a)
Smit et al., Andrologia 2022 (HAARLEM)	Prospective cohort, 100 men	Self-administered AAS cycle	During use: LDL-C +0.45 mmol/L (≈17 mg/dL), apo B +18.2 mg/dL, HDL-C −0.40 mmol/L (≈15 mg/dL), Lp(a) −37.6%. Back to baseline 3 months after the cycle

The pattern is consistent. Supraphysiological androgens, meaning doses above the body’s normal range, lower HDL-C. Apo B (a count of atherogenic particles) and LDL-C tend to rise, most clearly in cohorts of real-world users. A 2026 narrative review notes that oral androgens in particular are consistently linked to strong HDL suppression and LDL increases, while injectable testosterone and nandrolone at trial doses generally leave LDL-C unchanged (Bond et al., Clin Cardiol 2026). In contrast, testosterone at replacement doses in hypogonadal men produced only small falls in all three cholesterol measures (Whitsel et al., above).

Long-term AAS users also show more coronary atherosclerosis on imaging. In a cross-sectional study of 140 experienced male weightlifters, the 86 long-term AAS users had more coronary plaque volume than nonusers (median 3 vs 0 mL, p = 0.012). Plaque volume rose with cumulative years of use (Baggish et al., Circulation 2017).

What is not known:

No trial of statins in AAS users. The 2026 review states that empirical data on lipid-lowering or blood-pressure drugs specifically in androgen abusers are currently lacking. The authors assume these drugs work as they do in the general population, but no study has shown it (Bond et al., Clin Cardiol 2026).
HDL is not atorvastatin’s target. In the label’s dose-response trials, atorvastatin raised HDL-C by only 5–9%. That is far smaller than the HDL falls reported during AAS use. No study has measured whether atorvastatin changes AAS-related HDL or apo B shifts.
Outcome trials were in older people. The outcome trials above enrolled mostly middle-aged and older patients with established risk. Their results do not directly show benefit or harm in young athletes.

Side effects and risks

Atorvastatin has no boxed warning. The label’s warnings cover muscle injury, liver injury, blood sugar, and hemorrhagic stroke in people with a recent hemorrhagic stroke (FDA label).

Common side effects

In the label’s pooled placebo-controlled database (8,755 on atorvastatin, 7,311 on placebo; median 53 weeks), reactions seen in 2% or more and more often than with placebo included:

Reaction	Placebo	Atorvastatin, any dose
Nasopharyngitis	8.2%	8.3%
Arthralgia (joint pain)	6.5%	6.9%
Diarrhea	6.3%	6.8%
Pain in extremity	5.9%	6.0%
Urinary tract infection	5.6%	5.7%
Dyspepsia	4.3%	4.7%
Myalgia (muscle pain)	3.1%	3.5%
Muscle spasms	3.0%	3.6%

The differences from placebo were small. The most common reasons for stopping that occurred more often than with placebo were myalgia (0.7%), diarrhea (0.5%), nausea (0.4%) and liver enzyme increases (0.4% each for ALT and hepatic enzymes).

Muscle symptoms, myopathy and rhabdomyolysis

The label warns that atorvastatin can cause myopathy (muscle pain, tenderness or weakness with a raised creatine kinase, or CK, a muscle enzyme) and rhabdomyolysis (rapid muscle breakdown that can damage the kidneys). Rare deaths have occurred. Listed risk factors are age 65 or older, uncontrolled hypothyroidism, kidney impairment, interacting drugs (including other lipid-lowering drugs) and higher atorvastatin doses. The label says to stop the drug if CK is markedly raised or myopathy is diagnosed or suspected. It also advises pausing it during acute conditions that raise the risk of kidney failure from rhabdomyolysis, such as sepsis, major surgery, trauma or severe dehydration (FDA label).

Severe CK elevations were rare in the trials. In TNT, CK of 10 times the upper limit of normal or more occurred in 0.3% on 80 mg vs 0.1% on 10 mg. In SPARCL it occurred in 0.1% on 80 mg vs 0.0% on placebo.

The label also lists immune-mediated necrotizing myopathy (IMNM) as a rare reaction. IMNM is an autoimmune muscle disease with weakness and high CK that persists after the statin is stopped, and it may need immunosuppressive treatment.

How often do statins really cause muscle symptoms? Blinded trial data suggest much less often than people report:

CTT muscle meta-analysis (2022). This pooled 19 double-blind placebo-controlled trials (n = 123,940). Muscle pain or weakness was reported by 27.1% on a statin vs 26.6% on placebo (RR 1.03, 95% CI 1.01–1.06). The excess was concentrated in year 1 (RR 1.07) and absent after it. The authors concluded that over 90% of muscle-symptom reports in people on a statin were not caused by the statin. High-intensity regimens, which the authors defined as atorvastatin 40–80 mg or rosuvastatin 20–40 mg, carried a slightly higher risk (RR 1.08 vs 1.03) (CTT, Lancet 2022).
STOMP trial. 420 healthy, statin-naive adults took atorvastatin 80 mg or placebo for 6 months. Average strength and exercise capacity did not change. Myalgia was more frequent on atorvastatin (19 vs 10 participants, p = 0.05), and average CK rose by about 21 U/L, with no value over 10 times normal (Parker et al., Circulation 2013).

No study has measured statin muscle risk in AAS users.

Liver

Liver enzyme rises are the main liver finding. Persistent transaminase elevations (more than 3 times the upper limit of normal, on 2 or more occasions) occurred in 0.7% of trial patients overall. Rates rose with dose: 0.2%, 0.2%, 0.6% and 2.3% at 10, 20, 40 and 80 mg. One trial patient developed jaundice. Enzymes returned to or near baseline after dose reduction, interruption or stopping (FDA label).

Rare fatal and non-fatal liver failure has been reported after marketing. The label:

contraindicates atorvastatin in acute liver failure or decompensated cirrhosis;
notes higher risk with heavy alcohol use or a history of liver disease;
advises considering liver enzyme tests before starting and when clinically indicated.

No study has examined atorvastatin combined with oral 17α-alkylated anabolic steroids, which carry their own liver risks (see Anavar).

Blood sugar and diabetes risk

The label warns that statins, including atorvastatin, can raise HbA1c (a 3-month average of blood sugar) and fasting glucose. In SPARCL, diabetes was reported as an adverse reaction in 6.1% on atorvastatin 80 mg vs 3.8% on placebo (FDA label).

Analysis	Finding
Sattar et al., Lancet 2010: 13 trials, 91,140 people	9% higher risk of new diabetes (OR 1.09, 95% CI 1.02–1.17); 1 extra case per 255 people treated for 4 years
CTT, Lancet Diabetes Endocrinol 2024: low or moderate intensity vs placebo	New diabetes RR 1.10 (95% CI 1.04–1.16)
CTT 2024: high intensity vs placebo	New diabetes RR 1.36 (95% CI 1.25–1.48)
CTT 2024: people without diabetes	Mean HbA1c +0.06% (low/moderate) and +0.08% (high intensity)

In the CTT analysis, about 62% of new diabetes cases occurred in people whose blood sugar markers were already in the top quarter at baseline. The authors concluded that any effect of this small rise in glucose is already counted in the overall cardiovascular benefit seen in the trials.

Hemorrhagic stroke after a recent hemorrhagic stroke

In a post-hoc analysis of SPARCL, hemorrhagic stroke was more common on atorvastatin 80 mg than placebo (2.3% vs 1.4%; HR 1.68, 95% CI 1.09–2.59). Fatal hemorrhagic strokes were similar (17 vs 18). Patients who entered the trial with a hemorrhagic stroke had the highest rate (16% vs 4%). The label advises weighing risk and benefit of 80 mg in people with a recent hemorrhagic stroke (FDA label).

Other reported reactions

Postmarketing reports in the label include pancreatitis, tendon rupture, peripheral neuropathy, interstitial lung disease, severe skin reactions and anaphylaxis. The label also describes rare reports of cognitive impairment, such as memory loss or confusion, with all statins. These were generally nonserious and reversible after stopping, with a median of 3 weeks to resolve. It also lists rare new-onset or worsening myasthenia gravis.

Interactions

Atorvastatin is broken down by CYP3A4 and taken up into the liver by the transporters OATP1B1/1B3. Drugs that block these pathways raise atorvastatin levels and the risk of myopathy. The label gives these limits and measured effects (FDA label):

Co-administered drug	Effect on atorvastatin exposure (AUC ratio)	Label instruction
Cyclosporine	8.69×	Not recommended
Gemfibrozil	1.35× (plus its own myopathy risk)	Not recommended
Tipranavir plus ritonavir	9.36×	Not recommended
Glecaprevir plus pibrentasvir	8.28×	Not recommended
Clarithromycin	4.54×	Do not exceed 20 mg
Itraconazole	3.32×	Do not exceed 20 mg
Saquinavir plus ritonavir, darunavir plus ritonavir, fosamprenavir (with or without ritonavir), elbasvir plus grazoprevir, letermovir	1.9–3.9× across studies	Do not exceed 20 mg
Nelfinavir	1.74×	Do not exceed 40 mg
Grapefruit juice, 240 mL/day	1.37× (up to 2.5× with 750 mL–1.2 L/day)	Avoid over 1.2 L/day
Rifampin	Lower levels if doses are separated	Take at the same time

Other points from the label:

Other antifungals and macrolides. Other azole antifungals, such as ketoconazole, posaconazole and voriconazole, and erythromycin also raise atorvastatin levels. The label advises weighing risk and benefit and watching for muscle symptoms.
Other drugs that add myopathy risk. Fibrates, lipid-lowering doses of niacin (1 g/day or more), colchicine, and ledipasvir plus sofosbuvir have all been linked to myopathy or rhabdomyolysis when combined with atorvastatin.
Effects on other drugs. Atorvastatin 80 mg raised digoxin levels (AUC 1.15×). Atorvastatin 40 mg raised norethindrone and ethinyl estradiol exposure from an oral contraceptive (AUC 1.28× and 1.19×).
Warfarin. Atorvastatin had no clinically significant effect on prothrombin time in people on long-term warfarin.

Non-prescription products marketed for cholesterol can also interact with drugs. For example, berberine inhibits several drug-metabolizing enzymes; see that page for the evidence.

Who should not use it

Acute liver failure or decompensated cirrhosis: contraindicated.
Allergy to atorvastatin or tablet ingredients: contraindicated. Reported reactions include anaphylaxis, angioedema and Stevens-Johnson syndrome.
Pregnancy: the label says to stop when pregnancy is recognized, or to weigh the patient’s ongoing needs, because the drug may cause fetal harm by its mechanism.
Breastfeeding: not recommended during treatment.

Monitoring

The label recommends:

checking LDL-C as early as 4 weeks after starting or changing the dose;
considering liver enzyme tests before starting and when clinically indicated;
telling patients to report unexplained muscle pain, tenderness or weakness promptly, especially with fever or malaise.

The label also says to stop atorvastatin if CK is markedly raised or myopathy is diagnosed or suspected (FDA label).

Legal status

US: prescription-only drug, approved since 1996, with generics since 2011 (Drugs@FDA). It is not a controlled substance.
Sport: statins are not named on the WADA 2026 Prohibited List.

Key takeaways

Dose-dependent LDL lowering. In the label’s dose-response trials, LDL-C fell by about 39% at 10 mg and 60% at 80 mg after 6 weeks.
Proven to cut heart attacks and strokes. ASCOT-LLA, CARDS, PROVE IT, TNT and SPARCL showed fewer cardiovascular events, and 80 mg beat lower-intensity treatment in people with heart disease.
Muscle symptoms are real but mostly overcounted. Blinded trial data suggest that over 90% of muscle complaints on statins are not caused by the drug. Rhabdomyolysis is rare, and its risk rises with dose, age and interacting drugs.
Liver and glucose effects scale with dose. Persistent liver enzyme rises went from 0.2% at 10 mg to 2.3% at 80 mg. High-intensity statins raised new diabetes diagnoses by about 36% in trials.
Interactions matter. CYP3A4 and OATP1B1 inhibitors such as clarithromycin, itraconazole, cyclosporine and some antivirals can raise atorvastatin levels several-fold.
No data in steroid users. Anabolic steroids lower HDL and can raise LDL and apo B, but no trial has tested atorvastatin or any statin in this group.

Sources

Viatris Specialty LLC. Lipitor (atorvastatin calcium) tablets, for oral use: prescribing information. DailyMed setid a60cc18b-0631-4cf0-b021-9f52224ece65, version 8, July 2026. DailyMed.
US Food and Drug Administration. Drugs@FDA: NDA 020702 (Lipitor, original approval December 17, 1996) and ANDA 076477 (atorvastatin calcium, approved November 30, 2011). FDA NDA 020702; FDA ANDA 076477.
Sever PS, Dahlöf B, Poulter NR, et al. Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial–Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. Lancet. 2003;361(9364):1149–1158. PubMed.
Colhoun HM, Betteridge DJ, Durrington PN, et al. Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicentre randomised placebo-controlled trial. Lancet. 2004;364(9435):685–696. PubMed.
Cannon CP, Braunwald E, McCabe CH, et al. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med. 2004;350(15):1495–1504. PubMed.
LaRosa JC, Grundy SM, Waters DD, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352(14):1425–1435. PubMed.
Amarenco P, Bogousslavsky J, Callahan A 3rd, et al. High-dose atorvastatin after stroke or transient ischemic attack. N Engl J Med. 2006;355(6):549–559. PubMed.
Cholesterol Treatment Trialists’ (CTT) Collaboration, Baigent C, Blackwell L, et al. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010;376(9753):1670–1681. PubMed.
Cholesterol Treatment Trialists’ Collaboration. Effect of statin therapy on muscle symptoms: an individual participant data meta-analysis of large-scale, randomised, double-blind trials. Lancet. 2022;400(10355):832–845. PubMed.
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Sattar N, Preiss D, Murray HM, et al. Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. Lancet. 2010;375(9716):735–742. PubMed.
Cholesterol Treatment Trialists’ (CTT) Collaboration. Effects of statin therapy on diagnoses of new-onset diabetes and worsening glycaemia in large-scale randomised blinded statin trials: an individual participant data meta-analysis. Lancet Diabetes Endocrinol. 2024;12(5):306–319. PubMed.
Whitsel EA, Boyko EJ, Matsumoto AM, et al. Intramuscular testosterone esters and plasma lipids in hypogonadal men: a meta-analysis. Am J Med. 2001;111(4):261–269. PubMed.
Bhasin S, Woodhouse L, Casaburi R, et al. Testosterone dose-response relationships in healthy young men. Am J Physiol Endocrinol Metab. 2001;281(6):E1172–E1181. PubMed.
Kouri EM, Pope HG Jr, Oliva PS. Changes in lipoprotein-lipid levels in normal men following administration of increasing doses of testosterone cypionate. Clin J Sport Med. 1996;6(3):152–157. PubMed.
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World Anti-Doping Agency. The 2026 Prohibited List. In effect from January 1, 2026. WADA 2026 Prohibited List.

Atorvastatin (Lipitor)