Cholesterol on Steroids: Which Compounds Destroy HDL the Most?

Your HDL just came back at 18 mg/dL. You are six weeks into a cycle that includes an oral compound, and your lipid panel looks like it belongs to someone twice your age with a pack-a-day habit. The question is no longer whether steroids wreck your cholesterol. It is how badly, which compounds are the worst offenders, and what you can actually do about it.

Cardiovascular disease is the leading long-term health risk for steroid users, and lipid destruction is the primary driver. Yet most "cholesterol on steroids" content online either lists vague warnings without data or pushes supplements without evidence. This article takes a different approach: compound-by-compound rankings backed by clinical studies, specific lab value thresholds for decision-making, and a tiered management protocol based on what the research actually supports.

How steroids wreck your lipid profile

The damage is a two-front assault: HDL crashes while LDL climbs. Across the clinical literature, 17-alpha-alkylated oral AAS suppress the cardioprotective HDL2 subfraction by an average of 52%, with total HDL dropping as much as 78% in severe cases (Glazer, 1991). LDL rises an average of 36%. Documented cases in otherwise healthy bodybuilders include HDL as low as 14 mg/dL and LDL as high as 596 mg/dL, producing a three- to sixfold increase in estimated coronary artery disease risk (Achar et al., 2010).

To understand why this happens, you need to know about one enzyme: hepatic triglyceride lipase (HTGL).

The hepatic lipase mechanism

HTGL breaks down large, protective HDL2 particles into smaller, less useful HDL3 particles, accelerating their clearance from your blood. Oral steroids massively upregulate this enzyme. In a controlled study with stanozolol, HTGL activity spiked 62% on day one, 161% on day two, and 230% by day three, days before HDL even started dropping (Applebaum-Bowden et al., 1987). The enzyme surge drives the HDL collapse, not the other way around.

At just 6 mg/day of stanozolol, HDL fell from 59 to 29 mg/dL (a 51% reduction) while HTGL activity tripled. Both apolipoprotein A-I and A-II showed shortened plasma residence times, confirming the enzyme was actively clearing HDL particles from circulation (Haffner et al., 1983).

Why orals are worse than injectables

The difference is not subtle. In the landmark JAMA crossover trial, stanozolol (oral, 6 mg/day) reduced HDL by 33%, HDL2 by 71%, and raised LDL by 29%, with a 123% spike in HTGL activity. Testosterone enanthate (injectable, 200 mg/week) in the same subjects reduced HDL by only 9%, actually decreased LDL by 16%, and produced no statistically significant change in HTGL (Thompson et al., 1989).

The reason is first-pass metabolism. Oral 17-alpha-alkylated steroids resist liver breakdown, so they arrive at hepatocytes in full concentration, flooding the liver and triggering a massive HTGL response. Injectable esters absorb into the bloodstream first and reach the liver diluted, producing far less enzymatic stimulation.

This matters for practical cycle design. Every time you add an oral "kickstart" or cutting agent to an injectable base, you are not just adding another compound. You are introducing the class of drug most destructive to your lipids.

The aromatization factor: why crashing E2 makes it worse

Here is a counterintuitive finding: the estrogen that bodybuilders try to eliminate is actively protecting their cardiovascular system.

Estradiol directly suppresses hepatic lipase gene transcription through the estrogen receptor-alpha. In molecular studies, E2 reduced hepatic lipase gene expression by up to 50% (Jones et al., 2002). When you remove estradiol with an aromatase inhibitor, that brake on HTGL disappears entirely.

The data confirms this. In a controlled trial, adding an aromatase inhibitor to testosterone worsened HTGL elevation from 21% to 38% and deepened HDL suppression from 16% to 20%, compared to testosterone alone. Without the AI, estradiol rose 47%, partially protecting lipids (Zmuda et al., 1993).

The practical message: if you are running orals or high-dose injectables, aggressively crashing E2 with anastrozole or letrozole does not offset lipid damage. It compounds it. Manage estrogen sides with the minimum effective AI dose, not by driving E2 to the floor. For more on this balance, see our estradiol management guide.

Compound-by-compound HDL impact rankings

Not all steroids hit your lipids equally. The ranking below is based on available clinical data. Where controlled human studies exist, we cite specific percentage changes. Where they do not, placement is based on pharmacological class (17-alpha-alkylated oral vs. injectable ester) and documented case reports.

Tier 1: Severe HDL suppression

These compounds produce the fastest and most dramatic lipid destruction.

Stanozolol (Winstrol) is the most thoroughly documented lipid destroyer. In a controlled trial at just 6 mg/day: HDL -33%, HDL2 -71%, LDL +29%, HTGL +123% (Thompson et al., 1989). At higher bodybuilding doses, expect worse. Case reports document HDL values in the single digits.

Superdrol (Methyldrostanolone) has no controlled human lipid isolation studies, but its 17-alpha-alkylated structure, extreme androgenic potency, and case reports of catastrophic combined lipid panels place it firmly in Tier 1. Its hepatotoxicity is among the worst of any oral, and liver enzyme elevation typically accompanies severe lipid disruption.

Halotestin (Fluoxymesterone) shares the same structural class as stanozolol and superdrol. No dedicated lipid RCTs exist, but its extreme hepatotoxicity and potent androgenicity place it alongside the worst offenders.

Tier 2: Significant HDL suppression

These compounds substantially impair lipids, though generally less rapidly than Tier 1.

Oxymetholone (Anadrol) is a 17-alpha-alkylated oral with documented dramatic lipid worsening. Bodybuilder case reports show HDL values below 20 mg/dL during use (Achar et al., 2010).

Methandrostenolone (Dianabol) is another 17-alpha-alkylated oral. While it aromatizes heavily, which provides some estrogen-mediated lipid protection, the first-pass hepatic effect on HTGL overwhelms any benefit from estradiol production.

Trenbolone has no controlled human lipid isolation studies. Its 5x androgenic potency relative to testosterone, combined with non-aromatizing properties (no estrogen-mediated lipid protection), makes significant HDL suppression expected. Human case reports in polydrug users consistently show HDL in the single digits during trenbolone-containing cycles.

Tier 3: Moderate HDL suppression

Testosterone at 200 mg/week shows only a 9% HDL reduction in controlled data (Thompson et al., 1989). Aromatization to estradiol provides partial lipid protection. At supraphysiological bodybuilding doses (500+ mg/week), the impact increases but remains milder than oral compounds.

Nandrolone (Deca/NPP) is dose-dependent and variable. At 200 mg/week, one RCT found no statistically significant HDL change (Hartgens et al., 2004). At 100 mg/week in a different study, HDL fell 25-27% (Kuipers et al., 1991). At 300-600 mg/week in HIV patients, decreases of 8.7-10.6 mg/dL were observed (Sattler et al., 2002). Generally considered among the more cardiovascular-friendly injectables.

Boldenone (Equipoise) is injectable and non-17-alpha-alkylated, with an expected moderate lipid impact based on its androgenic profile. Limited controlled human data exists.

Tier 4: Mild HDL suppression

Primobolan (Methenolone) is often cited as the mildest AAS for lipids. The injectable form avoids first-pass hepatic effects. Oral primobolan exists but is rarely used at doses high enough to cause severe lipid disruption.

Oxandrolone (Anavar) has a reputation as "mild," but it does meaningfully suppress HDL. At cessation of 24 mg/day cycles, users showed HDL values of 24 mg/dL. Recovery was relatively fast, reaching 49 mg/dL by three months post-cycle. It is milder than stanozolol or superdrol but not lipid-neutral.

Masteron (Drostanolone) is injectable and non-17-alpha-alkylated. It does not aromatize, removing estrogen's protective effect, but avoids first-pass hepatic HTGL stimulation. Expected moderate impact based on class.

The ranking table

The oral vs. injectable divide matters more than the specific compound name. Any 17-alpha-alkylated oral will cause more HDL destruction than almost any injectable at comparable doses.

Beyond HDL numbers: cholesterol efflux and why your labs understate the damage

Here is the part that should concern you most. Standard lipid panels measure HDL quantity, the number of particles floating in your blood. But what actually prevents plaque buildup is HDL function: specifically, its ability to pull cholesterol out of artery walls through a process called cholesterol efflux.

A landmark 2014 study in the New England Journal of Medicine found that HDL-C quantity showed no association with cardiovascular events in adjusted analysis. But the highest quartile of cholesterol efflux capacity showed a 67% reduction in cardiovascular risk versus the lowest quartile (Rohatgi et al., 2014). The number on your lab report is not the number that determines plaque risk.

What the research shows in AAS users

De Souza et al. (2019) measured actual cholesterol efflux capacity in young male AAS users and found it was 20% versus 23% in strength-trained non-users and 24% in sedentary controls. That functional deficit existed even when HDL-C levels looked borderline acceptable (de Souza et al., 2019).

The same study found that 25% of AAS users had plaques in at least two coronary arteries. Zero percent of controls, both strength-trained lifters and sedentary men, had any plaques. These were young men whose standard lab panels might not have raised red flags.

The protein that drives efflux is apolipoprotein A-I (ApoA-I). Stanozolol cuts ApoA-I by 40% in six weeks. In polydrug stacks, ApoA-I dropped from 1.41 to 0.71 g/L, a 50% reduction (Hartgens et al., 2004). Without ApoA-I, HDL quantity is essentially irrelevant, because the particles cannot do their job.

What this means practically: a testosterone-only user with an HDL of 38 mg/dL is in a fundamentally different cardiovascular position than someone running stanozolol with the same HDL value. The testosterone user's HDL is still relatively functional. The stanozolol user's HDL is stripped of the protein it needs to protect artery walls.

How long do lipids take to recover?

The good news: lipid damage from AAS is generally reversible. The timeline depends on what you were running and for how long.

Testosterone only (near-therapeutic doses)

HDL largely normalizes within 4 weeks of stopping. In a controlled study of 200 mg/week testosterone enanthate for 20 weeks, HDL-C fell 13% during use and returned to baseline range within one month of cessation (Bagatell et al., 1994).

Injectable stacks (no hepatotoxic orals)

Expect 6-12 weeks for lipid normalization. A cross-sectional study found bodybuilders examined 3 months after stopping injectable-only cycles showed no differences in total cholesterol, HDL, or triglycerides compared to non-using controls (Hartgens et al., 1996).

Oral-containing stacks or heavy polydrug cycles

Lipid markers remain abnormal at 6 weeks post-cessation for multi-compound stacks (Hartgens et al., 2004). Full normalization takes 3-6 months (Baldo-Enzi et al., 1990). A longer follow-up study tracking 56 gym-attending men found lipid alterations persisting for up to 6 months after stopping intramuscular AAS, with complete normalization eventually achieved (Gårevik et al., 2011).

Bloodwork-gating: when is it safe to start another cycle?

The "time on equals time off" heuristic does not account for cardiovascular recovery. A more responsible approach: your HDL should return to within 10% of your personal baseline, and LDL should normalize before starting another cycle. Minimum 8-12 weeks off after oral-containing cycles regardless of how values look.

Lipid recovery is faster than endocrine recovery. Gårevik et al. found lipids normalizing before LH/FSH in many subjects. If you are tracking both compound logs and bloodwork on VitalMetrics, watch both timelines independently rather than assuming hormonal recovery means cardiovascular recovery (or vice versa).

One consistent finding: longer and heavier cycles produce slower recovery. Hartgens et al. (2004) found 14-week cycles produced slower lipid recovery than 8-week cycles. The longer your cycle, the longer your cardiovascular off-time needs to be.

On-cycle lipid management: what actually works

Not all interventions are equal. Here is a tiered protocol based on the quality of evidence, not forum popularity.

Tier 1: Aerobic exercise (strongest evidence)

A 2024 meta-analysis of 148 RCTs (8,673 participants) confirmed that exercise training raises HDL by approximately 2 mg/dL and lowers LDL by 7 mg/dL, triglycerides by 8 mg/dL, and VLDL by 4 mg/dL. Every additional weekly aerobic session reduced total cholesterol by a further 7.68 mg/dL (Smart et al., 2025).

More importantly, aerobic exercise improves HDL quality, not just quantity. Regular cardio upregulates LCAT activity (the enzyme that matures HDL particles), reduces CETP (which transfers cholesterol away from HDL), and improves overall cholesterol efflux capacity (Franczyk et al., 2023). Given that AAS users suffer impaired HDL function independent of particle count, this functional improvement is where cardio earns its place.

In a direct AAS-and-exercise animal study, aerobic exercise training (five sessions/week) blunted steroid-induced LDL and VLDL elevation, raised HDL, and attenuated pathological cardiac hypertrophy (Fontana & Oliveira, 2008).

30-45 minutes of moderate-intensity cardio (zone 2: you can hold a conversation), 4-5 sessions per week. This is the single most effective intervention and it costs nothing.

Tier 2: Omega-3 EPA/DHA (dose matters)

A 2023 dose-response meta-analysis of RCTs showed near-linear triglyceride reductions: -42.6 mg/dL at 2 g/day and -68.9 mg/dL at 3 g/day of combined EPA+DHA. HDL increased modestly (+1.7 mg/dL at 2 g/day). Non-HDL cholesterol fell linearly (Wang et al., 2023).

Beyond quantity, omega-3 supplementation improves HDL particle composition, shifting the balance toward larger, more functional HDL particles and enhancing sterol efflux capacity.

Take 3-4 g combined EPA+DHA per day. This is not the same as 3-4 g of fish oil capsules. Most 1 g capsules contain only 300-600 mg of actual EPA+DHA. Read the label and calculate the active ingredient content.

Tier 3: Citrus bergamot

The most evidence-backed natural LDL-lowering supplement. In a randomized, double-blind, placebo-controlled trial of 237 subjects over 30 days, bergamot polyphenolic fraction at 500 mg/day reduced total cholesterol by 21.8%, LDL by 24.1%, and raised HDL by 22.3%. At 1,000 mg/day: total cholesterol -29.4%, LDL -36%, HDL +40.1% (Mollace et al., 2011).

A follow-up study found that adding 1,000 mg/day bergamot to rosuvastatin 10 mg/day matched the LDL reduction of rosuvastatin 20 mg/day alone, suggesting a meaningful statin-sparing effect (Gliozzi et al., 2013).

One caveat worth noting: most bergamot trials are short (30 days), conducted by Italian research groups with financial conflicts of interest, and have not been independently replicated in large multicenter trials. The effect sizes are unusually large for a supplement. Use it as a complement to exercise and omega-3, not a replacement.

Dose: 500-1,000 mg bergamot polyphenolic fraction daily.

What about niacin?

Niacin raises HDL by approximately 30-35% and was long considered a first-line agent. Two large RCTs demolished this rationale. HPS2-THRIVE enrolled 25,673 high-risk patients and found that niacin produced no reduction in cardiovascular events despite raising HDL, with increased serious adverse events in the niacin arm (HPS2-THRIVE Collaborative Group, 2014).

The lesson: pharmacologically raising the HDL number on a lab report does not replicate the cardioprotective function of biologically normal HDL. Niacin is not an effective on-cycle lipid strategy. For AAS users specifically, its flush side effect, glucose intolerance, uric acid elevation, and hepatotoxicity risk are additional concerns. "Flush-free" inositol hexanicotinate has no reliable evidence for HDL elevation either.

The statin question

ACC/AHA guidelines recommend high-intensity statin therapy for all adults with LDL at or above 190 mg/dL regardless of estimated 10-year risk. This threshold is frequently exceeded by users of oral 17-alpha-alkylated compounds.

If your LDL is consistently above 190 mg/dL on cycle, a conversation with a physician about statins is warranted. Rosuvastatin or pravastatin are preferred for athletes due to their hydrophilic nature and lower myopathy risk compared to lipophilic statins like simvastatin or atorvastatin.

Ezetimibe (Zetia) reduces LDL by 15-25% via intestinal cholesterol absorption inhibition with no muscle or liver toxicity concerns. It is a useful adjunct when LDL remains above target on maximum tolerated statin, or for athletes who refuse statins.

A low-dose simvastatin study in steroid-using bodybuilders showed minimal improvement while the androgenic stimulus continued, suggesting that low-dose statin monotherapy is insufficient during active oral compound use. Higher-dose statins or combination therapy may be required.

When to worry: lab value red lines

Not every abnormal lipid result demands the same response. Here is a decision framework tied to specific numbers.

HDL below 25 mg/dL (0.65 mmol/L) puts you in high-risk territory. If running oral compounds, discontinue them. If injectable-only, reassess dose and add aggressive cardio and omega-3 supplementation. Recheck in 4 weeks.

LDL above 190 mg/dL (4.9 mmol/L) warrants statin consideration per ACC/AHA guidelines, alongside dietary and supplement intervention (bergamot, omega-3, reduced saturated fat).

A total cholesterol:HDL ratio above 5.0 reflects elevated cardiovascular risk. This ratio captures the combined damage of suppressed HDL and elevated LDL better than either number alone.

Non-HDL cholesterol that is significantly elevated captures all atherogenic particles including VLDL and is a better predictor of cardiovascular risk than LDL alone, especially when triglycerides are elevated from bulking diets or growth hormone use.

HDL below 15 mg/dL or LDL above 300 mg/dL: hard stop. Discontinue oral compounds immediately. These values represent extreme cardiovascular risk regardless of your training goals. No supplement or cardio protocol adequately compensates for lipid panels this severe while the suppressive compound continues.

Key takeaways

• Oral 17-alpha-alkylated steroids (stanozolol, superdrol, halotestin, oxymetholone, dianabol) are categorically worse for lipids than injectables. The mechanism is hepatic lipase upregulation from first-pass liver exposure.
• Stanozolol is the most documented offender: -33% HDL, -71% HDL2 at just 6 mg/day in controlled data.
• Injectable testosterone at 200 mg/week only reduces HDL by about 9%. The oral vs. injectable divide matters more than the specific compound name.
• Crashing estradiol with aromatase inhibitors removes a natural brake on hepatic lipase, worsening lipid damage. Use the minimum effective AI dose.
• HDL quantity on your lab report understates the real damage. Cholesterol efflux capacity is impaired in AAS users even when HDL-C looks borderline acceptable. 25% of young AAS users in one study had multi-vessel coronary plaques.
• Recovery takes 4 weeks for testosterone-only, 6-12 weeks for injectable stacks, and 3-6 months for oral-containing or heavy polydrug cycles. Wait for lipids to normalize before starting another cycle.
• Aerobic exercise is the single best intervention: it improves both HDL quantity and function. 30-45 minutes of zone 2 cardio, 4-5 times per week.
• Omega-3 at 3-4 g EPA+DHA per day reduces triglycerides and improves HDL particle quality. Citrus bergamot has promising but preliminary LDL-lowering data.
• Niacin does not reduce cardiovascular risk despite raising HDL numbers. Skip it.
• Hard lab value red lines: HDL below 15 or LDL above 300 means stop the oral compounds immediately.

---

References

1. Glazer, G. (1991). Atherogenic effects of anabolic steroids on serum lipid levels: A literature review. Archives of Internal Medicine, 151(10), 1925-1933. PubMed

2. Achar, S., Rostamian, A., & Narayan, S. M. (2010). Cardiac and metabolic effects of anabolic-androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions, and rhythm. American Journal of Cardiology, 106(6), 893-901. PubMed

3. Applebaum-Bowden, D., Haffner, S. M., & Hazzard, W. R. (1987). The dyslipoproteinemia of anabolic steroid therapy: Increase in hepatic triglyceride lipase precedes the decrease in high density lipoprotein2 cholesterol. Metabolism, 36(10), 949-952. PubMed

4. Haffner, S. M., Kushwaha, R. S., Foster, D. M., Applebaum-Bowden, D., & Hazzard, W. R. (1983). Studies on the metabolic mechanism of reduced high density lipoproteins during anabolic steroid therapy. Metabolism, 32(4), 413-420. PubMed

5. Thompson, P. D., Cullinane, E. M., Sady, S. P., Chenevert, C., Saritelli, A. L., Sady, M. A., & Herbert, P. N. (1989). Contrasting effects of testosterone and stanozolol on serum lipoprotein levels. JAMA, 261(8), 1165-1168. PubMed

6. Jones, D. R., Schmidt, R. J., Pickard, R. T., Foxworthy, P. S., & Eacho, P. I. (2002). Estrogen receptor-mediated repression of human hepatic lipase gene transcription. Journal of Lipid Research, 43(3), 383-391. PubMed

7. Zmuda, J. M., Fahrenbach, M. C., Younkin, B. T., Bausserman, L. L., Terry, R. B., Catlin, D. H., & Thompson, P. D. (1993). The effect of testosterone aromatization on high-density lipoprotein cholesterol level and postheparin lipolytic activity. Metabolism, 42(4), 446-450. PubMed

8. Hartgens, F., Rietjens, G., Keizer, H. A., Kuipers, H., & Wolffenbuttel, B. H. R. (2004). Effects of androgenic-anabolic steroids on apolipoproteins and lipoprotein (a). British Journal of Sports Medicine, 38(3), 253-259. PubMed

9. Kuipers, H., Wijnen, J. A., Hartgens, F., & Willems, S. M. (1991). Influence of anabolic steroids on body composition, blood pressure, lipid profile and liver functions in body builders. International Journal of Sports Medicine, 12(4), 413-418. PubMed

10. Sattler, F. R., Schroeder, E. T., Dube, M. P., Jaque, S. V., Martinez, C., Blanche, P. J., Azen, S., & Krauss, R. M. (2002). Metabolic effects of nandrolone decanoate and resistance training in men with HIV. American Journal of Physiology: Endocrinology and Metabolism, 283(6), E1214-E1222. PubMed

11. Rohatgi, A., Khera, A., Berry, J. D., Givens, E. G., Ayers, C. R., Wedin, K. E., Neeland, I. J., Yuhanna, I. S., Rader, D. R., de Lemos, J. A., & Shaul, P. W. (2014). HDL cholesterol efflux capacity and incident cardiovascular events. New England Journal of Medicine, 371(25), 2383-2393. PubMed

12. de Souza, F. R., Dos Santos, M. R., Porello, R. A., et al. (2019). Diminished cholesterol efflux mediated by HDL and coronary artery disease in young male anabolic androgenic steroid users. Atherosclerosis, 283, 100-105. PubMed

13. Bagatell, C. J., Heiman, J. R., Matsumoto, A. M., Rivier, J. E., & Bremner, W. J. (1994). Metabolic and behavioral effects of high-dose, exogenous testosterone in healthy men. Journal of Clinical Endocrinology & Metabolism, 79(2), 561-567. PubMed

14. Hartgens, F., Kuipers, H., Wijnen, J. A., & Keizer, H. A. (1996). Body composition, cardiovascular risk factors and liver function in long-term androgenic-anabolic steroids using bodybuilders three months after drug withdrawal. International Journal of Sports Medicine, 17(6), 429-433. PubMed

15. Baldo-Enzi, G., Giada, F., Zuliani, G., et al. (1990). Lipid and apoprotein modifications in body builders during and after self-administration of anabolic steroids. Metabolism, 39(2), 203-208. PubMed

16. Gårevik, N., Strahm, E., Garle, M., et al. (2011). Long term perturbation of endocrine parameters and cholesterol metabolism after discontinued abuse of anabolic androgenic steroids. Journal of Steroid Biochemistry and Molecular Biology, 127(3-5), 295-300. PubMed

17. Smart, N. A., Downes, D., van der Touw, T., et al. (2025). The effect of exercise training on blood lipids: A systematic review and meta-analysis. Sports Medicine, 55(1), 67-78. PubMed

18. Franczyk, B., Gluba-Brzozka, A., Cialkowska-Rysz, A., Lawinski, J., & Rysz, J. (2023). The impact of aerobic exercise on HDL quantity and quality: A narrative review. International Journal of Molecular Sciences, 24(5), 4653. PubMed

19. Fontana, K., & Oliveira, H. C. F. (2008). Adverse effect of the anabolic-androgenic steroid mesterolone on cardiac remodelling and lipoprotein profile is attenuated by aerobic exercise training. International Journal of Experimental Pathology, 89(5), 358-366. PubMed

20. Wang, T., Zhang, X., Zhou, N., et al. (2023). Association between omega-3 fatty acid intake and dyslipidemia: A continuous dose-response meta-analysis of randomized controlled trials. Journal of the American Heart Association, 12(11), e029512. PubMed

21. Mollace, V., Sacco, I., Janda, E., et al. (2011). Hypolipemic and hypoglycaemic activity of bergamot polyphenols: From animal models to human studies. Fitoterapia, 82(3), 309-316. PubMed

22. Gliozzi, M., Walker, R., Muscoli, S., et al. (2013). Bergamot polyphenolic fraction enhances rosuvastatin-induced effect on LDL-cholesterol, LOX-1 expression and protein kinase B phosphorylation in patients with hyperlipidemia. International Journal of Cardiology, 170(2), 140-145. PubMed

23. HPS2-THRIVE Collaborative Group. (2014). Effects of extended-release niacin with laropiprant in high-risk patients. New England Journal of Medicine, 371(3), 203-212. PubMed