Statins are more controversial than any other heart drug. The editors collected the most common myths about rosuvastatin and verified each of them with data from randomized trials and clinical guidelines.
Myth 1. "Cholesterol is not harmful, and statins are the invention of pharmaceutical companies"
This myth is popular in social networks and is often presented as a "hidden truth". The arguments usually go like this: the body needs cholesterol, half of the people who had a heart attack had "normal" cholesterol, and the statin studies were funded by the manufacturers.
Each of these statements is partially true, but the conclusion is false. Cholesterol is really necessary, but cells receive it in sufficient quantity even with low LDL in the blood. The role of LDL as a causative factor in atherosclerosis has been confirmed not only by statins, but also by genetic studies, studies of other drug classes (ezetimibe, PCSK9 inhibitors) and observations of people with congenital mutations.
Cholesterol Treatment Trialists meta-analyses combining individual data from tens of thousands of participants show that each 1 mmol/L reduction in LDL reduces the risk of major vascular events by approximately one-fifth (CTT, 2010). This pattern is stable regardless of the specific statin.
That many people with heart attacks had "normal" cholesterol is because normal values are calculated for the general population, not for people at high risk. For them, the target LDL levels are much lower.
Myth 2. "Everyone's muscles hurt from statins"
Muscle complaints are the most common reason people stop taking statins. However, blind studies give an unexpected picture. In the ASCOT-LLA study, during the blinded phase, the frequency of muscle symptoms was similar in the statin and placebo groups, and after disclosure of treatment, those who knew they were taking a statin complained more often (Gupta et al., 2017).
SAMSON enrolled people who had stopped statins because of symptoms. Participants received randomized monthly courses of atorvastatin 20 mg, matching placebo or no tablets. Statin and placebo were blinded; a no-tablet month could not be blinded. About 90% of the additional symptom burden on atorvastatin was also seen on placebo (Wood et al., 2020; Howard et al., 2021). This does not mean symptoms were imaginary or that true drug reactions never occur.
A large meta-analysis of 2022 confirmed: in the first year, statins give a small absolute increase in muscle complaints, and in the future the difference with placebo practically disappears (CTT Collaboration, 2022).
This does not mean that muscle side effects do not exist. Myopathy and rhabdomyolysis are real, albeit rare, conditions. But the statement "statins harm the muscles of everyone" does not correspond to the data.
Myth 3. "Statins destroy the liver and testosterone"
Statins can indeed mildly increase liver enzymes, but severe liver damage is very rare. That is why current guidelines recommend determining ALT before starting treatment, and then only if indicated, without mandatory regular monitoring in all patients (Newman et al., 2019).
Moreover, in people with nonalcoholic fatty liver disease, statins are generally considered safe and not contraindicated—in such patients, high cardiovascular risk is often a more important concern than liver status.
Regarding testosterone: the theoretical fear is understandable, because cholesterol is a precursor of steroid hormones. However, Leydig cells largely synthesize cholesterol themselves and take it from lipoproteins. A small decrease in testosterone during statins was described in some studies, but these data do not show clinically significant hypogonadism.
People who observe a worsening of their well-being should not refuse treatment on their own, but should take tests and discuss the results with a doctor.
Myth 4. "Statin protects against steroids and cleans blood vessels"
In the sports environment, there is a widespread idea that rosuvastatin can be "plugged in" as protection during anabolic steroids. The problem is that AAS reduce HDL the most, and statins have almost no effect on this indicator. In addition, the cardiac risks of AAS include myocardial hypertrophy, increased blood pressure, and hematocrit, which are not affected by statins (Pope et al., 2014).
There are no studies showing that statins reduce the incidence of heart attacks or sudden death in AAS users. So "protection" in such a scheme is psychological rather than proven.
The idea of “cleaning blood vessels” is misleading. In ASTEROID, intensive rosuvastatin treatment was associated with a mean reduction of 0.98 percentage points in percent atheroma volume over two years. This is a specific ultrasound measure, not a claim that all plaque disappeared or a universal percentage reduction in plaque volume.
Therefore, a statin is a tool for long-term prevention of atherosclerosis, not an antidote for pharmacological stress.
Other common myths in brief
Part of the myths concerns the how the medicine is taken. For example, it is common advice to take any statin only in the evening. It makes sense for short-acting simvastatin and lovastatin, but rosuvastatin with a half-life of about 19 hours can be taken at any convenient time of day (Crestor instructions).
Another myth: "if cholesterol has normalized, statin can be stopped." A statin does not cure hypercholesterolemia, but controls it. After withdrawal, LDL levels usually return to baseline within a few weeks.
It is also often said that "diet works no worse." A healthy diet does lower LDL and is important for everyone, but its effect is usually modest. For people with hereditary hypercholesterolemia or high risk, diet alone is usually not enough.
Finally, many people believe that "natural" remedies—garlic, turmeric, red yeast rice—are safe alternatives to statins. Most of them have weak or unproven effects on LDL, and red yeast rice contains monacolin K, which is actually the same lovastatin, but with unpredictable content and no quality control.
| Statement | What the data show |
|---|---|
| Statins are an invention of pharmaceutical companies | Benefit confirmed by meta-analyses and genetic studies |
| Everyone's muscles hurt | In blind studies, most symptoms are reproduced by placebo |
| Statins destroy the liver | Severe liver damage is very rare |
| Statins protect against AAS | Does not compensate for the drop in HDL and other cardio risks |
| Take only in the evening | For rosuvastatin, the time of administration is not essential |
| After normalization, you can quit | After withdrawal, LDL returns to baseline |
- true: Statins may increase the risk of diabetes, especially in people with prediabetes (Sattar et al., 2010);
- truth: when taking rosuvastatin, it is important to consider other drugs;
- true: severe muscle pain and dark urine is a reason to see a doctor immediately.
Editorial conclusions
Most of the popular myths about rosuvastatin are based on actual facts that have been twisted or taken out of context. Cholesterol is indeed needed by the body, side effects do exist, but data from blinded studies paint a much calmer picture than the forums.
At the same time, you should not go to the other extreme: a statin is not a "vitamin for the heart" and does not protect against the effects of anabolic steroids.
The decision to start, continue or stop treatment should be made on the basis of tests and risk assessment together with the doctor.
We also advise you to read our materials on rosuvastatin clinical studies, its side effects and why athletes are discussing it.
References
- Cholesterol Treatment Trialists' (CTT) Collaboration. 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.
- Gupta A, Thompson D, Whitehouse A, et al. Adverse events associated with unblinded, but not with blinded, statin therapy in the Anglo-Scandinavian Cardiac Outcomes Trial—Lipid-Lowering Arm (ASCOT-LLA). Lancet. 2017;389(10088):2473–2481.
- Wood FA, Howard JP, Finegold JA, et al. N-of-1 trial of a statin, placebo, or no treatment to assess side effects. N Engl J Med. 2020;383(22):2182–2184.
- 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.
- Newman CB, Preiss D, Tobert JA, et al. Statin safety and associated adverse events: a scientific statement from the American Heart Association. Arterioscler Thromb Vasc Biol. 2019;39(2):e38–e81.
- Pope HG Jr, Wood RI, Rogol A, et al. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341–375.
- Nissen SE, Nicholls SJ, Sipahi I, et al. Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial. JAMA. 2006;295(13):1556–1565.
- 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.
