Do Statins Lower Testosterone? The Honest Answer on Statins and Sex Drive
Share
Do statins lower testosterone? Yes, by a small amount that stays inside the normal range. Pooled across five randomized trials of 501 men, statins lowered testosterone by 0.66 nmol/L (95% CI minus 1.18 to minus 0.14) (Schooling et al., 2013), and a 2024 meta-analysis of five randomized trials measured a drop of 13.12 ng/dL while concluding that the decrease was not enough to reach levels below normal (Glina et al., 2024). The hormone moves. What happens to desire afterwards is a separate question, and the trials that asked it disagree with each other.
Read this part first: do not stop or change your cholesterol medication on your own.
Nothing on this page is a reason to skip a dose, halve a tablet, or quit a prescription. Statins are prescribed to lower cardiovascular risk and they do that job well. Any decision to change the dose, switch statins, or stop belongs to you and your prescriber. If your sex drive changed after you started one, book the conversation and bring the timeline.
- Statins lower total testosterone by a small amount: 0.66 nmol/L across five randomized trials of 501 men (95% CI minus 1.18 to minus 0.14), and 13.12 ng/dL in a 2024 meta-analysis that reported the decrease was not enough to reach levels below normal.
- The size of that drop depends heavily on study design: observational studies pooled to 55.02 ng/dL against 13.12 ng/dL from randomized trials, inside one paper.
- A Cochrane review of six randomized trials found no significant difference in men between atorvastatin and placebo (MD minus 0.20 nmol/L, 95% CI minus 0.77 to 0.37), at low to very low certainty.
- The two best randomized answers on sexual function disagree. Pooling 11 trials gave a rise of 3.4 points (95% CI 1.7 to 5.0); a trial of 2,153 men followed for a mean of 5.8 years found no difference between rosuvastatin and placebo (P = 0.74).
- Cochrane identified no studies at all in healthy women. Every confident answer about statins, testosterone, and a woman with normal hormone levels is an extrapolation from men or from women with polycystic ovary syndrome.
Figures from de Graaf et al. 2004 (PMID 15327593), Joseph et al. 2018 (PMID 29275880), and Shawish et al. 2021 (PMID 33482034).
Where the reputation came from: eight patients in a Dutch database
Almost every claim you will find about statins killing desire traces back to one short paper. In 2004, the Netherlands Pharmacovigilance Centre Lareb searched its adverse drug reaction database and found eight patients who had reported decreased libido while taking a statin. Testosterone was measured in two of them, and in both it came back low. The authors concluded that decreased libido is a probable adverse drug reaction of these drugs and that it is reversible, and they offered a mechanism: statins deplete intracellular cholesterol, the raw material the body builds testosterone from (de Graaf et al., 2004).
Eight case reports. That is the size of the direct-libido evidence base at the origin of a belief now held by millions of people. A spontaneous-report database collects what patients and doctors choose to send in, so it can tell you a thing has been noticed and nothing about how often it happens. The paper is honest about being a case series, and it then got quoted for twenty years as a frequency estimate. The mechanism deserves to be taken seriously even so, because it is chemically sensible: lower the precursor and the product might follow. Researchers have spent two decades testing that.
Do statins lower testosterone? What the randomized trials measured
They do, and the amount is small enough that the papers reporting it spend their conclusions explaining how small.
Schooling and colleagues ran a meta-analysis of placebo-controlled randomized trials on a hypothesis stated in advance: statins lower testosterone. Of 29 studies identified, 11 were eligible. Across five homogeneous trials of 501 men, mainly middle-aged with high cholesterol, statins lowered testosterone by 0.66 nmol/L (95% CI minus 1.18 to minus 0.14). Six heterogeneous trials of 368 young women with polycystic ovary syndrome showed a drop of 0.40 nmol/L (95% CI minus 0.75 to minus 0.05), and pooling everything gave 0.44 nmol/L (95% CI minus 0.75 to minus 0.13) (Schooling et al., 2013).
Hold on to which women those were: patients with polycystic ovary syndrome, a condition defined in part by elevated androgens, in whom lowering testosterone is often a clinical goal. We wrote about that condition and desire in our guide to PCOS and low sex drive. Those results do not transfer to a woman with normal hormone levels.
Glina and colleagues asked the same question of men in 2024 and split their evidence by design, which is what makes the paper useful. Six cross-sectional studies pooled to a reduction of 55.02 ng/dL (95% CI 39.40 to 70.64, I squared equal to 91%). Five randomized trials pooled to 13.12 ng/dL (95% CI 1.16 to 25.08, I squared equal to 0%). All 15 prospective studies gave 9.11 ng/dL (95% CI 0.16 to 18.06, I squared equal to 37%). Their conclusion: the decrease was not enough to reach levels below normal (Glina et al., 2024).
Same question, three study designs, one meta-analysis
Pooled reduction in total testosterone after statin use, by study design. All three estimates come from one 2024 systematic review, in men.
Source: Glina FPA, Lopes L, e Silva RS, et al., Int Braz J Urol 2024 (PMID 38386784). PROSPERO CRD42021270424. The cross-sectional arm carries an I squared of 91%, so treat it as the least reliable of the three.
That gap between 55.02 and 13.12 has a plain explanation. Cross-sectional studies compare men who happen to be taking statins against men who are off them, and men on statins are older, heavier, and more likely to have diabetes, metabolic syndrome, and cardiovascular disease. Every one of those lowers testosterone on its own, so the comparison picks up the reasons the prescription was written. Randomization removes the problem by deciding who gets the drug with a coin flip, which is why its estimate is roughly a quarter the size.
Cochrane then ran the strictest version of the test. Shawish and colleagues took only randomized trials of atorvastatin lasting at least three weeks and found six, covering 265 participants who completed. Two were in men, mean age 68, 140 in total, and there was no significant difference between atorvastatin and placebo (MD minus 0.20 nmol/L, 95% CI minus 0.77 to 0.37). The other four were in 125 women with polycystic ovary syndrome, mean age 32, where atorvastatin may reduce total testosterone by 0.27 nmol/L (95% CI minus 0.50 to minus 0.04). The authors rated the certainty low to very low for both comparisons and called for more trials (Shawish et al., 2021).
Three papers cut the data three ways and land on the same shape. The hormone moves down a little on average, and nobody has shown it moving far enough to drop a man out of the normal range.
Three study designs, three answers
| Study design | What it measured | What it found |
|---|---|---|
| Case reports from a side-effect database (de Graaf 2004) | Self-reported decreased libido, 8 patients | Called a probable adverse drug reaction and described as reversible. Testosterone was measured in two of the eight and was low. A case series carries no frequency information. |
| Observational studies pooled (Glina 2024, cross-sectional arm) | Total testosterone in 6 cross-sectional studies | 55.02 ng/dL lower (95% CI 39.40 to 70.64, I squared 91%). Men on statins differ from men off them in ways that lower testosterone by themselves. |
| Randomized trials pooled, hormone endpoint (Schooling 2013, Glina 2024, Shawish 2021) | Total testosterone, placebo-controlled | 0.66 nmol/L lower across 501 men; 13.12 ng/dL lower across 5 trials, called not enough to reach levels below normal; no significant difference in the Cochrane analysis of men (MD minus 0.20, 95% CI minus 0.77 to 0.37) at low to very low certainty. |
| Randomized trials pooled, sexual-function endpoint (Kostis 2014) | Score on the five-item IIEF questionnaire, 11 trials | Scores rose by 3.4 points (95% CI 1.7 to 5.0, P = 0.0001), a gain the authors put at one-third to one-half of a PDE-5 inhibitor. |
| One large long randomized trial (Joseph 2018, HOPE-3) | IIEF erectile function domain, 2,153 men, mean 5.8 years | Scores fell 1.4 points on rosuvastatin and 1.5 on placebo (P = 0.74). Blood pressure arm P = 0.10; combination P = 0.35. |
Trial data from PMIDs 15327593, 38386784, 23448151, 33482034, 24684744, and 29275880, listed in full below.
My doctor said it's not the statin
Your doctor has the larger half of the evidence behind them, and the honest version of the answer includes a genuine disagreement between two good randomized results.
Kostis and Dobrzynski pooled 11 randomized trials that measured sexual function on the five-item IIEF, a standard questionnaire about erectile function. Scores went up by 3.4 points with statins compared with control (95% CI 1.7 to 5.0, P = 0.0001), and the result held through a publication-bias analysis, a cumulative meta-analysis, and 11 repeated analyses with each study dropped in turn. The authors sized it against familiar comparisons: roughly one-third to one-half of what has been reported for a PDE-5 inhibitor, and larger than the effect of lifestyle modification (Kostis and Dobrzynski, 2014).
Then HOPE-3 tested the same idea inside one very large trial. Joseph and colleagues ran a pre-planned analysis of a 2 by 2 factorial randomization: 2,153 men aged 55 and over with a cardiovascular risk factor, assigned to rosuvastatin 10mg daily or placebo, and separately to candesartan with hydrochlorothiazide or placebo. Mean follow-up was 5.8 years and the baseline IIEF erectile function score averaged 23.0 (SD 5.6). Scores drifted down in every group, which is what happens to men over six years, and the drift was the same size in each: minus 1.4 on rosuvastatin against minus 1.5 on placebo (P = 0.74). The blood pressure comparison gave P = 0.10 and the combination P = 0.35 (Joseph et al., 2018).
So which one is right? Both results are real and they point in different directions. Kostis pooled 11 shorter trials in populations chosen partly because sexual difficulty was already present, where an improvement has room to show up. HOPE-3 followed a much larger group for nearly six years and found the two arms indistinguishable, concluding that cholesterol-lowering with a statin does not improve or adversely affect erectile function. The largest and longest randomized comparison is the most reliable answer on the table, and it found neither benefit nor harm.
That same trial is the cleanest evidence on the other drug class people blame. HOPE-3 randomized blood pressure treatment in the same men at the same time and found nothing there either, which lines up with the pooled trial data we went through in what the trials actually show about beta blockers and sex drive.
I started the pills and it just went: is it the pill or is it me
The experience is real. Something changed, you noticed it, and the timing pointed at the newest thing in your medicine cabinet. That is a reasonable first suspicion and it deserves a proper investigation.
Start with what else arrived that month. A statin prescription follows a cholesterol result, a risk score, or an event, and all three arrive with worry attached. People change their diet, sleep worse, drink differently, and sometimes leave with a second prescription. A drug started three weeks before your desire changed is a stronger suspect than one you have taken for six years, and a diagnosis delivered in the same appointment is a suspect too.
Then check the rest of the list, because statins are frequently the smallest contributor in a stack of things that each affect desire. Antidepressants have the clearest evidence of any prescription class, covered in antidepressants and low libido and in libido after stopping antidepressants. Stimulants have their own pattern, in Adderall and sex drive, and the newer weight-loss drugs are producing reports running in both directions, tracked in GLP-1 medications and libido. Blaming the statin and stopping there closes the file on sleep, alcohol, stress load, thyroid, mood, and every other tablet in the cabinet, on the strength of eight case reports from 2004.
Nobody has studied this in healthy women
This is where almost every page online is quietly making something up. The Cochrane review identified no studies in healthy females, meaning females with normal testosterone levels (Shawish et al., 2021).
Schooling's women were 368 young patients with polycystic ovary syndrome. Cochrane's were 125 patients with the same condition, mean age 32. Those trials existed because lowering androgens in PCOS can be therapeutic, so they were built around a population whose starting hormone levels are high. Glina's review, Kostis's meta-analysis, and HOPE-3 are all male, and HOPE-3 used the erectile function domain of the IIEF, an instrument with no female version at all.
A 54-year-old woman started on atorvastatin last spring, whose desire has since gone flat, stands outside every trial on this page. Any confident answer she is given is an extrapolation from 68-year-old men or from 32-year-old PCOS patients. Unmeasured is a worse position than measured and cleared, and that is where she stands.
Her question is open, so a clinician who takes it seriously is on solid ground. And the absence of evidence cuts both ways: nothing supports the idea that her statin ruined her sex drive, and nothing rules it out. What is left is her timeline and everything else in her life.
The numbers were fine and I still feel like crap
Cholesterol at target, blood pressure fine, testosterone in range, desire still gone. This is one of the most common ways the problem presents, and one of the most demoralizing: the tests that were supposed to explain it came back clean.
Part of the answer is that the conditions statins are prescribed for travel with sexual difficulty on their own, before any tablet is involved. The cross-sectional gap in Glina's review is the fingerprint of that: age, weight, metabolic health, and vascular disease were all already happening when the prescription was written.
A normal lab result and a normal life are also different measurements, a gap we went through in what to do when your labs come back normal and your libido has not, with the broader picture in our guide to low libido in men. Sleep is the item most often missing from that workup, and the link between sleep debt and testosterone is far better established than anything on this page: sleep, libido and testosterone.
Tired all the time
Exhaustion gets described as low libido more often than anything else on the list, because from the outside the two look identical. Someone flattened by 9pm has lost something that behaves exactly like lost desire, and the fix lives somewhere else entirely.
Muscle aches and fatigue are the side effects statins are actually known for, and they are worth raising with your prescriber in their own right, since dose changes and switching statins are routine responses. Cardiovascular conditioning improves the energy and the risk profile at once: the research on exercise and libido.
Once a man decides his testosterone is the problem, the internet offers to sell him something for it, and the evidence behind those products is thin: do testosterone boosters work. A drop of 13.12 ng/dL inside the normal range is a poor reason to start buying hormone products.
How to work out whether your statin is the cause
You can get most of the way to an answer before your appointment.
- Write the timeline. Days between the first dose and the change makes the drug a strong suspect; years makes it a weak one.
- List every medication and supplement you take, over the counter included, and bring the whole list. The statin is often the least likely item on it.
- Write down what else changed that month. A cholesterol diagnosis arrives with worry, dietary changes, disrupted sleep, and sometimes a second prescription.
- Separate desire from function. Wanting sex less and responding differently have different causes and different fixes.
- Ask for the tests that answer your question. A morning total testosterone, a thyroid panel, and a look at your sleep rule more in or out than another cholesterol panel.
- Ask about the statin itself. Dose, timing, and which statin you take are all adjustable, and that decision belongs to your prescriber.
What to say at the appointment
Where NUUD fits, and where it does not
The answer points away from most people reading this page.
NUUD's own product label carries this caution: avoid use if you are on blood pressure medication, have cardiovascular, renal, or pulmonary conditions, or if you are sensitive to any of the ingredients. A large share of statin readers fall inside that caution, because statins are usually prescribed alongside those exact conditions. If that describes you, talk to your doctor before taking anything of ours. We would sooner lose the sale than write around our own label.
Our supplements are built for people who want more desire and who sit outside that caution. For those readers the formula is anchored on the NUUD Mushroom Complex™ with Muira Puama, Boiled Rehmannia Root, Tribulus Terrestris, and Piper Nigrum for absorption, and our men's libido support capsules are the usual place to start. There is a women's version of the same capsule. They work on desire. No botanical supplement is an answer to a medication side effect, and nothing on this page should be read as one.
Frequently asked questions
Do statins lower testosterone?
Yes, by a small amount that stays inside the normal range. Across five randomized trials of 501 men, statins lowered testosterone by 0.66 nmol/L (95% CI minus 1.18 to minus 0.14). A 2024 meta-analysis of five randomized trials measured 13.12 ng/dL and concluded the decrease was not enough to reach levels below normal. A Cochrane review of six randomized trials found no significant difference in men between atorvastatin and placebo (MD minus 0.20 nmol/L, 95% CI minus 0.77 to 0.37), at low to very low certainty. Never change a cholesterol prescription on your own.
Do statins lower your sex drive?
The randomized evidence does not point that way, and it disagrees with itself about the direction. Pooling 11 randomized trials found sexual function scores rose by 3.4 points on the five-item IIEF (95% CI 1.7 to 5.0, P = 0.0001). A trial of 2,153 men followed for a mean of 5.8 years found scores fell equally on rosuvastatin and on placebo (P = 0.74), and its authors concluded that statins do not improve or adversely affect erectile function. The reputation traces back to a 2004 report of eight patients in a Dutch side-effect database.
My doctor said it's not the statin. Who is right?
The larger half of the evidence is on your doctor's side, and your experience still needs explaining. The biggest and longest randomized comparison, 2,153 men over a mean of 5.8 years, found no difference between rosuvastatin and placebo on sexual function scores. That leaves a timeline worth working through together: what else started that month, what else is on your prescription list, and whether sleep, mood, alcohol, or thyroid have been looked at. A cholesterol diagnosis arrives with worry attached, and worry is its own contributor.
Do statins affect testosterone or sex drive in women?
Nobody knows, because the studies have never been done. A 2021 Cochrane review states that it identified no studies in healthy females, meaning females with normal testosterone levels. The female evidence that exists comes from patients with polycystic ovary syndrome: 368 young women in one meta-analysis and 125 women of mean age 32 in the Cochrane review, populations where lowering androgens is often the clinical goal. Those results do not transfer to a woman with normal hormone levels, and the sexual-function trials here are entirely male.
I started the pills and my sex drive just went. Is this normal?
It is common, and the statin is often the wrong suspect. A drug started three weeks before the change is a stronger suspect than one you have taken for years, so the timeline matters most. Look at what else arrived that month, since a cholesterol diagnosis brings worry, dietary changes, and disrupted sleep with it, and check the rest of your prescription list, because antidepressants and several other classes have far stronger evidence behind them. Take the dates to your prescriber and ask for the rest of the workup.
References
- Joseph P, Lonn E, Bosch J, et al. Long-term Effects of Statins, Blood Pressure-Lowering, and Both on Erectile Function in Persons at Intermediate Risk for Cardiovascular Disease: A Substudy of the Heart Outcomes Prevention Evaluation-3 (HOPE-3) Randomized Controlled Trial. Can J Cardiol. 2018 Jan;34(1):38-44. https://pubmed.ncbi.nlm.nih.gov/29275880/
- Glina FPA, Lopes L, e Silva RS, et al. Do statins decrease testosterone in men? Systematic review and meta-analysis. Int Braz J Urol. 2024 Mar-Apr;50(2):119-135. https://pubmed.ncbi.nlm.nih.gov/38386784/
- Schooling CM, Au Yeung SL, Freeman G, Cowling BJ. The effect of statins on testosterone in men and women, a systematic review and meta-analysis of randomized controlled trials. BMC Med. 2013 Feb 28;11:57. https://pubmed.ncbi.nlm.nih.gov/23448151/
- Shawish MI, Bagheri B, Musini VM, et al. Effect of atorvastatin on testosterone levels. Cochrane Database Syst Rev. 2021 Jan 22;1(1):CD013211. https://pubmed.ncbi.nlm.nih.gov/33482034/
- Kostis JB, Dobrzynski JM. The effect of statins on erectile dysfunction: a meta-analysis of randomized trials. J Sex Med. 2014 Jul;11(7):1626-35. https://pubmed.ncbi.nlm.nih.gov/24684744/
- de Graaf L, Brouwers AH, Diemont WL. Is decreased libido associated with the use of HMG-CoA-reductase inhibitors? Br J Clin Pharmacol. 2004 Sep;58(3):326-8. https://pubmed.ncbi.nlm.nih.gov/15327593/
This article is for general education and is not medical advice. Never stop, reduce, or change a cholesterol medication without talking to the clinician who prescribed it. NUUD is a botanical supplement. These statements have not been evaluated by the Food and Drug Administration, and the product is not intended to diagnose, treat, prevent, or cure any disease. NUUD's label advises avoiding use if you are on blood pressure medication, have cardiovascular, renal, or pulmonary conditions, or are sensitive to any of the ingredients.
