Mortality has long been one of the greatest fears, concerns, and challenges humankind has faced throughout our long history. Current preventive medicine offers several prescription medications that, based on robust clinical evidence, may help men maintain better health for longer. This article examines two medications with strong supporting data — finasteride and rosuvastatin — as well as two emerging therapies that are attracting serious research interest.
This is an educational overview of the published science. These medications require a prescription and should only be taken under the supervision of a qualified healthcare provider. Everyone's body, health situation, and goals are different — any medication discussed here should be reviewed with your own doctor before considering it.
Table of Contents
Medication 1: Finasteride
Finasteride, typically used at either 1 mg or 5 mg, is a 5-alpha-reductase inhibitor with a compelling body of evidence for prostate cancer prevention in men.
One of the leading causes of death for men worldwide is prostate cancer. It is the second-most frequently diagnosed cancer in men and the fifth leading cause of cancer death worldwide. (By comparison, the first-most frequently diagnosed cancer in men is lung cancer.) Prostate cancer is also often asymptomatic, making it difficult to detect until well past the point where straightforward treatment is viable. Regular screening is recommended starting at age 45–50 for this reason, because outcomes are considerably better when the disease is caught early.
How does finasteride work? As a medication, it functions by blocking the conversion of the hormone testosterone into dihydrotestosterone. Dihydrotestosterone, or DHT, is an important hormone in male children, playing a vital role in sexual development throughout puberty — promoting prostate growth, body and facial hair growth, and other sex characteristics.
In adult life, however, DHT does not appear to play any significant physiological role, nor does it have a role in female physiology. For adult males, DHT primarily appears to do two things: promote male pattern baldness and stimulate prostate enlargement.
The clinical hypothesis is therefore that by lowering DHT levels in adult men, finasteride can help reduce prostate size and, correspondingly, reduce rates of prostate cancer. But does the evidence support this?
In 2003, a landmark study called the Prostate Cancer Prevention Trial (PCPT) was published. This study enrolled just under 19,000 men and compared a 5 mg daily dose of finasteride against placebo. After seven years, the prevalence of prostate cancer diagnoses was 24.8% lower in the finasteride group than in the control group (803 diagnoses out of 4,368 in the finasteride arm versus 1,147 out of 4,692 in the placebo arm).
Because of these positive results, the study continued to follow participants for up to 18 additional years of follow-up. The benefit persisted over time, with approximately a 30% reduction in prostate cancer diagnoses in the finasteride group across all follow-up points.
The picture is not entirely straightforward, however. Among men who did develop prostate cancer in the finasteride arm, there was a higher rate of high-grade cancer. Before interpreting this as finasteride causing more aggressive cancers, though, context is important.
Prostate cancer is graded using the Gleason scale, which ranges from 6 to 10. A score of 6 represents lower-grade, less aggressive disease; a score of 10 is high-grade and more aggressive. The higher the grade, the faster the cancer grows and the more difficult it may be to treat.
What the data suggest is that finasteride keeps the prostate smaller by reducing DHT levels — and a smaller prostate makes it easier to detect lumps and abnormalities during biopsy. Finasteride is not increasing the rate at which high-grade cancers develop; it is making existing high-grade cancers easier to detect. This phenomenon is well recognised as detection bias.
Does finasteride improve overall survival? The answer, based on current evidence, is nuanced. Finasteride itself does not appear to improve survival outcomes directly. However, early detection of cancer — including high-grade cancer — is known to improve treatment success. So while finasteride may not directly extend survival on its own, anything that facilitates earlier detection of aggressive prostate cancer is clinically valuable.
The overall picture from the evidence is therefore: finasteride reduces the development of prostate cancer by approximately 25–30%, appears to have no detrimental effect on overall survival, and increases early detection of high-grade prostate cancer — a net benefit profile that many preventive medicine specialists consider favourable when weighed against the side effect risks.
What about side effects? Finasteride lowers prostate-specific antigen (PSA) blood levels, which are a key marker used to screen for prostate abnormalities. Men taking finasteride will have a lower "normal" PSA range than the general population; a PSA reading that appears unremarkable by standard reference ranges may actually represent an elevated level for someone on finasteride. The commonly cited adjustment is to double the measured PSA to approximate the "true" value. This is a critical consideration that any clinician monitoring a patient on finasteride must account for when interpreting results and making screening decisions.
Another potential side effect: nearly all trials have shown a 2–4% increase in reported erectile dysfunction and gynaecomastia. These side effects may not fully resolve after stopping finasteride — a collection of persisting effects sometimes referred to as post-finasteride syndrome.
Some clinicians advocate starting at 1 mg (rather than the 5 mg used in the PCPT) when prescribing finasteride to younger men, on the basis that a lower dose may reduce side effect risk while still providing meaningful prostate benefit. This remains a discussion to have with a personal healthcare provider.
Medication 2: Rosuvastatin
Rosuvastatin is a statin medication. Statins are a class of drugs that reduce cholesterol production in the liver, and rosuvastatin is among the most potent. The evidence base underpinning statin use for cardiovascular risk reduction is one of the most extensive in all of clinical medicine.
Why does reducing LDL cholesterol matter? A comprehensive meta-analysis covering over 2 million participants — drawn from over 200 cohort studies, Mendelian randomisation studies, and randomised controlled trials — conclusively demonstrates that LDL (low-density lipoprotein) cholesterol contributes to the development of heart disease. It is not the only cause, but it is a highly significant and modifiable risk factor, consistently reproduced across a wide range of methodologies.
One of the most compelling studies is the PESA (Progression of Early Subclinical Atherosclerosis) study. Researchers specifically selected participants with ideal metrics across all other known cardiovascular risk factors, so that LDL cholesterol could be examined in isolation. Those with low LDL levels had zero or near-zero arterial blockages; as LDL values increased, the degree of subclinical atherosclerosis rose proportionally. The data are striking: LDL appears to be causally linked to plaque formation even in otherwise healthy individuals.
There is a growing clinical push to reduce LDL cholesterol more aggressively and earlier in life — before cardiovascular risk factors accumulate. This is the central argument of the American Journal of Preventive Cardiology's review, There is urgent need to treat atherosclerotic cardiovascular disease risk earlier, more intensively, and with greater precision: A review of current practice and recommendations for improved effectiveness. That article is available here.
Are LDL-lowering therapies safe at very low target levels? A 2023 meta-analysis of randomised trials examining intensive LDL lowering indicated no additional safety risks. And while cholesterol is essential to bodily function, further studies have established that reducing blood LDL levels does not reduce cholesterol availability in organs such as the brain, and thus does not contribute to cognitive issues such as dementia — a common concern that the evidence does not support.
What are the side effects of rosuvastatin? Two are frequently cited in the literature.
The first is muscle aches and weakness (myalgia). A large-scale Lancet meta-analysis confirmed this is a real side effect; however, it is rare, with an incidence of approximately 1–2 people per 100. Both the incidence and the severity are lower at lower doses, which is why lower-dose prescribing is sometimes preferred for individuals who do not yet have established cardiovascular disease.
The second risk is new-onset type 2 diabetes. Studies have confirmed this association, though the absolute risk is low: approximately 50–100 new cases of type 2 diabetes per 10,000 participants were seen in trials — and these trials predominantly used high doses (around 40 mg). At lower doses, this risk is further attenuated.
Rosuvastatin is often chosen over other available statins for two practical reasons. First, it is low-cost. Second — and more clinically meaningful — it is water-soluble (hydrophilic), which means it does not accumulate in fat and muscle tissue the way lipophilic statins (such as simvastatin or atorvastatin) can. This solubility profile is thought to contribute to its favourable muscle-safety record.
For some individuals, healthy lifestyle habits — including an evidence-based diet, regular exercise, and adequate sleep — are sufficient to achieve target LDL levels. For others, rosuvastatin at a low dose may be a clinically appropriate addition. A target of under 60–70 mg/dL is increasingly recommended in preventive cardiology for younger, low-absolute-risk individuals who nonetheless have persistently elevated LDL. This is a conversation to have directly with a healthcare provider, with full context of individual risk factors.
Medications Under Research
Two additional medications are generating significant interest in preventive medicine and are worth monitoring as the evidence base matures.
The first is Ezetimibe 10 mg. Rather than reducing cholesterol production in the liver (as statins do), ezetimibe works by preventing the gut from reabsorbing cholesterol from bile after fat digestion. It is known to be very well-tolerated, with the most commonly reported side effect being a mild upset stomach. Clinically, ezetimibe is a useful adjunct when statin therapy alone does not achieve target LDL levels: rather than escalating statin doses — and thereby increasing the risk of dose-dependent side effects such as myalgia or new-onset diabetes — adding ezetimibe provides additional LDL reduction through a complementary mechanism. A 2022 RACING trial analysis found that the combination of moderate-intensity statin plus ezetimibe was more effective and had fewer side effects than high-intensity statin monotherapy alone, supporting the value of combination therapy over simply doubling the statin dose.
The second is Empagliflozin 10 mg (an SGLT2 inhibitor, brand name Jardiance). This medication was originally developed for type 2 diabetes, but research has revealed broader effects. Studies show it can help slow the progression of kidney disease in non-diabetic individuals as well — a finding of considerable clinical interest given how common age-related renal decline is. SGLT2 inhibitors work by reducing glucose and sodium reabsorption in the kidney tubules, which lowers intra-glomerular pressure and thereby reduces the mechanical stress that progressively damages kidneys over time. Human trials are still ongoing to fully characterise these renal-protective benefits in individuals with less advanced kidney disease at baseline. Preclinical evidence from the NIA's Interventions Testing Program also showed a 14% increase in lifespan for male mice given an SGLT2 inhibitor, adding to the mechanistic interest in healthspan applications — though mouse data require cautious extrapolation to human populations. The field continues to watch evolving trial results closely.
Both of these medications require a prescription and are not currently indicated for healthy individuals without the conditions they were approved to treat. Anyone interested in emerging research in this area should discuss it thoroughly with their own physician, as evidence and guidelines continue to evolve.
Sources
- Epidemiology of Prostate Cancer: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6497009/
- Biochemistry, Dihydrotestosterone: https://www.ncbi.nlm.nih.gov/books/NBK557634/
- The influence of finasteride on the development of prostate cancer: https://pubmed.ncbi.nlm.nih.gov/12824459/
- Long-term survival of participants in the prostate cancer prevention trial: https://pubmed.ncbi.nlm.nih.gov/23944298/
- Finasteride and high-grade prostate cancer in the Prostate Cancer Prevention Trial: https://pubmed.ncbi.nlm.nih.gov/17848673/
- Long-Term Effects of Finasteride on Prostate Cancer Mortality: https://www.nejm.org/doi/10.1056/NEJMc1809961
- Use of 5-α-Reductase Inhibitors for Prostate Cancer Chemoprevention: American Society of Clinical Oncology/American Urological Association 2008 Clinical Practice Guideline: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2668556/
- Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel: https://pubmed.ncbi.nlm.nih.gov/28444290/
- Progression of Early Subclinical Atherosclerosis (PESA) Study: JACC Focus Seminar 7/8: https://www.sciencedirect.com/science/article/pii/S0735109721051159?via%3Dihub
- There is urgent need to treat atherosclerotic cardiovascular disease risk earlier, more intensively, and with greater precision: A review of current practice and recommendations for improved effectiveness: https://www.sciencedirect.com/science/article/pii/S2666667722000551?via%3Dihub
- Safety and efficacy of very low LDL-cholesterol intensive lowering: a meta-analysis and meta-regression of randomized trials: https://pubmed.ncbi.nlm.nih.gov/36102667/
- Aggressive LDL-C Lowering and the Brain: Impact on Risk for Dementia and Hemorrhagic Stroke: A Scientific Statement From the American Heart Association: https://www.ahajournals.org/doi/pdf/10.1161/ATV.0000000000000164
- Effect of statin therapy on muscle symptoms: an individual participant data meta-analysis of large-scale, randomized, double-blind trials: https://www.thelancet.com/article/S0140-6736(22)01545-8/fulltext
- Interpretation of the evidence for the efficacy and safety of statin therapy: https://pubmed.ncbi.nlm.nih.gov/27616593/
- Moderate-intensity statin with ezetimibe vs. high-intensity statin in patients with diabetes and atherosclerotic cardiovascular disease in the RACING trial: https://pubmed.ncbi.nlm.nih.gov/36529993/
- Determinants of the Evolution of Kidney Function with Age: https://www.sciencedirect.com/science/article/pii/S2468024921014650
- Canagliflozin extends life span in genetically heterogeneous male but not female mice: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7710304/
