Mortality has long been one of the greatest fears, concerns, and challenges humankind has faced throughout our long history. For my part, there are two medications I personally take to help me remain as healthy as possible for as long as possible. There are also a couple that I'm strongly considering taking in the future. Let's talk about each of them, the science behind them, and whether or not you should consider taking them as well.
Before we begin, my usual disclaimer: just because I take a particular medication doesn't mean you should take it as well. Everyone's body is different, everyone's health situation is different, and everyone's goals are different. Take the medications I mention here and bring them up with your own healthcare provider if you're interested in their benefits, and make the decision for yourself.
Table of Contents
Medication 1: Finasteride
The first medication is finasteride, in a 1 mg dose. I've taken this medication for the past 3-4 years. Why?
One of the leading causes of death for men worldwide is prostate cancer. It's the second-most frequently diagnosed cancer in men and the fifth leading cause of death worldwide. (If you're curious, the first-most frequently diagnosed is lung cancer.) Prostate cancer is also often asymptomatic, so it can be difficult to detect until well past the point where easy treatment is viable. Regular screening is recommended starting at age 45-50, specifically for this reason, because outcomes are much better when it's caught early.
Where does finasteride come into play? Well, as a medication, it functions by blocking the conversion of the hormone testosterone into dihydrotestosterone. Dihydrotestosterone, or DHT, is an incredibly important hormone in male children. It plays a vital role in the sexual development of young boys throughout puberty, promoting prostate growth, body and facial hair growth, and other sex characteristics.
What about after puberty? Well, in adult life, DHT doesn't seem to play any significant role, nor does it have a role in female physiology. For adult males, DHT seems to do two things: promote male pattern baldness and enlarge the prostate.
The theory, then, is that by lowering the amount of DHT in the body as an adult male, we can help reduce the size of the prostate and, correspondingly, reduce rates of prostate cancer. That's a great theory, but does it hold up in practice?
In 2003, a study called the Prostate Cancer Prevention Trial was published. This study involved a little under 19,000 men and tested a 5 mg dose of finasteride against a placebo. The results were very positive: after seven years, the prevalence of prostate cancer diagnoses was 24.8% lower in the finasteride group than in the control group (803 out of 4368 for finasteride, 1147 out of 4692 for control).
Because of these promising results, the study continued to follow these groups for up to 18 years of additional follow-up. The results continued over time, with about a 30% reduction in prostate cancer diagnoses in the finasteride group versus the control group across all points of the studies.
It's not all unmitigated good news, though. Through observation, it appears that finasteride reduces the chances of developing prostate cancer, but among those who do develop it, they had a higher rate of developing a high-grade version of the cancer. Before you assume that means finasteride causes higher-grade cancer, though, let's dig a bit deeper.
Prostate cancer is evaluated using the Gleason scale, which ranges from 6 to 10. A score of 6 is a lower-grade, less aggressive cancer, while a score of 10 is a high-grade and more aggressive cancer. This is important, because the higher grade the cancer is, the faster it grows and the more difficult it can be to treat.
What the study observed was that, among those diagnosed with prostate cancer, the finasteride group had a higher incidence of higher-grade cancers. However, something interesting is happening here. Finasteride keeps the prostate smaller by lowering levels of DHT. That makes it easier to detect lumps and bumps in the prostate. Finasteride isn't increasing the rates at which high-grade cancers occur; it's making it easier to detect them. This is known as detection bias.
A related question you might have is if finasteride improves outcomes and survival. The answer is both yes and no. Finasteride itself does not seem to improve survival outcomes, but early detection is beneficial for catching and treating cancers, so anything that makes it easier to detect prostate cancer – especially high-grade cancer – is beneficial.
So, essentially, it boils down to finasteride reducing the development of prostate cancer, having no detrimental effect on survival, and increasing early detection of high-grade prostate cancer.
What about side effects? Does finasteride have any meaningful side effects? Finasteride lowers prostate blood levels, which are used in detecting prostate problems via blood tests. That means if you're on finasteride, your normal range is lower; if your detected range is in the usual normal range, that actually means your levels are elevated. It's a bit of context that doctors will need to pay attention to when evaluating their patients.
Another potential side effect is that nearly all trials have shown a 2-4% increase in reported erectile dysfunction and gynecomastia. These side effects also may not go away entirely, even if you stop taking finasteride, in what is known as post-finasteride syndrome.
I've decided to take a lower dose than what was used in the study – 1 mg versus 5 mg – because I'm still young. My hope is that it will act as a proactive preventative without the same side effects, and I can always increase the dose later if it seems indicated that I should do so.
Medication 2: Rosuvastatin
The second medication I'm taking is 5 mg of rosuvastatin. I've been taking it for a little over a year, and I'm taking a very low dose. The typical maximum dose is 40 mg, so I'm taking a 1/8th dose. Again, just because I'm taking this medication does not mean you should as well. Always talk to your healthcare provider about your options and how they relate to your own health concerns.
What is rosuvastatin? It's a statin medication. Statins are a class of medications that work to reduce cholesterol in the body. Rosuvastatin specifically works on cholesterol in the liver.
Why is this important? Over 200 cohort studies, Mendelian randomization studies, and randomized trials were all evaluated through a meta-analysis covering over 2 million participants.
This massive amount of data shows conclusively that LDLs – low-density lipoproteins lead to the development of heart disease. They aren't the only cause of heart disease, but they are a significant contributing factor. This has been shown time and time again across a wide range of studies.
One of the most striking studies is the PESA study, which specifically selected a group of people with ideal metrics for all other known risk factors of heart disease but higher levels of LDL cholesterol. Those with low levels of LDL had zero or near-zero blockages, while the higher LDL values grew, the more blockages occurred.
I'm taking rosuvastatin because of this benefit in lowering LDL cholesterol. I'm taking a lower-than-normal dose because I'm taking it relatively early in life when other risk factors have not built up. There's a growing push to reduce LDL cholesterol more aggressively and earlier in life, as well. It's the core point of the American Journal of Preventive Cardiology's article 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. You can read that article here.
Are therapies that target LDL safe? Studies say yes. A meta-analysis from 2023 of studies into LDL-reducing therapies indicated no additional risks. Cholesterol is used throughout the body and is essential to life, but additional studies have shown that reducing blood LDL levels does not reduce those levels in organs like the brain and thus does not contribute to cognitive issues like dementia.
Are there side effects to rosuvastatin? Yes. Potentially, there were two that concerned me.
The first is muscle aches and weakness. A meta-analysis confirmed that this is a side effect; however, it's very rare, with an incidence of about 1-2 people per 100. Furthermore, both the incidence and the severity are lower the lower the dose of statins, hence my choice to opt for a low dosage.
The second risk is diabetes. Studies also confirmed this risk, but it's also very low; only around 50-100 new cases of Type II diabetes were diagnosed per 10,000 participants in studies, and again, they were taking a high 40 mg dose of statins. So, it is a low risk and can be further alleviated through a low dosage.
In my case, all of my healthy habits – diet, exercise, sleep – couldn't bring my LDL down to my target levels of under 60 mg/dl. Taking a low dose of rosuvastatin for a year, however, has helped me achieve that goal. I chose rosuvastatin out of all of the available statins for two reasons. The first is that it's very cheap, but the second and more important reason is that it's water-soluble, so it doesn't get transported to places in the body where I don't want it to go like a fat-soluble statin would.
Future Medications
There are two medications I'm keeping my eye on as potential future additions to my routine.
The first is Ezetimibe 10 mg. This medication prevents the gut from reabsorbing cholesterol from bile after digesting fat. It's known to be very well-tolerated, with the only side effect being a slightly upset stomach. I'm keeping this medication on my list in case my current regimen no longer keeps my LDL within my target range. Instead of just increasing rosuvastatin – and increasing the risk of side effects – I plan to simply add ezetimibe instead. As it turns out, the combination of ezetimibe and a statin is more effective and has fewer side effects than a statin alone.
The second medication I'm keeping an eye on is Empagliflozin 10 mg. This medication was designed for Type II diabetics, but as it turns out, it helps slow the progression of kidney disease in non-diabetics as well. Now, trials are still being conducted to validate these benefits and to study why and how they function. Some promising results have come from studies in mice as well, which showed a 14% increase in lifespan for male mice given the medication.
Again, I haven't started taking this medication yet. I'm currently waiting for the results of ongoing human studies to see if they show benefits for kidney disease, particularly in cases that aren't as advanced as the ones in existing studies.
For now, I'm happy to stick with a healthy diet, plenty of exercise, and great sleep, alongside MicroVitamin and medications such as rosuvastatin and finasteride. Again, I have to reiterate: just because I've chosen to take these medications does not mean you should as well. Consider the science, consider your own health and ongoing concerns, and talk to your own doctor about what you should take.
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/
