Prostate cancer doesn’t have a single cause. It develops when DNA in prostate cells mutates and triggers uncontrolled growth, but what drives those mutations varies from person to person. Most cases result from a combination of factors, some you can’t change (like age and genetics) and others tied to lifestyle and environment. Here are 10 well-established risk factors that contribute to prostate cancer.
1. Age
Age is the strongest risk factor for prostate cancer. The disease is rare before 40, and risk climbs sharply after 50. Incidence peaks in men aged 70 to 74, with a rate of 764 per 100,000 men in that age group. The vast majority of diagnoses occur in men over 65. This age-related increase likely reflects decades of accumulated DNA damage in prostate cells, combined with the ongoing hormonal stimulation that the prostate gland experiences throughout a man’s life.
2. Race and Ethnicity
Black men face the highest prostate cancer risk of any racial group, and the gap is significant. The incidence rate for non-Hispanic Black men is about 200 per 100,000, compared to 122 per 100,000 for non-Hispanic white men and 67 per 100,000 for Asian/Pacific Islander men. The disparity extends to mortality: Black men die from prostate cancer at roughly twice the rate of white men (36.2 vs. 18.1 per 100,000).
The reasons aren’t fully understood. Genetic differences, disparities in healthcare access, and variations in tumor biology all play a role. Notably, when prostate cancer does reach an advanced stage, Asian/Pacific Islander men actually have the highest five-year survival rate (42%) compared to Black men (31.6%) and white men (29.1%), suggesting the biology of the disease itself differs across populations.
3. Family History
Having a close relative with prostate cancer substantially increases your risk. A man with one first-degree relative (father or brother) diagnosed at any age has about 2.5 times the risk of the general population. If two or more first-degree relatives have been diagnosed, that risk jumps to roughly 4.4 times higher. The younger your relative was at diagnosis, the more it suggests a hereditary component that may affect you as well.
4. Inherited Gene Mutations
Family history reflects shared genetics, but specific inherited mutations can be pinpointed. Mutations in the BRCA1 and BRCA2 genes, better known for their link to breast cancer, also raise prostate cancer risk. BRCA2 mutations are particularly concerning because they’re associated with more aggressive, life-threatening forms of the disease. A third gene called HOXB13 carries a similar elevated risk profile.
These mutations follow an autosomal dominant pattern, meaning you only need to inherit one copy of the altered gene from one parent for your risk to increase. Dozens of other genes contribute smaller amounts of risk, often by interacting with the same biological pathways as BRCA1, BRCA2, and HOXB13. Genetic testing can identify these mutations if you have a strong family history.
5. Hormones
The prostate gland is fundamentally hormone-driven, and androgens (male sex hormones like testosterone) are the fuel that keeps prostate cells growing. Testosterone enters prostate cells and either binds directly to the androgen receptor or gets converted into dihydrotestosterone (DHT), which binds to that receptor even more tightly. Once the androgen receptor is activated, it switches on genes that tell prostate cells to multiply.
This mechanism operates in both normal and cancerous prostate tissue. It’s why hormone-suppressing therapy is a cornerstone of prostate cancer treatment: cutting off androgen supply can slow or shrink tumors. A lifetime of androgen exposure is part of why age matters so much. The prostate has been receiving growth signals for decades by the time most cancers appear.
6. Obesity
The relationship between body weight and prostate cancer is nuanced. Obesity doesn’t clearly raise the odds of getting any prostate cancer, but it does raise the odds of getting a dangerous one. Research shows an 8% to 11% increased risk of advanced prostate cancer and prostate cancer death in obese men, with about a 6% jump in advanced disease risk for every five-unit increase in BMI.
Overweight and obese men who are diagnosed also face worse outcomes overall: higher rates of recurrence after treatment, earlier progression to metastatic disease, more treatment side effects, and higher mortality. Excess body fat alters hormone levels, increases inflammation, and raises insulin, all of which can create a more favorable environment for aggressive tumors.
7. Diet and Calcium Intake
What you eat appears to influence prostate cancer risk, with dairy and calcium drawing the most research attention. Men consuming more than roughly 2,000 milligrams of dietary calcium per day (about the equivalent of six or more glasses of milk) showed a 34% higher risk compared to men consuming under 1,000 milligrams daily, according to a large National Cancer Institute screening trial. Low-fat dairy products specifically were linked to a 23% increased risk when intake exceeded about 2.75 servings per day.
The proposed mechanism involves vitamin D. High calcium intake can suppress your body’s production of the active form of vitamin D, which normally helps regulate cell growth in the prostate. Interestingly, calcium from supplements didn’t show the same association, suggesting that dairy itself may carry additional factors at play.
On the protective side, cruciferous vegetables like broccoli, cauliflower, and kale contain compounds called glucosinolates that break down into biologically active molecules during digestion. Some case-control studies have found that men eating more of these vegetables had lower prostate cancer risk, though large cohort studies in the U.S., Netherlands, and Europe have shown mixed results.
8. Geographic Location and Western Lifestyle
Where you live in the world dramatically affects your prostate cancer risk, and the differences are striking. In 2022, age-adjusted incidence rates ranged from 12.6 per 100,000 men in Asia to 82.8 per 100,000 in Northern Europe and 73.5 per 100,000 in North America. That’s a 13-fold gap between the highest and lowest regions worldwide.
These differences aren’t purely genetic. When men migrate from low-incidence countries (like Japan or China) to high-incidence countries (like the United States), their prostate cancer rates rise over time, often within a generation. This pattern points strongly to lifestyle factors, particularly the adoption of a Western diet that’s higher in processed foods, red meat, dairy, and overall calories. Rising obesity rates in traditionally low-incidence regions are also contributing to increasing prostate cancer diagnoses globally.
9. Chemical and Environmental Exposures
Certain toxic exposures are linked to prostate cancer, with Agent Orange being the most well-documented example. The National Academy of Sciences concluded there is limited but suggestive evidence of a positive association between prostate cancer and the herbicides used in Vietnam. A 2013 study from the Portland VA Medical Center found that veterans exposed to Agent Orange were not only at higher risk for prostate cancer but more likely to develop aggressive forms. The U.S. Department of Veterans Affairs recognizes this link and grants health care and disability benefits to exposed veterans with prostate cancer without requiring them to prove a direct connection.
Beyond Agent Orange, occupational exposure to pesticides, cadmium, and certain industrial chemicals has been investigated, though the evidence is less definitive. Firefighters, who face regular exposure to combustion byproducts, also show elevated rates.
10. Chronic Inflammation
Chronic inflammation of the prostate (prostatitis) has long been suspected as a cancer risk factor, since persistent inflammation can damage DNA and promote abnormal cell growth over time. Early studies suggested men with a history of prostatitis had roughly double the odds of developing prostate cancer. However, a systematic review and meta-analysis of 38 studies found that this association largely disappears when researchers account for detection bias. Men with prostatitis see doctors more frequently and undergo more testing, which catches cancers that would otherwise go undetected. After adjusting for this bias, the odds ratio dropped from 2.05 to a statistically neutral 1.16.
That said, inflammation at the cellular level still plays a theoretical role. Pathologists frequently find areas of inflammatory damage in prostate tissue removed during biopsies, and these areas sometimes sit adjacent to precancerous lesions. Whether this represents a true cause or simply a common companion remains an open question.
Screening Based on Your Risk
Because several of these factors overlap, the American Cancer Society tailors its screening recommendations accordingly. Men at average risk should discuss PSA testing with their doctor starting at age 50. Men at high risk, including Black men and those with a first-degree relative diagnosed before 65, should have that conversation at 45. Men at the highest risk, those with multiple close relatives diagnosed at an early age, should consider starting at 40.
If your PSA level comes back below 2.5 ng/mL, retesting every two years is generally sufficient. If it’s 2.5 or higher, annual screening is recommended. Screening doesn’t prevent prostate cancer, but it catches it earlier, when treatment options are broader and outcomes are significantly better.