PSA Test - What Your Result Means

PSA does not have a single "normal" cut-off - it must be interpreted by age, prostate size, ethnicity, and clinical context. Traditional threshold of 4.0 ng/mL misses 15–25% of cancers below this level and over-detects benign disease above it. Age-adjusted ranges are more useful: under 50 years: <2.5 ng/mL; 50–59 years: <3.5 ng/mL; 60–69 years: <4.5 ng/mL; 70+ years: <6.5 ng/mL. PSA density (PSA divided by prostate volume on MRI) and PSA velocity (rate of rise over time) add important context. A single PSA value cannot diagnose or exclude prostate cancer.

No. PSA (Prostate-Specific Antigen) is prostate-specific, not cancer-specific. The majority of men with a raised PSA do not have cancer. PSA is raised by: benign prostatic hyperplasia (BPH/enlarged prostate) - the most common cause; prostatitis (prostate infection or inflammation) - can cause dramatic PSA spikes; urinary tract infection; recent ejaculation (avoid 48 hours before the test); recent prostate biopsy or catheterisation; vigorous cycling or horseback riding (perineal pressure). After BPH and prostatitis are excluded, a persistently elevated PSA requires further evaluation with mpMRI and possibly biopsy.

PSA circulates in the blood in two forms - free (unbound) and complexed (bound to proteins). Prostate cancer tends to produce more complexed PSA, so men with cancer have a lower free PSA as a proportion of total PSA. A free/total ratio <10% is associated with higher cancer risk; >25% suggests lower risk. This ratio is particularly useful when total PSA is in the "grey zone" (4–10 ng/mL) where cancer and benign disease both occur commonly. The ratio helps triage which men need biopsy - it does not replace it.

PSA velocity is the rate of rise in PSA over time. A rise of more than 0.75 ng/mL per year (in men with PSA >4) or 0.4 ng/mL per year (in men with PSA 2–4) raises concern for cancer regardless of the absolute PSA level. PSA density is total PSA divided by prostate volume (measured on MRI or TRUS). A density >0.15 ng/mL/mL is associated with increased cancer risk. Both metrics help decide whether a raised PSA is likely due to a large benign prostate or whether cancer needs to be excluded. They require serial PSA measurements (velocity) or prostate imaging (density) to calculate.

Not automatically. Modern practice uses MRI-guided risk stratification before biopsy. A multiparametric MRI (mpMRI) of the prostate is performed first - if the scan shows a suspicious lesion (PIRADS 3–5), targeted biopsy of that lesion is performed in addition to systematic sampling. If the mpMRI is normal (PIRADS 1–2), biopsy may be safely deferred in low-risk cases - reducing unnecessary biopsies by approximately 30%. The MRI-first approach is now the standard of care in European and American guidelines. Dr. Nitin reviews mpMRI results with every raised-PSA patient before recommending biopsy.

Routine PSA screening is not universally recommended as population policy, but informed individual testing is appropriate for: men aged 50–70 at average risk who wish to be tested after understanding risks and benefits; men from age 45 with a family history of prostate cancer (father or brother); men of African descent from age 40–45 (higher risk population). A baseline PSA at age 40 is useful - men with PSA <1 ng/mL at 40 have very low cancer risk in the next decade; those with PSA 1–2 ng/mL at 40 should be monitored more closely. Dr. Nitin provides personalised guidance on testing intervals based on the baseline value.

No intervention has been conclusively proven to prevent prostate cancer. Lifestyle factors associated with lower risk include: maintaining a healthy weight (obesity increases risk of aggressive prostate cancer), regular exercise, a diet high in vegetables and low in red and processed meat, and moderate alcohol consumption. The REDUCE trial showed finasteride (a 5-ARI medication used for BPH) reduces detection of low-grade prostate cancer but may increase detection of high-grade cancers - it is not recommended as a preventive strategy outside clinical trials. Lycopene (in tomatoes), selenium, and Vitamin E have been studied but evidence is inconsistent.