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Benign Prostatic Hyperplasia · BPH
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In one pass The prostate is a ring of gland tissue wrapped around the outlet of the bladder.
Educational content, not medical advice — consult a clinician.
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Chapter 1
What an enlarged prostate is
The prostate is a ring of gland tissue wrapped around the outlet of the bladder. To leave the bladder, urine has to pass through the stretch of urethra the prostate encircles. When cells multiply in the part closest to the urethra (the transition zone), they squeeze that tube narrower. What drives the growth is mainly dihydrotestosterone (DHT) inside the gland, not the testosterone circulating in the blood.
This is benign prostatic hyperplasia (BPH): benign, not cancer, and not "kidney weakness". Getting up more at night and a thinner stream are usually this ring squeezing. Most of the time it can be handled without hurry. But if you suddenly cannot pass urine at all and your lower belly is painfully full, that is acute urinary retention — go to the emergency department now. Visible blood in the urine also needs a urologist soon.
This is benign prostatic hyperplasia (BPH): benign, not cancer, and not "kidney weakness". Getting up more at night and a thinner stream are usually this ring squeezing. Most of the time it can be handled without hurry. But if you suddenly cannot pass urine at all and your lower belly is painfully full, that is acute urinary retention — go to the emergency department now. Visible blood in the urine also needs a urologist soon.
Mechanism · Where it grows and why it squeezes
First get the location clear. The prostate sits directly below the bladder, wrapped like a doughnut around the first stretch of the urethra. To leave the bladder, urine has to pass through this ring; when the gland enlarges, the first thing it squeezes is this tube, and that is why urination is affected.Take the name apart: benign means not cancer, and not a precancerous lesion either; prostatic means it happens in this gland; hyperplasia means more cells (not bigger individual cells), forming nodules that push the gland larger.
Once you know this is simply the gland growing with age and pressing on the urethra, you will not treat it as "kidney weakness" and load up on remedies, and you will not scare yourself that every night-time trip means cancer. Why it does not turn into cancer is covered in the chapter Not cancer, and not prostatitis.
Numbers · How common it is, and two kinds of symptoms
How common it is under the microscope: Berry 1984 pooled 10 independent autopsy studies covering more than 1000 prostates. About 8% of men in their thirties (ages 31–40) already had hyperplasia on histology, and about 50% of men in their fifties (ages 51–60), and the share keeps rising with age. Live long enough and the prostate almost always enlarges. But hyperplasia on histology is not the same as symptoms: only about half of men are noticeably bothered by it.The symptoms are called lower urinary tract symptoms (LUTS), in two groups:
Voiding (obstructive): slow to start, a weak stream, a stream that stops and starts, feeling you have not emptied, dribbling afterward.Storage (irritative): needing to go often, nocturia (getting up at night to urinate), urgency.
Severity is scored with the International Prostate Symptom Score questionnaire (IPSS, also called the AUA-SI), from 0 to 35: under 8 is mild, 8–19 moderate, and 20 or more severe. It is also the ruler for deciding whether treatment is needed and whether it is working. Mild cases can be watched for many years and may even improve on their own; it does not turn into cancer, which is the first worry worth putting down.
Chapter 2
Why the prostate grows
The prostate does not enlarge for no reason; two conditions have to be met together — long-term exposure to testosterone, plus aging (Bartsch 2002). Men who lost their testes before puberty almost never develop benign prostatic hyperplasia.
The hormone that does the work is not testosterone in the blood but dihydrotestosterone (DHT) inside the gland: once testosterone enters the prostate, the enzyme type 2 5-alpha-reductase converts it. The growth happens mainly in the ring around the urethra (the transition zone). Poor flow comes from two forces: a static one, the bulk of the gland narrowing the tube, and a dynamic one, alpha-1 receptors on smooth muscle making the muscle contract and tighten the outlet further.
The hormone that does the work is not testosterone in the blood but dihydrotestosterone (DHT) inside the gland: once testosterone enters the prostate, the enzyme type 2 5-alpha-reductase converts it. The growth happens mainly in the ring around the urethra (the transition zone). Poor flow comes from two forces: a static one, the bulk of the gland narrowing the tube, and a dynamic one, alpha-1 receptors on smooth muscle making the muscle contract and tighten the outlet further.
Mechanism · DHT in the gland does the work
The key molecule is not testosterone but dihydrotestosterone (DHT). Once inside the prostate, testosterone is converted to DHT by 5-alpha-reductase (type 2). DHT binds the prostate's androgen receptors far more strongly than testosterone does, and it is the androgen that actually does the work in the gland.The interesting part: with age, testosterone in the blood falls, yet DHT inside the prostate holds up — which is exactly why 5-alpha-reductase inhibitors (finasteride, dutasteride) can work. Block this conversion step and the gland loses its signal to grow.
Both conditions are needed: long-term testosterone exposure, plus aging. Men who lost their androgens before puberty almost never get the disease, and this classic observation is the foundation of the whole mechanism (Bartsch 2002).
Mechanism · Why it grows in the ring around the urethra
Two kinds of tissue enlarge: the stroma (smooth muscle plus connective tissue) and the epithelium (the gland's lining cells). Both multiply together and form nodules. The location matters: it happens mainly in the transition zone, which is exactly the ring wrapped around the urethra (McNeal 1981).For contrast, prostate cancer arises mainly in the peripheral zone, away from the urethra. The hyperplasia that squeezes the tube and the cancer that often does not are not growing on the same patch of ground — that is the key to telling the two diseases apart.
Mechanism · The two parts of the blockage
Poor flow comes from two components of bladder-outlet obstruction. The static component is mechanical: the enlarged gland directly narrows the urethra. The dynamic component is muscle tone: the smooth muscle of the prostate and the bladder neck is dense with alpha-1 (mainly alpha-1A) adrenergic receptors. When the sympathetic nervous system fires (stress, cold, some medicines), that muscle contracts and tightens the outlet further.These two components match two classes of drug: 5-alpha-reductase inhibitors lower DHT and slowly shrink the static component (it takes months); alpha-blockers relax the dynamic component (they work within 1–2 weeks). Understand the two components and you understand why doctors sometimes use both drugs together (see the chapter Saw palmetto and medical treatment).
After the obstruction, the bladder changes too. With a narrowed outlet the bladder has to push harder to empty, and the muscle of its wall (the detrusor) thickens to compensate. A thickened bladder becomes unstable and easily irritated, and that is where the storage symptoms — frequency, urgency and night-time urination — come from. So the symptoms come not only from the narrowing but also from a bladder dragged along with it. If it can no longer compensate over the long term, more urine is left behind, leading to repeated infections, stones and, at worst, acute urinary retention (being unable to pass urine at all, which needs emergency care).
The whole chain: testosterone plus aging → DHT inside the prostate → growth of transition-zone stroma and epithelium → the urethra statically narrowed and dynamically tightened → the bladder forced to push harder and thicken → lower urinary tract symptoms. Every link corresponds to a piece of understanding or a treatment.
Chapter 3
Not cancer, and not prostatitis
Three conditions share the prostate, yet their mechanisms, locations and dangers are completely different. Benign prostatic hyperplasia grows in the transition zone around the urethra; it is benign and does not turn into cancer. Prostate cancer arises mainly in the peripheral zone, away from the urethra, and early on it often causes no urinary symptoms at all. The most common kind of prostatitis is mainly about pain, not painless narrowing.
Lumping them together either frightens you, or lets a real problem slide as "just an enlarged gland". Whether to test (PSA) and whether to be screened are decisions made with your doctor, not self-diagnosis.
Lumping them together either frightens you, or lets a real problem slide as "just an enlarged gland". Whether to test (PSA) and whether to be screened are decisions made with your doctor, not self-diagnosis.
Clinical · Telling BPH from prostate cancer
Benign prostatic hyperplasia (BPH): it grows in the transition zone (the ring around the urethra); it is benign, not cancer and not a precancerous lesion (Chughtai 2016). Some research suggests that the genetic variants that raise the risk of BPH and urinary symptoms overlap very little with those that raise the risk of prostate cancer — they are two different diseases. They often occur together mainly because both become common with age; having both does not mean one caused the other.Prostate cancer: it arises mainly in the peripheral zone (about 70–80%, McNeal 1981), which lies away from the urethra. That leads to a counter-intuitive but important fact: early prostate cancer usually causes no urinary symptoms. So having urinary symptoms does not mean you have cancer, and having none does not mean you do not. The vast majority of urinary symptoms come from BPH; only a small share are caused directly by cancer. Early cancer is mostly found through screening (a test) or a digital rectal exam (DRE, in which a doctor feels the prostate with a finger through the rectum and finds a hard nodule), not because the stream got weaker.
Clinical · Pain points to prostatitis
The US National Institutes of Health (NIH) classifies prostatitis into 4 categories (Krieger 1999): category I, acute bacterial; category II, chronic bacterial; category III, chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS); and category IV, inflammation without symptoms. The most common is category III: pain in the pelvis, the perineum or on ejaculation, usually with no bacteria found, not much related to age, and common in younger and middle-aged men.It is not the same thing as the painless obstruction of BPH: when pain dominates, think prostatitis; with age and a thinner stream, think BPH. Do not explain pain, blood in the urine or a sudden worsening as "just an enlarged prostate" — those have other causes. Leave telling them apart to a urologist; do not diagnose yourself.
Clinical · Reading PSA, and whether to screen
Prostate-specific antigen () is specific to the prostate, not to cancer: BPH, prostatitis, ejaculation, long bike rides and a digital rectal exam can all raise it. 5-alpha-reductase inhibitors lower PSA by about 50% (multiply by 2 to correct when reading it). So a single PSA number is easy to misread; it has to be combined with the rectal exam, the free-PSA ratio and the trend over time, with MRI or biopsy when needed, and read by a urologist.Screening is a shared decision; there is no standard answer to "should I be tested". The 2018 recommendation of the US Preventive Services Task Force (USPSTF) is this: for men aged 55–69, the USPSTF gives PSA screening a grade C recommendation, meaning the net benefit is small and each man should weigh it with his doctor — the benefit is catching a treatable high-risk cancer early, and the costs are false positives, overdiagnosis and overtreatment. For men aged 70 and over, the USPSTF gives a grade D, meaning routine screening is not recommended. Family history, ethnicity and life expectancy all shift this balance; it is a value judgment made together with your doctor.
To sum up: BPH is not cancer and not prostatitis. Do not assume an enlarged prostate means cancer, and do not explain every symptom as "just an enlarged gland".
Chapter 4
What lifestyle changes can do
Lifestyle cannot shrink a prostate that has already grown, but it can ease symptoms, may slow progression, and has no drug side effects. Do not expect it to shrink the gland, and do not skip it just because it cannot.
Metabolic syndrome and belly fat have an observed association with a larger prostate, so improving metabolism often pays off in several ways at once. The first things worth doing are behavioral: drink less before bed, cut back on alcohol and coffee, and read the ingredients before buying cold medicine. No food or supplement has been shown in large trials to shrink the prostate.
Metabolic syndrome and belly fat have an observed association with a larger prostate, so improving metabolism often pays off in several ways at once. The first things worth doing are behavioral: drink less before bed, cut back on alcohol and coffee, and read the ingredients before buying cold medicine. No food or supplement has been shown in large trials to shrink the prostate.
Evidence · How metabolism relates to prostate size
Metabolic syndrome and obesity really are linked to the prostate; this is not folklore. The Gacci 2015 (8 studies, 5403 men) found that men with metabolic syndrome had prostates that were on average 1.8 mL larger, more so among older men with obesity. Belly fat, insulin resistance and abnormal blood lipids are all associated with prostate enlargement.This places BPH in the same metabolic web as the age-related fall in male androgens, metabolic syndrome and type 2 diabetes, so the same lifestyle improvements often help across the board. To be honest about it: this is mostly observational evidence, an association that cannot prove cause, and an average difference of 1.8 mL is not large. Weight loss improves metabolism and helps symptoms, but do not expect the prostate to shrink noticeably.
In practice · Which habits to change first
Evidence-based symptom management is the tier worth doing first:Drink less in the evening: drinking less in the 2–3 hours before bed means fewer night-time trips.Cut back on alcohol, coffee and fizzy drinks: they both increase urine and irritate the bladder, so less of them eases frequency and urgency.Be careful with over-the-counter medicines: cold and allergy products with antihistamine or anticholinergic action, and nasal decongestants containing pseudoephedrine, can make urinating harder and can even trigger acute urinary retention — read the ingredients before you buy.Timed voiding, plus double voiding: after you finish, wait a moment and go again, to leave less urine behind.Bladder training: when urgency hits, hold on for 30 seconds before you go.Treat constipation, exercise regularly, lose weight: a full rectum makes symptoms worse, and people who are more physically active have fewer urinary symptoms (an observed association).
Evidence · Can supplements shrink the prostate?
No food or supplement has been shown in large to shrink the prostate or reliably improve urinary symptoms. Beta-sitosterol, rye-grass pollen extract (Cernilton), lycopene and pumpkin-seed oil have weak signals, small trials and inconsistent results — try them if you want, but they cannot replace an assessment and should not be relied on. Saw palmetto is the one in this group with the biggest gap between marketing and evidence, and it gets its own treatment in the chapter Saw palmetto and medical treatment.Do not buy a "prostate complex" bundle: with zinc, lycopene, pollen extract and saw palmetto mixed together, there is no way to tell which ingredient helps or which carries risk, and it is poor value.
Lifestyle is an adjunct and the first tier, most valuable for mild cases: fewer night-time trips, less urgency, and better metabolic health along the way. But it has a ceiling: do not use "I'm working on my lifestyle" to put off a proper assessment of moderate-to-severe symptoms or red-flag signs. People who understand the mechanism treat lifestyle and medical assessment as partners, not an either/or.
Chapter 5
Saw palmetto and medical treatment
This chapter is not a prescription: whether to take a drug, which one and at what dose must be decided by a doctor. It is here so you can follow why doctors treat in tiers, and why the best-selling natural option has a mechanism that sounds right yet failed in human trials.
In large, independent trials saw palmetto did no better than placebo, and the American Urological Association (AUA) guideline does not recommend it for urinary symptoms caused by an enlarged prostate. It is relatively safe, but in these trials it did not work (see Saw Palmetto). What has actually been tested in is the ladder of behavior → prescription drugs → surgery.
In large, independent trials saw palmetto did no better than placebo, and the American Urological Association (AUA) guideline does not recommend it for urinary symptoms caused by an enlarged prostate. It is relatively safe, but in these trials it did not work (see Saw Palmetto). What has actually been tested in is the ladder of behavior → prescription drugs → surgery.
Evidence · What the large saw palmetto trials found
Saw palmetto is the best-selling herbal supplement for an enlarged prostate, and its proposed mechanism (mild inhibition of 5-alpha-reductase, plus an anti-inflammatory effect) sounds plausible. But large, independently funded, rigorously blinded have all failed to beat placebo.The STEP trial (Bent 2006, NEJM): 225 men with moderate-to-severe symptoms took 320 mg a day for 1 year against placebo — there was no difference in symptom score, urine flow rate, prostate volume or quality of life.The CAMUS trial (Barry 2011): the dose was stepped up to 960 mg a day, and there was still no difference from placebo, which rules out the "not enough of it" excuse.A Cochrane systematic review (Tacklind 2012, 32 randomized controlled trials, 5666 men): pooled together, symptom scores and flow rates were no different from placebo.The AUA guideline amended in 2023 explicitly does not recommend saw palmetto for urinary symptoms caused by an enlarged prostate.
It is relatively safe: it will not harm you, and in these trials it did not treat you either. "Feeling much better" on it is mostly placebo plus the natural ups and downs of the symptoms. Why the early small trials came out positive is told in full in the saw palmetto story (see Saw Palmetto). Save the money and time you would spend on saw palmetto, and get to know the treatment ladder that has actually been tested in randomized controlled trials.
Clinical · How doctors tier treatment
Below is the tiered approach modern medicine takes to benign prostatic hyperplasia. For education only: whether to use a drug, which one and at what dose must be decided by a doctor based on your severity, prostate size, tolerance for side effects, plans for children and other medicines.Tier 0 · Watchful waiting
Mild symptoms (IPSS < 8) and no complications: many men stay stable for years, and regular review is enough.First, do the behavioral changes and weight loss from the chapter What lifestyle changes can do properly.
Tier 1 · Alpha-blockers (such as tamsulosin, alfuzosin, silodosin)
Mechanism: they relax the smooth muscle of the prostate and bladder neck, which carries alpha-1A receptors, and so address the dynamic component of the obstruction.They work fast (1–2 weeks); the symptom score (IPSS) often falls by about 30–40%, and flow rate improves.Side effects: dizziness and low blood pressure on standing, and retrograde ejaculation (semen going back into the bladder, especially common with silodosin). Tell your eye surgeon before cataract surgery, because these drugs can cause intraoperative floppy iris syndrome (IFIS).
Tier 2 · 5-alpha-reductase inhibitors (finasteride, dutasteride)
Mechanism: they block the making of DHT, so the prostate shrinks by about 20–25%, addressing the static component. They work slowly (3–6 months) and are most valuable for a large prostate.They change the course of the disease: in the PLESS trial (McConnell 1998, NEJM), finasteride cut the risk of acute urinary retention by about 57% and the risk of needing surgery by about 55%.Side effects: lower libido and erectile function (the Liu 2016 : at doses used for an enlarged prostate, the of sexual dysfunction was RR ≈ 2.56); they also lower by about 50% (correct for this when reading it).
Tier 3 · An alpha-blocker plus a 5-alpha-reductase inhibitor together
The MTOPS trial (McConnell 2003, NEJM, mean follow-up 4.5 years): the combination cut the risk of clinical progression by about 66%, better than either drug alone — suited to men with moderate-to-severe symptoms and a large prostate.
Tier 4 · Other drugs, and minimally invasive procedures or surgery
Low-dose daily tadalafil (which also helps erectile function).When an overactive-bladder component is present, a doctor may add an anticholinergic drug or a beta-3 agonist.Minimally invasive procedures or surgery: prostatic urethral lift (UroLift), water-vapor ablation (Rezūm), transurethral resection of the prostate (TURP), and laser surgery (HoLEP, GreenLight) — for drugs that do not work, repeated urinary retention, blood in the urine, stones, or kidney function that is being affected.
In short: the effective options are the ladder of behavior → prescription drugs → surgery, tested in large , not a supplement blend on the shelf. Once you understand the mechanism (the static and dynamic components), you can follow why a doctor orders them this way — but which tier you are on is decided by you and your doctor together.
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Chapter 6
When to see a doctor
Benign prostatic hyperplasia can usually be handled without hurry. But being unable to pass urine at all, or seeing blood in the urine, cannot wait at home or be handled with supplements. Urinary retention is a urological emergency. Visible blood in the urine, even once, needs assessment by a urologist (Barocas 2020); you cannot assume it is an enlarged prostate.
Understanding the mechanism keeps you calm, but understanding is not self-diagnosis. This is health education, not a diagnosis and not a prescription; the red-flag list, the routine path to a diagnosis and the full disclaimer are all in this chapter.
Understanding the mechanism keeps you calm, but understanding is not self-diagnosis. This is health education, not a diagnosis and not a prescription; the red-flag list, the routine path to a diagnosis and the full disclaimer are all in this chapter.
Red flag · Retention and visible blood cannot wait
Red flags needing prompt care / the ER:Cannot pass any urine + severe lower-abdominal distension = acute urinary retention: a urologic emergency — the trapped bladder needs catheter decompression → go to a clinic / ER immediatelyGross hematuria (visible blood or clots in urine): any single episode warrants urology evaluation, at any age — to rule out bladder, prostate, or kidney tumors (Barocas 2020). BPH can cause bleeding, but you cannot assume it is BPH yourselfRecurrent urinary tract infections, or fever + flank pain + chills: the upper tract / kidney may be involvedPersistent incomplete emptying + rising blood creatinine / hydronephrosis on ultrasound: obstruction is already affecting kidney functionPain-predominant picture (perineal / pelvic / ejaculatory pain): think prostatitis, not simple BPHBone pain + unexplained weight loss, or a hard nodule on DRE / clearly abnormal : needs a work-up for prostate cancer (note: what triggers the work-up is these systemic/exam signals, not LUTS itself)
Key to the abbreviations: BPH is benign prostatic hyperplasia; creatinine is a blood marker of kidney function; hydronephrosis means urine backing up and pooling in the kidney; DRE is a digital rectal exam; PSA is prostate-specific antigen; LUTS are lower urinary tract symptoms.
Clinical · The routine path to a diagnosis
The routine, non-emergency path (the one most people take): first record your International Prostate Symptom Score (IPSS) and a voiding diary (how often, night-time trips, the volume each time) — these are the most useful things to bring to the visit. A basic urology or primary-care assessment covers your history, a digital rectal exam, a urine test, when appropriate (a shared decision), and a flow-rate test with an ultrasound of the urine left behind. Start with behavioral changes plus watchful waiting, then discuss with your doctor, according to severity, whether to use medicine and at which tier.Practical summary: benign prostatic hyperplasia is common and mostly benign. Understanding the mechanism (DHT → transition-zone growth → bladder-outlet obstruction → lower urinary tract symptoms) keeps you calm and helps you see through pitches for "prostate miracle cures", "detox" or "natural shrinking". But understanding is not self-diagnosis: behind urinary symptoms there may be an enlarged prostate, cancer, prostatitis, an overactive bladder, the heavy urine output of diabetes, or a medicine — telling them apart needs a professional assessment. Lifestyle is a good first tier, but it has a ceiling; moderate-to-severe symptoms or red flags need the medical path.
Disclaimer: this page is health education, not a diagnosis and not a prescription, and it cannot replace an in-person assessment by a urologist or primary-care doctor. Whether to have PSA screening, which drug to use and whether to have surgery should all be decided together with your doctor. If red flags appear — being unable to pass urine, visible blood in the urine, fever with flank pain, abnormal kidney function — seek medical care immediately.
References · 12
- Berry, S. J., Coffey, D. S., Walsh, P. C., & Ewing, L. L. (1984). The development of human benign prostatic hyperplasia with age. Journal of Urology, 132(3), 474-479. Pooled data from 10 independent autopsy studies, more than 1,000 prostates. Pathological BPH prevalence is 8% in the fourth decade (ages 31-40) and 50% at ages 51-60; the abstract gives no figure for men in their 70s or 80s. Normal prostate ~20 ± 6 g at ages 21-30; only 4% of prostates in men over 70 exceed 100 g; BPH growth probably begins before age 30 (abstract, PMID 6206240). 10.1016/S0022-5347(17)49698-4
- Chughtai, B., Forde, J. C., Thomas, D. D. M., et al. (2016). Benign prostatic hyperplasia. Nature Reviews Disease Primers, 2, 16031. 10.1038/nrdp.2016.31
- Bartsch, G., Rittmaster, R. S., & Klocker, H. (2002). Dihydrotestosterone and the concept of 5alpha-reductase inhibition in human benign prostatic hyperplasia. World Journal of Urology, 19(6), 413-425. 10.1007/s00345-002-0248-5
- McNeal, J. E. (1981). The zonal anatomy of the prostate. The Prostate, 2(1), 35-49. 10.1002/pros.2990020105
- Krieger, J. N., Nyberg, L., Jr., & Nickel, J. C. (1999). NIH consensus definition and classification of prostatitis. JAMA, 282(3), 236-237. 10.1001/jama.282.3.236
- Grossman, D. C., Curry, S. J., Owens, D. K., et al. (US Preventive Services Task Force). (2018). Screening for prostate cancer: US Preventive Services Task Force recommendation statement. JAMA, 319(18), 1901-1913. 10.1001/jama.2018.3710
- Gacci, M., Corona, G., Vignozzi, L., et al. (2015). Metabolic syndrome and benign prostatic enlargement: a systematic review and meta-analysis. BJU International, 115(1), 24-31. 10.1111/bju.12728
- Sandhu, J. S., Bixler, B. R., Dahm, P., Goueli, R., Kirkby, E., Stoffel, J. T., & Wilt, T. J. (2024). Management of lower urinary tract symptoms attributed to benign prostatic hyperplasia: AUA guideline amendment 2023. Journal of Urology, 211(1), 11-19. AUA notes that the evidence does not support a benefit from saw palmetto and does not recommend it for LUTS/BPH. 10.1097/JU.0000000000003698
- Bent, S., Kane, C., Shinohara, K., Neuhaus, J., Hudes, E. S., Goldberg, H., & Avins, A. L. (2006). Saw palmetto for benign prostatic hyperplasia. New England Journal of Medicine, 354(6), 557-566. STEP trial: 320 mg/day saw palmetto × 1 yr vs placebo in 225 men with moderate-severe BPH — no difference in AUA-SI, max urinary flow, prostate size, or QoL. Saw palmetto extract 160 mg twice daily. Between-group differences: AUASI 0.04 point (-0.93 to 1.01) and maximal urinary flow 0.43 mL/min (-0.52 to 1.38); no difference in prostate size, post-void residual volume, quality of life or PSA (abstract, PMID 16467543). 10.1056/NEJMoa053085
- Barry, M. J., Meleth, S., Lee, J. Y., Kreder, K. J., Avins, A. L., Nickel, J. C., et al. (2011). Effect of increasing doses of saw palmetto extract on lower urinary tract symptoms: a randomized trial (CAMUS). JAMA, 306(12), 1344-1351. Dose-escalation 320 → 640 → 960 mg/day × 72 wk in 369 men — no benefit at any dose vs placebo. The group mean difference in AUASI change at 72 weeks was 0.79 points favouring placebo (upper bound of the one-sided 95% CI most favourable to saw palmetto 1.77; one-sided P = .91). Saw palmetto was no better for any secondary outcome - urinary bother, nocturia, peak uroflow, postvoid residual volume, PSA, global assessments, sexual function, continence, sleep and prostatitis symptoms; prostate volume is not among the listed outcomes (abstract, PMID 21954478; full text, PMC3326341). 10.1001/jama.2011.1364
- Tacklind, J., MacDonald, R., Rutks, I., Stanke, J. U., & Wilt, T. J. (2012). Serenoa repens for benign prostatic hyperplasia. Cochrane Database of Systematic Reviews, (12), CD001423. Updated meta of 32 trials, N=5,666: no difference vs placebo on urinary symptom scores or flow rate. 10.1002/14651858.CD001423.pub3
- Barocas, D. A., Boorjian, S. A., Alvarez, R. D., et al. (2020). Microhematuria: AUA/SUFU Guideline. Journal of Urology, 204(4), 778-786. 10.1097/JU.0000000000001297