References

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Here is a list of all of the medical journals and studies that we reference in order to back up everything we publish. We use only the peer-reviewed and double-blind scientific studies and evidence from a wide array of different sources to ensure that the information we publish is completely independent [last updated: 19/03/2018].

Serenoa repens

Study: Champault, G., Patel, J.C. and Bonnard, A.M., 1984. A double‐blind trial of an extract of the plant Serenoa repens in benign prostatic hyperplasia. British journal of clinical pharmacology, 18(3), pp.461-462.

This study was a double-blind randomised control trial, which examined the effects of plant Serenoa repens on BPH in 94 men. 50 of the men received 320 mg of Serenoa repens per day for 30 days.

The treatment group reduced the number of times they urinated per night, significantly improved flow rate and bladder emptying 30 days after treatment.

Di Silverio F, Monti S, Sciarra A, Varasano PA, Martini C, Lanzara S, D’Eramo G, Di Nicola S, Toscano V. Effects of long‐term treatment with Serenoa repens (Permixon®) on the concentrations and regional distribution of androgens and epidermal growth factor in benign prostatic hyperplasia. The Prostate. 1998 Oct 1;37(2):77-83.

“This in-vitro study looked at the mechanistic effects of serenoa repens. The study demonstrated that the decrease of DHT and the rise of T in BPH tissue of patients treated with Permixon® confirms the capacity of this drug to inhibit in vivo 5α-reductase in human pathological prostate. A marked decrease of EGF, associated with DHT reduction, was also observed.”

Beta sitosterol

Study: Klippel KF, Hiltl DM, Schipp B. A multicentric, placebo‐controlled, double‐blind clinical trial of β‐sitosterol (phytosterol) for the treatment of benign prostatic hyperplasia. BJU International. 1997 Sep 1;80(3):427-32.

Method: This study was a randomised double-blind placebo trial, which examined the effects of beta-sitosterol on the symptoms of BPH. 177 men with BPH were recruited to the study. 88 of the participants received allocated to the beta-sitosterol group and 89 to the placebo group. The beta-sitosterol group received 130mg of the treatment for 6 months.

Findings: The treatment group reported significantly better improvement in symptoms compared to the placebo group. There was also a significantly greater improvements in quality of life, bladder emptying and urine flow rate.

Study: Wilt TJ, MacDonald R, Ishani A. β-sitosterol for the treatment of benign prostatic hyperplasia: a systematic review. BJU international. 1999;83:976-83.

A systematic review examined randomised control trials that had looked to the effects of beta-sitosterol in men BPH between 1966 to 1998.

Method: There were 4 studies included in the review, in which a total of 519 men were included. The studies lasted between 4 to 26 weeks. The treatment dosages ranged from 60 to 195 mg per day.

Findings: 3 of the 4 studies showed significant improvements in symptoms of BPH. The one study that did not demonstrate a significant improvement was the only study to use pure beta-sitosterol beta-d glucoside.

Study: Berges RR, Kassen A, Senge T. Treatment of symptomatic benign prostatic hyperplasia with β‐sitosterol: an 18‐month follow‐up. BJU international. 2000 May 1;85(7):842-6.

Looked at the long-term effects of beta-sitosterol on BPH

Method: This was a follow-up study conducted 12 month after conclusion of a 6-month double blind placebo control trial with beta-sitosterol.

Findings: After the 6 months the treatment group significantly improved BPH symptoms. The 38 participants continued to use beta-sitosterol after the 6-month treatment maintained the improvement in symptoms. The 41 participants from the treatment group that did not continue to use beta-sitosterol reported slightly worse bladder emptying but no differences in flow rate. 27 of the participants from the placebo group who started using beta-sitosterol after the trial reported improvements in BPH to the same extent as participants in the treatment group. The 18 participants in the placebo group that chose no treatment showed no signs of improvement.

Testosterone

Study: Hubei Yike Daxue Xuebao 19 (1998), pp. 241-42

There is an important Chinese medical journal “Hubei Yike Daxue Xuebao” that is written in Chinese of course (vol. 19 in 1998). This had to be translated, so very few Westerners will ever learn of it. At the Hubei Medical University in the Wuhan Province doctors studied real men with BPH
and prostate cancer.

They took 96 men including 40 healthy subjects with no prostate disease. The doctors measured their levels of testosterone, estradiol, progesterone, LH and FSH. And what do you think they discovered? The men with BPH and prostate cancer had LOWER testosterone levels than the healthy men. They also had higher estrogen to testosterone ratios otherwise known as “estrogen dominance.

The lower the testosterone levels and the higher the estrogen levels the more prostate disease they had. The doctors clearly concluded that this imbalance of testosterone was largely
responsible for the pathogenesis of prostate disease.”

Vatten LJ, Ursin G, Ross RK, Stanczyk FZ, Lobo RA, Harvei S, Jellum E. Androgens in serum and the risk of prostate cancer: a nested case-control study from the Janus serum bank in Norway. Cancer Epidemiology and Prevention Biomarkers. 1997 Nov 1;6(11):967-9.

Looked at the relationship between androgens and prostate cancer

Method: Case-control study including 59 men who developed prostate cancer (cases) subsequent to blood donation and 180 men who were free of any diagnosed cancer (controls) in 1994 and were of similar age (± 1 year) and had similar blood storage time (±6 months) to the cases.

Findings: Neither T, DHT, nor the ratio T:DHT was associated with risk of developing prostate cancer. These results showed no association, positive or negative, between androgens measured in serum and the subsequent risk of developing prostate cancer.

Rhoden EL, Morgentaler A. Testosterone replacement therapy in hypogonadal men at high risk for prostate cancer: results of 1 year of treatment in men with prostatic intraepithelial neoplasia. The Journal of urology. 2003 Dec 31;170(6):2348-51.

Method: This study looked at the effects testosterone replacement therapy in hypoandrogen males, some of which were at a high risk of prostate cancer (had PIN without frank cancer). All 75 men were given TRT for a year.

Findings: The increased testosterone did not lead to an increase in PSA or significantly increase prostate cancer risk. This provides evidence that free testosterone is not the cause of prostate cancer.

Wu AH, Whittemore AS, Kolonel LN, John EM, Gallagher RP, West DW, Hankin J, Teh CZ, Dreon DM, Paffenbarger RS. Serum androgens and sex hormone-binding globulins in relation to lifestyle factors in older African-American, white, and Asian men in the United States and Canada. Cancer Epidemiology and Prevention Biomarkers. 1995 Oct 1;4(7):735-41. British Journal of Medicine 4 (1971), pp. 391-94

Method: This study examined differences levels of androgens and sex hormone binding globulin in healthy older mean of different ethnic groups. Since some ethnic groups are at a greater risk, the study looked to see if there were any differences in hormones between the ethnic groups.

Findings: The study found that androgen level decrease with age, again indicating that testosterone is not the cause of prostate cancer. African Americans, who are at the greatest risk of prostate cancer, had the highest DHT:testosterone ratio. Men with a history of BPH also had a higher DHT:testosterone ratio. These finding indicates that DHT may play a role in prostate disease, not testosterone. The levels of total and bioavailable testosterone were highest in Asian-Americans, intermediate in African-Americans, and lowest in whites. However, the DHT: testosterone ratio was highest in African-Americans, intermediate in whites, and lowest in Asian-Americans, corresponding to the respective incidence rates in these groups and providing indirect evidence for ethnic differences in 5a-reductase enzyme activity.

Daniell HW. A worse prognosis for men with testicular atrophy at therapeutic orchiectomy for prostate carcinoma. Cancer. 1998 Sep 15;83(6):1170-3.

Survival after therapeutic orchiectomy was determined for 78 men with prostate carcinoma and related to the histologic severity of testicular atrophy.

Method: Included in analysis were the presence or absence of prior radiation therapy, tumor grade and stage at diagnosis, host age, obesity, and smoking habits.

Findings: Testicular atrophy at the time of therapeutic orchiectomy for prostate carcinoma is associated with poor postorchiectomy prognosis in men with prior prostate bed radiation therapy and perhaps in men without prior radiation. The association may reflect a high frequency of inherently more aggressive tumors (often relatively nonandrogen‐dependent) among those tumors that are progressing in hypogonadal men.

Comstock GW, Gordon GB, Hsing AW. The relationship of serum dehydroepiandrosterone and its sulfate to subsequent cancer of the prostate. Cancer Epidemiology and Prevention Biomarkers. 1993 May 1;2(3):219-21. Akad. Med. Bialymstoku Supp. 42 (1984), p. 17

Study looked at the relationship between DHEA and prostate cancer

Method: Levels of DHEA and DHEA-sulphatein sera collected and frozen in 1974 were studied among 81 prostate cancer cases diagnosed in the following 12 years and 81 age- and race-matched controls without prostate cancer.

Findings: Although mean levels of DHEA were 11% lower among cases than controls and DHEA-S levels were 12% lower than among controls, no dose-response association was noted for either DHEA or DHEA-S. It seems unlikely that serum levels of DHEA or DHEA-S are important risk factors for prostate cancer. “

Hill P, Wynder EL, Garbaczewski L, Walker AR. Effect of diet on plasma and urinary hormones in South African black men with prostatic cancer. Cancer research. 1982 Sep 1;42(9):3864-9. Scand. J. Urol. Nephrol. 157 (1994) pp. 41-7

Looked at the effects of diet on hormones in black South African men with prostate cancer

Method: In this study, a comparison of serum and urinary levels of steroid hormones was carried out in healthy elderly rural vegetarian South African black men, a low-risk population, and a comparable group of men with prostatic cancer.

Findings: When transferred to a Western diet, plasma androgens showed a further decrease and a greater increase in estrone in prostatic cancer patients. In prostatic cancer patients, the total urinary androgen and estrogen levels were unaltered. However, in elderly healthy men, the Western diet decreased the excretion of estrogens and androgens. Thus, a Western diet supplemented the decrease in plasma androgens initially present in these patients. Evidence suggests that the decrease in plasma androgens increases the estrogeniandrogen ratio, which may lead to hyperplasia of the prostatic ductal epithelia, a change enhanced by a Western diet.”

ECKARDSTEIN S, Nieschlag E. Treatment of male hypogonadism with testosterone undecanoate injected at extended intervals of 12 weeks: a phase II study. Journal of andrology. 2002 May 6;23(3):419-25.

Looked at the efficacy and safety of testosterone injections on men with low T levels.

Method: This paper reports the result of an open-label, nonrandomized clinical trial investigating the efficacy and safety of an injectable preparation of testosterone undecanoate (TU) dissolved in castor oil and given over a 3.2-year period.

Findings: Compared with conventional testosterone enanthate or cypionate treatment requiring injection intervals of 2–3 weeks and resulting in supraphysiological serum testosterone levels, injections of TU at intervals of up to 3 months offer an excellent alternative for substitution therapy of male hypogonadism.

Prehn RT. On the prevention and therapy of prostate cancer by androgen administration. Cancer research. 1999 Sep 1;59(17):4161-4.

This article argued against the commonly-held view that suggests that high levels of androgens (testosterone) plays an in important role in the development of prostate cancer. The author provides evidence explains why testosterone is not the cause of prostate cancer, and that testosterone supplementation to people with low levels of testosterone may reduce prostate cancer risk. For example, when blood samples are analysed at the time the tumour is spotted, testosterone levels are low.

Schatzl G, Madersbacher S, Thurridl T, Waldmüller J, Kramer G, Haitel A, Marberger M. High‐grade prostate cancer is associated with low serum testosterone levels. The Prostate. 2001 Apr 1;47(1):52-8.

Method: The aim of this study was to assess whether low serum testosterone levels in men with newly diagnosed prostate cancer have an association to the endocrine status, prostate-specific antigen (PSA) levels, Gleason score, and androgen receptor expression.

Findings: Patients with high Gleason score prostate cancer had lower testosterone and estradiol serum levels.

Meikle AW, Stephenson RA, Lewis CM, Middleton RG. Effects of age and sex hormones on transition and peripheral zone volumes of prostate and benign prostatic hyperplasia in twins. The Journal of Clinical Endocrinology & Metabolism. 1997 Feb 1;82(2):571-5.

This study examined the relationship of sex hormones on volume of prostate zones in 214 male twins between 25 and 75 yr old.

Method: Volumes of the total prostate (TV), transition zone (TZ), and peripheral zones (PZ) were measured using transrectal ultrasound, and sex steroid concentrations were measured using RIA

Findings: The study found that elevated T and dihydrotestosterone concentrations do not predispose men to prostate enlargement or symptoms of benign prostatic hyperplasia.

Behre HM, Von Eckardstein S, Kliesch S, Nieschlag E. Long‐term substitution therapy of hypogonadal men with transscrotal testosterone over 7–10 years. Clinical Endocrinology. 1999 May 1;50(5):629-35.

Method: Eleven men aged at the beginning of the study were treated with transscrotal T patches because of primary or secondary hypogonadism.

Findings: The study demonstrated that Transscrotal testosterone patches are well-accepted and safe in long-term testosterone substitution therapy for male hypogonadism.”

Mulders PF, Dijkman GA, Del Moral PF, Theeuwes AG, Debruyne FM. Analysis of prognostic factors in disseminated prostatic cancer. An update. Cancer. 1990 Jun 15;65(12):2758-61.

Method: A statistical analysis of prognostic factors in 175 patients with hormonally treated disseminated prostatic cancer was done. The prognostic significance of performance status (PS), hemoglobin (Hb), alkaline phosphatase (AlkP), and testosterone was assessed.

Findings: The authors did not find significant prognostic value in age, tumor size or grade, prostatic acid phosphatase, or prostate-specific antigen in these patients.

Hu H, Odedina FT, Reams RR, Lissaker CT, Xu X. Racial differences in age-related variations of testosterone levels among US males: Potential implications for prostate cancer and personalized medication. Journal of racial and ethnic health disparities. 2015 Mar 1;2(1):69-76.

Method: analyzed data from the 1999–2004 National Health and Nutritional Examination Survey to compare agerelated variations in the testosterone levels of 355 black and 631 white males

Findings: Our study revealed that testosterone levels in black males decrease substantially with increasing age compared to those in white males. This rapid drop in testosterone levels may contribute to racial disparities in PCa.

Parsons JK, Sarma AV, McVary K, Wei JT. Obesity and benign prostatic hyperplasia: clinical connections, emerging etiological paradigms and future directions. The Journal of urology. 2009 Dec 1;182(6):S27-31.

Method: A review was carried out looked at the studies examined the relationship between obesity and physical activity and BPH and urinary tract symptoms.

Findings: The study found that obesity substantially increases the risk of BPH. Since physical activity decreases BPH risk, these observations support the development of novel strategies for BPH prevention and treatment targeted toward adiposity, weight loss and lifestyle interventions.

Douglas TH, Connelly RR, McLeod DG, Erickson SJ, Iii RB, Murphy GP. Effect of exogenous testosterone replacement on prostate‐specific antigen and prostate‐specific membrane antigen levels in hypogonadal men. Journal of surgical oncology. 1995 Aug 1;59(4):246-50.

The study looked at the effect of exogenous testosterone administration on the serum levels of PSA and PSMA in hypogonadal men.

Method: PSA, PSMA and total testosterone levels were obtained at intervals of every 2–4 weeks in 10 hypogonadal men undergoing treatment with exogenous testosterone

Findings: The statistical analysis failed to demonstrate a significant correlation between PSA or PSMA and testosterone levels. This study suggests that in hypogonadal men, neither PSMA nor PSA expression is testosterone-dependent.

Soloway MS, Ishikawa S, Van Der Zwaag R, Todd B. Prognostic factors in patients with advanced prostate cancer. Urology. 1989 May 1;33(5):53-6. New England Journal of Medicine 350 (2004) pp.482-92

Method: One hundred ten patients with metastatic prostate cancer (Stage D2) were analyzed to determine the associations among time until progression and the pretreatment testosterone level, extent of bone metastases as indicated by a semiquantitative grading scale for extent of disease, performance status, race, age, and the pretreatment level of prostatic acid phosphatase (PAP).

Findings: The following factors did not significantly correlate with progression free intervals: age, race, and PAP. However, patients with a pretreatment testosterone level of less than 300 ng/dL progressed more rapidly.

Schatzl G, Madersbacher S, Haitel A, Gsur A, Preyer M, Haidinger G, Gassner C, Ochsner M, Marberger M. Associations of serum testosterone with microvessel density, androgen receptor density and androgen receptor gene polymorphism in prostate cancer. The Journal of urology. 2003 Apr 30;169(4):1312-5.

This study investigated potential associations of serum testosterone with microvessel density, androgen receptor expression and AR gene polymorphism in men with untreated prostate cancer.

Method: luteinizing hormone, follicle-stimulating hormone, estradiol and testosterone were measured in men with newly diagnosed prostate cancer.

Findings: Low serum testosterone in men with newly diagnosed prostate cancer is associated with higher tumor microvessel and androgen receptor density as well as with higher Gleason score, suggesting enhanced malignant potential.

Harper ME, Pierrepoint CG, Griffiths K, British Prostate Study Group. Carcinoma of the prostate: relationship of pretreatment hormone levels to survival. European Journal of Cancer and Clinical Oncology. 1984 Apr 1;20(4):477-82.

Method: Pretreatment hormone levels were determined in 222 patients with prostatic cancer and their prognostic value assessed. The patients were grouped into yearly survival categories and only those whose cause of death was due to the disease were included in the study.

Findings: The pretreatment mean plasma testosterone concentrations were found to be higher as the survival period of the various groups lengthened. The indications from this study are that poor testicular function is associated with early death from prostatic carcinoma and that the measurement of blood levels of testosterone at diagnosis could provide a prognosis of subsequent life-span.

Swerdloff RS, Wang C. Three-year follow-up of androgen treatment in hypogonadal men: preliminary report with testosterone gel. The Aging Male. 2003 Jan 1;6(3):207-11.

Methods: This report provides a preliminary analysis of longer-term treatment with a testosterone gel (AndroGel ™ or Testogel®) in a group of men aged 19-67 years of age.

Findings: The positive effects of transdermal testosterone gel on bone mineral density previously identified at 6 months of treatment, continued with time. The positive effects on bone mineral density were greater in the spine than the hip. There were minimal effects on lipid levels. Levels of prostate-specific antigen (PSA) increased with testosterone treatment but, in general, remained in the normal range.”

Lowe FC, Dreikorn K, Borkowski A, Braeckman J, Denis L, Ferrari P, Gerber G, Levin R, Perrin P, Senge T. Review of recent placebo‐controlled trials utilizing phytotherapeutic agents for treatment of BPH. The Prostate. 1998 Nov 1;37(3):187-93.

Method: In order to assess the efficacy of phytotherapeutic agents for the treatment of benign prostatic hyperplasia (BPH), a review of recently published double‐blind placebo‐controlled trials was undertaken.

Findings: These studies suggest a possible benefit for the use of phytotherapeutic preparations in the treatment of BPH.”

Di Silverio F, D’eramo G, Lubrano C, Flammia GP, Sciarra A, Palma E, Caponera M, Sciarra F. Evidence that Serenoa repens extract displays an antiestrogenic activity in prostatic tissue of benign prostatic hypertrophy patients. European urology. 1992;21:309-14.

Method: A double-blind placebo-controlled study was performed in 35 benign prostatic hypertrophy (BPH) patients never treated before. The patients were randomized into two groups, the 1st (18 cases) receiving Serenoa repens extract ( 160 mg t.d.) for 3 months up to the day before the operation of transvesical adenomectomy and the 2nd (17 cases) receiving placebo.

Findings: S. repens extract is able to inhibit the nuclear estrogen receptors in prostatic tissue samples of BPH patients. The results obtained with the Scatchard analysis or the single saturating-dose assay are confirmed by ER-EIA and by PgR-EIA representing a marker of the estrogenic activity. A possible explanation for these findings is that S. repens extract contains at least two fractions, one with antiandrogenic, the other with antiestrogenic effect.”

Berges RR, Windeler J, Trampisch HJ, Senge TH, β-Sitosterol Study Group. Randomised, placebo-controlled, double-blind clinical trial of β-sitosterol in patients with benign prostatic hyperplasia. The Lancet. 1995 Jun 17;345(8964):1529-32.

Method: In a randomised, double-blind, placebo-controlled multi-centre study, 200 patients (recruited between April and October 1993) with symptomatic benign prostatic hyperplasia were treated with either 20 mg β-sitosterol (which contains a mixture of phytosterols) three times per day or placebo.

Findings: There was a greater decrease in IPSS points in the β-sitosterol-treated group vs  the placebo group and changes in urine flow parameters: β-sitosterol treatment resulted in increasing peak flow (15·2 [5·7] mL/s from 9·9 [2·5] mL/s), and decrease of mean residual urinary volume (30·4 [39·9] mL from 65·8 [20·8] mL). These parameters did not change in the placebo group. No relevant reduction of prostatic volume was observed in either group. Significant improvement in symptoms and urinary flow parameters show the effectiveness of β-sitosterol in the treatment of benign prostatic hyperplasia.”

Braeckman J. The extract of Serenoa repens in the treatment of benign prostatic hyperplasia: a multicenter open study. Current therapeutic research. 1994 Jul 1;55(7):776-85.

Method: The therapeutic effect of a 160-mg, twice-daily, oral dose of Serenoa repens extract was studied during a 3-month open trial in 505 patients with mild-to-moderate symptoms of BPH.

Findings: Traditional parameters for quantifying prostatism, such as the International Prostate Symptom Score, the quality of life score, urinary flow rates, residual urinary volume, and prostate size, were found to be significantly improved after only 45 days of treatment. After 90 days of treatment, a majority of patients (88%) and treating physicians (88%) considered the therapy effective. In addition, the serum prostate-specific antigen concentration was not modified by the drug.”

Zumoff B, Levin J, Strain GW, Rosenfeld RS, O’Connor J, Freed SZ, Kream J, Whitmore WS, Fukushima DK, Hellman L. Abnormal levels of plasma hormones in men with prostate cancer: Evidence toward a “two‐disease” theory. The Prostate. 1982 Jan 1;3(6):579-88.

Method: The 24-hr mean plasma concentrations of 13 hormones or hormone metabolites (cortisol, testosterone, dihydrotestosterone, dehydroisoandrosterone, dehydroisoandrosterone sulfate, androsterone, androsterone sulfate, estrone, thyroxine, triiodothyronine, LH, FSH, and prolactin) were measured in 16 rigorously screened patients (aged 55–80) with stage C or D prostate cancer and 36 normal men.

Findings: The cortisol/testosterone ratio almost completely separated prostate cancer patients under 65 from normal men, but did not discriminate patients 65 or older from normal.”

Rannikko S, Adlercreutz H. Plasma estradiol, free testosterone, sex hormone binding globulin binding capacity, and prolactin in benign prostatic hyperplasia and prostatic cancer. The Prostate. 1983 Jan 1;4(3):223-9.

Method: The nature of hormonal changes with age and the possible role of these changes in the development of benign prostatic hyperplasia (BPH) and prostatic cancer (PC) were studied by assaying the plasma levels of total and free testosterone (T), estradiol (E2), prolactin, and sex hormone binding globulin binding capacity (SHBG) in 20 normal healthy men aged 40-59 year.

Findings: The mean E2 was highly significantly lower in the PC patients and in the young controls than in the BPH patients. The mean free T was significantly higher in the young controls than in the BPH patients and PC patients. The PC patients had a slightly lower mean free T and mean E2/free T ratio than the BPH patients. The mean E2/free T ratio was significantly higher in the BPH patients and in the PC patients than in the young controls. It seems possible that the observed age-dependent significant increase in plasma estrogen concentration in the BPH patients may act as a protective factor against prostatic cancer.

Hulka BS, Checkoway H, Hammond JE, Ferdinando GD, Mickey DD, Fried FA, Stumpf WE, Beckman WC, Clark TD. Serum hormone levels among patients with prostatic carcinoma or benign prostatic hyperplasia and clinic controls. The Prostate. 1987 Jan 1;11(2):171-82.

This study sought to identify differences in serum hormone levels between prostatic cancer (Cap) patients, benign prostatic hyperplasia (BPH) patients, and clinic controls (CC)

Methods: Serum testosterone, estradiol, and prolactin values were obtained from 35 Cap, 42 BPH, and 161 CC patients attending a single medical center between January 1984 and April 1985.

Findings: Modest depression of serum testosterone and estradiol was noted for CaP patients compared to CC, although the differences were not statistically significant. This depression was interpreted to be a likely result of the malignant process rather than a cause of it, whereas the development of clinically evident BPH was felt to be a biologically plausible response to an elevated T/E ratio.”

Gann PH, Hennekens CH, Grodstein F, Stampfer MJ, Longcope C, Verhoek‐Oftedahl W. A prospective study of plasma hormone levels, nonhormonal factors, and development of benign prostatic hyperplasia. The prostate. 1995 Jan 1;26(1):40-9.

Method: Frozen plasma samples, collected at the study onset, were available for 320 men who developed surgically treated BPH up to 9 years later and for 320 age-matched controls. Plasma testosterone (T), dihydrotestosterone (DHT), androstenedione, estradiol (E2), and estrone (E1) were measured for each case-control pair.

Findings: Our results indicate that normal variation in circulating androgen levels does not influence development of BPH, but that variation in estrogen levels might be important.”

Morgentaler A, Bruning CO, DeWolf WC. Occult prostate cancer in men with low serum testosterone levels. Jama. 1996 Dec 18;276(23):1904-6.

Method: This retrospective cohort study determined the prevalence of occult prostate cancer in men with low serum total testosterone or free testosterone levels. Seventy-seven men with low total testosterone or free testosterone levels, with normal results of digital rectal examination and prostate-specific antigen (PSA) levels of 4.0 ng/mL or less. The mean age was 58 years.

Findings: A high prevalence of biopsy-detectable prostate cancer was identified in men with low total or free testosterone levels despite normal PSA levels and results of digital rectal examination.

Haapiainen R, Rannikko S, Alfthan O, Adlercreutz H. Pretreatment plasma levels of testosterone and sex hormone binding globulin binding capacity in relation to clinical staging and survival in prostatic cancer patients. The prostate. 1988 Jan 1;12(4):325-32.

Method: Pretreatment plasma concentrations of total testosterone (T), sex hormone binding globulin binding capacity (SHBG), T/SHBG ratio, and free testosterone (fT) were measured in 123 patients with prostatic cancer categorized into groups according to the UICC classification. The patients were randomized to orchiectomy or estrogen therapy and the mean follow-up time was 48 months.

Findings: This study supports the view that there are differences in the pretreatment T and fT levels in prostatic cancer patients in relation to the stage of tumor and that these hormone assays could be used as prognostic factors.“

Ribeiro M, Ruff P, Falkson G. Low serum testosterone and a younger age predict for a poor outcome in metastatic prostate cancer. American journal of clinical oncology. 1997 Dec 1;20(6):605-8.

This study was undertaken to determine which factors predict the course and outcome of patients treated with first line hormonal manipulation.

Method: A total of 144 patients with Stage D2 prostate cancer who received androgen deprivation therapy were studied. Pretreatment parameters analyzed were age, performance status, analgesia usage, concurrent disease, histologic differentiation, hemoglobin, leukocyte and platelet count, serum creatinine, alkaline phosphatase, lactate dehydrogenase, prostate specific antigen, total and prostatic acid phosphatase, serum testosterone, follicle stimulating and luteinizing hormone levels, number of metastatic sites and bone scan grade.

Findings: Both serum testosterone (26 vs. 20 months, p = 0.003), and age (28 vs. 17 months, p = 0.036) had a significant influence on overall survival. Low testosterone, indicating androgen independence, and a younger age, seem to result in a more aggressive disease and a poorer prognosis in advanced prostate cancer.

Schatzl G, Reiter WJ, Thürridl T, Waldmüller J, Roden M, Söregi S, Madersbacher S. Endocrine patterns in patients with benign and malignant prostatic diseases. The Prostate. 2000 Aug 1;44(3):219-24.

Method: Patients with newly diagnosed, untreated prostate cancer (PC) (n = 75) and, as a control population, those with untreated lower urinary tract symptoms (LUTS) due to benign prostatic hyperplasia (BPH) (n = 159) entered this prospective study. In all patients, the following parameters were obtained by serum analysis: prostate-specific antigen (PSA), human luteinizing hormone (hLH), human follicle-stimulating hormone (hFSH), testosterone, estradiol (E2), cortisol, and dehydroepiandrosterone-sulphate (DHEA-S). Serum samples were collected of fasting patients

Findings: Patients with newly diagnosed, untreated PC yielded significantly higher cortisol and lower estradiol serum concentrations than controls.”

Wayne Meikle A, Smith JA, West DW. Familial factors affecting prostatic cancer risk and plasma sex‐steroid levels. The Prostate. 1985 Jan 1;6(2):121-8.

Method: Whether familial factors affect the frequency of prostatic cancer and the plasma content of sex‐steroids was investigated.

Findings: Brothers (n = 257) of probands (n = 150) diagnosed with prostatic cancer before age 62 years had a fourfold higher risk for developing the disease than men in the general population The observations indicate that familial factors are potent risk factors for the development of prostatic cancer. They also suggest that plasma androgen values in families with prostatic cancer cluster in the lower range of normal and that plasma sex-steroid content is more similar in each brothers with or without prostatic cancer than among nonbrothers.”

Chodak GW, Vogelzang NJ, Caplan RJ, Soloway M, Smith JA. Independent prognostic factors in patients with metastatic (stage D2) prostate cancer. Jama. 1991 Feb 6;265(5):618-21.

Method: The independent prognostic factors affecting survival were assessed in 240 men undergoing treatment for metastatic prostate cancer as part of a randomized clinical trial comparing the gonadotropin releasing hormone analogue Zoladex (goserelin acetate implant) with castration.

Findings: In a multivariate analysis, the most highly significant predictors were the presence or absence of bone pain, serum testosterone levels, serum alkaline phosphatase levels, and performance status. Patients with all four factors favorable for survival had a 2-year survival rate of 84% as compared with only 8% for patients with none of the four factors favorable for survival. A separate analysis of serum testosterone levels revealed that the higher the pretreatment serum testosterone level, the greater the survival rate. Compared with patients with serum testosterone levels less than 6.9 nmol/L, significant differences in survival were observed for patients with serum testosterone levels of 10.4 to 13.9,13.9 to 17.3, and over 17.3 nmol/L.”

Meikle AW, Arver S, Dobs AS, Adolfsson J, Sanders SW, Middleton RG, Stephenson RA, Hoover DR, Rajaram L, Mazer NA. Prostate size in hypogonadal men treated with a nonscrotal permeation-enhanced testosterone transdermal system. Urology. 1997 Feb 1;49(2):191-6.

Method: As part of an open-label, multicenter study, prostate volume as measured by transrectal ultrasound and PSA were assessed in 29 hypogonadal men during treatment with intramuscular testosterone enanthate (+TE), followed by 8 weeks of androgen withdrawal (−T), and then during 1 year of therapy with Androderm Testosterone Transdermal System, a nonscrotal permeation-enhanced TTD system (+TTD).

Findings: Mean prostate volume decreased significantly from the +TE period (17 g) compared with the −T period (14 g). Prostate volume increased significantly from the −T period compared with the +TTD period (18 g). Maximum prostate size, comparable to that measured during +TE (P = 0.125), was reached by month 3 of + TTD therapy; prostate volume did not increase further during the remaining 9 months of + TTD therapy.”

Saroff J, Kirdani RY, Chu M, Wajsman Z, Murphy GP. Measurements of prolactin and androgens in patients with prostatic diseases. Oncology. 1980;37(1):46-52.

Method: Testosterone (T), dihydrotestosterone (DHT) and prolactin (HPr) levels were determined in normal males and females, in patients with benign prostatic hypertrophy (BPH) and in clinically stable patients with prostatic carcinoma (CAP), intact and orchiectomized.

Findings: The HPr levels were higher in prostatic cancer patients, in BPH patients, and in subjects on estrogen therapy. No significant differences were found between controls or patients treated with 5-Fu plus Cytoxan. The T and DHT levels were decreased in all noncontrol subjects. The levels of DHT in intact, untreated CAP patients or those receiving 5-FU plus Cytoxan were significantly higher than in BPH patients. Based on these observations, it appears that HPr could be involved with T and DHT in a feedback control role, especially in BPH.”

Ernst DS, Hanson J, Venner PM. Analysis of prognostic factors in men with metastatic prostate cancer. Uro-Oncology Group of Northern Alberta. The Journal of urology. 1991 Aug;146(2):372-6.

Method: This study determined the influence of the extent of disease on bone scan, serum testosterone, patient age, performance status, method of initial diagnosis, Gleason grade, clinical stage at diagnosis, serum acid phosphatase, serum prostate specific antigen (PSA) and primary hormonal treatment on survival. The clinical and hormonal data were obtained when the presence of metastatic disease was established and treatment was to be initiated in 162 men with metastatic prostate cancer.

Findings: We conclude that extent of disease on bone scan is the most important prognosticator of the analyzed factors and that serum testosterone may be of value.”

 

 

Lycopene

Key TJ, Silcocks PB, Davey GK, Appleby PN, Bishop DT. A case-control study of diet and prostate cancer. British journal of cancer. 1997 Sep;76(5):678.

Study: A Case Control Study of Diet and Prostate Cancer

Method: 328 men who had prostate cancer before the age of 75 were interviewed to see if their risk of prostate cancer would increase with a high intake of total or saturated fat, or decrease with Carotene or Lycopene.

Conclusion: This Study does not support the hypothesis that fat increases risk and is equivocal in relation to Carotene.

Marchand LL, Hankin JH, Kolonel LN, Wilkens LR. Vegetable and fruit consumption in relation to prostate cancer risk in Hawaii: a reevaluation of the effect of dietary beta-carotene. American journal of epidemiology. 1991 Feb 1;133(3):215-9.

Study: Vegetable and Fruit Consumption in relation to Prostate Cancer Risk in Hawaii: a Re-evaluation of the effect of dietary Beta-Carotene

Method: Analysis of case-control study of 452 prostate cancer cases and 899 population controls that were conducted in 1970-1983 among the multi ethnic population of Hawaii.

Conclusion: Intake of B-Carotene, lycopene, lutein, indols, phenols, or other phytochemicals is not associated with prostate cancer risk

Yoshizawa K, Willett WC, Morris SJ, Stampfer MJ, Spiegelman D, Rimm EB, Giovannucci E. Study of prediagnostic selenium level in toenails and the risk of advanced prostate cancer. JNCI: Journal of the National Cancer Institute. 1998 Aug 19;90(16):1219-24.

Study: Prediagnostic Selenium level in toenails and the risk of advanced prostate cancer

Method: On-going Prospective Cohort Study – We investigated the association between risk of prostate cancer and prediagnostic level of selenium in toenails, a measure of long-term selenium intake in 33,737 subjects.

Conclusion: Results support earlier findings that higher Selenium intakes may reduce the risk of prostate cancer.

Cohen JH, Kristal AR, Stanford JL. Fruit and vegetable intakes and prostate cancer risk. Journal of the National Cancer Institute. 2000 Jan 5;92(1):61-8.

Study: Fruit and Vegetable Intakes and Prostate Cancer Risk

Method: Data taken from population based case-control study of risk factors of Prostate Cancer

Conclusion: High consumption of vegetables, particularly cruciferous vegetables, is associated with a reduced risk of prostate cancer.

Hsing AW, Comstock GW, Abbey H, Polk BF. Serologic precursors of cancer. Retinol, carotenoids, and tocopherol and risk of prostate cancer. JNCI: Journal of the National Cancer Institute. 1990 Jun 6;82(11):941-6.

Study: Serologic Precursors of Cancer, Retinol, Carotenoids, and Tocopherol and risk of prostate cancer

Method: Investigated the associations of serum retinol, carotenoids B carotene and lycopene, and tocopheral (Vitamin E) with the risk of prostate cancer in a nested case-control study.

Conclusion: The data suggested an inverse relationship between serum retinol and risk of prostate cancer.

Nomura AM, Stemmermann GN, Lee J, Craft NE. Serum micronutrients and prostate cancer in Japanese Americans in Hawaii. Cancer Epidemiology and Prevention Biomarkers. 1997 Jul 1;6(7):487-91.

Study: Serum Micro-nutrients and Prostate Cancer in Japanese Americans in Hawaii

Method: Explored association between the intake of vitamins A and E and the risk of prostate cancer in a nested case control study.

Conclusion: Study does not support the observation of lycopene having a protective effect against prostate cancer.

Dorai T, Cao YC, Dorai B, Buttyan R, Katz AE. Therapeutic potential of curcumin in human prostate cancer. III. Curcumin inhibits proliferation, induces apoptosis, and inhibits angiogenesis of LNCaP prostate cancer cells in vivo. The prostate. 2001 Jun 1;47(4):293-303.

Study: Therapeutic Potential of Curcumin in human prostate cancer.

Method: Cancer cells were grown and injected into mice. Experimental group received a diet rich in Curcumin for six weeks. At end point tumours were evaluated for pathology, cell proliferation, apoptosis, and vascularity.

Conclusion: Could be a therapeutic anti-cancer agent, as it significantly inhibits prostate cancer growth and has potential to prevent progression of this cancer.

Kucuk O, Sarkar FH, Sakr W, Djuric Z, Pollak MN, Khachik F, Li YW, Banerjee M, Grignon D, Bertram JS, Crissman JD. Phase II randomized clinical trial of lycopene supplementation before radical prostatectomy. Cancer Epidemiology and Prevention Biomarkers. 2001 Aug 1;10(8):861-8.

Study: Phase II randomized clinical trial of lycopene supplementation before radical prostatectomy.

Method: Investigated the effects of lycopene supplementation in 26 patients with prostate cancer in a randomized clinical trial.

Conclusion: Results suggest the lycopene supplementation may suggest that lycopene supplementation may decrease the growth of prostate cancer. However, no firm conclusions can be drawn at this time because of the small sample size.

 

 

Betasitosterol

Di Silverio F, Monti S, Sciarra A, Varasano PA, Martini C, Lanzara S, D’Eramo G, Di Nicola S, Toscano V. Effects of long‐term treatment with Serenoa repens (Permixon®) on the concentrations and regional distribution of androgens and epidermal growth factor in benign prostatic hyperplasia. The Prostate. 1998 Oct 1;37(2):77-83.

Study: Effects of long term treatment with Serenoa repens on the concentrations and regional distribution of androgens and epidermal growth factor in Benign Prostatic Hyperplasia.

Method: BPH samples were sectioned in periurethral, subcapsular, and intermediate regions, in each region T, DHT, and EGF were determined by radioimmunoassay, after purification on celite columns or sep-pak c18 cartridges.

Conclusion: A possible speculation is that the preferential reduction of DHT and EGF content in the periurethral region is involved in the clinical improvement of the obstructive symptoms in BPH during LSESr therapy.

Berges RR, Kassen A, Senge T. Treatment of symptomatic benign prostatic hyperplasia with β‐sitosterol: an 18‐month follow‐up. BJU international. 2000 May 1;85(7):842-6.

Study: Treatment of Symptomatic benign prostatic hyperplasia with B-sitosteral: an 18 month follow up.

Method: At 18 months after enrolment in a six month multi-centre double-blind placebo-controlled clinical trial with B Sitosterol patients were re-evaluated.

Conclusion: The beneficial effects of B-sitosterol treatment recorded in the 6-month double blind trial were maintained for 18 months.

British Journal of Urology, V.83 (1993) pp. 976-83

Study: B-Sitosterol for the treatment of benign prostatic hyperplasia .

Method: Four trials comprising of 519 men. All were double-blind and lasted 4-26 weeks. Subjects given plant extracts which contained B-Sitosterols, whilst a control group were given placebo or pharmacological therapy. The treatment lasted 30 days.

Conclusion: B-sitosterol improves urological symptoms and flow measures.

Braeckman J. The extract of Serenoa repens in the treatment of benign prostatic hyperplasia: a multicenter open study. Current therapeutic research. 1994 Jul 1;55(7):776-85.

Study: The extract of Seronoa repens in the treatment of benign prostatic hyperplasia: a multicentre open study.

Method: Between December 23, 1992, and October 17, 1993, 112 urologists contributed to the enrolment of 505 patients with BPH into this study. The study received daily oral doses of the extract of Serenmoa Repens in 160mg capsules administered twice for a 3-month period. Medical visits for evaluations were scheduled for days 0, 45 and 90.

Conclusion:

The results obtained in this open study largely corroborate these recently reported in a placebo-controlled, double-blind, randomized clinical trial (unpublished data J.Braeckman et al, 1994) showing that the extract of Serenoa Repens is an effective treatment for the mictional problems associated with BPH.

British Journal of Urology, Volume 78 (1996) pp. 325-36

Study: Phytotherapy for the Prostate

Method: Review of studies which indicate the therapeutic potential of plant products, specifically Harzol, Tadenan, Permixon.

Conclusion:  There is now a considerable body of literature, including placebo controlled trials, indicating a significant benefit over placebo in up to 70% of patients.

Lowe FC, Dreikorn K, Borkowski A, Braeckman J, Denis L, Ferrari P, Gerber G, Levin R, Perrin P, Senge T. Review of recent placebo‐controlled trials utilizing phytotherapeutic agents for treatment of BPH. The Prostate. 1998 Nov 1;37(3):187-93.

Study: Review of recent placebo-controlled trials utilizing phytotheraputic agents for treatment of BPH.

Method: A review of recently published double-blind placebo-controlled trials was undertaken.

Conclusion: Studies suggest a possible benefit for the use of phytotheraputic preparations in the treatment of BPH.

Lancet, Volume 245 (1995), pp1529-32

Study: Randomised, placebo-controlled, double-blind clinical trial of beta-sitosterol in patients with benign prostate hyperplasia.

Method: 200 patients with symptomatic benign prostatic hyperplasia were treated with either 20mg B-sitosterol (which contains a mixture of phytosterols) three times per day or placebo.

Conclusion: Significant improvement in symptoms and urinary flow parameters show the effectiveness of B-sitosterol in the treatment of benign prostatic hyperplasia.

Urolage A, volume 24 (1985), pp 49-51

Study: Results of a double-blind study of the effectiveness of ERU (extractum radices urticase) capsules in conservative treatment of benign prostatic hyperplasia.

Methods: In 50 patients with prostatic hyperplasia the effect on symptomatology and objective findings of ERU- capsules versus placebo was investigated in a double-blind study over a 9 week treatment period.

Conclusion:  The improvement of the average flow in the ERU group was not significant.

British Journal of Urology, Volume 80 (1997), pp. 427-32

Study: A multicentric, placebo-controlled, double-blind clinical trial beta-sitosterol (phytosterol) for the treatment of benign prostatic hyperplasia.

Method: A randomized, double-blind and placebo-controlled clinical trial was conducted to assess the efficacy and safety 130mg free beta-sitosterol (phytosterol) daily, using the international prostate symptom score (IPSS) as the primary outcome variable.

Conclusion: These results show that beta-sitosterol is an effective option in the treatment of BPH.

Champault G, Patel JC, Bonnard AM. A double‐blind trial of an extract of the plant Serenoa repens in benign prostatic hyperplasia. British journal of clinical pharmacology. 1984 Sep 1;18(3):461-2.

Study: A double blind trial of an extract of the plant Serenoa repens in Benign Prostatic Hyperplasia

Method: The double-blind, placebo-controlled study was performed with 110 outpatients (55 PA109, 55 placebo). The symptoms of dysuria nocturia and frequent and poor urinary flow, present in all subjects, were assessed.

Conclusion: Both objective and subjective signs were improved. The improvement was significantly superior to that achieved with Placebo. PA109 would therefore appear to be a useful therapeutic tool in in the treatment of BPH.

Di Silverio F, D’eramo G, Lubrano C, Flammia GP, Sciarra A, Palma E, Caponera M, Sciarra F. Evidence that Serenoa repens extract displays an antiestrogenic activity in prostatic tissue of benign prostatic hypertrophy patients. European urology. 1992;21:309-14.

Study: Evidence that Serenoa repens extract displays an Antiestrogenic activity in prostatic tissue of benign prostatic hyperplasia patients.

Method: A double-blind placebo-controlled study was performed on 35 benign prostatic hypertrophy (BPH) patients never treated before. The patients were randomized into two groups, the 1st (18 cases) receiving Serenoa repens extract (160mg t.d) for three months up to the day before the operation of transvesical adenomectomy and the 2nd (17 cases) receiving placebo.

Conclusion: The findings show that S. repens extract is able to inhibit the nuclear estrogen receptors in prostatic tissue samples of BPH patients.

Ornish D, Weidner G, Fair WR, Marlin R, Pettengill EB, Raisin CJ, Dunn-Emke S, Crutchfield L, Jacobs FN, Barnard RJ, Aronson WJ. Intensive lifestyle changes may affect the progression of prostate cancer. The Journal of urology. 2005 Sep 1;174(3):1065-70.

Study: Intensive lifestyle changes may affect the progression of prostate cancer.

Method: A total of 93 volunteers with Serum PSA 4 to 10 ng/ml and cancer Gleason scores of less than 7 were randomly assigned to an experiment group that was asked to make comprehensive lifestyle changes or to a usual core control group.

Conclusion: Intensive lifestyle changes may affect the progression of early, low grade prostate cancer in men.

Seftel AD. Re: Effects of Testosterone Treatment in Older Men. The Journal of urology. 2016 Aug 1;196(2):516-9.

Study: Effects of Testosterone treatment in older men.

Method: 790 men over the age of 65 received either testosterone gel or placebo gel for one year. Each man participated in one or more of the trials – the sexual function trial, the physical function trial, and the vitality trial.

Conclusion: In symptomatic men 65 years or older, raising testosterone concentrations for 1 year from moderately low to the mid-normal range for men 19-40 years of age had a moderate benefit with respect to sexual function and some benefit with respect to mood and depressive symptoms.

Graff RE, Meisner A, Ahearn TU, Fiorentino M, Loda M, Giovannucci EL, Mucci LA, Pettersson A. Pre-diagnostic circulating sex hormone levels and risk of prostate cancer by ERG tumour protein expression. British journal of cancer. 2016 Apr;114(8):939.

Study: Pre-diagnostic circulating sex hormone levels and risk of Prostate Cancer by ERG tumour protein expression.

Method: Examined associations of 200 prostate cancer cases and 1057 controls in a nested case-control study between pre-diagnostic circulating levels of total testosterone, free testosterone, DHT, androstanediol glucouronide, estrodiol, and SHBG and risk of prostate cancer by TMPRSS2: ERG status.

Conclusion: These findings provide some suggestive evidence that higher pre-diagnostic free testosterone levels are associated with an increased risk of developing TMPRSS2: ERG – positive prostate cancer.

Khera M, Crawford D, Morales A, Salonia A, Morgentaler A. A new era of testosterone and prostate cancer: from physiology to clinical implications. European urology. 2014 Jan 1;65(1):115-23.

Study: A new era of testosterone and prostate cancer: from physiology to clinical implications.

Method: Review the current literature regarding the relationship of testosterone on PCa and in particular the effect of testosterone therapy on PCa progression and recurrence.

Conclusion: The long-held belief that PCa risk is related to high serum androgen concentrations can no longer be supported.

Hoffman MA, DeWOLF WC, Morgentaler A. Is low serum free testosterone a marker for high grade prostate cancer?. The Journal of urology. 2000 Mar 1;163(3):824-7.

Study: Is low serum free testosterone a marker for high grade prostate cancer?

Method: Investigated the relationship of serum free and total testosterone to the clinical and pathological characteristics of prostate cancer through retrospectively reviewing the clinical records of 117 patients.

Conclusion: Findings suggest that low serum free testosterone may be a marker for more aggressive disease.

Fwu CW, Eggers PW, Kirkali Z, McVary KT, Burrows PK, Kusek JW. Change in sexual function in men with lower urinary tract symptoms/benign prostatic hyperplasia associated with long-term treatment with doxazosin, finasteride and combined therapy. The Journal of urology. 2014 Jun 1;191(6):1828-34.

Study: Change in sexual function in men with lower urinary tract symptoms/ benign prostatic hyperplasia associated with long-term treatment with doxazosin, finasteride and combined therapy.

Method: Examined the effect of doxazosin, finasteride and combined therapy in men lower urinary tract symptoms associated with BPH on sexual function, as assessed by the Brief Male Sexual Function Inventory over 4 years.

Conclusion : Treatment with finasteride or combined therapy was associated with worsening sexual function while treatment with doxazosin alone was associated with minimal negative impact.

Journal of Urology, Volume 189 (2013), pp. 102-6

Study: Obesity and benign prostatic hyperplasia: Clinical connections, emerging paradigms and future directions.

Method: Structured, comprehensive literature review to identify studies of obesity, benign prostatic hyperplasia lower urinary tract symptoms and physical activity.

Conclusion: Obesity markedly increases the risk of benign prostatic hyperplasia.

Prostate Cancer, Volume 2013 (2013), pp. 1-12

Study: Global patterns of prostate cancer incidence, aggressiveness, and mortality in men of African descent.

Method:  Summarized publicly available CaP data and collected data from the men of African descent and Carcinoma of the Prostate (MADCap) consortium (AC3) to evaluate CaP incidence and mortality in men of African descent worldwide.

Conclusion: Data suggests that among men of African descent, CaP is most commin in AA and Caribbean men, and considerably less common in SSA.

Journal of Urology, Volume 90 (2016), pp. 112-8

Study: Age, body mass index, and frequency of sexual activity are independent predictors of testosterone deficiency in men with erectile dysfunction.

Method: retrospective review was conducted on 498 men evaluated for ED between January 2013 and July 2014. Testing for TD by early morning serum measurement was offered to all eligible men.

Conclusion: Men with ED and elevated BMI, advanced age, or infrequent sexual activity appear to be at high risk of TD, and such patients represent excellent potential candidates for targeted testosterone screening.

Hu H, Odedina FT, Reams RR, Lissaker CT, Xu X. Racial differences in age-related variations of testosterone levels among US males: Potential implications for prostate cancer and personalized medication. Journal of racial and ethnic health disparities. 2015 Mar 1;2(1):69-76.

Study: Racial differences in age-related variations of testosterone levels among US males: Potential implications for prostate cancer and personalized medication.

Method: Analysed data from the 1999-2004 National Health and Nutritional Examination Survey to compare age-related variations in the testosterone levels of 355 black and 631 white males.

Conclusion: Study revealed that testosterone levels in black males decrease substantially with increasing age compared to those in white males. Findings also suggest that personalized medication for hormone replacement therapy may be necessary to avoid sudden drops in testosterone levels, particularly for black males.