Androgen Replacement

Gan E, Pattman S, Pearce S, Quinton R. A UK epidemic of testosterone prescribing, 2001-2010. Clinical Endocrinology. A UK epidemic of testosterone prescribing, 2001-2010 - Gan - Clinical Endocrinology - Wiley Online Library

Context Testosterone replacement therapy is the standard treatment for male hypogonadism. There has lately been increased marketing in the medical media promoting testosterone replacement for men with erectile dysfunction or for older men with low serum testosterone, despite the lack of long-term safety and efficacy data. Therefore, we aimed to examine trends in testosterone prescribing in UK primary care over the last 10 years.

Methods Data about the use of testosterone preparations from the Departments of Health Prescription Cost Analysis for community pharmacies 2001-2010, for England, Scotland and Wales were collated. Community requests for serum total testosterone assay in males to the Biochemistry Department at the Newcastle upon Tyne Hospitals Trust were also examined over the same time period.

Results The number of prescriptions for testosterone preparations increased by nearly 90% from 157,602 to 298,134 dispensed items annually, over a 10-year period. However, due to a particularly significant (five-fold) increase in prescribing of (more expensive) transdermal preparations, the cost to the NHS showed a 267% escalation, from £3.2 to £11.7 million, annually over the same period. Local requests from primary care in the Newcastle and North Tyneside area for serum testosterone measurement in males also increased, from 347 requests in 2000 to 823 requests in 2010, a 137% increase. However, the number of men with likely unequivocal hypogonadism (testosterone less than 6.0 nmol/l) remained constant at 5.2% in 2000 and 6.3% in 2010.

Conclusion Many men in the UK might be receiving testosterone replacement therapy with neither clearly-established indications, nor robustly-diagnosed hypogonadism. A national registry for men treated with testosterone and further evidence to improve current guidance (national and/or international) on the indications for testosterone replacement would be beneficial.
 
Well, this certainly blew me away. New York (NY) classifies Testosterone (as well as all AAS) as a Schedule II drug!!! This means they are in the same class as opiates - morphine - and amphetamines. http://www.health.ny.gov/regulations/public_health_law/article/33/docs/33.pdf
 
Well, this certainly blew me away. New York (NY) classifies Testosterone (as well as all AAS) as a Schedule II drug!!! This means they are in the same class as opiates - morphine - and amphetamines. http://www.health.ny.gov/regulations/public_health_law/article/33/docs/33.pdf


Ridiculous! It's just more symbolism over substance that we've seen far too often from ignorant politicians and bureaucrats.

Politicians and diapers should be changed frequently and all for the same reason.
~José Maria de Eça de Queiroz
 
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[NO] Effect Of Testosterone On Mood And Well-Being In Men With Erectile Dysfunction

Spitzer M, Basaria S, Travison TG, Davda MN, Derogatis L, Bhasin S. The effect of testosterone on mood and well-being in men with erectile dysfunction in a randomized, placebo-controlled trial. Andrology. The effect of testosterone on mood and well-being in men with erectile dysfunction in a randomized, placebo-controlled trial - Spitzer - 2013 - Andrology - Wiley Online Library

The relationship between testosterone, well-being and mood is poorly understood. We investigated the effect of testosterone supplementation on mood, well-being, and self-reported health in men with erectile dysfunction (ED) and low serum testosterone levels.

This was a randomized, double-blind, placebo-controlled trial (ClinicalTrials.gov registration number NCT00512707), in which 140 men, 40-70 years, with ED and low serum testosterone levels were first optimized on sildenafil alone for 3-7 weeks and then randomized to receive either sildenafil plus testosterone gel (n = 70) or sildenafil plus placebo (n = 70) gel for 14 weeks. Using multiple imputations and generalized linear regression, we compared psychological changes in well-being, evaluated by the Psychological General Well-Being Index, and mood, evaluated by Derogatis Affects Balance Scale.

Mood and well-being scores were similar between the two groups at baseline and did not substantially change during the administration of sildenafil or after randomization to testosterone. Our findings show that the addition of testosterone to sildenafil in men with ED and low serum testosterone levels was not associated with improvement in either well-being or mood.
 
Why does this review isolate out older men! If anything, you would think younger men would be the group isolated, if at all.

Spitzer M, Huang G, Basaria S, Travison TG, Bhasin S. Risks and benefits of testosterone therapy in older men. Nat Rev Endocrinol. http://www.nature.com/nrendo/journal/vaop/ncurrent/full/nrendo.2013.73.html

In young men (defined as age <50 years) with classic hypogonadism caused by known diseases of the hypothalamus, pituitary or testes, testosterone replacement therapy induces a number of beneficial effects, for example, the development of secondary sex characteristics, improvement and maintenance of sexual function, and increases in skeletal muscle mass and BMD. Moreover, testosterone treatment in this patient population is associated with a low frequency of adverse events. Circulating testosterone levels decline progressively with age, starting in the second and third decade of life, owing to defects at all levels of the hypothalamic-pituitary-testicular axis. In cohort studies, testosterone levels are associated weakly but consistently with muscle mass, strength, physical function, anaemia, BMD and bone quality, visceral adiposity, and with the risk of diabetes mellitus, coronary artery disease, falls, fractures and mortality. However, the clinical benefits and long-term risks of testosterone therapy-especially prostate-related and cardiovascular-related adverse events-have not been adequately assessed in large, randomized clinical trials involving older men (defined as age >65 years) with androgen deficiency. Therefore, a general policy of testosterone replacement in all older men with age-related decline in testosterone levels is not justified.
 
Xu L, Freeman G, Cowling BJ, Schooling CM. Testosterone therapy and cardiovascular events among men: a systematic review and meta-analysis of placebo-controlled randomized trials. BMC Med 2013;11(1):108. BMC Medicine | Abstract | Testosterone therapy and cardiovascular events among men: a systematic review and meta-analysis of placebo-controlled randomized trials

BACKGROUND: Testosterone therapy is increasingly promoted. No randomized placebo-controlled trial has been implemented to assess the effect of testosterone therapy on cardiovascular events, although very high levels of androgens are thought to promote cardiovascular disease.

METHODS: A systematic review and meta-analysis was conducted of placebo-controlled randomized trials of testosterone therapy among men lasting 12+ weeks reporting cardiovascular-related events. We searched PubMed through the end of 2012 using "("testosterone" or "androgen") and trial and ("random*")" with the selection limited to studies of men in English, supplemented by a bibliographic search of the World Health Organization trial registry. Two reviewers independently searched, selected and assessed study quality with differences resolved by consensus. Two statisticians independently abstracted and analyzed data, using random or fixed effects models, as appropriate, with inverse variance weighting.

RESULTS: Of 1,882 studies identified 27 trials were eligible including 2,994, mainly older, men who experienced 180 cardiovascular-related events. Testosterone therapy increased the risk of a cardiovascular-related event (odds ratio (OR) 1.54, 95% confidence interval (CI) 1.09 to 2.18). The effect of testosterone therapy varied with source of funding (P-value for interaction 0.03), but not with baseline testosterone level (P-value for interaction 0.70). In trials not funded by the pharmaceutical industry the risk of a cardiovascular-related event on testosterone therapy was greater (OR 2.06, 95% CI 1.34 to 3.17) than in pharmaceutical industry funded trials (OR 0.89, 95% CI 0.50 to 1.60).

CONCLUSIONS: The effects of testosterone on cardiovascular-related events varied with source of funding. Nevertheless, overall and particularly in trials not funded by the pharmaceutical industry, exogenous testosterone increased the risk of cardiovascular-related events, with corresponding implications for the use of testosterone therapy.
 
The Worthless "Aging Males' Symptoms" Scale (AMS)

Zengerling F, Schrader AJ, Cronauer MV, Stemann H, Schrader M, Rinnab L. The "Aging Males' Symptoms" Scale (AMS): predictive value for lowered circulating androgens. Aging Male 2012;15(4):253-7. An Error Occurred Setting Your User Cookie

BACKGROUND: Symptoms of the "male climacteric" are often at least in part referred to an age-dependent decline of serum androgen levels. Therefore, we evaluated the relationship of climacteric symptoms as assessed by the "Aging Males' Symptoms" (AMS) Questionnaire with circulating androgen levels.

METHODS: 146 ambulatory men (age, 27-85 years) were surveyed with the AMS Questionnaire and sampled for serum values of total testosterone (tT) and sexual hormone binding globulin (SHBG). Free testosterone (fT) was calculated from tT and SHBG. A total AMS score >/=37 was considered pathological; the lower limits for tT and fT were set to 8 nmol/l and 180 pmol/l, respectively.

RESULTS: A significant deficit in tT and fT was shown in 25 (17.1%) and 34 (24.5%) men, respectively; the AMS Questionnaire showed pathological results for 66 (45.2%) men. In predicting a tT deficit, the AMS Questionnaire rendered a sensitivity of 76% and a specificity of 61.6%, only. However, multiple regression analysis revealed a significant correlation of lowered tT with a pathological somatovegetative and psychological AMS subscore (p = 0.042 and p = 0.01) and a correlation of lowered fT with a pathological sexual subscore (p = 0.039).

CONCLUSION: In predicting hypogonadism the AMS Questionnaire in total did not render a sufficient diagnostic efficiency.
 
It`s a throwback to the God created man in his own image, and hence shouldnt be tampered with, thinking.

fuck that! lol
we are all gods.
people use the term (in gods image) as if its some guy sitting in a cloud with a wrench! haha
I see it more like (to me) the sliver of DNA and energy of all life came from a microscopic DNA and evolution has grown that ( and yes still in gods image, we will all be at the level of god some day, if we don't wipe our selves out of course)
I hate the politics and bible thumpers of a book that WAS NOT WRITTEN BY GOD...
anyway vent over.

all politics to due with male hormones!
females can take birth control without a frown... but I cant take Dbol? WTF is that!?!?
 
Another thing is they DON'T want everyone healthy, there is more money in treatment then prevention or cure in most all cases of illness. why I think most cancer societies are just as bad as the cancer itself...
 
Glueck CJ, Richardson-Royer C, Schultz R, et al. Testosterone, Thrombophilia, and Thrombosis. Clin Appl Thromb Hemost. Testosterone, Thrombophilia, and Thrombosis

We describe thrombosis, deep venous thrombosis (DVT) pulmonary embolism (PE; n = 9) and hip-knee osteonecrosis (n = 5) that developed after testosterone therapy (median 11 months) in 14 previously healthy patients (13 men and 1 woman; 13 Caucasian and 1 African American), with no antecedent thrombosis and previously undiagnosed thrombophilia-hypofibrinolysis. Of the 14 patients, 3 were found to be factor V Leiden heterozygotes, 3 had high factor VIII, 3 had plasminogen activator inhibitor 1 4G4G homozygosity, 2 had high factor XI, 2 had high homocysteine, 1 had low antithrombin III, 1 had the lupus anticoagulant, 1 had high anticardiolipin antibody Immunoglobulin G, and 1 had no clotting abnormalities. In 4 men with thrombophilia, DVT-PE recurred when testosterone was continued despite therapeutic international normalized ratio on warfarin. In 60 men on testosterone, 20 (33%) had high estradiol (E2 >42.6 pg/mL). When exogenous testosterone is aromatized to E2, and E2-induced thrombophilia is superimposed on thrombophilia-hypofibrinolysis, thrombosis occurs. The DVT-PE and osteonecrosis after starting testosterone are associated with previously undiagnosed thrombophilia-hypofibrinolysis. Thrombophilia should be ruled out before administration of exogenous testosterone.
 
Ucak S, Basat O, Karatemiz G. Functional and Nutritional State in Elderly Men With Compensated Hypogonadism. J Am Med Dir Assoc. ScienceDirect.com - Journal of the American Medical Directors Association - Functional and Nutritional State in Elderly Men With Compensated Hypogonadism

OBJECTIVES: There are few data investigating the relationship between compensated hypogonadism and functional and nutritional status of elderly individuals. Impairment of functional and nutritional status of elderly men with compensated hypogonadism needs to be investigated. In this study, we tried to evaluate the association of functional and nutritional status with testosterone and LH levels in elderly with compensated hypogonadism.

DESIGN: A cross-sectional study was performed.

SETTING: A total of 1124 patients older than 70 years were screened.

PARTICIPANTS: A total of 250 patients (patient group) with compensated hypogonadism and 250 subjects (control group) with normal hormone levels were allocated in the study.

MEASUREMENTS: All parameters were compared in patient and control groups. The correlations between hormone levels and activities of daily living (ADL), instrumental activities of daily living (IADL), Mini Mental State Examination (MMSE), Mini Nutritional Assessment (MNA), and Geriatric Depression Scale (GDS) were evaluated.

RESULTS: ADL, IADL, MMSE, and MNA scores were significantly lower in the patient group. Testosterone and LH levels were correlated with ADL (R = 0.221 and R = -0.262), IADL (R = 0.210 and R = -0.277), MMSE (R = 0.331 and R = -0.341), MNA (R = 0.211 and R = -0.297), and GDS (R = -0.214 and R = -0.211) in the patient group independently from age and body mass index.

CONCLUSIONS: Our study showed that geriatric men with compensated hypogonadism had worse functionality, cognitive function, nutritional status, and mood compared with healthy controls.
 
Mortality Is Increased In Men Treated With Testosterone Compared To Age And Sex-Matched Controls
Mortality is increased in men treated with testosterone compared to age and sex-matched controls


Background: Symptomatic hypogonadism is frequent and associated with increased risk of cardiovascular events. Hypogonadism is often treated with testosterone replacement. In a recent meta-analysis on adverse events in randomised placebo controlled testosterone replacement trials (RPCT), no differences between testosterone or placebo/non-intervention groups with regards to cardiovascular events or risk factors was observed. Conversely, a contemporary RPCT in elderly immobile patients was prematurely stopped due to increased rate of cardiovascular events in the actively treated patients. The cardiovascular risk in men on long-term testosterone treatment is largely unsettled.

Aim and Method: We aimed at assessing the association between the exposure variable testosterone treatment and development of cardiovascular events in a cohort of all men in Denmark filing prescriptions for testosterone in the period 1997–2008. Three age and sex-matched controls per patient were randomly selected from the background population. Information on mortality, disease, drug use and social variables was acquired using four Danish nationwide registries.

Results: Seven thousand three hundred and thirty-three testosterone users were identified. Women and prior (before 1997) testosterone users were excluded, generating a study cohort of 4792 cases (aged 46.3±0.3; years±S.E.M.) and 14 376 controls (46.7±0.2 years), which was followed until December 2011. In the mean observation period (13.2±0.03 years) 858/1963 deaths were observed in cases/controls yielding an unadjusted total mortality odds-ratio of 1.38 (1.26–1.51, 95% CI, P<0.01) in cases vs controls and correspondingly a Cox proportional hazard-ratio of 1.36 (1.25–1.47, 95% CI). Unadjusted odds-ratio for cardiovascular death was 1.22 (1.04–1.43, 95% CI) in cases vs controls.

Conclusion: We found a significant 36% increased mortality in men treated with testosterone compared to age- and sex-matched controls. We also found an increased risk of cardiovascular death in the cases. However, in this on-going study additional analyses are needed to further clarify whether the observed increased mortality is connected with co-morbidity, concomitant drug.
 
Shahabi S, He S, Kopf M, et al. Free Testosterone Drives Cancer Aggressiveness: Evidence from US Population Studies. PLoS One 2013;8(4):e61955. PLOS ONE: Free Testosterone Drives Cancer Aggressiveness: Evidence from US Population Studies

Cancer incidence and mortality are higher in males than in females, suggesting that some gender-related factors are behind such a difference. To analyze this phenomenon the most recent Surveillance, Epidemiology and End Results (SEER) database served to access cancer survival data for the US population. Patients with gender-specific cancer and with limited information were excluded and this fact limited the sample size to 1,194,490 patients. NHANES III provided the distribution of physiologic variables in US population (n = 29,314). Cox model and Kaplan-Meier method were used to test the impact of gender on survival across age, and to calculate the gender-specific hazard ratio of dying from cancer five years following diagnosis. The distribution of the hazard ratio across age was then compared with the distribution of 65 physiological variables assessed in NHANES III. Spearman and Kolmogorov-Smirnov test assessed the homology. Cancer survival was lower in males than in females in the age range 17 to 61 years. The risk of death from cancer in males was about 30% higher than that of females of the same age. This effect was present only in sarcomas and epithelial solid tumors with distant disease and the effect was more prominent in African-Americans than Caucasians. When compared to the variables assessed in the NHANES III study, the hazard ratio almost exactly matched the distribution of free testosterone in males; none of the other analyzed variables exhibited a similar homology. Our findings suggest that male sex hormones give rise to cancer aggressiveness in patients younger than 61 years.
 
Gong Y, Xiao H, Li C, et al. Elevated t/e2 ratio is associated with an increased risk of cerebrovascular disease in elderly men. PLoS One 2013;8(4):e61598. PLOS ONE: Elevated T/E2 Ratio Is Associated with an Increased Risk of Cerebrovascular Disease in Elderly Men

OBJECTIVE: To investigate the relationship between sex hormones and the risk of vascular disease in elderly men and to evaluate the advantages and disadvantages of testosterone replacement.

METHODS: A total of 337 men, aged 60 to 91 years, were enrolled in this single-center, cross-sectional study, and their sex hormone levels were assessed. Linear and logistic regression analyses were utilized to compare the sex hormone levels between patients with and without vascular disease. The nonparametric K-sample test was used for inter-group comparisons.

RESULTS: Aging and abnormal metabolism were both significantly associated with an increased risk of vascular diseases and changes in sex hormone levels. Primary linear and logistic regression analyses showed no significant differences in sex hormone concentrations between patients with and without vascular diseases after adjusting for age. Logistic regression with abnormal metabolism as categorical variable showed that free testosterone (FT) and free estradiol (FE2) had significant relationships with CEVD risk (P<0.05). In further regression with all metabolic continuous variables included, the testosterone/estradiol (T/E2) ratio replaced FT and FE2 (P<0.05). Trend line analyses showed that T/E2 actually had a binomial linear correlation with the risk of cerebrovascular disease; its best protective effect occurred at values of 0.13-0.15, with an OR value extremely close to those of FT and FE2 (0.23 vs. 0.24-0.25).

CONCLUSION: T/E2 balance plays a key role in the relationship between sex hormones and the risk of cerebrovascular disease. The balance between T and E2 may be more important than their absolute quantities. Extremely low T/E2 and inappropriately high T/E2 ratio can both harm the brain blood vessels. Careful consideration should be given before beginning testosterone replacement treatment, and supplementing with estrogen seems to be a good way to protect blood vessels of the brain in elderly men.
 
Ya know doc. I hazzard to look in on this thread so often - BUT ALWAYS the same proverbial answer comes to mind with regard to the THREAD TITLE - "Because society fears testosterone usage due to misinformation and misnomer, finally resulting in FEAR for a MULTITUDE of vectors of INSANITY..

Its great that you posted it so we can all see how pathetic things really are for medical science. THIS PUBLICATION AND STUDY by these EXTREMISTS IS OFFENSIVELY DISGUSTING.... LOL. But a light show comparable to a FLOYD CONCERT... So lets get high and check it out.. LOL

Lets examine the ARTICLE title (not thread title)- "Free testosterone drives cancer aggressiveness".. And right out of the gate, they OMIT the fact that FREE TESTOSTERONE IS USELESS with respect to biological tissue action - until it is BOUND to protein for purpose. This is so disturbing it just fails to even Merit a hunt for reason or logic. But you know how I LOVE a good SNIPE HUNT... LOL:rolleyes:

After meandering through ENDLESS statistical and POORLY coded ABSTRACT with ONLY the Purpose of CONVOLUTING so that the legal LAYMAN has no chance of interpreting without the BIAS'd preparOR delivering their message (after all, cyphering is so damn taxing), I did come to denote that they are indeed accusing "free testosterone" as a culpret. Dont matter I got close enough, as thats all some bullshit like this merits. LOL

But did they even stop to even account for the fact that in most cases free testosterone is only what is LEFT OVER after the REQUIRED testosterone has been picked up by protein for delivery.? NO. And with consideration of no method of calculating REAL TIME Metabolism processing, the whole article is worth JACK SHIT...

But lets have some fun:
1. Did they stop to account for the fact that is the cancer we are talking about is a "GROWTH type" and not a "Deteriorative type" (please forgive my humble IGNORANCE oh mighty authors:D). - NO I doubt it..
2. Did they stop to consider the general condition of subject any further than GENERAL age classification and sex? - NO
3. Did they stop to attempt to qualify and quantify body types, BMI's, and physical work regimens/work histories? - NO
4. Did they consider extended backgrounds on these folks if available, and how far? Blood history? Doubtful...
5. ARE THEY EVEN REGISTERING A CHANGE IN FREE TESTOSTERONE AS RELATED TO TIME AND PRIOR TO DIAGNOSIS, OR WOULD IT MATTER? NO

Free testosterone can mean one of a few things:
1. A person is likely inclined to carry a given genetic propensity as physically manifested.
2. LESS Testosterone is being metabolized currently thus leaving an excess of free testosterone that will last about as long as it takes the body to adjust. This would mean LESS Cellular activity, and NOT More, which is what they would like to propose as they selfishly PreCLude a cellular cascade ensuing thus lacking all notions of normal control and APOPTOSIS action. IN SHORT that means that less cellular metabolish (tissue growth) is occurring as an indication of high FreeT.
3. It could mean that less testosterone is being metabolized around the entire body depending on the cancer.
4. It could simply mean that the testicles are now driven to produce MORE testosterone to FIX THE WOUND, and even though it is not able to use it. (Likely scenario)
5. It could be as specific as estrogen demands are up, but clearance is hindered by poor estrogen metabolism to higher proportions of negative derivatives.
6. SHIT - it could mean that SHBG, insulin, or IGF-1 is failing for all they know...!

Again, it doesnt matter that I am no more than an ARMCHAIR ASSHOLE who knows DICK. I am smart enough to see a pile of shit without smelling. The title "Free testosterone drives cancer aggressiveness".. is a poor fuckfest at best. The key operative word being DRIVES... The free T AINT even DRIVING Miss Daisy...!:rolleyes:;) With that said that article merits no more than my poor assessment at best.

So here are some new title proposals:
-" Free testosterone is found to correlate highly with aggressive cancers"; or
-"Free testosterone may be an indicator that endogenous hormone production is affected by aggressive cancers"; OR
- "Aggressive cancers stimulate testosterone production, or limit end receptor use potentially systemically."

The bottom line is that it is a BIG OL PILE O SHIT. The best part is that the authors MAY not even know what they are really looking at. Minimally, it is just a political spin to serve a current prinicple for Fund$$zzz. SADLY, there are really very FEW who are even TECHNICALLY QUALIFIED to Challenge or Debunk it, and due to the mystery that STEROID DEMONIZATION has caused and the damage now reaped in full. You could almost suspect that the groups doing this type research are nothing more than paid hit squads designed to produce custom tailored light shows for the highest bidder. "we're all so fuckig ignorant - just help us help us - we wont ask any questions massa...":D:p For the Romanest of Roman civilizations ever to grace the face of the planet, "modernized Medicine" was most likely handled with more sense and real purpose in the original times of Rome.

** You could show me where I remain ignorant and potentially off-base, but the name/title they attached really says it all..... ..... ...... !


Shahabi S, He S, Kopf M, et al. Free Testosterone Drives Cancer Aggressiveness: Evidence from US Population Studies. PLoS One 2013;8(4):e61955. PLOS ONE: Free Testosterone Drives Cancer Aggressiveness: Evidence from US Population Studies

Cancer incidence and mortality are higher in males than in females, suggesting that some gender-related factors are behind such a difference. To analyze this phenomenon the most recent Surveillance, Epidemiology and End Results (SEER) database served to access cancer survival data for the US population. Patients with gender-specific cancer and with limited information were excluded and this fact limited the sample size to 1,194,490 patients. NHANES III provided the distribution of physiologic variables in US population (n = 29,314). Cox model and Kaplan-Meier method were used to test the impact of gender on survival across age, and to calculate the gender-specific hazard ratio of dying from cancer five years following diagnosis. The distribution of the hazard ratio across age was then compared with the distribution of 65 physiological variables assessed in NHANES III. Spearman and Kolmogorov-Smirnov test assessed the homology. Cancer survival was lower in males than in females in the age range 17 to 61 years. The risk of death from cancer in males was about 30% higher than that of females of the same age. This effect was present only in sarcomas and epithelial solid tumors with distant disease and the effect was more prominent in African-Americans than Caucasians. When compared to the variables assessed in the NHANES III study, the hazard ratio almost exactly matched the distribution of free testosterone in males; none of the other analyzed variables exhibited a similar homology. Our findings suggest that male sex hormones give rise to cancer aggressiveness in patients younger than 61 years.
 
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Polackwich AS, Ostrowski KA, Hedges JC. Testosterone replacement therapy and prostate health. Curr Urol Rep 2013;13(6):441-6. Testosterone Replacement Therapy and Prostate Health - Springer

There is an emerging evolution in the understanding of the relationship between the prostate and testosterone. It has long been generally believed that with testosterone replacement therapy (TRT), increasing serum testosterone levels led to prostatic growth and worsening of voiding dysfunction and associated complications. A new theory, the Saturation Model of Testosterone and its effect on the Prostate has gained attention. This theory suggests that the prostate's response to increasing levels of serum testosterone reaches a limit beyond which there is minimal effect. This model predicts that testosterone replacement therapy occurs above this saturation point, and replacing testosterone to eugonadal levels should not worsen prostate related benign disease. We evaluated the recent published data, with an emphasis on clinical studies done within the last 3 years, for the effects of testosterone supplementation on benign prostatic disease.
 
The [VERY HIGH] Prevalence Of Prior Use Of Anabolic Androgenic Steroids In Young Hypogonadal Men [Abstract: 1395]
http://www.aua2013.org/abstracts/archive/printabstracts.cfm?id=1395

Introduction and Objectives - Testosterone replacement therapy (TRT) for hypogonadism has increased significantly in the past decade. In 2011, 1.3% of all 19-30 year olds reported prior use of anabolic androgenic steroids (AAS) (Johnson, 2012). This trend has led to a heightened sense of awareness surrounding AAS use and the potential for transient or permanent hypogonadotropic hypogonadism. The prevalence and attitudes of men with a history of prior AAS use presenting with symptomatic hypogonadism requiring TRT has never been reported.

Methods - An anonymous, prospective, IRB-approved survey was distributed to men with symptomatic hypogonadism over a 6-month period in 2012. Basic demographic information and choice of TRT was documented as was the nature and attitudes regarding prior AAS use. Statistical analysis was performed with student’s t-test and Fisher’s exact test with p<0.05 considered significant.

Results - A total of 138 men (mean age 45.7 ±11.7) currently receiving TRT for hypogonadism participated, and 31% (n=43; mean age 39.4 ±7.4) reported a history of prior AAS use. Among hypogonadal men ? 50 years old, 43.6% (n=41) used AAS in the past compared to 4.5% (n=2) in those >50 years old (p<0.001). Men with previous AAS use were 9.1 years younger on presentation than men without an AAS history (p<0.0001). The mean reported age of first AAS use was 24.6 ±6.8, and 21% started using AAS in their teens. Less than half understood the effects of AAS on natural testosterone production (49%) and fertility (47%), yet only 16% regretted using them.

In men with an AAS history, moving forward, treatment for hypogonadism via testosterone injections was preferred by 93%, while 46% without a history of AAS use preferred injections (p<0.0001). AAS users were more likely to experiment with their prescribed dose of TRT without notifying their physician (26%) and to use additional, non-prescribed substances like growth hormone (40%).

Conclusions - Prior AAS use is relatively common in men seeking treatment for symptomatic hypogonadism. Although this only represents one center, the prevalence was approximately ten times higher in hypogonadal men under age 50 years than those over. This information was not known prior to treatment and highlights the need to be cautious about prescribing TRT to younger patients. Perhaps prescription of alternative medications with lower likelihood for abuse (e.g. selective estrogen receptor modulators or aromatase inhibitors) would be more prudent in younger patients with symptomatic hypogonadism.
 
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