Showing posts with label testosterone complications. Show all posts
Showing posts with label testosterone complications. Show all posts

Monday, November 2, 2026

Testosterone Replacement Therapy Takes More Than A Blood Test...

 


Organization (Year)

Testing Requirement

Diagnostic Threshold and Notes

Endocrine Society (2018)

Fasting total testosterone measured on 2 separate mornings, both unequivocally low, plus consistent symptoms or signs

Lower limit 264 ng/dL (CDC-standardized assays). Measure free testosterone if SHBG may be altered (obesity, diabetes) or total testosterone is borderline

American Urological Association (2018)

Total testosterone measured on 2 separate early mornings, both low (Strong Recommendation, Grade A)

Consistently <300 ng/dL. Ideally the same lab and method for both samples

Society for Endocrinology and Association for Clinical Biochemistry and Laboratory Medicine, UK (2024)

Total testosterone measured on 2 consecutive fasting mornings, both low

Action threshold <8 nmol/L (~230 ng/dL). 8–12 nmol/L is a gray zone that needs careful clinical correlation

References:

 

1:  Sargis RM, Davis AM. Evaluation and Treatment of Male Hypogonadism. JAMA. 2018;319(13):1375–1376. doi:10.1001/jama.2018.3182

2:  Bhasin S, Brito JP, Cunningham GR, Hayes FJ, Hodis HN, Matsumoto AM, Snyder PJ, Swerdloff RS, Wu FC, Yialamas MA. Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2018 May 1;103(5):1715-1744. doi: 10.1210/jc.2018-00229. PMID: 29562364.

3:  Mulhall JP, Trost LW, Brannigan RE, Kurtz EG, Redmon JB, Chiles KA, Lightner DJ, Miner MM, Murad MH,       Nelson CJ, Platz EA, Ramanathan LV, Lewis RW. Evaluation and Management of Testosterone Deficiency: AUA Guideline. J Urol. 2018 Aug;200(2):423-432. doi: 10.1016/j.juro.2018.03.115. Epub 2018 Mar 28. PMID: 29601923.

4:  Zucker IJ, Masterson TA. Comparison of American Urological Association and Endocrine Society guidelines on testosterone replacement. Int J Impot Res. 2022 Nov;34(7):626-629. doi: 10.1038/s41443-021-00477-w. Epub 2021 Oct 18. PMID: 34663926.

5:  Jayasena CN, de Silva NL, O'Reilly MW, MacKenzie F, Marrington R, Jones H, Livingston M, Downie P, Hackett G, Ramachandran S, Tomlinson J, David J, Boot C, Patel M, Tarling J, Wu F, Quinton R. Standardising the biochemical confirmation of adult male hypogonadism: A joint position statement by the Society for Endocrinology and Association of Clinical Biochemistry and Laboratory Medicine. Clin Endocrinol (Oxf). 2024 Nov;101(5):531-534. doi: 10.1111/cen.14929. Epub 2023 Jul 1. PMID: 37393195.  (UK)

6:  Grossmann M, Jayasena CN, Anawalt BD. Approach to the Patient: The Evaluation and Management of Men ≥50 Years With Low Serum Testosterone Concentration. J Clin Endocrinol Metab. 2023 Aug 18;108(9):e871-e884. doi: 10.1210/clinem/dgad180. PMID: 36995891; PMCID: PMC10438885.

 

We are living in the age of testosterone – for the second or third time.  Some are taking it to caricature levels. I started writing about it on this blog 13 years ago – as a form of cheating in sports and health and wellness hype.  I have written about a study that carefully screened men for hypogonadism and demonstrated moderate benefit on sexual functioning and some benefit with mood and depressive symptoms but no effect on physical functioning or vitality.  Since then, testosterone prescribing has continued unabated and expanded with the growth of telemedicine and advertising to the target audience. As a psychiatrist working during that time, I saw men who were clearly taking supraphysiological doses of testosterone for the anabolic effects.  I did not have to speculate about that use when I saw men with obvious muscular hypertrophy who told me they were taking testosterone because they liked the interpersonal effects when people noticed they had muscle. 

 

The major guidelines for testosterone replacement therapy are produced in the above table. The indication for replacement is hypogonadism by clinical evaluation and laboratory determination.  The laboratory guidelines vary slightly between organizations but they are generally consistent.  The current guideline in UpToDate uses a determination of two morning determinations of testosterone and a diagnosis of hypogonadism that considers the many causes of primary and secondary hyopgonadism.  The indications for therapy are more concrete than many medications that are purportedly overprescribed.  Cultural factors are more prominent than ever with the current administration mandating testosterone screening (2) for active and reserve military to optimize human performance and address Operator Syndrome.  Interestingly the Operator Syndrome is a collection of physical and psychological injuries – some of which may have been pre-existing conditions.  The endocrine aspect of this syndrome is secondary hypogonadism from blast injuries.  There is a significant differential diagnosis of both secondary and primary hypogonadism that include functional etiologies like acute and chronic illnesses, malnutrition, other endocrinopathies, various drugs, infections, and various toxins. The  value of including this as a feature of a non-specific syndrome seems questionable to me.  The best approach to this problem is a comprehensive assessment by an endocrinologist – not a testosterone level. 

 

What about the mass screening aspects?  The pie diagram is from the EMAS study (4) of 3,369 men ages 40-79.  The interesting finding is that only 2% of that population has symptomatic hypogonadism that would be treated with testosterone.  5% had low testosterone that normalized on repeat.  10% had persistently low testosterone but no symptoms of hypogonadism. 83% had normal testosterone on the first test.            

 

 

After the DOD release, Hennigar, et al did a retrospective study of pre-existing health data on military personnel with a focus on testosterone (5).  The analysis was based on a sample of 479 men with an average age 29.9 years.  Weighted mean morning total testosterone, sex hormone–binding globulin, and free testosterone concentrations were determined.  Using 2 cutoff levels of <300 ng/dL and < 264 ng/dL – weighted prevalences of the sample were calculated for < 30 yrs old and ≥ 30 yrs old.  A separate non-obese group was estimated using the 264 ng/dL cutoff.  Extrapolating those prevalence figures to the active-duty US Army personnel gives a range of 57,788 to 100,691 service men.  Using the EMAS study estimate for symptomatic hypogonadism that number is 7,862.

 

The authors of this study qualify their results by saying that this is only one morning fasting testosterone level. 30% of the low levels are expected to normalize on repeat, but that would still leave about 20% of this sample in the low range. The sample was not screened for specific symptoms of low testosterone or moderate to severe head injury that has been associated with blast injuries and post-traumatic hypopituitarism (7).  Obesity and body composition contributes and they note the normal weight cohort has a lower prevalence of low testosterone.  The stress of some military conditions can also suppress testosterone.  Army Ranger training can reversibly suppress testosterone levels by 50% (8).  That is attributed to energy deficit, sleep restriction, heavy physical work, and psychological stress effects on gonadotropin-releasing hormone and luteinizing hormone pulsatility.  This is a critical observation that appears to be omitted from both the formulation of Operator Syndrome and the rationale for screening.  Treatment in this case would be removal from the stressful military conditions rather than testosterone replacement.  It would also seem to be a factor in determining the optimal time and status for diagnosing post-traumatic hypopituitarism.

 

All the factors mentioned so far suggest that testosterone is over prescribed in the US population. Since the US has no comprehensive pharmacosurveillance indirect estimates are made using other samples. In 2013 an estimated 2.3M men were using testosterone.  That dropped to about 1.15M men after an FDA warning about cardiovascular effects (9). From 2018-2022 the number of men being treated increased 27% from 1.22M to 1.66M.  The data in that study was from 25 state prescription data monitoring programs (PDMPs).  Remaining states were prohibited from sharing that information and the authors suggest that more populous states need to be included (10).      

 

The current population of men between the ages of 40 and 79 is estimated to be about 72 million and they make up 21.5% of the total population. Using the EMAS estimate for true hypogonadism (low total and free testosterone and 3 sexual symptoms of 2.1% yields a total of 1.53M men with true hypogonadism.  That number is lower than the estimate of 1.66M  from 25 states (10).  In that study the fastest growing testosterone use groups were 35–44 (+58%) and 45–54 (+35%) – groups that according to the EMAS study have the lowest prevalence of hypogonadism.  This age mismatch combined with missing or normal baseline testosterone levels, non-specific symptoms (fatigue, low energy), and low treatment rates in the target population of men ≥ 60 with the highest rates of hypogonadism suggests overprescribing.

 

There is additional indirect evidence available.  Every viewing of streaming channels on the Internet generally produces an advertisement about the easy availability of testosterone prescriptions by telemedicine.  A recent secret shopper study (17, 18) of online platforms offering testosterone therapy found that none of the assessments were done by a physician and despite normal total and free testosterone levels and wanting to father a child - 7 of 8 platforms prescribed testosterone.  The associated commentary says this highlights a problem and this technique might be used by state medical boards.  An earlier study looked at the relationship between advertising and prescriptions and noted that each additional testosterone ad exposure was associated with 14 new tests, 5 new initiations, and 2 initiations without testing per million men. Unbranded "low T" ads had a stronger effect than branded ads.  Advertising was also specifically associated with starting testosterone without a prior blood test. (19, 20).

 

At this point it goes without saying that testosterone and other anabolic steroids are considered performance enhancing drugs with other magical properties.  There is a fountain of youth myth and some men claim to take them for anti-aging effects. Excessive use can also occur associated with body dysmorphia and an anabolic androgenic steroid (AAS) use disorder (22, 23).  There is both pre-clinical data to support the use disorder diagnosis but it is not directly recognized in either the DSM or ICD.  Some studies suggest that 30% of casual users will go on to develop dependence on AAS.  It can also be recognized clinically because of the comorbidity with other substance use disorders most notably opioid use disorder.  In treatment settings, supraphysiological doses of testosterone can also be an indication.

 

To summarize, there is a clear indication for testosterone replacement therapy for hypogonadism that requires two fasting morning blood tests with specific cutoffs as noted in the table at the top of this post.  In reality, much more is required because of the causes of primary and secondary hypogonadism that can be both medical (like TBI) or functional (like the stressors of the military environment).  There is no indication for mass screening and no reason to believe that replacing testosterone in men with or without hypogonadism will enhance military effectiveness.  Testosterone has no anti-aging or vitality enhancing properties at physiological doses.  At supraphysiological doses, it is an androgenic anabolic steroid and cause muscle hypertrophy, irritability and aggression, and persistent hypogonadism when withdrawn.  In a study of quality of life in former AAS users abstinent for 2 years – the nonusing strength trainers had a quality of life score comparable to young adults with a previous ischemic stroke (16).

 

Any man considering testosterone replacement should adhere to the guidelines from the endocrine and urological societies.  For those members of the military that may not have a choice – I am hoping that you have access to a VA endocrinologist to make any treatment decisions.  They knew all about it in 1986 when I trained there and have been refining the guidelines for the past 40 years. 

 

George Dawson, MD, DFAPA

 

References:

 

1:  Hennigar SR, Heymsfield SB, Bukhari AS, Lieberman HR, Berryman CE. Testosterone Screening Thresholds in Active-Duty US Male Service Members. JAMA. Published online October 15, 2026. doi:10.1001/jama.2026.19794

 

2:  Health and human performance optimization to enhance military readiness.

Published July 15, 2026. Accessed 10/30/2026.  PDF

 

“Effective immediately, all Active Duty and Reserve Component personnel aged thirty

and older will be screened for testosterone deficiency as a mandatory element of their Periodic

Health Assessment (PHA). Service members under the age of thirty may also request this

screening during their PHA.

 

This enhanced screening protocol directly supports the Department's focus on Human

Performance Optimization while comprehensively addressing Operator Syndrome. Originally

identified among Special Forces in 2020 through collaborative research between the Department

of War (Do W) and leading academic institutions, Operator Syndrome represents a unique

convergence of health challenges that require proactive clinical intervention. Additionally,

applying lessons learned from treating Operator Syndrome across the Total Force including

targeted testosterone therapy directly optimizes Warfighter readiness….”

 

3:  Frueh BC, Madan A, Fowler JC, Stomberg S, Bradshaw M, Kelly K, Weinstein B, Luttrell M, Danner SG, Beidel DC. “Operator syndrome”: A unique constellation of medical and behavioral health-care needs of military special operation forces. The International Journal of Psychiatry in Medicine. 2020 Jul;55(4):281-95.

 

4:  Wu FC, Tajar A, Beynon JM, Pye SR, Silman AJ, Finn JD, O'Neill TW, Bartfai G, Casanueva FF, Forti G, Giwercman A, Han TS, Kula K, Lean ME, Pendleton N, Punab M, Boonen S, Vanderschueren D, Labrie F, Huhtaniemi IT; EMAS Group. Identification of late-onset hypogonadism in middle-aged and elderly men. N Engl J Med. 2010 Jul 8;363(2):123-35. doi: 10.1056/NEJMoa0911101. Epub 2010 Jun 16. PMID: 20554979.

 

5:  Hennigar SR, Heymsfield SB, Bukhari AS, Lieberman HR, Berryman CE. Testosterone Screening Thresholds in Active-Duty US Male Service Members. JAMA. 2026 Oct 15:e2619794. doi: 10.1001/jama.2026.19794. Epub ahead of print. PMID: 42879141; PMCID: PMC13673370.

 

7: Mubarak, M., Modgil, V. Routine testosterone screening in military personnel: an opportunity for evidence-based implementation in men’s health. Nat Rev Urol (2026). https://doi.org/10.1038/s41585-026-01181-4

 

8:  Friedl KE, Nindl BC, Potter AW. Stress-associated testosterone suppression: central adaptation or hypogonadism? J Clin Endocrinol Metab. 2026 Jul 15;111(8):e1951-e1960. doi: 10.1210/clinem/dgag181. PMID: 42044038; PMCID: PMC13368364.

 

9:  Walker RF, Zakai NA, MacLehose RF, et al. Association of Testosterone Therapy With Risk of Venous Thromboembolism Among Men With and Without Hypogonadism. JAMA Intern Med. 2020;180(2):190–197. doi:10.1001/jamainternmed.2019.5135

 

10:  Selinger S, Thallapureddy A. Cross-sectional analysis of national testosterone prescribing through prescription drug monitoring programs, 2018-2022. PLoS One. 2024 Aug 28;19(8):e0309160. doi: 10.1371/journal.pone.0309160. PMID: 39196907; PMCID: PMC11355536.

 

11:  Pope HG Jr, Wood RI, Rogol A, Nyberg F, Bowers L, Bhasin S. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014 Jun;35(3):341-75. doi: 10.1210/er.2013-1058. Epub 2013 Dec 17. PMID: 24423981; PMCID: PMC4026349.

 

12:  Kanayama G, Hudson JI, DeLuca J, Isaacs S, Baggish A, Weiner R, Bhasin S, Pope HG Jr. Prolonged hypogonadism in males following withdrawal from anabolic-androgenic steroids: an under-recognized problem. Addiction. 2015 May;110(5):823-31. doi: 10.1111/add.12850. Epub 2015 Feb 25. PMID: 25598171; PMCID: PMC4398624.

 

13:  Baggish AL, Weiner RB, Kanayama G, Hudson JI, Lu MT, Hoffmann U, Pope HG Jr. Cardiovascular Toxicity of Illicit Anabolic-Androgenic Steroid Use. Circulation. 2017 May 23;135(21):1991-2002. doi: 10.1161/CIRCULATIONAHA.116.026945. PMID: 28533317; PMCID: PMC5614517.

 

14:  Pope HG Jr, Kanayama G. Body Image Disorders and Anabolic Steroid Withdrawal Hypogonadism in Men. Endocrinol Metab Clin North Am. 2022 Mar;51(1):205-216. doi: 10.1016/j.ecl.2021.11.007. Epub 2022 Feb 8. PMID: 35216717.

 

15:  Bhasin S, Seidman S, Travison TG, Pencina KM, Lincoff AM, Nissen SE, Miller MG, Flevaris P, Li X, Wannemuehler KA, Pope HG. Depressive Syndromes in Men With Hypogonadism in the TRAVERSE Trial: Response to Testosterone-Replacement Therapy. J Clin Endocrinol Metab. 2024 Jun 17;109(7):1814-1826. doi: 10.1210/clinem/dgae026. PMID: 38205962.

 

16:  Pope HG Jr, Kanayama G. Reduced Quality of Life in Former Androgen Users: An Evolving Public-Health Concern. J Clin Endocrinol Metab. 2024 Apr 19;109(5):e1400-e1401. doi: 10.1210/clinem/dgad661. PMID: 37955864.

 

17:  Dubin JM, Jesse E, Fantus RJ, et al. Guideline-Discordant Care Among Direct-to-Consumer Testosterone Therapy Platforms. JAMA Intern Med. 2022;182(12):1321–1323. doi:10.1001/jamainternmed.2022.4928

 

18:  Woloshin S, Gill LL. Direct-to-Consumer Low-Testosterone Clinics—Where Is the Federation of State Medical Boards? JAMA Intern Med. 2023;183(4):288–289. doi:10.1001/jamainternmed.2022.7008

 

19: Kravitz RL. Direct-to-Consumer Advertising of Androgen Replacement Therapy. JAMA. 2017;317(11):1124–1125. doi:10.1001/jama.2017.1364

 

20:  Layton JB, Kim Y, Alexander GC, Emery SL. Association Between Direct-to-Consumer Advertising and Testosterone Testing and Initiation in the United States, 2009-2013. JAMA. 2017;317(11):1159–1166. doi:10.1001/jama.2016.21041

 

21:  Kanayama G, Brower KJ, Wood RI, Hudson JI, Pope Jr HG. Anabolic–androgenic steroid dependence: an emerging disorder. Addiction. 2009 Dec;104(12):1966-78.

 

22:  Kanayama G, Hudson JI, Pope Jr HG. Features of men with anabolic-androgenic steroid dependence: A comparison with nondependent AAS users and with AAS nonusers. Drug and alcohol dependence. 2009 Jun 1;102(1-3):130-7.

 

23:  Bhasin S, Storer TW, Berman N, Callegari C, Clevenger B, Phillips J, Bunnell TJ, Tricker R, Shirazi A, Casaburi R. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med. 1996 Jul 4;335(1):1-7. doi: 10.1056/NEJM199607043350101. PMID: 8637535.

 

 

Supplementary 1:  I was fortunate to train and work with many excellent endocrinologists at the Milwaukee VAMC and at St. Paul-Ramsey Medical Center/Regions Hospital.  I learned a lot in the process and ended up seeing many complex endocrine problems in clinical practice and serving on relevant committees with some of those same endocrinologists. Based on that experience I do not see any potential advantages to consider post TBI hypopituitarism as a feature of another syndrome. I personally saw it diagnosed and treated many times at the Milwaukee VAMC often associated with panhypopituitarism and recognized and treated several of those cases in clinical practice.  They were all secondary to TBI or neurosurgery complications.

 

Supplementary 2:  I was equally fortunate to train and work with many vets.  One of them described Jungle Warfare School to me. I will not attempt to recreate the scenarios he told me about -  and will only say it clearly puts members of the military at risk and places them under extreme physiological stress. The neuroendocrine system has always been an area of research in psychiatry. I was a research fellow in a program where we tested the HPA axis and adrenal responsiveness in patients stressed by depression.  A thorough characterization of some of these stressful training programs may be a batter place to start than just measuring testosterone levels and considering the patient to have hypogonadism.

 

The political atmosphere that these recommendations occur in cannot be ignored.  They are being made by a Department of War Secretary who has taken to lecturing experienced military personnel about fitness for duty and suggesting goals that are long on aggression and short on strategy.  Combined with the DOGE effects of reducing VAMC staffing and medical care I think it is reasonable to be concerned about whether members of the military will get adequate assessments for any abnormal tests rather than just a prescription. Congress should be watching this as an experiment if the guidelines for testosterone replacement are not met and if the effects of testosterone are not carefully followed.   

 


Sunday, February 21, 2016

Testosterone Study Is Disappointing For More Than The Obvious Reasons

Testosterone

Testosterone replacement has been a controversial issue, despite a large number of physicians who prescribe it, FDA approval of products for mass marketing, and a number of advocates that see it as an anti-aging and performance enhancing drug for aging men.  The science behind is has been surprisingly slow.  In an era where inequities in health care are often argued by race or sex, this seems to be one where the science at least lags far behind what is known for women.  Expert opinion about testosterone replacement has changed very little over the years, despite much popular literature about how this has occurred for years in Europe and there is widespread benefit for physical and emotional well being of men as they age.  From a clinical perspective, psychiatrists are seeing more and more middle-aged men on testosterone replacement.  This treatment modality has significant implications for any medical treatment provided by psychiatrists as well as associated comorbidity.  From a psychiatric perspective it is also important to determine if the testosterone use is more than indicated, is associated with increasing muscle mass and body image changes, and if it occurring in the context of unreasonable expectations like preserving youth , reversing the effects of aging, or athletic performance enhancement.

In the most recent study of men 65 years of age and older the authors examined the effects of treatment with testosterone gel for a period of one year (1).  The total number of subjects was 790 out of a total of 51,085 men who were screened.  In order to qualify for the trial testosterone level had to be sufficiently low (less than 275 ng/dl) on one of two samples and that eliminated 85% of all of the screened men.  The trial was designed to look at physical function, sexual function, and vitality.  The treatment resulted in testosterone levels that were in the mid-normal range for 19 to 40 year old men.  Despite considerable medical comorbidity in the recruited patients there were clear cutoffs for medical comorbidity.  Those cutoffs included a history of prostate cancer or risk of prostate cancer on the Prostate Cancer Risk Calculator, other conditions known to cause hypogonadism, medications known to effect the concentration of testosterone, high cardiovascular and severe depression (PHQ-9 score >20).   The overall results showed that there was moderate benefit on sexual functioning and some benefit with mood and depressive symptoms but no effect on physical functioning or vitality.  A look at these measurements is instructive.

Physical Function was assessed using the 6 minute walk.  Recent normative data has been established for various age cohorts using subjects from several countries.   That data establishes normative curves for age cohort stratified by sex.  The six-minute walk distance (6MWD) ranged from 559 +/- 80 meters in 60-69 year old men to 514 +/- 71 meters in 70-80 year old men.  On two trials subjects usually walked on average 12 meter farther on the second trial.  In the present study, the criterion for a positive effects from testosterone was a walking distance increase of 50 meters.  When compared with controls, the testosterone treated men had significantly more men increasing the distance walked by 50 meters, the percentage of men exceeding this measure, the change from baseline, and the percentage of men with higher scores on the physical function domain test (PF-10) from the Medical Outcomes Study 36-Item Short Form Instrument (SF-36).  One of the concerns I had reading this methodology is the use of testosterone for physical performance enhancement.  Is it effective without using a training program?  Were the subjects in this study advised to extend their walking distances or speed?  Without it I am skeptical that it would have much of an effect.

Vitality was determined by measures on the FACIT-Fatigue score as the primary outcome measure.  Interestingly FACIT stands for Functional Assessment of Cancer Treatment and their web page links to an extensive list of modified rating scales.  I could not tell if the rating scale had been validated in normal 65 year old men without a cancer diagnosis.  No significant differences were noted between testosterone treated men and controls.  On secondary measures testosterone treated men were more likely to report higher energy at the end of the trial, but that measure was unspecified and may have been a line item in the SF-36.

Sexual Function was measured primarily by question 4 of the Psychosexual Daily Questionnaire.  This item is a 12 item yes-no checklist of male sexual behaviors, thoughts, and fantasies.  Greater testosterone levels achieved in treatment correlated with higher testosterone levels.  A secondary measure - the Derogatis Interview for Sexual Functioning in Men-II (DISF-M-II) also documented increased sexual desire and it was also used as a screen for participants in the Sexual Function arm of the trial.  The sexual function measures do appear to be more straightforward, but they are all self report measures over considerable time frames.

One of the most interesting aspects of this trial was an analysis of the side effects.  One of the main concerns in treating men with testosterone is the risk of prostate cancer that is sensitive to testosterone levels.   I have had personal communication with physicians who were treating patients with testosterone who developed widely metastatic prostate cancer.  The significant adverse effects in this trial were all summarized in a table.  There were 394 placebo treated men compared with 394 testosterone treated men.  The events were summarized according to prostate-specific antigen (PSA) level increases, diagnoses of prostate cancer, elevations of hemoglobin, myocardial infarction, stroke, all cause cardiovascular death, death and hospitalization.  Although there were a greater number of PSA elevations in the testosterone treated men, there was only 1 case of prostate cancer (compared to 0 in the controls) during the year of study and 2 cases of prostate cancer in the testosterone group and one in the placebo group in the subsequent year of the study.

The rationale for this study was try to to add to the results of previous trials that showed inconsistent results of testosterone replacement on muscle mass, body fat, sexual function, energy level, and physical function.  It is disappointing to read through all of these details and find out that there was not much of an effect and that the methodology in the 21st century is so weak.  The only good news that I can find in the article is that it is relatively safe to replace testosterone in 65 year old men who are rigorously screened for hypogonadism and prostate cancer risk.  Although selection bias for a project like this is certainly a consideration, I asked myself whether men self-selected for replacement by low testosterone ads would be rejected at the 85% level by their physicians.  Of course the researchers here point out that the risk over the long run can only be determined by larger trials or (my opinion) post marketing surveillance.  But post marketing surveillance as suggested by the FDA is really a blunt instrument compared with any type of organized pharmacosurveillance or screening all new cases of prostate cancer on a particular electronic health record for testosterone prescriptions. At some level,  I wonder if the research questions would have been answered more completely by trials focused solely on each groups, but there were a very large number of investigators.  Many of the investigators have the appearance of conflict of interest through affiliations with pharmaceutical companies and many do not.

The results of this study are consistent with what clinical psychiatrists see in their practice.  It is not uncommon to see men taking supraphysiological doses of testosterone and not wanting to reduce those doses.  It is common to see men on testosterone who stop taking it because there is no clear efficacy and/or because they are concerned that the women and girls in their life will accidentally come into contact with testosterone.  But let's face it - this is really not about hypoandrogenism.  That is not what is fueling the debate.  I am not an advocate of aging gracefully and accepting what happens.  I think if you have been dieting and exercising through the first 65 years of life it would be useful if medical science could provide something to help you maintain an active lifestyle and prevent the kind of morbidity that slows you down, leads to deconditioning and the host of metabolic factors that hasten aging and death.  Preventing that pathway of physical deterioration depends on maintaining attitude, muscle, joints, and bone.  This is another paper documenting that there is no clear solution to that array of problems.

It is unfortunate that medicine does not have a scientific solution at this point - even after hearing all of the unscientific hype about testosterone and growth hormone for the past 30 years.    

                  

George Dawson, MD, DLFAPA



References:

1:  Snyder PJ, Bhasin S, Cunningham GR, Matsumoto AM, Stephens-Shields AJ, Cauley JA, Gill TM, Barrett-Connor E, Swerdloff RS, Wang C, Ensrud KE, Lewis CE, Farrar JT, Cella D, Rosen RC, Pahor M, Crandall JP, Molitch ME, Cifelli D, Dougar D, Fluharty L, Resnick SM, Storer TW, Anton S, Basaria S, Diem SJ, Hou X, Mohler ER 3rd, Parsons JK, Wenger NK, Zeldow B, Landis JR, Ellenberg SS; Testosterone Trials Investigators. Effects of Testosterone Treatment in Older Men. N Engl J Med. 2016 Feb 18;374(7):611-24. doi: 10.1056/NEJMoa1506119. PubMed PMID: 26886521.

2:  Casanova C, Celli BR, Barria P, Casas A, Cote C, de Torres JP, Jardim J, LopezMV, Marin JM, Montes de Oca M, Pinto-Plata V, Aguirre-Jaime A; Six Minute Walk Distance Project (ALAT). The 6-min walk distance in healthy subjects: reference standards from seven countries. Eur Respir J. 2011 Jan;37(1):150-6. PubMed PMID: 20525717.

3:  Lee KK, Berman N, Alexander GM, Hull L, Swerdloff RS, Wang C. A simple self-report diary for assessing psychosexual function in hypogonadal men. J Androl. 2003 Sep-Oct;24(5):688-98. PubMed PMID: 12954659.


Brief Video:

The two minute NEJM video summarizing this trial can be found at this link.  Interestingly the video attributes sexual function, vitality, and physical function to testosterone decrease with age and yet full replacement to the point where it is equivalent to levels in much younger men does nothing for physical function or vitality.


Sunday, November 24, 2013

"Low T Syndrome" and the Fountain of Youth

Psychiatrists are seeing increasing numbers of male patients who are being treated for low testosterone.  The symptoms of "Low T" are being promoted as a reason to get assessed and treated with testosterone.  Not surprisingly, "Low T" is a highly successful pharmaceutical company promotion.  So successful that testosterone seems to have disappeared from the vernacular, replaced by "T".  I have had the opportunity to follow this controversy for the last 30 years.  Back in the days when there were a subgroup of psychiatrists who considered themselves to be "microendocrinologists" testosterone, LH, FSH, and GnRH were studied along with the components of the hypothalamic-pituitary-adrenal and hypothalamic-pituitary-thyroid axes,  particularly in depressives.  Despite a lengthy but low intensity research effort on gonadal steroids in both men and women the data on baseline neuroendocrine correlates and results of supplemental treatments are equivocal.  That said, most psychiatrists have encountered women who have often had a significant response to treatment with gonadal steroids.  Seeing a consistent treatment effect is difficult.

As a clinical psychiatrist, I have found that the clearest information on drugs is available in the FDA approved package insert.  In the case of the product being marketed by the "Low T" ads is a form of testosterone gel that is available in two different strengths.  The only indication for the the product according to that package insert is primary hypogonadism (congenital or acquired) or hypogonadotropic hypogonadism (congential or acquired).  Any use for treating depression or augmenting antidepressants is off label use.  If testosterone was effective as an augmenting agent it would join the ranks of most antidepressant augmenting agents as being an off label prescription.  There are three related issues.

The first is the diagnosis of primary or hypogonadotropic hypogonadism.  In most cases, my speculation would be that a middle aged man sees or hears about the "Low T" ad and goes in to see their primary care physician and a testosterone level is ordered.  Most authoritative sources like UpToDate state that testosterone replacement should only occur in men who are hypogonadal.  Making that determination generally requires two low testosterone levels or in the indeterminant cases some expertise in the hypothalamic-pituitary-gonadal axis (HPG), as well as access to a laboratory with some specialized endocrine capabilities.  This is the level where most assessments seem to break down.  The range I am used to seeing is total testosterone levels ranging from about 300-1,000 ng/ml.  Scattergrams of testosterone versus behavioral parameters of interest like libido, aggression, and energy usually show low levels of correlation.  Many men are getting treated for (like the commercial suggests) low testosterone, or a level in the low normal range but not in the deficient range.  That takes treatment into the realm of off label indications because they do not have a diagnosis of hypogonadism.  A definitive algorithm (1) from endocrinologists is available including when to refer to an endocrinologist.

The second issue is whether there is any evidence testosterone either treats depression or is an effective agent to augment the effects of antidepressants.  That would conceivably move testosterone to the level of the augmenting agents used in the STAR*D study of depression.  The best guidance in the literature comes from Pope, et al (2) article on testosterone replacement in men 65 years of age or younger taking serotonergic antidepressants, a total testosterone level of less than or equal to 350 ng/ml, a PSA less than 4.0 ng/ml and an incomplete response to the antidepressant.  The author's conclude that there were no significant differences in response to testosterone or placebo gel.  Their conclusion is that the current practice of testosterone supplementation of antidepressants is not supported, but that there may be identifiable subgroups in larger studies.

Pope's observations are also critical in that he is an expert in anabolic androgenic steroid (AAS) abuse and has observed a euphorigenic hypomanic response to both AAS and prescription testosterone.  In his article he cites this response occurring in about 4.8% of 105 volunteers taking the equivalent of 500 mg/week of testosterone or an equivalent.  These observations are critical because they factor in addictive behaviors associated with substance use and Pope's group has proposed criteria for anabolic-androgenic steroid dependence.  The criteria highlight that fact that there are a number of associated mood symptoms including depression during the withdrawal phase.  Screening for an AAS use disorder and associated comorbidity like muscle dysmorphia

The third issue is the risk benefit analysis and that makes testosterone as an augmenting agent more unique than the other STAR*D agents.  Testosterone has unique medical risks beyond any risk of an additive effect with an antidepressant.  The main risk with other augmenting agents is usually rare cases of serotonin syndrome or side effects specific to the agent.  They are essentially being prescribed for the same indication.  With testosterone, there is no professional body advocating for supplementation in men with a eugonadal state and the risks may be significant starting with the contraindications (breast cancer, known or suspected prostate cancer) and warnings (benign prostatic hypertrophy, exposure to women and children, edema, sleep apnea, and the need to monitor a number of biochemical parameters).  There have also been recent articles showing a possible correlation with a number concerns about increased myocardial infarction, ischemic stroke, and other mortality (3,4,5).

So for all of you psychiatrists out there who are being referred men who are being treated for "Low T" or being sent to you with a question about testosterone there are a couple of necessary steps at this point.  Make sure that a diagnosis of hypogonadism has been established.  Let your patient know that testosterone supplementation of antidepressants in eugonadal men at this time is experimental and carries risks.  I would also inquire about a past history of anabolic androgenic steroid use, their conscious experience of that use ranging from mood changes to body image concerns and any prior psychiatric history including a history of addictions or using performance enhancing drugs.  For men considering an evaluation and treatment for "Low T" it is much more complex than filling out an online questionnaire on pharmaceutical company website.  Have realistic expectations about what you can expect, especially if someone is suggesting that testosterone supplementation is a treatment for depression.  Take a good look at the risk and consider that there will probably never be a major study that takes a good look at this issue with a large population of men.  The prospective studies will probably be similar to Pope, et al of about 100 men followed for a short period of time and the retrospective studies will have some innovative designs but they will also be limited by selection factors and significant stratification factors.  That generally means that additional information about risk may only be available in the form of FDA warnings from post marketing surveillance or their own analysis of data that may not be publicly available.

George Dawson, MD, DFAPA

References:

1.  Dandona P, Rosenberg MT. A practical guide to male hypogonadism in the primary care setting. Int J Clin Pract. 2010 May;64(6):682-96. doi: 10.1111/j.1742-1241.2010.02355.x. Review. PubMed PMID: 20518947; PubMed Central PMCID: PMC2948422

2.  Pope HG Jr, Amiaz R, Brennan BP, Orr G, Weiser M, Kelly JF, Kanayama G, Siegel A, Hudson JI, Seidman SN. Parallel-group placebo-controlled trial of testosterone gel in men with major depressive disorder displaying an incomplete response to standard antidepressant treatment. J Clin Psychopharmacol. 2010 Apr;30(2):126-34. doi: 10.1097/JCP.0b013e3181d207ca. PubMed PMID: 20520285

3.  Vigen R, O’Donnell CI, Barón AE, et al. (2013) Association of testosterone therapy with mortality, myocardial infarction, and stroke in men with low testosterone levels. JAMA 310:1829-1836.

4.  Basaria S, Coviello AD, Travison TG, et al.  Adverse events associated with testosterone administration. N Engl J Med. 2010 Jul 8;363(2):109-22. doi: 10.1056/NEJMoa1000485. Epub 2010 Jun 30. PubMed PMID: 20592293; PubMed Central PMCID: PMC3440621.

5. Cappola AR. Testosterone therapy and risk of cardiovascular disease in men.  JAMA. 2013 Nov 6;310(17):1805-6. doi: 10.1001/jama.2013.280387. PubMed PMID: 24193077.

Tip:  Follow the lead authors of these references on Medline and you will have a comprehensive look at the literature in this area.