Low Testosterone: Symptoms and Ways to Increase Levels

ContributorsProf. Dr. Mustafa ÖzdoğanAuthor · Medical review · Editorial approval

PublishedMar 25, 2025

UpdatedOct 18, 2026

30 min read

Low Testosterone: Symptoms and Ways to Increase Levels

In this article

Low testosterone is one of the most exaggerated and misunderstood men's health topics online. The reality is that genuinely symptomatic testosterone deficiency affects approximately 2% of men aged 40-79 — claims such as “one third” or “half” are incorrect. In patients with cancer, however, the picture is different: among men receiving hormone suppression for prostate cancer, allhave testosterone deficiency; among patients taking long-term opioids, two thirdsdo; among testicular cancer survivors, one fifth are affected. This article examines the issue using current data from both general men's health and cancer treatment perspectives.

Article Summary

“Normal testosterone is 300-1000 ng/dL” is an old laboratory range. The internationally standardized reference range is 264-916 ng/dL, and guideline thresholds differ.
“Andropause” is not a term used by any guideline. The appropriate terms are “late-onset hypogonadism” or “functional hypogonadism.”
The age-related decline is real but small; the main determinant is weight. Losing weight restores testosterone.
Proven benefits of treatment concern sexual desire, anemia and bone density. Fatigue, mood, walking performance, and cognitive function did not improve.
There is no evidencethat testosterone therapy causes prostate cancer; however, it is contraindicated in active prostate cancer.
In Turkey, testosterone does not require a red prescription, but since November 2024 it has been subject to restricted distribution by TİTCK , explicitly to “prevent misuse.”

Terminology First: There Is No Diagnosis Called “Andropause”

Menopause is the cessation of ovarian function at a certain age in almost all women. There is no equivalent eventin men. Testosterone decreases gradually, partially, and with considerable individual variation. Most of the decline is due to accompanying weight gain and disease rather than age itself.

This is why no guideline uses “andropause.” The Endocrine Society uses “age-related testosterone decline”; the European Association of Urology uses “late-onset hypogonadism” and “functional hypogonadism”; the American Urological Association uses “testosterone deficiency.” The Turkish Urological Association guideline uses “Late-Onset Testosterone Deficiency.” The UK's National Health Service states directly: “The ‘male menopause’ (sometimes called andropause) is an unhelpful term used in the media.”

What Is Normal? Even Guidelines Disagree

The “300-1000 ng/dL” range in older articles comes from older, nonstandardized measurement methods. A harmonization study combining 9054 men from four major cohorts found the following range for healthy, nonobese men aged 19-39 :

Percentile	Total testosterone
2.5th percentile (lower limit)	264 ng/dL
Median	531 ng/dL
97.5th percentile (upper limit)	916 ng/dL

Notably: the lower limit decreases with age, while the upper limit remains almost unchanged. In nonobese men, the 2.5th percentile is 267 at ages 19-39, 219 at ages 50-59, and 218 ng/dL at ages 70-79.

Guideline	Diagnostic threshold	Note
Endocrine Society (2018)	264 ng/dL	Diagnosis is based on symptoms + repeatedly low measurements together, rather than a number alone. In the general population, it does not recommend screening.
AUA (2018, validity confirmed in 2024)	300 ng/dL	It requires two separate morning measurements on different days.
EAU (European Association of Urology)	~346 ng/dL (12 nmol/L)	The highest threshold. The greatest benefit is expected below 231 ng/dL .
Turkish Urological Association	Morning total T >350 ng/dL normal	Free testosterone >7 ng/dL

A diagnosis is not made from a single measurement. Testosterone fluctuates during the day and is highest in the morning; an evening blood sample can be misleadingly low. Acute illness, fever, extreme fatigue, and fasting can also cause temporary decreases. The rule is: between 7-11 in the morning, fasting, on at least two separate days. For borderline results, free testosterone and SHBG are measured; LH and FSH distinguish a testicular problem (high LH) from a central problem in the brain (low/normal LH).

“One Third of Men” Is Incorrect

The frequently repeated claim that “one third of men at age 60 and half of those over 80 have low testosterone” comes from an old cohort that assessed only blood levels , and most of these men had no symptoms. The true prevalence when symptoms are included is much lower.

How Common Is Testosterone Deficiency?

How do results change in the same age group when the definition changes?

Low blood level alone — over age 80

~50%

Low blood level alone — over age 70

~30%

Low blood level alone — over age 60

~20%

Symptoms + blood level — ages 40-79

2.1%

The bottom row comes from EMAS, which followed 3369 European men. Its definition required three sexual symptoms together (loss of morning erections, reduced sexual desire, and erectile dysfunction) and low levels of both total and free testosterone. The result: only 2.1% of men aged 40-79 had true late-onset hypogonadism, approximately one man in fifty.

Age or Weight? In the longitudinal EMAS analysis following 2395 men for 4.4 years, total testosterone declined by an average of only 0.1 nmol/L per year. By contrast, weight change was decisive: testosterone increased in proportion to weight loss and decreased with weight gain. More strikingly, changes in the number of accompanying diseases did not significantly affect the hormonal axis. The authors concluded: “Weight management appears important for maintaining circulating testosterone in aging men, and obesity-related hormonal changes are reversible with weight loss.”

A meta-analysis of 24 studies quantified this reversal: with a low-calorie diet, testosterone increased by an average of +83 ng/dL, with bariatric surgery, by +252 ng/dL. The strongest predictor was the amount of weight lost. Much of “I am older, so my testosterone has fallen” therefore actually means “I have gained weight.”

Symptoms and Causes

Symptoms of testosterone deficiency are nonspecific; the same complaints occur with thyroid disease, depression, sleep apnea, anemia, and cancer itself. Symptoms therefore do not establish a diagnosis; they only warrant testing.

Sexual symptoms

These are the most meaningful for diagnosis : reduced sexual desire, loss of morning erections, and erectile dysfunction. The EMAS definition requires all three together.

Physical symptoms

Reduced muscle mass and strength, abdominal fat accumulation, decreased bone density, anemia, hot flashes, and enlarged breast tissue.

Psychological symptoms

Fatigue, loss of motivation, low mood, and difficulty concentrating. These are the least specific symptoms and do not, on their own, indicate a testosterone problem.

Cause	Explanation
Obesity	The most common and most reversible cause. Aromatase in fatty tissue converts testosterone to estrogen, suppressing stimulation from the brain.
Type 2 diabetes and metabolic syndrome	Among men with type 2 diabetes, at least 25% have low free testosterone with inappropriately normal or low LH and FSH.
Cancer treatments	Discussed in the next section: hormone suppression for prostate cancer, treatment for testicular cancer, chemotherapy, and radiotherapy.
Opioid painkillers	An often-overlooked cause, discussed in detail below.
Corticosteroids	Long-term use suppresses the hypothalamic-pituitary axis.
Anabolic steroid use	When high doses of hormones are taken externally, the body stops its own production. After they are stopped, testicular shrinkage, infertility, and sometimes permanent hypogonadism may remain. For details, see our article on anabolic steroids .
Insufficient sleep	In 10 healthy young men, 8 nights of less than 5 hours of sleep reduced daytime testosterone by 10-15% . This is a small study, but its direction is clear.
Testicular causes	Trauma, orchitis (after mumps), a history of undescended testes, and genetic conditions such as Klinefelter syndrome.
Central causes	Pituitary adenoma, high prolactin, head trauma, and radiotherapy to the head.

Cancer and Testosterone: The Most Important Section

Symptomatic testosterone deficiency affects one man in fifty in the general population, but it is many times more common in patients with cancer. It often goes unnoticed because fatigue, muscle loss, and low mood are attributed directly to cancer.

Hormone Suppression for Prostate Cancer (ADT)

Androgen deprivation therapy deliberately lowers testosterone to castrate levels (<50 ng/dL). In these patients, hypogonadism is therefore not an adverse effect but the aim of treatment. Its consequences are nevertheless serious and require management.

Effect	Figure
Loss of sexual desire	More than 95%
Erectile dysfunction	More than 80%
Hot flashes	34-80%. They peak at approximately month 4 ; after treatment ends, they resolve after a median of 7.6 months . Of patients, 27% describe them as the most troublesome adverse effect.
Bone loss	In the first 12 months, spinal bone loss is 4.0%, and hip bone loss is 2.5%. Annual loss in healthy men is 0.5-1.0%. Loss is concentrated in the first year.
Fractures	Among those surviving longer than 5 years, fractures occurred in 19.4%of ADT recipients versus 12.6% of nonrecipients (a registry study of 50613 people).
Muscle and fat	Lean tissue mass decreases annually by 2.0-3.6%; in men over 70, the loss is three times that of younger men. Fat mass increases by more than 11% annually. The fastest changes occur in the first 6 months.
Diabetes	In those using a GnRH analogue, HR 1.44 (a Medicare analysis of 73196 people).
Coronary heart disease / myocardial infarction	HR 1.16 / HR 1.11
Anemia	An average hemoglobin decrease of 1.11 g/dL ; with leuprolide alone, 1.66 g/dL.
Dementia risk	A meta-analysis of 21 studies involving 2.3 million patients found an overall HR of 1.14. However, no significant association was found with LHRH analogues or orchiectomy; the signal mainly concerns antiandrogens. These are observational data.

What Should Be Done for Patients Receiving ADT?

Bone: Assess fracture risk at baseline using FRAX and DEXA when needed. In patients with advanced disease scheduled for more than 6 months of ADT, or when a next-generation hormonal drug is added, treatment without waiting for further risk stratification may be considered because FRAX and DEXA underestimate risk in this group.
Calcium and vitamin D: At least 1 g of elemental calcium + 800 IU of vitamin D daily.
Medication: First choice: a weekly oral bisphosphonate (risedronate 35 mg or alendronate 70 mg); second choice: zoledronic acid once yearly or denosumab every 6 months. When denosumab is stopped, a bisphosphonate must be started (risk of rebound fractures).
Evidence: In a randomized trial of 1468 patients, denosumab reduced new vertebral fractures at month 36 from 3.9% to 1.5% (RR 0.38).
Exercise: On 2-3 days per week, resistance training + weight-bearing aerobic exercise. In the guideline's words, this should be “an essential component.”
Hot flashes: They can be treated. Megestrol acetate, medroxyprogesterone, venlafaxine, and gabapentin have demonstrated efficacy.
Monitoring: Hemoglobin, HbA1c, lipids, blood pressure, and waist circumference.

Testicular Cancer Survivors

This is the article's most overlooked topic. Testicular cancer affects young men and has excellent survival — a man surviving seminoma at age 30 will live another 50 years. Spending those 50 years with untreated hypogonadism carries a substantial metabolic cost.

After orchiectomy, with or without chemotherapy, approximately 20% develop primary testosterone deficiency.
The increase in risk when standard chemotherapy is added: OR 1.8; with high-dose chemotherapy, OR 3.1; with subdiaphragmatic radiotherapy, OR 1.6.
Comparing those with versus without deficiency: cholesterol medication use 20% versus 6%, erectile dysfunction 20% versus 12%, and hypertension 19% versus 11%.
Deficiency may appear late — new cases can be identified even an average of 18 years after treatment. Follow-up is therefore lifelong.

Recommendation: Annual screening of testosterone and SHBG, HbA1c, renal function, blood pressure, waist circumference, body mass index, and lipids.

Opioid Painkillers: The Most Frequently Missed Cause

A meta-analysis of 52 studies involving 18428 people found hypogonadism in 63% of men taking long-term opioids (69% when restricted to studies at low risk of bias). Mean total testosterone was 172 ng/dLwith high-dose opioids, 266 ng/dL with low doses, and, without opioid use, 449 ng/dL.

The effect differs by drug: compared with hydrocodone, the likelihood of testosterone deficiency with fentanyl was 25.7 times higher, with methadone 7.3 times higher, and with oxycodone 3.2 times higher. Rates were 57% among long-acting opioid users and 35% among short-acting users.

Why Does It Matter? When a patient taking long-acting opioids for cancer pain develops fatigue, low mood, loss of sexual desire, and muscle loss, these are almost automatically attributed to cancer or its treatment. Yet in two out of three patients, opioid-induced testosterone deficiency contributes to the picture, and this is measurable and can be addressed.

Does Testosterone Therapy Cause Prostate Cancer?

The short answer: there is no evidence supporting this. The old view that “testosterone pours fuel on the fire” arose from observations in a small number of men with metastatic disease in the 1940s. Today, three independent sources of evidence point in the same direction:

Evidence	Result
TRAVERSE prostate substudy (5204 men, mean follow-up 33 months)	High-grade prostate cancer 0.19% versus 0.12%; HR 1.62 (95% CI 0.39-6.77; p=0.51). Any prostate cancer: HR 1.07. PSA increased more only during the first 12 months , with no difference afterward.
Meta-analysis of 41 randomized trials (11161 participants, 2026)	Prostate cancer OR 0.88 (0.52-1.51); clinically significant prostate cancer: OR 1.13. Short- to medium-term safety is supported.
Swedish national registry study (38570 cases, 192838 controls)	Overall prostate cancer OR 1.03 — no association. The slight increase in low-risk disease (OR 1.35) was attributed to screening bias ; for aggressive disease, risk was lower (OR 0.50).

By contrast, testosterone therapy is contraindicated in active, untreated prostate cancer , and this is not disputed. Guidelines differ after treated prostate cancer: the Endocrine Society advises against starting it, the AUA considers the evidence insufficient, and the EAU says it may be considered in low-risk patients treated surgically, with undetectable PSA for at least a year and no signs of recurrence, after detailed counseling . All data in this setting are retrospective; there are no randomized trials.

Cancer Cachexia and Fatigue

Testosterone has not been shownto improve muscle loss and fatigue in patients with cancer. In a randomized trial in hypogonadal men with advanced cancer, 4 weeks of testosterone produced no significant difference in the primary fatigue-scale endpoint (p=0.11). Two large phase 3 trials of the SARM enobosarm in non-small cell lung cancer (POWER 1 and 2) also failed on their co-primary endpoints. There is therefore no androgen treatment approved for cachexia.

Does Low Testosterone Increase Cancer Risk? A 2026 pooled analysis of more than 26000 men from 11 cohorts found that men in the lowest testosterone quintile had an 18% higher risk of cancer-related death years later. However, the researchers' own warning is clear: this does not demonstrate cause and effect; low testosterone is probably a marker of poor overall health, and an undetected illness may itself suppress the hormone. As the lead researcher put it: “We have no evidence yet that giving men testosterone would reduce this risk.” For prostate cancer specifically, no association with blood testosterone levels was found.

Ways to Increase Testosterone: What Works and What Does Not?

Method	Evidence
Weight loss	The strongest evidence. An average increase of +83 ng/dL with diet and +252 ng/dL with bariatric surgery. The effect is proportional to weight lost.
Resistance exercise	Increases muscle mass and insulin sensitivity and supports weight loss. A large, sustained testosterone increase should not be expected; the main benefit is indirect.
Sleep habits	A small study showed that restricted sleep lowers testosterone. Sleep apnea, if present, should be treated.
Vitamin D supplementation	Does not work. In two randomized trials, 20000 IU of vitamin D was given weekly for 12 weeks: neither those with normal testosterone (n=98) nor those with low testosterone (n=94) showed any effect. In the first study, insulin sensitivity worsened slightly.
Tribulus terrestris (puncture vine)	Does not work. A systematic review of 10 studies involving 483 participants found no change in androgen levels in 8 of the studies. The authors concluded: “To date, there is no robust evidence that Tribulus boosts testosterone.” Some benefit has been reported in mild to moderate erectile dysfunction.
Ashwagandha	Weak and exaggerated. The best study was manufacturer-funded and involved 43 participants; testosterone increased by 14.7% over 8 weeks. There is no pooled meta-analysis and no evidence that it treats hypogonadism. These products may also produce positive doping-test results.
Zinc	Replacing it makes sense in people with deficiency. For people without deficiency, insufficient randomized trial evidence has been found to show that it increases testosterone.
Stopping smoking and reducing alcohol	Appropriate for overall health; effects on testosterone are indirect and modest.

The common problem with marketed “natural testosterone boosters” is that none treats hypogonadism. While a man with genuinely low testosterone wastes time on these products, the underlying cause, such as obesity, sleep apnea, pituitary disease, or a drug effect, remains uninvestigated. In addition, undeclared addition of pharmaceutical active ingredients is a known problem about which Turkey's Ministry of Agriculture and Forestry has issued warnings.

Testosterone Replacement Therapy (TRT): What Does It Do, and What Does It Not Do?

The best answer comes from a program involving 790 men over 65 and 7 substudies: the T Trials . Results after one year of testosterone gel were:

Domain	Result
Sexual function	Improved. Moderate effect (0.45). The clearest benefit concerned sexual desire; improvement in erections was smaller.
Anemia	Improved. Unexplained anemia resolved in 58.3% versus 22.2%.
Bone density	Increased. Spinal trabecular bone density increased by 6.8%, and estimated bone strength by 8.5%. No fracture data.
Walking performance	Did not improve. The primary endpoint was not met.
Vitality / fatigue	Did not improve. The primary endpoint was not met.
Cognitive function	Did not improve.
Coronary arteries	An adverse signal: Noncalcified coronary plaque volume increased more in testosterone recipients (p<0.003).

This table summarizes the difference between how testosterone is marketed and what it does. The promised energy, mood, vitality, and performancedid not improve in controlled trials. Improvements were in sexual desire, anemia, and bone density.

Cardiovascular Safety: TRAVERSE and the FDA Label Change

In 5246 men with cardiovascular disease or high risk, TRAVERSE found a primary cardiac event rate over a mean 33-month follow-up of 7.0%in the testosterone arm and 7.3% in the placebo arm (HR 0.96; 95% CI 0.78-1.17). Testosterone therefore did not increase myocardial infarction risk as previously thought.

But that is not the whole story. The same study found the following unplanned differences: atrial fibrillation: 3.5% versus 2.4% (p=0.02), acute kidney injury: 2.3% versus 1.5% (p=0.04), and pulmonary embolism: 0.9% versus 0.5%. In the fracture substudy, contrary to the bone-density result in the T Trials, fractures were more frequent in the testosterone arm: 3.50% versus 2.46% (HR 1.43); more than 80% of fractures were due to falls.

On February 28, 2025, the FDA changed the labels of all testosterone products: it removed the boxed warning about cardiovascular risk, but at the same time added a new class warning about increased blood pressure and retained the restriction that they are not indicated for age-related low testosterone. Reports mentioning only the first part are misleading.

Monitoring and Contraindications

Hematocrit: At baseline, treatment is not started if it exceeds 48%. During treatment, it is stopped if hematocrit exceeds 54% or the dose is reduced. This is the most common serious adverse effect.
PSA and prostate: PSA and digital rectal examination at baseline; after treatment, at months 3-12, then annually. Refer to a urologist if PSA increases by more than 1.4 ng/mL from baseline or exceeds 4.0 ng/mL.
When treatment should not be started: Breast or prostate cancer, a palpable prostate nodule, PSA >4 ng/mL, elevated hematocrit, untreated severe sleep apnea, severe urinary symptoms, uncontrolled heart failure, myocardial infarction or stroke within the last 6 months, a clotting disorder, and plans to have children in the near future.

The Least-Discussed Risk: Infertility Externally administered testosterone suppresses LH and FSH signals from the brain; intratesticular testosterone falls sharply, and sperm production stops. This is a known and predictable consequence of TRT, but patients are often not told.

In a pooled analysis of 1549 healthy men, the probability of sperm counts returning to normal after treatment stopped was 67% at 6 months, 90% at 12 months, and 100% at 24 months; the median time was 3.4 months. However, these data come from healthy men in contraceptive studies of limited duration and cannot be considered a guarantee for someone who has used TRT for years.

For men wishing to have children, alternatives to TRT include hCG, clomiphene and similar options. Note: enclomiphene is not FDA-approved — it received a rejection letter in 2015, and development stopped in 2021. Clomiphene is also not approved for any indication in men and is used off-label.

The Situation in Turkey

Restricted distribution since November 2024. In its announcement dated November 20, 2024, TİTCK placed testosterone-containing medicines, GnRH analogues, and products containing estrogen alone at doses of 2 mg or more under restricted distribution . The stated reason was explicit: “to prevent misuse.” In practice, this means that medicines are dispensed only with an electronic prescription through the Reçetem System and tracked through the Pharmaceutical Tracking System.

Testosterone is not subject to red-prescription requirements in Turkey; it is prescribed on a normal (white) prescription. However, the restricted-distribution arrangement described above has effectively tightened pharmacy access.

Reimbursement: Under Article 40 of SUT Annex-4/F, testosterone may be prescribed without a report by specialists in urology, endocrinology, and pediatric surgery ; all other physicians may prescribe it only on the basis of a specialist physician's report from one of these three specialties.

Main preparations available in Turkey: Intramuscular injections include Nebido (testosterone undecanoate, every 3 months), Sustanon 250 and the generic Tesroject (mixed testosterone esters, every 2-4 weeks); skin gels include Testogel and Tostran; the oral preparation is Virigen Testocaps. A common mistake is using the American name “Androgel” for Turkey, where the corresponding product is Testogel.

Frequently Asked Questions

I am tired and have low desire. Is my testosterone low?: Possibly, but the likelihood is lower than you may think. Among men aged 40-79, only 2.1% have symptomatic testosterone deficiency. The same complaints occur with thyroid disease, sleep apnea, anemia, depression, and vitamin D deficiency. Get tested, but do not regard testosterone as the only possible explanation.
My testosterone result was 280. Should I receive treatment?: A single measurement does not establish a diagnosis. Testing should be repeated in the morning, fasting, on at least two separate days . The number is also assessed together with symptoms , not alone: guidelines diagnose the combination of symptoms and low values rather than a number. For a borderline result, first investigate the cause, such as weight, sleep apnea, or medication.
Will testosterone therapy rejuvenate me or increase my energy?: No. In controlled studies involving 790 men over 65, fatigue, walking performance, and cognitive function did not improve. Sexual desire, anemia, and bone density improved. The FDA also retains the restriction that testosterone is not indicated for age-related low levels.
Does testosterone therapy cause infertility?: Yes, it does — and this is the issue most often overlooked. Externally administered testosterone stops sperm production. After stopping, it recovers within 6-12 months in most men, but this is not guaranteed. Men wishing to have children should discuss alternatives such as hCG or clomiphene rather than TRT.
Is it the same as the injections used in gyms?: The active ingredient may be similar, but the use is completely different. Medical treatment aims to restore a deficient hormone to normal; performance-enhancing doses are many times higher , and the body's own production may stop permanently. The consequences include testicular shrinkage, infertility, gynecomastia , and cardiovascular risk. This misuse is precisely why testosterone was placed under restricted distribution in Turkey.
I have had prostate cancer. Can I take testosterone?: In active, untreated prostate cancer, no. After treated disease, guidelines differ: the Endocrine Society advises against starting it, the AUA considers the evidence insufficient, and the EAU says it may be considered after detailed counseling in low-risk patients without recurrence for at least a year. In this setting, there are no randomized trials; decisions should be made case by case with your urologist and oncologist.
I am receiving hormone suppression. Must I tolerate the adverse effects?: No. Calcium, vitamin D, and, when necessary, bisphosphonates/denosumab are available for bone loss; drugs with demonstrated efficacy for hot flashes; and resistance exercise for muscle loss. ADT adverse effects should be managed rather than simply accepted. Raise these issues at follow-up appointments.
I take painkillers. Could that be related?: Very possibly. Among men using long-term opioids, 63% have been found to have hypogonadism, and the effect increases with dose. If you use long-acting opioids for cancer pain, some fatigue and low desire may stem from this. Measuring testosterone is reasonable.

A Brief Glossary

Hypogonadism: Inadequate sex hormone production. It is called “primary” when the problem is in the testes and “secondary” when it involves the pituitary/hypothalamus in the brain.
Late-onset hypogonadism: Testosterone deficiency arising in adulthood with both symptoms and laboratory findings. This is the guideline equivalent of “andropause.”
Functional hypogonadism: Deficiency caused by obesity, disease, or medication without a structural problem in the testes or pituitary. Usually reversible.
Total / free testosterone: Total testosterone includes all testosterone in the blood. Free testosterone is the portion not bound to proteins that can enter cells.
SHBG: The binding protein that carries testosterone in blood. Because it increases with age and certain diseases, free testosterone may be low even when total testosterone appears normal.
LH and FSH: Hormones secreted by the pituitary that stimulate the testes. High levels suggest a testicular problem; low or inappropriately normal levels suggest a central problem.
ADT (androgen deprivation therapy): Treatment that lowers testosterone to castrate levels in prostate cancer.
Hematocrit: The cellular density of blood. Elevation of this value is the most common serious adverse effect of testosterone therapy.
SARM: Selective androgen receptor modulator. Tested for cachexia but unsuccessful in phase 3 trials; no approved product is available.

DROZDOGAN Academy Commentary

Testosterone is a topic with a particularly large gap between medical evidence and popular narratives. We share our assessment below.

⚡ Why does this matter?

Because two different errors are occurring simultaneously. On one side is unnecessary treatment : testosterone is marketed on social media as an elixir of youth and performance, and healthy men begin treatment after testing yields “borderline” values. On the other side, and more importantly for us, is failure to provide needed treatment : hypogonadism is almost the rule among men receiving hormone suppression for prostate cancer, taking long-term opioids, or surviving testicular cancer, yet it is not discussed.

The figures show this asymmetry clearly: symptomatic deficiency in the general population affects one man in fifty; among long-term opioid users, two men in three. Our attention is focused in the wrong place.

✅ Strengths / positive developments

High-quality studies have been conducted in this field over the last decade. The T Trialsused randomization to distinguish what the hormone does and does not improve. TRAVERSEsettled the decade-long cardiovascular safety debate with 5246 patients. This is a level of evidence not found in nutrition or supplements.

The second positive development is growing acceptance of functional hypogonadism . Knowing that obesity-related low testosterone is reversible changes the logic of treatment: remove the cause rather than supply the hormone externally. Increases of 83 with diet and 252 ng/dL with bariatric surgery exceed what most supplements promise.

Third, Turkey placed testosterone under restricted distribution in November 2024. The explicit rationale was “preventing misuse”; given the extent of gym-related use, this is an appropriate step.

⚠️ Limitations / what should not be exaggerated

TRAVERSE's conclusion of “cardiovascular safety” is being reported incompletely. In the same study, atrial fibrillation, acute kidney injury, and pulmonary embolism were more common in the testosterone arm; in the fracture substudy, fractures were more frequent despite the T Trials showing increased bone density. If bone density and fractures both increase, something remains unexplained. The FDA's addition of a new blood-pressure warning while removing the cardiovascular warning completes this picture.

Second, testosterone has not demonstrated benefit in patients with cancer. Cachexia and fatigue studies failed on their primary endpoints, and the SARM phase 3 program failed. An association between low testosterone and cancer death is not a treatment rationale either; it most likely represents reverse causation: an undetected illness suppresses the hormone rather than the hormone causing the illness.

Third, regarding TRT after treated prostate cancer, there is not a single randomized trial. All available data are retrospective and subject to selection bias: physicians give testosterone to patients who already appear low risk, then we are surprised that recurrence is uncommon.

🩺 Our Position in Practice

We start a bone-health plan when ADT begins. Calcium, vitamin D, fracture-risk assessment, and a resistance-exercise prescription are discussed on the first day; bone loss is fastest in the first year and is not made up later.
We measure testosterone in men taking long-acting opioids. It is a value worth checking before automatically attributing fatigue to cancer.
We plan lifelong follow-up after testicular cancer. Deficiency can arise even 18 years after treatment; annual testosterone, HbA1c, lipid, and blood-pressure monitoring should be standard for this group.
For borderline values, we investigate the cause first. Weight, sleep apnea, opioids, corticosteroids, excessive alcohol. In functional hypogonadism, the solution lies in the cause rather than the hormone.
We explain expectations accurately. We do not promise increased energy or rejuvenation; proven benefits concern sexual desire, anemia, and bone density. Incorrect expectations are the greatest source of unnecessary treatment.
We always ask about plans for children. TRT stops sperm production. Failing to provide this information before starting treatment is an irreversible mistake.

❓ Open Questions

Why did fractures increase when bone density improved? This contradiction remains unresolved; whether patients became more prone to falls or fell more because they became more active is unknown. Whether testosterone is safe after treated prostate cancer will not be answered without a randomized trial , and conducting such a study is difficult. Are ADT's cognitive effects real or due to confounding in observational studies? A signal with antiandrogens but not LHRH analogues makes this question even more interesting. Specifically in Turkey, we know neither the prevalence of hypogonadism nor the rate of steroid use in gyms; these two gaps stand in stark contrast to how much the topic is discussed in the country.

Our Brief Verdict: Testosterone is discussed too much in healthy men and far too little in patients with cancer. The correct statement is: testosterone is not a youth hormone; it is a hormone that should be replaced when deficiency causes symptoms — and in oncology, we create that deficiency more than anyone, so monitoring it is our responsibility.

Transparency Note. Points that could not be established in this article:

The overall EMAS prevalence of 2.1%was verified; the frequently cited breakdown by age decade was not included because it could not be confirmed from the primary source.
The claim that “low testosterone is twice as common in men with diabetes” could not be verified; the verified statement that “at least 25% have low free testosterone” was used instead.
The numerical risk ratio circulating for an association between ADT and depression was not included because it could not be linked to a primary source.
The proposed castrate-level target of <20 ng/dL is disputed; because no primary source showing guideline-level adoption was found, only the established <50 ng/dL definition was used.
For pelvic radiotherapy, verified data on scatter dose to the testes and the subsequent rate of hypogonadism could not be found; rates after stem cell transplantation are also inconsistent. Neither topic was therefore quantified.
For zinc supplementation in men without deficiency, no randomized trial was found; the wording is “insufficient evidence,” not “ineffective.”
The list of preparations in Turkey was compiled from secondary drug databases and could not be verified against TİTCK's official list of licensed products. Some products may no longer be marketed.
The information that testosterone is not subject to red-prescription requirements was inferred from its absence from the red-prescription list; it should be confirmed directly against TİTCK's current controlled-medicines list.
The text of SUT Annex-4/F, Article 40 was verified through two secondary sources, not the current official SUT text.
In Turkey, no published data on hypogonadism prevalence or the rate of anabolic steroid use could be found. The figures in the Turkish Urological Association guideline are international data.
The legal consequences in Turkey of possessing anabolic steroids could not be verified; the article mentions only general rules concerning sale and manufacture and gives no penalty.
This article provides general information and does not replace assessment by your physician.

References

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EAU Guidelines on Sexual and Reproductive Health — Male Hypogonadism. European Association of Urology, 2026
Türk Üroloji Derneği. Hipogonadizm Tanı, Tedavi ve Takip Kılavuzu
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Sosyal Güvenlik Kurumu Sağlık Uygulama Tebliği, Annex-4/F, Article 40

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