Testosterone vs Estrogen in Men: Why You Need Both, How Testosterone Becomes Estradiol, and When Estrogen Becomes a Problem

Testosterone vs estrogen in men is not a contest between opposites. Most of a man's estradiol is made from his own testosterone, and controlled trials show estrogen handles fat and bone while testosterone handles muscle and strength. Both run sexual function.

Testosterone vs estrogen in men is less of a rivalry than the supplement aisle suggests. In men, testosterone is the main raw material for estradiol, the most active estrogen, and only about 20% of a man's circulating estradiol is secreted directly by the testes, according to a review by Alex Vermeulen and colleagues in The Aging Male in 2002. The rest is made from testosterone inside fat, bone, brain and other tissues by an enzyme called aromatase.

That shared origin is why the two hormones are hard to study separately. Joel Finkelstein and colleagues at Massachusetts General Hospital solved the problem in a trial published in the New England Journal of Medicine in 2013. They shut down hormone production in healthy men, gave testosterone back at set doses, and blocked its conversion to estradiol in half the men. The findings show which symptoms of low testosterone are really symptoms of low estrogen.

Testosterone is an androgen and estradiol is an estrogen, but in a man the second is mostly built from the first. Testosterone acts on androgen receptors in muscle, skin, the prostate and the brain. Estradiol acts on estrogen receptors in bone, fat, blood vessels and the brain. A man's body runs on both hormones at once, and the ratio between them shifts with age and body fat.

The amounts are very different. Vermeulen's review puts plasma estradiol in men at 2 to 3 ng/dL, a small fraction of a typical testosterone level, yet still significantly higher than in postmenopausal women. Small amounts matter because estradiol is potent at its receptors and because some of it is made and used inside tissues without ever reaching the bloodstream. Vermeulen noted that plasma estradiol does not necessarily reflect tissue-level activity for exactly this reason.

Yes, testosterone is the main source of estradiol in men, and the conversion happens through aromatase in tissues. The Vermeulen review describes testosterone as the major source of plasma estradiol in males. Testosterone that is tightly bound to sex hormone-binding globulin (SHBG) circulates in a less available form, while the unbound and loosely bound share can enter cells, which is where aromatase works. A separate pathway converts androstenedione, mostly from the adrenal glands, into estrone, a weaker estrogen.

Body fat changes how much testosterone gets converted. Vermeulen reported that estradiol in men is significantly related to body fat mass, especially subcutaneous abdominal fat. The same review found that aromatase activity in omental fat, the visceral fat around the gut, is only one tenth of the activity in gluteal fat. More fat tissue means more aromatase in total, which is one reason estradiol tends to hold steady in heavier and older men even as testosterone drops.

The clearest answer comes from the Finkelstein trial. Testosterone controls muscle size and strength, estrogen controls body fat and bone, and both are needed for sexual function. The researchers gave 198 healthy men aged 20 to 50 goserelin, a drug that switches off the body's own testosterone and estradiol. The men then received placebo gel or 1.25 g, 2.5 g, 5 g or 10 g of testosterone gel daily for 16 weeks. Another 202 men got the same treatments plus anastrozole, which blocks the conversion of testosterone to estradiol.

Body fat went up in the men taking placebo, 1.25 g or 2.5 g of testosterone without anastrozole. Their mean testosterone levels were 44, 191 and 337 ng/dL. That last figure sits inside the range many labs call normal, yet these men still gained fat. Lean mass and thigh muscle shrank only with placebo or the lowest dose, and leg-press strength fell only with placebo. The authors concluded that estrogen deficiency primarily accounted for increases in body fat, while androgen deficiency accounted for losses in lean mass, muscle size and strength.

The practical point is that a man's symptoms do not map neatly onto a testosterone number. Finkelstein's team found that the amount of testosterone required to maintain lean mass, fat mass, strength and sexual function varied widely between men. Someone who gains belly fat on a low testosterone level may be short on the estradiol that testosterone would normally supply, not only on testosterone itself.

Estrogen in men is necessary, and bone is where the evidence is strongest. In a follow-up analysis of the same hormone clamp trial, published in the Journal of Clinical Investigation in 2016, Finkelstein's group found that bone density on quantitative CT of the spine fell substantially in every testosterone dose group in which aromatization was also blocked. The fall happened regardless of the testosterone dose. Estradiol deficiency also disrupted cortical bone structure at the wrist and shin.

The same study gave rough floors. Estradiol levels above 10 pg/mL and testosterone levels above 200 ng/dL were generally sufficient to prevent increases in bone breakdown and decreases in bone density in these men. The authors wrote that testosterone and estradiol levels must decline substantially to impact the skeleton. Our guide to bone density in men and DEXA scans covers how that risk is read in practice.

Rare genetic cases show what a male skeleton looks like with no estrogen at all. Akira Morishima and colleagues described a man with aromatase deficiency in the Journal of Clinical Endocrinology and Metabolism in 1995. At age 24 his testosterone was 2015 ng/dL, far above normal, but his estradiol was below 7 pg/mL. He stood 204 cm tall because his growth plates had never closed, his bone age was 14 years, and the bone density at his wrist was 4.7 standard deviations below the average for men his age. High testosterone could not stand in for the missing estrogen.

High estradiol in men is linked to worse outcomes in some groups, but so is low estradiol, and the strongest data show a U-shaped curve rather than a simple rule that more estrogen is harmful. Ewa Jankowska and colleagues followed 501 men with chronic heart failure, mean age 58, for 3 years and published the results in JAMA in 2009. There were 171 deaths (34%). The men were split into five groups by estradiol level, with the middle group (21.80 to 30.11 pg/mL) as the reference.

Men in the lowest estradiol group had a mortality hazard ratio of 4.17 compared with the middle group, and men in the highest group had a hazard ratio of 2.33. The two extremes looked different clinically. The low-estradiol men had more advanced heart failure, poorer kidney function and less body fat, while the high-estradiol men had raised liver enzymes and bilirubin. That pattern suggests estradiol was partly a marker of how sick each man was, so these numbers cannot show that changing estradiol would change survival.

Estradiol holds up with age because aromatase activity and body fat both increase as men get older. Vermeulen's review found that the age-associated decrease in testosterone is scarcely reflected in plasma estradiol for this reason. Free and bioavailable estradiol do fall modestly with age, and so does the ratio of free testosterone to free estradiol, which the authors read as evidence of more conversion with age.

Weight is one of the strongest drivers of low testosterone. The European Male Aging Study surveyed 3200 men aged 40 to 79 in eight countries and published the baseline results in the Journal of Clinical Endocrinology and Metabolism in 2008. Compared with men with a BMI under 25, men with a BMI of 25 to under 30 had total testosterone 2.32 nmol/L lower, and men with a BMI of 30 or more had total testosterone 5.09 nmol/L lower. The hormone pattern pointed to a signalling problem in the brain and pituitary, not only in the testes.

Blocking estrogen with an aromatase inhibitor raises testosterone in older men, but the trials found no gain in muscle or strength and a loss of spine bone density. Anastrozole stops aromatase, so more testosterone stays as testosterone and the brain senses less estradiol and pushes the testes harder. In a 12 week trial by Benjamin Leder and colleagues (JCEM, 2004), anastrozole 1 mg daily raised total testosterone from 343 to 572 ng/dL and lowered estradiol from 26 to 17 pg/mL. Erectile function scores did not change.

The bone result is the warning sign. In the 69 men studied by Sherri-Ann Burnett-Bowie and colleagues, spine bone density on anastrozole fell from 1.121 to 1.102 g/cm2, while the placebo group rose from 1.180 to 1.189 g/cm2. The authors concluded that aromatase inhibition does not improve skeletal health in aging men with low or low normal testosterone. Our article on estradiol during TRT covers why routine estrogen blocking during testosterone therapy is questioned for the same reason.

In women the roles are reversed in size: estrogen is the dominant sex hormone and testosterone is present in much smaller amounts. Low estrogen after menopause and low testosterone in women are different problems with different evidence behind them. The Global Consensus Position Statement on testosterone therapy for women, endorsed by groups including The Endocrine Society, recommended testosterone only for postmenopausal women with hypoactive sexual desire disorder, as summarised in the 2021 International Society for the Study of Women's Sexual Health guideline. Low libido is the one use with consensus support; mood, energy and bone are not established indications.

A man trying to sort out testosterone vs estrogen problems needs both numbers measured properly, plus SHBG. Estradiol in men is low enough that assay choice matters, and our guide to SHBG and free testosterone explains why total testosterone alone can mislead. The steps below are a general framework for a conversation with a clinician, not a treatment plan.

This article is for educational purposes only and is not medical advice. Nothing here diagnoses, treats, cures or prevents any disease, including hypogonadism, osteoporosis or heart failure. Testosterone therapy and aromatase inhibitors are prescription drugs discussed only in terms of what published research reported. Speak with a licensed physician before starting, stopping or changing any medication.

• Finkelstein JS et al. Gonadal steroids and body composition, strength, and sexual function in men. New England Journal of Medicine, 2013. https://doi.org/10.1056/NEJMoa1206168
• Finkelstein JS et al. Gonadal steroid-dependent effects on bone turnover and bone mineral density in men. Journal of Clinical Investigation, 2016. https://doi.org/10.1172/JCI84137
• Jankowska EA et al. Circulating estradiol and mortality in men with systolic chronic heart failure. JAMA, 2009. https://doi.org/10.1001/jama.2009.639
• Burnett-Bowie SA et al. Effects of aromatase inhibition on bone mineral density and bone turnover in older men with low testosterone levels. Journal of Clinical Endocrinology and Metabolism, 2009. https://doi.org/10.1210/jc.2009-0739
• Burnett-Bowie SA et al. Effects of aromatase inhibition in hypogonadal older men: a randomized, double-blind, placebo-controlled trial. Clinical Endocrinology, 2009. https://doi.org/10.1111/j.1365-2265.2008.03327.x
• Leder BZ et al. Effects of aromatase inhibition in elderly men with low or borderline-low serum testosterone levels. Journal of Clinical Endocrinology and Metabolism, 2004. https://doi.org/10.1210/jc.2003-031467
• Morishima A et al. Aromatase deficiency in male and female siblings caused by a novel mutation and the physiological role of estrogens. Journal of Clinical Endocrinology and Metabolism, 1995. https://doi.org/10.1210/jcem.80.12.8530621
• Vermeulen A et al. Estradiol in elderly men. The Aging Male, 2002. https://pubmed.ncbi.nlm.nih.gov/12198740/
• Wu FC et al. Hypothalamic-pituitary-testicular axis disruptions in older men are differentially linked to age and modifiable risk factors: the European Male Aging Study. Journal of Clinical Endocrinology and Metabolism, 2008. https://doi.org/10.1210/jc.2007-1972
• Parish SJ et al. International Society for the Study of Women's Sexual Health Clinical Practice Guideline for the Use of Systemic Testosterone for Hypoactive Sexual Desire Disorder in Women. Journal of Sexual Medicine, 2021. https://doi.org/10.1016/j.jsxm.2020.10.009

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