Testosterone: When Too Little — or Too Much — Becomes a Problem

Testosterone is usually associated with libido and sexual function. But its influence reaches much further. In men, testosterone contributes to the maintenance of muscle mass and strength, bone density, red blood cell production, fat distribution, sperm production, sexual function and general physical wellbeing. Like most hormones, the goal is not simply to have “more”: both too little testosterone and excessive androgen activity can cause problems — and some of testosterone’s effects depend on what happens to it after it is produced.

When testosterone is too low

Testosterone production is controlled through a communication pathway between the hypothalamus, pituitary gland and testes. A problem anywhere along that pathway can lower testosterone.

Sometimes the testes themselves cannot produce sufficient testosterone. This is known as primary hypogonadism and may occur following testicular injury, infection, chemotherapy or radiotherapy, or because of certain genetic conditions.

In other men, the problem originates higher up — the pituitary or hypothalamus is not providing enough stimulation to the testes. This is termed secondary hypogonadism.

But there is another increasingly important category: functional suppression of testosterone.

Obesity and metabolic dysfunction are strongly associated with lower testosterone, and particularly with secondary hypogonadism. Chronic systemic illness, liver disease, excessive alcohol use, some medications — notably opioids and glucocorticoids — hyperprolactinaemia, iron overload and pituitary disorders can also interfere with testosterone production.

Ageing matters too, but a falling testosterone concentration should not automatically be dismissed as “just getting older”. Current European guidance emphasises investigating associated disease, medication and metabolic factors rather than assuming age alone is responsible.

What might low testosterone feel like?

Symptoms vary considerably, and many are nonspecific. Some of the more suggestive changes include:

• reduced sexual desire
• fewer spontaneous or morning erections
• erectile difficulties
• reduced muscle mass and strength
• increased body fat, particularly visceral fat
• reduced energy and physical performance
• reduced motivation or low mood
• difficulty concentrating
• reduced bone density
• infertility
• sometimes anaemia

Sexual symptoms tend to be among the more specific indicators of true androgen deficiency; fatigue, poor concentration and low mood have many other possible causes. That distinction is important. A tired 50-year-old man with abdominal weight gain and poor concentration does not automatically have testosterone deficiency. Sleep apnoea, thyroid dysfunction, anaemia, diabetes, depression, medication effects, chronic disease and metabolic dysfunction can produce a very similar picture.

But can testosterone be too high?

Yes — although markedly excessive testosterone arising naturally is much less common than low testosterone. Clinically, excessive androgen exposure is more often encountered through testosterone treatment, anabolic-androgenic steroid use or excessive supplementation.

This creates an interesting paradox. Very high external doses of testosterone can produce some of the effects people are trying to achieve — such as greater muscle mass — while simultaneously switching down the body's own testosterone and sperm production. High-dose anabolic-androgenic steroid exposure is associated with:

• acne and oily skin
• accelerated androgen-dependent hair loss
• increased red blood cell production and potentially erythrocytosis
• fluid retention
• changes in blood pressure and blood lipids
• irritability, aggression or mood changes at high doses
• testicular shrinkage
• reduced sperm production
• subfertility or infertility
• sometimes gynaecomastia

The last point may seem counterintuitive: taking testosterone can actually reduce male fertility because external testosterone suppresses LH and FSH signalling from the pituitary, reducing the stimulation needed inside the testes for normal sperm production. This is why testosterone therapy is not used as a fertility treatment and is specifically discouraged in men actively wishing to father a child.

And then there is DHT

Testosterone is not the end of the story. In certain tissues, testosterone can be converted by the enzyme 5-alpha-reductase into dihydrotestosterone, or DHT.

DHT binds strongly to the androgen receptor and produces particularly important androgenic effects in tissues including the: prostate • skin • sebaceous glands • hair follicles.

DHT is essential to normal male development. In adulthood, however, high local androgen activity can contribute to some familiar androgen-related problems:

Male-pattern hair loss
In genetically susceptible scalp follicles, DHT contributes to progressive follicular miniaturisation.

Oily skin and acne
Androgen signalling stimulates sebaceous gland activity.

Prostate growth
DHT is a major androgen within prostate tissue and contributes to prostate development and growth.

Increased facial and body hair
DHT contributes to terminal hair growth in androgen-sensitive areas.

This helps explain why two men with apparently similar blood testosterone concentrations can sometimes display quite different androgenic characteristics. It isn't simply “how much testosterone?” It is also: How much is biologically available? How much is converted into other hormones? How sensitive are the target tissues to those hormones?

Testosterone can also take another route

Some testosterone is converted through the enzyme aromatase into estradiol. Men require estradiol too. It contributes particularly to bone health and normal reproductive and metabolic physiology. The balance therefore involves far more than testosterone alone: testosterone ↔ DHT ↔ estradiol along with SHBG, pituitary signalling, body composition, metabolic health and androgen-receptor sensitivity.

This is one reason indiscriminately attempting to “boost testosterone” — or aggressively block its conversion into DHT or estradiol — can oversimplify a much more complex endocrine system.

So what should actually be tested?

A single testosterone measurement is rarely enough to establish hypogonadism. Current guidelines recommend diagnosing testosterone deficiency only when compatible symptoms or signs occur alongside repeatedly low testosterone concentrations. As testosterone varies considerably during the day and from one day to another, measurements are generally repeated in the morning, ideally under standardised conditions.

Depending on the clinical picture, investigation may include:

Total testosterone
SHBG
Calculated or measured free testosterone
LH and FSH
Prolactin

and, where relevant:

Estradiol
Thyroid function
Full blood count / haematocrit
Glucose and HbA1c
Liver function
Ferritin and iron studies
PSA and prostate assessment where appropriate

SHBG deserves particular attention because changes in SHBG can make total testosterone misleading. Obesity and type 2 diabetes, for example, may lower SHBG and therefore lower measured total testosterone even when free testosterone is less affected.

The Clinical Insight

When a man presents with fatigue, reduced libido, declining muscle mass, abdominal weight gain or poorer physical performance, asking “Is his testosterone low?” is only the beginning. The more useful questions are:

Why has it changed?

Is the problem originating in the testes, the pituitary–hypothalamic axis, or from metabolic and systemic illness?

What is happening to testosterone once it reaches its target tissues?

Are we looking at testosterone itself — or the wider physiology that controls it?

More is not necessarily better with male hormones. Balance, signalling and the underlying cause matter far more than chasing a number.

This article is for educational purposes and is not a substitute for individual medical assessment. Symptoms of testosterone deficiency or excess should be properly investigated rather than treated on symptoms alone.

References

1. Bhasin S, Brito JP, Cunningham GR, et al. Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2018;103(5):1715–1744. doi:10.1210/jc.2018-00229.
2. Endocrine Society. Testosterone Therapy for Hypogonadism Guideline Resources. Clinical Practice Guideline. 2018.
3. Jimbo M, Gomella LG. Male Hypogonadism. Merck Manual Professional Edition. Reviewed 2025; updated February 2026. Useful for primary vs secondary hypogonadism, obesity, systemic illness, medications, iron overload, alcohol and pituitary causes, as well as clinical symptoms and diagnostic testing.
4. Jimbo M, Gomella LG. Male Reproductive Endocrinology. Merck Manual Professional Edition. 2025. Covers hypothalamic–pituitary–gonadal regulation and normal male reproductive endocrine physiology.
5. Merck Manual Professional Edition. Anabolic Androgenic Steroids. Covers adverse effects of supraphysiological androgen exposure, including acne, alopecia, hypertension, dyslipidaemia, erythrocytosis, gonadal suppression, reduced sperm production, testicular atrophy and infertility.
6. Swerdloff RS, Dudley RE, Page ST, Wang C, Salameh WA. Dihydrotestosterone: Biochemistry, Physiology, and Clinical Implications of Elevated Blood Levels. Endocr Rev. 2017;38(3):220–254. doi:10.1210/er.2016-1067. An excellent detailed review of testosterone-to-DHT conversion, 5α-reductase, tissue-specific DHT production, prostate and skin physiology.