Most men who come to our clinic in Hull know that testosterone is important. They know it’s connected to energy, muscle, libido, and mood. But when you ask them where testosterone is actually produced — and, critically, what controls that production — the answer is usually a blank stare or a vague reference to “the testes.”
That’s an understandable gap. The male hormone system is not something most of us are taught in any useful detail. And yet understanding how testosterone is produced, regulated, and distributed throughout the body is genuinely useful — both for men who are experiencing symptoms of deficiency and for anyone trying to make sense of their blood test results or treatment options.
As a leading TRT Clinic in Hull, we believe that informed patients make better decisions. In this article, we’ll explain exactly where testosterone is produced, how its production is controlled, what can go wrong with that system, and what the clinical implications are when production fails. Written clearly enough for anyone to follow — but with enough detail to be genuinely informative.
The Primary Site: The Testes
The vast majority of testosterone in men — approximately 95% of total circulating levels — is produced in the testes. Specifically, it is synthesised by a specialised population of cells called Leydig cells, which are located in the interstitial tissue between the seminiferous tubules (the tubes within the testes responsible for sperm production).
Leydig cells contain the enzymatic machinery to convert cholesterol — the universal steroid precursor — through a series of biochemical steps into testosterone. This conversion pathway involves multiple enzymes and intermediate molecules, ultimately producing testosterone as the final product ready for release into the bloodstream.
The testes are the dominant site of testosterone production for a straightforward reason: the volume of Leydig cells present, and their capacity for testosterone synthesis, far exceeds that of any other tissue in the body. In a healthy adult man, this system produces between 3 and 10 milligrams of testosterone per day under normal conditions — enough to maintain physiological function across all the bodily systems that depend on it.
Why Testicular Location Matters for Temperature
One physiologically interesting feature of testicular testosterone production is its sensitivity to temperature. The testes are housed outside the body in the scrotal sac specifically because optimal testosterone synthesis (and sperm production) occurs at a temperature approximately 2–3°C below core body temperature. Conditions that chronically raise testicular temperature — such as varicocele (enlarged testicular veins), prolonged sedentary posture, or obesity — can impair both testosterone production and sperm quality over time.
The Secondary Site: The Adrenal Glands
A smaller but physiologically meaningful contribution to androgen production comes from the adrenal glands — a pair of small glands that sit above each kidney and are primarily known for producing cortisol and adrenaline.
The adrenal cortex produces weak androgens — principally dehydroepiandrosterone (DHEA) and androstenedione — which can be converted into testosterone and oestrogen in peripheral tissues throughout the body. However, the amount of testosterone directly attributable to adrenal androgen conversion is relatively modest in healthy men — typically representing no more than 5% of circulating testosterone levels.
The clinical relevance of adrenal androgens becomes more significant in specific situations: in men who have undergone surgical removal of the testes (for example, due to testicular cancer), adrenal androgens represent the remaining endogenous source of androgenic activity. In women with certain adrenal disorders, excessive adrenal androgen production can produce masculine characteristics.
For most men assessed at our Hull clinic, adrenal androgen production is a minor contributor to overall testosterone levels — but understanding its existence helps explain why testosterone levels are not simply zero in men who have had surgical castration or who are on medications that suppress testicular function.
The Control System: The Hypothalamic-Pituitary-Gonadal (HPG) Axis
The most important concept for understanding testosterone production — and the one most directly relevant to clinical assessment and treatment — is not where testosterone is made, but how its production is controlled. That control system is called the hypothalamic-pituitary-gonadal axis, universally abbreviated to the HPG axis.
The HPG axis is a three-level hormonal signalling cascade that coordinates testosterone production with extraordinary precision. Understanding it is the key to understanding why testosterone deficiency occurs, how blood tests interpret the underlying cause, and how different treatment approaches work.
Level 1 — The Hypothalamus: GnRH
The hypothalamus is a small but critically important region at the base of the brain. It serves as the master regulator of the HPG axis, releasing gonadotropin-releasing hormone (GnRH) in pulsatile bursts — typically every 60 to 120 minutes — directly into the portal blood vessels that connect it to the pituitary gland.
GnRH release is not constant — it is pulsatile, and the frequency and amplitude of those pulses directly controls how much downstream hormone is produced. This pulsatile nature is essential: continuous GnRH exposure actually suppresses the downstream response (a mechanism exploited medically in certain hormone-sensitive cancers). The hypothalamus integrates signals from numerous sources — including circulating testosterone levels, body weight, stress hormones, sleep patterns, nutritional status, and neural inputs — to calibrate GnRH output accordingly.
Level 2 — The Pituitary Gland: LH and FSH
GnRH signals travel to the anterior pituitary gland — a pea-sized structure at the base of the brain — where it stimulates the release of two critical hormones: luteinising hormone (LH) and follicle-stimulating hormone (FSH).
For testosterone production, LH is the primary driver. LH travels through the bloodstream to the testes, where it binds to receptors on Leydig cells and activates the enzymatic machinery responsible for converting cholesterol into testosterone. The more LH present, the more testosterone the Leydig cells produce — up to their maximum capacity.
FSH, by contrast, acts primarily on Sertoli cells within the seminiferous tubules, where it supports sperm production (spermatogenesis). FSH does not directly stimulate testosterone production, but it is measured in clinical assessments because its level — alongside LH — helps distinguish between different types of hypogonadism
Level 3 — The Testes: Testosterone
In response to LH stimulation, Leydig cells produce testosterone, which enters the bloodstream and circulates throughout the body to exert its wide-ranging effects. Testosterone also feeds back to the hypothalamus and pituitary, reducing GnRH and LH release when levels are adequate — a classic negative feedback mechanism that keeps testosterone within a physiological range under normal conditions.
This feedback loop is the reason that testosterone replacement therapy suppresses the body’s own production: when exogenous testosterone is introduced, circulating levels rise, the hypothalamus and pituitary detect sufficient testosterone, and they reduce GnRH and LH output accordingly — shutting down the endogenous signal to the Leydig cells.
What Happens to Testosterone Once It Is Produced?
Once secreted from the Leydig cells into the bloodstream, testosterone does not simply float freely to its target tissues. The majority of circulating testosterone is bound to carrier proteins — primarily sex hormone-binding globulin (SHBG) and albumin. Only a small fraction circulates in its free, biologically active form.
Total vs. Free Testosterone — Why the Distinction Matters
| Fraction | Binding | Biological Activity | Approximate Proportion |
|---|---|---|---|
| Bound to SHBG | Tightly bound | Inactive — cannot enter cells | ~45% |
| Bound to Albumin | Loosely bound | Weakly available — can dissociate | ~50–54% |
| Free Testosterone | Unbound | Fully active — enters cells directly | ~1–3% |
This is clinically significant because a man can have a total testosterone level that appears normal on a standard blood test while still experiencing genuine deficiency — if his SHBG is elevated, a disproportionately high fraction of that testosterone is bound and inactive, leaving insufficient free testosterone to drive the physiological effects that actually matter.
This is one of the core reasons why at Vitalis Luxe Clinic in Hull we always measure SHBG alongside total testosterone. A comprehensive panel that includes free testosterone calculation gives a far more accurate picture of a man’s actual androgenic status than a total testosterone figure alone.
Testosterone Conversion: DHT and Oestradiol
Testosterone is not the end of the story. In many tissues, it undergoes further conversion into other active hormones:
- Conversion to dihydrotestosterone (DHT) via the enzyme 5-alpha reductase — DHT is approximately three to five times more potent than testosterone at the androgen receptor and is particularly active in the prostate, skin, hair follicles, and genitalia. It is the primary androgen responsible for male pattern hair loss in genetically susceptible individuals.
- Conversion to oestradiol (E2) via the enzyme aromatase — a proportion of testosterone is converted to the primary oestrogen, oestradiol, in adipose tissue, liver, muscle, and other peripheral tissues. In men, oestradiol is essential for bone health, cardiovascular function, libido, and cognitive function — but excessive conversion (particularly from visceral fat) can suppress testosterone through negative feedback and produce unwanted effects.
Both of these conversion pathways are measured as part of a comprehensive hormone panel at our Hull clinic — DHT is not routinely assessed in standard panels, but oestradiol is included in our protocol as a standard safety and balance marker.
Daily and Lifelong Patterns of Testosterone Production
The Circadian Rhythm of Testosterone
Testosterone production follows a consistent daily rhythm in healthy men. Levels are highest in the early morning — typically peaking between 7am and 10am — and decline steadily through the afternoon and evening, reaching their lowest point late at night before the cycle resets during sleep.
This daily variation is significant enough to affect blood test interpretation. A testosterone level taken at 2pm will typically be 20–30% lower than the same man’s level taken at 8am. This is why clinical guidelines recommend that testosterone blood testing is performed in the morning, ideally fasting, for reliable and comparable results. At Vitalis Luxe Clinic, we apply this protocol consistently for all hormone assessments.
The Lifelong Arc of Testosterone Production
Beyond the daily cycle, testosterone follows a broader lifelong pattern in men:
- Foetal development: testosterone is produced in small amounts from around the 8th week of gestation, driving the differentiation of male reproductive organs
- Early childhood: very low levels, with a transient mini-puberty in male infants in the first months of life
- Puberty (roughly ages 11–17): dramatic rise in testosterone production, driving sexual development, muscle growth, voice deepening, and other secondary male characteristics
- Peak production: late teens to late twenties — highest lifetime testosterone levels
- Gradual decline from age 30: approximately 1–2% per year on average, though with significant individual variation
- Accelerating decline from 50s onwards: increasingly common for levels to fall below clinical thresholds, particularly free testosterone as SHBG tends to rise with age
This lifelong pattern is why age-appropriate reference ranges matter when interpreting testosterone blood tests — a level of 12 nmol/L is entirely different in clinical significance for a 25-year-old compared to a 65-year-old.
What Goes Wrong: How Testosterone Production Fails
With a clear picture of how testosterone production works, it becomes much easier to understand how and why it fails — and what the clinical implications are.
Primary Hypogonadism — The Testes Fail
In primary hypogonadism, the problem lies within the testes themselves. The Leydig cells are unable to produce sufficient testosterone despite receiving adequate LH stimulation from the pituitary. The pituitary responds by producing more LH and FSH in an attempt to compensate — which is why men with primary hypogonadism typically have elevated LH and FSH on their blood tests, alongside low testosterone.
Causes include genetic conditions (Klinefelter syndrome), previous testicular injury, orchitis following viral infection, testicular cancer treatment (surgery or chemotherapy), and idiopathic Leydig cell failure. Primary hypogonadism is less common than secondary hypogonadism but is well-managed with TRT.
Secondary Hypogonadism — The Signal Fails
In secondary hypogonadism, the testes are capable of producing testosterone but are not receiving adequate stimulation. The problem lies in the signalling chain — either at the hypothalamic level (insufficient GnRH) or the pituitary level (insufficient LH). Because the testes are not being adequately stimulated, testosterone falls — but so do LH and FSH, which is the diagnostic pattern that distinguishes secondary from primary hypogonadism.
Secondary hypogonadism is the more common presentation in younger men presenting to our Hull clinic, and it is frequently driven by modifiable factors: obesity, chronic stress, elevated cortisol, poor sleep, insulin resistance, nutritional deficiency, excessive alcohol, and certain medications. It can also result from pituitary tumours, elevated prolactin, or systemic illness.
The Clinical Importance of Distinguishing the Two
This distinction has real clinical consequences. A man with secondary hypogonadism due to a pituitary adenoma needs different management to a man with the same low testosterone level resulting from lifestyle factors. A man with elevated prolactin may respond better to a prolactin-lowering medication than to TRT alone. And a younger man with secondary hypogonadism who wishes to maintain fertility may benefit from an approach that stimulates his own testosterone production rather than replacing it exogenously.
This is why the LH and FSH values in a comprehensive hormone panel are not just academic — they are clinically essential for understanding the underlying cause of deficiency and directing the most appropriate treatment.
What Testosterone Replacement Therapy Does to This System
Understanding the HPG axis makes it straightforward to understand what happens when TRT is introduced.
When exogenous testosterone is administered — whether by injection, gel, or oral preparation — circulating testosterone levels rise. The hypothalamus and pituitary detect this through their testosterone receptors and reduce their output of GnRH and LH accordingly — the standard negative feedback response. With less LH reaching the testes, Leydig cell activity reduces and the body’s own testosterone production declines, sometimes to near-zero.
This is an expected and managed consequence of TRT, not a dangerous side effect. It explains why men on TRT have suppressed LH and FSH on their blood tests — this is the intended pharmacological mechanism, not a sign that something has gone wrong. It also explains the fertility consideration: with FSH suppressed, sperm production is significantly reduced during TRT.
For men on TRT at Vitalis Luxe Clinic, we monitor LH, FSH, and the full hormone panel at regular intervals — not because we expect problems, but because responsible clinical oversight requires understanding what the system is doing at every stage of treatment.
Frequently Asked Questions
Where is testosterone produced in the male body?
Approximately 95% of testosterone in men is produced by Leydig cells within the testes, in response to stimulation by luteinising hormone (LH) from the pituitary gland. A smaller contribution — around 5% — comes from the adrenal glands, which produce weak androgens that can be converted to testosterone in peripheral tissues.
What are Leydig cells?
Leydig cells are specialised cells located in the interstitial tissue of the testes, between the sperm-producing seminiferous tubules. They contain the enzymatic machinery to convert cholesterol into testosterone and are the primary testosterone-producing cells in the male body. Their function is directly regulated by luteinising hormone (LH) from the pituitary gland.
What controls testosterone production?
Testosterone production is controlled by the hypothalamic-pituitary-gonadal (HPG) axis — a three-level signalling cascade. The hypothalamus releases GnRH, which stimulates the pituitary to release LH. LH travels to the testes and stimulates Leydig cells to produce testosterone. Testosterone then feeds back to the hypothalamus and pituitary to regulate its own production — a classic negative feedback loop.
What is the difference between total and free testosterone?
Total testosterone measures all circulating testosterone in the blood, including the majority that is bound to carrier proteins (SHBG and albumin). Free testosterone is the small fraction — roughly 1–3% — that circulates unbound and is immediately available to enter cells and exert biological effects. Free testosterone is often a more clinically meaningful measure than total testosterone, particularly in men with elevated SHBG.
Why is testosterone measured in the morning?
Testosterone follows a daily circadian rhythm, with levels peaking between approximately 7am and 10am and declining through the afternoon and evening. A morning blood sample captures testosterone at or near its highest daily level, providing the most accurate and reproducible result for comparison against reference ranges. Afternoon testing can give readings 20–30% lower than morning levels in the same individual.