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Clinical Diagram

The Three Axes

The adrenal, thyroid and gonadal axes are usually drawn separately, as though they were three systems. They share a hypothalamus and a pituitary. Once you see that, a great deal of confusing clinical presentation stops being confusing.

SHARED CONTROL HYPOTHALAMUS PITUITARY ACTH TSH LH / FSH ADRENAL CORTEX cortisol · DHEA THYROID T4 → T3 GONADS oestrogen · testosterone HPA AXIS HPT AXIS HPG AXIS dashed = negative feedback WHERE THE AXES INTERFERE Cortisol suppresses T4→T3 and raises reverse T3 Cortisol suppresses LH and FSH — reproduction is deprioritised Low T3 slows cortisol clearance Shared precursor: pregnenolone THE CLINICAL POINT One hypothalamus. One pituitary. Three outputs. Sustained demand on one axis is not contained within it. This is why stress presents as a thyroid problem, or as a cycle problem, or as both.

Why this matters clinically

A patient arrives with fatigue, cold hands, weight that will not shift and a cycle that has become irregular. Thyroid bloods come back normal. So does everything else. They are told there is nothing wrong.

What has usually happened is that sustained demand on one axis has spilled into the others — because the control is shared, and the body triages.

Under sustained threat, the body funds survival and defers everything that can wait. Reproduction can wait. Metabolic rate can be lowered. Neither of those is a malfunction — they are a system doing exactly what it evolved to do, for longer than it was designed to do it.

The three interference points

HPA → HPT
Cortisol and T3 conversion
T4 is largely inert until converted to T3. Glucocorticoids inhibit that conversion and shunt more T4 toward reverse T3, which occupies the receptor without activating it. The result is a normal TSH, a normal T4, a low free T3, and a person who is cold and exhausted.
HPA → HPG
Cortisol and reproduction
Sustained cortisol suppresses GnRH signalling and therefore LH and FSH. Cycles lengthen, become irregular or stop; libido falls; testosterone drops in men. This is the mechanism behind exercise-associated menstrual disturbance and it is not a gynaecological fault.
HPT → HPA
Low T3 slows clearance
Thyroid status influences how quickly cortisol is metabolised. Low thyroid output slows clearance, so free cortisol can look adequate or high while total production is modest — one of the patterns that is invisible on a single reading.
SHARED SUBSTRATE
Pregnenolone
Cortisol and the sex hormones share pregnenolone as a precursor. The idea that stress "steals" it is stated far more confidently than the evidence supports — steroidogenesis is tissue-specific and locally regulated. Treat it as a plausible contributor, not a proven mechanism.

What this changes about testing

If the three axes share control, then testing one in isolation answers a narrower question than the one the patient is asking. A TSH tells you very little about why someone is cold and tired if the problem is conversion rather than production — and conversion is influenced by cortisol, ferritin, selenium, zinc and inflammatory load.

In practice that means reading the cortisol curve and total production alongside free T3 and reverse T3, alongside sex hormones and their metabolites, rather than sequentially and separately.

And it means the treatment order matters. Supporting thyroid output while the axis is being suppressed from above tends to disappoint. The demand usually has to come down first.

What this diagram is not

It is a simplification. Each axis has more feedback loops than shown, tissue-level regulation matters as much as circulating levels, and the interference is bidirectional in ways a flat diagram cannot capture. It is drawn to make one point clearly: these are not three separate systems, and a symptom appearing in one of them does not mean the problem originated there.

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