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Hormones

Hormone Optimisation in Wimbledon

Hormonal symptoms are not the problem — they are the signal. Irregular cycles, fatigue, low mood, weight that will not shift, night sweats, poor recovery, a libido that has quietly disappeared: each points to something upstream. My work is to find what that something is, read the whole hormonal axis rather than one result at a time, and treat the terrain the hormones are being produced in.

Who this is for

Women with cycle or fertility concerns — irregular or absent cycles, short luteal phases, PMOS (polyendocrine metabolic ovarian syndrome, renamed from PCOS in 2026), thyroid dysfunction, or hormone results that come back “normal” while you continue to feel unwell.

Women in the perimenopausal and menopausal transition — vasomotor symptoms, disrupted sleep, mood and cognitive change, joint pain, weight redistribution and the metabolic shift that tends to accompany all of it. Whether or not you are taking HRT.

Men in midlife — persistent fatigue, loss of morning erections and libido, poor training recovery, central weight gain, low mood or irritability: the cluster often labelled “andropause”. The accurate term is age-related decline in testosterone, or late-onset hypogonadism where it is confirmed — and, as set out below, it is assumed far more often than it is present.

How I approach hormone work

I begin with data, not assumption. Symptoms tell me where to look, not what is happening: two women with identical fatigue and cycle irregularity can have opposite underlying pictures — one with impaired thyroid conversion and a flattened cortisol curve, another with compensatory hyperinsulinaemia and raised androgens. So the sequence is history and examination, then testing where it will change what I do, then a plan built on what the testing showed — not the reverse.

Hormones are a network, not a list. A single result becomes meaningful only in three relationships — to the other hormones on its pathway, to its place in the hierarchy, and to the time it was measured. Cortisol, progesterone, DHEA, testosterone and oestradiol are built from one cholesterol precursor along competing branches, so pulling on one changes the others; and because thyroid and insulin set the metabolic pace and fuel handling, a reproductive panel read without them is read out of order.

Hormone output depends on energy status. The first committed step of steroid synthesis takes place on the inner mitochondrial membrane and depends on the mitochondrion producing energy adequately; the conversion of T4 to active T3 falls in illness, inflammation and sustained energy restriction. Where energy production is compromised, hormone output falls.

Alongside the results I assess how you generate and spend energy (temperature, resting heart rate, exercise tolerance and recovery, and the structural and myofascial load found on examination), nutritional status and substrate, and gut function — because oestrogens conjugated in the liver can be deconjugated by bacterial β-glucuronidase and reabsorbed rather than excreted.

Testing — what I use and why

Standard reference ranges are built to catch disease, not to describe how well your system is regulated — a result can sit inside the range and still be part of why you feel unwell.

A serum test measures the concentration at the moment the needle went in — for hormones that swing across the day or the cycle, a single frame from a film. Cortisol is the clearest case: its meaning lives in its shape — a sharp waking rise, then a decline to a low at night — which a mid-range 9 a.m. reading cannot show. Timed dried-urine collection resolves that rhythm and adds metabolites: not just how much oestradiol is present but which route it is being cleared down, and the same for androgens.

NICE advises identifying peri- and menopause without laboratory tests in otherwise healthy women aged over 45 with menopausal symptoms.¹ Testing here answers a different question: it characterises the metabolic, adrenal and thyroid picture underneath the transition.

Panel	What it adds
Steroid Hormone Testing (dried urine)	Adrenal and sex steroids with metabolites — cortisol diurnal pattern, cortisol vs cortisone, progesterone, androgens, and oestrogen metabolism down each hydroxylation route
Complete Thyroid (blood)	TSH, free T4, total T4, free T3 and both antibody classes, with lipids and vitamin D — conversion and autoimmunity read against the metabolic terrain, not just pituitary signalling
CardioMetabolic Assay (blood)	Fasting insulin, leptin, adiponectin and an extended lipid picture — the metabolic regulation that drives much of what looks purely hormonal

Specifications, laboratories and fees for every panel are on the functional lab testing page. Which panel is useful — and whether any is — depends on your history; testing is selected after evaluation and according to individual needs.

What treatment involves

Treatment is built from what the assessment showed and targeted at the specific picture identified — never a generic protocol or a stock supplement stack.

• Food first — nutritional targets met with whole foods, adequate protein and enough total energy before anything is supplemented. Supplements do not substitute for real food.
• Acupuncture — applied for autonomic regulation, local circulation, and the structural and myofascial restrictions found on examination.
• Herbal prescription — where a compound-level rationale exists for the picture in front of me.
• Circadian and sleep optimisation — morning light, evening darkness and sufficient sleep: a direct input to the cortisol rhythm the rest of the plan depends on. The relationship runs both ways: the body clock times hormone release, and hormones in turn reset the clock.⁷ When hormones change, sleep changes too; the night sweats of perimenopause are the familiar example. Sleep also changes with age, with less deep sleep and more waking in the night.⁸

Perimenopause and menopause

What changes in perimenopause is not only oestradiol. Insulin sensitivity typically falls, body composition shifts, thyroid conditions are more likely to surface, sleep architecture changes, and the adrenal contribution to hormone production becomes proportionally more important as ovarian output declines. A woman whose perimenopause is difficult very often has a metabolic and adrenal picture that was already marginal and is now being stress-tested. That terrain is the part I work on — supporting the shifts driving the symptoms rather than suppressing the symptoms alone.

Men in midlife — testosterone, energy and recovery

Testosterone is where the gap between the marketing and the physiology is widest. It does decline with age, at roughly 1% a year from the fourth decade — but when the European Male Ageing Study applied a rigorous definition, only about 2% of men aged 40 to 79 met it.² The symptoms are extremely common; confirmed hypogonadism is not.

Far more often, a low reading in a midlife man is secondary — a consequence of visceral adiposity, insulin resistance, poor sleep, sleep apnoea or sustained under-recovery, rather than a primary testicular problem. The Endocrine Society guideline is explicit that reversible causes should be identified and addressed first.³ So the work here is the same: read the metabolic picture, correct the terrain, and let the axis recover where it can.

Diminished ovarian reserve and premature ovarian insufficiency

A low AMH or a raised FSH is a measurement, not a verdict — and neither measures egg quality. Reserve markers describe quantity and recruitment, not the energetic capacity of the oocytes that remain, which is what determines whether a cycle produces a competent embryo. Where premature ovarian insufficiency has been diagnosed, it is worth looking further than the hormone panel: it is autoimmune in an appreciable minority of cases and clusters with autoimmune thyroid and adrenal disease, which warrants proper investigation, as the international guideline sets out.⁴

What to expect

Initial consultation — your full hormonal and health history, physical and structural assessment, review of any existing results, and a decision together about whether further testing would add anything. You leave with a plan.

Testing — where indicated, panels are arranged after that consultation and interpreted with you personally in an interpretation consultation. You receive the reasoning, not just the report.

Key takeaways

• Hormonal symptoms are downstream signals; the diagnostic question is what produces them, and answering it needs data, not pattern-matching.
• A hormone result means something only in three relationships: to its pathway, to its place in the hierarchy, and to the time it was measured — with thyroid and insulin read before the sex steroids.
• Steroid synthesis depends on the mitochondrion producing energy, and T4-to-T3 conversion falls in illness, inflammation and sustained energy restriction.
• A single blood draw gives a level; timed dried urine gives a rhythm and a clearance pattern, frequently the actionable part.
• Most low testosterone in midlife men is secondary to metabolic factors; confirmed late-onset hypogonadism is uncommon.

Frequently Asked Questions

References

1. National Institute for Health and Care Excellence. Menopause: identification and management (NG23). Published 12 November 2015; updated 2026. Recommendations 1.3.1, 1.3.4, 1.3.6. https://www.nice.org.uk/guidance/ng23 [Established — clinical guideline] ↩︎

2. Wu FCW, Tajar A, Beynon JM, et al. Identification of late-onset hypogonadism in middle-aged and elderly men. N Engl J Med. 2010;363(2):123–135. doi:10.1056/NEJMoa0911101 [Established — human observational] ↩︎

3. 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 [Established — clinical guideline] ↩︎

4. Panay N, Anderson RA, Bennie A, et al; ESHRE, ASRM, CREWHIRL and IMS Guideline Group on POI. Evidence-based guideline: premature ovarian insufficiency. Hum Reprod Open. 2024;2024(4):hoae065. doi:10.1093/hropen/hoae065 [Established — clinical guideline] ↩︎

5. World Health Organization Task Force on Methods for the Regulation of Male Fertility. Contraceptive efficacy of testosterone-induced azoospermia in normal men. Lancet. 1990;336(8721):955–959. doi:10.1016/0140-6736(90)92416-f [Established — human trial] ↩︎

6. Liu PY, Swerdloff RS, Christenson PD, Handelsman DJ, Wang C; Hormonal Male Contraception Summit Group. Rate, extent, and modifiers of spermatogenic recovery after hormonal male contraception: an integrated analysis. Lancet. 2006;367(9520):1412–1420. doi:10.1016/S0140-6736(06)68614-5 [Established — pooled analysis] ↩︎

7. Begemann K, Rawashdeh O, Olejniczak I, Pilorz V, de Assis LVM, Osorio-Mendoza J, Oster H. Endocrine regulation of circadian rhythms. npj Biol Timing Sleep. 2025;2:10. doi:10.1038/s44323-025-00024-6 [Established — review of animal and human studies] ↩︎

8. Ohayon MM, Carskadon MA, Guilleminault C, Vitiello MV. Meta-analysis of quantitative sleep parameters from childhood to old age in healthy individuals: developing normative sleep values across the human lifespan. Sleep. 2004;27(7):1255–1273. doi:10.1093/sleep/27.7.1255 [Established — human observational, meta-analysis] ↩︎

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Agnes Ryu, OMD, MATCM is the founder of Dr Ryu Natural Medicine in Wimbledon, South West London. She qualified as a Licensed Oriental Medicine Physician in Korea in 1995 — a six-year medical degree — and holds an MSc in Human Physiology. She worked as a clinician and as a research biochemist at the Natural Products Research Institute, Seoul National University, and lectured in physiology and diagnostics at the Asante Academy of Chinese Medicine, Middlesex University, before moving into private practice. Her clinical focus has been on endocrine regulation, energy metabolism and fertility. She has over 30 years in clinical medicine and close to two decades focused on fertility. Member, Association of Traditional Chinese Medicine and Acupuncture UK (ATCM) — FM0200004.

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