The Metabolic-Bioenergetic Approach to Fertility

Most people arrive at fertility treatment having already been given a number. An AMH result, an FSH level, a follicle count, an age-related percentage. The number is often presented as a verdict. A number says where you stand; it does not say why. This article explains the approach I use, which starts from that second question.

If you have been investigated and told your infertility is “unexplained”, or handed a diagnosis with no mechanism attached to it, you already know the gap I am describing. My work looks at what those numbers sit on: the metabolic and energetic terrain they are downstream of.

What “metabolic-bioenergetic” actually means

The phrase is precise, not decorative.

Metabolic refers to how your body produces, regulates, and uses energy and nutrients — insulin signalling, thyroid function, inflammation, and the broader regulation of fuel.

Bioenergetic refers to energy production at the level of the cell: how reliably a cell can turn fuel and oxygen into ATP, the cell’s energy currency, through oxidative phosphorylation in its mitochondria, and how much it has left over once the basic business of staying alive is paid for.

These two belong together in fertility because reproduction is energetically expensive. An egg maturing over its final months, an embryo dividing in its first days, a uterine lining preparing to receive it — each depends on a reliable energy supply, and the oocyte is the richest cell in the body in mitochondria [Established — review].¹ When the metabolic environment is disturbed, fertility can be affected before anything shows up as an abnormal hormone result [Theoretical].

That is the heart of the approach: fertility is treated as a downstream expression of metabolic and energetic health, not as an isolated reproductive problem.

Why standard fertility care often stops short

Conventional investigation is built to identify clear, nameable obstacles: blocked tubes, absent ovulation, low sperm parameters, structural problems. When it finds one, it is genuinely useful — and where it finds one, it should be acted on.

The difficulty arises when it does not. When every standard result sits within range and the couple is told their infertility is “unexplained”.

Standard panels also work from population reference ranges — the band within which most results fall. A result inside that band is reported as normal. But “within the normal range for the population” and “the range that changes the decision for you” are not the same statement. Thyroid function is the everyday example. In sixteen healthy men tested monthly for a year, each man’s own range for thyroid hormones was about half as wide as the range for the group as a whole, the kind of range laboratory limits are built from; so a result inside the laboratory range is not necessarily normal for that person [Established — human observational, small].³ That is a reason to measure and compare over time, not to treat a number: in the TABLET trial, levothyroxine for 952 women with normal thyroid function and TPO antibodies did not raise live births (37.4% against 37.9%), and T4LIFE found the same in women with recurrent miscarriage [Established — human RCT, null].⁴⁵

The three systems I look at first

When I assess a fertility case, I am usually looking at three systems and, more importantly, at how they are interacting. They are not separate problems.

Cellular energy production

Eggs spend their final months maturing, and that maturation is energetically expensive. Where a cell’s capacity to produce energy is compromised — often alongside oxidative stress — egg quality and early embryo development can be affected [Emerging — human and animal].¹ It is one reason the same chronological age carries very different fertility pictures in different people: the underlying energetic terrain is not the same [Theoretical].

Steroid hormone production begins inside the mitochondrion, where the enzyme P450scc converts cholesterol to pregnenolone [Established — review].⁶

Insulin and metabolic regulation

Insulin resistance is best documented in PMOS, where it is common at every body weight [Established — human, meta-analysis],⁷ but it is not confined to it [Clinical Heuristic]. When cells stop responding crisply to insulin, the pancreas makes more of it, so blood glucose can stay normal while insulin runs high; that extra insulin acts on the ovary, raising androgen production and disturbing ovulation [Established].⁸ PCOS is now PMOS sets out the ovarian side.

The thyroid and stress axes

Thyroid function and the HPA (stress) axis sit close to reproduction and influence it directly. Cortisol, raised in stress, acts on the hypothalamus, the pituitary and the ovary to slow reproduction [Established — review].⁹ On the thyroid side, a single in-range result can miss a change that matters for one person, for the reason given above [Established — human observational, small].³

What can actually be changed

Everything I do is ultimately aimed at the same place: the cell’s capacity to make energy. That is the target. What differs — enormously — is the route to it.

You cannot reach into an organelle and adjust it by hand. What you can change is every condition it depends on, and there are a great many of those. Digestion and absorption, so the raw material actually arrives. Nutritional repletion, so the cofactors the machinery needs are present. Thyroid function — measured as TSH, free T4, free T3 and TPO antibodies, with basal temperature kept as a supplementary record, never a substitute — because T3, the active thyroid hormone, sets much of the body’s metabolic rate [Established — review].¹⁰ Circadian signalling: light in the morning, darkness at night, sleep long enough to run repair. Blood sugar stability and insulin sensitivity, so glucose is actually oxidised rather than stored. Inflammatory load. Stress physiology, so that cortisol keeps its daily rhythm, high in the morning and low at night, rather than staying high. Clearance — liver phase I and II metabolism, bile flow and bowel transit, the route by which oestrogen and other hormones leave the body. Endocrine-disrupting chemical exposure. Movement, which is both a demand on the system and a signal to expand it.

That list is deliberately long, because which of those levers moves the needle is highly individual. In one person the limiting factor is structural — a mechanical restriction, a breathing pattern, a postural load. In another it is neurological, endocrine, immunological, or simply that nothing has been absorbed properly for years. Working out which is most of what a first consultation is for [Clinical Heuristic].

How this changes what happens in practice

Because the approach treats fertility as downstream of these systems, the work looks different from the first consultation onwards.

The first consultation is longer and goes wider. I take a full history — reproductive, but also metabolic, nutritional and lived — examine you, and review the results you already have through that lens. The aim is to build a picture of the terrain, not to confirm a diagnosis.

Testing is selected, not ordered off a list. A test is added only where its answer would change what we do; tests take time and money, and a result you already hold is not repeated without reason. For some people the first work is nutrition, energy, sleep and stress. How I use testing: functional lab testing.

Treatment is built around what the terrain reveals. Acupuncture, herbal medicine and nutritional therapy come in here — not as a fixed protocol applied to everyone, but as tools directed at the specific findings in your case.

Who comes to this approach

• People told their infertility is unexplained after normal standard results
• People with low AMH or raised FSH who want to know what else in their physiology can be measured
• People with PMOS (formerly PCOS),¹¹ irregular cycles or a metabolic history
• People preparing for IVF, or recovering from a cycle, who want the metabolic picture measured alongside it — see IVF support
• People who want a mechanism, not only a number

Where the method came from

This approach did not come from a single tradition. I qualified as a Licensed Oriental Medicine Physician in Korea in 1995, worked as a research biochemist at the Natural Products Research Institute, Seoul National University, and worked in stroke care and rehabilitation before moving into private practice in South West London in 2004. That combination — laboratory science, hospital medicine, and a systems view of the body — is what the method is built on.

It is also why the language here stays close to mechanism. I would rather explain how something works than ask you to take it on trust. More on the about page.

Key takeaways

• The oocyte is the richest cell in the body in mitochondria, and it relies on them to become competent for fertilisation and early development [Established — review].
• When energy is short, from under-eating or heavy training, or under prolonged stress, the hypothalamus can switch ovulation off: functional hypothalamic amenorrhoea [Established — clinical guideline].
• In sixteen healthy men tested monthly for a year, each man’s own range for thyroid hormones was about half as wide as the range for the group as a whole [Established — human observational, small].
• In the TABLET trial of 952 women with normal thyroid function and TPO antibodies, levothyroxine did not raise live births: 37.4% against 37.9% [Established — human RCT, null].
• Which system limits fertility differs from person to person, so the work starts from the person’s own history and results, not from a fixed protocol [Clinical Heuristic].

Frequently asked questions

References

1. May-Panloup P, Boucret L, Chao de la Barca JM, Desquiret-Dumas V, Ferré-L’Hotellier V, Morinière C, et al. Ovarian ageing: the role of mitochondria in oocytes and follicles. Hum Reprod Update. 2016;22(6):725–743. doi:10.1093/humupd/dmw028. PMID: 27562289. [Established — review] ↩︎↩︎

2. Gordon CM, Ackerman KE, Berga SL, Kaplan JR, Mastorakos G, Misra M, et al. Functional hypothalamic amenorrhea: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2017;102(5):1413–1439. doi:10.1210/jc.2017-00131. PMID: 28368518. [Established — clinical guideline] ↩︎

3. Andersen S, Pedersen KM, Bruun NH, Laurberg P. Narrow individual variations in serum T4 and T3 in normal subjects: a clue to the understanding of subclinical thyroid disease. J Clin Endocrinol Metab. 2002;87(3):1068–1072. doi:10.1210/jcem.87.3.8165. PMID: 11889165. [Established — human observational, small] ↩︎↩︎

4. Dhillon-Smith RK, Middleton LJ, Sunner KK, Cheed V, Baker K, Farrell-Carver S, et al. Levothyroxine in women with thyroid peroxidase antibodies before conception. N Engl J Med. 2019;380(14):1316–1325. doi:10.1056/NEJMoa1812537. PMID: 30907987. [Established — human RCT, null] ↩︎

5. van Dijk MM, Vissenberg R, Fliers E, van der Post JAM, van der Hoorn MP, de Weerd S, et al. Levothyroxine in euthyroid thyroid peroxidase antibody positive women with recurrent pregnancy loss (T4LIFE trial): a multicentre, randomised, double-blind, placebo-controlled, phase 3 trial. Lancet Diabetes Endocrinol. 2022;10(5):322–329. doi:10.1016/S2213-8587(22)00045-6. PMID: 35298917. [Established — human RCT, null] ↩︎

6. Miller WL, Auchus RJ. The molecular biology, biochemistry, and physiology of human steroidogenesis and its disorders. Endocr Rev. 2011;32(1):81–151. doi:10.1210/er.2010-0013. PMID: 21051590. [Established — review] ↩︎

7. Cassar S, Misso ML, Hopkins WG, Shaw CS, Teede HJ, Stepto NK. Insulin resistance in polycystic ovary syndrome: a systematic review and meta-analysis of euglycaemic-hyperinsulinaemic clamp studies. Hum Reprod. 2016;31(11):2619–2631. doi:10.1093/humrep/dew243. PMID: 27907900. [Established — human, meta-analysis] ↩︎

8. Diamanti-Kandarakis E, Dunaif A. Insulin resistance and the polycystic ovary syndrome revisited: an update on mechanisms and implications. Endocr Rev. 2012;33(6):981–1030. doi:10.1210/er.2011-1034. PMID: 23065822. [Established — review] ↩︎

9. Whirledge S, Cidlowski JA. Glucocorticoids, stress, and fertility. Minerva Endocrinol. 2010;35(2):109–125. PMID: 20595939. [Established — review, animal and human] ↩︎

10. Mullur R, Liu YY, Brent GA. Thyroid hormone regulation of metabolism. Physiol Rev. 2014;94(2):355–382. doi:10.1152/physrev.00030.2013. PMID: 24692351. [Established — review] ↩︎

11. Teede HJ, Bahri Khomami M, Morman R, Laven JSE, Joham AE, Costello MF, et al. Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process. Lancet. 2026;407(10545):2329–2339. doi:10.1016/S0140-6736(26)00717-8. PMID: 42119588. [Established — consensus statement] ↩︎

Related reading

• PCOS is now PMOS — the metabolic story behind the condition
• How does acupuncture work? — the mechanism beneath the needle