Female Athlete Triad / RED-S

Functional hypothalamic amenorrhoea is a diagnosis of exclusion, and labelling an athlete's missing periods as "just her training" without testing is a real clinical error - it delays the diagnosis of conditions that need entirely different treatment.

• Always exclude pregnancy first with a beta-hCG. It is the commonest cause of secondary amenorrhoea in a woman of reproductive age, athlete or not.
• Thyroid disease and hyperprolactinaemia - TSH and prolactin. A prolactinoma presents exactly this way and will not respond to eating more.
• Polycystic ovary syndrome, which is common and can coexist with athletic training; clinical hyperandrogenism and testosterone help separate it. The distinction matters because PCOS is not a state of oestrogen deficiency and does not carry the same bone risk.
• Premature ovarian insufficiency - an elevated FSH points away from a hypothalamic cause, since functional hypothalamic amenorrhoea produces low or inappropriately normal LH and FSH with low oestradiol.
• Coeliac disease and inflammatory bowel disease, which cause inadvertent energy deficiency through malabsorption rather than through under-eating.

Alongside these, check full blood count, ferritin, vitamin D, calcium and renal function, and consider T3 - a low T3 is one of the more useful markers of ongoing energy deficiency. DXA is indicated after six or more months of amenorrhoea, after a bone stress injury, with disordered eating, or at a very low BMI.

The single point most likely to be tested, and most often got wrong, concerns the combined oral contraceptive pill.

The combined oral contraceptive does not treat this condition. Prescribing it to an amenorrhoeic athlete is intuitive and wrong for two reasons. First, it has not been shown to restore bone mineral density in functional hypothalamic amenorrhoea, because the problem is not simply absent oestrogen - low energy availability independently suppresses bone formation through low IGF-1 and low T3, and no amount of exogenous oestrogen corrects an energy deficit. Second, and more insidiously, it produces a withdrawal bleed that looks like a period, which masks the single best clinical marker of recovery: the spontaneous return of menses. An athlete on the pill can appear to be improving while her energy deficit continues untreated.

What to do instead:

• Restoring energy availability is the treatment, and the return of spontaneous menstruation is the endpoint that tells you it has worked. Everything else is adjunctive.
• Calcium and vitamin D to recommended intakes, correcting a measured deficiency.
• Where pharmacological oestrogen is judged necessary - typically a persistently low BMD with continuing bone stress injuries despite genuine attempts at nutritional restoration - transdermal 17-beta-oestradiol with cyclic progestogen is preferred over the oral pill, because it avoids the hepatic first-pass effect that suppresses IGF-1 and therefore does not blunt bone formation in the way oral ethinyl oestradiol does.
• Bisphosphonates are generally avoided in young women of childbearing potential: the evidence in this population is thin, and their very long skeletal half-life raises unresolved concerns about a future pregnancy.
• If the athlete needs contraception for contraception's sake, that is a legitimate separate indication - but it should be prescribed knowing it neither treats the bone nor allows menses to be used as a recovery marker.

Use the threshold as a concept, not as a test

Two cautions belong with those numbers. The 30 kcal/kg figure comes from short-term laboratory studies in small groups of young women, and it describes the point at which measurable disruption appeared in that setting - it was never validated as an individual diagnostic cut-off. In practice, energy availability is also very hard to measure accurately in a free-living athlete, because it compounds the well-known unreliability of self-reported dietary intake with an estimate of exercise energy expenditure and a body-composition measurement, so a calculated EA carries a wide margin of error.

The 2023 IOC consensus reflects this by moving away from a single threshold toward a physiological model that distinguishes adaptable from problematic low energy availability, modified by individual factors - the same calculated EA may be benign in one athlete over a short period and damaging in another sustained for months. The practical consequence for the exam and the clinic is the same: a calculated EA above 30 does not exclude the diagnosis in an athlete who has stopped menstruating and is breaking bones. Treat the number as a way of understanding the mechanism and framing the dietary conversation, not as a rule-in or rule-out test.

Which bone stress injuries should raise the question

Not every stress fracture points to an energy deficit, and knowing which ones do is what makes the screening decision practical. Bone stress injuries at trabecular (cancellous) sites - the sacrum, pubic rami, femoral neck and calcaneus - are the ones most associated with low bone mineral density and hormonal disruption, because trabecular bone has a high surface area and turns over fast, so it registers oestrogen deficiency early. Injuries at predominantly cortical sites - the tibial shaft and metatarsals - are more often explained by training load, surface, footwear and biomechanics. A sacral or femoral neck stress fracture in a young female endurance athlete should therefore trigger a full RED-S assessment almost reflexively, while a second metatarsal stress fracture in a runner who has just doubled her mileage may be exactly what it looks like. Multiple or recurrent stress injuries at any site, and any stress injury in an athlete with menstrual disturbance, warrant the workup regardless. Note this is a different axis from the familiar high-risk versus low-risk classification, which describes the risk of non-union and the need for aggressive treatment rather than the likelihood of an underlying energy deficit - see Stress Fractures.