Short Cycles, Long Cycles, No Cycles: They're All Reading the Same Signal

A few weeks ago I wrote about the twenty years my own cycle spent telling me things nobody else was reading: heavy and painful from the start, gone entirely through an eating disorder, gone again in my early thirties under a load of stress I didn't know how to put down, and finally settling into something quiet and unremarkable once I addressed what was actually underneath it. If you haven't read that piece, it's here, and I'd start there for the fuller arc, along with the biology of how a system in the brain runs a constant energy audit and decides, cycle by cycle, whether reproduction is worth funding.

What I want to do here is something narrower, and I think more useful: name the framework that explains why so many women spend years, sometimes over a decade, being investigated for the wrong thing.

Cycles Change Before They Stop

Here's a pattern I see constantly in clinic, and it rarely gets named as a pattern at all. A woman's cycle starts changing years before anyone calls it a problem. Sometimes that looks like shortening: a cycle that used to run 28 days settles into 23, then 21, and nobody flags it because she's still bleeding on a roughly predictable schedule. A luteal phase of ten days or less is the clinical threshold for a luteal phase defect, and a shortening cycle is very often a shortening luteal phase in disguise: ovulation still happening, but the corpus luteum unable to sustain a full second half.

Just as often, the pattern runs the other way. Cycles stretch out and become unpredictable, skipping months before stopping altogether. Even well short of full amenorrhoea, sustained energy deficit is associated with a shortened luteal phase and reduced progesterone production, often long before a cycle stops arriving at all, and the same underlying calculation can show up as a system running faster and thinner, or as one slowing down and eventually stopping. Which direction a given body's cycle moves in seems to depend on where the load is landing most (how much is coming from restriction specifically, how much from stress, how much from inflammation), but the direction matters less than the fact of the change itself.

The point I want to make before anything else: "still bleeding" is not the same as "still ovulating properly," and a cycle doesn't need to disappear to be telling you something. It only needs to change.

The Calculation Underneath

I went into the mechanics of this in detail in the last piece, so I'll keep this part brief. The reproductive system is metabolically expensive to run, and the brain is constantly auditing whether it's currently worth funding. More than 95% of the neurons that release GnRH, the hormone that drives the entire reproductive cascade, carry AMPK, a fuel gauge that activates when cellular energy runs low, and when AMPK switches on, it suppresses the signalling that keeps that cascade firing in a steady rhythm.

There's a hard number attached to this, too. Below roughly 30 kilocalories of energy availability per kilogram of lean body mass per day, a threshold established in controlled research on regularly menstruating women, LH pulse frequency drops off and pulse amplitude increases. And the disruption is more pronounced in women who already run short luteal phases. Energy availability here means intake minus what's spent on exercise, not intake alone, which is why this shows up in women who are eating what looks like enough on paper but training hard, or carrying enough chronic stress that the body is effectively running the same shortfall as if the food weren't there.

This is a calculation, not a malfunction. The hypothalamus is reading the conditions and deciding whether this is a safe moment to spend resources on something as costly as reproduction. Functional hypothalamic amenorrhoea, where the cycle shuts down in response to inadequate energy, psychosocial stress, or the combination, is the best-documented clinical example of this calculation running to its conclusion. What I want to spend the rest of this piece on is everything that happens before a cycle gets anywhere near that endpoint, and why almost none of it gets read as part of the same story.

The Framework That Exists, If You're an Athlete

This calculation already has a name. It just doesn't reach most of the women living inside it.

In 2014, the International Olympic Committee's medical commission formally introduced Relative Energy Deficiency in Sport (RED-S), replacing the older Female Athlete Triad model with something broader: a syndrome, not a triad, in which low energy availability disrupts not just menstrual function but bone density, immunity, cardiovascular health, gastrointestinal function, and cognitive function, all off the same root cause. The framework was updated in 2018 and again in a substantially expanded 2023 consensus statement, which frames low energy availability as a spectrum from adaptable to genuinely problematic rather than a single cutoff, and sets out conceptual models for how it interacts with an individual's specific risk factors. Alongside it sits the RED-S Clinical Assessment Tool, a structured way for sports medicine clinicians to grade an athlete's risk and decide what happens next, itself updated in 2023 into a more nuanced four-level version.

I want to be precise about what's notable here, because it isn't the existence of a syndrome. It's that the syndrome has clinical infrastructure. RED-S has diagnostic criteria, a validated assessment tool, published management pathways, and a body of literature built specifically to support clinicians using them. A menstrual cycle that shortens, lengthens, or disappears gets read, systematically, as one data point inside a bigger physiological picture, rather than an isolated complaint managed on its own.

And the mechanism underneath RED-S isn't sport-specific. It's energy physiology: the same hypothalamic calculation, the same AMPK-linked fuel gauge, the same threshold Loucks and Thuma measured in sedentary women who had never competed in anything. RED-S gets diagnosed in athletes because sports medicine built a framework to catch it, not because the underlying biology only happens to people who train.

RED-L: The Same Physiology, Still Unnamed

Here's the hypothesis I want to put forward, and I want to be upfront that it is one. I think the physiology described by RED-S is operating in a much larger population of women who will never set foot in a sports medicine clinic. Women under chronic stress. Women undereating without identifying as restricting, because their intake looks reasonable and their weight hasn't obviously changed. Women in high-cognitive-load jobs or caregiving roles. Women in perimenopause. Women recovering from chronic illness, where the energy budget is already stretched thin by something else entirely.

I don't think there's currently a name for this population's version of the syndrome, so for now I'm calling it RED-L: Relative Energy Deficiency in Life. Same underlying calculation as RED-S. Same downstream cascade. Different population, defined not by sport but by the ordinary, unglamorous ways a modern life can run a chronic energy deficit without anyone, including the woman living it, recognising it as one.

I want to be honest that RED-L isn't a term with a consensus statement behind it, and I'm not presenting it as an established diagnosis. The closest existing clinical frame is functional hypothalamic amenorrhoea, and the Endocrine Society's own clinical practice guideline on FHA recognises exactly this picture: stress, weight change, or exercise, alone or combined, suppressing the hypothalamic-pituitary-gonadal axis in non-athletes as well as athletes. But FHA, as currently used in clinical practice, tends to get named only at the extreme end of the spectrum, once periods have stopped altogether. The subclinical version, the years of shortening and lengthening and lower fertility and worse PMS that happen before a cycle disappears, has no name and no referral pathway. RED-S doesn't reach these women because they don't fit its intake criteria. FHA doesn't reach them because they're still bleeding. They fall into the gap between two frameworks each built to catch a narrower slice of the same physiology.

From both myn personal and clinical experience, that gap has real clinical consequences, which is what the next two sections are about.

One Pattern, Three Diagnoses

Here's what I actually see in clinic, and it's the reason I think this gap matters more than a naming exercise. The same underlying load state (this is the phrase I keep coming back to: not a disease, a state the whole system is currently operating under) can express as a shortened luteal phase in one woman, adrenal-driven PMOS in another, unexplained infertility in a third, and heavy, painful, endometriosis-suspicious bleeding in a fourth. Compartmentalised medicine investigates each of these as its own condition, referred to a different specialist, worked up with a different panel, treated in isolation from the others.

This isn't a claim that endometriosis, PMOS, and luteal insufficiency are secretly the same disease. They aren't, and I'm not suggesting a unifying diagnosis where none exists. What I am pointing to is that these conditions already share more physiological ground than the separate referral pathways suggest. Luteal phase deficiency and PCOS/PMOS have been shown to share overlapping pathophysiology, including hyperinsulinaemia, excess AMH, and impaired angiogenesis in the developing corpus luteum, despite being treated as entirely independent disorders. If the diagnostic labels already overlap at the level of mechanism, it isn't a stretch to ask whether an upstream energy and stress load, sitting underneath several of them at once, ever gets investigated in any of the separate workups. In my experience, it usually doesn't, because none of the specialists a woman sees are looking upstream of their own specialty.

A woman with heavy, painful, irregular cycles might collect a gynaecology diagnosis, an endocrinology diagnosis, and a mental health diagnosis across three separate consultations, when a real chunk of what's driving all three sits in the same place: a body that has been calculating, for years, that it doesn't have enough spare energy to run reproduction cleanly.

When the Bleeding Is Removed and the Cause Isn't

I want to be careful here, because this section can easily read as a critique of a procedure rather than what I actually mean it as: a critique of a pathway.

Hysterectomy is a legitimate, sometimes essential, intervention. Severe endometriosis, adenomyosis, cancer, prolapse, and life-threatening haemorrhage are all real indications, and nothing here is an argument against the surgery itself. What concerns me is hysterectomy used as a first-line response to heavy or dysfunctional bleeding before anyone has investigated what's actually driving it.

Hysterectomy rates in Australia have fallen over the past decade, but the country's own safety and quality commission has been direct about what the remaining variation suggests: many women are still having hysterectomies for heavy menstrual bleeding rather than being offered the less invasive, conservative options first. The most common indications for benign hysterectomy remain prolapse, pain, and abnormal uterine bleeding, and the rate varies as much as sixfold between different regions of the country. That’s a spread that tracks practice patterns far more closely than it tracks any real difference in how much disease exists from one postcode to the next.

I see women in clinic after a hysterectomy who still carry almost everything they walked in with, minus the bleeding: the fatigue, the pain elsewhere in the body, the sleep that never settles, the anxiety that spikes premenstrually except there's no longer a premenstrual phase for it to spike around. The bleeding was the endpoint of the load, not its cause. Removing the organ that was expressing the signal doesn't touch whatever was generating it. When a cycle has been telling a RED-L story for years and nobody has read it, hysterectomy answers a question that was never actually asked.

What This Looked Like In My Own Body

I told the earlier chapters of my own story in the last piece: the heavy periods from adolescence, the eating disorder that took my cycle with it, the years in my twenties where restriction and adequate eating traded off and my cycle tracked the trade almost exactly.

The part I want to add here is what came after all of that had resolved on paper. In my late twenties and early thirties, I was eating consistently and exercising consistently, by any conventional measure doing everything right, and my period still nearly vanished: two or three times a year, while I ran a business under more sustained pressure than I'd registered as pressure at the time. Looking back at that stretch through this framework, I'd call it a clean case of RED-L. Nothing was wrong with my ovaries. My body was running a chronic energy deficit that had nothing to do with food and everything to do with a nervous system that never got to come off duty.

Closing the business didn't fix it immediately either, which is worth naming honestly. My cycle came back within weeks, but with the heaviest bleeding and worst pain of my life, because removing the external pressure hadn't automatically resolved the internal state my body had been running in for years. It took deliberate nervous system work, not a single hormone protocol, before things settled into something close to a textbook 28 days.

I’m not unique in my ability to recover from this either: over the last few years, I’ve worked with numerous female clients who have seen their periods go from non-existent to regular or from as short as 14 days to 26-28 days. I’m yet to meet a woman whose cycle doesn’t respond to correcting metabolic bottlenecks and lifestyle patterns that contribute to RED-L. This includes the clients I’ve worked with going through perimenopause.

What an Actual RED-L Workup Looks Like

If any of this sounds like your own history, here's what I think a proper investigation looks like, rather than the piecemeal version most women get.

Start with the cycle itself: length, pattern, and how both have changed over years, not just the last few months. Layer in a full functional hormone panel with cycle-day timing, which I've written about here, because the timing of the draw changes what the result can actually tell you. Add metabolic markers (fasting insulin, HOMA-IR, HbA1c, lipids, hs-CRP), a full thyroid panel, and core nutrient status: iron studies, vitamin D, B12, folate, zinc, and red cell magnesium. None of these are exotic tests. Most are simply never ordered together, or never read together.

I put together a bloodwork guide that walks through exactly this: when to test each marker in your cycle, what an optimal range looks like rather than just a technically normal one, and how to read the patterns in your own results.

Then add the two pieces standard testing skips entirely. The first is an honest look at energy availability specifically (intake relative to exercise expenditure and lean mass, not calorie counting for its own sake), because this is the number the hypothalamus is actually responding to. The second is basal body temperature (BBT) charted over two to three cycles, which shows the pattern a single blood draw can't: whether ovulation is happening at all, and whether the rise that follows it holds for long enough to mean anything.

Download my free BBT guide here

Recovery from a genuine RED-L state is slow, usually six to eighteen months once the actual constraints are addressed, and it isn't a hormone replacement story. It's a restoring-the-conditions story: enough energy, a nervous system that gets to come off duty sometimes, and enough time for a system that adapted intelligently to start recalculating.

The Signal Was Never The Problem

If your cycle has been shortening, lengthening, or disappearing, that's information, not a variation you can file away because you're still bleeding on some kind of schedule. If you've been told nothing's wrong because your labs came back "normal," the bleeding pattern is a symptom, not a diagnosis in itself. And if you've been handed a hysterectomy referral for heavy or dysfunctional bleeding without anyone investigating the load underneath it, you're allowed to ask for that investigation before you consent to a definitive surgery.

Your body has been calculating this the whole time. It's never too late to learn to read what it's been telling you.

If you'd like a proper look at what's actually driving your cycle, I work with women one-on-one to look at the whole picture: hormones, nutrient status, gut health, and the nervous system underneath all of it, rather than any one piece in isolation.