Why You Have Hot Flushes — and How to Calm Them

A wave of heat rises through your chest and face. Your skin prickles and dampens. Your heart picks up. Half a minute later it passes, and leaves you flushed, clammy, and thrown off for the rest of the day. At night it wakes you — damp sheets, a racing heart, sleep gone.

Hot flushes are the most familiar sign of menopause, and often the most dismissed: because of falling oestrogen, to be handled with HRT or waited out. But falling oestrogen is only half the story.

Not every woman gets hot flushes

If hot flushes were simply the result of falling oestrogen, every woman going through menopause would have them. They do not. Some barely notice the transition; others are floored by it — and that difference is the clue to what is really going on.

The sharpest evidence comes from a study of rural Mayan women in the Yucatán. Researchers measured their hormones directly: the women were as oestrogen-deprived as women in the United States or Europe — low oestradiol, high FSH, the same hormonal picture — yet reported essentially no hot flushes. The authors concluded plainly that the difference was not in the women’s endocrinology; the hormone fall was identical [1]. Something in their diet and way of life meant the same hormonal change produced almost no symptoms. Women who later moved to the towns were reported to begin having flushes.

So the question is not whether oestrogen is falling, but what condition the brain is in, when it falls.

What the research shows: insulin and the brain’s fuel

That state is largely metabolic and it’s clearest marker is insulin.

In a 2026 analysis of more than 700 women in the long-running SWAN study, those with higher insulin in early perimenopause went on to have hot flushes that started earlier and lasted longer — and this held independently of body weight [2]. Insulin, the hormone that manages blood sugar, was one of the earliest signals of who would struggle.

The reason runs through how the brain is fuelled. The brain can burn two fuels: glucose, from carbohydrates, and ketones, which the liver makes from body fat. Oestrogen runs the glucose side — it raises the GLUT transporters that carry glucose across into brain cells, and keeps the mitochondria that burn it working efficiently [9]. As oestrogen falls, that glucose system winds down, and brain scans show it directly: glucose use drops measurably across the menopausal transition, in the same regions each time [10]. The brain is built to make up the shortfall by turning to its second fuel, ketones.

But ketones are only made when insulin is low. Insulin is the signal that sugar is available; while it stays high — kept up by a diet of frequent bread, pasta, rice, sugar and processed food, and by insulin resistance, where the body’s cells respond less to insulin so it has to make more to do the same job — the liver cannot make ketones. High insulin itself also pushes up the stress hormones ACTH and cortisol, independently of blood sugar [11]. This transition has a name — the Energy Shift: the brain moving from running fully on glucose to depending, in part, on ketones. It is a normal, built-in change, and set out in full on The Energy Shift →. The trouble comes when the Shift is blocked. High insulin holds the ketone side shut, so the brain cannot complete the move — the glucose system has wound down, the ketone system will not open, and the brain is left short of steady fuel, caught between the two. That block is the state the Mayan diet avoided, and the state that higher insulin creates.

How a flush is made: the thermostat and the neurons that run it

Deep in the brain, the hypothalamus holds your core temperature inside a narrow band — an internal thermostat. Slightly too warm, and it opens the skin’s blood vessels and starts a light sweat to shed heat; slightly too cool, and it conserves. The width of that comfortable band has a name — the thermoneutral zone — and most of the time small changes in warmth stay inside it, unnoticed.

The zone is set by a cluster of cells in the hypothalamus called KNDy neurons, named for the three messengers they carry: kisspeptin, neurokinin B, and dynorphin. Two of these drive the neurons’ activity up — kisspeptin and neurokinin B — and one holds it back: dynorphin, the internal brake. The balance between them sets how hard the neurons fire. They pass that signal on, chiefly through neurokinin B, to the brain’s temperature-control hub, the median preoptic area, which sets how wide the thermoneutral zone sits and triggers heat-shedding — opening the skin’s blood vessels — when its upper edge is crossed.

Oestrogen keeps the system calm. KNDy neurons carry the oestrogen receptor (ERα), and oestrogen acts on it as a brake, restraining how much kisspeptin and neurokinin B the neurons produce. So while oestrogen is present, the neurons stay quiet, the thermoneutral zone stays wide, and ordinary warmth passes unnoticed.

As oestrogen falls, that brake lifts. In the menopausal hypothalamus these neurons enlarge, raise their kisspeptin and neurokinin B, and make less of their own dynorphin — more accelerator, less brake — so their neurokinin B signal to the preoptic area climbs. This primes the brain for hot flushes.

But priming is not the same as firing. On its own, oestrogen withdrawal would predict that every woman flushes as her oestrogen falls, and flushes equally. They do not. The brake lifts for all of them; whether the primed system then tips into a flush, and how hard, varies far more than the hormone change alone can account for. That difference — the part the oestrogen-only account leaves out — is set by the rest of what these neurons read.

KNDy neurons are not only temperature controllers. They sit in the arcuate nucleus, the hypothalamus’s metabolic control room, and they carry the receptors to read the body’s fuel and stress state alongside its hormones: receptors for insulin and leptin, the signals of fuel and appetite, and for cortisol and its trigger CRH, the signals of stress. The same arcuate KNDy neurons that set temperature have been shown to also carry oestrogen’s effect on body weight and energy balance [6], and to carry glucocorticoid and CRH receptors directly [7]. These are cells built to read three things at once: oestrogen, fuel, and stress.

While oestrogen is present, it is the loudest of the three, and it holds the neurons steady regardless of the rest. When it withdraws, that dominant signal is gone — and the neurons are left governed by the inputs that remain, fuel and stress, which oestrogen had been overriding. The metabolic and stress state now does its work by two routes. Directly: the low-fuel signal of a brain short on glucose and blocked from making ketones, and the high-cortisol signal of a loaded stress system, act on the receptors these neurons carry. And through the flush itself: the heat-shedding response is carried out by the sympathetic “fight-or-flight” system — the same system cortisol and adrenaline drive — so a body already running high on stress hormones keeps that response primed, lowering the threshold at which it goes off. Cortisol then feeds back onto the fuel side, raising blood sugar and insulin and deepening the shortage. Fuel and stress are not two separate problems here; they are one self-reinforcing loop.

Push the primed neurons hard enough, by either route, and their neurokinin B tips the thermoneutral zone past its edge: the heat-shedding response fires, skin vessels open, heat rushes to the surface, sweat breaks, and the heart picks up. That is the flush — the thermostat working exactly as built, inside a zone that has narrowed.

What makes hot flushes worse

Nowadays, the menopausal shift rarely arrives in a well-resourced body. Many women reach it already carrying years of load that keeps insulin and cortisol high — the very signals that push the primed thermostat toward firing:

• decades of blood sugar instability on a high-carbohydrate diet
• chronic stress, sustained through demanding work, caregiving, and compressed lives
• sleep already broken before menopause began
• too little protein, and a reliance on quick carbohydrates
• gut problems built up over years of poor diet or antibiotics
• low-grade inflammation from processed food, too little omega-3, low vitamin D
• a stress system already running close to its limit

By the time the brain begins its shift, it is working in a far more depleted setting than the one the shift was built for. That is what makes the shift so symptomatic: the biology is doing exactly what it is designed to do, but it is meeting a body pushed to the edge of its metabolic reserves. And day to day, the same factors turn the dial — a high-sugar meal, several strong coffees, a stressful week, a run of broken nights all raise insulin and cortisol and lower the threshold the thermostat fires at.

It is the flip side of the Mayan finding: a steady, low-sugar diet and an active life kept those reserves intact, so the same hormone fall passed through without tipping the thermostat into flushing.

Hot flushes rarely travel alone

Hot flushes are the most visible sign of this, but they seldom come by themselves. Night sweats, disturbed sleep, anxiety, heart palpitations, brain fog, low mood, and fatigue tend to arrive together — and large symptom-tracking studies show they cluster in consistent patterns rather than at random [3, 4]. They travel together because they share a root: one metabolic transition showing up in different systems. Address the root, and the group tends to ease together rather than one symptom at a time.

What HRT and the new drugs do

HRT relieves hot flushes for many women, and that relief is real. By restoring oestrogen, it steadies the KNDy neurons and widens the thermoneutral zone again, so the thermostat settles. What it does not do is change the metabolic factors underneath — the insulin, the fuel supply, the cortisol load — which is why flushes can return when it is stopped. Whether HRT is right is an individual decision, made with your own doctor, weighing your history and what matters to you.

The newest non-hormonal prescription drug works further downstream: it blocks neurokinin B at the thermostat itself. Veozah (fezolinetant), approved by NICE in March 2026, reduces hot flushes by approximately 2.5 events per day above placebo (SKYLIGHT 1 and 2 trials, ICER review 2023). The published threshold for an effect a woman would actually notice is 3.57 events per day. Veozah falls short of clinical significance by its own field’s standards. The FDA added a warning about rare serious liver injury in September 2024. The drug blocks the KNDy neuron pathway rather than resolving the underlying fuel deficit — it mutes the alarm without fixing the fire.

Veozah takes twelve weeks to bring daily hot flushes down by about 2.5 over placebo, and even then leaves most women still flushing. Working on the drivers underneath — the fuel supply and the stress load — most women I see get their hot flushes down to none, or close to it, within about four weeks.

What calms hot flushes

The work is to lift the load the thermostat is reading: bring insulin down by cutting refined carbohydrates and sugar, with enough protein and quality fat to steady blood sugar between meals; take the pressure off cortisol through stress, caffeine and sleep; and correct what a blood panel shows is missing — B12, folate, vitamin D, an underactive thyroid — while supporting the gut that has to absorb it all. Reverse enough of the load and the primed thermostat settles.

The nutritional framework I use in clinic — MenoKeto — is built around lowering insulin while keeping protein and nutrients high, and is adjusted to each woman’s own picture and tolerances. It is not permanent restriction: once the system is steady, many women reintroduce carbohydrates to their own tolerance.

What this looks like in practice

Worked this way — lowering the metabolic load and steadying the stress side together — most women I see have their flushes fall substantially, often within the first few weeks, with the remaining flushes becoming shorter and milder. One woman, after weeks of daily flushes, described what was left as “more like a warmth in the chest” than the old adrenaline surge. The pace varies with how much stress, caffeine and sleep disruption are working against it, and what a blood panel turns up — which is why the approach is built around the individual rather than a fixed plan.

Work with me

This is the work I do — finding the specific reasons your hot flushes are firing, and bringing them down, step by step. If they are disrupting your sleep, your work, and your days, that is where we start.

The discovery call is free, thirty minutes, no obligation. We go through your symptoms, your history, and what you have already tried, and you leave with a clear picture of what is driving your flushes and what the first steps look like — whether you work with me or not.

Book a discovery call →

References

References

1. Martin MC, Block JE, Sanchez SD, Arnaud CD, Beyene Y. Menopause without symptoms: the endocrinology of menopause among rural Mayan Indians. Am J Obstet Gynecol. 1993;168(6):1839–1845. (Postmenopausal Mayan women were oestrogen-deprived — low oestradiol/oestrone, high FSH — yet reported no hot flushes; authors conclude the absence of symptoms is not attributable to a difference in endocrinology.)
2. Athar F, Gregory S, Houston EJ, Templeman NM. Insulin levels early in perimenopause inform vasomotor symptom incidence across the menopausal transition. J Clin Endocrinol Metab. 2026. doi:10.1210/clinem/dgaf699. (SWAN analysis, 704 women; higher fasting insulin at age 47 predicted earlier onset and longer duration of hot flashes/night sweats, independent of BMI — an association, not a demonstrated causal mechanism.)
3. Aras SG, Grant AD, Konhilas JP. Clustering of symptom logs reveals distinct pre, peri, and menopausal phenotypes. Sci Rep. 2025;15:640. doi:10.1038/s41598-024-84208-3. (Menopause symptoms cluster in consistent patterns; hot flushes co-occur with sleep disruption, mood change and cognitive symptoms.)
4. Harlow SD, et al. The Study of Women’s Health Across the Nation (SWAN). Menopause. (Longitudinal cohort; vasomotor, sleep and mood symptoms track together, supporting shared underlying mechanisms.)
5. Lederman S, et al. Fezolinetant for treatment of moderate-to-severe vasomotor symptoms associated with menopause (SKYLIGHT 1): a phase 3 randomised controlled trial. Lancet. 2023;401:1091–1102. FDA approval May 2023; boxed warning for rare serious liver injury added 2024. (NK3-receptor antagonism reduced hot flushes by ~2/day vs placebo, meeting the accepted clinical threshold — and validates the KNDy/neurokinin B mechanism of the flush.)
6. Mittelman-Smith MA, Williams H, Krajewski-Hall SJ, McMullen NT, Rance NE. Arcuate kisspeptin/neurokinin B/dynorphin (KNDy) neurons mediate the estrogen suppression of gonadotropin secretion and body weight. Endocrinology. 2012;153(6):2800–2812. doi:10.1210/en.2012-1045. (The same arcuate KNDy neurons that control temperature also mediate oestrogen’s effects on energy balance and body weight — the anatomical basis for these neurons integrating oestrogen and fuel status. Animal model.)
7. Takumi K, Iijima N, Higo S, Ozawa H. Immunohistochemical colocalization of corticotropin-releasing hormone receptor and glucocorticoid receptor in kisspeptin neurons in the hypothalamus of female rats. Neurosci Lett. 2012. PMID 23069671. See also Thorson JF, Prezotto LD. Front Physiol. 2024;15:1372944 — KNDy neurons express metabolic receptors (leptin, insulin, IGF-1) and act as metabolic sensors. (KNDy/kisspeptin neurons carry receptors for stress signals (CRH, glucocorticoids) and metabolic signals — the machinery for fuel and stress to act on these cells. Largely animal data; the thermoregulatory application is a model.)
8. Rance NE, Dacks PA, Mittelman-Smith MA, Romanovsky AA, Krajewski-Hall SJ. Modulation of body temperature and LH secretion by hypothalamic KNDy neurons: a novel hypothesis on the mechanism of hot flushes. Front Neuroendocrinol. 2013;34:211–227. (Establishes the KNDy/neurokinin B thermoregulatory mechanism of hot flushes.)
9. Brinton RD, Yao J, Yin F, Mack WJ, Cadenas E. Perimenopause as a neurological transition state. Nat Rev Endocrinol. 2015;11(7):393–405. doi:10.1038/nrendo.2015.82. (Oestrogen regulates brain glucose transporters and mitochondrial function; its withdrawal initiates a shift in brain fuel use from glucose toward ketones.)
10. Mosconi L, et al. Perimenopause and emergence of an Alzheimer’s bioenergetic phenotype in brain and periphery. PLoS One. 2017;12(10):e0185926. (FDG-PET: reduced cerebral glucose metabolism across the menopausal transition.)
11. Fruehwald-Schultes B, et al. Hyperinsulinemia, but not hypoglycemia, acutely increases hypothalamic-pituitary-adrenal axis activity in humans. J Clin Endocrinol Metab. 1999. (Experimental hyperinsulinaemia raises ACTH and cortisol independently of blood glucose.)
12. Mittelman-Smith MA, Williams H, Krajewski-Hall SJ, Lai J, Ciofi P, McMullen NT, Rance NE. Role for kisspeptin/neurokinin B/dynorphin (KNDy) neurons in cutaneous vasodilatation and the estrogen modulation of body temperature. Proc Natl Acad Sci USA. 2012;109(48):19846–19851. doi:10.1073/pnas.1211517109. (Ablating KNDy neurons reduced tail-skin temperature — direct evidence that these neurons drive the cutaneous vasodilation of a flush; with the postmenopausal hypertrophy, increased kisspeptin/NKB and reduced dynorphin gene expression driven by oestrogen withdrawal.)