Menopause Brain Fog is an Energy Problem
The brain fog that starts in late perimenopause — losing words, forgetting why you walked into a room, reading the same line three times — has a specific, physical cause: the brain running short of the energy it needs for you to think clearly. Here is how that happens, and what changes it.

By Sandra Ishkanes, Functional Medicine Practitioner, specialising in perimenopause and menopause. I hold a BSc in Molecular Biology from King’s College London, MA in Social Anthropology from SOAS, trained in nutritional therapy and functional medicine at the Institute of Optimum Nutrition, and I am a registered member of the Association of Naturopathic Practitioners (ANP).
You reach for a word you use all the time, and it is gone. You walk into a room and cannot remember why. You read the same paragraph three times and none of it stays. For many women this starts in their forties, and it is one of the most distressing parts of the menopause transition.
There is a specific, physical reason for it. Menopause brain fog is a fuel problem: the brain is short of the energy it needs to think clearly. This is how that happens — and what changes it.
Your brain uses a lot of energy
The brain is about 2% of your body weight, and it uses 20 to 25% of your energy — most of it spent sending the electrical signals between nerve cells. It runs at that rate all day, even while you sleep.
An organ that hungry depends completely on its fuel supply.
Your brain can run on two fuels
The brain can run on two different fuels. One is glucose — the sugar that comes from carbohydrates: bread, pasta, rice, fruit, anything sweet. The other is ketones, which the liver makes from fat when carbohydrates are low.
A body that moves easily between the two keeps the brain fed whether you have just eaten or not. That ability to switch has a name — metabolic flexibility.
Oestrogen keeps the fuel system running
Oestrogen does two specific jobs in this system. It helps glucose get into brain cells, through carrier proteins called GLUT transporters. And it keeps the machinery that turns fat into ketones in good working order. It also keeps the mitochondria — the parts of each cell that produce energy — working efficiently.
While oestrogen is steady, all of this runs in the background without you noticing.
Perimenopause triggers a fuel change
As menopause approaches, oestrogen falls, and the system it was running changes with it.
The glucose side winds down: fewer GLUT transporters, less of the machinery that burns sugar, and mitochondria that work less efficiently. At the same time, the brain is set up to lean more on ketones. It is meant to shift toward running on ketones instead of glucose. This is a normal, built-in change.
You can see it on brain scans. Across the menopause transition, the amount of glucose the brain uses falls — highest before menopause, lower through perimenopause, lowest after — in the same regions involved in Alzheimer’s, along with a measurable drop in mitochondrial activity [4, 8].
Ketones are only made when insulin is low
There is a catch in how ketones are made.
Ketones are produced in the liver, from fat. When carbohydrates are low, fat is released from your fat stores into the blood, the liver takes it up and breaks it down, and turns it into ketones that feed the brain. Every step depends on one thing: insulin being low.
Insulin is the signal that sugar is available. While insulin is high, it does two things — it keeps fat locked in storage, and it stops the liver making ketones.
High insulin leaves the brain short — and that is the fog
Whether your insulin runs high depends mostly on how you eat. A diet high in refined carbohydrates and sugar, with frequent snacking, keeps insulin up through the day. A lower-carbohydrate way of eating keeps it low. (Oestrogen also influences insulin sensitivity, but diet is the larger factor, and the one you can change.)
So when the brain’s glucose system winds down at menopause and the brain turns to ketones, the ketones may not be there. Insulin is high, fat stays locked away, the liver cannot make ketones, and nothing comes down the line.
That shortfall is brain fog: nerve cells trying to work without enough fuel. Glucose is not getting in as easily as it did, and ketones are not being made to take its place. The brain is caught between two fuels, with too little of either.
A brain short of fuel starts using its own myelin
When the brain runs short of fuel and none is coming, it looks closer to home.
In animal studies, the ageing female brain starts breaking down its own myelin — the fatty coating around nerve fibres that lets signals travel quickly — and turns it into ketones on the spot. In those studies, ketone levels rose inside the brain while falling in the blood: the brain making fuel out of its own wiring. Whether it happens the same way in women is not yet known [7].
When myelin is damaged, signals slow and misfire. On an MRI this can show up as white-matter changes. These become more common through the menopause transition, and other factors — including blood-vessel health — contribute too [9, 10, 11, 12]. This is why acting early matters, while the system is still easy to shift.
Brain fog rarely comes alone
Brain fog usually arrives with other symptoms, and they share a cause. Hot flushes, broken sleep, and low mood come from the same energy shortfall showing up in different parts of the brain:
- the hypothalamus feels it as an unstable thermostat → hot flushes
- the cortex feels it as slowed thinking → brain fog
- the limbic system feels it as unsteady mood → anxiety and low mood
- the stress axis feels it as raised night-time cortisol → broken sleep
Because they share a root, working on that root tends to ease the whole group together, rather than one symptom at a time [13, 14, 15, 16].
Why cutting carbohydrates may not be enough
Lowering insulin so the brain can use ketones addresses the glucose side. For many women that is most of it. There is a second part.
The shift to ketones is never complete. The brain does not run purely on fat — ketones add to glucose, they do not fully replace it, and a large part of the brain still runs on glucose. So the brain still has to get glucose into its cells. And that step needs oestradiol: it maintains the GLUT transporters that carry glucose in [6]. Even with ketones available, if oestradiol is low, glucose uptake stays low, and part of the fog stays with it.
So once the ovaries have wound down, where does the brain get oestradiol? It makes its own, through a process called intracrinology. It starts with DHEA, made in the adrenal glands and released into the blood. Tissues around the body take up DHEA and convert it into testosterone, estrone, and other steroid hormones. The brain then takes up testosterone and converts it to oestradiol using the enzyme aromatase [17], and takes up estrone and converts it to oestradiol using the enzyme 17β-HSD [18].
Testosterone is not only a stepping stone to oestradiol, though. The brain carries receptors for it, and testosterone is thought to support memory and concentration directly. So the DHEA the brain draws on feeds two things the thinking brain uses: the oestradiol that lets glucose in, and the testosterone that acts on the brain itself. When adrenal DHEA runs low, both fall together — and while the evidence linking testosterone to cognition in women is still limited [20], it means part of the fog can sit on the androgen side, which topping up glucose alone will not reach.
So the brain’s ability to top up its own oestradiol rests on the adrenal glands producing DHEA well. Where adrenal output is low — after long periods of chronic stress, broken sleep, and high cortisol demand — there is less raw material to work with, and cutting carbohydrates does not replace it.
Two things support this: a steady supply of DHEA from the adrenal glands, and the raw materials the conversion enzymes need to work. Aromatase is an iron-dependent enzyme, built around an iron core, and it runs on energy delivered by cofactors the body makes from the B vitamins; the step that turns estrone into oestradiol depends on the same kind of cofactors. So the foundations the fuel side already needs — the B vitamins, magnesium, and iron — also support the brain in making its own oestrogen.
This is where heavy perimenopausal bleeding enters the picture. Months of heavy periods drain iron, and iron sits at the centre of two things the brain depends on: the machinery that produces energy inside every cell, and the aromatase enzyme that makes the brain’s own oestradiol. Low iron can work against clear thinking on both fronts, and it is one of the most common and most overlooked findings at this age. (Covered in more depth in Heavy Bleeding in Perimenopause →.)
There are two supply lines, then: the fuel side (insulin and the ketone switch) and the hormonal side (adrenal DHEA feeding the brain’s own oestradiol, which lets glucose in). A low-carbohydrate diet moves the first. It can leave the second where it was. (The steps in this pathway are well established; how much each one contributes to brain fog is still being researched.)
What deepens the fog, and what lifts it
A handful of factors decide how deep the shortfall goes, and each one runs both ways.
- Carbohydrate load — the main one. A diet high in refined carbohydrates and sugar keeps insulin up and the ketone supply shut off; heavy fog after a carb-heavy meal is that shortfall in real time. Bringing refined carbohydrates and sugar down — with enough protein and quality fat at each meal — lets insulin fall and steadies blood sugar between meals.
- Sleep. Broken sleep raises cortisol, which raises blood sugar, which raises insulin — keeping the fat door shut. This is one reason fog is often worst after a poor night.
- Stress. The same cortisol–sugar–insulin loop, running through the day. Calming the stress system takes load off the fuel switch.
- Adrenal reserve. Once the ovaries have wound down, the brain builds its own oestrogen — and its testosterone — from a raw material made by the adrenal glands. Protecting sleep and easing the pressure is what keeps it topped up.
- Thyroid. An underactive thyroid slows the whole metabolic rate. If fog is severe and does not shift with diet, thyroid function is worth checking with a full panel, not TSH alone.
- Nutrients. An iron panel can show whether iron is low — worth checking, given how common it is at this stage. Magnesium and the B vitamins are needed for the enzymes that produce and use energy, and when they are low, even a good change of diet gives a smaller response.
Work with me
This is the work I do — finding the specific reason a woman’s brain fuel supply has faltered, and rebuilding it, step by step. In my clinic, brain fog usually clears within about eight weeks, because the work covers both lines at once — steadying the fuel side and supporting the adrenal and hormonal side together.
If brain fog is the symptom worrying you most, that is where we begin.
The discovery call is free, thirty minutes, no obligation.
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FAQ’s
Is menopause brain fog permanent?
Usually not. It tends to improve when the drivers behind it — the fuel side and the hormonal side — are addressed, and research shows that cognition tends to recover after the transition. It is a stage, not a fixed state.
Could my brain fog be early dementia?
This is the fear many women bring, and it is understandable, because the brain changes of menopause share some scan features with early Alzheimer’s — which is why researchers have looked closely at the link. But menopause brain fog is a functional state driven by the fuel shortfall, and it responds to metabolic and hormonal change. If cognitive symptoms are severe, getting worse quickly, or come with other neurological signs, see your GP.
Does HRT help brain fog?
For some women, partly. Oestrogen supports glucose getting into the brain, so extending it can ease some of the fuel shortfall. But HRT does not lower insulin, start the ketone switch, or restore the testosterone side, so brain fog can persist on HRT when those have not been addressed.
Do I need to cut out carbohydrates completely?
No. The aim is to bring insulin down far enough for the ketone switch to work, not to remove all carbohydrates. For most women, a real reduction in refined carbohydrates and sugar, with enough protein and quality fat, is what matters. The right approach is individual.
References
- Epperson CN, Sammel MD, Freeman EW. Menopause effects on verbal memory: findings from a longitudinal community cohort. J Clin Endocrinol Metab. 2013;98(9):3829–3838. doi:10.1210/jc.2013-1808. See also Greendale GA, et al. Am J Epidemiol. 2010;171(11):1214–1224.
- Brinton RD. The healthy cell bias of estrogen action: mitochondrial bioenergetics and neurological implications. Trends Neurosci. 2008;31(10):529–537. doi:10.1016/j.tins.2008.07.003
- Mergenthaler P, Lindauer U, Dienel GA, Meisel A. Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends Neurosci. 2013;36(10):587–597. doi:10.1016/j.tins.2013.07.001
- Mosconi L, Berti V, Dyke J, et al. Menopause impacts human brain structure, connectivity, energy metabolism, and amyloid-beta deposition. Sci Rep. 2021;11:10867. doi:10.1038/s41598-021-90084-y — 161 women across the transition; brain metabolic markers stabilised and grey matter recovered post-menopause, correlating with preserved cognition.
- Cunnane SC, et al. Can ketones compensate for deteriorating brain glucose uptake during aging? Ann N Y Acad Sci. 2016;1367(1):12–20. doi:10.1111/nyas.12999
- Mauvais-Jarvis F, Clegg DJ, Hevener AL. The role of estrogens in control of energy balance and glucose homeostasis. Endocr Rev. 2013;34(3):309–338. doi:10.1210/er.2012-1055
- Klosinski LP, Yao J, Yin F, et al. White matter lipids as a ketogenic fuel supply in aging female brain. EBioMedicine. 2015;2(12):1888–1904. doi:10.1016/j.ebiom.2015.11.002 — animal model: myelin lipids are broken down to make ketones locally; not yet shown in women.
- Mosconi L, Berti V, Quinn C, et al. Perimenopause and emergence of an Alzheimer’s bioenergetic phenotype in brain and periphery. PLoS One. 2017;12(10):e0185926. doi:10.1371/journal.pone.0185926 — FDG-PET in 43 women; reduced brain glucose metabolism and mitochondrial activity, worsening across the transition.
- Tari AR, et al. Cardiometabolic health across menopausal years and white matter hyperintensities. Front Glob Womens Health. 2024. PMC10783171
- Guo W, et al. Menopause status, brain perfusion, white matter hyperintensities and cerebral blood flow. Stroke. 2024. doi:10.1161/STROKEAHA.123.044841
- Thurston RC, et al. Menopausal hot flashes and white matter hyperintensities. Menopause. 2016;23(1):1–7. doi:10.1097/GME.0000000000000530
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- Aras SG, Grant AD, Konhilas JP. Clustering of >145,000 symptom logs reveals distinct pre, peri, and menopausal phenotypes. Sci Rep. 2025;15:640. doi:10.1038/s41598-024-84208-3
- Zouabi A, et al. Advances in understanding of cognitive symptoms during menopause. Lancet Reg Health — Womens Health. 2026. doi:10.1016/S3050-5038(26)00043-9
- Maki PM, Jaff NG. Brain fog in menopause: a guide for decision-making and counselling on cognition. Climacteric. 2022;25(6):570–578. doi:10.1080/13697137.2022.2122792
- Lang MJ, et al. Menopause-related brain fog as a midlife window in women’s brain aging. Front Hum Neurosci. 2026. doi:10.3389/fnhum.2026.1814092
- Azcoitia I, Yague JG, Garcia-Segura LM. Aromatase in the human brain. Neuroscience. 2011;191:139–147; and Bixo M, et al. J Steroid Biochem Mol Biol. 1995;55:297–303 (PMID 8541226) — human brain converts testosterone/androstenedione to oestradiol locally.
- Steckelbroeck S, et al. Estrogenic 17β-hydroxysteroid dehydrogenase (17β-HSD) activity in the human brain. J Steroid Biochem Mol Biol. 2003;86(1):79–92. PMID 12943747 — human brain interconverts estrone and oestradiol.
- Labrie F, et al. Intracrinology: DHEA-metabolising enzymes in human physiology. — after menopause, circulating androgens and estrone are made in peripheral tissues from adrenal DHEA. See also Lasley BL, et al. Menopause. 2012, PMID 22415563 (SWAN: DHEA-S and androgens rise across the transition).
- Davis SR, Baber R, Panay N, et al. Global Consensus Position Statement on the Use of Testosterone Therapy for Women. J Clin Endocrinol Metab. 2019;104(10):4660–4666. PMID 31498871 — testosterone is a biologically active hormone in women with actions in the brain; evidence for testosterone therapy improving cognition is rated insufficient (not negative), and the panel called for adequately powered trials.