Why does body composition change during perimenopause?

Why Does Body Composition Change During Perimenopause?

For many women, the first sign that their body composition is beginning to change during perimenopause is not necessarily a dramatic change on the scales. Often, it is something much more subtle. A pair of jeans that has always fitted comfortably begins to feel a little tighter around the waist. Muscle that once seemed relatively easy to maintain feels as though it requires more attention. Or perhaps the number on the scales has barely changed at all, yet the familiar shape and feel of the body somehow seems different.

It can be confusing, particularly when there has been no obvious change in the way someone is eating or exercising. And because these changes tend to arrive during the same years that menstrual cycles begin to change, they are often gathered together under the familiar description of “menopausal weight gain.” Yet body weight is only one part of what is happening. Across the menopausal transition, women can experience changes in fat mass, lean tissue and, importantly, where fat is being stored, meaning that the scales may tell only a small part of the story (Greendale et al., 2019; Marlatt et al., 2022).

To understand why, we need to look beyond weight itself and begin with the hormonal transition taking place underneath it.

Perimenopause begins as a change in reproductive function, but the hormones involved have never worked exclusively within the reproductive system. Oestrogen, in particular, has effects throughout the body. It influences adipose tissue and the way fat is stored and mobilised, contributes to the maintenance and function of skeletal muscle, and is involved in aspects of glucose and lipid metabolism. So, as ovarian hormone production begins to change, it makes sense that the consequences of that change can eventually be felt well beyond the menstrual cycle (Motlani et al., 2023; Lobato et al., 2026).

There is another part of this story that is worth keeping in mind. Perimenopause arrives during midlife, which means the hormonal transition is unfolding against a background of ageing that would have been occurring regardless. Muscle mass and energy requirements can change with age. Sleep and movement may change. Metabolic and cardiovascular risk can change too. Ovarian ageing and chronological ageing are therefore occurring alongside one another, sometimes influencing the same tissues and outcomes, but not necessarily contributing to them in exactly the same way (Greendale et al., 2019; Marlatt et al., 2022).

This is part of what makes body-composition changes during perimenopause more intricate than the familiar explanation that “oestrogen falls and women gain weight.” Oestrogen does eventually decline, but even that is not a smooth or particularly orderly process.

It begins with changing ovarian hormones

When we think about menopause, it is easy to imagine oestrogen gradually falling until menstrual periods eventually stop. Perimenopause rarely behaves quite so neatly. Long before the ovaries stop producing meaningful amounts of oestradiol, the hormonal conversation between the ovaries and the brain has already begun to change, and for several years that conversation can become increasingly variable from one cycle to the next (Motlani et al., 2023; Lobato et al., 2026).

At the centre of this transition is the gradual decline in the ovarian follicle pool. Developing follicles produce inhibin B, which normally provides part of the negative feedback that helps regulate follicle-stimulating hormone, or FSH. As fewer follicles remain and inhibin B begins to decline, some of that feedback is lost. In response, FSH rises and becomes more variable as the pituitary works harder to stimulate the remaining follicles (Motlani et al., 2023; Lobato et al., 2026).

But the ovaries have not stopped responding. At least not yet.

While responsive follicles remain, some cycles can still produce quite substantial amounts of oestradiol. In one cycle, oestradiol exposure may be relatively high; in another, considerably lower. This is why thinking about early perimenopause simply as a state of “low oestrogen” can be misleading. What often best characterises these years is variability. Follicular development becomes less predictable, the amount of oestradiol produced can vary considerably between cycles, and cycles that once followed a relatively familiar pattern can begin to look quite different from one month to the next. Ovulation may still occur, but it becomes progressively less consistent as the transition continues (Motlani et al., 2023; Lobato et al., 2026).

Progesterone changes as part of this same process, because ovarian progesterone production is closely tied to ovulation. After an egg is released, the follicle that has released it becomes the corpus luteum, which produces progesterone during the luteal phase of the cycle. If ovulation does not occur, that normal post-ovulatory rise in progesterone does not occur in the same way. As ovulation becomes less predictable and anovulatory cycles become more common through the menopausal transition, progesterone exposure can therefore become lower and increasingly inconsistent from one cycle to another (Motlani et al., 2023; Lobato et al., 2026).

Eventually, the remaining ovarian follicles become less able to respond to the increasing stimulation from FSH, and oestradiol production becomes more persistently reduced. Normally, ovarian hormones provide feedback to the hypothalamus and pituitary, helping to regulate how much FSH is released. As ovarian oestradiol and inhibin production decline, considerably less of that negative feedback is returning to the brain. The pituitary continues to release FSH in an attempt to stimulate ovaries that are now much less responsive, which is why FSH remains elevated as a woman passes through her final menstrual period and into postmenopause (Motlani et al., 2023; Lobato et al., 2026).

There is another change occurring within this hormonal landscape that becomes particularly relevant when we begin thinking about body composition. Oestrogen and androgens do not change in parallel across the menopausal transition. The reduction in oestradiol is considerably greater than the corresponding change in circulating androgens, which alters the relative balance between oestrogenic and androgenic signalling. The result is what is often described as a relatively more androgenic hormonal environment. This does not necessarily mean that a woman suddenly begins producing more androgens; rather, their influence is now occurring against a background of substantially lower oestrogen exposure (Motlani et al., 2023; Palacios et al., 2024).

Why does this relative change between oestrogen and androgens matter when we are talking about menopausal body composition?

Because sex hormones are one of the influences on where adipose tissue tends to be deposited. During the reproductive years, women typically carry a greater proportion of subcutaneous fat around the hips, thighs and buttocks, a gluteofemoral pattern of fat storage that is, at least in part, driven by the more oestrogenic premenopausal sex-hormone environment. As ovarian oestradiol production declines and the relative balance shifts towards greater androgenicity, this pattern of adipose deposition can begin to change. Fat storage increasingly shifts away from the predominantly gluteofemoral pattern and towards greater central and visceral deposition around the abdomen (Motlani et al., 2023; Palacios et al., 2024).

The relative hormonal balance is only part of the explanation, however, because oestrogen also acts directly within the tissues whose behaviour is changing.

Oestrogen does not only act on the ovaries. Oestrogen receptors are distributed throughout the body, including within adipose tissue and skeletal muscle. During the reproductive years, these tissues have therefore been responding to oestrogen signalling all along. Within adipose tissue, oestrogen is involved in processes that influence adipocyte function, lipid storage and mobilisation and insulin sensitivity, while within skeletal muscle it contributes to processes involved in muscle function, metabolism and maintenance. As oestrogen exposure becomes increasingly variable and eventually settles at much lower levels, the hormonal environment surrounding these tissues changes with it (Motlani et al., 2023; Kodete et al., 2024).

This is the point at which a transition that began with ovarian ageing starts to become visible as something much broader.

The change is not simply about gaining weight

One of the more visible consequences of this changing hormonal environment is a gradual shift in where body fat tends to be stored.

During the reproductive years, women tend to store a greater proportion of subcutaneous fat around the hips, thighs and buttocks. As we have just seen, this gluteofemoral pattern is influenced, at least in part, by the more oestrogenic hormonal environment of the premenopausal years. As oestradiol exposure changes and the relative balance between oestrogenic and androgenic signalling shifts through perimenopause and into postmenopause, fat deposition can begin to move towards a more central pattern, with a greater proportion accumulating around the abdomen and within the visceral compartment surrounding the abdominal organs (Motlani et al., 2023; Palacios et al., 2024).

This redistribution is unlikely to be explained by the relative androgenic shift alone. Adipocytes themselves contain oestrogen receptors, which means adipose tissue has been responding directly to oestrogen signalling throughout the reproductive years. Oestrogen influences aspects of lipid storage and mobilisation, adipocyte function and insulin sensitivity, so the decline in ovarian oestradiol alters the metabolic environment within adipose tissue itself. Rising FSH has also attracted interest as another possible contributor to adipose tissue biology, although direct FSH effects in human adipose tissue remain less firmly established and are probably better regarded as an evolving area of research rather than a settled explanation for menopausal changes in body fat (Motlani et al., 2023; Palacios et al., 2024).

What all of this begins to show is why looking only at kilograms can be misleading.

The scales can tell us whether total body weight has changed, but they cannot tell us what that weight is made up of. They cannot tell us whether fat mass has increased while lean tissue has declined, or whether fat that was once stored predominantly beneath the skin around the hips and thighs is increasingly being carried around the abdomen. A woman can therefore look and feel quite different in her body without seeing an equally dramatic change when she steps on the scales.

We have an unusually useful window into this process through the Study of Women’s Health Across the Nation, or SWAN, a large longitudinal study that has followed women through midlife and across the menopausal transition (Greendale et al., 2019). Rather than taking a group of younger premenopausal women and comparing them with a different group of older postmenopausal women, the longitudinal design allows researchers to observe changes occurring within women as they approach, pass through and move beyond their own final menstrual period. This gives us a much clearer picture of when changes in fat mass, lean mass and body weight begin to occur in relation to menopause itself (Greendale et al., 2019).

When Greendale et al. (2019) examined the longitudinal body-composition data from SWAN, the story told by the scales was not quite the same as the story told by body composition. Beginning approximately two years before the final menstrual period, the rate of fat gain accelerated while lean mass began to decline. Those changes continued through the menopausal transition before slowing approximately two years after the final menstrual period (Greendale et al., 2019).

Body weight did not show the same acceleration.

Women had already been gaining weight before this window, and that trajectory continued rather than suddenly speeding up as menopause approached (Greendale et al., 2019). This distinction is important because it suggests that some of the changes particularly associated with the menopausal transition are occurring not simply in how much the body weighs, but in what that weight consists of.

That helps make sense of something many women describe during these years: “My weight hasn't changed that much, but my body has.”

There can be a physiological basis for that experience. Fat mass may be increasing at the same time that lean mass is declining, while some of that adipose tissue is also being redistributed away from the predominantly gluteofemoral pattern of the reproductive years and towards greater central and visceral storage. The number on the scales may therefore change relatively little while the proportions and distribution of the tissues underneath that number are gradually becoming quite different (Greendale et al., 2019; Marlatt et al., 2022).

And these changes in body composition matter for reasons that extend well beyond body shape.

Fat tissue and skeletal muscle are not metabolically interchangeable tissues. Skeletal muscle is one of the body's major sites for glucose uptake and disposal and contributes to insulin sensitivity and energy metabolism, while visceral adipose tissue has a different metabolic and endocrine profile from the subcutaneous fat stored around the hips and thighs. So when lean tissue begins to decline at the same time that fat mass increases and a greater proportion of that fat is being stored viscerally, the metabolic consequences can be quite different from simply gaining the same amount of weight while maintaining muscle and predominantly subcutaneous fat stores (Kodoth et al., 2022; Marlatt et al., 2022).

This is where the body-composition story begins to become a cardiometabolic one. Changes in the relative amounts of muscle and adipose tissue, together with where that adipose tissue is stored, can influence insulin sensitivity, glucose regulation, lipid metabolism and inflammatory signalling. It is one of the reasons that understanding what happens to body composition across perimenopause is more useful than focusing on body weight alone (Kodoth et al., 2022; Marlatt et al., 2022).

Why a changing waistline matters

As body fat begins to shift towards a more central pattern during the menopausal transition, the change that becomes visible around the waist can also reflect changes occurring more deeply within the abdomen. Not all abdominal fat is the same. Some remains subcutaneous, sitting beneath the skin, while visceral adipose tissue is stored deeper within the abdominal cavity, surrounding the internal organs. It is the tendency towards greater visceral fat accumulation that becomes particularly relevant when we begin thinking about the metabolic changes that can accompany and follow the menopausal transition (Kodoth et al., 2022; Marlatt et al., 2022).

This is important because adipose tissue does considerably more than simply store energy. We now understand it as an active endocrine and metabolic tissue, capable of communicating with other parts of the body through hormones, adipokines and inflammatory signalling molecules. The way adipose tissue behaves also differs depending on where it is stored. Visceral adipose tissue has a different metabolic profile from the predominantly subcutaneous fat stored around the hips and thighs and is more closely associated with insulin resistance, altered lipid metabolism and cardiovascular risk (Kodoth et al., 2022; Marlatt et al., 2022).

One of the places where these differences begin to matter is in the way the body responds to insulin. Insulin helps regulate the movement of glucose from the circulation into tissues where it can be used or stored, and skeletal muscle is particularly important in this process. After a meal, muscle provides a large reservoir into which glucose can be taken up in response to insulin. As visceral adiposity increases, however, changes in fatty-acid metabolism, adipokine secretion and inflammatory signalling can begin to interfere with normal insulin action. The body may compensate for some time by producing more insulin, helping to keep circulating glucose within a relatively normal range, but if insulin sensitivity continues to deteriorate, maintaining that balance can become progressively more difficult (Kodoth et al., 2022; Lobato et al., 2026).

This becomes even more relevant when we remember what may be happening to skeletal muscle at the same time. In the longitudinal SWAN data discussed earlier, the acceleration in fat gain around the final menstrual period occurred alongside a decline in lean mass (Greendale et al., 2019). So, rather than thinking about the metabolic effects of increasing abdominal fat in isolation, we may have two changes occurring together: an increase in visceral adipose tissue associated with a less favourable metabolic environment, alongside a gradual reduction in lean tissue that plays an important role in glucose disposal and insulin sensitivity.

The changes do not stop with glucose metabolism. Lipid profiles can also begin to shift across the menopausal transition, with longitudinal research showing increases in LDL cholesterol and apolipoprotein B around the final menstrual period. Increasing visceral adiposity and changing body composition sit within this broader cardiometabolic picture, alongside the direct effects of changing ovarian hormones and the effects of ageing itself (Marlatt et al., 2022).

It is worth keeping that last point in mind. Menopause does not suddenly become responsible for every change in glucose, cholesterol, blood pressure or cardiovascular risk that occurs during midlife. Chronological ageing continues alongside the menopausal transition, while genetics, diet, movement, sleep, smoking, alcohol intake and existing metabolic health all contribute to the picture. What changes through perimenopause is one important part of a much larger physiological story.

This is why the conversation around body composition during perimenopause needs to extend beyond whether body weight has increased, or whether a woman's body looks different from the way it did earlier in adulthood. The more meaningful change is occurring within the composition and distribution of those tissues. When visceral adipose tissue increases at the same time that lean tissue begins to decline, the balance between two metabolically very different tissues is changing, with potential consequences for insulin sensitivity, glucose and lipid metabolism and longer-term cardiometabolic health (Kodoth et al., 2022; Marlatt et al., 2022).

And this is also why maintaining skeletal muscle becomes such an important part of the story.

What happens to lean mass?

While increasing abdominal and visceral adiposity may be one of the more visible changes in body composition during perimenopause, another change can be occurring at the same time that is much less obvious. Lean mass can begin to decline across midlife, and the SWAN findings suggest that the menopausal transition may represent a particularly important period within that longer trajectory. As we saw earlier, the acceleration in fat gain beginning around two years before the final menstrual period occurred alongside a decline in lean mass. Body composition can therefore be changing in two directions at once, with fat mass increasing while lean tissue is gradually being lost (Greendale et al., 2019).

Part of this decline is related to ageing itself. Skeletal muscle mass and strength gradually change as we get older, influenced by changes in physical activity, muscle protein turnover, neuromuscular function and the way muscle responds to the usual anabolic signals provided by nutrition and exercise. Perimenopause arrives during this same period of life, which makes it difficult to draw a neat dividing line between changes associated with chronological ageing and those associated more specifically with ovarian ageing. What we do know, however, is that skeletal muscle is responsive to the sex-hormone environment, meaning the substantial change in oestrogen exposure across the menopausal transition is occurring within a tissue already undergoing age-related change (Marlatt et al., 2022; Kodete et al., 2024).

Oestrogen receptors are present within skeletal muscle, where oestrogen signalling is involved in processes that help regulate muscle protein turnover, mitochondrial function and energy metabolism, muscle repair and regeneration, and aspects of glucose metabolism. Its influence also appears to extend beyond how much muscle tissue is present to how well that muscle functions. This distinction matters because changes in muscle through midlife are not simply about the amount of lean mass present; muscle quality, strength and metabolic function are part of the picture too (Kodete et al., 2024).

As oestrogen exposure becomes increasingly variable through perimenopause and then remains substantially lower after menopause, skeletal muscle is therefore being maintained within a hormonal environment that is quite different from the one present during the reproductive years. This is occurring alongside the effects of chronological ageing, as well as differences in movement, physical activity and other individual factors that influence muscle over time. Rather than there being one hormonal explanation for the decline in lean mass, it is more useful to think about ovarian ageing and chronological ageing occurring together, with changing oestrogen exposure adding another influence to the longer-term changes already taking place within skeletal muscle (Marlatt et al., 2022; Kodete et al., 2024).

Why does this loss of lean tissue matter when we are talking about the changing body composition of perimenopause?

Skeletal muscle is one of the body's largest metabolically active tissues and a major site of insulin-stimulated glucose uptake. It provides an important destination for glucose leaving the circulation, contributes to energy expenditure and plays a role in insulin sensitivity and broader metabolic health. A reduction in lean mass therefore represents more than a change in strength or physical function; it also changes the amount of metabolically active tissue available to participate in these processes (Marlatt et al., 2022; Lobato et al., 2026).

This becomes particularly important when we place the two sides of the body-composition change beside one another. Across the menopausal transition, lean tissue may be declining at the same time that fat mass is increasing and a greater proportion of that fat is being stored viscerally. These tissues have very different metabolic roles. The result is not simply a different body shape or a change in the number on the scales, but a gradual shift in the relative amounts and distribution of tissues involved in glucose regulation, insulin sensitivity, energy metabolism and cardiometabolic health (Kodoth et al., 2022; Marlatt et al., 2022).

Body composition changes during perimenopause, then, because several physiological changes are unfolding at the same time. Ovarian ageing alters the hormonal environment, oestrogen becomes increasingly variable before eventually declining, and the balance between oestrogenic and androgenic signalling changes. These hormonal changes influence where adipose tissue is stored and occur alongside changes in skeletal muscle, while the effects of chronological ageing continue in the background (Marlatt et al., 2022; Motlani et al., 2023; Palacios et al., 2024).

This is why describing the experience simply as “menopausal weight gain” misses so much of what is actually happening. For some women, the scales may change relatively little while underneath that number fat mass is increasing, lean mass is declining and a greater proportion of adipose tissue is being stored centrally. It is this change in the composition and distribution of body tissue, rather than body weight alone, that helps connect the menopausal transition with changes in insulin sensitivity, glucose and lipid metabolism and longer-term cardiometabolic health (Greendale et al., 2019; Marlatt et al., 2022).

Understanding what is changing does not mean that every change in body composition during midlife can be attributed to menopause, nor that the body should be expected to remain unchanged across the lifespan. It does, however, give us a much more useful way of understanding why the body can begin to look, feel and behave differently through perimenopause and beyond.

References

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