If you have PMOS (the condition previously known as PCOS), you have probably been told at some point to "just lose weight". Maybe more than once.
It is well-meaning advice, but it often misses what is actually happening inside the body. For many women with PMOS, the issue isn't really how much weight the body is carrying but where it is being carried, and there is a fascinating piece of hormone science behind that which almost never gets explained properly. So let's explain it.
If you're new to PMOS or the recent change of name from PCOS, you may find it helpful to start with my article PCOS is now PMOS: what the new name means for your health.
Fat isn't just fat
It is easy to think of body fat as one single thing: extra padding, stored energy, the number that moves (or doesn't) on the scales. But fat tissue is not uniform, and it behaves very differently depending on where it sits.
Fat stored under the skin around the hips, thighs and bottom, sometimes described as a "pear" shape, tends to be metabolically fairly quiet. It stores energy steadily and is generally considered the body's safest storage space; more fat in this area is even associated with better insulin sensitivity. Fat stored around the abdomen and internal organs, an "apple" shape often called visceral fat, behaves quite differently. It is more metabolically active, contains more immune and inflammatory cells, drains directly to the liver, and is far more closely linked with insulin resistance, type 2 diabetes and cardiovascular disease.
This distinction matters enormously in PMOS, because androgens, the hormones that tend to run higher in PMOS, influence which type of fat storage the body favours.
The insulin paradox that explains so much
You may have been told you have "insulin resistance". Quite reasonably, you might assume that means your body has become resistant to insulin across the board: one hormone, one problem, one effect everywhere it acts. That isn't quite what happens in PMOS, and the detail matters.
Insulin has more than one job. The one most of us have heard of is helping move sugar out of the bloodstream and into cells, where it can be used for energy. Far less talked about is its role as a signal to the ovaries, where it works alongside another hormone, luteinising hormone (LH), to encourage the production of androgens. Insulin also tells the liver to make less sex hormone-binding globulin (SHBG), the protein that keeps testosterone bound up and inactive in the blood, so higher insulin means more testosterone is free to act.
In PMOS, the body becomes resistant to insulin's blood sugar job, while the ovaries remain responsive to its androgen-producing signal. Researchers call this "selective" insulin resistance, and it has been traced to a fault in the signalling pathway inside cells that affects some of insulin's actions but not others. I think it is one of the most genuinely interesting pieces of the PMOS puzzle.
Picture insulin sending the same instruction out to two different departments in the body. One department, the muscles and liver that are largely responsible for blood sugar, starts tuning the message out. The other department, the ovaries, keeps listening. Because the blood sugar department has stopped listening properly, the pancreas does the only thing it can and produces more insulin to get the message through. Blood sugar often stays perfectly normal as a result, which is part of why insulin resistance in PMOS can go unnoticed on a standard blood test for years.
But that extra insulin doesn't just circulate uselessly. It also reaches the ovaries, which never stopped listening, and now there is more of the signal arriving than ever. The result is more androgen production, driven directly by insulin resistance that a routine test may miss entirely.
This is why "you can't have insulin resistance, your bloods are normal" is a phrase I'd love to retire. Fasting glucose is often the last thing to change, not the first sign that something is happening.
Androgens are directing traffic
Testosterone and related androgens don't just sit quietly in the background. They influence where the body stores incoming energy, and in PMOS that influence tends to lean towards the abdomen. Imaging studies have found that women with PMOS carry more fat in the deeper abdominal depots than women without the condition, a pattern the researchers described as partly "masculinised". There seem to be a few reasons for this.
Abdominal fat is more responsive to androgens. Visceral fat cells carry more androgen receptors than fat cells under the skin, so they are, in a sense, listening more closely to that hormonal signal.
Androgens change how fat cells behave. They influence how fat cells grow, mature and release their contents, and they encourage the low-grade inflammation that makes fat tissue less healthy. Visceral fat is also quicker to release fatty acids, and because it drains directly to the liver, it can add to the liver's workload. Over time this contributes to the changes in cholesterol and triglycerides that often show up on blood tests. It is worth adding that researchers still debate how much of visceral fat's effect comes through this direct route to the liver, and how much it is a marker of fat being stored in the wrong places more generally.
Androgens may limit the body's safest storage space. Androgens can slow the development of new fat cells. One theory is that this makes it harder for the hip-and-thigh depot to expand comfortably, so the body has fewer safe places to put extra energy and ends up storing more of it centrally. This idea is still being researched, but it fits well with what is often seen in clinic.
Put simply, it isn't that women with PMOS store more fat because of some failure of willpower. Androgens are influencing where the body chooses to put it, often somewhere far more metabolically demanding.
And then it becomes a loop
Here is the part I think is genuinely important for anyone trying to make sense of their own body. Visceral fat isn't just a passive result of this process; it becomes an active participant in it.
Fat tissue produces its own chemical messengers. Unhealthy abdominal fat releases more inflammatory signals and less of a hormone called adiponectin, which normally helps the body stay sensitive to insulin. Women with PMOS tend to have lower adiponectin than women of a similar weight without the condition, and the difference is linked to insulin resistance. Androgens themselves also appear to make tissues less sensitive to insulin, so the sequence looks something like this:
Higher androgens → more fat stored centrally → central fat further reduces insulin sensitivity → more insulin → more androgens.
Researchers increasingly describe this two-way relationship between androgens and fat tissue as a central "vicious cycle" in PMOS. It is a loop rather than a straight line, and once you can see it that way, a lot about PMOS starts to make sense. That includes why "eat less, move more" so often fails to shift things for women with this pattern: It doesn't address the loop at all.
Where oestrogen fits
You may have come across the idea that oestrogen protects women from carrying weight centrally, and there is truth in that. Oestrogen tends to favour the hip-and-thigh storage pattern, which is part of why fat often shifts towards the middle through and after the menopause, when oestrogen levels fall.
In PMOS, higher androgen activity can tip that balance in a similar direction well before the menopause. It isn't the main driver of the picture (the androgen and insulin story above is the bigger piece), but it helps explain why this pattern can show up relatively early in life for some women with PMOS. It also means the metabolic side of PMOS deserves particular attention as women move into perimenopause.
If you're slim, this still applies
Because this article is about weight, it would be easy to assume it only matters for women in larger bodies. It doesn't. Insulin resistance is reported in around 85% of women with PMOS overall, and in roughly three-quarters of those in a healthy weight range. Women with PMOS who are not overweight also tend to show the same shifts in fat-tissue hormones, including lower adiponectin, as their heavier counterparts.
A healthy BMI can also hide a less healthy distribution. It is possible to carry relatively more fat around the organs while the overall number on the scales looks unremarkable, and the international PMOS guideline recommends metabolic checks for all women with the condition, whatever their size. That said, PMOS varies a great deal from one woman to the next, and some slimmer women do have normal insulin sensitivity, which is one more reason why individual assessment matters more than assumptions in either direction.
If you are slim with PMOS and have been told your weight means you don't need to think about the metabolic side, it may be worth a second conversation with your GP.
Why this matters more than the scales do
If you take one thing away from this article, I'd like it to be this: Where body fat is stored tells us more about metabolic health than how much of it there is. Two women can weigh exactly the same and have very different metabolic pictures because one carries more of her weight centrally. That isn't visible on a set of scales, and "eat less" doesn't fix it, because it was never really about quantity in the first place.
This is why I don't lead with weight-loss advice when working with women who have PMOS. I lead with the question underneath it: What is the metabolic environment doing, and how do we support it? The international guideline takes a similar view, recommending healthy lifestyle support for all women with PMOS regardless of weight, without favouring any one diet.
In practice, that usually means focusing on the things that improve insulin sensitivity directly:
Building and maintaining muscle, as muscle is one of the main places the body uses glucose
Regular movement, including resistance training. Exercise reduces visceral fat even when weight barely changes: in one large analysis, exercise without weight loss reduced visceral fat by about 6%, while dieting without weight loss made almost no difference [13]
Eating enough protein and fibre, within regular, balanced meals
Decent sleep and stress management, both of which affect insulin and appetite
Not because these things are a moral improvement project, but because they are genuine levers on the exact mechanism described above. Sometimes weight on the scales changes as a result. Sometimes it doesn't change much at all, while the metabolic picture, the thing that actually matters for long-term health, improves anyway.
Your body isn't working against you
I think this is worth saying plainly: If you have PMOS and have struggled to shift weight from your middle despite doing "everything right", this isn't a personal failing. Your hormones are giving your body a very specific set of instructions, and those instructions can be worked with once you understand what they are.
Want to understand your own picture more clearly?
If you have PMOS and want support that works with your metabolic picture, rather than generic weight-loss advice that was never going to touch the underlying mechanism, my Hormone Insights & Support Service is designed for exactly that, or you can book a session with me here.
And if you'd like more explanations like this one, grounded in the science without the overwhelm, my newsletter goes out every fortnight, and it's free.
References and further reading
Booth Andrea, et al.Review of central versus lower-body adipose tissue distribution and metabolic risk. Horm Mol Biol Clin Investig. 2014. doi:10.1515/hmbci-2014-0009.
Ibrahim MM. Subcutaneous and visceral adipose tissue: structural and functional differences. Obes Rev. 2010;11(1):11–18.
Diamanti-Kandarakis E, Dunaif A. Insulin resistance and the polycystic ovary syndrome revisited: an update on mechanisms and implications. Endocr Rev. 2012;33(6):981–1030.
Borruel S, et al. Global adiposity and thickness of intraperitoneal and mesenteric adipose tissue depots are increased in women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2013;98(3):1254–1263.
de Medeiros SF, et al. The interplay between androgens and adipocytes: the foundation of comorbidities of polycystic ovary syndrome. GREM. 2022;3(1):2–8.
Klein S. Is visceral fat responsible for the metabolic abnormalities associated with obesity? 2010.
Toulis KA, et al. Adiponectin levels in women with polycystic ovary syndrome: a systematic review and a meta-analysis. Hum Reprod Update. 2009.
Lin K, et al. Circulating adipokine levels in nonobese women with polycystic ovary syndrome and in nonobese control women: a systematic review and meta-analysis. Front Endocrinol. 2021;11:537809.
Muchu N et al. Adipose-androgen crosstalk in polycystic ovary syndrome: mechanisms and therapeutic implications. Front Endocrinol. 2025.
Klein S. Mini review: sex hormones, oestrogens and differences in body fat distribution. Front Endocrinol. 2022.
Teede HJ, et al. Recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. J Clin Endocrinol Metab. 2023;108:2447–2469. Guideline summary.
Verheggen RJ, et al. A systematic review and meta-analysis on the effects of exercise training versus hypocaloric diet: distinct effects on body weight and visceral adipose tissue. Obes Rev. 2016;17(8):664–690.
