Insulin resistance and PMOS

If you have a PCOS diagnosis, what you have is now formally called PMOS (polyendocrine metabolic ovarian syndrome), the new name confirmed by global consensus in May 2026. The diagnostic criteria did not change. The clinical condition did not change. The name became more accurate, and a large part of why it became more accurate is the role of insulin resistance.

In the 2026 Lancet rename consensus, insulin resistance was moved from a "common feature" to one of the defining mechanisms of the condition. The paper cites a prevalence figure of approximately 85 percent of people with PMOS overall, and approximately 75 percent of women with PMOS at a lean body weight (BMI of 25 or below). These are the highest-quality summary figures currently available, and they reshape how the condition is best understood. Insulin resistance is not a complication that sometimes shows up. It is part of how PMOS shows up in most people who have it.

This is not a substitute for a conversation with a clinician. It is meant to give you the vocabulary and the questions for one.

Insulin, in 90 seconds

When you eat, your blood glucose rises. Your pancreas releases insulin, a hormone that signals your cells to absorb that glucose and use it for fuel or store it for later. In a body with typical insulin sensitivity, a small amount of insulin gets a large response from the cells.

In insulin resistance, the cells respond less efficiently to the same signal. The pancreas compensates by releasing more insulin. Glucose levels in the blood may stay in the normal range for years, sometimes decades, because the extra insulin is doing the work. The result is chronically elevated insulin, often called compensatory hyperinsulinaemia, alongside cells that become progressively less responsive over time.

This is the loop that the word "insulin resistance" describes. In PMOS, this loop has effects that reach well beyond blood sugar.

What insulin resistance does in PMOS

Insulin in PMOS is not just a metabolic story. It is also a hormonal one. Four mechanisms are well established in the research literature.

Insulin signals the ovaries to make more androgens. Elevated insulin acts on the theca cells of the ovary and increases their production of testosterone and other androgens. This is a long-established pathway, first characterised in the late 1990s and consistently replicated since. It is part of the mechanism behind the androgen-driven features of PMOS: acne, unwanted hair growth, hair thinning in androgen-sensitive patterns, and contributions to cycle irregularity.

Insulin lowers SHBG, which raises free testosterone.Sex hormone-binding globulin (SHBG) is a protein produced by the liver that binds testosterone in the bloodstream and keeps it inactive. Insulin suppresses SHBG production. When SHBG drops, more of the testosterone that is in circulation becomes biologically active, reaching skin, hair follicles, and ovarian tissue. Total testosterone on a lab report can look unremarkable while free testosterone is elevated. This is one of the reasons "normal" labs can coexist with clear androgenic symptoms.

Insulin interferes with the LH-to-FSH balance that drives ovulation.Ovulation depends on a coordinated release pattern of luteinising hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary. Insulin disrupts this rhythm, contributing to long cycles, missed ovulations, and the accumulation of immature follicles that gave the condition its now-retired "polycystic" name. Treating insulin resistance often improves ovulation, though the response varies considerably between people and over time.

Insulin is a fat-storage signal.When insulin is chronically elevated, the body is being repeatedly told to store rather than mobilise energy. This is part of why weight changes in PMOS often respond differently to standard "eat less, move more" advice than they do in people without insulin resistance. It is not a willpower problem and it is not a permanent state. It is a signal-receiving problem in a system that is being asked to do the impossible.

A clarifying note: not every feature of PMOS is downstream of insulin. Some androgenic features have adrenal as well as ovarian sources. Some cycle irregularity has hypothalamic-pituitary contributions that are not solely insulin-driven. Mood, sleep, and other features have multifactorial origins. What the 2026 Lancet consensus does say is that insulin resistance is a central, common, mechanistically connected piece of the picture in most people with PMOS. It is the part of the story most worth understanding, not the only part.

Why the standard test misses it

The test most commonly ordered in a primary-care setting is fasting glucose. It measures the level of glucose in the blood after roughly eight or more hours without food. For people who already have type 2 diabetes or who are very close to it, fasting glucose is informative. For early and moderate insulin resistance, it is often not.

The reason is the compensation pattern described above. As insulin resistance develops, the pancreas releases more insulin to keep glucose in range. Glucose stays "normal" while insulin climbs. A glucose-only test cannot see this. By the time fasting glucose finally elevates above the normal range, the dysfunction has typically been present for years.

The 2023 International Guideline for PMOS recommends a broader assessment that includes insulin-aware tests where insulin resistance is suspected. The 2026 Lancet rename consensus reinforces this. The tests that are more informative than fasting glucose alone include:

• Fasting insulin. A single fasting blood draw that measures insulin rather than glucose. A high fasting insulin in the context of normal fasting glucose is suggestive of compensatory hyperinsulinaemia.
• HOMA-IR. A calculation based on fasting glucose and fasting insulin together. It produces a single number that can be tracked over time. It is widely used in research and increasingly available in clinical settings.
• Oral glucose tolerance test with insulin measurement. A two-hour test that tracks both glucose and insulin response after a standardised glucose drink. This is the most detailed of the common options and the most likely to surface insulin resistance that fasting tests miss.

Not every clinician orders these by default, even when the 2023 Guideline recommends them. If you have a PMOS diagnosis and your workup has only included fasting glucose, it is reasonable to ask about adding fasting insulin, HOMA-IR, or an OGTT with insulin to the next set of labs. The care-prep guide on talking to a clinician about PMOS labs has more on how to frame this.

What the evidence supports

Insulin resistance in PMOS responds to several well-studied interventions. The interventions stack. Most of them are inexpensive, accessible, and low-risk. A few involve medication and require a clinician.

The list below is not a treatment plan. It is a description of what the evidence supports, with relative strength noted. Specific decisions belong with your clinician.

Sleep. Restricted sleep reduces insulin sensitivity quickly and substantially. A single night of sleep under approximately five hours can lower insulin sensitivity meaningfully the following day; chronic sleep restriction compounds the effect. This is one of the most consistent findings in metabolic research and one of the most overlooked. The intervention is not a sleep tracker; it is sleep. Most people with PMOS who improve their sleep notice metabolic effects within weeks.

Meal composition and sequencing. What you eat with carbohydrates, and the order in which you eat them, materially changes the insulin response to the same meal. Eating fibre, protein, and fat before the carbohydrate portion of a meal lowers the post-meal insulin spike by roughly 30 to 50 percent in studies of people with insulin resistance. Same food, same calories, different metabolic signal. This is the closest thing to a free intervention in the list.

Resistance training. Strength training increases skeletal muscle, which is the largest single site of insulin-mediated glucose uptake in the body. Two to three resistance sessions a week improves insulin sensitivity in PMOS. The evidence is consistent that resistance training is at least as effective as aerobic exercise for insulin sensitivity in this context, and may be more effective in some studies, though comparative head-to-head trials are not extensive.

Inositol. The supplement with the largest evidence base for PMOS. The most-studied form is myo-inositol with a small proportion of d-chiro-inositol, in roughly a 40-to-1 ratio. Multiple randomised trials and meta-analyses report improvements in insulin sensitivity, androgen levels, and ovulation rates over three to six months in many users. Side-effect profile is favourable. Inositol is over-the-counter in most jurisdictions; pregnancy and conception contexts warrant a clinician conversation. See the evidence summary on inositol for the fuller picture.

Metformin. A prescription medication that reduces glucose production by the liver and improves cellular insulin sensitivity. It is one of the longest-used interventions in PMOS, with decades of clinical experience and a substantial trial base. It is commonly used for women preparing to conceive when insulin resistance is part of the picture. Gastrointestinal side effects are common in the first weeks and usually settle. Decisions about metformin belong with a clinician.

GLP-1 receptor agonists. Newer medications (including semaglutide and tirzepatide, sold under several brand names) act through different mechanisms and have shown effects on insulin sensitivity, weight, and cardiometabolic markers in people with PMOS. The PMOS-specific evidence base is growing but is not as deep as for inositol or metformin. Use in PMOS is increasingly common but remains a clinician-led decision with access, cost, and side-effect considerations. See the evidence summary on GLP-1s in PMOS.

A note on what is not on this list: there is no "PMOS diet" with strong trial support. Specific elimination patterns (gluten, dairy, all carbohydrates) have not consistently outperformed general-quality dietary patterns in trials. What does have evidence is meal composition, meal sequencing, fibre, protein, and the overall pattern of eating, rather than the elimination of food categories. Approaches that introduce food restriction or moralised eating language are out of scope here, both because the evidence does not support them and because they can deepen patterns that are harder to recover from than insulin resistance is.

What to ask a clinician

If insulin resistance has not come up in your PMOS care, or if you are not sure what is currently being measured, a few questions are worth bringing to the next appointment.

Have we tested for insulin resistance specifically, not just fasting glucose? If the answer is fasting glucose only, ask about adding fasting insulin, HOMA-IR, or an OGTT with insulin measurement.

What do my SHBG and free testosterone look like, not just total testosterone? SHBG is one of the most reliable indirect markers of insulin status in PMOS. Free testosterone often tells a different story than total testosterone.

Are the interventions we are discussing aimed at insulin specifically, or at symptoms? Some PMOS care addresses cycle irregularity or androgenic features without addressing the upstream insulin contribution. Knowing which one you are getting clarifies what to expect from it.

These questions are not about challenging a clinician. They are about making sure the workup matches what the current evidence considers central. The care-prep guide on labs goes into more detail.

What is still uncertain

The 85 percent overall and 75 percent in lean PMOS figures from the 2026 Lancet consensus are the strongest summary numbers currently available, but they are summary numbers. Insulin resistance in PMOS varies in severity, in measurable markers, and in response to intervention. Some people with PMOS show very high HOMA-IR; others sit close to the normal range. Some respond strongly to inositol; others respond more to resistance training or to metformin. The mechanism is consistent enough to be central; the individual presentation is heterogeneous.

There is also active debate about whether PMOS subtypes can be defined by insulin status (some researchers propose "insulin-resistant" and "reproductive" subtypes), and whether assay variability in insulin testing limits the comparability of HOMA-IR across labs. The 2028 International Guideline update is the next likely inflection point on both questions.

When citing the 2026 Lancet rename consensus for these figures, it is also relevant context that several individual authors declared honoraria from pharmaceutical companies with adjacent commercial interests (including Novo Nordisk and Eli Lilly, both GLP-1 manufacturers, alongside others). The consensus itself was not pharma-funded; the disclosures are standard for senior endocrinology authors and appear in the paper. This is context, not a reason to discount the figures.

Why this matters

Insulin resistance in PMOS is invisible without the right test. It is also one of the most consequential pieces of the condition to understand, both because it sits upstream of several other features and because it responds to interventions that are accessible to most people. Sleep is free. Meal sequencing is free. Resistance training requires time but minimal equipment. Inositol is inexpensive. Metformin and GLP-1s are clinician-led decisions that follow from these, not replacements for them.

The science was visible before the rename. The 2026 rename to PMOS made it harder to keep out of view. The point of the name change, in the words of the consensus paper, was to put the centre of the condition in the centre of the name.