She was 48, in perimenopause, and on paper she was doing fine.
Her fasting glucose was 93 mg/dL, comfortably normal. Her coronary calcium score was zero, meaning no calcified plaque was visible in the arteries of her heart. Her LDL cholesterol was 130 mg/dL, not ideal but not alarming.
Then I looked more closely.
Her A1c, a three-month average of blood sugar, was 6.0%.
Her HDL cholesterol was 42 mg/dL.
Her triglycerides were 147 mg/dL, just under the cutoff of 150.
Her blood pressure was 139/87.
Her liver enzyme ALT was mildly elevated at 44, with a normal AST of 36.
At 173 cm and 90 kg, her BMI was 30.
And one more detail in her history tied it all together. Years earlier, she had been diagnosed with PCOS.
If you have ever been told your blood sugar is “fine” while another number quietly says otherwise, this article is for you. Her numbers were not a sudden midlife surprise. They may have been the latest chapter of a story that began decades earlier, and perimenopause is a time when that story can speed up.
A normal glucose, an A1c that disagrees
Fasting glucose and A1c both measure your blood sugar, but in different ways. Fasting glucose is a single snapshot taken after a night without food. A1c reflects your average blood sugar over the past two to three months, including the rises after every meal. ¹
The American Diabetes Association defines prediabetes as a fasting glucose of 100 to 125 mg/dL or an A1c of 5.7% to 6.4% ¹. By her fasting glucose, she was normal. By her A1c, she was well inside the prediabetes range.
These tests capture different aspects of glucose regulation. Insulin resistance may be part of the picture, but this mismatch alone does not tell us how much insulin her body is producing. ¹ Our sister publication, The Integrative Cardiologist, explores that hidden effort in depth in “When Blood Sugar Doesn’t Tell the Whole Story.”
The short version is this: insulin resistance is not just a blood sugar problem. The metabolic changes that come with it can contribute to fat buildup in the liver, a more harmful mix of cholesterol-carrying particles in the blood, and inflammation, all of which matter for the arteries. ²
PMOS: the first chapter
You may know this condition as PCOS, polycystic ovary syndrome. In May 2026, after a global consensus process involving 56 organizations and more than 14,000 patients and health professionals, it was formally renamed polyendocrine metabolic ovarian syndrome, or PMOS ³.
The new name matters for your heart. The old one focused on ovarian “cysts,” which are not actually cysts. The new name puts the word “metabolic” front and center, because insulin resistance, abnormal blood sugar, high blood pressure, cholesterol changes and fatty liver are central to the condition, not side effects of it ⁴.
Here is what we know about the metabolic side of PMOS:
Insulin resistance is common. Most women with PMOS have it, usually along with higher insulin levels as the body compensates. Estimates range from about 60% to 70% in one review ⁵ to as high as 85% in others ⁶. Obesity is not required: about half of women with PMOS are not obese ⁵.
High insulin helps drive the condition itself. It encourages the ovaries to produce extra androgens, the hormones behind many of PMOS’s familiar symptoms ⁵.
Diabetes risk is higher. A BMJ review reports that PMOS carries nearly three times the odds of type 2 diabetes. It also describes a long-term study in which 19% of women with PMOS developed type 2 diabetes over 24 years, compared with 1% of women without it ⁷ ⁸.
What happens as women with PMOS reach midlife? A 2023 meta-analysis found that higher androgen levels tend to persist during the late reproductive years and after menopause. Heart attack and stroke were more common in women with PMOS, but mostly in studies where they were also heavier than the comparison group. Overall, most of the cardiometabolic differences were tied to the frequent combination of PMOS and excess weight, and the quality of the evidence was low ⁹.
So a history of PMOS does not guarantee heart disease. It is a strong reason to look more closely, and what it has in common with the years ahead is insulin.
The four-year window
For years, we described the menopause transition mainly through hot flashes, sleep and mood. Research now shows it is also a metabolic event.
A study published in October 2026 followed 1,315 women who were 42 to 52 years old and before or early in perimenopause when it began in 1995 and 1996. Researchers estimated their insulin resistance using HOMA-IR, a measure calculated from fasting glucose and insulin, up to 12 times over the following two decades. Insulin resistance rose fastest over a four-year span, from about a year and a half before the final menstrual period to two and a half years after it ¹⁰.
For the study’s modeled reference woman, the BMI-adjusted HOMA-IR increases were:
About 1.2% per year in the years before the window
About 4.3% per year during the window
About 0.9% per year after it
The reference woman was White, had her final period at 52, had a starting BMI of 25.6, did not smoke, and did not use hormone therapy or statins. These model estimates accounted for changes in BMI; they are not a forecast for every woman. ¹⁰ The acceleration was not simply a matter of weight gain on the scale.
That does not mean body composition was irrelevant. BMI cannot tell us where fat is stored, and body shape shifts over these same years. A 2026 review reports that, in unadjusted estimates from a separate SWAN Heart analysis, fat around the abdominal organs grows about 8.2% per year in the two years before the final period and 5.8% per year afterward. ¹¹ In the Study of Women’s Health Across the Nation (SWAN), lean mass shifted from slight gain to slight loss during the transition ¹² ¹³.
Our patient, at 48 and perimenopausal, had good reasons for a closer metabolic assessment. Her age and symptoms alone could not tell us exactly where she was in relation to her final menstrual period. The study gives us a reason to pay attention during this transition, not proof that prevention works better only during these four years. ¹⁰
What estrogen was doing all along
Why would the menopause transition speed up insulin resistance? Part of the answer may be what estrogen had been quietly doing for decades.
Laboratory and animal research shows that estrogen helps the liver respond to insulin by restraining how much glucose it releases. It also supports the insulin-producing beta cells of the pancreas, helps them release insulin and protects them from inflammation and cell death ¹⁴. Before menopause, women also tend to store more fat on the hips and thighs and less deep in the abdomen. ¹⁵
As estrogen levels fall and fluctuate during perimenopause, those protections weaken:
Fat storage shifts toward the abdomen and around the organs. ¹²
Lean muscle begins to decline ¹², and muscle is a major site of insulin-stimulated glucose uptake. ²
Fat around the heart itself increases in late perimenopause and after menopause ¹⁶.
For a woman with PMOS, this has a particular meaning. She may enter perimenopause with insulin resistance already in place. Then the transition takes away a layer of protection she may have been relying on without knowing it.
Belly fat and the liver
Fat stored deep in the abdomen behaves differently from fat stored under the skin. It is more metabolically active, and part of its blood supply drains toward the liver. The fatty acids and inflammatory signals it releases may make the liver more resistant to insulin and more likely to store fat. ² The Integrative Cardiologist article walks through this process step by step.
Not every woman follows the same path, and not every study finds metabolic worsening across the transition. One analysis found that insulin sensitivity fell in the women who gained the most abdominal fat ¹⁵.
Our patient’s ALT of 44 with a normal AST fits a picture of possible fat in the liver. But a mildly raised liver enzyme does not diagnose fatty liver on its own. It is a clue, not a conclusion. ¹⁷
Hot flashes and insulin
Hot flashes may be more than a nuisance. They may also be a metabolic signal.
In SWAN, higher fasting insulin levels at age 47 were associated with earlier onset and longer duration of hot flashes ¹⁸. Women whose hot flashes were frequent or persistent across the transition had roughly 40% to 50% higher risk of developing diabetes ¹⁹.
These are associations, not proof that hot flashes cause diabetes. But if your hot flashes are frequent or long-lasting, it is a reasonable prompt to ask about your metabolic numbers too.
Why this matters for your heart
Look again at our patient’s results as a group:
HDL of 42: below the threshold of 50 for women.
Blood pressure of 139/87: above the threshold of 130/85.
Triglycerides of 147: just under the threshold of 150.
A1c of 6.0%: in the prediabetes range, though her fasting glucose of 93 was below the threshold of 100.
Metabolic syndrome is diagnosed when three or more of five measures are abnormal: waist size, triglycerides, HDL, blood pressure and fasting glucose ²⁰. She clearly met two. Her triglycerides sat at the edge of a third. That is a pattern worth following closely during the menopause transition.
Her triglyceride-to-HDL ratio, 147 divided by 42, was about 3.5. In a Stanford study of overweight adults without diabetes, a ratio of 3.0 or higher was one of the most useful simple markers of insulin resistance ²¹.
Then there is her calcium score of zero. It helps to know what a calcium scan sees. It detects calcium deposits in the walls of the heart arteries. It does not detect plaque that has not calcified, so a zero score means no calcified plaque was found, not proof that the arteries are completely free of plaque. ²²
Research shows why that distinction matters. In the Multi-Ethnic Study of Atherosclerosis, adults whose calcium score was zero but who had plaque in their neck arteries had about 66% higher risk of coronary heart disease events over 16 years than those without it, although absolute event rates stayed low. The researchers described a zero score as “low risk,” not “no risk” ²³.
That study included older men and women, and our patient did not have imaging of her neck arteries. It does not tell us anything about her own arteries. It shows that a zero score answers one question, not every question.
Her calcium score was zero. Her A1c, HDL, blood pressure and PMOS history were still part of the same assessment.
Later this month, we will look at why diabetes erodes women’s natural cardiovascular advantage more than it does men’s, and why catching insulin resistance before it becomes diabetes matters so much for women. ²⁴
What to measure and ask
If you are in your 40s or early 50s, especially with a history of PMOS, these are worth reviewing with your doctor:
A1c alongside fasting glucose. As our patient showed, the two can disagree. ¹
With a history of PMOS, ask whether a 75-g oral glucose tolerance test would be more informative. It is the most accurate test for assessing blood sugar in this condition, regardless of BMI. ²⁵
Your waist, measured the same way each time and tracked over time. A commonly used US threshold for women is 88 cm, or about 35 inches, though the appropriate cutoff can vary by ancestry and guideline. ²⁰
Your triglyceride-to-HDL ratio. Divide your triglycerides by your HDL when both are reported in mg/dL. It is a clue, not a diagnosis of insulin resistance. ²¹
Your liver enzymes, especially if ALT is creeping up. ¹⁷
Your blood pressure at home, since perimenopause can make readings less predictable (see “The Menopause Blood Pressure Rollercoaster”).
Your PMOS history. Mention it to every doctor you see, including your cardiologist. It is a recognized risk factor for type 2 diabetes ⁷, and it is easy for it to fall out of the conversation once fertility questions are behind you. ²⁵
First steps during the window
The useful part of these findings is knowing when change may accelerate. This is a reason to act, not a deadline after which prevention stops helping. The study did not test whether lifestyle changes have a larger effect during these four years. ¹⁰
The foundations will be familiar, and they remain worth reviewing now:
Strength training, to protect and build the muscle that clears glucose from your blood. ²⁵
Protein spread across the day, to support that muscle. ¹²
Fiber-rich, whole foods. In a major Lancet analysis, people who ate the most fiber had 15% to 30% lower rates of cardiovascular death, coronary disease, stroke and type 2 diabetes ²⁶.
Sleep, which perimenopause often disrupts and which affects insulin sensitivity. ¹²
Alcohol, kept modest.
Stress, acknowledged and managed rather than ignored.
We will go deeper into strength training, protein and the role of hormone therapy later this month. Hormone therapy has a complicated relationship with diabetes risk, and it deserves a full, balanced discussion rather than a passing line.
The takeaway
Her fasting glucose was normal, and her calcium score was zero. But her A1c of 6.0%, her HDL, her blood pressure and her history of PMOS told a fuller story, one that may have started years earlier and could speed up in the years ahead.
If you are in perimenopause, you are living through one of the most metabolically important periods of your adult life. If you also have a history of PMOS, that history adds another reason to review your metabolic health.
It is not a reason for fear. It is a reason to look closely now, without treating menopause as a deadline for prevention.
This post is for general educational purposes only. It is not medical advice, is not a substitute for care from your own physician, and does not create a physician-patient relationship. Do not start, stop, or change any treatment based on what you read here. If you think you may have a medical emergency, call 911 or go to the nearest emergency department.
Also from Cordate Press: The Integrative Cardiologist, our flagship publication for broad prevention
Also by Dr. Azhak: Lower Your Blood Pressure: Help Your Doctor Reduce Your Medication, by Sameer Azhak, MD, FACC. Available on Amazon in paperback and Kindle.
© 2026 Cordate Press
References
American Diabetes Association Professional Practice Committee for Diabetes. 2. Diagnosis and classification of diabetes: Standards of Care in Diabetes—2026. Diabetes Care. 2026;49(Suppl 1):S27–S49. doi:10.2337/dc26-S002. PubMed Central
Petersen MC, Shulman GI. Mechanisms of Insulin Action and Insulin Resistance. Physiol Rev. 2018;98(4):2133–2223. doi:10.1152/physrev.00063.2017. PubMed Central
Teede HJ, Bahri Khomami M, Morman R, et al.; Global Name Change Consortium. Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process. Lancet. 2026;407(10545):2329–2339. doi:10.1016/S0140-6736(26)00717-8. PubMed
Dalamaga M. What’s in a name? From PCOS to polyendocrine metabolic ovarian syndrome: A metabolic reframing, promise, controversies, and challenges ahead. Metabol Open. 2026;30:100479. doi:10.1016/j.metop.2026.100479. PubMed Central
Abhinethri B, Harindranathan DN, Kurian SJ. Insulin Resistance in Polycystic Ovary Syndrome: Mechanistic Insights and Therapeutic Perspectives Independent of Obesity. Gynecol Minim Invasive Ther. 2026;15(3):199–206. doi:10.4103/gmit.GMIT-D-25-00185. PubMed Central
White L. PCOS Gets a New Name: Polyendocrine Metabolic Ovarian Syndrome (PMOS). American Family Physician Community Blog. June 1, 2026. American Family Physician
Hanna F, Wu P, Heald A, Fryer A. Diabetes detection in women with gestational diabetes and polycystic ovarian syndrome. BMJ. 2023;382:e071675. doi:10.1136/bmj-2022-071675. BMJ
Forslund M, Landin-Wilhelmsen K, Trimpou P, Schmidt J, Brännström M, Dahlgren E. Type 2 diabetes mellitus in women with polycystic ovary syndrome during a 24-year period: importance of obesity and abdominal fat distribution. Hum Reprod Open. 2020;2020(1):hoz042. doi:10.1093/hropen/hoz042. PubMed
Millán-de-Meer M, Luque-Ramírez M, Nattero-Chávez L, Escobar-Morreale HF. PCOS during the menopausal transition and after menopause: a systematic review and meta-analysis. Hum Reprod Update. 2023;29(6):741–772. doi:10.1093/humupd/dmad015. Oxford Academic
Karlamangla AS, Han WJ, Srikanthan P, et al. Development of insulin resistance in women over the menopause transition. JCI Insight. In-Press Preview, October 6, 2026. doi:10.1172/jci.insight.206342. JCI Insight
Samargandy S, Matthews KA, Brooks MM, et al. Abdominal visceral adipose tissue over the menopause transition and carotid atherosclerosis: the SWAN heart study. Menopause. 2021;28(6):626–633. doi:10.1097/GME.0000000000001755. PubMed Central
Bonnes SLR, Nordhues H, Sood R, et al. Metabolic Changes of Perimenopause and Nutritional Advice. Curr Nutr Rep. 2026;15(1):69. doi:10.1007/s13668-026-00788-8. PubMed Central
Greendale GA, Sternfeld B, Huang M, et al. Changes in body composition and weight during the menopause transition. JCI Insight. 2019;4(5):e124865. doi:10.1172/jci.insight.124865. JCI Insight
Hairi HA, Ibrahim NI, Sadikan MZ, Jayusman PA, Shuid AN. Deciphering the role of classical oestrogen receptor in insulin resistance and type 2 diabetes mellitus: From molecular mechanism to clinical evidence. Bioimpacts. 2025 collection;15:30378. Published online August 4, 2024. doi:10.34172/bi.30378. PubMed Central
Marlatt KL, Pitynski-Miller DR, Gavin KM, et al. Body composition and cardiometabolic health across the menopause transition. Obesity (Silver Spring). 2022;30(1):14–27. doi:10.1002/oby.23289. PubMed Central
Nair AR, Pillai AJ, Nair N. Cardiovascular Changes in Menopause. Curr Cardiol Rev. 2021;17(4):e230421187681. doi:10.2174/1573403X16666201106141811. PubMed Central
European Association for the Study of the Liver; European Association for the Study of Diabetes; European Association for the Study of Obesity. EASL-EASD-EASO Clinical Practice Guidelines on the Management of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD). Obes Facts. 2024;17(4):374–444. doi:10.1159/000539371. PubMed Central
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;111(6):e1544–e1553. doi:10.1210/clinem/dgaf699. Journal of Clinical Endocrinology & Metabolism
Hedderson MM, Liu EF, Lee C, et al. Vasomotor Symptom Trajectories and Risk of Incident Diabetes. JAMA Netw Open. 2024;7(10):e2443546. doi:10.1001/jamanetworkopen.2024.43546. PubMed Central
Alberti KGMM, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120:1640–1645. doi:10.1161/CIRCULATIONAHA.109.192644. Circulation
McLaughlin T, Abbasi F, Cheal K, Chu J, Lamendola C, Reaven G. Use of metabolic markers to identify overweight individuals who are insulin resistant. Ann Intern Med. 2003;139(10):802–809. doi:10.7326/0003-4819-139-10-200311180-00007. PubMed
American College of Radiology and Radiological Society of North America. Cardiac CT for Calcium Scoring. RadiologyInfo.org. Reviewed July 15, 2026. RadiologyInfo
Mehta A, Rigdon J, Tattersall MC, et al. Association of Carotid Artery Plaque with Cardiovascular Events and Incident Coronary Artery Calcium in Individuals with Absent Coronary Calcification: The Multi-Ethnic Study of Atherosclerosis (MESA). Circ Cardiovasc Imaging. 2021. doi:10.1161/CIRCIMAGING.120.011701. PubMed Central
Peters SAE, Huxley RR, Woodward M. Diabetes as risk factor for incident coronary heart disease in women compared with men: a systematic review and meta-analysis of 64 cohorts including 858,507 individuals and 28,203 coronary events. Diabetologia. 2014;57(8):1542–1551. doi:10.1007/s00125-014-3260-6. PubMed
Teede HJ, Tay CT, Laven JJE, 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(10):2447–2469. doi:10.1210/clinem/dgad463. PubMed Central
Reynolds A, Mann J, Cummings J, Winter N, Mete E, Te Morenga L. Carbohydrate quality and human health: a series of systematic reviews and meta-analyses. Lancet. 2019;393(10170):434–445. doi:10.1016/S0140-6736(18)31809-9. PubMed