Insulin Resistance & Hormones: A Guide for Women
If you’ve heard the term “insulin resistance” but aren’t quite sure what it means or how it connects to your hormones, you’re not alone. The relationship between insulin resistance and women’s health is significant. The good news: understanding the basic mechanisms helps you recognise the signs early and make realistic, meaningful changes that actually make a difference.
What Is Insulin and Insulin Resistance
Insulin is a hormone produced by the pancreas that works like a key: it unlocks your cells so they can absorb glucose (sugar) from the blood and use it for energy.
Insulin resistance means your cells stop responding as well to this key. When this happens, the pancreas produces more insulin so cells can still access the energy they need. This excess insulin manages to keep blood sugar levels normal, sometimes for years. However, chronically elevated insulin has downsides: it contributes to weight gain, stimulates androgen production from the ovaries — which explains the link with PMOS/PCOS — and, over time, can place strain on the pancreas, raising the risk of prediabetes or type 2 diabetes. The opposite of insulin resistance, insulin sensitivity, means cells respond effectively to insulin, so the body only produces as much as it actually needs — in other words, the body is working as it should.
Important: insulin resistance is not something you did wrong. It’s strongly influenced by genetic and hormonal factors — as we’ll see below — that are largely outside your control.
How Hormones Connect to Insulin
Oestrogen protects insulin sensitivity
Oestrogen helps cells respond better to insulin through several mechanisms: in the liver (limiting excess glucose production), and in muscle and fat tissue (improving insulin signalling). This is part of why women of reproductive age typically have better insulin sensitivity than men of the same age — an advantage that reduces after menopause as estrogen declines.
Testosterone has the opposite effect in women
In men, testosterone is associated with protection against insulin resistance. In women, however, excess androgens (as seen in PCOS/PMOS) have the opposite effect — increasing the risk of insulin resistance. It’s one of the clearest examples of how the same hormone can act differently depending on the body’s hormonal environment.
Insulin Resistance in PMOS/ PCOS
Polycystic Ovary Syndrome, now known as PMOS (Polyendocrine Metabolic Ovarian Syndrome), has insulin resistance as a core feature — independent of body weight. Even women with a normal weight and PMOS often show insulin resistance.
Worth knowing: international guidelines note that blood tests aren’t reliable enough to be used alone for diagnosis of insulin resistance. This means “normal” test results doesn’t necessarily rule out the condition.
Insulin Resistance in Pregnancy
During pregnancy, the placenta produces hormones that deliberately reduce the mother’s insulin sensitivity — this isn’t dysfunction, but a normal mechanism that ensures more glucose remains available for the baby. In a healthy pregnancy, the pancreas compensates by producing significantly more insulin.
In women with pre-existing insulin resistance (e.g. from PMOS or prediabetes), this normal increase can outpace the pancreas’s ability to compensate, raising the risk of gestational diabetes. Here too, the same principle applies: it’s not always something that could be prevented through diet and lifestyle alone — it’s a combination of hormonal physiology and individual predisposition.
Insulin Resistance in Perimenopause/Menopause
As oestrogen declines, there’s a gradual increase in abdominal fat mass and a decrease in muscle mass — changes directly linked to worsening insulin sensitivity. Recent research even shows that higher insulin levels early in perimenopause are associated with more intense hot flashes — showing just how connected metabolic and classic menopausal symptoms are.
Insulin Resistance Signs
- Intense fatigue or drowsiness after a carbohydrate-rich meal
- Reactive hypoglycemia: dizziness, shakiness, intense hunger or sugar cravings, 2-5 hours after a meal
- Difficulty losing weight, particularly abdominal fat, despite genuine efforts
- Acanthosis nigricans: dark, velvety patches of skin at the neck or underarms
What You Can Do
The good news: the Mediterranean diet is associated with improvements across many metabolic health markers, with some studies showing improvement in insulin sensitivity specifically. In women with PMOS particularly, a recent study found that a non-restrictive Mediterranean approach was feasible and well accepted, with larger effectiveness trials currently underway.
Some small, realistic changes supported by current research:
The type, amount, distribution, and combination of carbohydrates matter. You don’t need to eliminate carbohydrates to improve insulin sensitivity. What appears to matter more is:
- Type: slow-release carbohydrates (legumes, wholegrains) cause a gentler blood sugar rise compared to refined carbohydrates (white bread, sugar)
- Amount per meal and distribution across the day: spreading carbohydrates into smaller portions helps you digest and absorb them more evenly
- Combination: pairing carbohydrates with protein, fibre, or healthy fats (e.g. bread with egg or cheese, fruit with yogurt) moderates the blood sugar rise
In other words, the strategy isn’t “cut all carbohydrates,” but smart choices around type, timing across the day, and combination — which is much more sustainable long-term.
Breakfast plays an important role. The body is naturally more insulin-resistant in the morning, so the type and amount of carbohydrate you choose matters more at this meal. A breakfast with adequate protein (e.g. eggs, yoghurt, cheese) and complex carbohydrates (e.g. wholegrain bread, oats) rather than refined ones (white bread, sugary cereals) helps not just with that particular meal, but with blood sugar control for the rest of the day.
The order you eat in matters. Studies show that when vegetables and protein are eaten before carbohydrates in a meal (rather than together or after), the rise in blood sugar and insulin is significantly smaller.
A short walk after meals. Research shows that even 10-15 minutes of gentle walking after a meal noticeably reduces blood sugar spikes. No intense exercise needed — a walk around the block, or even some house chores, is enough.
Muscle mass supports blood sugar regulation. Strength training (twice a week) improves insulin sensitivity, since muscle is the body’s main site for glucose uptake. Building muscle mass increases both the “storage capacity” for glucose and the mechanisms that transport it into the cell.
Important: you don’t need to change everything at once. Small, consistent changes that fit your lifestyle make a bigger difference long-term than a “perfect” but unrealistic plan. Progress, not perfection, is what counts.
When to Talk to a Specialist
If you recognise any of these signs and you are concerned, the first step is a conversation with your doctor, who will review your history and clinical picture as a whole.
A dietitian can complement that care, helping you translate general recommendations into practical, everyday choices — taking into account your circumstances, preferences, and lifestyle.
If you’d like to explore how I could help, you can learn more about my PCOS Nutrition Programme, Perimenopause & Menopause Support Programme, Fertility & Pregnancy Nutrition Programme, or book a free discovery call.
This article is for educational and informational purposes only and does not replace individualised medical or dietary advice. Please consult your doctor or dietitian regarding your own health history.
References
- 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. PMID: 37580314
- Teede HJ, Bahri Khomami M, Morman R, et al. Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome. Lancet. 2026. PMID: 42119588
- Yan H, et al. Estrogen Improves Insulin Sensitivity and Suppresses Gluconeogenesis via the Transcription Factor Foxo1. Diabetes. 2019;68(2):291-304. PMID: 30487265 (animal model study)
- Morford J, Wu S, Mauvais-Jarvis F. The impact of androgen actions in neurons on metabolic health and disease. Mol Cell Endocrinol. 2017;465:92-102. PMID: 28882554
- Mumm H, et al. Prevalence and possible mechanisms of reactive hypoglycemia in polycystic ovary syndrome. Hum Reprod. 2016;31(5):1105-12. PMID: 27008892
- Catalano PM, Shankar K. Obesity and pregnancy: mechanisms of short- and long-term adverse consequences for mother and child. BMJ. 2017;356:j1
- [Author names TBC]. Insulin levels early in perimenopause inform vasomotor symptom incidence across the menopausal transition. 2025. PMID: 40963750
- Scannell N, et al. A Pilot Randomized Control Trial Evaluating the Feasibility of a 12-Week Mediterranean Diet Intervention Without Caloric Restriction in Women with PCOS. J Clin Med. 2025;14(16):5842
- Mazzocchi A, et al. The Secrets of the Mediterranean Diet. Does [Only] Olive Oil Matter? Nutrients. PMC7692768
- Moran LJ, et al. Efficacy, Feasibility and Acceptability of a Mediterranean Diet Intervention on Hormonal, Metabolic and Anthropometric Measures in Overweight and Obese Women with PCOS: Study Protocol. Nutrients. 2020. PMC9029422
- Shukla AP, et al. Effect of Food Order on Ghrelin Suppression. Diabetes Care. 2015;38(7):e98-e99
- Engeroff T, Groneberg DA, Wilke J. After Dinner Rest a While, After Supper Walk a Mile? A Systematic Review with Meta-analysis on the Acute Postprandial Glycemic Response to Exercise. Sports Med. 2023;53(4):849-869. PMID: 36715875
- Kanaley JA, et al. Effect of increasing the protein content of breakfast on postprandial glycemic control in adults with type 2 diabetes. J Nutr. 2015
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