Insulin resistance
Insulin resistance is the most common yet most under-tested metabolic condition today. It develops 10–20 years before type 2 diabetes and is an independent risk factor for cardiovascular disease, Alzheimer’s, PCOS, fatty liver, and several cancers.
- Develops 5–10 years before glucose rises
- Routine bloodwork (glucose, HbA1c) does not rule it out
- Reversible – if caught early enough
What is insulin resistance?
Insulin is a hormone released by the pancreas after meals. Its job is to move glucose from blood into cells – mainly muscle, liver, and fat tissue. When cells stop responding normally, insulin resistance sets in.
To compensate, the pancreas releases more and more insulin. This state – compensatory hyperinsulinaemia – can last 10–20 years before glucose starts to rise. That is why ‘normal blood sugar’ is far from a guarantee of metabolic health.
Kraft, and later Crofts & Schofield (BMJ Open Diabetes 2016), showed that up to 75% of adults with ‘normal glucose’ have hyperinsulinaemia – missed unless insulin is actually measured.
Signs worth noticing
- Fat around the waist – over 94 cm in men, over 80 cm in women (measure in the morning, at navel level)
- Strong sugar cravings, especially in the afternoon and evening
- Energy drops 2–3 hours after eating; sleepiness after lunch
- Hard to concentrate, a foggy head after bread, pasta or sweets
- Weight won’t move even though you eat less
- Dark velvety patches on the neck or under the arms (doctors call this acanthosis nigricans)
- In women: irregular periods, polycystic ovary syndrome (PCOS), trouble conceiving
- Blood test shows a triglyceride to ‘good cholesterol’ (HDL) ratio above 1.5
Why cells stop listening to insulin
Cells protect themselves from too much energy. When sugar and fat keep pouring into the blood, the cell closes the door: fewer ‘doors’ (transporters) are left on its surface for sugar to enter.
Deep belly fat – the fat stored around the organs – is not just a storage depot. It releases inflammatory substances that block insulin’s message inside the cell (Petersen & Shulman, Physiol Rev 2018).
Main drivers
- Eating spread over more than 14 hours a day – if something goes into your mouth from early morning to late evening, the pancreas never rests
- Liquid carbs: juice, sweet drinks, smoothies – they raise blood sugar faster than the same food eaten whole
- Deep belly fat (fat around the organs). It can be there at a normal weight too – someone thin outside but fatty inside is called a TOFI type
- Fatty liver – fat stored in the liver that is not caused by alcohol. It affects roughly one in four adults, often with no symptoms
- Sleep debt – a single bad night already cuts insulin’s effect by about a quarter (Donga, JCEM 2010)
- Long-term stress – the stress hormone cortisol tells the liver to release sugar into the blood, even when you haven’t eaten
- Little muscle – muscle is the biggest place sugar goes after a meal. Less muscle means less room for sugar
- Lots of bright screen light in the evening – it suppresses the sleep hormone melatonin and shifts the body’s internal clock, so you handle sugar worse the next morning
- Too little daylight during the day – a weak internal clock, lower vitamin D, and poorer energy production in cells
- Hormone-disrupting chemicals: BPA and PFAS in drinking water, plastic softeners (phthalates), pesticide residues on food, preservatives and fragrance in cosmetics, aluminium salts in deodorants. These substances imitate or block the body’s own hormones
- Synthetic clothing and microplastics – polyester, acrylic and viscose shed plastic softeners onto the skin; tiny plastic particles in water and seafood are linked to silent inflammation in the body
- Heavy metals (mercury, lead, cadmium) and mould toxins – they disturb energy production in cells and insulin’s signal
A holistic approach
Insulin resistance is a lifestyle condition, not a genetic verdict. Four pillars that work together:
Nutrition
Cut liquid and fast-absorbing carbs. Raise protein to 1.2–1.6 g per kg body weight. Eat 2–3 times daily, no snacking. Eating window 8–10 h. Plenty of non-starchy vegetables, omega-3, fiber.
Movement
8,000–10,000 steps daily as a baseline. Strength training 2–3× per week directly increases muscle GLUT4 and insulin sensitivity. A 10-minute walk after meals blunts glucose spikes by ~30%.
Supplements that support insulin sensitivity
Supplements do not replace lifestyle changes, but well-chosen ones can support insulin signalling and reduce metabolic inflammation. Discuss with your clinician before starting, especially if you take medications.
- Berberine – a plant alkaloid that activates the AMPK enzyme and improves glucose and lipid metabolism. Some studies show effects comparable to metformin, but it can interact with medications (e.g., blood thinners).
- Curcumin (turmeric) – a potent antioxidant and anti-inflammatory that supports insulin signalling.
- Gymnema sylvestre – reduces sugar cravings and supports pancreatic beta-cell function.
- Magnesium – involved in insulin-receptor function; deficiency is linked to poorer glucose tolerance.
- Vitamin D – supplementation may improve insulin sensitivity when baseline levels are low.
- Omega-3 fatty acids – reduce metabolic inflammation and improve lipid profiles.
- Chromium – supports glucose-transport proteins.
- Alpha-lipoic acid (ALA) – improves insulin sensitivity and acts as an antioxidant.
Fasting and time-restricted eating
A time-restricted eating window (e.g., 8–10 hours) and intermittent fasting give the pancreas and liver a rest, lower insulin levels, and promote fat burning.
Sutton et al. (2018, Cell Metabolism) showed that early time-restricted feeding (a 6-hour eating window during the day) improved insulin sensitivity, blood pressure, and oxidative stress in men with prediabetes compared with a standard eating schedule.
Start carefully: shorten the eating window gradually, drink enough water, and monitor sleep, energy, and blood sugar. Fasting is not suitable during pregnancy, breastfeeding, eating disorders, or with certain medications.
Labs worth discussing
- Fasting insulin (optimal < 6 mU/L, warning > 10)
- HOMA-IR: (glucose × insulin) / 22.5 (optimal < 1.0)
- Fasting glucose and HbA1c (baseline, not the diagnosis)
- Triglycerides and HDL – ratio > 1.5 flags insulin resistance
- hs-CRP (low-grade inflammation)
- ALT, AST, GGT (metabolic status of the liver)
- Waist circumference and body composition
- Kraft test or 5-hour OGTT with insulin – can add information in selected clinical situations, but is not a universal diagnostic standard
Insulin resistance webinars
Recorded sessions ‘Insulin resistance in clinical practice’ and ‘Insulin resistance in women’ – Dr Saadi’s own clinical view, with lab interpretation and practical steps.
HOMA-IR, insulin and glucose norms
Practical lab values for adults (non-pregnant, non-diabetic)
| Marker | Optimal | Borderline | Insulin resistant |
|---|---|---|---|
| HOMA-IR | < 1.0 | 1.0–2.5 | > 2.5 |
| Fasting insulin | < 6 µU/ml | 6–10 µU/ml | > 10 µU/ml |
| Fasting glucose | 4.4–5.0 mmol/l | 5.1–5.6 mmol/l | > 5.6 mmol/l |
| HbA1c | < 5.3 % | 5.4–5.6 % | ≥ 5.7 % |
| Triglycerides / HDL | < 1.5 | 1.5–2.5 | > 2.5 |
| Waist (M / F) | < 94 / 80 cm | 94–102 / 80–88 cm | > 102 / 88 cm |
HOMA-IR
- Optimal
- < 1.0
- Borderline
- 1.0–2.5
- Insulin resistant
- > 2.5
Fasting insulin
- Optimal
- < 6 µU/ml
- Borderline
- 6–10 µU/ml
- Insulin resistant
- > 10 µU/ml
Fasting glucose
- Optimal
- 4.4–5.0 mmol/l
- Borderline
- 5.1–5.6 mmol/l
- Insulin resistant
- > 5.6 mmol/l
HbA1c
- Optimal
- < 5.3 %
- Borderline
- 5.4–5.6 %
- Insulin resistant
- ≥ 5.7 %
Triglycerides / HDL
- Optimal
- < 1.5
- Borderline
- 1.5–2.5
- Insulin resistant
- > 2.5
Waist (M / F)
- Optimal
- < 94 / 80 cm
- Borderline
- 94–102 / 80–88 cm
- Insulin resistant
- > 102 / 88 cm
Ranges based on IDF 2005 metabolic syndrome criteria and Dr Saadi’s clinical practice.
Frequently asked questions
Go deeper: related material
Articles
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Metabolic health is interconnected – explore the other deep-dives:
Overweight
Why calorie counting fails – hormones, insulin, leptin and adipose tissue.
ReadVagus nerve
The rest-and-repair system – digestion, heart, inflammation, stress.
ReadCholesterol & ApoB
Expanded lipid panel – ApoB, Lp(a), homocysteine, A vs B phenotype.
ReadSleep
The foundation of metabolic health – hormones, cortisol, insulin, brain recovery.
ReadChronic inflammation
The ‘silent fire’ behind cardiovascular disease, diabetes and autoimmunity.
ReadLow-carb and keto
Carbohydrate restriction – IR, T2D, fatty liver, metabolic syndrome.
ReadScientific references
- DeFronzo RA, Tripathy D. Skeletal muscle insulin resistance is the primary defect in type 2 diabetes. Diabetes Care, 2009. doi.org/10.2337/dc09-S302
- Matthews DR et al. Homeostasis model assessment: insulin resistance and beta-cell function. Diabetologia, 1985. pubmed.ncbi.nlm.nih.gov/3899825/
- Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes, 1988. pubmed.ncbi.nlm.nih.gov/3056758/
- Petersen MC, Shulman GI. Mechanisms of Insulin Action and Insulin Resistance. Physiological Reviews, 2018. doi.org/10.1152/physrev.00063.2017
- Spiegel K et al. Impact of sleep debt on metabolic and endocrine function. Lancet, 1999. pubmed.ncbi.nlm.nih.gov/10543671/
- Sutton EF et al. Early time-restricted feeding improves insulin sensitivity. Cell Metabolism, 2018. doi.org/10.1016/j.cmet.2018.04.010
- Volek JS et al. Carbohydrate restriction improves the atherogenic profile in metabolic syndrome. Lipids, 2009. pubmed.ncbi.nlm.nih.gov/19082851/
- Sattar N, Preiss D. HbA1c in metabolic syndrome and prediabetes. Diabetologia, 2019. doi.org/10.1007/s00125-018-4767-z
Dr Sergey Saadi – insulin resistance specialist in Estonia
Dr Sergey Saadi is a physician with more than 15 years of clinical practice.
- Daily clinical work in insulin resistance and metabolic health
- Author of ‘Dangerous secrets of blood sugar’ (Varrak, EST · RU)
- Clinical approach: HOMA-IR + Kraft insulin test + lifestyle audit
- Regular media presence and educator to other physicians
Want to see your real metabolic status?
In consultation we review your labs, calculate HOMA-IR, assess body composition and put together an individual plan that you can then discuss with your GP or other treating specialists.
Booking information and contactThis page is educational and general in nature. It is not personal medical advice, a diagnosis, or a treatment plan. Consult your physician before changing your lifestyle, medications, or supplements.