Insulin resistance: signs, causes and how to test for it

Excess visceral fat and abdominal adiposity

Visceral fat stored around the abdomen and organs is metabolically distinct from subcutaneous fat. It releases inflammatory cytokines and free fatty acids directly into the portal circulation, impairing the liver's ability to respond to insulin and suppressing insulin signalling in muscle cells. A waist circumference above 88cm in women or 102cm in men is associated with significantly elevated insulin resistance risk, independent of overall body weight. Waist measurement is more informative than BMI alone when assessing metabolic risk.

Sedentary behaviour and low muscle mass

Skeletal muscle is the primary site of glucose disposal in the body: when you eat, muscle cells absorb the majority of circulating glucose in response to insulin. People with low muscle mass or who are predominantly sedentary have reduced glucose disposal capacity, which means the pancreas must produce more insulin to achieve the same blood glucose clearance. Regular resistance training and aerobic exercise improve insulin sensitivity through multiple pathways, including increased GLUT4 transporter expression in muscle cell membranes.

High intake of refined carbohydrates and ultra-processed foods

Diets high in refined carbohydrates, added sugars, and ultra-processed foods produce rapid and large post-meal glucose spikes, requiring repeated high-insulin responses that over time desensitise cells to insulin's signal. Chronically elevated insulin levels also prevent fat breakdown between meals, which drives further fat storage and worsens the metabolic cycle. Fructose specifically, found in high concentrations in sugary drinks and fruit juice, is processed primarily by the liver and drives hepatic de novo lipogenesis and insulin resistance through a distinct pathway from glucose.

Poor sleep and circadian disruption

Sleep deprivation and irregular sleep timing impair insulin sensitivity, even in people who eat well and exercise regularly. A single night of poor sleep can reduce insulin sensitivity by up to 25 per cent in healthy adults. Chronic sleep restriction raises cortisol and growth hormone, both of which antagonise insulin action. Shift workers and people with irregular circadian patterns have significantly elevated rates of insulin resistance and type 2 diabetes compared to the general population, independent of diet and weight.

Chronic stress and elevated cortisol

Cortisol counteracts insulin by raising blood glucose and suppressing insulin signalling in peripheral tissues, a mechanism evolved for short-term stress but damaging when chronically activated. People with high psychological stress, high-pressure jobs, or ongoing financial or relational stressors show measurable insulin resistance even in the absence of other risk factors. The HPA axis (hypothalamic-pituitary-adrenal) and metabolic insulin signalling pathways are directly interconnected, meaning that addressing stress is not a peripheral wellness suggestion but a mechanistically important metabolic intervention.

Genetic predisposition

Some individuals are genetically predisposed to insulin resistance through variants in genes involved in glucose metabolism, adipogenesis, and insulin signalling. MTHFR variants can affect methylation and homocysteine metabolism in ways that compound metabolic risk. Certain ethnic groups, including South Asian, Black African, and Caribbean populations, develop insulin resistance at lower BMI thresholds than the general population, reflecting genetic differences in fat distribution, muscle composition, and metabolic rate.

PCOS and hormonal factors

Polycystic ovary syndrome (PCOS) and insulin resistance are closely connected: up to 70 per cent of women with PCOS have some degree of insulin resistance, even in the absence of excess weight. Insulin resistance in PCOS drives elevated androgen production by the ovaries, which worsens the hormonal and reproductive features of the condition. Managing insulin resistance through diet, exercise, and sometimes medication is central to PCOS treatment because the hormonal abnormalities frequently normalise as insulin sensitivity improves.

Standard NHS testing for metabolic health typically includes HbA1c and sometimes fasting glucose. Both markers become elevated only once insulin resistance has progressed to pre-diabetes or diabetes stage, by which point insulin levels may have been elevated for five to ten years. This means that for a large proportion of adults with insulin resistance, routine testing returns a "normal" result despite a significant and ongoing metabolic problem.

A more sensitive approach assesses the markers that reflect insulin's function before glucose regulation breaks down:

HbA1c reflects average blood glucose over the preceding two to three months. It identifies pre-diabetes (42 to 47mmol/mol) and diabetes (48mmol/mol and above), but misses the earlier phase of insulin resistance where glucose is still normal.

Fasting glucose measures blood sugar after an overnight fast. As with HbA1c, it tends to rise only once the pancreas can no longer fully compensate for insulin resistance through increased insulin output.

Fasting insulin is the marker that identifies insulin resistance before glucose becomes affected. When cells resist insulin, the pancreas produces more to compensate: elevated fasting insulin alongside normal fasting glucose is the hallmark of early insulin resistance. This combination can be assessed using the HOMA-IR calculation (fasting glucose multiplied by fasting insulin, divided by a constant), developed by researchers at Oxford University. A HOMA-IR score below 1.0 indicates good insulin sensitivity. A score above 1.9 suggests early insulin resistance, and above 2.9 indicates significant insulin resistance.

Triglycerides and HDL cholesterol provide an indirect but accessible window into insulin resistance. High triglycerides combined with low HDL (the triglyceride-to-HDL ratio) is a recognised surrogate marker for insulin resistance used in cardiovascular research. This pattern reflects impaired lipoprotein metabolism driven by excess insulin and is visible in a standard lipid panel.

CRP (C-reactive protein) measures systemic inflammation, which both accompanies and compounds insulin resistance. Chronically elevated insulin promotes inflammatory cytokine release, and inflammation in turn worsens insulin signalling.

If your results suggest insulin resistance, a fasting insulin test can be added to calculate your HOMA-IR score with precision. This is most useful for people who want to track metabolic improvement over time as they make dietary, exercise, or lifestyle changes, since fasting insulin responds faster to intervention than HbA1c and identifies progress before glucose markers shift.

Dietary carbohydrate quality and meal timing

Shifting from refined carbohydrates to whole foods with lower glycaemic impact is the most consistently evidence-supported dietary intervention for insulin resistance. This means replacing white bread, pasta, rice, sugary drinks, and ultra-processed snacks with whole grains, legumes, vegetables, and quality protein sources. Time-restricted eating (consuming all meals within an 8 to 10 hour window) has been shown in several controlled trials to improve fasting insulin and HOMA-IR independently of calorie reduction, primarily by extending the overnight fast and allowing insulin levels to remain low for longer periods.

Resistance training and movement

Muscle is the primary site of insulin-stimulated glucose uptake. Resistance training increases the number and activity of GLUT4 transporters in muscle cell membranes, improving glucose disposal independently of weight loss. Even two to three sessions of resistance training per week produce measurable improvements in insulin sensitivity within four to six weeks. Breaking prolonged sitting with short bouts of walking every 30 to 60 minutes also reduces postprandial glucose and insulin spikes in people who are predominantly desk-based.

Sleep quality and duration

Consistently achieving seven to nine hours of good-quality sleep is one of the most underestimated metabolic interventions. Addressing sleep apnoea, establishing consistent sleep and wake times, and reducing blue light exposure in the two hours before bed all have direct, measurable effects on fasting insulin and insulin sensitivity. Tracking biomarkers before and after addressing sleep issues often reveals larger metabolic improvements than dietary changes alone for people whose primary driver is sleep disruption.

Stress reduction and cortisol management

Interventions that reliably reduce cortisol output, including regular low-to-moderate intensity exercise, mindfulness practice, structured recovery time, and adequate sleep, all improve insulin sensitivity through the HPA-metabolic axis connection. The effect is dose-dependent and cumulative: the more consistently stress is managed, the more pronounced the improvement in insulin sensitivity over time. This is not a peripheral lifestyle recommendation but a mechanistically direct metabolic intervention for people in whom chronic stress is a primary driver.