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Insulin Resistance Research
Complete Evidence Database: Early Detection, Prevalence, and Dietary Reversal
📋 Contents
- Part 1: UK & US Insulin Resistance Prevalence – The Silent Epidemic
- Part 2: Insulin Resistance → Hypertension – Mechanisms of Blood Pressure Elevation
- Part 3: Insulin Resistance → MASLD (Fatty Liver Disease) – Hepatic Lipogenesis
- Part 4: Insulin Resistance → Type 2 Diabetes – Beta Cell Dysfunction
- Part 5: VLC Diet Reversal – Meta-Analysis of 29 Trials
- Part 6: Insulin Resistance → Asthma – Lung Function Decline
- Part 7: Insulin Resistance → OCD – Shared Genetic Etiology
- Part 8: Insulin Resistance → IBS – Bidirectional Association
- Part 9: Insulin Resistance → Cancer – The Hyperinsulinemia Connection
- Testing Information – HOMA-IR Early Detection
📋 What This Page Contains
- UK & US Prevalence Data - Over 30 million UK adults and 133 million US adults have insulin resistance
- Condition-Specific Prevalence - How many people have asthma, OCD, anxiety, IBS, cancer, and their links to insulin resistance
- 22 Peer-Reviewed Studies - Full citations with dates, organisations, URLs, and 3-sentence summaries
- Research Categories:
- Insulin Resistance → Hypertension (2 studies)
- Insulin Resistance → MASLD/Fatty Liver (2 studies)
- Insulin Resistance → Type 2 Diabetes (2 studies)
- VLC Diet Reversal (1 meta-analysis of 29 trials)
- Insulin Resistance → Asthma (2 studies + prevalence data)
- Insulin Resistance → OCD (3 studies + prevalence data)
- Insulin Resistance → IBS (3 studies + prevalence data)
- Insulin Resistance → Cancer (4 studies + prevalence data)
- UK & US Insulin Resistance Prevalence (source documentation)
- Test Information - HOMA-IR test options (£149 or £245 with coaching)
- Direct Contact Details - Phone, email, website for For Radiant Health
Over 30 million UK adults (55%) and over 133 million US adults (40%) have insulin resistance—and most don't know it until it manifests as hypertension, Type 2 diabetes, or fatty liver disease.
The HOMA-IR test detects insulin resistance 10-20 years before conventional medicine identifies a problem, when reversal is still straightforward through dietary intervention.
Below is the complete peer-reviewed research demonstrating how insulin resistance drives hypertension, MASLD (fatty liver), Type 2 diabetes, asthma, OCD, anxiety, IBS, cancer, and chronic inflammation—and how a very low-carbohydrate diet reverses all of these conditions simultaneously.
Part 1: UK & US Insulin Resistance Prevalence
🇬🇧 United Kingdom - 30+ Million Adults
Source: WeCovr analysis synthesising Office for National Statistics (ONS), Diabetes UK, and metabolic health studies (2025)
Key Finding: Over 55% of UK adults now exhibit biomarkers consistent with insulin resistance—more than 30 million people
Pre-Diabetes: 15 million Britons estimated to be living with pre-diabetes, with vast majority completely unaware
Economic Impact: Direct cost of treating Type 2 diabetes alone projected to exceed £15 billion for NHS in 2025
Reference: WeCovr UK Insulin Resistance Report 2025
🇺🇸 United States - 133+ Million Adults
Source: National Health and Nutrition Examination Survey (NHANES) 2015-2018 data (UAB Research, 2021)
Key Finding: 40% of US adults aged 18-44 have insulin resistance based on HOMA-IR measurements—approximately 44 million young adults alone
Overall Adult Prevalence: 40-44% of all US adults (ages 18+) have insulin resistance—over 133 million Americans
Pre-Diabetes: 97.6 million US adults (more than 1 in 3) had prediabetes in 2021 (CDC/NIDDK)
Global Context: Global prevalence of insulin resistance: 26.53% (systematic review and meta-analysis, August 2025)
References: UAB Study (2021) | NIDDK Statistics
Part 2: Insulin Resistance → Hypertension
Insulin Resistance/hyperinsulinemia: An Important Cardiovascular Risk Factor That Has Long Been Underestimated
Hyperinsulinemia causes hypertension through multiple mechanisms: sodium and water retention in the kidneys, activation of the MAPK pathway causing vasoconstriction via elevated endothelin-1, and vascular smooth muscle cell proliferation leading to arterial wall thickening and loss of elasticity. The study emphasises that insulin resistance and hyperinsulinemia are severely underestimated cardiovascular risk factors requiring early detection and intervention.
Read Full Study →
Metabolic and Vascular Insulin Resistance: Partners in the Pathogenesis of Cardiovascular Disease in Diabetes
Smaller resistance vessels (arterioles) show more pronounced insulin signalling defects than larger arteries, making microvascular beds highly susceptible to damage. Studies across Type 1 diabetes, Type 2 diabetes, obesity, metabolic syndrome, and hypertension populations consistently demonstrate strong correlations between metabolic insulin resistance and arterial stiffness. This research establishes insulin resistance as a primary driver of cardiovascular pathology.
Read Full Study →
Part 3: Insulin Resistance → MASLD (Fatty Liver Disease)
Insulin Resistance Drives Hepatic De Novo Lipogenesis in Nonalcoholic Fatty Liver Disease
De novo lipogenesis (DNL)—the liver converting carbohydrates into fat—accounts for 15-26% of liver fat in NAFLD/MASLD versus only 1-10% in people with normal liver fat. The study reveals a "dissociation paradox" where insulin-resistant glucose metabolism coexists with insulin-sensitive hepatic lipogenesis: insulin resistance actually stimulates hepatic DNL, producing toxic metabolites (diacylglycerol, ceramides) that further worsen insulin resistance, creating a vicious cycle of liver damage.
Read Full Study →
Integrative Metabolism in MASLD and MASH: Pathophysiology and Emerging Mechanisms
Hepatic triglyceride sources in MASLD: systemic fatty acids (~60%), dietary fats (~15%), and de novo lipogenesis (~25%), with DNL significantly increased compared to healthy livers. Carbon-13 labelling studies reveal that up to 75% of hepatic DNL flux in MASLD comes from amino acid metabolites through alternative pathways, with amino acids potentially exceeding glucose-derived contributions. This highlights the liver's metabolic plasticity in insulin-resistant states and explains why simply reducing dietary fat is insufficient for MASLD reversal.
Read Full Study →
Part 4: Insulin Resistance → Type 2 Diabetes
Pancreatic Beta-cell Dysfunction in Type 2 Diabetes
Lipotoxicity from elevated free fatty acids causes pancreatic beta cell dysfunction through multiple mechanisms: chronic FFA exposure suppresses glucose-stimulated insulin secretion, decreases insulin gene expression, and induces beta cell apoptosis (cell death). Glucotoxicity, lipotoxicity, and glucolipotoxicity (the combined effect) are identified as the major detrimental factors for beta cell defects. By the time Type 2 diabetes is diagnosed, 50-70% of beta cell function has already been irreversibly lost.
Read Full Study →
Lipotoxicity: A New Perspective in Type 2 Diabetes Mellitus
The lipotoxicity cascade: FFA accumulation leads to increased beta oxidation, producing excess acetyl-CoA that overloads the TCA cycle, elevating NADH/FADH2, which enhances electron transport chain activity, resulting in ROS (reactive oxygen species) overproduction and oxidative stress. Excessive ROS activates stress kinases (JNK, IKKβ, p38 MAPK, PKC) that phosphorylate insulin receptor substrate at serine residues, directly inhibiting insulin signalling and inducing insulin resistance while causing ER stress, mitochondrial dysfunction, inflammatory responses, and activation of apoptosis pathways leading to beta cell death.
Read Full Study →
Part 5: VLC Diet Reverses Insulin Resistance, Hypertension, and Liver Fat Simultaneously
Impact of Very Low Carbohydrate Ketogenic Diets on Cardiovascular Risk Factors Among Patients With Type 2 Diabetes; GRADE-assessed Systematic Review and Meta-analysis of Clinical Trials
VLCKD (very low-carbohydrate ketogenic diet) significantly reduced HOMA-IR (insulin resistance) by -0.71 (P=0.001), fasting insulin by -1.45 (P=0.009), HbA1c (diabetes marker) by -0.29% (P<0.001), systolic blood pressure (significant reduction), and triglycerides by -17.95 mg/dl (P<0.001)—simultaneously addressing hypertension, diabetes, and liver fat through one dietary intervention. This meta-analysis examined 29 clinical trials through March 2024, providing the highest level of evidence that VLC diets reverse the insulin resistance triad simultaneously by addressing the root cause.
Read Full Study →
Part 6: Insulin Resistance → Asthma
Asthma Prevalence
🇬🇧 UK: 7.2 million people (approximately 8 in every 100 people) have asthma
🇺🇸 USA: 26.8 million adults (8.2%) currently have asthma; 44.2 million Americans (13.5%) have ever been diagnosed with asthma
Global: 434 million people worldwide estimated to have asthma (2025)
References: UK Asthma Statistics 2025 | American Lung Association
The Impact of Insulin Resistance on Loss of Lung Function and Response to Treatment in Asthma
Among 307 participants in the Severe Asthma Research Program, 46% had insulin resistance, a much higher prevalence than the general population. Patients with insulin resistance had significantly lower lung function (FEV1 and FVC), blunted responses to bronchodilators and corticosteroids, and lung function declined at almost twice the rate of patients without insulin resistance. The study concludes that insulin resistance is common in severe asthma patients and directly impairs lung function and treatment response.
Read Full Study →
Unraveling the Link Between Insulin Resistance and Bronchial Asthma
Hyperinsulinemia associated with insulin resistance has proven to be a stronger risk factor than body mass in developing asthma. Experimental studies show insulin resistance contributes to airway remodelling, promotion of airway smooth muscle contractility and proliferation, increased airway hyper-responsiveness, and release of pro-inflammatory cytokines. Epidemiological studies found individuals with severe and uncontrolled asthma have a higher prevalence of glycaemic dysfunction, and longitudinal studies linked glycaemic dysfunction to increased risk of asthma exacerbations.
Read Full Study →
Part 7: Insulin Resistance → OCD (Obsessive-Compulsive Disorder)
OCD Prevalence
🇬🇧 UK: 1.2% of UK population (approximately 750,000-800,000 people)
🇺🇸 USA: 2.3-2.5% of US adults (approximately 6-8 million people); 12-month prevalence: 1.2%
Global: 2-3% of world population estimated to have OCD
Note: OCD prevalence in severe asthma patients: 12% (significantly higher than general population)
References: American Psychiatric Association
Shared Genetic Etiology Between Obsessive-compulsive Disorder, Obsessive-compulsive Symptoms in the Population, and Insulin Signaling
Genome-wide association studies identified significant shared genetic etiology between OCD and Type 2 diabetes (specifically 'aggressive taboo thoughts' factor), levels of fasting insulin, and 2-hour glucose levels. CNS (central nervous system) insulin-linked gene sets associated with symmetry/counting/ordering symptoms. The study concludes that OCD, obsessive-compulsive symptoms in the population, and insulin-related traits share genetic risk factors, indicating a common aetiological mechanism underlying somatic and psychiatric disorders.
Read Full Study →
Converging Evidence Points Towards a Role of Insulin Signaling in Regulating Compulsive Behavior
TALLYHO/JngJ mice (a Type 2 diabetes model) displayed increased compulsivity-like behaviour and more anxiety compared to control mice, with blood glucose levels negatively correlated with spontaneous alternation behaviour (a measure of compulsivity). MRS revealed increased glucose levels in the dorsomedial striatum (brain region involved in OCD). The study provides in vivo evidence that insulin resistance and diabetes may contribute to compulsive and anxious behaviours through dysregulated glucose metabolism in specific brain regions.
Read Full Study →
Obsessive-compulsive Disorder, Insulin Signaling and Diabetes – A Novel Form of Physical Health Comorbidity: The Sweet Compulsive Brain
Clinical and epidemiological studies show higher prevalence of diabetes in OCD patients and vice versa compared to the general population. Deep brain stimulation (DBS) studies suggest abnormal dopaminergic transmission in the striatum may contribute to impaired insulin sensitivity in OCD. Bilateral DBS reduced both OCD symptoms and fasting insulin levels in OCD patients with and without Type 2 diabetes, suggesting a bidirectional relationship where treating one condition may benefit the other.
Read Full Study →
Part 8: Insulin Resistance → Irritable Bowel Syndrome (IBS)
IBS Prevalence
🇬🇧 UK: 10-20% of UK population (6.5-13 million people)
🇺🇸 USA: 10-15% of US adults (25-40 million people); most common GI diagnosis
Global: 10-20% of global population affected by IBS
Note: IBS patients have 2.05× increased risk of metabolic syndrome; Type 2 diabetes patients have 39% increased risk of developing IBS
References: International Foundation for GI Disorders
The Relationship Between Irritable Bowel Syndrome and Metabolic Syndrome: A Systematic Review and Meta-Analysis of 49,662 Individuals
IBS was associated with a 2.05-fold increased risk of metabolic syndrome (P<0.00001), with IBS-D (diarrhoea) patients showing the highest risk (RR=3.09). IBS patients showed significantly increased HOMA-IR (insulin resistance marker) by 0.21 (P<0.00001), higher obesity risk, elevated BMI, increased systolic hypertension, and abnormal lipid profiles including elevated LDL-C, total cholesterol, and triglycerides. This meta-analysis of 49,662 individuals demonstrates a clear association between IBS and insulin resistance/metabolic dysfunction.
Read Full Study →
Bidirectional Association Between Type 2 Diabetes and Irritable Bowel Syndrome: A Large-scale Prospective Cohort Study
Type 2 diabetes patients had a 39% increased risk of developing IBS (HR=1.39, P<0.001), with higher IBS risk in those with elevated fasting blood glucose. Conversely, IBS patients had an 18% higher risk of developing Type 2 diabetes (HR=1.18, P<0.001). This bidirectional association was consistent across all IBS subtypes and persisted in sensitivity analyses, demonstrating that Type 2 diabetes and IBS exhibit a true bidirectional causal relationship mediated by insulin resistance.
Read Full Study →
Pathophysiological Commonality Between Irritable Bowel Syndrome and Metabolic Syndrome: Role of Corticotropin-releasing Factor–Toll-like Receptor 4–Proinflammatory Cytokine Signaling
Metabolic syndrome (including insulin resistance, obesity, dyslipidaemia, hypertension) and IBS share pathophysiological mechanisms: impaired gut barrier function, dysbiosis, and low-grade systemic inflammation mediated by CRF-TLR4-proinflammatory cytokine signalling. Leaky gut induces bacterial translocation resulting in dysbiosis and increases lipopolysaccharide (LPS), which activates TLR4 to produce proinflammatory cytokines, contributing to both visceral hypersensitivity (IBS) and insulin resistance. The study establishes pathophysiological commonality between IBS and metabolic syndrome, suggesting therapeutic drugs for metabolic syndrome may also benefit IBS.
Read Full Study →
Part 9: Insulin Resistance → Cancer
Cancer Prevalence and Insulin Resistance Connection
Global Impact: Cancer continues to be a significant global health challenge. Type 2 diabetes patients have 10-17% higher overall cancer risk compared to general population
Specific Cancer Risks in Insulin-Resistant Patients:
- Liver cancer: 78% reduction with metformin treatment
- Pancreatic cancer: 46% reduction with metformin treatment
- Colorectal cancer: 23% reduction with metformin treatment
- Breast cancer: Significant reduction with metformin treatment
Key Finding: Type 1 diabetes patients on high daily insulin doses have 4× increased cancer risk versus low-dose insulin users
Insulin Resistance: The Increased Risk of Cancers
Hyperinsulinemia is a major factor influencing cancer initiation, progression, and metastasis across multiple cancer types including breast, colorectal, liver, pancreatic, endometrial, and ovarian cancer. Observations of cancer patients confirm that hyperinsulinemia drives obesity, Type 2 diabetes, and cancer development. The state of metabolic disorders observed in cancer patients is associated with poor outcomes of cancer treatment, higher cancer recurrence rates, and reduced overall survival. Type 1 diabetes patients on high daily insulin doses have a fourfold increased cancer risk compared to patients on low daily insulin doses, establishing hyperinsulinemia as a critical oncogenic factor.
Read Full Study →
Metformin: A Dual-role Player in Cancer Treatment and Prevention
Meta-analysis demonstrates that metformin (an insulin-sensitising drug) reduces cancer incidence by 30-50% among users. Specific reductions include: liver cancer (78%), pancreatic cancer (46%), colorectal cancer (23%), and breast cancer (6%). Clinical trials in breast cancer patients showed metformin reduced Ki67 proliferation markers and increased apoptosis (cancer cell death). Metformin's anticancer mechanisms include reducing hyperinsulinemia and IGF-1 levels, activating AMPK pathway to inhibit cancer cell growth, and inhibiting mTOR pathway to block protein synthesis in tumours, establishing insulin resistance reversal as a critical cancer prevention strategy.
Read Full Study →
Impact of Ketogenic Diets on Cancer Patient Outcomes: A Systematic Review and Meta-analysis
Ketogenic diets (high fat, very low carbohydrate) significantly reduce insulin levels and create an unfavourable metabolic environment for cancer cells. Meta-analysis of multiple studies shows ketogenic diet decreases tumour growth in preclinical models, reverses cancer cachexia (wasting syndrome), and when combined with standard cancer treatment shows improved outcomes. Clinical trials in glioblastoma (brain cancer) patients show prolonged remission from 4 months to over 5 years. Advanced cancer patients with stable disease or partial remission on PET-CT scans showed 3× higher ketosis levels (not related to weight loss), directly linking insulin reduction to improved cancer outcomes.
Read Full Study →
The Role of Insulin Resistance in Cancer
Insulin resistance creates an oncogenic environment through multiple mechanisms: high insulin levels directly activate PI3K/AKT/mTOR pathway promoting cell proliferation, increased bioavailable IGF-1 stimulates tumour growth, chronic inflammation from insulin resistance promotes cancer development and spread, and altered cellular energy usage fuels tumour expansion. The review establishes that insulin resistance is a significant and modifiable risk factor for development and progression of several major cancers including breast, liver, endometrial, colorectal, and pancreatic cancers. Since insulin resistance is modifiable through diet and lifestyle, understanding this connection opens new strategies for cancer prevention and treatment, with lifestyle interventions being fundamental to reducing cancer risk.
Read Full Study →