Insulin Resistance & OCD — USA & UK 1975–2022

Insulin Resistance & OCD

Prevalence trajectories in the USA and United Kingdom, 1975–2022. OCD affects an estimated 2–3% of the global population and is classified by the WHO as one of the leading causes of disability worldwide. Unlike purely metabolic conditions in this series, OCD does not show a dramatic parallel rise alongside insulin resistance — yet a clinically significant mechanistic link has emerged through shared neuroinflammatory and serotonergic pathways. The correlation is meaningful rather than dominant, and is increasingly relevant to integrative treatment approaches targeting the gut–brain–metabolic axis.

Why the two curves don't track each other exactly — even when the correlation is very high:

The solid line shows the percentage of adults with insulin resistance across the entire population — everyone with measurable insulin resistance, regardless of what condition it causes them. Because insulin resistance is the upstream root cause of many different diseases — type 2 diabetes, fatty liver, cognitive decline, cardiovascular disease and more — this curve rises relatively gradually as it reflects a burden shared across all of those outcomes.

The dotted line shows the prevalence of the specific condition studied on this page — in this case, only the people for whom insulin resistance has expressed itself as that particular disease. This curve can rise more steeply because it captures decades of accumulated cases: someone may develop insulin resistance at 35 but not manifest this condition until their 50s, so even a modest early rise in insulin resistance translates into a much larger rise in diagnosed cases years later.

The r value (e.g. r = 0.97) is a correlation coefficient. It doesn't measure whether the two lines are the same height — it measures how consistently they move together over time. An r of 0.97 means that 97% of the rise in this condition over the past five decades is statistically explained by the parallel rise in insulin resistance.

What the r value tells you:
0.50–0.70 — Modest connection. The two trends are related but many other factors are involved.
0.70–0.90 — Strong connection. Insulin resistance is a major driver, alongside other contributing causes.
0.90 and above — Dominant connection. Insulin resistance accounts for the overwhelming majority of the trend. At this level, it is difficult to argue that other factors are primarily responsible. The values seen across these studies — consistently 0.90 to 0.97 — place insulin resistance firmly in this category for every condition shown.

United States

USA — Insulin Resistance vs OCD

1975 – 2022  |  % of population
Insulin Resistance (%)
OCD Prevalence (%)
United Kingdom

UK — Insulin Resistance vs OCD

1975 – 2022  |  % of population
Insulin Resistance (%)
OCD Prevalence (%)
r = 0.73
USA
IR ↔ OCD
r = 0.76
UK
IR ↔ OCD
2–3%
OCD prevalence
both countries
1.5× ♀
Women affected
slightly more often
An honest reading of this correlation: OCD is distinct from purely metabolic conditions in this series. Its lifetime prevalence has been relatively stable at approximately 2–3% of the Western population across the study period — it did not surge dramatically in parallel with the metabolic crisis of the late 20th century. This means the correlation with rising insulin resistance is moderate (r ≈ 0.73–0.76) rather than the near-perfect correlation seen in T2DM (r = 0.98) or the strong correlation in ADHD (r = 0.94). Diagnosis rates have edged upward as awareness increased and diagnostic criteria were refined (DSM-III 1980, DSM-IV 1994, DSM-5 2013), but the dramatic parallel rise visible in other charts in this series is not present here. OCD is better understood as a condition whose severity and treatment resistance are worsened by metabolic dysfunction, rather than one primarily caused by it.
The neuroinflammatory & serotonergic pathway: Despite the more modest correlation, the mechanistic link is scientifically compelling. High refined carbohydrate and sugar consumption — the same dietary pattern that drives insulin resistance — elevates systemic lipopolysaccharide (LPS) through leaky gut and activates TLR4-driven proinflammatory cytokine signalling (TNF-α, IL-6, IL-1β). This neuroinflammatory cascade directly impairs serotonin (5-HT) synthesis and receptor sensitivity in the cortico-striato-thalamo-cortical (CSTC) circuits — the neural loops considered central to OCD symptomatology. Research in Frontiers in Psychiatry (2021) and Neuroscience & Biobehavioral Reviews (2022) identifies elevated CRP, IL-6, and TNF-α in OCD patients compared to controls. Insulin resistance amplifies this inflammatory burden by impairing insulin signalling in the prefrontal cortex and basal ganglia, disrupting dopaminergic and serotonergic regulation, and suppressing BDNF — a key modulator of synaptic plasticity implicated in OCD treatment response. Additionally, the gut microbiome produces approximately 90% of the body's serotonin precursors; gut dysbiosis — the same microbial signature associated with insulin resistance — reduces tryptophan availability for 5-HT synthesis. The GAPS protocol used in integrative remission programmes targets this gut–brain–metabolic axis directly. Sources: Fountas et al. (2022); Özdemir et al. (2021); Kleinridders et al. (2014); Turna et al. (2020).
Data sources
OCD USA — historical prevalence: Epidemiologic Catchment Area (ECA) Study 1980–1985 (Robins et al.): lifetime OCD prevalence 2.5–3.0%. National Comorbidity Survey (NCS-R 2001–2003, Kessler et al.): 12-month prevalence 1.0%, lifetime 1.6% by DSM-IV strict criteria. Estimates using DSM-5 structured clinical interview converge at 1.2–2.3%; broader symptom-level estimates reach 2–3%. WHO Global Burden of Disease 2019: OCD among top 10 causes of years lived with disability globally.
https://pubmed.ncbi.nlm.nih.gov/3736028/
https://pubmed.ncbi.nlm.nih.gov/15939837/
https://www.who.int/news-room/fact-sheets/detail/obsessive-compulsive-disorder
OCD UK — historical prevalence: OPCS Survey of Psychiatric Morbidity 1993–1995 (Meltzer et al.): OCD 1.2% in adults. Adult Psychiatric Morbidity Survey (APMS) 2007 & 2014 (McManus et al.): 1.3% consistent. NHS Digital 2014: community prevalence 1.1–1.3%. OCD UK charity estimates ~750,000 adults affected at any one time.
https://digital.nhs.uk/data-and-information/publications/statistical/adult-psychiatric-morbidity-survey
https://www.ocduk.org/ocd/how-many-people-have-ocd/
Global OCD burden: Ruscio et al. systematic review, Molecular Psychiatry 2010 (global prevalence 1.3%). WHO World Mental Health Surveys (Kessler et al. 2012): cross-national 12-month OCD 1.1–1.8%. GBD 2019: OCD affecting ~70 million people worldwide.
https://pubmed.ncbi.nlm.nih.gov/19529964/
https://pmc.ncbi.nlm.nih.gov/articles/PMC3188445/
OCD–Insulin Resistance & neuroinflammatory mechanistic link: Fountas et al., Neuroscience & Biobehavioral Reviews 2022 (elevated CRP, IL-6, TNF-α in OCD). Özdemir et al., Frontiers in Psychiatry 2021 (neuroinflammation via TLR4–cytokine pathway). Kleinridders et al., Cell Metabolism 2014 (insulin signalling in brain & psychiatric disorders). Bhatt et al., Progress in Neuropsychopharmacology & Biological Psychiatry 2020 (BDNF, IR and OCD treatment response).
https://pubmed.ncbi.nlm.nih.gov/35314183/
https://www.frontiersin.org/articles/10.3389/fpsyt.2021.665782/full
https://pubmed.ncbi.nlm.nih.gov/24768741/
Gut–brain axis, tryptophan & serotonin in OCD: Yano et al., Cell 2015 (gut bacteria regulate host serotonin biosynthesis). Turna et al., Neuropsychopharmacology 2020 (altered gut microbiota in OCD). Simpson et al., Biological Psychiatry 2021 (microbiota–gut–brain axis and OCD).
https://pubmed.ncbi.nlm.nih.gov/25860609/
https://pubmed.ncbi.nlm.nih.gov/31761722/
Insulin Resistance USA & UK: NHANES III 1988–94; NHANES 1999–2018 (Hirode & Wong, JAMA 2020); NHS Health Survey England 2003–2021; GBD 2019 metabolic risk; Diabetes UK; Frontiers meta-analysis 2025.
https://pmc.ncbi.nlm.nih.gov/articles/PMC11601873/
https://www.diabetesuk.org/professionals/position-statements-reports/statistics/
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