Field notes · Anxiety & OCD · Food & eating

The doubting disease. What OCD is, where it comes from, how it tangles with anorexia, and how exposure therapy loosens its grip — with a practice you can try.

A 22-minute read, with five interactive tools · Reid Robison, MD

Nineteenth-century French psychiatrists called it la folie du doute, the madness of doubt. It's a better name than the modern one. Obsessive-compulsive disorder isn't about liking things tidy. It's a brain that can't accept "probably fine," and a person who spends hours trying to make a feeling of uncertainty go away. This post covers what OCD is and isn't, what causes it, how it's measured, why it travels so often with anorexia nervosa, and the treatment that works best: exposure and response prevention.

TL;DR

OCD is common and often hidden. About 2.3% of people meet criteria over a lifetime, usually starting by early adulthood¹. Nearly everyone has intrusive thoughts; OCD is getting stuck on them².
It's about half genetic. Family studies put heritability near 47%, and a 2025 study of 53,660 cases found 30 risk regions in the genome^3,⁴.
OCD and anorexia are genetic cousins. Their genetic correlation is about 0.5, roughly 1 in 5 people with anorexia have OCD at some point, and people with OCD are about 17 times more likely to be diagnosed with anorexia^4,^5,⁶.
The Y-BOCS is the standard measure. You can take the self-report version here and track change over time against expert definitions of response and remission^7,⁸.
Exposure and response prevention (ERP) is the first-line treatment, with large effects in trials. Added to medication, ERP helped 80% of people in one trial, versus 23% for an antipsychotic^9,¹⁰.
You can try a gentle ERP practice below: build a fear ladder, run a short exposure, and see how your prediction compares with what actually happened.

What OCD is

OCD has two parts. Obsessions are intrusive, unwanted thoughts, images or urges that cause anxiety or disgust. Compulsions are repeated behaviors or mental acts a person feels driven to perform to neutralize the obsession or prevent something bad from happening. To be a disorder, they take up a lot of time (more than an hour a day is the DSM's example) or cause real distress or impairment¹¹.

Three things are often misunderstood:

Intrusive thoughts are normal. In a study across 13 countries on six continents, about 94% of people reported at least one unwanted intrusive thought in the past three months². Having a disturbing thought isn't the problem. Treating it as dangerous and trying to neutralize it is.
Compulsions can be invisible. Mental reviewing, counting, praying, replacing a bad thought with a good one and seeking reassurance all count.
Insight varies. Many people know their fears are excessive; some are less sure, and a few are convinced. The DSM records this as good, poor or absent insight. It also notes when someone has a current or past tic disorder¹¹.

OCD usually starts in childhood, the teens or early adulthood. In the US National Comorbidity Survey Replication, the average age of onset was about 19.5, a quarter of cases started by age 14, and boys tended to start earlier than girls¹. Since 2013 the DSM has placed OCD in its own chapter with related conditions: body dysmorphic disorder, hoarding disorder, trichotillomania and skin-picking disorder¹¹.

Research finds that OCD symptoms cluster into four broad dimensions¹²:

Contamination

ObsessionGerms, illness, bodily fluids, chemicals

CompulsionWashing, cleaning, avoiding touch

Responsibility for harm

ObsessionCausing a fire, an accident, a mistake

CompulsionChecking, re-checking, seeking reassurance

Unacceptable thoughts

ObsessionUnwanted violent, sexual or religious thoughts

CompulsionMental rituals, neutralizing, avoidance

Symmetry, "just right"

ObsessionThings feel incomplete, uneven or wrong

CompulsionOrdering, arranging, repeating until it feels right

Where it comes from

Genes. In a Swedish study of more than 24,000 people with OCD and their relatives, heritability was about 47%, and risk rose with genetic closeness³. The largest genetic study to date (53,660 cases and more than 2 million controls) found 30 risk regions and estimated that thousands of common variants each add a tiny amount of risk. Common variants explained about 7% of risk on their own⁴.
Brain circuits. OCD involves loops linking the orbitofrontal cortex, the striatum and the thalamus, circuits that flag errors and help us decide when something is "done." The same 2025 study found OCD risk genes concentrated in neurons of these circuits⁴.
Learning. A compulsion brings quick relief. That relief teaches the brain the ritual was necessary, which makes the next urge stronger. It's a textbook case of negative reinforcement.
Thinking patterns. The cognitive model says intrusive thoughts become obsessions when a person reads them as meaningful and feels responsible for preventing harm: "If I thought it, it might happen, and it would be my fault"¹³.

Tool · why rituals backfire

An illustration of the OCD loop. Compare what anxiety does when you ritualize versus when you stay with it.

Screening, diagnosis and tracking

Screening. Brief self-report questionnaires like the 18-item Obsessive-Compulsive Inventory–Revised (OCI-R) and the 20-item Dimensional Obsessive-Compulsive Scale (DOCS) are good first passes^14,¹². Two quick clinician questions are often enough to open the door: Do you have thoughts that bother you and that you can't get rid of? Do you have to do things over and over, or check things, to feel okay?

Diagnosis comes from a clinical interview. The clinician-rated Yale-Brown Obsessive Compulsive Scale (Y-BOCS), published in 1989, is still the standard: a symptom checklist plus ten severity items (time, interference, distress, resistance and control, for obsessions and for compulsions separately), each scored 0–4 for a total of 0–40⁷.

Tracking. Repeating the Y-BOCS every few weeks shows whether treatment is working. An international expert consensus defines response as at least a 35% drop (25–35% is partial response) and remission as a score of 12 or less, each sustained for at least a week alongside a clinician's global rating⁸.

Tool · Y-BOCS self-report

The same ten severity items as the clinician scale, answered about the past week. Nothing is saved or sent anywhere. Bands: 0–7 subclinical, 8–15 mild, 16–23 moderate, 24–31 severe, 32–40 extreme.

Tool · am I responding to treatment?

Enter a starting Y-BOCS score and a current one. This applies the 2016 consensus definitions (it can't include the clinician's global rating).

Starting score (0–40) Current score (0–40)

OCD and anorexia: the overlap

In my work with eating disorders, OCD comes up constantly. The science says that isn't a coincidence.

~1 in 5people with anorexia have OCD at some point in their lives (19% lifetime, 14% currently). In studies that followed people over time, the figure was 44%⁵.

17×higher risk of an anorexia diagnosis for people with OCD than for matched controls, in a Danish national cohort of more than 15,000 people with either diagnosis⁶.

~0.5genetic correlation between OCD and anorexia, among the highest between any two psychiatric conditions^15,⁴.

Genetic correlation (r_g) between anorexia nervosa and OCD in three genome-wide studies. Zero means no shared common-variant genetics; 1 means fully shared. Each new, larger study has found about the same answer^16,^15,⁴. The combined AN–OCD genetic signal is concentrated in the basal ganglia and its medium spiny neurons, the same habit and reward circuitry both conditions involve¹⁵.

Why they overlap

Shared traits that come first. Perfectionism, harm avoidance, intolerance of uncertainty and a need for things to feel "just right" often appear in childhood, before either illness¹⁵.
Cognitive inflexibility. People with anorexia, like many with OCD, show measurable difficulty switching mental sets, which makes rules and routines feel safer than change¹⁷.
Habit circuitry. One leading model of why anorexia persists is that restriction starts as a goal but becomes a habit, run by the same striatal circuits that drive compulsions¹⁸.
Starvation itself. In the Minnesota Starvation Experiment of the 1940s, healthy young men on a semi-starvation diet developed food obsessions, rituals and rigidity that faded only with refeeding¹⁹. Low weight amplifies obsessionality, which is one reason nutrition comes first.

Tool · where the symptoms overlap

Tap any symptom to see how it shows up in OCD, in anorexia, or in both.

Is it OCD or the eating disorder?Two questions clinicians ask

What is the ritual about? Rituals focused only on food, weight or shape (counting calories, cutting food a certain way, body checking) are usually part of the eating disorder. Rituals about germs, harm, symmetry or unacceptable thoughts that have nothing to do with food point to OCD. Many people have both.

How does it feel? OCD obsessions usually feel unwanted and senseless, and people want them gone. Anorexia's rules often feel justified, even like part of who the person is, at least early on. That difference changes how treatment is framed, though exposure works for both.

What works for OCD

Exposure and response prevention (ERP) is the first-line psychotherapy. Across randomized trials, CBT with ERP has large effects compared with waitlist or placebo control conditions, and in a network meta-analysis psychotherapy outperformed medication^9,²⁰. In a landmark trial, ERP outperformed clomipramine and placebo, and combining ERP with clomipramine did no better than ERP alone²¹.
SSRIs (fluoxetine, fluvoxamine, sertraline, paroxetine, escitalopram) and clomipramine help many people. OCD usually needs higher doses than depression, and higher doses work better²². A fair trial is 8–12 weeks at a good dose.
When the first steps aren't enough: adding ERP to an SSRI is the best-supported next step. Low-dose antipsychotics such as aripiprazole or risperidone give a modest additional benefit for some people^10,²³.
Neuromodulation. Deep TMS was FDA-cleared for OCD in 2018 after a sham-controlled trial²⁴. Deep brain stimulation is reserved for severe, treatment-resistant cases.

Response rates in key OCD trials. Top: people already on an SSRI who still had symptoms were randomized to add ERP, risperidone or placebo for 8 weeks; response was a Y-BOCS drop of at least 25%¹⁰. Middle: deep TMS versus sham, response = at least 30% drop²⁴. Bottom: a residential program combining ERP with eating disorder treatment for people with both conditions²⁵.

How ERP works

ERP has two halves. Exposure means deliberately approaching the trigger: touching the doorknob, leaving the stove unchecked, letting the "wrong" thought stay. Response prevention means not doing the ritual afterward, including the mental ones. People work up a ladder from easier to harder steps, usually with a therapist.

The older explanation was habituation: stay with the fear long enough and it fades. That happens, but it doesn't predict who gets better. The current model is inhibitory learning: exposure teaches the brain a new, competing lesson ("I touched it and nothing bad happened; I can handle not knowing"), and that lesson grows stronger when an expectation is clearly violated. So modern ERP focuses less on waiting for anxiety to drop and more on testing predictions, varying the exposures, and dropping safety behaviors²⁶.

ERP when anorexia is part of the picture

It can work for both at once. In a residential program that combined ERP with eating disorder treatment for 56 adults with OCD and an eating disorder, 80% improved meaningfully on OCD symptoms, half reached mild or minimal OCD by discharge, and eating disorder symptoms improved too. People with bulimia improved more than those with anorexia^25,²⁷.
Exposure can target fear of food itself. A pilot randomized trial applied ERP to eating-related fear in anorexia after weight restoration, building ladders of feared foods and eating situations, and found it feasible and promising²⁸.
Nutrition comes first. Starvation amplifies obsessions and rigidity¹⁹, and fluoxetine did not prevent relapse in anorexia after weight restoration²⁹. In practice, weight restoration, ERP and family or team support carry most of the load. Medication can still help OCD once weight is restored.

Try it: a guided exposure practice

This is a small taste of an ERP session: build a ladder, pick a low step, make a prediction, do the exposure without the ritual, rate your distress as you go, and compare what you predicted with what happened.

Tool · the ERP practice lab

Start low and stay safe. Pick a step rated 40 or lower. Never do anything actually dangerous. If OCD is severe, or if you have an eating disorder, do exposures with your therapist or treatment team, not alone. If distress ever comes with thoughts of harming yourself, stop and call or text 988.

1 · Choose a theme to load an example ladder. Edit any step or its distress rating (SUDS, 0–100), or add your own.

Where to start

If your Y-BOCS self-report is 16 or higher, or OCD is costing you an hour a day, look for a therapist who specifically does ERP. The International OCD Foundation (iocdf.org) keeps a directory.
Ask any therapist directly: "Do you use exposure and response prevention for OCD?" General talk therapy and reassurance can make OCD worse.
If an eating disorder is part of the picture, make sure your team addresses both. Treating one and ignoring the other is a common reason recovery stalls.
Medication is a reasonable partner to ERP, at OCD doses and for long enough.

Related: The worry engine, on generalized anxiety and the anxiety family, and the anxiety & OCD and food & eating topic pages.

Sources

Ruscio AM, Stein DJ, Chiu WT, Kessler RC. The epidemiology of obsessive-compulsive disorder in the National Comorbidity Survey Replication. Mol Psychiatry. 2010;15(1):53–63.
Radomsky AS, Alcolado GM, Abramowitz JS, et al. Part 1 — You can run but you can't hide: intrusive thoughts on six continents. J Obsessive Compuls Relat Disord. 2014;3(3):269–279.
Mataix-Cols D, Boman M, Monzani B, et al. Population-based, multigenerational family clustering study of obsessive-compulsive disorder. JAMA Psychiatry. 2013;70(7):709–717.
Strom NI, Gerring ZF, Galimberti M, et al. Genome-wide analyses identify 30 loci associated with obsessive–compulsive disorder. Nat Genet. 2025;57:1389–1401.
Mandelli L, Draghetti S, Albert U, De Ronchi D, Atti AR. Rates of comorbid obsessive-compulsive disorder in eating disorders: a meta-analysis of the literature. J Affect Disord. 2020;277:927–939.
Zhu LY, et al. Predictors of anorexia nervosa and obsessive-compulsive disorder comorbidity and order of diagnosis in a Danish national cohort. Int J Eat Disord. 2025;58(9):1817–1829.
Goodman WK, Price LH, Rasmussen SA, et al. The Yale-Brown Obsessive Compulsive Scale. I. Development, use, and reliability. Arch Gen Psychiatry. 1989;46(11):1006–1011.
Mataix-Cols D, Fernández de la Cruz L, Nordsletten AE, Lenhard F, Isomura K, Simpson HB. Towards an international expert consensus for defining treatment response, remission, recovery and relapse in obsessive-compulsive disorder. World Psychiatry. 2016;15(1):80–81.
Öst LG, Havnen A, Hansen B, Kvale G. Cognitive behavioral treatments of obsessive-compulsive disorder. A systematic review and meta-analysis of studies published 1993–2014. Clin Psychol Rev. 2015;40:156–169.
Simpson HB, Foa EB, Liebowitz MR, et al. Cognitive-behavioral therapy vs risperidone for augmenting serotonin reuptake inhibitors in obsessive-compulsive disorder: a randomized clinical trial. JAMA Psychiatry. 2013;70(11):1190–1199.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR). Washington, DC: APA Publishing; 2022. Obsessive-Compulsive and Related Disorders chapter.
Abramowitz JS, Deacon BJ, Olatunji BO, et al. Assessment of obsessive-compulsive symptom dimensions: development and evaluation of the Dimensional Obsessive-Compulsive Scale. Psychol Assess. 2010;22(1):180–198.
Salkovskis PM. Obsessional-compulsive problems: a cognitive-behavioural analysis. Behav Res Ther. 1985;23(5):571–583.
Foa EB, Huppert JD, Leiberg S, et al. The Obsessive-Compulsive Inventory: development and validation of a short version. Psychol Assess. 2002;14(4):485–496.
Yilmaz Z, Halvorsen M, Bryois J, et al. Examination of the shared genetic basis of anorexia nervosa and obsessive-compulsive disorder. Mol Psychiatry. 2020;25(9):2036–2046.
Watson HJ, Yilmaz Z, Thornton LM, et al. Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa. Nat Genet. 2019;51(8):1207–1214.
Roberts ME, Tchanturia K, Stahl D, Southgate L, Treasure J. A systematic review and meta-analysis of set-shifting ability in eating disorders. Psychol Med. 2007;37(8):1075–1084.
Steinglass JE, Walsh BT. Neurobiological model of the persistence of anorexia nervosa. J Eat Disord. 2016;4:19.
Keys A, Brožek J, Henschel A, Mickelsen O, Taylor HL. The Biology of Human Starvation. Minneapolis: University of Minnesota Press; 1950.
Skapinakis P, Caldwell DM, Hollingworth W, et al. Pharmacological and psychotherapeutic interventions for management of obsessive-compulsive disorder in adults: a systematic review and network meta-analysis. Lancet Psychiatry. 2016;3(8):730–739.
Foa EB, Liebowitz MR, Kozak MJ, et al. Randomized, placebo-controlled trial of exposure and ritual prevention, clomipramine, and their combination in the treatment of obsessive-compulsive disorder. Am J Psychiatry. 2005;162(1):151–161.
Bloch MH, McGuire J, Landeros-Weisenberger A, Leckman JF, Pittenger C. Meta-analysis of the dose-response relationship of SSRI in obsessive-compulsive disorder. Mol Psychiatry. 2010;15(8):850–855.
Veale D, Miles S, Smallcombe N, Ghezai H, Goldacre B, Hodsoll J. Atypical antipsychotic augmentation in SSRI treatment refractory obsessive-compulsive disorder: a systematic review and meta-analysis. BMC Psychiatry. 2014;14:317.
Carmi L, Tendler A, Bystritsky A, et al. Efficacy and safety of deep transcranial magnetic stimulation for obsessive-compulsive disorder: a prospective multicenter randomized double-blind placebo-controlled trial. Am J Psychiatry. 2019;176(11):931–938.
Simpson HB, Wetterneck CT, Cahill SP, et al. Treatment of obsessive-compulsive disorder complicated by comorbid eating disorders. Cogn Behav Ther. 2013;42(1):64–76.
Craske MG, Treanor M, Conway CC, Zbozinek T, Vervliet B. Maximizing exposure therapy: an inhibitory learning approach. Behav Res Ther. 2014;58:10–23.
Leonard RC, Riemann BC. Treatment of obsessive-compulsive disorder with comorbid eating disorders. International OCD Foundation, expert opinion.
Steinglass JE, Albano AM, Simpson HB, et al. Confronting fear using exposure and response prevention for anorexia nervosa: a randomized controlled pilot study. Int J Eat Disord. 2014;47(2):174–180.
Walsh BT, Kaplan AS, Attia E, et al. Fluoxetine after weight restoration in anorexia nervosa: a randomized controlled trial. JAMA. 2006;295(22):2605–2612.

Educational only. This isn't medical advice and isn't a substitute for care. Self-report scales can't diagnose a condition. If you're struggling or thinking about ending your life, call or text 988 (US, 24/7).