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Clinical Atlas Prestige · Evidence-first

Psych MEQs / SAQsFoundations — epidemiologic methods for psychiatry

Psych MEQs / SAQs · Foundations — epidemiologic methods for psychiatry

Epidemiologic measures and inference in psychiatry (MEQ)

FRANZCP/MRCPsych-style MEQ on frequency measures, RR/OR/PAF, bias families, screening base rates, and causal language.

20 marks20 min
On this page & tools

Target exams

FRANZCPMRCPsychABPNMD-DNB

Target exams

FRANZCPMRCPsychABPNMD-DNB
Prompt
You are the psychiatry registrar preparing a teaching session for core trainees after a journal club abstract claimed that 'childhood adversity causes 40% of adult depression' based on a cross-sectional survey OR of 2.8 and a quoted population attributable fraction of 40%. Separately, the local public health unit asks whether a new online depression screen (sensitivity 90%, specificity 90%) should be rolled out to all adults in a region where true major depression prevalence is about 2%. (i) Define point prevalence, period prevalence, cumulative incidence, and incidence rate, and state which measure best describes current community caseload for service planning. (ii) Explain the difference between a relative risk, an odds ratio, and a population attributable fraction, including when OR may mislead if read as RR. (iii) List three major bias families that could distort the adversity–depression association and give a psychiatry-specific example of each. (iv) Using the screening numbers above, explain qualitatively why PPV will be low in community rollout and what programme criteria (Wilson–Jungner tradition) you would require before endorsing screening. (v) Outline how you would rewrite the journal club causal claim in scientifically defensible language. (20 marks)

Model answer

Reveal model answer

(i) Frequency measures. Point prevalence: existing cases at one time / population. Period prevalence: people who were cases during an interval (for example 12 months) / population. Cumulative incidence: new cases over a fixed period / population initially at risk. Incidence rate: new cases / person-time at risk.[1] Current community caseload for service planning is best informed by period (especially 12-month) prevalence plus severity/need, not lifetime prevalence or crude hospital counts alone.[1]

(ii) RR, OR, PAF. RR compares risks (risk_exposed / risk_unexposed). OR compares odds; in case-control work it is the natural association measure and approximates RR when the outcome is uncommon, but overstates relative risk if misread as RR when outcomes are common.[1] PAF estimates the proportion of population cases attributable to an exposure if the association is causal and estimates are unbiased; it depends on exposure prevalence and association strength and is easily misused when assumptions fail or correlated factors are naively summed.[3]

(iii) Bias families (examples). Selection: non-response or clinic-only sampling enriching trauma and depression co-occurrence.[2][8] Information: recall bias — depressed adults over-reporting childhood adversity relative to controls.[2][8] Confounding: childhood socioeconomic disadvantage as a common cause of adversity exposure and later depression risk, distorting the crude OR if uncontrolled.[2]

(iv) Screening. With Sn and Sp both 90% but prevalence about 2%, false positives greatly outnumber true positives among screen-positives, so PPV is low — most “positives” are not cases.[4][5] Before rollout, require Wilson–Jungner-style programme conditions: important condition, acceptable accurate test, agreed pathway and capacity for assessment/treatment, acceptable false-positive burden, cost balance, and quality-assured continuous programme — not test marketing alone.[6]

(v) Rewrite claim. Defensible language: “In this cross-sectional survey, childhood adversity was associated with higher odds of adult depression (OR 2.8). A model-based PAF near 40% would require strong causal assumptions, absence of major bias/confounding, and correct exposure prevalence; cross-sectional data cannot establish temporality. Longitudinal and intervention evidence are needed before claiming that adversity causes 40% of depression cases.” Use Hill viewpoints as weight-of-evidence, not proof.[2][3][7]

Common errors

Equating lifetime prevalence with current need; treating PAF as assumption-free; reading OR as RR when caseness is common; listing only “bias” without naming selection/information/confounding; endorsing community screens from Sn/Sp alone; asserting causation from a single cross-section.[1][2][3][5]

References

  1. [1]Grimes DA, Schulz KF An overview of clinical research: the lay of the land Lancet, 2002.PMID 11809203
  2. [2]Grimes DA, Schulz KF Bias and causal associations in observational research Lancet, 2002.PMID 11812579
  3. [3]Rockhill B, Newman B, Weinberg C Use and misuse of population attributable fractions Am J Public Health, 1998.PMID 9584027
  4. [4]Altman DG, Bland JM Diagnostic tests. 1: Sensitivity and specificity BMJ, 1994.PMID 8019315
  5. [5]Altman DG, Bland JM Diagnostic tests 2: Predictive values BMJ, 1994.PMID 8038641
  6. [6]Andermann A, Blancquaert I, Beauchamp S, Déry V Revisiting Wilson and Jungner in the genomic age: a review of screening criteria over the past 40 years Bull World Health Organ, 2008.PMID 18438522
  7. [7]Hill AB The environment and disease: association or causation? Proc R Soc Med, 1965.PMID 14283879
  8. [8]Sackett DL Bias in analytic research J Chronic Dis, 1979.PMID 447779