Transition Rates in Treatment-as-Usual Arms of Ultra-High-Risk Trials

confidence: high · 2 sources

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Working research — not a recommendation.

This page records what the evidence says a policy does, not what anyone should do about it. It has been synthesized from the cited sources but has not been independently reviewed.

What the evidence says

The sources on this page give transition rates for people at clinical high risk for psychosis (CHR-P) in general. They do not report rates for the treatment-as-usual (TAU) arms of ultra-high-risk trials as a separate quantity. The closest figure is a pooled estimate: CHR-P individuals have an up to 20% risk of developing psychosis within 2 years (95% CI: 17%–25%). The source does not say whether this figure comes from untreated natural history, from treated populations, or from a mix of trial arms. Read it as an upper bound for CHR-P samples, not as a TAU-arm baseline.

A second meta-analysis compares CHR-P-positive help-seekers with CHR-P-negative help-seekers. The estimated transition rate was 14.7% (95% CI, 9.7–21.7%) among CHR-P-positive individuals and 1.6% (95% CI, 0.8–3.2%) among CHR-P-negative individuals. Across 14 studies, CHR-P status was associated with an almost ten-fold increased risk of transition (RR 9.8; 95% CI, 4.5–21.82). The wide interval reflects heterogeneous methods across those studies. These figures are associational. They show that the CHR-P label separates higher-risk from lower-risk help-seekers. They do not show what any particular control condition produces.

The only evidence on how an intervention changes the transition rate comes from a meta-analysis of randomized controlled trials. It found that short-term (6–12 month) psychological interventions can halve the risk of illness onset at 12 months. The effect is not sustained at 24 months and longer. The authors say this may reflect delayed rather than prevented onset. This is the one causal claim on the page, and the source does not specify what the TAU or control condition was in those trials.

Evidence is thin on the page's central question. The claims give no transition rate measured in a TAU arm alone, no breakdown of TAU arms by what care they received, and no trend in TAU-arm rates over time.

Where the evidence splits

No contradictions in the current sources.

Thresholds and dose-response

No threshold established in the current sources.

Open empirical questions

Findings

CHR-P status increases the measured 2-year risk of transition to psychosis, up to 20%

confidence — direction: highconfidence — magnitude: highconsensus: thin for TAU arms specifically. The weight leans toward a 2-year risk near the stated range for CHR-P samples generally.
mechanism
not established in the claims. The risk comes from selecting help-seekers who meet CHR-P criteria. The sources give no causal pathway.
effect
up to 20% 2-year risk of developing psychosis (95% CI: 17%–25%) in CHR-P individuals.
conditions / moderators
the source does not say whether the figure reflects natural history, treated populations, or mixed trial arms. It is not a TAU-arm-specific rate.

CHR-P-positive status is associated with higher transition rates than CHR-P-negative status

confidence — direction: highconfidence — magnitude: mediumconsensus: settled on direction. The magnitude carries a wide interval.
mechanism
not established in the claims. The comparison is between help-seekers who do and do not meet CHR-P criteria.
effect
transition rate 14.7% (95% CI, 9.7–21.7%) in CHR-P-positive individuals versus 1.6% (95% CI, 0.8–3.2%) in CHR-P-negative individuals. The pooled risk ratio is 9.8 (95% CI, 4.5–21.82) across 14 studies.
conditions / moderators
the claims report consistent findings with no moderation by follow-up duration or sample characteristics. The wide risk-ratio interval reflects heterogeneous methods across studies.

Short-term psychological interventions decrease the 12-month risk of illness onset, and the decrease is not sustained at 24 months

confidence — direction: highconfidence — magnitude: mediumconsensus: thin. This is a single meta-analysis of randomized controlled trials, cited in a review.
mechanism
not established. The source suggests the result may reflect delayed rather than prevented onset.
effect
the 12-month risk of illness onset is halved relative to a control condition. The preventive effect is not sustained at 24 months and longer.
conditions / moderators
applies to short-term (6–12 month) interventions in CHR-P individuals. The source does not say what the TAU or control condition was. The authors advise interpreting the findings cautiously.