Trial reportJAMA psychiatry2025

Semaglutide Treatment of Antipsychotic-Treated Patients With Schizophrenia, Prediabetes, and Obesity: The HISTORI Randomized Clinical Trial.

Ashok A Ganeshalingam, Nicolai Uhrenholt, Sidse Arnfred, Peter Gæde, Signe Düring, Elsebeth N Stenager, Nick Bünger, Andreas K Pedersen, Niels Bilenberg, Jan Frystyk

Registry-linked trialAbstract readClinical Trial, Phase IIRandomized Controlled Trial
In one paragraph

Trial report in JAMA psychiatry, 2025. The graph read 6 numbers from its abstract, feeding 4 cells of the map: it supports the treatment in 3, finds no clear difference in 1. It reports registered trial NCT05193578. Cited by 13 papers.

6numbers the graph read from it
4cells of the map it votes in
13citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

← favours the treatmentfavours the comparator →
-55.818.50 · no effect
Change in HbA1conce-weekly subcutaneous semaglutide vs placebofavours the treatment · obesity, t2dfeeds one cell of the map
Δ -0.46-0.56 to -0.36
Semaglutide reduced HbA1c by 0.46% of total hemoglobin (95% CI, -0.56% to -0.36%) and body weight by 9.21 kg (95% CI, -11.68 to -6.75).
Triglyceridesonce-weekly subcutaneous semaglutide vs placebono clear difference · obesity, t2dfeeds one cell of the map
Δ -29.2-55.8 to 2.65.03
An HbA1c less than 5.7% of total hemoglobin was achieved in 81% vs 19% of patients treated with semaglutide and placebo, respectively (P < .001); improvements in high-density cholesterol by 10.81 mg/dL (95% CI, 2.70-18.53; P = .007) and triglycerides by -29.20 mg/dL (95% CI, -55.75 to 2.65; P = .03) (to convert to millimoles per liter, multiply by 0.0113) were also observed.
Quality of life & behaviourfavours the treatment · against placebo · obesity, t2dfeeds one cell of the map
improved 2.001.52 to 5.98P = .001
Finally, semaglutide improved physical QoL by 3.75 points on the SF-36v2 (95% CI, 1.52-5.98; P = .001) but had no significant effect on mental QoL scores or PANSS-6 score.
Physical QoLonce-weekly subcutaneous semaglutide vs placebofavours the treatment · obesity, t2dfeeds one cell of the map
Δ 3.751.52 to 5.98.001
Finally, semaglutide improved physical QoL by 3.75 points on the SF-36v2 (95% CI, 1.52-5.98; P = .001) but had no significant effect on mental QoL scores or PANSS-6 score.
Change in body weightonce-weekly subcutaneous semaglutide vs placebofavours the treatment · obesity, t2dfeeds one cell of the map
Δ -9.21-11.7 to -6.75
Semaglutide reduced HbA1c by 0.46% of total hemoglobin (95% CI, -0.56% to -0.36%) and body weight by 9.21 kg (95% CI, -11.68 to -6.75).
High-density cholesterolonce-weekly subcutaneous semaglutide vs placebofavours the treatment · obesity, t2dfeeds one cell of the map
improvements 10.82.70 to 18.5P = .007
An HbA1c less than 5.7% of total hemoglobin was achieved in 81% vs 19% of patients treated with semaglutide and placebo, respectively (P < .001); improvements in high-density cholesterol by 10.81 mg/dL (95% CI, 2.70-18.53; P = .007) and triglycerides by -29.20 mg/dL (95% CI, -55.75 to 2.65; P = .03) (to convert to millimoles per liter, multiply by 0.0113) were also observed.

clause the extractor read what became the number

2 · Its place on the map

Where it lands on the map

Rows are treatments, columns are outcomes. The coloured squares are the cells this paper feeds, coloured by the vote it casts there. Click one to jump to what this paper adds to it.

supports the treatmentfavours the comparatorno clear differenceread, but no usable result
3 · What it changes

What it adds to each cell

For every cell the paper feeds: the belief in the claim with and without this paper, and this paper's estimate drawn against every other readable study in the cell. The ringed dot is this paper.

GLP-1 receptor agonists×lipids

InconclusiveOpen on the map →What to test next →

9 readable studies in this cell: 3 favour the treatment, 6 find no difference, 0 favour the comparator.

Belief with this paper
0.50one trial · 1 family supports, 0 contradict · against placebo
Without it
0.50This paper does not move the number.
← favours the comparatorfavours the treatment →
0 · no effect
This paper154 enrolled · 2022
improvements 10.82.70 to 18.5
NCT00676338820 enrolled · 2008
Δ -0.01-0.18 to 0.15
NCT00781937422 enrolled · 2008
Treatment Contrast -0.11-0.20 to -0.01
NCT04019197108 enrolled · 2019
β coefficient -7.17-22.2 to 7.85
NCT0488111060 enrolled · 2021
Δ -4.80-32.6 to 22.9
NCT0062028249 enrolled · 2008
Least squares mean -2.24-17.8 to 13.4
NCT0331578012 enrolled · 2017
Δ -15.4-118 to 87.6

GLP-1 receptor agonists×quality of life & behaviour

SupportsOpen on the map →What to test next →

14 readable studies in this cell: 4 favour the treatment, 6 find no difference, 4 favour the comparator.

Belief with this paper
0.44contested · 4 families support, 5 contradict · against placebo
Without it
0.37This paper moves it by +0.07.
← favours the comparatorfavours the treatment →
0 · no effect
This paper154 enrolled · 2022
Δ 3.751.52 to 5.98
NCT017204463,297 enrolled · 2013
Δ 0.50-0.48 to 1.47
NCT039879191,879 enrolled · 2019
Δ -0.24-0.50 to 0.03
NCT02963935282 enrolled · 2017
Δ 0.16-1.19 to 1.52
NCT05564039282 enrolled · 2022
Δ 4.10-1.00 to 9.20
NCT03951753117 enrolled · 2019
Δ -246-358 to -133
NCT04311411114 enrolled · 2020
Δ 6.63-1.53 to 14.8
NCT04019197108 enrolled · 2019
β coefficient 420-1012 to 1852
NCT0304179261 enrolled · 2017
Δ -236-322 to -149
weight loss -6.50-10.2 to -2.90

GLP-1 receptor agonists×glycemic control

SupportsOpen on the map →What to test next →

40 readable studies in this cell: 97 favour the treatment, 16 find no difference, 10 favour the comparator.

Belief with this paper
0.91replicated · 68 families support, 7 contradict · against placebo
Without it
0.91This paper does not move the number. It would be established.
← favours the treatmentfavours the comparator →
0 · no effect
This paper154 enrolled · 2022
Δ -0.46-0.56 to -0.36
NCT017204463,297 enrolled · 2013
Δ -0.66-0.80 to -0.52
NCT036893742,274 enrolled · 2018
Δ -0.29-0.38 to -0.20
NCT039879191,879 enrolled · 2019
Δ -0.51-0.64 to -0.38
NCT026078651,864 enrolled · 2016
Δ -0.50-0.60 to -0.40
NCT013360231,663 enrolled · 2011
Treatment contrast -0.64-0.75 to -0.53
NCT040178321,441 enrolled · 2019
Δ -0.20-0.30 to -0.10
NCT018365231,398 enrolled · 2013
Δ -0.20-0.32 to -0.07
NCT019301881,231 enrolled · 2013
Δ -1.06-1.21 to -0.91
NCT007344741,202 enrolled · 2008
Δ -0.71-0.87 to -0.55
NCT020581471,170 enrolled · 2014
Δ -0.29-0.38 to -0.19
NCT003184611,091 enrolled · 2006
Δ -1.09-1.30 to -0.88
NCT021289321,089 enrolled · 2014
Δ -0.81-0.96 to -0.67

GLP-1 receptor agonists×body weight & composition

SupportsOpen on the map →What to test next →

40 readable studies in this cell: 83 favour the treatment, 15 find no difference, 11 favour the comparator.

Belief with this paper
0.90replicated · 64 families support, 7 contradict · against placebo
Without it
0.90This paper does not move the number.
← favours the treatmentfavours the comparator →
0 · no effect
This paper154 enrolled · 2022
Δ -9.21-11.7 to -6.75
NCT012722193,731 enrolled · 2011
Δ -5.39-5.82 to -4.95
Δ -17.3-18.1 to -16.6
NCT017204463,297 enrolled · 2013
Δ -2.95-3.47 to -2.44
NCT035489351,961 enrolled · 2018
Δ -12.4-13.4 to -11.5
NCT039879191,879 enrolled · 2019
Δ -1.70-2.60 to -0.70
NCT026078651,864 enrolled · 2016
Δ -2.50-3.00 to -2.00
NCT056467061,407 enrolled · 2023
Δ -14.8-16.2 to -13.4
NCT018365231,398 enrolled · 2013
Δ -4.90-5.65 to -4.16
NCT035527571,210 enrolled · 2018
Δ -6.21-7.28 to -5.15
NCT007344741,202 enrolled · 2008
Δ -1.50-2.08 to -0.92
Δ -10.4-11.2 to -9.50
NCT020581471,170 enrolled · 2014
Δ 14.38.37 to 20.3
4 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT05193578 phase2completed

Home-based Intervention With Semaglutide Treatment Of Neuroleptica-Related Prediabetes

Ran2022Enrolled154Registered outcomes17Posted comparisons0ConditionsPrediabetic State, SchizophreniaArmsPlacebo, Semaglutide, 1.34 mg/mL
Open the trial in the graph
5 · Its place in the literature

Who cites it

13 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
6 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

7 · Who and what money

Authors and funding

10 authors.

Ashok A GaneshalingamDepartment of Endocrinology, Odense University Hospital, Odense, Denmark.
Nicolai UhrenholtDepartment of Clinical Research, Faculty of Health Science, University of Southern Denmark, Odense, Denmark.
Sidse ArnfredPsychiatric Research Unit, Copenhagen University Hospital-Psychiatry Region Zealand, Slagelse, Denmark.
Peter GædeDepartment of Internal Medicine, Geriatrics and Neurology M3, Slagelse, Denmark.
Signe DüringPsychiatric Research Unit, Copenhagen University Hospital-Psychiatry Region Zealand, Slagelse, Denmark.
Elsebeth N StenagerUnit of Mental Health Research, Southwest Denmark, Department of Regional Health Services, University of Southern Denmark, Aabenraa, Denmark.
Nick BüngerMental Health Services in the Region of Southern Denmark, Department of Psychiatry Odense-Svendborg, Svendborg, Denmark.
Andreas K PedersenOdense University Hospital, Open Patient data Explorative Network (OPEN), Odense, Denmark.
Niels BilenbergDepartment of Clinical Research, Faculty of Health Science, University of Southern Denmark, Odense, Denmark.
Jan FrystykDepartment of Endocrinology, Odense University Hospital, Odense, Denmark.

Funding

No grant is acknowledged in the PubMed record.

8 · The paper itself

Abstract

The marked sentences are the ones the graph read a number from.

Importance: Patients with schizophrenia have reduced life expectancy due to cardiovascular disease and obesity-related type 2 diabetes, exacerbated by second-generation antipsychotic (SGA) medication. Existing interventions have shown limited effect. Objectives: To assess the effect of the once-weekly glucagon-like peptide-1 receptor agonist semaglutide in SGA-treated adults (aged 18-60 years) with schizophrenia, prediabetes (glycosylated hemoglobin A1c [HbA1c], 5.7%-6.4% of total hemoglobin) (to convert HbA1c from percentage of total hemoglobin to mmol/mol, use the following formula: (HbA1c % - 2.152)/0.09148), and overweight or obesity (body mass index [BMI], calculated as weight in kilograms divided by height in meters squared, ≥27). Design, Setting, and Participants: This placebo-controlled, double-blinded randomized clinical trial was conducted from January 2022 to May 2024, with 30 weeks of follow-up, among regional community-based mental health services in 2 regions of Denmark (Region of Southern Denmark and Region of Zealand). SGA-treated patients with schizophrenia, prediabetes, and overweight or obesity were randomized to semaglutide or placebo. Data analysis was completed from May 2024 to January 2025. Intervention: Once-weekly subcutaneous semaglutide or placebo for 30 weeks; semaglutide was titrated up to 1.0 mg/week over 8 weeks. Main Outcomes and Measures: The primary outcome was change in HbA1c. Secondary end points included changes in body weight, schizophrenia symptoms based on Positive and Negative Syndrome Scale 6 (PANSS-6) score, and physical and mental quality of life (QoL) (assessed via the 36-item Short Form Survey, version 2 [SF-36v2]). Results: A total of 154 patients were recruited and randomized 1:1 to semaglutide or placebo (87 female participants (56.5%); mean [SD] age, 38.3 [10.7] years). Of 154 randomized patients, 141 (91.5%) completed the trial-74 of 77 patients randomized to semaglutide (96%) and 67 of 77 randomized to placebo (87%). Semaglutide reduced HbA1c by 0.46% of total hemoglobin (95% CI, -0.56% to -0.36%) and body weight by 9.21 kg (95% CI, -11.68 to -6.75). An HbA1c less than 5.7% of total hemoglobin was achieved in 81% vs 19% of patients treated with semaglutide and placebo, respectively (P < .001); improvements in high-density cholesterol by 10.81 mg/dL (95% CI, 2.70-18.53; P = .007) and triglycerides by -29.20 mg/dL (95% CI, -55.75 to 2.65; P = .03) (to convert to millimoles per liter, multiply by 0.0113) were also observed. Finally, semaglutide improved physical QoL by 3.75 points on the SF-36v2 (95% CI, 1.52-5.98; P = .001) but had no significant effect on mental QoL scores or PANSS-6 score. Gastrointestinal symptoms were more frequent in semaglutide-treated patients. A few semaglutide-treated patients were hospitalized more frequently than observed in the placebo-treated group, but the number of serious adverse effects did not differ between groups. Conclusions and Relevance: In this multicenter, double-blinded randomized clinical trial, 30 weeks of administration of semaglutide, up to 1.0 mg/week, was safe, lowered blood glucose (as measured by HbA1c) and weight, and improved physical QoL in SGA-treated patients with schizophrenia, prediabetes, and obesity without worsening mental health. Trial Registration: ClinicalTrials.gov Identifier: NCT05193578.

Indexed as

Antipsychotic AgentsGlucagon-Like PeptidesObesityPrediabetic StateSchizophreniaAdolescentAdultDouble-Blind MethodFemaleGlucagon-Like Peptide 1Glucagon-Like Peptide-1 Receptor AgonistsGlycated HemoglobinHumansMaleMiddle AgedSemaglutideAntipsychotic AgentsGlucagon-Like Peptide 1Glucagon-Like Peptide-1 Receptor AgonistsGlucagon-Like PeptidesGlycated HemoglobinSemaglutide

Identifiers

PMID40900607
PMCPMC12409653

What Socratic holds

Texttitle and abstract
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.