Schizophrenia: an integrated sociodevelopmental-cognitive model
Open accessAbstract
Schizophrenia remains a major burden on patients and society. The dopamine hypothesis attempts to explain the pathogenic mechanisms of the disorder, and the neurodevelopmental hypothesis the origins. In the past 10 years an alternative, the cognitive model, has gained popularity. However, the first two theories have not been satisfactorily integrated, and the most influential iteration of the cognitive model makes no mention of dopamine, neurodevelopment, or indeed the brain. In this Review we show that developmental alterations secondary to variant genes, early hazards to the brain, and childhood adversity sensitise the dopamine system, and result in excessive presynaptic dopamine synthesis and release. Social adversity biases the cognitive schema that the individual uses to interpret experiences towards paranoid interpretations. Subsequent stress results in dysregulated dopamine release, causing the misattribution of salience to stimuli, which are then misinterpreted by the biased cognitive processes. The resulting paranoia and hallucinations in turn cause further stress, and eventually repeated dopamine dysregulation hardwires the psychotic beliefs. Finally, we consider the implications of this model for understanding and treatment of schizophrenia.
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The demographic factors are likely to drive the groups' appraisals of their psychotic experiences and environments.
“These factors are likely to drive the groups' appraisals of their psychotic experiences and their environments, as would be predicted by biopsychosocial models of psychosis.7, 8”
From Clinical relevance of appraisals of persistent psychotic experiences in people with and without a need for care: an experimental study (2017) · cites this paper as [7]
The ‘Cognitive theories and their link to dopaminergic dysfunction’ section says social adversity can bias schemas through which people interpret their experiences and see the world as threatening. The integrated-model section likewise links social adversity to psychotic interpretations. These passages support a prediction about appraisals, but do not establish that the citing paper’s demographic factors drive differences between its groups. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe study's results support biopsychosocial models that emphasize the importance of environmental and psychological factors in the aetiology of psychosis and need for care.
“These results support biopsychosocial models 21,22,37 that emphasize the importance of environmental and psychological factors in the aetiology of psychosis and need for care.”
From Clinical, socio‐demographic and psychological characteristics in individuals with persistent psychotic experiences with and without a “need for care” (2016) · cites this paper as [22]
The Abstract and the ‘Cognitive theories and their link to dopaminergic dysfunction’ section describe how social adversity, stress, and cognitive processes contribute to psychosis. The ‘Implications and future directions’ section discusses psychological and social interventions, but the passages do not establish that these factors determine a need for care. (LLM, conf=0.83)
Experimental — accuracy not yet measuredStress-vulnerability and integrated cognitive models posit a role for social, environmental and psychological factors in the aetiology of psychosis, in addition to genetic and neurodevelopmental features such as a family history of psychosis and low IQ.
“Stress-vulnerability and integrated cognitive models 21,22 posit a role for social, environmental and psychological factors in the aetiology of psychosis, in addition to genetic and neurodevelopmental features such as a family history of psychosis and low intelligence quotient (IQ).”
From Clinical, socio‐demographic and psychological characteristics in individuals with persistent psychotic experiences with and without a “need for care” (2016) · cites this paper as [22]
Persistent psychotic experiences only become problematic in the context of pre-existent vulnerabilities.
“it is likely that persistent PEs only become problematic in the context of pre-existent vulnerabilities, as suggested by contemporary aetiological models of psychosis 21,22,37”
From Clinical, socio‐demographic and psychological characteristics in individuals with persistent psychotic experiences with and without a “need for care” (2016) · cites this paper as [22]
Adverse experiences may increase the likelihood of developing psychosis in two ways: early adversity could increase the persecutory content of predictions, and adversity is often stressful and stress sensitises the dopamine system.
“Adverse experiences may increase the likelihood of developing psychosis in two ways. First, early adversity could increase the persecutory content of predictions(68, 105). Second, adversity is often stressful, and as reported above, there is evidence that stress sensitises the dopamine system(118). This could result in higher presynaptic dopamine synthesis and release capacity(123).”
From Aberrant Salience, Information Processing, and Dopaminergic Signaling in People at Clinical High Risk for Psychosis (2020) · cites this paper as [68]
Chronic psychosocial adversity increases the risk of mental illnesses including schizophrenia and depression.
“Chronic psychosocial adversity increases the risk of mental illnesses including schizophrenia and depression (van Os et al., 2010; Howes and Murray, 2014; Parker, 1983).”
From The effects of psychosocial stress on dopaminergic function and the acute stress response (2019) · cites this paper as Howes and Murray, 2014
One common component underlying psychosocial risk factors is exposure to psychosocial stress via activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system as part of the normal biological stress response.
“One common component underlying these factors is exposure to psychosocial stress (Howes and Murray, 2014) via activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system as part of the normal biological stress response (Taylor, 2010).”
From The effects of psychosocial stress on dopaminergic function and the acute stress response (2019) · cites this paper as Howes and Murray, 2014
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Howes, O. H., & Kaar, S. J. (2018) · World Psychiatry · doi:10.1002/wps.20522 · Cited by 24 · see citing works
Self-citationAdverse effects associated with antipsychotic use in older adults
Khalid, J., & Aparasu, R. R. (2024) · Expert Opinion on Drug Safety · doi:10.1080/14740338.2024.2386377 · Cited by 17 · see citing works
Underwood, R., Kumari, V., & Peters, E. (2016) · Psychological Medicine · doi:10.1017/s0033291715002780 · Cited by 14 · see citing works
The second agent effect: interpersonal predictive coding in people with schizophrenia
Okruszek, Ł., Piejka, A., Wysokiński, A., Szczepocka, E., & Manera, V. (2019) · Social Neuroscience · doi:10.1080/17470919.2017.1415969 · Cited by 12 · see citing works
Baumeister, D., Peters, E., Pruessner, J., Howes, O., & Chadwick, P. (2022) · Schizophrenia Research · doi:10.1016/j.schres.2019.07.019 · Cited by 6 · see citing works
Self-citation
- Authors
- Howes, O. D., & Murray, R. M.
- Affiliations
- King's College London (GB)
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2014-05
- Volume
- 383
- Issue
- 9929
- Pages
- 1677-1687
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- PMC
- PMC4127444
- OpenAlex
- W2146809691
- Cited by
- 864
- References
- 137
- Citations by year
- 2026: 46 · 2025: 55 · 2024: 95 · 2023: 70 · 2022: 69 · 2021: 93 · 2020: 89 · 2019: 79 · 2018: 53 · 2017: 49 · 2016: 74 · 2015: 72 · 2014: 19
- FWCI
- 7.50
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Lancet (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- Medical Research Council UK (MC-A656–5QD30)
- Wellcome Trust (094849/Z/10/Z)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Social Sciences › Arts and Humanities › Philosophy › Mental Health and Psychiatry
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- schizophrenia, dopamine hypothesis, neurodevelopmental hypothesis, childhood adversity, genetic variants, dopamine dysregulation, hallucinations, stress, social adversity
- MeSH terms
- Brain, Cognition, Dopamine, Hallucinations, Humans, Paranoid Disorders, Schizophrenia, Social Environment
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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