ArticleProceedings. Biological sciences2014
Opposite risk patterns for autism and schizophrenia are associated with normal variation in birth size: phenotypic support for hypothesized diametric gene-dosage effects.
Article in Proceedings. Biological sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 59 citations in OpenAlex.
- The Evolutionary Misfit: Evolution, Epigenetics, and the Rise of Non-Communicable Diseases.Epigenomes · 2025Review
- On the varieties of conscious experiences: Altered Beliefs Under Psychedelics (ALBUS).Neuroscience of consciousness · 2025Article
- Perinatal nutrition as a key regulator of genomic imprinting: a new paradigm for maternal-child health.Frontiers in nutrition · 2025Article
- Maternal-fetal conflict and the timing of birth.Evolution, medicine, and public health · 2025Review
- Evolutionary psychiatry: foundations, progress and challenges.World psychiatry : official journal of the World Psychiatric Association (WPA) · 2023Article
- Generalized Simultaneous Localization and Mapping (G-SLAM) as unification framework for natural and artificial intelligences: towards reverse engineering the hippocampal/entorhinal system and principles of high-level cognition.Frontiers in systems neuroscience · 2022Article
- Sex-Dependent Shared and Nonshared Genetic Architecture Across Mood and Psychotic Disorders.Biological psychiatry · 2022Article
- Phenotypic Trade-Offs: Deciphering the Impact of Neurodiversity on Drug Development in Fragile X Syndrome.Frontiers in psychiatry · 2021Article
- Kinesin Kif3b mutation reduces NMDAR subunit NR2A trafficking and causes schizophrenia-like phenotypes in mice.The EMBO journal · 2020Article
- Why and How Imprinted Genes Drive Fetal Programming.Frontiers in endocrinology · 2019Article
- Comparative psychopharmacology of autism and psychotic-affective disorders suggests new targets for treatment.Evolution, medicine, and public health · 2019Review
- Baby food and bedtime: Evidence for opposite phenotypes from different genetic and epigenetic alterations in Prader-Willi and Angelman syndromes.SAGE open medicine · 2019Review
- The genome, microbiome and evolutionary medicine.CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne · 2018Article
- Older fathers' children have lower evolutionary fitness across four centuries and in four populations.Proceedings. Biological sciences · 2017Article
- Time from pre-eclampsia diagnosis to delivery affects future health prospects of children.Evolution, medicine, and public health · 2017Article
- Dopamine-prolactin pathway potentially contributes to the schizophrenia and type 2 diabetes comorbidity.Translational psychiatry · 2016Review
- Opposite differential risks for autism and schizophrenia based on maternal age, paternal age, and parental age differences.Evolution, medicine, and public health · 2016Article
- Diametrical diseases reflect evolutionary-genetic tradeoffs: Evidence from psychiatry, neurology, rheumatology, oncology and immunology.Evolution, medicine, and public health · 2015Review
- Using visual lateralization to model learning and memory in zebrafish larvae.Scientific reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Opposite phenotypic and behavioural traits associated with copy number variation and disruptions to imprinted genes with parent-of-origin effects have led to the hypothesis that autism and schizophrenia share molecular risk factors and pathogenic mechanisms, but a direct phenotypic comparison of how their risks covary has not been attempted. Here, we use health registry data collected on Denmark's roughly 5 million residents between 1978 and 2009 to detect opposing risks of autism and schizophrenia depending on normal variation (mean ± 1 s.d.) in adjusted birth size, which we use as a proxy for diametric gene-dosage variation in utero. Above-average-sized babies (weight, 3691-4090 g; length, 52.8-54.3 cm) had significantly higher risk for autism spectrum (AS) and significantly lower risk for schizophrenia spectrum (SS) disorders. By contrast, below-average-sized babies (2891-3290 g; 49.7-51.2 cm) had significantly lower risk for AS and significantly higher risk for SS disorders. This is the first study directly comparing autism and schizophrenia risks in the same population, and provides the first large-scale empirical support for the hypothesis that diametric gene-dosage effects contribute to these disorders. Only the kinship theory of genomic imprinting predicts the opposing risk patterns that we discovered, suggesting that molecular research on mental disease risk would benefit from considering evolutionary theory.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.