A comparison of selected risk factors for unipolar depressive disorder, bipolar affective disorder, schizoaffective disorder, and schizophrenia from a Danish population-based cohort
ABSTRACT Growing evidence of an etiologic overlap between schizophrenia and bipolar disorder has become increasingly difficult to disregard. In this study, we examined paternal age, urbanicity of place of birth, being born "small for gestational age," and parental loss as risk factors for primarily schizophrenia and bipolar disorder, but also unipolar depressive disorder and schizo-affective disorder. Furthermore, we examined the incidence of the disorders in a population-based cohort and evaluated our results in the context of the Kraepelinian dichotomization.
We established a register-based cohort study of more than 2 million persons born in Denmark between January 1, 1955, and July 1, 1987. Overall follow-up began on January 1, 1973 and ended on June 30, 2005. Relative risks for schizophrenia, bipolar disorder, unipolar depressive disorder, and schizoaffective disorder (ICD-8 or ICD-10) were estimated by survival analysis, using Poisson regression.
Differences were found in age-specific incidences. Loss of a parent (especially by suicide) was a risk factor for all 4 disorders. High paternal age and urbanization at birth were risk factors for schizophrenia. Children born pre-term had an excess risk of all disorders except schizophrenia if they were born "small for gestational age."
An overlap in the risk factors examined in this study was found, and the differences between the phenotypes were quantitative rather than qualitative, which suggests a genetic and environmental overlap between the disorders. However, large gender differences and differences in the age-specific incidences in the 4 disorders were present, favoring the Kraepelinian dichotomization.
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- "While many studies have identified alleles associated with depression, to our knowledge no study has shown an association between increased mutation rate and MDD. In one sample, for instance, paternal age was shown to be a risk factor for schizophrenia, but not unipolar depressive disorder (Laursen et al., 2007). This suggests that MDD is less likely than other psychiatric disorders to be caused by de novo genetic mutations that lead to biological malfunction. "
ABSTRACT: Major depressive disorder (MDD) presents with a variety of symptoms and responds to a wide range of treatment interventions. Diagnostic criteria collapse multiple syndromes with distinct etiologies into the same disorder. MDD is typically understood as a malfunction of neurotransmission or brain circuitry regulating mood, pleasure and reward, or executive function. However, research from an evolutionary perspective suggests that the “normal” functioning of adaptations may also generate symptoms meeting diagnostic criteria. Functioning adaptations may be an underappreciated etiological pathway to MDD. Many adaptive functions for depressive symptoms have been suggested: biasing cognition to avoid losses, conserving energy, disengaging from unobtainable goals, signaling submission, soliciting resources, and promoting analytical thinking. We review the potential role of these adaptive functions and how they can lead to specific clusters of depressive symptoms. Understanding MDD from such a perspective reduces the heterogeneity of cases and may help to select the best intervention for each patient. We discuss the implications of different adaptive and maladaptive etiological pathways for the use of antidepressants and various modes of psychotherapy. In particular, instances of MDD caused by functioning adaptations may benefit most from treatments that support the adaptive function, or that target the precipitating causal stressor. We conclude that an evolutionary approach to the study of MDD may be one of the more promising approaches to reduce its heterogeneity and to better match patients and treatment.Journal of Affective Disorders 09/2014; 172. DOI:10.1016/j.jad.2014.09.032 · 3.71 Impact Factor
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- "However, to our knowledge, no previous study has offered a lifecourse perspective examining whether the possible effects of late preterm birth on mental disorders extend across adult ages from young to old adulthood. Some studies suggest that the increased risk for mental disorders associated with preterm birth may characterize especially those preterm individuals who were born small for gestational age [SGA; defined as birth size at 42 standard deviations (S.D.s) or below the 5th or 10th percentile of that predicted by their gestational age; Laursen et al. 2007; Räikkönen et al. 2008; Strang-Karlsson et al. 2008; Monfils Gustafsson et al. 2009]. In fact, previous studies have shown that at least until young adulthood, individuals born SGA are at increased risk of severe mental disorders independently of their gestational age (Abel et al. 2010; Niederkrotenthaler et al. 2012; Nosarti et al. 2012). "
ABSTRACT: Late preterm births constitute the majority of preterm births. However, most evidence suggesting that preterm birth predicts the risk of mental disorders comes from studies on earlier preterm births. We examined if late preterm birth predicts the risks of severe mental disorders from early to late adulthood. We also studied whether adulthood mental disorders are associated with post-term birth or with being born small (SGA) or large (LGA) for gestational age, which have been previously associated with psychopathology risk in younger ages.Psychological Medicine 09/2014; 45(05):1-15. DOI:10.1017/S0033291714001998 · 5.43 Impact Factor
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- "Risk factors for these sets of disorders are shared [migration and ethnicity (Cantor-Graae & Selten, 2005; Fearon et al. 2006) and childhood traumas (Laursen et al. 2007)] and unique [e.g. urban birth and upbringing (Mortensen et al. 1999), paternal age (Laursen et al. 2007), developmental delays ( Jones et al. 1994) and impaired pre-morbid cognition in schizophrenia (Reichenberg et al. 2002)], suggesting that there may be both overlapping and distinct aetiological pathways to psychotic disorder. "
ABSTRACT: The extent to which different symptom dimensions vary according to epidemiological factors associated with categorical definitions of first-episode psychosis (FEP) is unknown. We hypothesized that positive psychotic symptoms, including paranoid delusions and depressive symptoms, would be more prominent in more urban environments. We collected clinical and epidemiological data on 469 people with FEP (ICD-10 F10-F33) in two centres of the Aetiology and Ethnicity in Schizophrenia and Other Psychoses (AESOP) study: Southeast London and Nottinghamshire. We used multilevel regression models to examine neighbourhood-level and between-centre differences in five symptom dimensions (reality distortion, negative symptoms, manic symptoms, depressive symptoms and disorganization) underpinning Schedules for Clinical Assessment in Neuropsychiatry (SCAN) Item Group Checklist (IGC) symptoms. Delusions of persecution and reference, along with other individual IGC symptoms, were inspected for area-level variation. Reality distortion [estimated effect size (EES) 0.15, 95% confidence interval (CI) 0.06-0.24] and depressive symptoms (EES 0.21, 95% CI 0.07-0.34) were elevated in people with FEP living in more urban Southeast London but disorganized symptomatology was lower (EES -0.06, 95% CI -0.10 to -0.02), after controlling for confounders. Delusions of persecution were not associated with increased neighbourhood population density [adjusted odds ratio (aOR) 1.01, 95% CI 0.83-1.23], although an effect was observed for delusions of reference (aOR 1.41, 95% CI 1.12-1.77). Hallucinatory symptoms showed consistent elevation in more densely populated neighbourhoods (aOR 1.32, 95% CI 1.09-1.61). In people experiencing FEP, elevated levels of reality distortion and depressive symptoms were observed in more urban, densely populated neighbourhoods. No clear association was observed for paranoid delusions; hallucinations were consistently associated with increased population density. These results suggest that urban environments may affect the syndromal presentation of psychotic disorders.Psychological Medicine 01/2014; 44(11):1-12. DOI:10.1017/S0033291713003188 · 5.43 Impact Factor