ESEARCHERS LIKE TO BE surprised by the data. When new data challenge old beliefs, the field becomes primed for discovery. The aim of this commentary is to let the broader psychiatric community know about recent discoveries in schizophrenia epidemiology, and to speculate on how best to leverage these discoveries to advance knowledge. For those who do not follow the literature closely, recent research in the epidemiology of schizophrenia may come as a surprise. The once cardinal notions that schizophrenia affects men and women equally and is found in all societies with comparable (or equal) incidence are no longer supported by the data. Schizophrenia is not the egalitarian disorder that we once thought it was.1
"Schizophrenia is a common and devastating mental illness with a lifetime incidence rate of about 1% throughout the global population . Temporal, geographic, and population variations in this incidence rate have yielded clues to some of the possible etiologies of schizophrenia . Perhaps the most well established variation in the topography of schizophrenia incidence rates is the increased rate associated with a winter-spring birth (in the northern hemisphere ) , which is roughly 10% higher than the 1% yearly base incidence rate for schizophrenia (i.e., the absolute winter-spring risk is 1.1%). "
[Show abstract][Hide abstract] ABSTRACT: The season of birth risk factor for schizophrenia exerts a pervasive effect on the global population, particularly at northerly latitudes. The winter infection hypothesis and the low vitamin D hypothesis are both compelling but lack conclusive clinical data. The present work develops a maternal–fetal chronobiological hypothesis for this season of birth risk factor and its prevention by maternal bright light treatment. Around the winter solstice, due to decreased sunlight, the chronobiological apparatus of the at-risk second trimester mother is characterized by a reduced amplitude circadian pacemaker, and a reduced maximum of her nocturnal plasma melatonin concentrations (MTmax) and an increased minimum of her nocturnal core body temperatures (Tmin)—both of which exert adverse effects on the fetal hippocampus and dorsal striatum. The consequences for the fetus include reduced volume and increased excitability of the hippocampus, ventral striatal dysfunction, increased presynaptic nigrostriatal dopamine transmission, and increased propensity for pathological nigrostriatal neuronal phasic firing. Thus, the maternal–fetal chronobiological hypothesis fully accounts for the fetal precursors of the major pathognomonic abnormalities in adults with schizophrenia. Bright light treatment for the second trimester mother around the winter solstice, by increasing maternal circadian amplitude, could possibly prevent the fetal hippocampal and striatal abnormalities and eliminate the season of birth risk factor for schizophrenia.
Medical Hypotheses 10/2014; 83(6). DOI:10.1016/j.mehy.2014.10.014 · 1.07 Impact Factor
"Psychosis, and psychotic disorders such as schizophrenia, is characterized by the presence of hallucinations (false perceptions) and delusions (false beliefs). It has become clear in recent years that the marked heterogeneity in the rates of schizophrenia and psychotic disorders across population groups  can be partly explained by urban birth and upbringing, migration, ethnicity, and what Cantor-Graae and Selten have termed “social defeat” [2, 3]. A particularly important recent body of research is the MRC AESOP study that demonstrated a twentyfold rate increase in the incidence of psychosis in London, compared with Nottingham and Bristol, and the very highest rates being within the Black and ethnic minority groups [4–8]. "
[Show abstract][Hide abstract] ABSTRACT: Psychotic disorders carry social and economic costs for sufferers and society. Recent evidence highlights the risk posed by urban upbringing and social deprivation in the genesis of paranoia and psychosis. Evidence based psychological interventions are often not offered because of a lack of therapists. Virtual reality (VR) environments have been used to treat mental health problems. VR may be a way of understanding the aetiological processes in psychosis and increasing psychotherapeutic resources for its treatment. We developed a high-fidelity virtual reality scenario of an urban street scene to test the hypothesis that virtual urban exposure is able to generate paranoia to a comparable or greater extent than scenarios using indoor scenes. Participants (n = 32) entered the VR scenario for four minutes, after which time their degree of paranoid ideation was assessed. We demonstrated that the virtual reality scenario was able to elicit paranoia in a nonclinical, healthy group and that an urban scene was more likely to lead to higher levels of paranoia than a virtual indoor environment. We suggest that this study offers evidence to support the role of exposure to factors in the urban environment in the genesis and maintenance of psychotic experiences and symptoms. The realistic high-fidelity street scene scenario may offer a useful tool for therapists.
"Environmental factors linked to schizophrenia include winter parturition , maternal stress during pregnancy [10,11], second trimester and postnatal infection, labour and perinatal traumas, immigration, residency in urban areas and so on [12,13], and paternal occupation and age . Paternal age has been linked to schizophrenia since 1958 . "
[Show abstract][Hide abstract] ABSTRACT: Since 1958 many, but not all studies have demonstrated that paternal age is a risk factor for schizophrenia. There may be many different explanations for differences between studies, including study design, sample size, collection criteria, heterogeneity and the confounding effects of environmental factors that can for example perturb epigenetic programming and lead to an increase in disease risk. The small number of children in Western families makes risk comparisons between siblings born at different paternal ages difficult. In contrast, more Eastern families have children both at early and later periods of life. In the present study, a cross-sectional population study in an Iranian population was performed to compare frequency of schizophrenia in younger offspring (that is, older paternal age) versus older offspring.
A total of 220 patients with the diagnosis of schizophrenia (cases) from both psychiatric hospitals and private clinics and 220 individuals from other hospital wards (controls), matched for sex and age were recruited for this study. Patients with neurological problem, substance abuse, mental retardation and mood disorder were excluded from both groups.
Birth rank comparisons revealed that 35% vs 24% of the cases vs the controls were in the third or upper birth rank (P = 0.01). Also, the mean age of fathers at birth in case group (30 ± 6.26 years) was significantly more than the control group (26.45 ± 5.64 years; P = 0.0001). The age of 76 fathers at birth in case group was over 32 versus 33 fathers in control group. Individuals whose fathers' age was more than 32 (at birth) were at higher risk (2.77 times) for schizophrenia versus others (P < 0.0001, 95% CI 1.80 to 4.27). The maternal age at parturition of the case versus controls groups was 26.1 ± 5.41 vs 25.07 ± 4.47 (P = 0.02). Logistic regression analysis suggests that maternal age is less likely to be involved in the higher risk of schizophrenia than advanced parental age.
This study demonstrates a relationship between paternal age and schizophrenia in large families of an Iranian population. Arguments have been put forth that DNA bases changes or epigenetic changes in sperm account for the increased risk associated with older fathers. However, it would not be surprising that both de novo germline mutations and epigenetic changes contribute to disease occurrence because DNA replication and DNA methylation are closely linked at both the macromolecular level (that is, methylation closely follows replication), and at the metabolic level (both processes require folate), and susceptible to modulation by the environment. Further research on samples such as those collected here are needed to sort out the contributions of de novo mutations versus epigenetic changes to schizophrenia.
Annals of General Psychiatry 04/2011; 10(1):15. DOI:10.1186/1744-859X-10-15 · 1.40 Impact Factor
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