Academic literature on the topic 'Early-Life-Urbanicity'

ObjectivesWe aimed to study the association of childhood urbanicity with depressive symptoms in late adulthood.Design, setting and participantsWe used linear and logistic regressions to analyse data drawn from 20 400 respondents from the Survey of Health, Ageing and Retirement in Europe, a panel dataset incorporating a representative sample of the 50+ population in 13 European countries.Outcomes and analysisChildhood urbanicity was determined using self-reports of the respondents’ circumstances at age 10, and late-adulthood depression using the EURO-D scale. We conditioned on circumstances early in life as well as later in life, most importantly late-adulthood urbanicity. We estimated the associations using linear regression models and limited dependent variable models.ResultsA pooled regression of both men and women suggested that childhood urbanicity is associated non-monotonically with depression in late adulthood and is particularly apparent for those spending their childhoods in suburban settings. We found that individuals who spend the longest time in their childhood in a suburban home exhibit an average increase in probability of 3.4 (CI 1.1 to 5.7) percentage points in reporting four or more depressive symptoms. The association was robust to the inclusion of a host of household characteristics associated with childhood urbanicity and was independent of current urbanicity and current income. When broken down by gender, we found some evidence of associations between depressive outcomes and urban living for men, and stronger evidence of such associations with urban and suburban living for women who exhibit an increase of 5.6 (CI 2.2 to 9.0) percentage points in reporting four or more depressive symptoms.ConclusionsOur analysis reveals a relationship between childhood urbanicity and depression in late adulthood. The evidence presented on the nature of this relationship is not straightforward but is broadly suggestive of a link, differing by gender, between greater urbanicity and higher levels of depressive symptoms. The life-long nature of this association may potentially inform policy agendas aimed at improving urban and suburban living conditions.

BackgroundCannabis use is considered a component cause of psychotic illness, interacting with genetic and other environmental risk factors. Little is known, however, about these putative interactions. The present study investigated whether an urban environment plays a role in moderating the effects of adolescent cannabis use on psychosis risk.MethodProspective data (n=1923, aged 14–24 years at baseline) from the longitudinal population-based German Early Developmental Stages of Psychopathology cohort study were analysed. Urbanicity was assessed at baseline and defined as living in the city of Munich (1562 persons per km2; 4061 individuals per square mile) or in the rural surroundings (213 persons per km2; 553 individuals per square mile). Cannabis use and psychotic symptoms were assessed three times over a 10-year follow-up period using the Munich version of the Composite International Diagnostic Interview.ResultsAnalyses revealed a significant interaction between cannabis and urbanicity [10.9% adjusted difference in risk, 95% confidence interval (CI) 3.2–18.6, p=0.005]. The effect of cannabis use on follow-up incident psychotic symptoms was much stronger in individuals who grew up in an urban environment (adjusted risk difference 6.8%, 95% CI 1.0–12.5, p=0.021) compared with individuals from rural surroundings (adjusted risk difference −4.1%, 95% CI −9.8 to 1.6, p=0.159). The statistical interaction was compatible with substantial underlying biological synergism.ConclusionsExposure to environmental influences associated with urban upbringing may increase vulnerability to the psychotomimetic effects of cannabis use later in life.

IntroductionResearch has established that there are high rates of first episode psychosis (FEP) in immigrant populations. These findings could indicate that socio-environmental risk factors, such as individual social class, social capital, early trauma, life events, neighborhood deprivation could be relevant in explaining the differences in incidence rates observed between migrants and natives, following the socio-developmental model of Morgan et al. (2010). Some preliminary results also indicate that migration history itself versus ethnicity could implicate higher risk of the onset of psychotic disorders.AimsTo present preliminary findings from the EUGEI European Network of National Schizophrenia Networks Studying Gene Environment Interactions study.MethodsPopulation based FEP incidence/case control study. Comparison of the incidence rate of FEP and of the distribution of several risk factors (e.g. substance abuse, neighborhood deprivation, urbanicity and trauma) in natives and migrants in different countries across Europe.ResultsPreliminary results of the EUGEI study will be discussed in comparison with previous evidences.ConclusionThe EUGEI study allows a deeper understanding of the excess of FEP found among migrants in Europe.Disclosure of interestThe authors have not supplied their declaration of competing interest.

AbstractBackgroundAccording to the multidimensional model of schizophrenia, three basic psychopathological dimensions constitute its clinical structure: positive symptoms, negative symptoms and disorganization. The latter one is the newest and the least studied. Our aim was to discriminate disorganization in schizophrenia clinical picture and to identify its distinctive biological and socio-psychological particularities and associated genetic and environmental factors.MethodsWe used SAPS/SANS psychometrical scales, scales for the assessment of patient's compliance, insight, social functioning, life quality. Neuropsychological tests included Wisconsin Card Sorting Test (WCST), Stroop Color-Word test. Neurophysiological examination included registration of P300 wave of the evoked cognitive auditory potentials. Environmental factors related to patient's education, family, surrounding and nicotine use, as well as subjectively significant traumatic events in childhood and adolescence were assessed. Using PCR we detected SNP of genes related to the systems of neurotransmission (COMT, SLC6A4 and DRD2), inflammatory response (IL6, TNF), cellular detoxification (GSTM1, GSTT1), DNA methylation (MTHFR, DNMT3b, DNMT1).ResultsDisorganization is associated with early schizophrenia onset and history of psychosis in family, low level of insight and compliance, high risk of committing delicts, distraction errors in WCST, lengthened P300 latency of evoked cognitive auditory potentials, low-functional alleles of genes MTHFR (rs1801133) and DNMT3b (rs2424913), high level of urbanicity and psychotraumatic events at early age.ConclusionsSevere disorganization at the stage of schizophrenia clinical outcome is associated with the set of specific biological and social–psychological characteristics that indicate its epigenetic nature and maladaptive social significance.

Abstract Background Drug (ab)use and substance use disorders are frequently observed in patients with psychiatric illness, but the underlying causes remain widely unknown. A number of environmental risk factors have been proposed to affect the use of one or multiple drugs in the general population and adolescents. Whereas most previous studies focused on the influence of single risk factors on the use of one or a few selected drugs, the effect of accumulated environmental risk in early life on multiple drug use remains to be studied. Similarly, evidence on genetic susceptibility to the (ab)use of a single drug, e.g. nicotine, alcohol, cocaine, is abundant, while the role of genetic predisposition for multiple drug use - in particular during early life - is yet to be explored. Thus, the current work aims to study the role of environmental as well as genetic risk factors for multiple drug abuse (‘polytoxicomania’) in a large sample of schizophrenic/schizoaffective patients. Methods Information from ~2000 schizophrenia/schizoaffective patients on (preadult) multiple drug use (> 2 drugs) and environmental risk factors was extracted from the Göttingen Research Association for Schizophrenia (GRAS) data collection – currently the largest data base of deeply phenotyped patients with schizophrenia/schizoaffective disorder or other neuropsychiatric diseases. In addition, genetic data from these patients and 2111 healthy blood donors were used in a novel genetic approach that employs multiple genome-wide association studies (GWAS) to identify genetic associations with preadult multiple drug use. Genotyping was performed on a semi-custom Axiom MyDesign Genotyping Array (Affymetrix, Santa Clara, CA, USA), based on a CEU (Caucasian residents of European ancestry from UT, USA) marker backbone. Results The accumulation of environmental risk factors, i.e. sexual abuse, physical abuse, migration, urbanicity, together with alcohol and cannabis consumption as secondary risk factors, in early life (< 18 years) were strongly associated with lifetime multiple drug use (p = 3.48 x 10^-44, extreme group comparison odds ratio (OR) = 31.8). When the sample was split into preadult and adult multiple drug users, there was a remarkable association of the number of preadult environmental risk factors with preadult multiple drug use (p = 1.12 x 10^-25, OR = 243.6). Furthermore, preadult environmental risk accumulation strongly predicted onset of multiple drug use in adulthood (> 18 years; p = 6.27 x 10^-18, OR = 19.4). The application of the novel genetic approach yielded 35 single-nucleotide variants (SNPs) that potentially confer susceptibility to preadult multiple drug use. Out of these, 14 were located in gene-coding regions. Interestingly, 9 of these genes are implicated in neuronal development/function or metabolite transport/transformation. Additional gene-based analyses identified another 4 genes relevant for metabolite transport/transformation as well as 4 genes that play a role in hypoxia signaling. Discussion The present results show that an accumulation of environmental risk factors during early life (< 18 years) is a strong predictor of multiple drug use during adolescence and later life. These findings suggest that exposure to accumulated environmental risk during early life is not only associated with violent aggression – as previously reported by our lab – but is also an important predictor of multiple drug use. Moreover, we present first evidence of a genetic susceptibility to preadult multiple drug use, which will benefit from future replication in suitable samples of patients with mental illness or the general population.

Abstract Background There is replicated evidence of a shared genetic load between affective and non-affective psychosis, but much less is known of whether affective psychosis is affected by the same environmental risk factors as well. The aim of this review and meta-analysis is to study the association between specific environmental risk factors of interest previously associated with schizophrenia and later affective psychoses (bipolar disorder and psychotic depression). Methods A systematic search of prospective studies was conducted in MEDLINE, EMBASE and PsycINFO databases, supplemented by hand searching. Selected exposures included: paternal age, maternal infection, obstetric and perinatal factors, childhood trauma, childhood infection, urbanicity, migration, stressful life events, head injury and cannabis or substance use. Relevant studies were selected systematically among those fulfilling inclusion criteria, and effect sizes were extracted. Pooled information was presented for those factors with enough number studies to combine extracted effect sizes, while the rest were presented in a narrative way. Results Approximately 60 studies addressing the associations between environmental risk factors of interest and later affective psychoses were identified. The compiled studies showed that paternal age, early gestational age, lifetime cannabis use, parental death during childhood and ethnic minority in UK are associated with future development of affective psychosis. Discussion These results show that, as per genetics, there may be some overlap in the environmental load between schizophrenia and affective psychosis, suggesting general risks for psychosis rather than diagnostic specific risks. Nonetheless, publish studies for some factors in this subgroup of patients are still scarce. More longitudinal studies addressing specific association between environmental risk factors and affective psychosis are warranted.

Preterm birth occurs at excessively high and disparate rates in the United States. In 2016, the National Institutes of Health (NIH) launched the Environmental influences on Child Health Outcomes (ECHO) program to investigate the influence of early life exposures on child health. Extant data from the ECHO cohorts provides the opportunity to examine racial and geographic variation in effects of individual- and neighborhood-level markers of socioeconomic status (SES) on gestational age at birth. The objective of this study was to examine the association between individual-level (maternal education) and neighborhood-level markers of SES and gestational age at birth, stratifying by maternal race/ethnicity, and whether any such associations are modified by US geographic region. Twenty-six ECHO cohorts representing 25,526 mother-infant pairs contributed to this disseminated meta-analysis that investigated the effect of maternal prenatal level of education (high school diploma, GED, or less; some college, associate’s degree, vocational or technical training [reference category]; bachelor’s degree, graduate school, or professional degree) and neighborhood-level markers of SES (census tract [CT] urbanicity, percentage of black population in CT, percentage of population below the federal poverty level in CT) on gestational age at birth (categorized as preterm, early term, full term [the reference category], late, and post term) according to maternal race/ethnicity and US region. Multinomial logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CIs). Cohort-specific results were meta-analyzed using a random effects model. For women overall, a bachelor’s degree or above, compared with some college, was associated with a significantly decreased odds of preterm birth (aOR 0.72; 95% CI: 0.61–0.86), whereas a high school education or less was associated with an increased odds of early term birth (aOR 1.10, 95% CI: 1.00–1.21). When stratifying by maternal race/ethnicity, there were no significant associations between maternal education and gestational age at birth among women of racial/ethnic groups other than non-Hispanic white. Among non-Hispanic white women, a bachelor’s degree or above was likewise associated with a significantly decreased odds of preterm birth (aOR 0.74 (95% CI: 0.58, 0.94) as well as a decreased odds of early term birth (aOR 0.84 (95% CI: 0.74, 0.95). The association between maternal education and gestational age at birth varied according to US region, with higher levels of maternal education associated with a significantly decreased odds of preterm birth in the Midwest and South but not in the Northeast and West. Non-Hispanic white women residing in rural compared to urban CTs had an increased odds of preterm birth; the ability to detect associations between neighborhood-level measures of SES and gestational age for other race/ethnic groups was limited due to small sample sizes within select strata. Interventions that promote higher educational attainment among women of reproductive age could contribute to a reduction in preterm birth, particularly in the US South and Midwest. Further individual-level analyses engaging a diverse set of cohorts are needed to disentangle the complex interrelationships among maternal education, neighborhood-level factors, exposures across the life course, and gestational age at birth outcomes by maternal race/ethnicity and US geography.

Preterm birth occurs at excessively high and disparate rates in the United States. In 2016, the National Institutes of Health (NIH) launched the Environmental influences on Child Health Outcomes (ECHO) program to investigate the influence of early life exposures on child health. Extant data from the ECHO cohorts provides the opportunity to examine racial and geographic variation in effects of individual- and neighborhood-level markers of socioeconomic status (SES) on gestational age at birth. The objective of this study was to examine the association between individual-level (maternal education) and neighborhood-level markers of SES and gestational age at birth, stratifying by maternal race/ethnicity, and whether any such associations are modified by US geographic region. Twenty-six ECHO cohorts representing 25,526 mother-infant pairs contributed to this disseminated meta-analysis that investigated the effect of maternal prenatal level of education (high school diploma, GED, or less; some college, associate’s degree, vocational or technical training [reference category]; bachelor’s degree, graduate school, or professional degree) and neighborhood-level markers of SES (census tract [CT] urbanicity, percentage of black population in CT, percentage of population below the federal poverty level in CT) on gestational age at birth (categorized as preterm, early term, full term [the reference category], late, and post term) according to maternal race/ethnicity and US region. Multinomial logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CIs). Cohort-specific results were meta-analyzed using a random effects model. For women overall, a bachelor’s degree or above, compared with some college, was associated with a significantly decreased odds of preterm birth (aOR 0.72; 95% CI: 0.61–0.86), whereas a high school education or less was associated with an increased odds of early term birth (aOR 1.10, 95% CI: 1.00–1.21). When stratifying by maternal race/ethnicity, there were no significant associations between maternal education and gestational age at birth among women of racial/ethnic groups other than non-Hispanic white. Among non-Hispanic white women, a bachelor’s degree or above was likewise associated with a significantly decreased odds of preterm birth (aOR 0.74 (95% CI: 0.58, 0.94) as well as a decreased odds of early term birth (aOR 0.84 (95% CI: 0.74, 0.95). The association between maternal education and gestational age at birth varied according to US region, with higher levels of maternal education associated with a significantly decreased odds of preterm birth in the Midwest and South but not in the Northeast and West. Non-Hispanic white women residing in rural compared to urban CTs had an increased odds of preterm birth; the ability to detect associations between neighborhood-level measures of SES and gestational age for other race/ethnic groups was limited due to small sample sizes within select strata. Interventions that promote higher educational attainment among women of reproductive age could contribute to a reduction in preterm birth, particularly in the US South and Midwest. Further individual-level analyses engaging a diverse set of cohorts are needed to disentangle the complex interrelationships among maternal education, neighborhood-level factors, exposures across the life course, and gestational age at birth outcomes by maternal race/ethnicity and US geography.

AbstractConsidering the immense societal and personal costs and suffering associated with multiple drug use or “polytoxicomania”, better understanding of environmental and genetic causes is crucial. While previous studies focused on single risk factors and selected drugs, effects of early-accumulated environmental risks on polytoxicomania were never addressed. Similarly, evidence of genetic susceptibility to particular drugs is abundant, while genetic predisposition to polytoxicomania is unexplored. We exploited the GRAS data collection, comprising information on N~2000 deep-phenotyped schizophrenia patients, to investigate effects of early-life environmental risk accumulation on polytoxicomania and additionally provide first genetic insight. Preadult accumulation of environmental risks (physical or sexual abuse, urbanicity, migration, cannabis, alcohol) was strongly associated with lifetime polytoxicomania (p = 1.5 × 10−45; OR = 31.4), preadult polytoxicomania with OR = 226.6 (p = 1.0 × 10−33) and adult polytoxicomania with OR = 17.5 (p = 3.4 × 10−24). Parallel accessibility of genetic data from GRAS patients and N~2100 controls for genome-wide association (GWAS) and phenotype-based genetic association studies (PGAS) permitted the creation of a novel multiple GWAS–PGAS approach. This approach yielded 41 intuitively interesting SNPs, potentially conferring liability to preadult polytoxicomania, which await replication upon availability of suitable deep-phenotyped cohorts anywhere world-wide. Concisely, juvenile environmental risk accumulation, including cannabis and alcohol as starter/gateway drugs, strongly predicts polytoxicomania during adolescence and adulthood. This pivotal message should launch more effective sociopolitical measures to prevent this deleterious psychiatric condition.