Increased Risk of Affective Disorders in Males after Second Trimester Prenatal Exposure to the Dutch Hunger Winter of 1944–45

1995 ◽  
Vol 166 (5) ◽  
pp. 601-606 ◽  
Author(s):  
Alan S. Brown ◽  
Ezra S. Susser ◽  
Shang P. Lin ◽  
Richard Neugebauer ◽  
Jack M. Gorman
Keyword(s):  
Prenatal Exposure ◽  
Affective Disorders ◽  
Separate Analysis ◽  
Second Trimester ◽  
Birth Cohorts ◽  
Affective Psychosis ◽  
Affective Psychoses ◽  
Increased Risk ◽  
Famine Exposure ◽  
Prenatal Famine

BackgroundPrenatal and perinatal factors have been linked to affective disorders. We therefore undertook an exploratory study to determine whether prenatal exposure to severe famine was associated with an increased risk of affective disorders.MethodMonthly birth cohorts that were exposed and unexposed to the Dutch Hunger Winter of 1944–45 were identified. The cumulative incidences of affective psychoses and neurotic depression (ICD–9 criteria) were compared between exposed and unexposed cohorts during each trimester of gestation.ResultsThe relative risk (RR) of affective psychosis (broad and restricted definitions) among persons exposed to famine during the second trimester was significantly increased (broad: RR (95% confidence interval) = 1.62 (1.19, 2.20); restricted: 1.59 (1.14, 2.21)). Separate analysis by gender showed a significant association among males (broad: 2.26 (1.43, 3.57); restricted: 2.40 (1.49, 3.89)), but not females (broad: 1.28 (0.84, 1.94); restricted: 1.17 (0.73, 1.86)). The risk of neurotic depression was not increased after prenatal famine exposure.ConclusionsThese results suggest a possible relationship between prenatal famine during the second trimester and affective psychosis, lending plausibility to reports that have associated affective psychoses with prenatal exposures. Further studies of this relationship are warranted.

Prenatal famine exposure, health in later life and promoter methylation of four candidate genes

2012 ◽  
Vol 3 (6) ◽  
pp. 450-457 ◽  
Author(s):  
M. V. Veenendaal ◽  
P. M. Costello ◽  
K. A. Lillycrop ◽  
S. R. de Rooij ◽  
J. A. van der Post ◽  
...  
Keyword(s):  
Candidate Genes ◽  
Promoter Methylation ◽  
Peripheral Blood ◽  
Methylation Status ◽  
Later Life ◽  
Proximal Promoter ◽  
Promoter Regions ◽  
Increased Risk ◽  
Famine Exposure ◽  
Prenatal Famine

Poor nutrition during fetal development can permanently alter growth, cardiovascular physiology and metabolic function. Animal studies have shown that prenatal undernutrition followed by balanced postnatal nutrition alters deoxyribonucleic acid (DNA) methylation of gene promoter regions of candidate metabolic control genes in the liver. The aim of this study was to investigate whether methylation status of the proximal promoter regions of four candidate genes differed between individuals exposed to the Dutch famine in utero. In addition, we determined whether methylation status of these genes was associated with markers of metabolic and cardiovascular disease and adult lifestyle. Methylation status of the GR1-C (glucocorticoid receptor), PPARγ (peroxisome proliferator-activated receptor gamma), lipoprotein lipase and phosphatidylinositol 3 kinase p85 proximal promoters was investigated in DNA isolated from peripheral blood samples of 759 58-year-old subjects born around the time of the 1944–45 Dutch famine. We observed no differences in methylation levels of the promoters between exposed and unexposed men and women. Methylation status of PPARγ was associated with levels of high-density lipoprotein cholesterol and triglycerides as well as with exercise and smoking. Hypomethylation of the GR promoter was associated with adverse adult lifestyle factors, including higher body mass index, less exercise and more smoking. The previously reported increased risk of cardiovascular and metabolic disease after prenatal famine exposure was not associated with differences in methylation status across the promoter regions of these candidate genes measured in peripheral blood. The adult environment seems to affect GR and PPARγ promoter methylation.

Comparing cohort incidence of schizophrenia with that of bipolar disorder and affective psychosis in individuals born in Stockholm County 1955–1967

2015 ◽  
Vol 45 (16) ◽  
pp. 3433-3439 ◽  
Author(s):  
J. Söderlund ◽  
S. Wicks ◽  
L. Jörgensen ◽  
C. Dalman
Keyword(s):  
Risk Factors ◽  
Bipolar Disorder ◽  
Birth Cohort ◽  
Socioeconomic Development ◽  
Incidence Rates ◽  
Birth Cohorts ◽  
Affective Psychoses ◽  
Increased Risk ◽  
National Patient ◽  
Incident Cases

Background.Perinatal factors are associated with increased risk for both schizophrenia and bipolar disorder. Improvements in obstetric and maternal healthcare and positive socioeconomic development in Sweden from the 1950s onwards could be expected to affect incidence estimates. However, commonly incidence rates are calculated during a specific year, i.e. time of diagnosis, which mirrors proximal precipitating risk factors. To examine whether incidence estimates are compatible with the hypothesis of an impact of perinatal exposures on the risk of the different disorders we here instead calculate incidence rates for consecutive birth cohorts born between 1955 and 1967. We hypothesized that schizophrenia incidence would be more affected compared to bipolar disorder and other affective psychoses since most perinatal risk factors are more pronounced in schizophrenia aetiology.Method.Birth cohorts of individuals born in Sweden and resident in Stockholm (N = 2 16 322), were followed in The National Patient Register regarding incident inpatient episodes Incident cases/10 000 person-years and birth cohort were calculated. Linear regression was used to estimate change in incidence rate.Results.We found stable birth cohort-based incidence estimates for bipolar disorder and other affective psychoses, but a continuous reduction in incidence estimates for schizophrenia as well as other non-affective psychoses in subsequent birth cohorts from 1955 to 1967.Conclusions.The consecutive birth cohort-based incidence estimates unveiled patterns that are compatible with the hypothesis of an impact of early life exposures decreasing over time, in the aetiology of schizophrenia, whereas this pattern is less apparent in affective psychoses..

scholarly journals Association between prenatal exposure to analgesics and risk of schizophrenia

2004 ◽  
Vol 185 (5) ◽  
pp. 366-371 ◽  
Author(s):  
Holger J. Sørensen ◽  
Erik L. Mortensen ◽  
June M. Reinisch ◽  
Sarnoff A. Mednick
Keyword(s):  
Prenatal Exposure ◽  
Viral Infections ◽  
Second Trimester ◽  
Parental History ◽  
Central Register ◽  
Increased Risk ◽  
Wide Range ◽  
History Of ◽  
The Central Nervous System ◽  
Using Data

BackgroundDisturbances in the central nervous system originating during foetal life may increase the risk of schizophrenia.AimsTo illuminate the hypothesis that prenatal exposure to analgesics may affect foetal neurodevelopment, leading to increased risk of schizophrenia in adulthood.MethodUsing data from the Copenhagen Perinatal Cohort and from the Danish Psychiatric Central Register, we studied the relationship between prenatal exposure to analgesics and the risk of schizophrenia. The effect of prenatal exposure was adjusted for parental history of schizophrenia, second-trimester viral infections, concomitant drug treatment during pregnancy, an index of pregnancy complications, parental social status and parental age.ResultsIn a risk set of 7999 individuals, 116 cases of schizophrenia were found (1.5%). Prenatal exposure to analgesics in the second trimester was associated with an elevated risk (adjusted odds ratio 4.75, 95% CI1.9–12.0). Independent of the covariates, the effect remained statistically significant.ConclusionsIndependent of a wide range of possible confounders, a significant association between second-trimester exposure to analgesics and increased risk of schizophrenia was observed.

scholarly journals CACNA1C Polymorphism (rs2283291) Is Associated with Schizophrenia in Chinese Males: A Case-Control Study

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Xiaojing Zhu ◽  
Rixin Li ◽  
Guojun Kang ◽  
Qi Kang ◽  
Wenwang Rao ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Gene Interaction ◽  
Environment Interaction ◽  
Gender Stratification ◽  
Gene Environment ◽  
Increased Risk ◽  
Genetic Level ◽  
Famine Exposure ◽  
Male Patients ◽  
Prenatal Famine

Recent research has shown that prenatal famine exposure may be one of the risk factors for schizophrenia and that people born in famine years may be at an increased risk of schizophrenia due to alteration of the DNA methylation of genes. In this study, the association of rs2283291/rs4648635 and the incidence of schizophrenia and prenatal famine exposure at the genetic level were investigated to provide clues to the pathogenesis of schizophrenia. A total of 960 participants were recruited, comprising 473 prenatal famine-exposed individuals (225 patients and 248 controls) and 487 prenatal non-famine-exposed individuals (220 patients and 267 controls). The association of prenatal famine, schizophrenia, and their interaction with DNA methylation levels was analyzed using SPSS and GMDR software. Gender stratification analysis revealed a significant association between the rs2283291 genotype and schizophrenia in male patients (P=0.017), and difference still existed after correction by the Bonferroni method. It was also found that an increasing risk of schizophrenia was associated with rs2283291 in males (OR: 1.62, 95% CI: 1.13-2.33, P=0.0086, AIC=669.7) in an overdominant model. The results of gene-environment interaction and gene-gene interaction revealed no association with the risk of schizophrenia. This study reported for the first time that rs2283291 was associated with schizophrenia in Chinese males.

Effects of prenatal exposure to the 1983–1985 Ethiopian great famine on the metabolic syndrome in adults: a historical cohort study

2020 ◽  
Vol 124 (10) ◽  
pp. 1052-1060
Author(s):  
Getachew Arage ◽  
Tefera Belachew ◽  
Habtamu Hassen ◽  
Mubarek Abera ◽  
Fedilu Abdulhay ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Prenatal Exposure ◽  
Fasting Blood Glucose ◽  
International Diabetes Federation ◽  
Birth Date ◽  
Historical Cohort ◽  
The Metabolic Syndrome ◽  
Great Famine ◽  
Famine Exposure ◽  
Prenatal Famine

AbstractThe Ethiopian great famine was one of the severe forms of global famines ever documented in Africa as well as in the recent history of the world. Earlier famine studies, as natural experiments, had tested the association between prenatal famine exposure and the metabolic syndrome and reported heterogeneous findings. Hence, this study aimed at evaluating the effects of prenatal exposure to the 1983–1985 Ethiopian great famine on the metabolic syndrome in adults. Self-reported birth date and age of the study subjects were used to classify the status of famine exposure. The International Diabetes Federation criterion was used to assess the metabolic syndrome. Multivariable logistic regression models were fitted to examine relationship between prenatal famine exposure and the metabolic syndrome. The findings showed that, adjusted for covariates, adults who had prenatal exposure to famine were 2·94 times more likely to develop the metabolic syndrome compared with non-exposed groups (adjusted OR (AOR) 2·94, 95 % CI 1·66, 5·27). More specifically, famine exposure during prenatal life was associated with increased waist circumference (AOR 2·27 cm, 95 % CI 0·28, 4·26), diastolic blood pressure (AOR 2·47 mmHg, 95 % CI 0·84, 4·11), TAG (AOR 0·20 mmol/l, 95 % CI 0·10, 0·28) and fasting blood glucose (AOR 0·24 mmol/l, 95 % CI 0·04, 0·43) compared with the control groups. Higher proportion of the metabolic syndrome, risky anthropometric and dyslipidaemic parameters were observed among exposed groups. This finding adds further evidence on fetal origin of adult diseases hypothesis. The finding may imply that one potential means of preventing adulthood metabolic syndrome is to optimise maternal nutrition during pregnancy.

scholarly journals Overweight and obesity at age 19 after pre-natal famine exposure

2021 ◽  
Author(s):  
L. H. Lumey ◽  
Peter Ekamper ◽  
Govert Bijwaard ◽  
Gabriella Conti ◽  
Frans van Poppel
Keyword(s):  
Social Class ◽  
Prenatal Exposure ◽  
Rural Areas ◽  
Fertility Decline ◽  
Military Service ◽  
Later Life ◽  
Overweight And Obesity ◽  
Study Results ◽  
Famine Exposure ◽  
Prenatal Famine

Abstract Background Weight for height has been used in the past as an indicator of obesity to report that prenatal exposure to the Dutch famine of 1944–1945 determined subsequent obesity. Further evaluation is needed as unresolved questions remain about the possible impact of social class differences in fertility decline during the famine and because being overweight is now defined by a Body Mass Index (BMI: kg/m2) from 25 to <30 and obesity by a BMI of 30 or more. Methods We studied heights and weights of 371,100 men in the Netherlands born between 1943 and 1947 and examined for military service at age 19. This group includes men with and without prenatal exposure to the Dutch famine. Results There was a 1.3-fold increase in the risk of being overweight or obese in young adults at age 19 after prenatal famine exposure in early gestation. The increase was only seen in sons of manual workers born in the large cities of Western Netherlands and not among those born in smaller cities or rural areas in the West. Social class differentials in fertility decline during the famine did not bias study results. Conclusions The long-term adverse impact of prenatal famine on later life type 2 diabetes and mortality through age 63 is already showing at age 19 in this population as a significant increase in overweight risk.

Association between psychotic disorder and urban place of birth is not mediated by obstetric complications or childhood socio-economic position: a cohort study

2003 ◽  
Vol 33 (4) ◽  
pp. 723-731 ◽  
Author(s):  
G. HARRISON ◽  
D. FOUSKAKIS ◽  
F. RASMUSSEN ◽  
P. TYNELIUS ◽  
A. SIPOS ◽  
...  
Keyword(s):  
Maternal Education ◽  
Disease Risk ◽  
Hazard Ratio ◽  
Obstetric Complications ◽  
Place Of Birth ◽  
Urban Place ◽  
Affective Psychosis ◽  
Affective Psychoses ◽  
Increased Risk ◽  
Economic Position

Background. Although urban place of birth has been identified as a risk factor for schizophrenia, the extent to which this association is mediated by socially patterned risk factors such as obstetric complications and childhood socio-economic position is unclear. The diagnostic specificity of the association within the clinical psychotic syndromes is also unclear.Method. A population cohort of 696025 males and females, born in Sweden between 1973 and 1980 and with linked birth and socio-economic data was followed up from age 16 for up to 9·8 years. Hospitalized cases of schizophrenia and other non-affective psychosis were identified from the Swedish Inpatient Discharge Register. We examined associations of these disorders with a three-level measure of urbanicity of birthplace before and after controlling for measures of foetal nutrition, obstetric complications and level of maternal education.Results. Urban compared to rural birthplace was associated both with increased risk of adult onset schizophrenia (hazard ratio 1·34, CI 0·91–1·96) and other non-affective psychoses (hazard ratio 1·63, CI 1·18–2·26). None of these associations was greatly affected by adjustment for obstetric complications or maternal educational level. In the group of other non-affective psychoses urban–rural differences in disease risk were strongest among those born in the winter months.Conclusion. Urbanization of birthplace is associated with increased risk of non-affective psychosis but this is not confined to narrowly defined cases. The magnitude of the association in Sweden is lower than that reported in other studies. Causal factors underlying this association appear to operate independently of risks associated with obstetric complications and parental educational status.

Ageing and Affective Disorders: The Age at First Onset of Affective Disorders in Scotland, 1969–1978

1985 ◽  
Vol 147 (2) ◽  
pp. 180-187 ◽  
Author(s):  
John M. Eagles ◽  
Lawrence J. Whalley
Keyword(s):  
Affective Disorder ◽  
Affective Disorders ◽  
Steady Increase ◽  
Social Psychological ◽  
Affective Psychosis ◽  
Affective Psychoses ◽  
Admission Rates ◽  
Clear Cut ◽  
Psychiatric Units ◽  
First Onset

SummaryFirst admission rates from 1969–78 for Scottish psychiatric units were calculated for discharge diagnoses of affective psychosis for each five-year age-group from 15 years to over 74 years. There were clear-cut linear increases in rates of depressive psychoses, mania, and all affective psychoses, consistent with a relatively steady increase in the rate of first-onset affective psychoses with increasing age. These findings are discussed in terms of social, psychological, and biological hypotheses of the causes of affective disorder. It is argued that no single factor could produce the observed linear increases with age and that the data appear more consistent with an integrative aetiological model of affective disorder.

Age-at-First-Registration and Heterogeneity in Affective Psychoses

2003 ◽  
Vol 37 (1) ◽  
pp. 66-69 ◽  
Author(s):  
Joy L. Welham ◽  
Richard Thomis ◽  
John J. Mcgrath
Keyword(s):  
Affective Disorders ◽  
Age Of Onset ◽  
Age Distribution ◽  
Unipolar Depression ◽  
Linear Increase ◽  
Diagnostic Group ◽  
Affective Psychosis ◽  
Affective Psychoses ◽  
Background Population ◽  
Age Range

Background: Previous research into age of onset in affective disorders has produced conflicting results. This paper examines the influence of heterogeneity on the age-at-firstregistration distribution for the ICD-9 diagnostic group ‘affective psychosis’. Method: For 1979–1991, data for age-at-first-registration for 4985 individuals diagnosed with affective psychosis (ICD-9 296.x) were extracted from a name-linked mental health register. These data were divided into (i) ‘296.1 only’, a category used to code unipolar depression (males = 700; females = 1321); and (ii) ‘296 other’, all 296 cases other than 296.1 (males = 1280; females = 1684). Inception rates for each 5-year age division were adjusted for the background population age-structure as a rate per 100 000 population. Results: The age-at-first-registration distribution for affective psychosis has a wide age range, with women outnumbering men. There is a near-linear increase in inception rates for both men and women with 296.1 only, while the bulk of those with affective psychoses (296 other) have an inverted U-shaped age distribution. Males have an earlier modal age-atfirst-registration for 296 other compared to females. Conclusion: The heterogeneity in terms of subtypes and sex in affective psychosis clouds the interpretation of age-at-first-registration. Separating those with unipolar psychotic depression from other subclassifications and differentiating by sex may provide clues to factors that precipitate the onset of affective psychosis.

scholarly journals In Silico Exploration of the Potential Role of Acetaminophen and Pesticides in the Etiology of Autism Spectrum Disorder

Toxics ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 97
Author(s):  
Tristan Furnary ◽  
Rolando Garcia-Milian ◽  
Zeyan Liew ◽  
Shannon Whirledge ◽  
Vasilis Vasiliou
Keyword(s):  
Autism Spectrum Disorder ◽  
Prenatal Exposure ◽  
Pesticide Exposure ◽  
Neurodevelopmental Disorder ◽  
Autism Spectrum ◽  
Biomedical Literature ◽  
Spectrum Disorder ◽  
Biological Processes ◽  
Genetic Associations ◽  
Increased Risk

Recent epidemiological studies suggest that prenatal exposure to acetaminophen (APAP) is associated with increased risk of Autism Spectrum Disorder (ASD), a neurodevelopmental disorder affecting 1 in 59 children in the US. Maternal and prenatal exposure to pesticides from food and environmental sources have also been implicated to affect fetal neurodevelopment. However, the underlying mechanisms for ASD are so far unknown, likely with complex and multifactorial etiology. The aim of this study was to explore the potential effects of APAP and pesticide exposure on development with regards to the etiology of ASD by highlighting common genes and biological pathways. Genes associated with APAP, pesticides, and ASD through human research were retrieved from molecular and biomedical literature databases. The interaction network of overlapping genetic associations was subjected to network topology analysis and functional annotation of the resulting clusters. These genes were over-represented in pathways and biological processes (FDR p < 0.05) related to apoptosis, metabolism of reactive oxygen species (ROS), and carbohydrate metabolism. Since these three biological processes are frequently implicated in ASD, our findings support the hypothesis that cell death processes and specific metabolic pathways, both of which appear to be targeted by APAP and pesticide exposure, may be involved in the etiology of ASD. This novel exposures-gene-disease database mining might inspire future work on understanding the biological underpinnings of various ASD risk factors.

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