Season of birth and biomarkers of early‐life environment

Author(s):  
Karolina Miłkowska ◽  
Ilona Nenko ◽  
Magdalena Klimek ◽  
Andrzej Galbarczyk ◽  
Grazyna Jasienska
2017 ◽  
Vol 41 (S1) ◽  
pp. S570-S570
Author(s):  
T. Duarte ◽  
A. Ferreira ◽  
S. Paulino ◽  
L. Câmara Pestana

IntroductionSeason of birth, an exogenous indicator of early life environment, has been related to higher risk of adverse psychiatric outcomes. According to literature, an excess of 5–8% of winter-spring births is found in individuals who later develop schizophrenia and bipolar disorder; this seasonal birth excess is also found in schizoaffective disorder (winter), major depression (March–May), and autism (March).ObjectivesThe objective of this study was to analyze the seasonal birth patterns of in-patients with psychiatric disorders.AimsUnderstand the relation between psychiatric disorders and season of birth during a 10 year period in a Portuguese University Hospital.MethodsAnalyze the birth date distribution of 2202 in-patients between 2007 and 2016 and compare with the psychiatric diagnosis.ResultsPatients’ diseases analyzed by birthday season: 60% of patients with schizoaffective disorder were born in winter-spring, 48.4% of mental retarded patients were born in autumn, 37% of dementia patients in winter, 77% of patients with delusional disorder in winter-spring, 78% of patients with Cluster A personality disorder in spring-summer and 71% of patients with substance abuse conditions in autumn-winter. No seasonal birth excess was found for bipolar affective disorder, schizophrenia, alcohol abuse, major depressive disorder or Cluster B personality disorder.ConclusionsOur sample data shows evidence for a potential link between season of birth and risk for schizoaffective disorder, dementia, mental retardation, Cluster A personality disorder, delusional disorder and substance abuse. The attempt to explain seasonal birth patterns in psychiatric illnesses could serve to clarify the etiological bases of such disorders.Disclosure of InterestThe authors have not supplied their declaration of competing interest.


2011 ◽  
Vol 140 (5) ◽  
pp. 835-841 ◽  
Author(s):  
L. H. MORTENSEN ◽  
A. B. MAIER ◽  
P. E. SLAGBOM ◽  
G. PAWELEC ◽  
E. DERHOVANESSIAN ◽  
...  

SUMMARYHuman cytomegalovirus (CMV) is a common herpesvirus establishing lifelong persisting infection, which has been implicated in immunosenescence and mortality in the elderly. Little is known about how and when susceptibility to CMV infection is determined. We measured CMV seroprevalence in two genetically informative cohorts. From the Leiden Longevity Study (LLS) we selected long-lived sib-pairs (n=844) and their middle-aged offspring and the offspring's partners (n=1452). From the Longitudinal Study of Aging Danish Twins (LSADT) 604 (302 pairs) same-sex monozygotic (MZ) and dizygotic (DZ) twins aged 73–94 years were included (n=302 pairs). Offspring of the long-lived LLS participants had significantly lower seroprevalence of CMV compared to their partners (offspring: 42%vs. partners: 51%,P=0·003). Of 372 offspring living with a CMV-positive partner, only 58% were infected. The corresponding number for partners was 71% (P<0·001). In the LSADT, MZ and DZ twins had high and similar CMV-positive concordance rates (MZ: 90%vs. DZ: 88%,P=0·51) suggesting that shared family environment accounts for the similarity within twin pairs. Our findings suggest that susceptibility to CMV infection – even under continuous within-partnership exposure – appears to be more strongly influenced by early-life environment than by genetic factors and adult environment.


2017 ◽  
Vol 8 (5) ◽  
pp. 513-519 ◽  
Author(s):  
T. Bianco-Miotto ◽  
J. M. Craig ◽  
Y. P. Gasser ◽  
S. J. van Dijk ◽  
S. E. Ozanne

Developmental origins of health and disease (DOHaD) is the study of how the early life environment can impact the risk of chronic diseases from childhood to adulthood and the mechanisms involved. Epigenetic modifications such as DNA methylation, histone modifications and non-coding RNAs are involved in mediating how early life environment impacts later health. This review is a summary of the Epigenetics and DOHaD workshop held at the 2016 DOHaD Society of Australia and New Zealand Conference. Our extensive knowledge of how the early life environment impacts later risk for chronic disease would not have been possible without animal models. In this review we highlight some animal model examples that demonstrate how an adverse early life exposure results in epigenetic and gene expression changes that may contribute to increased risk of chronic disease later in life. Type 2 diabetes and cardiovascular disease are chronic diseases with an increasing incidence due to the increased number of children and adults that are obese. Epigenetic changes such as DNA methylation have been shown to be associated with metabolic health measures and potentially predict future metabolic health status. Although more difficult to elucidate in humans, recent studies suggest that DNA methylation may be one of the epigenetic mechanisms that mediates the effects of early life exposures on later life risk of obesity and obesity related diseases. Finally, we discuss the role of the microbiome and how it is a new player in developmental programming and mediating early life exposures on later risk of chronic disease.


2014 ◽  
Vol 109 ◽  
pp. S486
Author(s):  
Abra Guo ◽  
Robin Wilson ◽  
Betsy Stevens ◽  
Caitlin Russell ◽  
Melissa Cohen ◽  
...  

2011 ◽  
Vol 77 (4) ◽  
pp. 626-632 ◽  
Author(s):  
Fritha H. Milne ◽  
Debra S. Judge ◽  
David B. Preen ◽  
Phil Weinstein

Heredity ◽  
2017 ◽  
Vol 118 (6) ◽  
pp. 534-541 ◽  
Author(s):  
L Canario ◽  
N Lundeheim ◽  
P Bijma

Author(s):  
Luba Sominsky ◽  
Adam K. Walker ◽  
Deborah M. Hodgson

2004 ◽  
Vol 25 ◽  
pp. S385 ◽  
Author(s):  
Tina L. Huang ◽  
Michelle Carlson ◽  
Annette L. Fitzpatrick ◽  
Linda Fried ◽  
Lewis H. Kuller ◽  
...  

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