scholarly journals Prenatal Developmental Origins of Future Psychopathology: Mechanisms and Pathways

2019 ◽  
Vol 15 (1) ◽  
pp. 317-344 ◽  
Author(s):  
Catherine Monk ◽  
Claudia Lugo-Candelas ◽  
Caroline Trumpff
Keyword(s):  
Maternal Distress ◽  
Developmental Origins ◽  
Neurodevelopmental Outcomes ◽  
Fetal Origins ◽  
Behavior Development ◽  
Increased Risk ◽  
Health And Disease ◽  
Brain And Behavior ◽  
And Behavior ◽  
The Impact

The developmental origins of health and disease hypothesis applied to neurodevelopmental outcomes asserts that the fetal origins of future development are relevant to mental health. There is a third pathway for the familial inheritance of risk for psychiatric illness beyond shared genes and the quality of parental care: the impact of pregnant women's distress—defined broadly to include perceived stress, life events, depression, and anxiety—on fetal and infant brain–behavior development. We discuss epidemiological and observational clinical data demonstrating that maternal distress is associated with children's increased risk for psychopathology: For example, high maternal anxiety is associated with a twofold increase in the risk of probable mental disorder in children. We review several biological systems hypothesized to be mechanisms by which maternal distress affects fetal and child brain and behavior development, as well as the clinical implications of studies of the developmental origins of health and disease that focus on maternal distress. Development and parenting begin before birth.

scholarly journals Using fathers as a negative control exposure to test the Developmental Origins of Health and Disease Hypothesis: A case study on maternal distress and offspring asthma using Swedish register data

2017 ◽  
Vol 45 (17_suppl) ◽  
pp. 36-40 ◽  
Author(s):  
Bronwyn K. Brew ◽  
Tong Gong ◽  
Dylan M. Williams ◽  
Henrik Larsson ◽  
Catarina Almqvist
Keyword(s):  
Negative Control ◽  
Maternal Distress ◽  
Control Analysis ◽  
Developmental Origins ◽  
Unmeasured Confounding ◽  
Paternal Exposure ◽  
Health And Disease ◽  
The Impact

Background: Developmental Origins of Health and Disease Hypothesis (DOHaD) studies are often observational in nature and are therefore prone to biases from loss to follow-up and unmeasured confounding. Register-based studies can reduce these issues since they allow almost complete follow-up and provide information on fathers that can be used in a negative control analysis to assess the impact of unmeasured confounding. Aim: The aim of this study was to propose a causal model for testing DOHaD using paternal exposure as a negative control, and its application to maternal distress in pregnancy and offspring asthma. Methods: A causal diagram including shared and parent-specific measured and unmeasured confounders for maternal (fetal) and paternal exposures is proposed. The case study consisted of all children born in Sweden from July 2006 to December 2008 ( n=254,150). Information about childhood asthma, parental distress and covariates was obtained from the Swedish national health registers. Associations between maternal and paternal distress during pregnancy and offspring asthma at age five years were assessed separately and with mutual adjustment for the other parent’s distress measure, as well as for shared confounders. Results: Maternal distress during pregnancy was associated with offspring asthma risk; mutually adjusted odds ratio (OR) (OR 1.32, 95% CI 1.23, 1.43). The mutually adjusted paternal distress−offspring asthma analysis (OR 1.05, 95% CI 0.97, 1.13) indicated no evidence for unmeasured confounding shared by the mother and father. Conclusions: Using paternal exposure in a negative control model to test the robustness of fetal programming hypotheses can be a relatively simple extension of conventional observational studies but limitations need to be considered.

Epigenetics and DOHaD: how translation to predictive testing will require a better public understanding

2021 ◽  
pp. 1-7
Author(s):  
Fiona Lynch ◽  
Sharon Lewis ◽  
Ivan Macciocca ◽  
Jeffrey M. Craig
Keyword(s):  
Health Professionals ◽  
Early Life ◽  
Predictive Testing ◽  
Public Understanding ◽  
Future Research ◽  
Developmental Origins ◽  
Needed Information ◽  
Genes And Environment ◽  
Increased Risk ◽  
Health And Disease

Abstract Epigenetics is likely to play a role in the mediation of the effects of genes and environment in risk for many non-communicable diseases (NCDs). The Developmental Origins of Health and Disease (DOHaD) theory presents unique opportunities regarding the possibility of early life interventions to alter the epigenetic makeup of an individual, thereby modifying their risk for a variety of NCDs. While it is important to determine how we can lower the risk of these NCDs, it is equally important to understand how the public’s knowledge and opinion of DOHaD and epigenetic concepts may influence their willingness to undertake such interventions for themselves and their children. In this review, we provide an overview of epigenetics, DOHaD, NCDs, and the links between them. We explore the issues surrounding using epigenetics to identify those at increased risk of NCDs, including the concept of predictive testing of children. We also outline what is currently understood about the public’s understanding and opinion of epigenetics, DOHaD, and their relation to NCDs. In doing so, we demonstrate that it is essential that future research explores the public’s awareness and understanding of epigenetics and epigenetic concepts. This will provide much-needed information which will prepare health professionals for the introduction of epigenetic testing into future healthcare.

scholarly journals Homage to the ‘H’ in developmental origins of health and disease

2016 ◽  
Vol 8 (1) ◽  
pp. 8-29 ◽  
Author(s):  
C. S. Rosenfeld
Keyword(s):  
Female Offspring ◽  
Postnatal Period ◽  
Environmental Chemicals ◽  
Primary Concern ◽  
Developmental Origins ◽  
Adult Health ◽  
Fetal Origins ◽  
Adult Disease ◽  
Remediation Strategies ◽  
Health And Disease

Abundant evidence exists linking maternal and paternal environments from pericopconception through the postnatal period to later risk to offspring diseases. This concept was first articulated by the late Sir David Barker and as such coined the Barker Hypothesis. The term was then mutated to Fetal Origins of Adult Disease and finally broadened to developmental origins of adult health and disease (DOHaD) in recognition that the perinatal environment can shape both health and disease in resulting offspring. Developmental exposure to various factors, including stress, obesity, caloric-rich diets and environmental chemicals can lead to detrimental offspring health outcomes. However, less attention has been paid to date on measures that parents can take to promote the long-term health of their offspring. In essence, have we neglected to consider the ‘H’ in DOHaD? It is the ‘H’ component that should be of primary concern to expecting mothers and fathers and those seeking to have children. While it may not be possible to eliminate exposure to all pernicious factors, prevention/remediation strategies may tip the scale to health rather than disease. By understanding disruptive DOHaD mechanisms, it may also illuminate behavioral modifications that parents can adapt before fertilization and throughout the neonatal period to promote the lifelong health of their male and female offspring. Three possibilities will be explored in the current review: parental exercise, probiotic supplementation and breastfeeding in the case of mothers. The ‘H’ paradigm should be the focus going forward as a healthy start can indeed last a lifetime.

The establishment of DOHaD working groups in Australia and New Zealand

2016 ◽  
Vol 7 (5) ◽  
pp. 433-439 ◽  
Author(s):  
S. L. Prescott ◽  
K. Allen ◽  
K. Armstrong ◽  
C. Collins ◽  
H. Dickinson ◽  
...  
Keyword(s):  
New Zealand ◽  
Early Life ◽  
Developmental Origins ◽  
Effect Change ◽  
Cohort Group ◽  
Disease Outcomes ◽  
Working Groups ◽  
Health And Disease ◽  
Translational Strategies ◽  
The Impact

The evidence underpinning the developmental origins of health and disease (DOHaD) is overwhelming. As the emphasis shifts more towards interventions and the translational strategies for disease prevention, it is important to capitalize on collaboration and knowledge sharing to maximize opportunities for discovery and replication. DOHaD meetings are facilitating this interaction. However, strategies to perpetuate focussed discussions and collaborations around and between conferences are more likely to facilitate the development of DOHaD research. For this reason, the DOHaD Society of Australia and New Zealand (DOHaD ANZ) has initiated themed Working Groups, which convened at the 2014–2015 conferences. This report introduces the DOHaD ANZ Working Groups and summarizes their plans and activities. One of the first Working Groups to form was the ActEarly birth cohort group, which is moving towards more translational goals. Reflecting growing emphasis on the impact of early life biodiversity – even before birth – we also have a Working Group titled Infection, inflammation and the microbiome. We have several Working Groups exploring other major non-cancerous disease outcomes over the lifespan, including Brain, behaviour and development and Obesity, cardiovascular and metabolic health. The Epigenetics and Animal Models Working Groups cut across all these areas and seeks to ensure interaction between researchers. Finally, we have a group focussed on ‘Translation, policy and communication’ which focusses on how we can best take the evidence we produce into the community to effect change. By coordinating and perpetuating DOHaD discussions in this way we aim to enhance DOHaD research in our region.

Advanced maternal age and the impact on maternal and offspring cardiovascular health

2019 ◽  
Vol 317 (2) ◽  
pp. H387-H394 ◽  
Author(s):  
Christy-Lynn M. Cooke ◽  
Sandra T. Davidge
Keyword(s):  
Cardiovascular Disease ◽  
Maternal Age ◽  
Cardiovascular Health ◽  
Advanced Maternal Age ◽  
Limited Information ◽  
In Utero Environment ◽  
Increased Risk ◽  
Health And Disease ◽  
The Impact

Delaying pregnancy, which is on the rise, may increase the risk of cardiovascular disease in both women and their children. The physiological mechanisms that lead to these effects are not fully understood but may involve inadequate adaptations of the maternal cardiovascular system to pregnancy. Indeed, there is abundant evidence in the literature that a fetus developing in a suboptimal in utero environment (such as in pregnancies complicated by fetal growth restriction, preterm birth, and/or preeclampsia) is at an increased risk of cardiovascular disease in adulthood, the developmental origins of health and disease theory. Although women of advanced age are at a significantly increased risk of pregnancy complications, there is limited information as to whether advanced maternal age constitutes an added stressor on the prenatal environment of the fetus, and whether or not this is secondary to impaired cardiovascular function during pregnancy. This review summarizes the current literature available on the impact of advanced maternal age on cardiovascular adaptations to pregnancy and the role of maternal age on long-term health risks for both the mother and offspring.

Cardiovascular diseases in grandparents and the risk of congenital heart diseases in grandchildren

2014 ◽  
Vol 5 (2) ◽  
pp. 152-158 ◽  
Author(s):  
K. P. J. Wijnands ◽  
S. A. Obermann-Borst ◽  
E. J. G. Sijbrands ◽  
M. F. Wildhagen ◽  
W. A. Helbing ◽  
...  
Keyword(s):  
Metabolic Pathways ◽  
Congenital Heart ◽  
Family Study ◽  
Heart Diseases ◽  
Case Control ◽  
Fetal Origins ◽  
Increased Risk ◽  
Health And Disease ◽  
Control Family ◽  
Detailed Questionnaire

Hyperglycemia, dyslipidemia and hyperhomocysteinemia are associated with both adult cardiovascular disease (CVD) and having a child with a congenital heart disease (CHD). We investigated associations between CVD in grandparents and the risk of CHD in grandchildren. In a case–control family study, we obtained detailed questionnaire information on CVD and CHD in 247 families with a CHD child and 203 families without a CHD child. Grandparents with CVD or intermittent claudication (IC) were significantly associated with an increased risk for CHD in grandchildren [OR 1.39 (95% CI 1.03–1.89) and OR 2.77 (95% CI 1.02–7.56), respectively]. The risk of CHD grandchildren was particularly increased in paternal grandfathers with CVD [OR 1.85 (95% CI 1.01–3.37)]. Overall, having a grandparent with CVD increased the risk for CHD in the grandchild by 1.65 (95% CI 1.12–2.41). After adjustment for potential maternal confounders, this risk was 1.44 (95% CI 0.94–2.21). Having two or more grandparents with CVD was associated with an approximately threefold risk for CHD grandchildren [OR adjusted 2.72 (95% CI 1.08–6.89)]. Our data suggest that CVD and IC in grandparents are associated with an increased risk of having a CHD grandchild. These first findings may be explained by shared causality of derangements in metabolic pathways and are in line with the fetal origins of health and disease.

scholarly journals Sex Differences in the Developmental Origins of Cardiovascular Disease

Physiology ◽  
2014 ◽  
Vol 29 (2) ◽  
pp. 122-132 ◽  
Author(s):  
Suttira Intapad ◽  
Norma B. Ojeda ◽  
John Henry Dasinger ◽  
Barbara T. Alexander
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Sex Differences ◽  
Cardiovascular Risk ◽  
Early Life ◽  
Experimental Models ◽  
Developmental Origins ◽  
Proof Of Concept ◽  
Increased Risk ◽  
Health And Disease

The Developmental Origins of Health and Disease (DOHaD) proposes that adverse events during early life program an increased risk for cardiovascular disease. Experimental models provide proof of concept but also indicate that insults during early life program sex differences in adult blood pressure and cardiovascular risk. This review will highlight the potential mechanisms that contribute to the etiology of sex differences in the developmental programming of cardiovascular disease.

scholarly journals Gonadal steroids, brain, and behavior: role of context

2002 ◽  
Vol 4 (2) ◽  
pp. 123-137 ◽  
Keyword(s):  
Mood Disorders ◽  
Steroid Hormones ◽  
Differential Susceptibility ◽  
Reproductive Function ◽  
Gonadal Steroids ◽  
Wide Range ◽  
Reproductive Endocrine ◽  
Brain And Behavior ◽  
And Behavior ◽  
The Impact

The nature and extent of the impact of gender and reproductive function on mood has been the subject of speculation and controversy for centuries. Over the past 50 years, however, it has become increasingly clear that not only is the brain a major target of reproductive steroid hormones, but additionally, the steroid hormones, as neuroregulators, create a context thai influences a broad range of brain activities; ie, neural actions and resultant behaviors are markedly different in the presence and absence of gonadal steroids. In turn, the actions of gonadal steroids are themselves context-dependent. Thus, even where it can be demonstrated thai gonadal steroids trigger mood disorders, the triggers are normal levels of gonadal steroids (to be contrasted with the mood disturbances accompanying endocrinopathies), and the mood disorders appear only in a subset of susceptible individuals. The context specificity and differential susceptibility to affective dysregulation seen in women with reproductive endocrine-related mood disorders are undoubtedly important underlying characteristics of a wide range of psychiatric disorders in which the triggers have not yet been identified. Consequently, reproductive endocrine-related mood disorders offer unparalleled promise for the identification of those contextual variables that permit biological stimuli to differentially translate into depression in individuals at risk.

23 Pulmonary Hypertension Associated with Bronchopulmonary Dysplasia and Neurodevelopmental Outcomes: A Systematic Review and Meta-Analysis

2021 ◽  
Vol 26 (Supplement_1) ◽  
pp. e16-e17
Author(s):  
Soumya Thomas ◽  
Prashanth Murthy ◽  
Amuchou Soraisham ◽  
Abhay Lodha
Keyword(s):  
Systematic Review ◽  
Pulmonary Hypertension ◽  
Cerebral Palsy ◽  
Cohort Studies ◽  
Quality Assessment ◽  
Developmental Delay ◽  
Bronchopulmonary Dysplasia ◽  
Neurodevelopmental Outcomes ◽  
Increased Risk ◽  
The Impact

Abstract Primary Subject area Neonatal-Perinatal Medicine Background Pulmonary Hypertension (PH) is estimated to occur in 1 in 4 infants with Bronchopulmonary Dysplasia (BPD). The impact of PH in infants with BPD on their neurodevelopmental (ND) outcomes is uncertain. Objectives This systematic review aims to evaluate whether PH in infants with BPD is associated with ND delay. Design/Methods A systematic literature search was performed to identify studies that reported ND outcomes of infants with BPD (based on NIH definition) and PH (based on echocardiographic findings of PH at 36 weeks PMA). The primary outcome was ND delay in infants with pulmonary hypertension associated with BPD compared with BPD alone. Standardized developmental tests evaluated ND outcomes at 18-24 months corrected age (CA) and three years of age. Quality assessment of the studies was done using the Newcastle-Ottawa Quality Assessment for Cohort studies. Results Three retrospective cohort studies met the inclusion criteria. Two studies reported ND outcomes based on Bayley Scales of Infant and Toddler Development-III Edition in cognitive, language, and motor domains at 18-24 months CA (Table 1 and Figure 1). One study reported outcomes at 3 years, including overall developmental delay (Kyoto Scale of Psychological Development [KSPD] scores < 70) and cerebral palsy. The quality of all 3 studies was rated between good, fair, and poor. Pooled data from the 2 studies reporting outcomes at 18-24 months showed no difference between the 2 infant groups for Bayley cognitive score < 85 (Odds ratio [OR]: 3.78; 95% CI 0.87-16.52), Bayley language score < 85 (OR: 1.19; 95% CI0.57-2.49), and Bayley motor score < 85 (OR: 2.04; 95% CI 0.89-4.67). At 3 years of age, children in the BPD-PH group had an increased risk of developmental delay (DQ < 70 in all areas) compared with the BPD group (OR: 4.37; 95% CI 1.16-16.46), but no difference in the risk of cerebral palsy (OR: 0.57; 95%0.03-12.39). Conclusion PH in BPD is not associated with a developmental delay compared to BPD alone at 18-24 months CA. However, a single study showed infants in BPD-PH had delayed development at 3 years of age. A large prospective cohort study with longer multidisciplinary follow-up is required to confirm this.

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