scholarly journals Maternal and early life exposures and their potential to influence development of the microbiome

2022 ◽  
Vol 14 (1) ◽  
Author(s):  
Erin E. Bolte ◽  
David Moorshead ◽  
Kjersti M. Aagaard

AbstractAt the dawn of the twentieth century, the medical care of mothers and children was largely relegated to family members and informally trained birth attendants. As the industrial era progressed, early and key public health observations among women and children linked the persistence of adverse health outcomes to poverty and poor nutrition. In the time hence, numerous studies connecting genetics (“nature”) to public health and epidemiologic data on the role of the environment (“nurture”) have yielded insights into the importance of early life exposures in relation to the occurrence of common diseases, such as diabetes, allergic and atopic disease, cardiovascular disease, and obesity. As a result of these parallel efforts in science, medicine, and public health, the developing brain, immune system, and metabolic physiology are now recognized as being particularly vulnerable to poor nutrition and stressful environments from the start of pregnancy to 3 years of age. In particular, compelling evidence arising from a diverse array of studies across mammalian lineages suggest that modifications to our metagenome and/or microbiome occur following certain environmental exposures during pregnancy and lactation, which in turn render risk of childhood and adult diseases. In this review, we will consider the evidence suggesting that development of the offspring microbiome may be vulnerable to maternal exposures, including an analysis of the data regarding the presence or absence of a low-biomass intrauterine microbiome.

Author(s):  
Markus J Haapanen ◽  
Juulia Jylhävä ◽  
Lauri Kortelainen ◽  
Tuija M Mikkola ◽  
Minna Salonen ◽  
...  

Abstract Background Early life exposures have been associated with the risk of frailty in old age. We investigated whether early life exposures predict the level and rate of change in a frailty index (FI) from midlife into old age. Methods A linear mixed model analysis was performed using data from three measurement occasions over 17 years in participants from the Helsinki Birth Cohort Study (n=2000) aged 57-84 years. A 41-item FI was calculated on each occasion. Information on birth size, maternal body mass index (BMI), growth in infancy and childhood, childhood socioeconomic status (SES), and early life stress (wartime separation from both parents), was obtained from registers and healthcare records. Results At age 57 years the mean FI level was 0.186 and the FI levels increased by 0.34 percent/year from midlife into old age. Larger body size at birth associated with a slower increase in FI levels from midlife into old age. Per 1kg greater birth weight the increase in FI levels per year was -0.087 percentage points slower (95% CI=-0.163, -0.011; p=0.026). Higher maternal BMI was associated with a higher offspring FI level in midlife and a slower increase in FI levels into old age. Larger size, faster growth from infancy to childhood, and low SES in childhood were all associated with a lower FI level in midlife but not with its rate of change. Conclusions Early life factors seem to contribute to disparities in frailty from midlife into old age. Early life factors may identify groups that could benefit from frailty prevention, optimally initiated early in life.


2021 ◽  
pp. 108705472110367
Author(s):  
Bob Cattoi ◽  
Ingrid Alpern ◽  
Jeffrey S. Katz ◽  
David Keepnews ◽  
Mary V. Solanto

Recent research has increasingly documented the adverse effects of ADHD on physical health in addition to its well-known effects on emotional health. Responding to this concern, CHADD organized a summit meeting of health care providers, governmental and other health-related organizations, and health care payers. A White Paper generated from the meeting reviewed the adverse health outcomes, economic burden and public health implications of unmanaged ADHD. Here we summarize the resulting Calls to Action to the various stakeholder groups including: increased awareness and education of providers; development of professional guidelines for diagnosis and treatment; insurance coverage of the relevant services; support of research targeting the role of ADHD in the etiology and treatment of physical illness; and public education campaigns.


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.


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