scholarly journals Maternal Obesity, Birth Size, and Risk of Childhood Cancer Development

2019 ◽  
Vol 188 (8) ◽  
pp. 1503-1511 ◽  
Author(s):  
Shaina L Stacy ◽  
Jeanine M Buchanich ◽  
Zhen-qiang Ma ◽  
Christina Mair ◽  
Linda Robertson ◽  
...  
Keyword(s):  
Childhood Cancer ◽  
Early Life ◽  
Maternal Obesity ◽  
Birth Certificate ◽  
Cancer Development ◽  
Related Factors ◽  
Early Life Exposure ◽  
Increased Risk ◽  
Development Accounting ◽  
Newborn Size

Abstract Infants and children are particularly vulnerable to in utero and early-life exposures. Thus, a mother’s exposures before and during pregnancy could have important consequences for her child’s health, including cancer development. We examined whether birth certificate–derived maternal anthropometric characteristics were associated with increased risk of subsequent childhood cancer development, accounting for established maternal and infant risk factors. Pennsylvania birth and cancer registry files were linked by the state Department of Health, yielding a virtual cohort of births and childhood cancers from 2003 through 2016. The analysis included 1,827,875 infants (13,785,309 person-years at risk), with 2,352 children diagnosed with any cancer and 747 with leukemia before age 14 years. Children born to mothers with a body mass index (weight (kg)/height (m)2) of ≥40 had a 57% (95% confidence interval: 12, 120) higher leukemia risk. Newborn size of ≥30% higher than expected was associated with 2.2-fold and 1.8-fold hazard ratios for total childhood cancer and leukemia, respectively, relative to those with expected size. Being <30% below expected size also increased the overall cancer risk (P for curvilinearity < 0.0001). Newborn size did not mediate the association between maternal obesity and childhood cancer. The results suggest a significant role of early-life exposure to maternal obesity- and fetal growth–related factors in childhood cancer development.

scholarly journals Maternal Obesity and Developmental Programming of Metabolic Disorders in Offspring: Evidence from Animal Models

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
M. Li ◽  
D. M. Sloboda ◽  
M. H. Vickers
Keyword(s):  
Animal Models ◽  
Early Life ◽  
Metabolic Disorders ◽  
Maternal Obesity ◽  
Maternal Weight ◽  
Critical Window ◽  
Obesity Epidemic ◽  
Obesity And Overweight ◽  
Increased Risk ◽  
Maternal Overnutrition

The incidence of obesity and overweight has reached epidemic proportions in the developed world as well as in those countries transitioning to first world economies, and this represents a major global health problem. Concern is rising over the rapid increases in childhood obesity and metabolic disease that will translate into later adult obesity. Although an obesogenic nutritional environment and increasingly sedentary lifestyle contribute to our risk of developing obesity, a growing body of evidence links early life nutritional adversity to the development of long-term metabolic disorders. In particular, the increasing prevalence of maternal obesity and excess maternal weight gain has been associated with a heightened risk of obesity development in offspring in addition to an increased risk of pregnancy-related complications. The mechanisms that link maternal obesity to obesity in offspring and the level of gene-environment interactions are not well understood, but the early life environment may represent a critical window for which intervention strategies could be developed to curb the current obesity epidemic. This paper will discuss the various animal models of maternal overnutrition and their importance in our understanding of the mechanisms underlying altered obesity risk in offspring.

scholarly journals Prenatal and early-life exposure to the Great Chinese Famine increased the risk of tuberculosis in adulthood across two generations

2020 ◽  
Vol 117 (44) ◽  
pp. 27549-27555
Author(s):  
Qu Cheng ◽  
Robert Trangucci ◽  
Kristin N. Nelson ◽  
Wenjiang Fu ◽  
Philip A. Collender ◽  
...  
Keyword(s):  
Incidence Rate ◽  
Early Life ◽  
Food System ◽  
Cohort Analysis ◽  
Host Susceptibility ◽  
Sexually Transmitted ◽  
Global Food Security ◽  
Household Transmission ◽  
Early Life Exposure ◽  
Increased Risk

Global food security is a major driver of population health, and food system collapse may have complex and long-lasting effects on health outcomes. We examined the effect of prenatal exposure to the Great Chinese Famine (1958–1962)—the largest famine in human history—on pulmonary tuberculosis (PTB) across consecutive generations in a major center of ongoing transmission in China. We analyzed >1 million PTB cases diagnosed between 2005 and 2018 in Sichuan Province using age–period–cohort analysis and mixed-effects metaregression to estimate the effect of the famine on PTB risk in the directly affected birth cohort (F1) and their likely offspring (F2). The analysis was repeated on certain sexually transmitted and blood-borne infections (STBBI) to explore potential mechanisms of the intergenerational effects. A substantial burden of active PTB in the exposed F1 cohort and their offspring was attributable to the Great Chinese Famine, with more than 12,000 famine-attributable active PTB cases (>1.23% of all cases reported between 2005 and 2018). An interquartile range increase in famine intensity resulted in a 6.53% (95% confidence interval [CI]: 1.19–12.14%) increase in the ratio of observed to expected incidence rate (incidence rate ratio, IRR) in the absence of famine in F1, and an 8.32% (95% CI: 0.59–16.6%) increase in F2 IRR. Increased risk of STBBI was also observed in F2. Prenatal and early-life exposure to malnutrition may increase the risk of active PTB in the exposed generation and their offspring, with the intergenerational effect potentially due to both within-household transmission and increases in host susceptibility.

scholarly journals 180 Early Life Exposure to Maternal Obesity Perturbs Renal Morphology in Mice

Heart ◽  
2016 ◽  
Vol 102 (Suppl 6) ◽  
pp. A125.1-A125
Author(s):  
Adele Pinnock ◽  
Heather Blackmore ◽  
Tom Ashmore ◽  
Susan Ozanne
Keyword(s):  
Early Life ◽  
Maternal Obesity ◽  
Early Life Exposure ◽  
Renal Morphology

scholarly journals Maternal Residential Proximity to Major Roadways and the Risk of Childhood Acute Leukemia: A Population-Based Case-Control Study in Texas, 1995–2011

2019 ◽  
Vol 16 (11) ◽  
pp. 2029 ◽  
Author(s):  
Erin C. Peckham-Gregory ◽  
Minh Ton ◽  
Karen R. Rabin ◽  
Heather E. Danysh ◽  
Michael E. Scheurer ◽  
...  
Keyword(s):  
Acute Leukemia ◽  
Early Life ◽  
Childhood Leukemia ◽  
Lymphoblastic Leukemia ◽  
Birth Certificate ◽  
Population Based ◽  
Residential Proximity ◽  
Early Life Exposure ◽  
Proximity Measures ◽  
Childhood Acute Leukemia

Acute leukemia is the most common pediatric malignancy. Some studies suggest early-life exposures to air pollution increase risk of childhood leukemia. Therefore, we explored the association between maternal residential proximity to major roadways and risk of acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). Information on cases with acute leukemia (n = 2030) was obtained for the period 1995–2011 from the Texas Cancer Registry. Birth certificate controls were frequency matched (10:1) on birth year (n = 20,300). Three residential proximity measures were assessed: (1) distance to nearest major roadway, (2) residence within 500 meters of a major roadway, and (3) roadway density. Multivariate logistic regression was used to generate adjusted odds ratios (aOR) and 95% confidence intervals (CI). Mothers who lived ≤500 meters to a major roadway were not more likely to have a child who developed ALL (OR = 1.03; 95% CI: 0.91–1.16) or AML (OR = 0.84; 95% CI: 0.64–1.11). Mothers who lived in areas characterized by high roadway density were not more likely to have children who developed ALL (OR = 1.06, 95% CI: 0.93–1.20) or AML (OR = 0.83, 95% CI: 0.61–1.13). Our results do not support the hypothesis that maternal proximity to major roadways is strongly associated with childhood acute leukemia. Future assessments evaluating the role of early-life exposure to environmental factors on acute leukemia risk should explore novel methods for directly measuring exposures during relevant periods of development.

scholarly journals Developmental Programming of Nonalcoholic Fatty Liver Disease: The Effect of Early Life Nutrition on Susceptibility and Disease Severity in Later Life

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Minglan Li ◽  
Clare M. Reynolds ◽  
Stephanie A. Segovia ◽  
Clint Gray ◽  
Mark H. Vickers
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Early Life ◽  
Fatty Liver Disease ◽  
Maternal Obesity ◽  
Later Life ◽  
Developmental Programming ◽  
Nonalcoholic Fatty Liver ◽  
Increased Risk

Nonalcoholic fatty liver disease (NAFLD) is fast becoming the most common liver disease globally and parallels rising obesity rates. The developmental origins of health and disease hypothesis have linked alterations in the early life environment to an increased risk of metabolic disorders in later life. Altered early life nutrition, in addition to increasing risk for the development of obesity, type 2 diabetes, and cardiovascular disease in offspring, is now associated with an increased risk for the development of NAFLD. This review summarizes emerging research on the developmental programming of NAFLD by both maternal obesity and undernutrition with a particular focus on the possible mechanisms underlying the development of hepatic dysfunction and potential strategies for intervention.

scholarly journals Pregnancy, obesity and insulin resistance: maternal overnutrition and the target windows of fetal development

2013 ◽  
Vol 15 (1) ◽  
Author(s):  
Beverly S. Muhlhausler ◽  
Jessica R. Gugusheff ◽  
Zhi Yi Ong ◽  
Mini A. Vithayathil
Keyword(s):  
Insulin Resistance ◽  
Early Life ◽  
Maternal Obesity ◽  
Nutrient Supply ◽  
Personal Perspective ◽  
Human Populations ◽  
Maternal Undernutrition ◽  
Increased Risk ◽  
Maternal Overnutrition ◽  
The Impact

AbstractA substantial body of literature has demonstrated that the nutritional environment an individual experiences before birth or in early infancy is a key determinant of their health outcomes across the life course. This concept, the developmental origins of health and disease (DOHaD) hypothesis, was initially focused on the adverse consequences of exposure to a suboptimal nutrient supply and provided evidence that maternal undernutrition, fetal growth restriction, and low birth weight were associated with heightened risk of central adiposity, insulin resistance, and cardiovascular disease. More recently, the epidemic rise in the incidence of maternal obesity has seen the attention of the DOHaD field turn toward identifying the impact on the offspring of exposure to an excess nutrient supply in early life. The association between maternal obesity and increased risk of obesity in the offspring has been documented in human populations worldwide, and animal models have provided critical insights into the biological mechanisms that drive this relationship. This review will discuss the important roles that programming of the adipocyte and programming of the central neural networks which control appetite and reward play in the early life programming of metabolic disease by maternal overnutrition. It will also highlight the important research gaps and challenges that remain to be addressed and provide a personal perspective on where the field should be heading in the coming 5–10 years.

The impact of early life gut colonization on metabolic and obesogenic outcomes: what have animal models shown us?

2015 ◽  
Vol 7 (1) ◽  
pp. 15-24 ◽  
Author(s):  
J. G. Wallace ◽  
W. Gohir ◽  
D. M. Sloboda
Keyword(s):  
Animal Models ◽  
Gut Microbiota ◽  
Early Life ◽  
Maternal Obesity ◽  
Communicable Disease ◽  
Critical Periods ◽  
Early Life Adversity ◽  
Gut Colonization ◽  
Increased Risk ◽  
The Impact

The rise in the occurrence of obesity to epidemic proportions has made it a global concern. Great difficulty has been experienced in efforts to control this growing problem with lifestyle interventions. Thus, attention has been directed to understanding the events of one of the most critical periods of development, perinatal life. Early life adversity driven by maternal obesity has been associated with an increased risk of metabolic disease and obesity in the offspring later in life. Although a mechanistic link explaining the relationship between maternal and offspring obesity is still under investigation, the gut microbiota has come forth as a new factor that may play a role modulating metabolic function of both the mother and the offspring. Emerging evidence suggests that the gut microbiota plays a much larger role in mediating the risk of developing non-communicable disease, including obesity and metabolic dysfunction in adulthood. With the observation that the early life colonization of the neonatal and postnatal gut is mediated by the perinatal environment, the number of studies investigating early life gut microbial establishment continues to grow. This paper will review early life gut colonization in experimental animal models, concentrating on the role of the early life environment in offspring gut colonization and the ability of the gut microbiota to dictate risk of disease later in life.

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