Obesogenic Endocrine Disrupting Chemicals: Identifying Knowledge Gaps

Veiga-López, Almudena; Pu, Yuehua; Gingrich, Jeremy; Padmanabhan, Vasantha

doi:10.1016/j.tem.2018.06.003

Cited by 87 publications

(39 citation statements)

References 165 publications

(232 reference statements)

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“…These data fit within a broadening context of multigenerational and transgenerational effects of multiple EDC classes on various endocrine and metabolic tissues [7,[26][27][28][29]. Recently, studies have demonstrated that changes in the expression and methylation of imprinted genes in the brain persist across three generations after BPA exposure in mice [30].…”

Section: Exposures During Sensitive Developmental Windowssupporting

confidence: 58%

Environmental neglect: endocrine disruptors as underappreciated but potentially modifiable diabetes risk factors

2019

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Type 2 diabetes prevalence is increasing dramatically across the globe, imposing a tremendous toll on individuals and healthcare systems. Reversing these trends requires comprehensive approaches to address both classical and emerging diabetes risk factors. Recently, environmental toxicants acting as endocrine-disrupting chemicals (EDCs) have emerged as novel metabolic disease risk factors. EDCs implicated in diabetes pathogenesis include various inorganic and organic molecules of both natural and synthetic origin, including arsenic, bisphenol A, phthalates, polychlorinated biphenyls and organochlorine pesticides. Indeed, evidence implicates EDC exposures across the lifespan in metabolic dysfunction; moreover, specific developmental windows exhibit enhanced sensitivity to EDC-induced metabolic disruption, with potential impacts across generations. Importantly, differential exposures to diabetogenic EDCs likely also contribute to racial/ethnic and economic disparities. Despite these emerging links, clinical practice guidelines fail to address this underappreciated diabetes risk factor. Comprehensive approaches to stem the tide of diabetes must include efforts to address its environmental drivers.

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Section: Exposures During Sensitive Developmental Windowssupporting

confidence: 58%

Environmental neglect: endocrine disruptors as underappreciated but potentially modifiable diabetes risk factors

2019

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“… 30 Thus, EDCs with estrogenic, antiandrogenic, or obesogenic actions may have differing associations with puberty in boys and girls. 27 , 31 , 32 To what extent EDCs contribute to the secular trend in male pubertal timing presented in this study is not clear. Our findings indicate that there is a robust secular trend for earlier pubertal timing in boys that is explained by other unknown factors than the obesity epidemic and demographic changes.…”

Section: Discussionmentioning

confidence: 88%

Secular Trends in Pubertal Growth Acceleration in Swedish Boys Born From 1947 to 1996

et al. 2019

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IMPORTANCE A secular trend for earlier menarcheal age has been established in girls but there are few studies of pubertal timing for boys. OBJECTIVE To determine if there is a secular trend for earlier pubertal timing among boys. DESIGN, SETTING, AND PARTICIPANTS For this population-based retrospective cohort study conducted in Gothenburg, Sweden, we collected heights and weights from school health records for boys born consecutively from January 1 and onwards in 1947 and every 5 years from 1951 to 1996 (n = 375 for each birth cohort from 1947-1991, n = 340 for the birth cohort in 1996, and n = 4090 for the total cohort). We estimated age at the peak height velocity (PHV), the maximum growth velocity during puberty, and childhood body mass index (BMI) at age 8 years for all study participants. The data were analyzed during 2018 and 2019. Boys were eligible if they had a complete personal identity number and data to calculate their age at PHV and childhood BMI. Approximately 2.4% of the original study population was excluded because they lacked a personal identity number, and in the remaining study population, 4090 (69%) had sufficient data to calculate childhood BMI and age at PHV. EXPOSURES The exposure was birth year and a potential confounding factor was childhood BMI. MAIN OUTCOMES AND MEASURES The outcome was age at PHV. RESULTS Of the 4090 participants, most were white and the mean (SD) age at PHV was 13.9 (1.1) years. A linear regression model revealed a significant association between year of birth and age at PHV. Age at PHV was 1.5 months earlier for every decade increase in birth year (95% CI, −1.72 to −1.19; P < .001). After adjusting for childhood BMI, age at PHV was 1.2 months earlier per decade increase in birth year (95% CI, −1.41 to −0.89). All analyses were repeated in the subgroup of boys born in Sweden and with parents born in Sweden with similar results, indicating that the secular trend was not explained by demographic changes in the population between 1947 and 1996. CONCLUSIONS AND RELEVANCE We provide evidence of a secular trend for earlier pubertal timing in boys that is partially explained by an increased childhood BMI, but other factors that are unknown contribute.

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“…114 EDCs appear to work through a variety of mechanisms, including direct binding to hormone receptors, disrupting mitochondrial function, altering the intestinal microbiome, and modifying the epigenome. 115,116 Screening and Diagnosis…”

Section: Environmental Exposuresmentioning

confidence: 99%

Nonalcoholic Fatty Liver Disease in Children: Unique Considerations and Challenges

Goldner

Lavine

2020

Gastroenterology

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Obesogenic Endocrine Disrupting Chemicals: Identifying Knowledge Gaps

Cited by 87 publications

References 165 publications

Environmental neglect: endocrine disruptors as underappreciated but potentially modifiable diabetes risk factors

Environmental neglect: endocrine disruptors as underappreciated but potentially modifiable diabetes risk factors

Secular Trends in Pubertal Growth Acceleration in Swedish Boys Born From 1947 to 1996

Nonalcoholic Fatty Liver Disease in Children: Unique Considerations and Challenges

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