Search

AimsExposure to endocrine-disrupting chemicals (EDCs) during critical neurodevelopmental windows has been associated with the risk of autistic traits. This systematic review of epidemiological studies examined the association between maternal exposure to EDCs during pregnancy and the risk of autism spectrum disorder (ASD) in the offspring.MethodsWe searched PubMed, Web of Science, Scopus, and Google Scholar from inception to November 17, 2022, for studies investigating the association between prenatal exposure to EDCs and outcomes related to ASD. Two independent reviewers screened studies for eligibility, extracted data, and assessed the risk of bias. The review was registered in PROSPERO (CRD42023389386).ResultsWe included 27 observational studies assessing prenatal exposure to phthalates (8 studies), polychlorinated biphenyls (8 studies), organophosphate pesticides (8 studies), phenols (7 studies), perfluoroalkyl substances (6 studies), organochlorine pesticides (5 studies), brominated flame retardants (3 studies), dioxins (1 study), and parabens (1 study). The number of examined children ranged from 77 to 1,556, the age at the assessment of autistic traits ranged from 3 to 14 years, and most studies assessed autistic traits using the Social Responsiveness Scale. All but one study was considered to have a low risk of bias. Overall, there was no association between maternal exposure to specific ECDs during pregnancy and the occurrence of autistic traits in offspring.ConclusionsFindings from the epidemiological studies evaluated here do not support an association between prenatal exposure to ECDs and the likelihood of autistic traits in later in life. These findings should not be interpreted as definitive evidence of the absence of neurodevelopment effects of EDCs affecting ASD risk, given the limitations of current studies such as representative exposure assessment, small sample sizes, inadequacy to assess sexually dimorphic effects, or the effects of EDC mixtures. Future studies should carefully address these limitations.

Obesity is now a worldwide pandemic. The usual explanation given for the prevalence of obesity is that it results from consumption of a calorie dense diet coupled with physical inactivity. However, this model inadequately explains rising obesity in adults and in children over the past few decades, indicating that other factors must be important contributors. An endocrine-disrupting chemical (EDC) is an exogenous chemical, or mixture that interferes with any aspect of hormone action. EDCs have become pervasive in our environment, allowing humans to be exposed daily through ingestion, inhalation, and direct dermal contact. Exposure to EDCs has been causally linked with obesity in model organisms and associated with obesity occurrence in humans. Obesogens promote adipogenesis and obesity, in vivo, by a variety of mechanisms. The environmental obesogen model holds that exposure to obesogens elicits a predisposition to obesity and that such exposures may be an important yet overlooked factor in the obesity pandemic. Effects produced by EDCs and obesogen exposure may be passed to subsequent, unexposed generations. This "generational toxicology" is not currently factored into risk assessment by regulators but may be another important factor in the obesity pandemic as well as in the worldwide increases in the incidence of noncommunicable diseases that plague populations everywhere. This review addresses the current evidence on how obesogens affect body mass, discusses long-known chemicals that have been more recently identified as obesogens, and how the accumulated knowledge can help identify EDCs hazards.

Background: Heart failure, a complex clinical syndrome with high morbidity and mortality, has become a significant burden on public health. Recently, a new class of antidiabetic agents-the sodium-glucose cotransporter 2 (SGLT2) inhibitors-was associated with a significant reduction on mortality and hospitalization in HF with reduced ejection fraction (HFrEF) when added to standard pharmacological treatment. Considering the lack of data on its cost-effectiveness, the present study aims to estimate the incremental cost-effectiveness ratio of add-on dapagliflozin treatment for HFrEF from the Brazilian public healthcare system perspective., Methods: We built a Markov model to estimate the clinical outcomes and costs of 1,000 hypothetical subjects with established HFrEF in a lifetime horizon. The model inputs were based on the Dapagliflozin and Prevention of Adverse Outcomes in Heart Failure (DAPA-HF) trial and local data. The main outcome was the incremental cost-effectiveness ratio (ICER) per quality-adjusted life year (QALY) gained. Deterministic and probabilistic sensitivity analyses, as well as scenario analyses, were performed., Findings: The addition of dapagliflozin to standard care treatment in 1,000 HFrEF patients yielded an expected value of 366.99 additional QALYs at an incremental cost of US$ 1,517,878.49, resulting in an ICER of US$ 4,136.08 per QALY gained, being a cost-effective strategy considering the Brazilian official cost-effectiveness threshold (US$ 8,000/QALY). In probabilistic sensitivity analyses, 96.60% of the simulations were also cost-effective. In the scenario analyses, results were similar for individuals with and without diabetes., Interpretation: Dapagliflozin is likely to be cost-effective when added to standard HFrEF therapy in Brazil., Funding: This study was supported by the National Institute of Science and Technology for Health Technology Assessment (Instituto de Avaliação de Tecnologias em Saúde-IATS)., Competing Interests: None declared., (© 2024 The Author(s).)

Emergent evidence suggests that the long-term healthy lifestyle of master athletes may attenuate aging. We compared telomere length (TL) of high-level master sprinters and non-athlete age-matched controls, and analyzed the relationships of TL with performance and body fat. Elite master sprinters (n=11; aged 50.1±9.2yrs) and healthy untrained controls (n=10; aged 45.4±10.9yrs) had blood samples collected for biochemical and biomolecular analyses. Master sprinters had longer TL, lower body fat and BMI, and a better lipid profile than age-matched controls (p<0.05). A large effect size was verified comparing TL between athletes vs. controls (Cohen's d=1.039), with a significant negative correlation between TL and performance decline per decade (r=-0.624, p<0.01) and a positive correlation of TL and actual performance level (r=0.641, p<0.01). In conclusion, TL of elite master sprinters was longer than their untrained peers, and seems to be not only a marker of health status, but also an indicator of sports longevity since both actual performance level and its decrease over years were related to TL. Further research might assess the TL of elite master endurance athletes for comparison with sprinters, and also investigate the underlying mechanisms by which the attenuation of telomere shortening occurs in master athletes., Competing Interests: Disclosure The authors report no conflicts of interest in this work., (© Georg Thieme Verlag KG Stuttgart · New York.)