Toxicology in Vitro, Journal Year: 2016, Volume and Issue: 40, P. 66 - 78
Published: Dec. 12, 2016
Language: Английский
Toxicology in Vitro, Journal Year: 2016, Volume and Issue: 40, P. 66 - 78
Published: Dec. 12, 2016
Language: Английский
PLoS ONE, Journal Year: 2018, Volume and Issue: 13(5), P. e0197244 - e0197244
Published: May 10, 2018
Objective Many people are exposed to perfluoroalkyl substances (PFASs) because these widely used as industrial products. Although epidemiological studies suggest that PFASs can disrupt thyroid hormones, the association between PFAS exposure and function remains inconclusive. Therefore, we performed a comprehensive meta-analysis investigate hormones. Methods We searched medical literature databases for articles on PFASs–perfluorooctanesulfonic acid (PFOS), perfluorooctanoic (PFOA), perfluorohexane sulfonic (PFHxS)–and hormone levels in adults. Twelve were included meta-analysis, pooled z values calculated with correlation or regression coefficients. Results The blood PFOS concentration was positively correlated free T4. value 0.05 (95% confidence interval (CI): 0.03, 0.08). negatively total T4 T3 when excluding outlier studies. In subgroup analysis stratified by mean concentration, observed be associated TSH intermediate group (8–16 ng/mL). PFOA (z value, -0.06; 95% CI: -0.09, -0.03) after omitting one study. PFHxS also showed negative -0.04; -0.07, -0.01). A of pregnant women there no Conclusions Our suggests T4, their effect different depending concentration.
Language: Английский
Citations
118Environmental Health Perspectives, Journal Year: 2018, Volume and Issue: 126(5)
Published: May 21, 2018
There is growing concern that phthalate exposures may have an impact on child neurodevelopment. Prenatal exposure to phthalates has been linked with externalizing behaviors and executive functioning defects suggestive of attention-deficit hyperactivity disorder (ADHD) phenotype.We undertook investigation into whether prenatal was associated clinically confirmed ADHD in a population-based nested case-control study the Norwegian Mother Child Cohort (MoBa) between years 2003 2008.Phthalate metabolites were measured maternal urine collected at midpregnancy. Cases (n=297) obtained through linkage MoBa National Patient Registry. A random sample controls (n=553) from population obtained.In multivariable adjusted coexposure models, sum di-2-ethylhexyl (∑DEHP) monotonically increasing risk ADHD. Children mothers highest quintile ∑DEHP had almost three times odds diagnosis as those lowest [OR=2.99 (95% CI: 1.47, 5.49)]. When modeled log-linear (natural log) term, for each log-unit increase exposure, increased by 47% [OR=1.47 1.09, 1.94)]. We detected no significant modification sex or mediation thyroid function preterm delivery.In this clinical ADHD, urinary concentrations DEHP Additional research needed evaluate potential mechanisms linking https://doi.org/10.1289/EHP2358.
Language: Английский
Citations
117Philosophical Transactions of the Royal Society B Biological Sciences, Journal Year: 2019, Volume and Issue: 374(1770), P. 20180115 - 20180115
Published: Feb. 25, 2019
Maternal effects can adaptively modulate offspring developmental trajectories in variable but predictable environments. Hormone synthesis is sensitive to environmental factors, and maternal hormones are thus a powerful mechanism transfer cues the next generation. Birds have become key model for study of hormone-mediated because embryo develops outside mother's body, facilitating measurement manipulation prenatal hormone exposure. At same time, birds excellent models integration both proximate ultimate approaches, which better understanding evolution effects. Over past two decades, surge studies on has revealed an increasing number discrepancies. In this review, we discuss role environment, genetic factors social interactions causing these discrepancies provide framework resolve them. We also explore largely neglected modulating signal, as well costs benefits expression different family members. conclude by highlighting fruitful avenues future research that opened up thanks new theoretical insights technical advances field. This article part theme issue ‘Developing differences: early-life evolutionary medicine’.
Language: Английский
Citations
111Current Nutrition Reports, Journal Year: 2019, Volume and Issue: 8(2), P. 99 - 107
Published: April 5, 2019
Language: Английский
Citations
91Toxicology and Applied Pharmacology, Journal Year: 2018, Volume and Issue: 354, P. 196 - 214
Published: March 18, 2018
Language: Английский
Citations
87International Journal of Developmental Neuroscience, Journal Year: 2019, Volume and Issue: 73(1), P. 41 - 49
Published: Jan. 8, 2019
Abstract Background During development, the placenta can be said to most important organ, however, poorly researched. There is currently a broader understanding of how specific insults during development affect fetal brain, and also importance placental signaling in neurodevelopmental programming. Epigenetic responses maternal signals are an obvious candidate for transforming early life inputs into long‐term programmatic outcomes. As mediator environmental developing fetus, epigenetic processes within particularly powerful such that alterations gene expression, downstream function, signalling foetal have potential dramatic changes developmental Summary In this article, we reviewed emerging evidence role prenatal programming with focus on nutrient stress integration chromatin changes; new understanding, hope will provide means lowering developmentally based disorder risk, therapeutic targets treatment adulthood. Key messages Based review, potent micro‐environmental player neurodevelopment as it orchestrates series complex maternal–foetal interactions. Maternal microenvironment impair these disrupt brain resulting disorders. These findings should inspire advance animal model human research drive appraise gene–environment impacts pregnancy target cause adult‐onset mental
Language: Английский
Citations
86The Journal of Clinical Endocrinology & Metabolism, Journal Year: 2020, Volume and Issue: 105(12), P. 3821 - 3841
Published: Aug. 18, 2020
Abstract Context Previous studies suggested a potential link of maternal thyroid dysfunction with adverse neurocognitive outcomes and impaired development internal organs in offspring. Objective To review the association between risk Data Sources PubMed, EMBASE, Cochrane Library. Study Selections Eligible reported hormone function their children. Extraction Reviewers extracted data on study characteristics results independently. Synthesis Estimates were pooled as odds ratio (OR) 95% confidence interval (CI). I2 tests applied to assess heterogeneity across studies. Results We identified 29 eligible articles found an hyperthyroidism attention deficit hyperactivity disorder (ADHD) (OR: 1.18, CI: 1.04-1.34, = 0%) epilepsy 1.19, 1.08-1.31, offspring; well hypothyroidism increased ADHD 1.14, 1.03-1.26, 25%), autism spectrum 1.41, 1.05-1.90, 63%), 1.21, 1.06-1.39, Conclusion Routine measurement timely treatment should be considered for pregnant women.
Language: Английский
Citations
81The Journal of Clinical Endocrinology & Metabolism, Journal Year: 2020, Volume and Issue: 106(3), P. 883 - 892
Published: Dec. 22, 2020
Abstract Both hyperthyroidism and hypothyroidism can have adverse effects in pregnancy. The most common causes of thyrotoxicosis pregnancy are gestational transient Graves’ disease. It is important to distinguish between these entities as treatment options differ. Women reproductive age who diagnosed with disease should be counseled regarding the impact on a potential Although absolute risk small, antithyroid medications teratogenic effects. Propylthiouracil appears less severe teratogenicity compared methimazole therefore favored during first trimester if medication needed. advised delay for at least 6 months following radioactive iodine minimize from radiation ensure normal thyroid hormone levels prior conception. As critical fetal development, associated obstetric child neurodevelopmental outcomes. overt treated levothyroxine (LT4) thyrotropin (thyroid-stimulating hormone; TSH) goal <2.5 mIU/L. There mounting evidence associations maternal hypothyroxinemia subclinical loss, preterm labor, lower scores cognitive assessment. there minimal LT4 keep TSH within pregnancy-specific reference range, mild hypofunction remains controversial, given lack clinical trials showing improved outcomes treatment.
Language: Английский
Citations
71BMC Endocrine Disorders, Journal Year: 2021, Volume and Issue: 21(1)
Published: Feb. 27, 2021
Abstract Background Levothyroxine replacement therapy may decrease the risk of adverse pregnancy outcomes among women with subclinical hypothyroidism (SCH). The aim this study is to conduct a systematic review and meta-analysis examine pregnancy, perinatal, early childhood SCH treated levothyroxine. Methods A literature search was conducted using Ovid-Medline, Ovid-EMBASE, Pubmed (non-Medline), Ebsco-CINAHL Plus full text Cochrane Library databases. Randomized controlled studies (RCTs) observational examining association between treatment during our interest were included. Studies that compared levothyroxine versus no eligible for inclusion. Data from included extracted quality assessment performed by two independent reviewers. Results Seven RCTs six met inclusion criteria. total 7342 individuals in these studies. demonstrated several sources bias, lack blinding participants or research personnel; only one fully blinded. In studies, there moderate serious bias due adjustment certain confounding variables, participant selection, selective reporting results. Pooled analyses showed decreased loss (RR: 0.79; 95% CI: 0.67 0.93) neonatal death 0.35; 0.17 0.72) associated SCH. There associations labour delivery, cognitive status children at 3 5 years age. Conclusion Treatment risks death. Given paucity available data heterogeneity additional are needed address benefits use pregnant
Language: Английский
Citations
65Brain Sciences, Journal Year: 2023, Volume and Issue: 13(7), P. 1010 - 1010
Published: June 29, 2023
Humans have lived in a dynamic environment fraught with potential dangers for thousands of years. While fear and stress were crucial the survival our ancestors, today, they are mostly considered harmful factors, threatening both physical mental health. Trauma is highly stressful, often life-threatening event or series events, such as sexual assault, war, natural disasters, burns, car accidents. can cause pathological metaplasticity, leading to long-lasting behavioral changes impairing an individual’s ability cope future challenges. If individual vulnerable, tremendously traumatic may result post-traumatic disorder (PTSD). The hypothalamus critical initiating hormonal responses stressful stimuli via hypothalamic–pituitary–adrenal (HPA) axis. Linked prefrontal cortex limbic structures, especially amygdala hippocampus, acts central hub, integrating physiological aspects response. Consequently, hypothalamic functions been attributed pathophysiology PTSD. However, apart from well-known role HPA axis, also play different roles development PTSD through other pathways, including hypothalamic–pituitary–thyroid (HPT) hypothalamic–pituitary–gonadal (HPG) axes, well by secreting growth hormone, prolactin, dopamine, oxytocin. This review aims summarize current evidence regarding neuroendocrine hypothalamus, which correlated A better understanding could help develop treatments this debilitating condition.
Language: Английский
Citations
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