A prospective, cross-sectional study of the protective and risk psychological factors of successful in vitro fertilisation outcome: preliminary results in a Greek sample

The aim of this prospective, cross-sectional study was to examine the protective and risk psychological factors associated with the successful outcome of In vitro fertilisation (IVF). Various psychological factors that may affect the IVF outcome were measured to a sample of 61 infertile women (mean age 37.2 ± 4.4), who started their first or consecutive IVF treatment cycle in an IVF Unit in Greece. Over half of the participants (50.8%) became pregnant. A binary logistic regression analysis (stepwise) was conducted on pregnancy as the outcome, with various variables as predictors. The model was statistically significant (Omnibus Chi-square = 27.324, df = 5, p < .001), explained 54.7% of the variance, and correctly classified 84.6% of the cases. Life purpose (odds ratio [OR] = 1.35, 95% CI = 1.02–1.78) and negative emotions (e.g. discontent, sorrow) (OR = 1.76, 95% CI = 1.19–2.60) were associated with increased pregnancy rates, whereas autonomy (OR = 0.57, 95% CI = 0.39–0.82), and stress (OR = 0.69, 95% CI = 0.55–0.88) were associated with decreased pregnancy rates. It has been concluded that the relationship between psychological factors and successful IVF outcome is more complex than commonly believed. The identification of the risk and protective psychological factors could contribute to increased pregnancy rates and foster the implementation of tailored therapeutic interventions.Impact statement What is already known on this subject? High levels of infertility stress and/or depression have been associated with lower pregnancy rates. However, little is known on the impact of emotions, personality characteristics and other psychological variables on in vitro fertilisation (IVF) outcome. What the results of this study add? A combination of commonly believed ‘negative’ factors (e.g. stress) and ‘positive’ ones (e.g. well-being) may diversely affect the IVF outcome. Otherwise believed to be positive aspects of human life (i.e. autonomy) may decrease the likelihood of pregnancy, and other factors believed to be ‘negative’ (e.g. negative emotions) may increase pregnancy rates. What the implications of these findings are for clinical practice and/or further research? The findings invite researchers to further examine the role of the psychological factors which could potentially affect pregnancy rates. Modifiable factors, such as well-being, stress and emotions, should guide tailored interventions aimed at increasing the pregnancy rates in infertile women

Endocrine Disruptors Leading to Obesity and Related Diseases

The review aims to comprehensively present the impact of exposure to endocrine disruptors (EDs) in relation to the clinical manifestation of obesity and related diseases, including diabetes mellitus, metabolic syndrome, cardiovascular diseases, carcinogenesis and infertility. EDs are strong participants in the obesity epidemic scenery by interfering with cellular morphological and biochemical processes; by inducing inflammatory responses; and by presenting transcriptional and oncogenic activity. Obesity and lipotoxicity enhancement occur through reprogramming and/or remodeling of germline epigenome by exposure to EDs. Specific population groups are vulnerable to ED exposure due to current dietary and environmental conditions. Obesity, morbidity and carcinogenicity induced by ED exposure are an evolving reality. Therefore, a new collective strategic approach is deemed essential, for the reappraisal of current global conditions pertaining to energy management

Endocrine Disruptors Acting on Estrogen and Androgen Pathways Cause Reproductive Disorders through Multiple Mechanisms: A Review

Increasing contamination of the environment by toxic compounds such as endocrine disrupting chemicals (EDCs) is one of the major causes of reproductive defects in both sexes. Estrogen/androgen pathways are of utmost importance in gonadal development, determination of secondary sex characteristics and gametogenesis. Most of the EDCs mediate their action through respective receptors and/or downstream signaling. The purpose of this review is to highlight the mechanism by which EDCs can trigger antagonistic or agonistic response, acting through estrogen/androgen receptors causing reproductive defects that lead to infertility. In vitro, in vivo and in silico studies focusing on the impact of EDCs on estrogen/androgen pathways and related proteins published in the last decade were considered for the review. PUBMED and PUBCHEM were used for literature search. EDCs can bind to estrogen receptors (ERα and ERβ) and androgen receptors or activate alternative receptors such as G protein-coupled receptors (GPCR), GPR30, estrogen-related receptor (ERRγ) to activate estrogen signaling via downstream kinases. Bisphenol A, dichlorodiphenyltrichloroethane, dichlorodiphenyldichloroethylene, polychlorinated biphenyls and phthalates are major toxicants that interfere with the normal estrogen/androgen pathways leading to infertility in both sexes through many ways, including DNA damage in spermatozoids, altered methylation pattern, histone modifications and miRNA expression

DNA Damage Estimation after Chronic and Combined Exposure to Endocrine Disruptors: An In Vivo Real-Life Risk Simulation Approach

Exposure to chemical substances has always been a matter of concern for the scientific community. During the last few years, researchers have been focusing on studying the effects resulting from combined exposure to different substances. In this study, we aimed to determine the DNA damage caused after chronic and combined exposure to substances characterized as endocrine disruptors using comet and micronuclei assays, specifically glyphosate (pure and commercial form), bisphenol A, parabens (methyl-, propyl- and butylparaben), triclosan and bis (2-ethylhexyl) phthalate. The highest mean tail intensity was observed in the group exposed to a high-dose (10 × ADI) mixture of substances (Group 3), with a mean value of 11.97 (11.26–13.90), while statistically significant differences were noticed between the groups exposed to low-dose (1 × ADI) (Group 2) and high-dose (10 × ADI) (Group 3) mixtures of substances (p = 0.003), and between Group 3 and both groups exposed to high doses (10 × ADI) of the pure and commercial forms of glyphosate (Groups 4 (p = 0.014) and 5 (p = 0.007)). The micronuclei assay results were moderately correlated with the exposure period. Group 5 was the most impacted exposure group at all sampling times, with mean MN counts ranging between 28.75 ± 1.71 and 60.75 ± 1.71, followed by Group 3 (18.25 ± 1.50–45.75 ± 1.71), showing that commercial forms of glyphosate additives as well as mixtures of endocrine disruptors can enhance MN formation. All exposure groups showed statistically significant differences in micronuclei counts with an increasing time trend