Endocrine-disrupting chemicals (EDCs) are natural or synthetic chemicals that mimic, block, or interfere with the hormones in the body. The most common and well- studied EDCs are bisphenol A, phthalates, and persistent organic pollutants including polychlorinated biphenyls, polybrominated diphenyl ethers, per- and polyfluoroalkyl substances, other brominated flame retardants, organochlorine pesticides, dioxins, and furans. Starting in embryonic life, humans are constantly exposed to EDCs through air, diet, skin, and water. Fetuses and newborns undergo crucial developmental processes that allow adaptation to the environment throughout life. As developing organisms, they are extremely sensitive to low doses of EDCs. Many EDCs can cross the placental barrier and reach the developing fetal organs. In addition, newborns can be exposed to EDCs through breastfeeding or formula feeding. Pre- and postnatal exposure to EDCs may increase the risk of childhood diseases by disrupting the hormone-mediated processes critical for growth and development during gestation and infancy. This review discusses evidence of the relationship between pre- and postnatal exposure to several EDCs, childbirth, and neurodevelopmental outcomes. Available evidence suggests that pre- and postnatal exposure to certain EDCs causes fetal growth restriction, preterm birth, low birth weight, and neurodevelopmental problems through various mechanisms of action. Given the adverse effects of EDCs on child development, further studies are required to clarify the overall associations.

Purpose of Review: Endocrine disruptors (EDs) can mimic or interfere with hormones in the body, leading to non-communicable diseases, such as obesity, diabetes, and metabolic syndrome. Susceptibility to EDs increases during prenatal and postnatal life, a critical time window. This review aims to summarize the latest evidence on the relation of early life exposure to some EDs with obesity and the other metabolic disorders. Recent Findings: There is increasing evidence that early life exposure to EDs may impair adipogenesis by increasing the number and size of adipocytes, thereby increasing susceptibility to obesity in childhood. It is stated that exposure to EDs during the prenatal and postnatal period may raise the risk of type 2 diabetes in adulthood by disrupting glucose, lipid, and insulin homeostasis in the offspring. They can also accelerate the development of type 1 diabetes through various mechanisms, like immunomodulation, gut microbiota, and vitamin D pathways. Summary: There is a growing understanding that ED exposure during critical stages of life could play an important role in the development of obesity and metabolic disorders. We suggest setting national goals, global standards, and policies to reduce environmental exposure to pregnant and lactating women, and babies, considered sensitive populations.

Type 2 diabetes mellitus (T2DM) is a multifactorial metabolic disorder described by chronic hyperglycemia, insulin resistance, as well as low-grade inflammation. Recent research highlights the vital role of the gut microbiota in the pathogenesis and progression of T2DM. Dysbiosis can impair intestinal barrier integrity, promote systemic inflammation, and contribute to insulin resistance and glucose metabolism dysfunction. This review article investigates the mechanisms by which probiotics interact with gut microbiota and host signaling pathways to impact the onset and complications of T2DM. Databases were searched, and related articles were added, to get a thorough overview of the relationship between probiotics and T2DM and its complications. Probiotics have appeared as potential modulators of the gut microbiome, capable of restoring microbial balance and strengthening intestinal barrier function. Probiotics can influence glucose homeostasis through their multifaceted effects on the gut microbiota and host metabolism. Through the production of beneficial metabolites, suppress α-glucosidase activity, enhance short-chain fatty acid (SCFA) levels, competitive inhibition of pathogenic bacteria, regulation of gut-derived neurotransmitters such as serotonin, improve intestinal, and immune functions, probiotics may alleviate key mechanisms involved in T2DM development and its complications.

Purpose of Review: Environmental pollutants in air, water, soil, and food are a significant concern due to their potential adverse effects on fetuses, newborns, babies, and children. These chemicals, which pass to fetuses and babies through trans-placental transfer, breast milk, infant formula, dermal transfer, and non-nutritive ingestion, can cause health problems during childhood. This review aims to discuss how exposure to various environmental pollutants in early life stages can disrupt reproductive health in children. Recent Findings: Environmental pollutants can affect Leydig cell proliferation and differentiation, decreasing testosterone production throughout life. This may result in cryptorchidism, hypospadias, impaired semen parameters, and reduced fertility. Although many studies on female reproductive health cannot be interpreted to support causal relationships, exposure to pollutants during critical windows may subsequently induce female reproductive diseases, including early or delayed puberty, polycystic ovary syndrome, endometriosis, and cancers. Summary: There is growing evidence that fetal and early-life exposure to environmental pollutants could affect reproductive health in childhood. Although diet is thought to be the primary route by which humans are exposed to various pollutants, there are no adopted nutritional interventions to reduce the harmful effects of pollutants on children's health. Therefore, understanding the impact of environmental contaminants on various health outcomes may inform the design of future human nutritional studies.

Oxylipins are oxidized fatty acids, both saturated and unsaturated, formed through pathways that involve singlet oxygen or dioxygen-mediated oxygenation reactions and are primarily produced by enzyme families such as cyclooxygenases, lipoxygenases, and cytochrome P450. These lipid-based complex bioactive molecules are pivotal signal mediators, acting in a hormone-like manner in the pathophysiology of numerous diseases, especially cardiometabolic diseases via modulating plenty of mechanisms. It has been reported that omega-6 and omega-3 oxylipins are important novel biomarkers of cardiometabolic diseases. Moreover, collected literature has noted that diet and dietary components, especially fatty acids, can modulate these oxygenated lipid products since they are mainly derived from dietary omega-3 and omega-6 polyunsaturated fatty acids (PUFAs) or linoleic acid and α-linolenic by elongation and desaturation pathways. This comprehensive review aims to examine their correlations to cardiometabolic diseases and how diets modulate oxylipins. Also, some aspects of developing new biomarkers and therapeutical utilization are detailed in this review.

Giriş ve Amaç: Gelecek nesillere yaşanabilir bir dünya bırakmak için bireylerin sürdürülebilir ve sağlıklı beslenme davranışlarının arttırılması gerekmektedir. Bu çalışma, yetişkin bireylerin sürdürülebilir ve sağlıklı beslenme davranışları ile e-sağlıklı beslenme okuryazarlığı ve beslenme bilgi düzeyleri arasındaki ilişkinin değerlendirilmesi amacıyla yürütülmüştür. Gereç ve Yöntemler: Araştırmanın örneklemini, yaşları 18-65 yıl arasında değişen 110 erkek ve 102 kadın olmak üzere toplam 222 birey oluşturmaktadır. Çalışma verileri anket aracılığıyla toplanmıştır. Bireylerin sürdürülebilir ve sağlıklı beslenme davranışlarını belirlemek amacıyla “Sürdürülebilir ve Sağlıklı Beslenme Davranışları Ölçeği”, elektronik sağlıklı beslenme okuryazarlık düzeyini değerlendirmek amacıyla “e-Sağlıklı Beslenme Okuryazarlık Ölçeği (e-SBO)” ve beslenme bilgi düzeyini belirlemek amacıyla “Yetişkinler için Beslenme Bilgi Düzeyi Ölçeği (YETBİD)” kullanılmıştır. Bulgular: Kadınlarda sürdürülebilir ve sağlıklı beslenme davranışları ölçeği toplam puanı 4,0±1,05 ve erkeklerde 3,9±0,87’dir (p>0,05). Kadınların e-SBO düzeyleri (41,4±7,26) erkeklerden (38,6±7,20) daha yüksektir (p