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Congenital heart diseases (CHDs) are the most common birth defects and the leading cause of non-infectious deaths in infants, with an unknown etiology. We aimed to assess the association of genetic variations in UCP2 gene, dietary factors, and their interactions with the risk of CHDs in offspring. The hospital-based case-control study included 464 mothers of children with CHDs and 504 mothers of healthy children. The exposures of interest were maternal dietary factors in early pregnancy and UCP2 genetic variants. Logistic regression analyses were used to assess the association and interaction of UCP2 gene and dietary factors with CHDs. Our results found that the polymorphisms of UCP2 gene at rs659366 and rs660339, together with maternal dietary factors including excessive intake of pickled vegetables and smoked foods were associated with increased risks of CHDs in offspring. Regular intake of fresh meat, fish and shrimp, and milk products were associated with lower risks of CHDs in offspring. Besides, positive interaction between the dominant model of rs659366 and excessive intake of pickled vegetables was found in the additive interaction model (RERI = 1.19, P = 0.044). These findings provide the theoretical basis for gene screening and a new clue for the prevention of CHDs in offspring.
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http://dx.doi.org/10.1038/s41598-021-88057-2 | DOI Listing |
Arterioscler Thromb Vasc Biol
September 2025
Vascular Biology Program, Boston Children's Hospital and Harvard Medical School, MA (K. Cui, B.Z., B.W., S.E.-B., A.V., H.C.).
Background: Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipid-laden foam cells and plaques within the arterial wall. Dysfunctional vascular smooth muscle cells (VSMCs), fibroblasts, endothelial cells, and macrophages contribute to disease progression. Here, we report that macrophage-specific expression of epsins, highly conserved endocytic adaptor proteins involved in clathrin-mediated endocytosis, accelerates atherosclerosis in Western diet-fed mice.
View Article and Find Full Text PDFBrain Behav
September 2025
Department of Neuroscience, School of Translational Medicine, Monash University, Melbourne, Australia.
Background: Migraine pathophysiology involves a constellation of metabolic abnormalities. These interlinked contributory factors include mitochondrial dysfunction, an altered gut microbiome, neuroinflammation, oxidative stress, weight imbalance, and altered glucose metabolism. The ketogenic diet is an emerging therapy which may restore hypometabolism seen in chronic migraine.
View Article and Find Full Text PDFMol Nutr Food Res
September 2025
Institute of Nutritional Science, Justus-Liebig University Giessen, Giessen, Germany.
Hypertension represents a major risk factor for cardiovascular diseases. As a diet high in sodium chloride is associated with hypertension, so-called "blood pressure salts" are attracting increasing scientific interest. These are characterized by a partial replacement of sodium chloride by other salts, mainly potassium and magnesium compounds.
View Article and Find Full Text PDFJDR Clin Trans Res
September 2025
School of Dentistry, Faculty of Health and Behavioural Sciences, The University of Queensland, Brisbane, Queensland, Australia.
Objectives: Socioeconomic status (SES) has a significant effect on the burden of early childhood caries (ECC), yet addressing SES disparities remains challenging. This study aimed to identify and quantify the most impactful mediator linking SES effect to the occurrence of ECC using advanced causal mediation analysis, to inform targeted interventions that reduce SES-related disparities in ECC.
Methods: Data were drawn from the Study of Mothers' and Infants' Life Events, a cohort of 2,182 mother-child dyads recruited from Adelaide's 3 largest public hospitals (2013-2014).
Geroscience
September 2025
NUS Bia-Echo Asia Centre for Reproductive Longevity and Equality, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
In the past century, the human Lifespan has doubled. However, this is not equivalent to Healthspan which refers to the number of years spent healthy and free from disease. Women have an additional level of complexity on the path to optimal healthspan where health resilience dramatically decreases following menopause and this is due to their ovaries aging by midlife.
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