Recent research highlights that adverse parental factors can profoundly affect fetal development and long-term health through epigenetic regulation. The concept of 'Paternal Origins of Health and Disease' (POHaD) shifts the focus toward the significance of paternal health in embryonic development, pregnancy, and offspring growth. Specifically, a father's lifestyle and dietary choices before conception can alter the epigenetic marks of sperm, thereby influencing gene expression in the child. Evidence from preclinical studies, particularly in animal models, demonstrates that paternal dietary patterns such as fasting, low-protein diets, and excessive intake of fats, sugars, and oils can impact pregnancy outcomes and metabolic processes in offspring. These alterations, mediated by epigenetic mechanisms, are associated with an increased risk of chronic diseases. This article comprehensively reviews findings from both preclinical and limited clinical studies, analyzing how paternal dietary and lifestyle factors shape epigenetic regulatory mechanisms and contribute to transgenerational health impacts. These insights underscore the need to optimize fathers' diets and lifestyles and provide important scientific evidence for the prevention and treatment of diseases originating from paternal influences on fetal health.

Objectives: To investigate the association between free and total 25(OH)D levels and fetal growth during pregnancy, and to evaluate whether free 25(OH)D is a better indicator of vitamin D status compared to total 25(OH)D. Methods: A total of 160 pregnant women and their newborns were consecutively recruited from a Jiangsu hospital (March–May 2019). Maternal blood was collected before delivery, and cord blood was collected after umbilical cord disconnection. Serum free and total 25(OH)D were measured by ELISA. Clinical data, including pregnancy records, neonatal assessments, and 6-month follow-ups, were extracted from electronic medical records. Associations between vitamin D levels and developmental outcomes were analyzed using univariate correlation analysis and multivariable linear regression in SPSS 20.0 (p<0.05). Results: Maternal-umbilical free 25(OH)D correlation was stronger than total (rho=0.699 vs. 0.475; both p<0.001). Maternal free 25(OH)D showed stronger associations with early pregnancy femur length (11.37 ± 3.39 mm; β=2.053), late pregnancy biparietal diameter (82.65 ± 4.60 mm; β=−0.273), and femur length growth efficiency (0.89 ± 0.15 mm/week; β=−0.289) than total 25(OH)D (all p<0.05). Umbilical free 25(OH)D correlated with mid-pregnancy transverse cerebellar diameter (22.0[21.0–23.0] mm; β=−0.231) and femur length growth efficiency (0.92[0.78–1.05] mm/week; β=−0.224) (p<0.05 and p<0.01). Maternal free 25(OH)D negatively associated with late pregnancy head circumference (330.11 ± 7.89 mm; β=−9.050, p<0.01). Conclusions: Compared to total 25(OH)D, free 25(OH)D in maternal and umbilical blood may be more strongly associated with early-life physical growth parameters.