An increasing number of studies highlight the critical role of both maternal and paternal nutrition and body weight before conception in shaping offspring health. Traditionally, research has focused on maternal factors, particularly in utero exposures, as key determinants of chronic disease development. However, emerging evidence underscores the significant influence of paternal preconception health on offspring metabolic outcomes. While maternal health remains vital, with preconception nutrition playing a pivotal role in fetal development, paternal obesity and poor nutrition are linked to increased risks of metabolic disorders, including type 2 diabetes and cardiovascular disease in children. This narrative review aims to synthesize recent findings on the effects of both maternal and paternal preconception health, emphasizing the need for integrated early interventions. The literature search utilized PubMed, UNF One Search, and Google Scholar, focusing on RCTs; cohort, retrospective, and animal studies; and systematic reviews, excluding non-English and non-peer-reviewed articles. The findings of this review indicate that paternal effects are mediated by epigenetic changes in sperm, such as DNA methylation and non-coding RNA, which influence gene expression in offspring. Nutrient imbalances during preconception in both parents can lead to low birth weight and increased metabolic disease risk, while deficiencies in folic acid, iron, iodine, and vitamin D are linked to developmental disorders. Additionally, maternal obesity elevates the risk of chronic diseases in children. Future research should prioritize human studies to explore the influence of parental nutrition, body weight, and lifestyle on offspring health, ensuring findings are applicable across diverse populations. By addressing both maternal and paternal factors, healthcare providers can better reduce the prevalence of metabolic syndrome and its associated risks in future generations.

Depression is a major global health concern expected to worsen by 2030. In 2019, 28 million individuals were affected by depressive disorders. Dietary and supplemental vitamins show overall favorable preventative and therapeutic effects on depression. B vitamins are crucial for neurological function and mood regulation. Deficiencies in these vitamins are linked to depression. Studies on individual B vitamins show promise in improving depressive symptoms, particularly thiamin, riboflavin, niacin, and folate. Vitamin C deficiency may heighten depressive symptoms, but its exact role is not fully understood. Seasonal Affective Disorder (SAD) is associated with insufficient sunlight exposure and vitamin D deficiency. Vitamin D supplementation for SAD shows inconsistent results due to methodological variations. Further investigation is needed to understand the mechanisms of vitamins in depression treatment. Moreover, more research on SAD and light therapy’s efficacy and underlying mechanisms involving photoreceptors, enzymes, and immune markers is needed. Although dietary and supplemental vitamins show overall favorable preventative and therapeutic effects on depression, dietitians treating psychiatric disorders face challenges due to diverse study designs, making direct comparisons difficult. Therefore, this article reviews the current literature to assess the role of dietary and supplemental vitamins in the prevention and treatment of depression. This review found that, although evidence supports the role of B vitamins and vitamins C and D in preventing and treating depression, further research is needed to clarify their mechanisms of action and determine the most effective intervention strategies.

Gestational obesity, defined as obesity during pregnancy or a pre-pregnancy BMI ≥30, is a growing global health challenge with profound implications for both maternal and offspring health. This narrative review synthesizes current evidence on the mechanistic pathways by which maternal obesity affects pregnancy outcomes and intergenerational health trajectories. For mothers, gestational obesity increases the risk of gestational diabetes, hypertensive disorders, cesarean delivery, and postpartum weight retention. Offspring exposed to maternal obesity face higher risks of obesity, metabolic syndrome, cardiovascular disease, and neurodevelopmental disorders, many of which persist across the lifespan. The underlying mechanisms include metabolic dysregulation, insulin resistance, chronic inflammation, oxidative stress, and alterations in placental function. Epigenetic modifications, such as DNA methylation, histone changes, and non-coding RNA expression, play central roles in fetal programming, while maternal gut dysbiosis and alterations in breast milk microbiota further shape infant health outcomes. Importantly, maternal obesity not only influences pregnancy and early life but also perpetuates an intergenerational cycle of obesity and related comorbidities. Preventive strategies targeting preconception and prenatal health, combined with interventions to optimize lactation and maternal diet, may mitigate long-term risks. Future research should prioritize longitudinal and mechanistic studies to refine interventions aimed at disrupting the transmission of obesity-related disease across generations.