Introduction: Neural tube defects occur when the embryonic neural tube fails to close properly during early gestational development, leading to conditions like spina bifida or anencephaly. Adequate intake of folate prevents these malformations by supporting DNA synthesis and rapid cell division required for fetal CNS maturation. A. Lutein is a carotenoid with antioxidant properties primarily localized within the macula of the eye. While it plays a significant role in filtering blue light and protecting retinal photoreceptors from oxidative stress, it does not possess a recognized therapeutic role in preventing congenital structural malformations or neural tube defects in neonates. B. Vitamin D is a fat-soluble vitamin essential for intestinal calcium absorption and bone mineralization through the regulation of serum phosphorus levels. While maternal Vitamin D status is critical for fetal skeletal development and preventing neonatal rickets, it is not the primary supplement indicated for the reduction of neural tube defects. C. Folic acid, a synthetic form of Vitamin B9, is a mandatory supplement for women of childbearing age to facilitate the conversion of homocysteine to methionine. It is crucial for the closure of the neural tube within the first 28 days of gestation, significantly reducing the incidence of neonatal CNS defects. D. Omega-3 fatty acids, including docosahexahenoic acid and eicosapentaenoic acid, are long-chain polyunsaturated fats essential for fetal neurodevelopment and retinal function. Although they support cognitive outcomes and visual acuity in the infant, they do not provide the specific biosynthetic pathways required to prevent primary structural neural tube closure failures.