PROTECTIVE ROLE OF VITAMIN D/OMEGA-3 IN MATERNAL HYPOTHYROIDISM-INDUCED NEUROBEHAVIORAL CHANGES

Abstract

Maternal hypothyroidism, a prevalent endocrine disorder during pregnancy, negatively affects fetal neurodevelopment and has ensuing neurobehavioral effects. Neuronal migration, proliferation, synaptogenesis, myelination, and neurotransmitter modulation all depend on thyroid hormones (THs) (triiodothyronine and thyroxine), especially from the start stages of pregnancy when the fetal thyroid axis is still developing. By interfering with neurotrophic signaling, oxidative stress, neuroinflammation, and epigenetic changes, maternal TH insufficiency has been connected to cognitive impairment, motor impairments, and behavioral abnormalities in offspring. Potential neuroprotective dietary therapies include omega-3 fatty acids (n-3) polyunsaturated fatty acids (PUFAs) and Vitamin D (Vit-D). Through Vit-D receptor-mediated pathways, Vit-D modifies neurogenesis, lowers inflammation, and strengthens antioxidant defenses. Brain-derived neurotrophic factor/tropomyosin receptor kinase B signaling, synaptic plasticity, and the integrity of neuronal membranes are all supported by n-3 PUFAs, especially docosahexaenoic acid. Pre-clinical research shows that these nutrients lessen oxidative stress, neuroinflammation, and defective neurotrophic signaling, which in turn reduces thyroid deficiency-induced neurodevelopmental harm. However, because of variations in dosage, timing, baseline nutritional status, and evaluation techniques, clinical evidence is still inconclusive. The neuroprotective functions of Vit-D and omega-3 in maternal hypothyroidism-induced neurobehavioral changes are integrated in this review, which also identifies potential avenues for further research