Type 3 diabetes (T3D) is characterized by chronic insulin resistance and insulin deficiency in the brain, leading to neuronal death, inflammation, oxidative stress, apoptosis, and synaptic dysfunction. These pathological processes contribute to cognitive decline and neurodegenerative disorders such as Alzheimer’s disease. However, despite increasing evidence that links insulin resistance to cognitive impairment, the precise mechanisms that underly T3D remain largely unknown. This highlights a critical gap in research and potential therapeutic strategies. Given the significant impact of diet on metabolic health, investigating the correlation between the gut–brain axis may offer novel insights into the prevention and management of T3D. This review aims to elucidate the potential connections between insulin resistance and cognitive decline while also proposing interventions to slow aging and reduce the risk of early cognitive decline. At the same time, we acknowledge that the classification of type 3 diabetes is debatable and there is uncertainty as to whether insulin resistance is a primary driver or secondary manifestation of neurodegeneration.

One in 36 children were identified with autism in 2020, a 22% increase from 2018 and a 98% increase from 2010. Simultaneously, attention-deficit/hyperactivity disorder (ADHD) diagnoses increased 36% from 2003 to 2016–2019. Despite this surge, their etiologies remain largely unknown. However, numerous studies document higher incidences of mitochondrial abnormalities in affected individuals. Additionally, acetaminophen has been implicated in these disorders in longitudinal studies and murine models. This paper is a compilation of literature aiming to explore a theoretical framework for acetaminophen-induced mitochondrial damage in utero. It focuses on a toxic metabolite of acetaminophen, N-acetyl-p-benzoquinone imine (NAPQ1), and its role in neuroinflammation. Based on our findings, we recommend further research studying fetal mitochondria after maternal acetaminophen usage.

Maternal nutrition is a key determinant of fetal development, particularly in the context of neural regulation and maturation. Omega-3 polyunsaturated fatty acids, especially docosahexaenoic acid (DHA), play an essential role in neural differentiation, synaptogenesis, myelination, and neuroprotection. While the neurodevelopmental benefits of DHA are well-documented, the effects of excessive maternal DHA intake and the potential long-term consequences on offspring neurophysiology remain poorly understood. The purpose of this review is to synthesize current findings on the role of DHA in fetal neural development, emphasizing biochemical mechanisms and developmental outcomes. It further explores emerging concerns associated with excessive intake, the varied responses to intake, the varied sources of supplements, and the influence of maternal metabolic conditions, such as diabetes, on DHA bioavailability and fetal brain development. Finally, the review highlights the need for individualized supplementation strategies in maternal nutrition and considers the potential epigenetic implications of prenatal DHA exposure, to ultimately inform future research and therapeutic strategies in maternal–fetal health and neurodevelopmental biology.