3 papers indexed here
We haven’t gathered this author’s papers yet. Follow them and we’ll fetch their work.
Not the right person? Other researchers publish under this name.
Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by persistent deficits in social communication and restricted, repetitive patterns of behavior. Recent claims linking prenatal exposure to paracetamol (acetaminophen), the most commonly analgesic during pregnancy, to increased risk of ASD. This review aims to critically evaluate the validity of these associations, clarify potential biological mechanisms, and provide a balanced, evidence-based perspective to inform clinical practice. Although several observational cohort studies report statistical associations between in utero paracetamol exposure and ASD, these findings are often limited by confounding. Maternal conditions necessitating pain treatment, such as infection or fever, are themselves established risk factors for adverse neurodevelopmental outcomes. Greater emphasis here is therefore placed on robust study designs, particularly sibling-comparison analyses, which account for shared genetic and environmental influences. These epidemiological studies control for unmeasured confounders and consistently demonstrate attenuation or absence of previously reported associations, suggesting that paracetamol exposure is unlikely to be causative. This review also examines proposed mechanistic pathways, including mitochondrial dysfunction and inhibition of ribonucleotide reductase, but finds insufficient evidence to support a clinically meaningful effect in humans. Given the known risks of alternative therapies, particularly non-steroidal anti-inflammatory drugs during pregnancy, paracetamol remains the recommended first-line treatment for pain and fever. Overall, current evidence does not support a significant increase in ASD risk, and clinical guidelines should remain unchanged.
INTRODUCTION Parasitic infections remain a major global health challenge involving complex interactions between pathogens and host immunity. Emerging evidence indicates that epigenetic mechanisms, including DNA methylation, histone modifications, chromatin remodeling, and non-coding RNAs, critically regulate immune responses and influence host susceptibility, resistance, and disease progression. METHODS This review synthesizes current evidence on epigenetic regulation of host immunity during parasitic infections, focusing on mechanisms underlying immune activation, immune evasion, host susceptibility, and parasite persistence. Emerging epigenetic biomarkers and therapeutic strategies targeting epigenetic pathways are also considered. RESULTS Parasites can manipulate host epigenetic machinery to evade immune surveillance, suppress protective responses, and establish persistent infections. Conversely, epigenetic regulation in immune cells modulates cytokine production, macrophage polarization, T-cell differentiation, and immune memory, thereby influencing infection outcomes. Parasite-derived epigenetic factors and non-coding RNAs may additionally contribute to immune modulation and immunopathology. Epigenetic signatures associated with disease severity and treatment response show potential as biomarkers, while targeting epigenetic pathways may enhance antiparasitic immunity. DISCUSSION Epigenetic regulation represents a central mechanism governing host-parasite interactions. Integrating advanced approaches, including single-cell epigenomics and spatial transcriptomics, may clarify cell-specific mechanisms and identify novel biomarkers and therapeutic targets. These advances could support personalized strategies to improve antiparasitic treatment and disease outcomes.
We use cookies to run the site and, with your consent, for analytics and to show ads. See our Cookie Policy.
