Sounding the alarm: Could stadium crowd noise contribute to amyotrophic lateral sclerosis risk in soccer and football players?

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder of largely unknown etiology. Epidemiological data have consistently shown a disproportionately higher incidence of ALS among professional soccer and American football players, yet the specific environmental triggers remain unclear. While factors such as head trauma, extreme physical activity, and doping have been proposed, none of them fully explain the occupational and geographical clustering observed. Here, we propose a novel, underexplored hypothesis: repeated exposure to high-decibel stadium crowd noise may transiently disrupt the blood–brain barrier (BBB), facilitating entry of neurotoxic substances produced during extreme physical activity, such as stress–related metabolites (e.g. lactate and ammonia) and pro–inflammatory cytokines, into the central nervous system and contributing to ALS pathogenesis. Animal studies have shown that sound pressure levels of 90–100 dB can significantly increase BBB permeability. Stadium crowd noise can generate sound pressure peaks of 140 dB and professional players are chronically exposed to these acoustic conditions over many years, especially in high-attendance leagues. This hypothesis suggests a potential association of the observed ALS incidence with stadium crowd noise, as this risk appears to increase in countries and leagues with higher crowd attendance and louder stadium environments. To test this hypothesis, future studies should incorporate in vivo models exposed to crowd-like noise patterns, alongside neuroimaging to evaluate blood–brain barrier (BBB) permeability before and after acute and chronic sound exposure. Additionally, wearable decibel meters could enable real-time sound pressure level monitoring and correlation with neurovascular stress markers and potential ALS onset. Overall, this hypothesis offers a novel framework linking environmental stressors to sporadic ALS and could open new avenues for prevention and neuroprotection.