Non-alcoholic fatty liver diseases (NALFD) and unexplained decompression sickness (DCS) in divers: is there a relationship?

Non-alcoholic fatty liver diseases (NAFLD) and unexplained decompression sickness (DCS) in divers: is there a relationship? Decompression sickness (DCS) remains one of the most intriguing and multifactorial conditions in diving medicine. Although the introduction of standardized decompression algorithms has significantly reduced its incidence, a substantial number of “undeserved” DCS cases still occur in divers who strictly adhere to safety procedures. This observation suggests the presence of individual biological factors that modulate susceptibility to bubble formation and endothelial injury. Non-alcoholic fatty liver disease (NAFLD), currently recognized as a multisystem metabolic disorder, is characterized by chronic low-grade inflammation, oxidative stress, and endothelial dysfunction — all mechanisms potentially influencing vascular gas kinetics during decompression. This doctoral research aimed to explore the possible physiological link between NAFLD and individual vulnerability to “undeserved” DCS through an integrated in vitro and in vivo approach. The in vitro phase employed HepG2 hepatocyte models exposed to a controlled mixture of palmitic and oleic acids to reproduce hepatic steatosis. Cellular and molecular analyses demonstrated increased lipid accumulation, mitochondrial injury, and upregulation of pro-inflammatory cytokines (TNF-α, IL-6, IL-8, MCP-1), along with oxidative stress markers (MDA, 4-HNE) and reduced antioxidant defenses. These findings outline a pro-inflammatory and pro-thrombotic cellular microenvironment capable of impairing endothelial homeostasis and potentially facilitating gas nucleation at the vascular interface. The in vivo study involved 30 recreational divers who underwent standardized dry hyperbaric chamber dives (30 m / 25 min at 4 ATA). All subjects received pre-dive hepatic ultrasound assessment to identify and grade NAFLD. Post-dive transthoracic echocardiography was performed to detect venous gas emboli (VGE), quantified according to the Modified Spencer Scale. Preliminary statistical evaluations have identified emerging patterns suggesting that divers with sonographic evidence of NAFLD tend to exhibit a higher post-dive VGE load compared to those without hepatic steatosis. These data indicate a potential metabolic-endothelial interaction influencing bubble dynamics and vascular response to decompression. Further analyses are underway to refine the correlation and to delineate the underlying physiological mechanisms.