Omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have been investigated for their potential to support or treat fibrosis, which refers to the excessive formation of connective tissue in organs such as the liver, lungs, heart, and kidneys. The scientific rationale centers on the anti-inflammatory and anti-fibrotic properties of omega-3s. Studies have shown that omega-3 fatty acids can modulate immune responses, decrease the production of pro-inflammatory cytokines, and inhibit the activation of stellate cells (key drivers of fibrosis in the liver), as well as reduce collagen deposition, which is central to the fibrotic process.

Animal studies in models of liver, lung, and cardiac fibrosis have demonstrated that omega-3 supplementation can attenuate fibrosis progression. Human data are more limited but suggest potential benefits. For example, small clinical trials in patients with non-alcoholic fatty liver disease (NAFLD), which can progress to liver fibrosis, have reported improvements in liver enzymes and imaging markers of fibrosis with omega-3 supplementation. However, large-scale, definitive clinical trials specifically targeting established fibrosis are lacking.

Overall, while there is a plausible mechanistic basis and promising preclinical data, the evidence in humans is moderate and not yet conclusive. Omega-3 fatty acids are not a primary therapy for fibrosis but may be considered as adjunctive support, especially in metabolic or inflammatory contexts. Further research is needed to establish efficacy and optimal dosing in fibrotic diseases.