Synopsis

Source of validity: Scientific
Rating (out of 5): 2

Palmitoylethanolamide (PEA) is an endogenous fatty acid amide that has been studied for its anti-inflammatory and analgesic properties. In the context of fibrosis, preclinical studies (mainly in animal models and in vitro) have shown that PEA may help reduce fibrotic processes by modulating inflammation, inhibiting mast cell activation, and regulating the activity of pro-fibrotic cytokines such as TGF-β1. These actions are relevant because chronic inflammation and excessive activation of pro-fibrotic pathways are central to the development of fibrosis in organs such as the liver, lungs, and kidneys.

There are several animal studies suggesting that PEA administration can attenuate fibrosis in models of pulmonary and renal fibrosis, primarily by dampening inflammatory responses and interfering with the signaling mechanisms that mediate tissue remodeling and fibrogenesis. However, as of mid-2024, there is a lack of robust clinical trial data in humans specifically assessing PEA for the treatment of established fibrosis in any organ system. Most human data with PEA relate to pain and inflammatory conditions rather than direct anti-fibrotic effects.

Therefore, while there is scientific rationale and some experimental evidence supporting the potential role of PEA in modulating fibrosis, its clinical application for this purpose remains unproven. The current evidence base rates as low to moderate (2/5), pending further clinical trials.

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