Biological aging, sedentariness, adiposity, and chronic illness can negatively impact the body’s natural production of PRMs. In addition, dietary intakes of omega-3 fatty acid precursors of PRMs are commonly insufficient, while consumption of proinflammatory lipids (like some saturated and omega-6 fats) tends to be quite generous in the typical diet. Inflammation can proceed unabated if the body lacks the building blocks and preconditions needed for resolving inflammatory responses.
The discovery of specialized pro-resolving mediators (called SPMs or PRMs) has changed our fundamental understanding of inflammation as well as our approaches to resolving chronic inflammation. Much as various substances termed ‘antioxidants’ can act in either pro-oxidant or anti-oxidant capacities under different circumstances, lipid mediators can encourage either the development or the resolution of an inflammatory response. All of these lipid mediators play crucial roles in the inflammatory response, yet lifestyle factors heavily influence the availability of the dietary precursors needed for forming pro-resolving species.
Lipid mediator metabolites of arachidonic acid include prostaglandins, thromboxanes, and leukotrienes. These molecules that tend to build inflammation, while lipoxins, also produced from arachidonic acid, have lower proinflammatory potential. Metabolites of eicosapentaenoic acid (EPA) include E-series resolvins possessing moderate to high pro-resolving potential in different tissue environments, while the PRM metabolites of docosahexaenoic and docosapentaenoic acids (DHA and DPA) include D-series resolvins, protectins, and maresins having higher pro-resolving potential.
The Spectrum of Pro-Resolving Mediators (PRMs)
Dietary provision of omega-3 fatty acid precursors of pro-resolving mediators can potentially heighten levels of crucial PRMs in various body compartments. It may also increase the activities of enzymes required for PRM production, and improve the status of PRM-specific receptors needed for effective immune signaling.