Beneficial Outcomes of Omega-6 and Omega-3 Polyunsaturated Fatty Acids on Human Health: An Update for 2021

Abstract

Oxidative stress and inflammation have been recognized as important contributors to the risk of chronic non-communicable diseases. Polyunsaturated fatty acids (PUFAs) may regulate the antioxidant signaling pathway and modulate inflammatory processes. They also influence hepatic lipid metabolism and physiological responses of other organs, including the heart. Longitudinal prospective cohort studies demonstrate that there is an association between moderate intake of the omega-6 PUFA linoleic acid and lower risk of cardiovascular diseases (CVDs), most likely as a result of lower blood cholesterol concentration. Current evidence suggests that increasing intake of arachidonic acid (up to 1500 mg/day) has no adverse effect on platelet aggregation and blood clotting, immune function and markers of inflammation, but may benefit muscle and cognitive performance. Many studies show that higher intakes of omega-3 PUFAs, especially eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are associated with a lower incidence of chronic diseases characterized by elevated inflammation, including CVDs. This is because of the multiple molecular and cellular actions of EPA and DHA. Intervention trials using EPA + DHA indicate benefit on CVD mortality and a significant inverse linear dose-response relationship has been found between EPA + DHA intake and CVD outcomes. In addition to their antioxidant and anti-inflammatory roles, omega-3 fatty acids are considered to regulate platelet homeostasis and lower risk of thrombosis, which together indicate their potential use in COVID-19 therapy.

Keywords: COVID-19; inflammation; omega-3 fatty acids; omega-6 fatty acids; oxidative stress.

Figure 1

The bidirectional links between inflammation and oxidative stress. Reactive oxygen species (ROS) can act as inflammatory trigger initiating inflammation. On the other hand, inflammation induces oxidative stress. Abbreviations used: IkB, inhibitory subunit of NFkB; MAPK, mitogen-activated protein kinase; NFkB, nuclear factor kappa-light-chain-enhancer of activated B cells; P, phosphate; ROS, reactive oxygen species. Reproduced from [7].

Figure 2

Schematic overview of how polyunsaturated fatty acids (PUFAs) affect cell responses.

Figure 3

Pathway of conversion of essential fatty acids to their more unsaturated and longer chain derivatives.

Figure 4

Overview of the cyclooxygenase, lipoxygenase and cytochrome P450 pathways of conversion of arachidonic acid to bioactive mediators. DHET, dihydroxyeicosatrienoic acid; EET, epoxyeicosatrienoc acid; HETE, hydroxyeicosatetraenoic acid; HpETE, hydroperoxyeicosatetraenoic acid; LX, lipoxin; LT, leukotriene; PG, prostaglandin; TX, thromboxane.

Figure 5

Overview of the conversion of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) to lipid mediators, including specialized pro-resolving mediators (resolvins, protectins, maresins). COX, cyclooxygenase; LOX, lipoxygenase.