Flaxseed reduces the production of major systemic markers of inflammatory activity, including eicosanoids, cytokines and platelet-activating factor. Regular consumption of flaxseed may influence the progression of atherosclerosis, an inflammatory disease.

Atherosclerosis is an inflammatory disease. Its origins are in infancy and childhood when the earliest lesions, called fatty streaks, begin to develop in arteries. Fatty streaks consist only of monocyte-derived macrophages and T lymphocytes—two types of immune cells whose presence in arterial walls provides evidence that the inflammatory response contributes to atherosclerosis. Recognizing the role of inflammation in atherosclerosis suggests a new approach to cardiovascular disease prevention and treatment: Developing interventions that alleviate chronic
inflammation and may retard the progression of atherosclerosis.

Flaxseed inhibits the production of pro-inflammatory cytokines and lipid mediators derived from arachidonic acid (an omega-6 fatty acid) and thus reduces inflammatory responses. This effect is likely due to one or both of the following constituents present in flaxseed: alpha-linolenic acid (ALA), the essential omega-3 fatty, and lignans, which are phytoestrogens that exhibit antioxidant, antimitotic and antifungal activity. With its unique fatty acid profile, flaxseed is the richest source of ALA in the North American diet— ALA constitutes 57% of the total fatty acids in flaxseed. It is also the richest source of lignans, providing 75-800 times more lignans than other plant foods such as legumes, cereals, vegetables and fruits. ALA and lignans appear to influence inflammatory responses by different mechanisms.