Fish Oil for Heart Health
Two prominent human studies have shown tremendous benefit of fish oil supplementation for cardiovascular health. The largest study supplemented 18645 people with either 1800mg of EPA or placebo for a period of 5 years. The next largest study supplemented 11323 people with either 850mg per day of combined EPA and DHA or placebo for a period of 2 years. Both studies showed tremendously positive benefit from supplementation with fish oil.
The American Heart Association actively promotes intake of EPA and DHA. They state that through diet or through supplementation, intake of EPA and DHA are beneficial for cardiovascular health. Since this time a number of very important studies have been conducted.
Can cytokines also impact heart health?
The Response-to-Injury Hypothesis of Atherosclerosis is used by scientists to describe how hardening and thickening of the arteries occurs. What was first observed in animals and then shown in humans was a process in which the human body attempts to repair injury to the inner lining of arteries. The result includes inflammation and LDL-cholesterol deposited within the injured area of the artery. One mechanism by which fish oil is believed to benefit cardiovascular health is by preventing the inflammation which occurs at the site of arterial injury.
The immune cell known as a monocyte is the first cell to arrive at a site of arterial injury. The monocyte attaches to the damaged arterial cells and proceeds to migrate into the lining of the artery. Once within the artery the cell matures into a “macrophage” where it begins to perform two key functions; accumulates oxidized LDL-cholesterol, and releases cytokines which attract more monocytes to the site of injury.
One way in which EPA and DHA benefit cardiovascular health is through inhibition of inflammation. By replacing arachidonic acid within cell membranes, EPA and DHA reduce the amount of inflammatory cytokines produced by macrophages. The result appears to be fewer monocytes attracted to the site of injury and thus the process of atherosclerosis progresses at a slower rate.
As the macrophage accumulates LDL-cholesterol the area is now referred to as a “fatty streak”. The fatty streak continues to grow. The outer layer of the artery (the smooth muscle layer) begins to thicken. The combination of a fatty streak with a thickened smooth muscle layer is referred to as an “atherosclerotic plaque”.
EPA and DHA further impact the process of atherosclerosis by impacting the thickening of the smooth muscle layer. Inflammatory cytokines produced by the macrophages not only attract additional monocytes to the site of injury but they also stimulate the thickening of the smooth muscle layer. By altering cytokine metabolism EPA and DHA appear able to slow the rate at which the smooth muscle layer thickens.
