DPA Reduces Vascular and Systemic Inflammation
There are several possible explanations as to why DPA is able to reduce vascular inflammation and prevent atherosclerosis. Consider the following:
• DPA leads to the production of its own anti-inflammatory molecules known as “resolvins” and “protectins.”
• DPA may be more effective than either EPA or DHA in reducing C-reactive protein and other markers of inflammation.
• DPA is more effective than EPA or DHA in inhibiting platelet aggregation, a key factor in the development of atherosclerosis.
• DPA enhances EPA’s ability to repair damaged blood vessels.
Let’s take a more in depth look at each of these mechanisms. First, one of the interesting downstream metabolites of omega-3 fatty acids are compounds known as resolvins and protectins. Resolvins are given that name because of their ability to resolve inflammation while protectins protect against inflammation from ever starting. Resolvins (Rv), protectins (PD) and another class of compounds, maresins (MaR), are now termed specialized pro-resolving mediators (SPMs).
The discovery of SPMs has helped understand why fish oil supplementation reduces inflammatory conditions and promote true healing. The different omega-3s give rise to different series of resolvins. EPA gives rise to the E series: DPA and DHA the D series. There is emerging data that the DPA-derived resolvins and protectins exert more significant effects. This has been demonstrated on the vascular endothelium, lining of the intestines, and systemically. DPA may hold the key to preventing and resolving inflammation.9
C-reactive protein is a well-known biological marker of inflammation. In the classic response to injury or infection, the injured area becomes red, swollen, hot and painful. But, there is another type of inflammation that is not so obvious. This silent inflammation reflects an underlying low-grade stimulation of the inflammatory process with no outwards signs of inflammation. Silent inflammation is a major factor in the development of virtually every major chronic degenerative disease including cardiovascular disease (CVD), type 2 diabetes, cancer, and Alzheimer’s disease. High sensitivity C-reactive protein (hsCRP), a blood marker that reflects different degrees of inflammation, has been identified as an independent risk factor for CVD. In fact, it is about 4 times more significant that measuring LDL-cholesterol.
DPA appears to exert significant effects in reducing both CRP and blood triglyceride levels. One group of researchers evaluated whether n-3 DPA content of red blood cells (RBC) influenced CRP and triglyceride levels if subject took an omega-3 supplement. The study was divided into two separate studies. Study 1enrolled 115 subjects, aged 20-44 years, body mass index (BMI) 20-30 kg/m2, TG = 34-176 mg/dL; Study 2 enrolled 28 subjects, aged to two 22-65 years, BMI 24-37 kg/m2, TG = 141-339 mg/dL). The dose-response effects of n-3 fatty acid supplementation on RBC n-3 DPA after five months of supplementation with over-the-counter omega-3 triglycerides (Study 1: 0, 300, 600, 900, and 1800 mg/day EPA + DHA) and eight weeks of prescription omega-3 ethyl esters (Study 2: 0, 850, and 3400 mg/day EPA + DHA). In both studies, RBC levels of DPA were inversely correlated with CRP and with fasting triglycerides. In other words, the higher the DPA content in RBCs, the lower the CRP and triglycerides. The only shortcoming of the study was using fish oils with low levels of DPA. Even so, both groups saw DPA levels rise.
DPA Prevents Platelets from Becoming “Stick”
DPA also exerts more favorable effects on platelets compared to EPA and DHA. Platelets are tiny blood cells that help your body form clots to stop bleeding. If one of your blood vessels gets damaged, it sends out signals that are picked up by platelets. The platelets then rush to the site of damage and form clot to help repair the damage. However, if the platelets are too “sticky” and easy to aggregate it is a problem. Excessive platelet aggregation, like CRP, is another independent risk factor for heart disease and stroke. Once platelets aggregate, they release potent compounds that dramatically promote the formation of the atherosclerotic plaque, or they can form a clot that can lodge in small arteries and produce a heart attack or stroke. The adhesiveness of platelets is determined largely by the type of fats in the diet and the level of antioxidants. While saturated fats and cholesterol increase platelet aggregation, omega-3 fatty acies (both short-chain and long-chain) and monounsaturated fats have the opposite effect. Among the long-chain omega-3 fatty acids it appears DPA exerts the most favorable effects in inhibiting excessive platelet aggregation.11
