The normal human body can produce all of the fatty acids it needs except for omega-3 (ALA or alpha-linolenic) and omega-6 (LA or linoleic acid). Therefore, these are called essential fatty acids and must be consumed. Dietary sources of LA are sunflower oil, safflower oil, corn oil, cereals, animal fat, and wholegrain bread. Dietary sources of ALA are green leafy vegetables, flaxseed, rapeseed (or canola*), and fish.
Essential fatty acids and their derivatives serve many functions in the human body for immunity and inflammation. In general, omega-6 and its derivatives are inflammatory, and omega-3 and its derivatives, DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid), are anti-inflammatory. Both of these fatty acids produce signaling chemicals called eicosanoids**, which must balance each other for health. These signs of inflammation caused by omega-6 eicosanoids include clumping of platelets, bleeding, constriction, and dilation of blood vessels.
In recent decades, diets have changed so much in industrialized countries that we now consume an excess of omega-6 and trans fats, as well as insufficient omega-3. Ancestral diets contained 20-30% of energy needs as fatty acids. Now, Europeans consume 28-42% of their energy needs as fatty acids. This increase has been supplied mainly by an increase in omega-6 rich vegetable oils without an increase in omega-3 sources. The omega-6/omega-3 ratio should be 1-4/1. The ratio now tends to be 10-20/1.
While our diets are becoming increasingly high in omega-6, we are increasingly afflicted by inflammatory diseases, such as cardiovascular disease, obesity, inflammatory bowel disease, rheumatoid arthritis, cancer, Alzheimer’s disease, and depression. Studies confirm that a shift in the diet from omega-3 to omega-6 results in more spasms of blood vessels, blood viscosity, inflammation, and related diseases, such as metabolic syndrome. Replacing omega-3, DHA, and EPA in the diet has been shown to replace the inflammatory omega-6 in the cell membranes in a variety of cells to reduce inflammation.
Non-alcoholic fatty liver disease (NAFLD) appears to have inflammation as its basis. Nutritional factors are important in the start of NAFLD in a stage called liver steatosis. Patients with NAFLD have deficiency of liver omega-3. An oversupply of omega-6 fatty acids in the liver leads to further derangement of liver cells. Supplementation with fish oil is beneficial to patients with NAFLD.
Cardiovascular disease, atherosclerosis and coronary heart disease are associated with inflammation. When cells have an excess of omega-6, inflammation increases, and the resulting damage leads to atherosclerosis. The Japanese, who eat more fish with omega-3 in their diet than Americans, have lower risk of acute heart attacks and atherosclerosis.
Inflammatory bowel diseases (IBD), such as Crohn’s disease (CD) and ulcerative colitis (UC), are diseases in which the underlying causes are inflammation of the digestive tract. Fatty components of the diet act as triggers for IBD. Prevalence of omega-3 from fish in the diets of Greenland Eskimos results in low rates of IBD.
Rheumatoid arthritis (RA) is an inflammatory disease which can be improved by changing to a lactovegetarian diet to reduce the omega-6 intake to 90 mg/day. Supplementation with omega-3 has been shown to reduce factors associated with cartilage destruction in RA.
Alzheimer’s disease (AD) is a disease of complex origin, but diet seems to play a role. DHA has been shown to give some protection from AD in animal models of the disease. Studies suggest that a diet low in omega-6 and high in omega-3 may be preventive in the development of AD.
CONCLUSION: Changes in the Western diet with increased amounts of omega-6 and reduced amounts of omega-3 may be the cause of the current great increase of inflammatory disease. A more balanced omega-3/omega-6 ratio may be therapeutic.
NOTE: *Canola is one cultivator of rapeseed.
**Eicosanoids are chemicals derived from omega-3 and omega-6 which signal cells, such as inflammatory and immune cells, on how to react.
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