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Omega-3 Fatty Acids Lower Inflammation
Controlling Inflammation with Fats
Our discussion of anti-inflammatory foods must begin with fats. This is because fatty acids are the building blocks of almost all our cells and these same fatty acids are the source of our inflammatory process.
[INSERT FIGURE OF PROGRESSION OF CELL MEMBRANE TO INDIVIDUAL FATTY ACID TO A FOOD LIKE FISH] [this one is a placeholder]
Fatty acids form the backbone of our inflammatory cascade. To understand why this is the case, we have to first look at our basic cellular make-up. Each cell is comprised of a two-layered membrane that is made from fatty acids. When our cells get bumped, poked, torn, or traumatized in some way, the fatty acids break loose and are acted upon by enzymes of the inflammatory cascade. In short, fatty acids from our cell membranes are like unlit matches that, when struck, light up the inflammatory cascade. To further understand why this is so important, we have to understand how extensively the fatty acids permeate all our cells. Consider the total surface area of some of the body structures noted below:
There no longer any question about whether fatty acids help control your inflammatory system. This is now basic biochemistry. Among the fats, omega-3 fatty acids have received a great deal of attention for their potential role in helping people with arthritis.
A recent study published in the journal Pain looked at 17 clinical research trials of omega-3 fatty acids used to manage symptoms in people with joint pain. They showed that supplementation with these fatty acids for 3 to 4 months reduced patient reported joint pain intensity, minutes of morning stiffness, number of painful and/or tender joints, and the use of anti-inflammatory drugs.
[Goldberg, RJ, Katz, J. A meta-analysis of the analgesic effects of omega-3 polyunsaturated fatty acid supplementation for inflammatory joint pain. Pain. 2007;129(1-2):210-23.]
Fatty Acids Control Our Fat-Burner Genes
Since belly fat and excess weight are linked to joint pain and inflammation, it is important to understand that fatty acids have immense control over our fat-burning genes. Put another way, whenever we make a choice about the fat we consume (and actually consume that fat) we are driving the expression of genes with a widespread impact on metabolism. It is safe to say that if we do not gain control over the type of fat we consume, we lose control over our genes and our inflammatory system. Not only do fatty acids regulate our immune, inflammatory, and repair system, they greatly influence whether we will store fat in our bellies, or burn fat and remain lean.
For example, omega-3 fatty acids up-regulate (switch up) gene transcription for proteins involved in fatty acid oxidation (burning fat as fuel), such as carnitine palmitoyltransferase and acyl-CoA oxidase. At the same time, omega-3 fatty acids down-regulate (dial down) the transcription of genes that code for proteins involved in the manufacture of fat (such as fatty acid synthase.) In this regard, n-3 fatty acids are being referred to as “fuel partitioners,” because of the ways in which they do the following:
- Omega-3 fatty acids direct fat away from triglyceride storage
- Omega-3 fatty acids direct fat toward fat burning
- Omega-3 fatty acids enhance glucose conversion to the storage form called glycogen
- Omega-3 fatty acids control the fat-burning capacity by activating the transcription factor PPARα (peroxisome proliferator-activated receptor alpha).
Unsaturated fatty acids control an array of fat-making (lipogenic) genes. This means that the right forms of fatty acids can actually limit the amount of fat the body makes for storage.
Fat-making genes controlled by fatty acids include:
- Hepatic glucokinase
- Pyruvate kinase
- Pyruvate dehydrogenase
- Fatty acid synthase
- Adipocyte fatty acid synthase
Unsaturated fatty acids also control an array of fat-burning (lipolytic) genes. This means that the right forms of fatty acids, such as omega-3 fatty acids can actually accelerate fat burning.
Fat-burning genes controlled by fatty acids include:
- Carnitine palmitoyltransferse
- Mitochondrial HMG-CoA synthase
- Peroxisomal acyl-CoA oxidase
- Fatty acid binding proteins
- Fatty acid transporter
- UCP-3 (mitochondrial uncoupling protein-3)
Mechanisms by which fatty acids accomplish the above include (but are not limited to):
- Fatty acids improve insulin sensitivity
- Fatty acids upregulate genes that code for proteins that enhance fat burning
- Fatty acids downregulate genes that code for proteins involved in fat synthesis
Specific recommendations to improve postprandial glucose and triglycerides are as follows:
- Select high-fiber carbohydrates with low glycemic index, including vegetables, fruits, whole grains, legumes, and nuts.
- At all 3 meals, consume lean protein.
- Eat approximately 1 handful of nuts daily (using a closed fist), consumed with vegetables, grains, berries, or other fruits.
- Eat salad daily, consisting of leafy greens with dressing of vinegar and virgin olive oil.
- Avoid highly processed foods and beverages, particularly those containing sugar, high-fructose corn syrup, white flour, or trans fats.
- Limit portion sizes to modest quantities.
- Maintain normal weight and avoid overweight or obesity. Waist circumference should be less than one half of height in inches.
- Perform physical activity for at least 30 minutes or more daily, of at least moderate intensity.
- For those with no history of substance abuse, consuming 1 alcoholic beverage before or with an evening meal may be considered.
Study Highlights
- The glycemic index of a food is defined as the incremental increase in the area under the postprandial glucose curve after ingestion of 50 g of a specific amount of food vs that associated with 50 g of oral glucose. Ideal carbohydrates with a low glycemic index include green leafy vegetables such as broccoli and spinach and fruits such as grapefruits and cherries.
- Excess intake of processed carbohydrates leads to a vicious cycle of transient spikes in blood glucose levels, increased insulin production, and reactive hypoglycemia.
- Berries, dark chocolate, red wine, tea, and pomegranates reduce postprandial oxidant stress and inflammation.
- When paired with a high-glycemic-index meal, cinnamon slows gastric emptying and reduces postprandial glucose excursion.
- Nuts also slow gastric emptying and can reduce the impact of high-glycemic-index carbohydrates by as much as half. Nuts also reduce postprandial oxidative protein damage, and consumption of nuts at least 5 times weekly can reduced the risks for coronary artery disease and diabetes by 20% to 50%.
- Vinegar can reduce postprandial glycemia and promotes satiety.
- Lean protein reduces postprandial glucose excursion and improves satiety. Such protein includes egg whites, game meat, skinless poultry breast meat, and whey protein or other nonfat dairy protein.
- Drinking 0.5 to 1 alcoholic drink per day for women and 1 to 2 alcoholic drinks per day for men can reduce cardiovascular risk, and 1 to 2 drinks before a meal can reduce postprandial glucose and insulin levels. However, higher levels of drinking can impair glucose metabolism.
- Exercise acutely lowers glucose and triglyceride levels in a dose-dependent fashion.
January 22 issue of the Journal of the American College of Cardiology.




















