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P r o v i d i n g C l i n i c a l N u t r i t i o n , P r o g r ams a n d S e r v i c e s S i n c e 1 9 2 4

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Combating Lifelong Chronic Inflammation

Chronic inflammation is a biochemical "state" that develops within the body due to poor lifestyle choices. A lack of exercise, a lack of sleep, and poor dietary choices are important modifiable causes of the chronic pro-inflammatory state.

The chronic pro-inflammatory state consists of 3 interrelated components (10):

1. Reduced energy production due to impaired mitochondrial function.
2. Oxidative stress. This term refers to an increased production of cell damaging free radicals.
3. Increased production of inflammatory chemicals.

The expression of multiple conditions, such as those listed in Table 1, has been linked to the pro-inflammatory state (1,4-12,14-17).

Table 1 - Examples of diseases promoted by a chronic pro-inflammatory state

Alzheimer's disease

Cardiovascular disease



Unhealthy aging

Cognitive decline

Kidney stones

Parkinson's disease


Crohn's disease

Macular degeneration



Depression & anxiety


Renal insufficiency


Dry eye syndrome

Migraine headaches

Skin cancer



Multiple sclerosis





Ulcerative colitis

Research has demonstrated that an unhealthy, pro-inflammatory diet can lead to the generation and perpetuation of the chronic pro-inflammatory state. Each of the 3 components will be discussed in more detail below. A more thorough discussion is also provided in the Clinician section of our website.

1. Reduced cellular energy production

Inside each cell are structures called mitochondria that function to produce energy for all metabolic processes. The produced energy is a chemical called adenosine triphosphate (ATP), which is needed for every activity we perform.

In the image below, we see an electron microscope image of skeletal muscle from a type 2 diabetic patient on the left and a healthy lean individual on the right. Notice the substantial lack of mitochondria in the type 2 diabetic patient compared to the lean individual (Ritov). A similar loss of mitochondria was found in obese subjects.

Type 2 diabetic patient who lacks Mitochondria. Lean healthy individual with adequate mitochondria.

Diabetic and obese patients common complain of fatigue. Based on this image that demonstrates a lack of mitochondria in these individuals, it should not be a surprise that fatigue is complaint.

The loss of mitchondria is a gradual process. If you eat too much sugar, flour, and refined oils and do not exercise adequately, then you are moving toward a biochemical state in which you will have less mitochondria and less ATP (energy) production. You will feel less vital compared to when you were younger. As you eat anti-inflammatory foods and less calories, and exercise more, you will be able to regenerate your mitochondria (2,3).

2. Oxidative stress - excess free radicals

Free radicals are substances that damage cells. We most commonly think about free radicals in the context of taking supplemental antioxidants, such as vitamin C and E, to protect against free radicals.

In fact, the greatest source of free radicals is overeating. When we pig out on sugar, flour, and fatty food, we get an immediate elevation of blood sugar and fats. The greater the rise in blood sugar and fat, there is an associated greater production of free radicals (12). Most chronic diseases are associated with an excessive production of free radicals, so it is very important to keep their production within the normal range. When we eat vegetables, fruit, fish and lean meats, we do not produce an excess of free radicals (12).

This means that the best antioxidant is a healthy, anti-inflammatory diet. We can support a healthy diet by taking unique antioxidants, such as lipoic acid and coenzyme Q10, which will be discussed in the supplement section of our website.

3. Increased production of inflammatory chemicals

A loss of mitochondria and overeating increases free radical production, which excites cells to produce inflammatory chemicals called eicosanoids, cytokines, adhesion molecules, and growth factors. Do not worry about the details of these chemicals. The important, real-life concern that we must embrace is that, overtime, our bodies become inflammation producing machines, especially as our bodyweight increases, blood pressure rises, and as we move closer to pre-diabetes and diabetes.

We also directly increase the production of inflammatory chemicals by eating the wrong types of fats. Approximately 18% of the calories consumed by Americans come from seed/legume oils that are rich in omega-6 fatty acids. Examples of such oils include corn, safflower, sunflower, cottonseed, peanut and soybean oil.

It takes between 10-15 ears of corn to get 1 tablespoon of corn oil. No one eats this much corn, so there is no concern for eating corn on the cob. However, in just one serving of potato chips or corn chips, we get almost a tablespoon of oil.

Most people are aware that omega-3 fatty acids are anti-inflammatory, which is why omega-3 fish oil has become so popular in recent years. However, what many people are unaware of is that anyone who is not watching what they eat, is likely to consume excessive amounts of omega-6 fatty acids from foods that contain too much of the omega-6 seed/legume oils.

The seed/legume oils contain an omega-6 fatty acid called linoleic acid. When we eat linoleic acid, our bodies convert it into arachidonic acid. We also get excessive amounts of arachidonic acid from fatty meats and certain fish, such as farm-raised tilapia and catfish (4,18). The problem is that our bodies convert arachidonic acid into multiple inflammatory chemicals. One example is prostaglandin E2 (PGE2), which causes pain and inflammation.

Interestingly, the conversion of diet-derived arachidonic acid into pro-inflammatory PGE2 is inhibited by aspirin, Tylenol, Celebrex, ibuprofen, Advil, Alleve, and other anti-inflammatory drugs. This means that if you get relief from these medications, it is likely that you are eating an excess of inflammatory foods.

As illustrated in the image above, linoleic acid (LA) and arachidonic acid are omega-6 fatty acids. The consumption of pro-inflammatory omega-6 foods leads to an accumulation of arachidonic acid in the body, which is converted into pro-inflammatory chemicals [eicosanoids], including PGE2, TXA2, and LTB4.

The anti-inflammatory drugs listed above inhibit the conversion of dietary arachidonic acid into pain and inflammation producing PGE2. Aspirin is recommended by physicians to inhibit the conversion of diet-derived arachidonic acid into vascular constricting and platelet-clumping TXA2 (thromboxane A2). Singulair is taken by asthma and allergy patients to inhibit the activity of LTB4 (leukotriene B4) that is produced from diet-derived arachidonic acid.

If we minimize the consumption of the illustrated pro-inflammatory foods, this will lead to a reduced production of the pro-inflammatory eicosanoids. We also need to eat more green vegetables that contain anti-inflammatory omega-3 (n-3) alpha-linolenic acid (ALA) and animal proteins that contain omega-3 eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).

When we eat adequate omega-3 foods, we will produce anti-inflammatory chemicals [eicosanoids] from the omega-3 fatty acids EPA/DHA, which resolve inflammation (resolvins) and protect the nervous system (neuroprotectins). The PGE3, TXA3, and LTB5 eicosanoids from EPA are not inflammatory and antagonize the activity of the pro-inflammatory eicosanoids PGE2, TXA2, and LTB4 from arachidonic acid.


To combat the chronic pro-inflammatory state, we need to adopt a healthy lifestyle, part of which involves healthy eating and nutritional supplementation. Appropriate Diet and Supplementation are discussed in separate sections of our website.


1. Aggarwal BB, Shishodia S. Suppression of the nuclear factor-kB activation pathway by spice-derived phytochemicals. Reasoning for the seasoning. Ann NY Acad Sci. 2004;1030:434-41.
2. Civitarese AE, Smith SR, Ravussin E. Diet, energy metabolism and mitochondrial biogenesis. Curr Opin Clin Nutr Metab Care. 2007; 10(6):679-87.
3. Conley KE, Marcinek DJ, Villarin J. Mitochondrial dysfunction and age. Curr Opin Clin Nutr Metab Care. 2007; 10(6):688-92.
4. Cordain L, Eaton SB, Sebastian A et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005;81:341-54.
5. Franco OH, Bonneux L, de Laet C, Peeters A, Steyerberg EW, Mackenbach JP. The Polymeal: a more natural, safer, and probably tastier (than the Polypill) strategy to reduce cardiovascular disease by more than 75%. Brit Med J. 2004; 329:1447-50.
6. Giugliano D, Ceriello A, Esposito K. The effects of diet on inflammation: emphasis on the metabolic syndrome. J Am Coll Cardiol. 2006;48(4):677-85.
7. Joseph J, Cole G, Head E, Ingram D. Nutrition, brain aging, and neurodegeneration. J Neurosci. 2009;29(41):12795-12801.
8. Lekander M, Elofsson S, Neve IM, Hansson LO, Unden AL. Self-rated health is related to levels of circulating cytokines. Psychosom Med. 2004;66(4):559-63.
9. Lopez-Garcia E, Schulze MB, Fung TT et al. Major dietary patterns are related to plasma concentrations of markers of inflammation and endothelial dysfunction. Am J Clin Nutr. 2004;80:1029-35.
10. Kumar V, Abbas AK, Fausto N. Robbins and Cotran: pathologic basis of disease. 7th ed. Philadephia: Elsevier Saunders; 2005: p.4-118.
11. Nicklas BJ, You T, Pahor M. Behavioural treatments for chronic system inflammation: effects of dietary weight loss and exercise training. Can Med Assoc J. 2005;172(9):1199-209.
12. O'Keefe JH, Gheewala NM, O'Keefe JO. Dietary strategies for improving post-prandial glucose, lipids, inflammation, and cardiovascular health. J Am Coll Cardiol. 2008;51:249-55.
13. Ritov VB et al. Deficiency of subsarcolemmal mitochondria in obesity and type 2 diabetes. Diabetes 2005; 54(1):8-14.
14. Seaman DR. The diet-induced pro-inflammatory state: a cause of chronic pain and other degenerative diseases? J Manipulative Physiol Ther. 2002;25:168-79.
15. Shapira N. Nutritional approach to sun protection: a suggested complement to external strategies. Nutr Rev. 2009;68(2):75-86.
16. Simopoulos AP. The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases. Exp Biol Med. 2008;233:674-88.
17. Warnberg J, Gomez-Martinez S, Romeo J, Diaz LE, Marcos A. Nutrition, inflammation, and cognitive decline. Ann NY Acad Sci. 2009;1153:164-75.
18. Weaver KL, Ivester P, Chilton JA, Wilson MD, Pandey P, Chilton FH. The content of favorable and unfavorable polyunsaturated fatty acids found in commonly eaten fish. J Am Diet Assoc. 2008;108:1178-85.


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