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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
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
Depression & anxiety
Dry eye syndrome
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.
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
|Type 2 diabetic patient who lacks Mitochondria.
||Lean healthy individual with adequate mitochondria.
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
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
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
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.
2. Civitarese AE, Smith SR, Ravussin E. Diet, energy metabolism and
mitochondrial biogenesis. Curr Opin Clin Nutr Metab Care. 2007;
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.
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.
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.
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
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
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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