Low-Grade Systemic Inflammation: The Perpetual Heat

We get two main types of inflammation: it will be either (1) acute, or (2) chronic. Put simply, acute = good, chronic = bad!

Inflammation is essentially a protective and healing process that the body undergoes when it encounters anything from a paper cut to a broken bone. Acute inflammation (immediately after the injury) triggers a biochemical cascade in order to increase blood flow to the area. All your nerve endings and cells at the sit of the injury then send messages to recruit your body’s defense mechanisms – your white blood cells! These little superheroes then come to fight off any foreign bacteria. When you have a red, swollen patch that is a little tender around your paper cut – this is inflammation. It is necessary and very normal in a healthy individual.

Low-grade systemic inflammation however, is very different. This type of inflammation is chronic and plays a very different role in the body. Consider the many different autoimmune disease (such as SLE or Rheumatoid Arthritis) where your immune system is unable to “turn off” the little superheroes even when there is nothing to fight off! Low-grade systemic inflammation also plays an obvious role in conditions such as asthma, and the inflammatory bowel diseases (IBD) Crohn’s disease and ulcerative colitis.

Other conditions where low-grade systemic inflammation is implicated may be less obvious. It is considered a causal factor in the development and progression of:
– atherosclerosis
– metabolic syndrome (or syndrome X)
– cardiovascular diseases [1, 2, 3, 4, 5, 6, 7]
In type 2 diabetes and obesity, low-grade systemic inflammation is a key role-player in the development of peripheral insulin resistance, which in turn causes tissue deterioration and a health decline.[8] Low-grade systemic inflammation has also been implicated in the development of Alzheimer’s disease. It is possible that dementia and the underlying dysfunction within the brain may be exacerbated or driven by chronic inflammation, however further research is warranted. [8] Furthermore, chronic inflammation has also been implicated in the development of bladder cancer. [9]

It doesn’t sound great, right? So let’s prevent this! Here are some of the known causes of this inflammation:

  • Hypokinesis: this is really just a fabulous word for low physical activity or a sedentary lifestyle. As you exercise, your skeletal muscles produce and release anti-inflammatory substances into the blood. [10, 11] You do need a good, hard workout to reap the benefits mind you! But regular physical activity will definitely decrease your inflammation.
  • Obesity: the fat cells themselves have been shown to play a role in inflammation, and obese individuals have higher blood levels of inflammatory markers. [12, 13, 14] So the more fat you accumulate, the greater inflammation you may experience!
  • Poor Diet: refined and processed foods, including products high in simple sugars are implicated. [15, 16, 17, 18] In combination, diets high in red meat and low in antioxidant vitamins E and C may also perpetuate chronic inflammation. [19, 20] On the other hand, omega-3 fatty acid intake is a known anti-inflammatory and this is an essential part of a healthy diet. [21]
  • Infection: the implicated bacteria and viruses include H. Pylori (which is a cause of peptic ulcer disease), chlamydia pneumoniae and herpes simplex virus.

Final Points

Low-grade systemic inflammation places you at risk for heart disease, metabolic syndrome, Alzheimer’s disease, and even cancer, and also plays a role in many more conditions! As chronic inflammation may be induced by poor lifestyle choices, the treatment is quite simple. Most importantly – learn to make better lifestyle choices by being active and eating healthy, nutritious food!

References:

  1. Packard RRS, Libby P. Inflammation in atherosclerosis: from vascular biology to biomarker discovery and risk prediction. Clin Chem 2008; 54:24–38.
  2. Tamakoshi K, Yatsuya H, Kondo T, Hori Y, Ishikawa M, Zhang H, Murata C, Otsuka R, Zhu S, Toyoshima H. The metabolic syndrome is associated with elevated circulating C-reactive protein in healthy reference range, a systemic low-grade inflammatory state. Int J Obes Relat Metab Disord 2003;27:443–9.
  3. Ford ES. The metabolic syndrome and C-reactive protein, fibrinogen, and leukocyte count: findings from the Third National Health and Nutrition Examination Survey. Atherosclerosis 2003;168:351–8.
  4. Pickup JC. Inflammation and activated innate immunity in the patho- genesis of type 2 diabetes. Diabetes Care 2004;27:813–23.
  5. Dehghan A, Kardys I, de Maat MPM, Uitterlinden AG, Sijbrands EJG, Bootsma AH, Stijnen T, Hofman A, Schram MT, Witteman JCM. Genetic variation, C-reactive protein levels, and incidence of diabetes. Diabetes 2007;56:872–8.
  6. Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA 2001;286:327–34.
  7. De Ferranti SD, Rifai N. C-reactive protein: a nontraditional serum marker of cardiovascular risk. Cardiovasc Pathol 2007;16:14–21.
  8. De Felice FG, Ferreira ST. Inflammation, defective insulin signaling, and mitochondrial dysfunction as common molecular denominators connecting type 2 diabetes to Alzheimer disease. Diabetes. 2014 Jul;63(7):2262-72. doi: 10.2337/db13-1954. Epub 2014 Jun 
  9. Gakis G. The role of inflammation in bladder cancer. Adv Exp Med Biol. 2014;816:183-96. doi: 10.1007/978-3-0348-0837-8_8.
  10. Febbraio MA, Pedersen BK. Muscle-derived interleukin-6: mechanisms for activation and possible biological roles. J FASEB 2002; 16: 1335-47.
  11. Febbraio MA, Pedersen BK. Contraction-induced myokine production and release: is skeletal muscle an endocrine organ? Ex sport sci rev 2005; 33: 114-9
  12. Das UN. Is obesity an inflammatory condition? Nutr 2001; 17: 953-66.
  13. Trayhurn P, Wood IS. Adipokines: inflammation and the pleiotropic role of white adipose tissue. Br J Nutr 2004; 92: 347-55.
  14. Florez H, Castillo-Florez S, Mendez A, Casanova-Romero P, Larreal-Urdaneta C, Lee D, et al. C-reactive protein is elevated in obese patients with the metabolic syndrome. Diabetes research and clinical practice 2006; 71: 92-100.
  15. Calder PC, Kew S. The immune system: a target for functional foods? Br J Nutr 2002; 88 Suppl 2: S165-77.
  16. Salmeron J, Ascherio A, Rimm EB, Colditz GA, Spiegelman D, Jenkins DJ, et al. Dietary fiber, glycemic load, and risk of NIDDM in men. Diabetes care 1997; 20: 545-50.
  17. Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett WC. Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. JAMA 1997; 277: 472-7.
  18. Liu S, Manson JE, Buring JE, Stampfer MJ, Willett WC, Ridker PM. Relation between a diet with a high glycemic load and plasma concentrations of high-sensitivity C-reactive protein in middle-aged women. Am J Clin Nutr 2002; 75: 492-8.
  19. Ford ES, Giles WH, Mokdad AH, Ajani UA. Microalbuminuria and concentrations of antioxidants among US adults. Am J Kid Dis 2005; 45: 248-55.
  20. Accinni R, Rosina M, Bamonti F, Della Noce C, Tonini A, Bernacchi F, et al. Effects of combined dietary supplementation on oxidative and inflammatory status in dyslipidemic subjects. Nutr Met Cardio 2006; 16: 121-7.
  21. Ferrucci L, Cherubini A, Bandinelli S, Bartali B, Corsi A, Lauretani F, et al. Relationship of plasma polyunsaturated fatty acids to circulating inflammatory markers. J Clin Endo Met 2006; 91: 439-46.

 

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