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Inflammation: friend or foe?

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Immune system cells systemic inflammation
 Key learnings:
  • What is systemic inflammation, and why we should avoid it
  • Common causes and consequences of chronic inflammation
  • Practical strategies to fight inflammation effectively

Did you know inflammation is an important aspect of our immune response? In a healthy body, it will be triggered and last only for as long as it is required. However, in the presence of oxidative stress, inflammation can become chronic and wreak havoc in the body.
 

What is inflammation?

Inflammation is triggered as part of our body’s innate immune response and it certainly isn’t always ‘bad.’  In fact, without any inflammation, we wouldn’t have made it this far as a species.

Inflammation is one part of the body’s defense against pathogenic organisms such as bacteria, viruses and fungi as well as against the body’s own damaged cells. Inflammation assists in the removal of these micro-organisms and damaged cells and promotes healing within the body.

During acute inflammation, the capillaries dilate, and immune cells seep through the bloodstream to the site of injury or damage to protect the body. This inflammatory response causes pain, redness, heat, oedema and potentially a temporary loss of function in the injured area. When the area has sufficiently healed, the body stops the inflammatory response.

Chronic systemic inflammation occurs when the body has not eliminated the cause of injury or damage, or is not getting the message to shut off the inflammatory response. Two common biomarkers of systemic inflammation are the C-Reactive Protein (CRP) and Erythrocyte sedimentation rate (ESR).

 

What causes it?

There are many individual causes of inflammation, but at their root they all have one thing in common: Oxidative Stress.

Any stressor on the body, physical, mental or chemical, causes an increase in the production of reactive oxygen species (ROS), known as oxidation. Like inflammation, not all oxidation is ‘bad.’ In fact, one of the reasons that exercising improves our health is that the generation of ROS triggers the body to adapt and improve. 

Our body has mechanisms of dealing with ROS, however there are times when there is an imbalance between production and elimination. This, at the root cause is the contributor to chronic inflammation.

Below are some of the potential causes of oxidative stress and inflammation:

  1. Environmental toxic exposure: Heavy metals such as mercury and aluminium are known to contribute to inflammatory states within the body (1, 2). Even, excess levels of free iron can contribute to inflammation (3).
  1. Diet: Consuming foods that trigger an immune or allergic response in the body can lead to inflammation.  This will vary per person, for instance, eggs may cause an inflammatory response for you and have no such effect on your neighbour. Then there are some foods which trigger these responses indiscriminately, including, refined seed oils, alcohol and a diet with a high omega-6 to omega-3 ratio, such as the Standard American Diet (4).
  1. Poor gut health: While there is a link between inflammation and intestinal permeability, a causal relationship hasn’t been proven. It is postulated that due to the inadequate breakdown of foods, large particles slip through the tight junctions of the gut and into the bloodstream. The immune system recognises these large food particles as foreign invaders, triggering an inflammatory response within the body (5).
  1. Genetics: Certain individuals are more susceptible to higher levels of inflammation due to their genetics.  Genes such as the ARG1 and TREM2 variations have been associated with higher levels of CRP (6, 7). However, genetics by themselves aren’t a sentence for permanently high inflammation. Our diet, lifestyle and overall environment determines whether or not these genes get expressed, known as epigenetic triggers.
  1. Blood sugar dysregulation: When the body is unable to adequately regulate blood sugar, such as for diabetics or those with insulin resistance, inflammation can be a consequence. Interestingly enough, inflammation can also further exacerbate blood sugar dysregulation, making this a vicious cycle to break (8).
  1. Weight issues: Being overweight or obese can increase levels of inflammation. Fat acts as an endocrine gland within our body, meaning it secretes a number of chemicals and hormones, one group of which are inflammatory cytokines (9). Another vicious cycle.

 

What does chronic inflammation lead to? (10)

  • Tissue damage
  • Fatigue
  • Fever
  • Pain
  • Rash
  • Blood vessels swell and lose function
  • Insulin resistance

 

A number of chronic diseases, such as:

  • Cardiovascular diseases including atherosclerosis, heart attack and stroke (11)
  • Diabetes and other blood sugar related complications such as neuropathy and retinopathy (8)
  • Musculoskeletal diseases such as osteoporosis and osteoarthritis (12)
  • Cancers including lung, colon, prostate and lymphoma (13)
  • Asthma (14)
  • Intestinal permeability (5)
  • Fatty liver (15)
  • Neurological disorders such as Alzheimer’s, Parkinson’s disease and dementia (16)

What can be done?

Antioxidants

Seeing as chronic inflammation is triggered by an increased production of ROS, it makes sense that reducing the levels of these ROS should be a major step in your inflammation protocol.

Antioxidants, as the name suggests, are designed to quench these ROS. These include the antioxidants we get from food and supplements, as well as the ones we make on our own, such as glutathione.

 

Glutathione

Lower levels of glutathione lead to an imbalance between ROS production and elimination, leading to chronic levels of inflammation (17). Thus, increasing glutathione levels should be a top priority in managing inflammation.

By increasing levels of glutathione we can more readily control inflammation by decreasing ROS.  Increasing glutathione levels should be approached from two directions:  One, decrease exposure to stressors when possible, this reduces the depletion of glutathione. Two, increase production of glutathione. 

One of the most effective ways to increase glutathione is to consume bioavailable amounts of the precursors glutamate, glycine and cysteine, with cysteine being the most important (18). Undenatured whey is one source of these bioavailable glutathione precursors and has been shown to improve glutathione levels (18).

On top of directly targeting glutathione, it is imperative to live a healthy lifestyle by

  • Moving often
  • Eating according to what is best for you
  • Reducing mental and emotional stress
  • Getting to the root of any health issues and addressing them
  • Balancing blood sugar levels

Conclusion

Chronic inflammation is a risk factor for many diseases and can certainly decrease quality of life.  Reversing states of chronic inflammation is possible, but it usually requires approaches from many angles, as chronic inflammation can be a vicious cycle that promotes more inflammation. From reducing the sources of ROS, such as stress, infection and blood sugar dysregulation, and increasing our body’s glutathione production, chronic inflammation can be quelled.

As with most things health related, prevention seems to be easier than reversing chronic inflammation. 

 

References

  1. Houston, M.C., 2011. Role of mercury toxicity in hypertension, cardiovascular disease, and stroke. The Journal of Clinical Hypertension13(8), pp.621-627.
  2. Campbell, A., 2002. The potential role of aluminium in Alzheimer's disease. Nephrology Dialysis Transplantation17(suppl_2), pp.17-20.
  3. Pietrangelo, A., 2006. Molecular insights into the pathogenesis of hereditary haemochromatosis. Gut55(4), pp.564-568.
  4. Simopoulos, A.P., 2002. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomedicine & pharmacotherapy56(8), pp.365-379.
  5. Bischoff, S.C., Barbara, G., Buurman, W., Ockhuizen, T., Schulzke, J.D., Serino, M., Tilg, H., Watson, A. and Wells, J.M., 2014. Intestinal permeability–a new target for disease prevention and therapy. BMC gastroenterology14(1), p.189.
  6. Reiner, A.P., Beleza, S., Franceschini, N., Auer, P.L., Robinson, J.G., Kooperberg, C., Peters, U. and Tang, H., 2012. Genome-wide association and population genetic analysis of C-reactive protein in African American and Hispanic American women. The American Journal of Human Genetics91(3), pp.502-512.
  7. Vinayagamoorthy, N., Hu, H.J., Yim, S.H., Jung, S.H., Jo, J., Jee, S.H. and Chung, Y.J., 2014. New variants including ARG1 polymorphisms associated with C-reactive protein levels identified by genome-wide association and pathway analysis. PLoS One9(4), p.e95866.
  8. Shoelson, S.E., Lee, J. and Goldfine, A.B., 2006. Inflammation and insulin resistance. The Journal of clinical investigation116(7), pp.1793-1801.
  9. Berg, A.H. and Scherer, P.E., 2005. Adipose tissue, inflammation, and cardiovascular disease. Circulation research96(9), pp.939-949.
  10. Schuppan, D., Pickert, G., Ashfaq-Khan, M. and Zevallos, V., 2015. Non-celiac wheat sensitivity: differential diagnosis, triggers and implications. Best Practice & Research Clinical Gastroenterology29(3), pp.469-476.
  11. Ridker, P.M., Rifai, N., Cook, N.R., Bradwin, G. and Buring, J.E., 2005. Non–HDL cholesterol, apolipoproteins AI and B100, standard lipid measures, lipid ratios, and CRP as risk factors for cardiovascular disease in women. Jama294(3), pp.326-333.
  12. Spector, T.D., Hart, D.J., Nandra, D., Doyle, D.V., Mackillop, N., Gallimore, J.R. and Pepys, M.B., 1997. Low‐level increases in serum C‐reactive protein are present in early osteoarthritis of the knee and predict progressive disease. Arthritis & Rheumatism: Official Journal of the American College of Rheumatology40(4), pp.723-727.
  13. Allin, K.H., Bojesen, S.E. and Nordestgaard, B.G., 2009. Baseline C-reactive protein is associated with incident cancer and survival in patients with cancer. Journal of clinical oncology27(13), pp.2217-2224.
  14. Takemura, M., Matsumoto, H., Niimi, A., Ueda, T., Matsuoka, H., Yamaguchi, M., Jinnai, M., Muro, S., Hirai, T., Ito, Y. and Nakamura, T., 2006. High sensitivity C-reactive protein in asthma. European Respiratory Journal27(5), pp.908-912.
  15. Oruc, N., Ozutemiz, O., Yuce, G., Akarca, U.S., Ersoz, G., Gunsar, F. and Batur, Y., 2009. Serum procalcitonin and CRP levels in non-alcoholic fatty liver disease: a case control study. BMC gastroenterology9(1), p.16.
  16. McGeer, P.L., McGeer, E.G. and Yasojima, K., 2000. Alzheimer disease and neuroinflammation. In Advances in Dementia Research(pp. 53-57). Springer, Vienna.
  17. Rose, S., Melnyk, S., Pavliv, O., Bai, S., Nick, T.G., Frye, R.E. and James, S.J., 2012. Evidence of oxidative damage and inflammation associated with low glutathione redox status in the autism brain. Translational psychiatry2(7), p.e134.
  18. Bounous, G. and Gold, P., 1991. The biological activity of undenatured dietary whey proteins: role of glutathione. Clin Invest Med14(4), pp.296-309.

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