Part Two of 4 part Blog series: In the last blog we explained inflammation and mentioned that systemic inflammation can create injury to the body and go on to become a chronic disease. Guess what else turns out to be an inflammatory disease - Diabetes. The medical profession should have guessed it over 100 years ago when, in 1896, Ebstein discovered that aspirin could abolish symptoms of diabetes. They should have noticed it again in 1957 when high dose aspirin given for rheumatic fever completely reversed the need for insulin in affected diabetic patients. Only recently does modern medicine appreciate inflammation in the genesis of diabetes, and research is now in full swing.
What’s the injury involved with diabetes? Often times it is obesity (more kindly called “overnutrition”…). “It is recognized that a chronic low-grade inflammation and an activation of the immune system are involved in the pathogenesis of obesity-related insulin resistance and type 2 diabetes.”(2) Excessive accumulation of lipids in fat cells is itself a type of injury causing inflammation in the fatty tissue of the body.
So, fat cells become enlarged and, well, fat. Think of this as an injury, causing the fat cells to release inflammatory substances called inflammatory cytokines. The pathways from this point are myriad and complex. The bottom line is that these inflammatory substances attract inflammation cells called macrophages to the fat, skeletal muscle, liver and pancreas. Normally, macrophages are helpful in killing bacteria, cleaning up bacterial debris, old cell parts, etc. by digesting them and disassembling them. But when mistakenly called by inflammatory cytokines from enlarged fat cells, macrophages come to do their job – destroy and clean up- where it is not needed. The macrophages release their own destructive substances setting up chronic low-level inflammation. Eventually, this damages cells’ ability to respond to insulin. This is called insulin resistance, often thought of as “pre-diabetes.”
Unfortunately, this inflammation strikes elsewhere, as well. Macrophages normally living in the liver become “remotely activated” by the cytokine chemicals, setting up inflammation in the liver, causing non-alcoholic fatty liver and eventually cirrhosis. The problem with fatty liver is that the liver can no longer regulate itself. It cannot shut off glucose production properly and releases glucose when you don’t need it.
So, now you have a situation where body cells do not respond properly to insulin and cannot take in blood glucose. Plus, the liver is dumping out more glucose than it should. And, the pancreas (where insulin is produced) can fall victim to the inflammation, resulting in impaired insulin production. The final result: elevated blood glucose. In its early or pre-diabetic stage, this is called glucose intolerance, and when advanced, diabetes mellitus.
At this point, it is helpful to remember that it has been clearly shown that high dose aspirin (and some other anti-inflammatory drugs) can temporality reverse this inflammation, glucose intolerance, diabetic level glucose. This has led to the current inflammatory model of diabetes prompting the development of novel anti-inflammatory diabetes drugs.
However, that would only treat the symptom and not the cause. We believe that only permanent and meaningful lifestyle changes in nutrition, low intensity exercise, stress management and quality sleep patterns can control and eliminate systemic inflammation. Eliminate systemic inflammation and eliminate the problems that it causes.
- The Journal of Inflammation, Sep 27, 2004, 1:1, Punchard, et.al. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1074343/
- Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes, http://orbi.ulg.ac.be/bitstream/2268/168482/1/1-s2.0-S0168822714001879-main.pdf (hyperlink to original manuscript)
- Obesity, inflammation, and insulin resistance--a mini-review.
Zeyda M1, Stulnig TM. http://www.ncbi.nlm.nih.gov/pubmed/19365105
- Inflammation, Metabolic Syndrome and Melatonin: A Call for Treatment Studies http://www.karger.com/Article/Abstract/446543
- Inflammation and Insulin Resistance, Journal of Clinical Investigation, 166, 7, July 2006, Shoelson, et al, pp 1793 – 1801. www.jci.org
- Mechanisms Linking Inflammation to Insulin Resistance , International Journal of Endocrinology, 2015, Chen, et al.