Thus, the brain is now “blind” such that these cells without insulin signaling “think” there is not enough sugar.  At the level of the arteries the increased blood sugar causes reduced nitrous oxide (NO) production. 6,7

NO is a substance that our body uses to dilate arteries to increase blood flow and oxygen to the body’s organs. Insulin itself promotes the release of NO in muscle cells blood vessels. 8 So, if cells are resistant to its effect like type II diabetes or insulin is absent like in type I diabetes NO production will decrease.

Increased blood sugar also causes increase in the concentration of free radicals. 9 Free radicals are what are called reactive molecules as they can and do react with cells in the body. They can and do damage cells including its DNA that can result in cell death.

The cells that make up the lining of arteries and veins which is called the endothelium is particularly vulnerable. The body sends immune cells to these damaged areas in the arteries to repair them. But as chronically damaged this causes the body to find a more durable fix. Like with a chronically damaged part of the body like a herniated disc.

Where over years of chronic inflammation and thus the body is not able to repair it. The body eventually attempts to isolate it by encapsulating it in calcium. In my opinion this is like why plaque in arteries forms due to chronic inflammation causing chronic damage that cannot be repaired.

Plaque is made up of calcium but also cholesterol. Not sure why cholesterol but it may be the body substance that best allows blood cells, platelets and other substances to flow through the artery without being damaged, altered or sticking to the artery walls.

This narrows the arteries, also causing them to become more rigid and prone to clog. All bad.  As those with type II diabetes are usually obese, they are already in a chronic inflamed state. 10 Chronic inflammation also damages the inner walls of arteries.

In fact, the latest research is demonstrating chronic inflammation is cause of type II diabetes. Overeating causes chronic inflammation. For example, those with chronic inflammation like rheumatoid arthritis 11 or hepatitis C are more prone to develop type II diabetes. As the immune system and metabolic system are closely tied. 12

So, the issue is inflammation. Well inflammation causes lots of issues with metabolism which many believe leads to diabetes. 13 High blood sugar levels lead to inflammation which causes the gut to have leptin and insulin resistance. Here is the gut again causing issues.

As inflammation is a catabolic process (breaks things down) and insulin (and Leptin) are anabolic (build things up). The though in one theory it is the bodies efforts to balance and maintain a healthy weight, so it initiates a catabolic process inflammation when there are higher levels of leptin and insulin.

The elevated leptin and insulin causing excess anabolic activity. The other theory is that overeating causes the body stress like an infection, so the body reacts in the same way it would to an infection. Thus, stimulating the immune system to cause inflammation.

A much deeper explanation of these theories and other more detailed and beyond what I am trying to do can be found in an excellent article (as well as many other topics I believe he covers extremely well) by #ChrisKresser. 14

Thus, the combination of obesity, inflammation and now elevated blood sugar accelerate the process of atherosclerosis. This is what makes how vitamin D3 helps in reversing this as well as preventing it a bit complex. More in next post.

   

  1. Tessari P, Cecchet D, Vedovato M, et al. (September 2010). Nitric oxide synthesis is reduced in subjects with type 2 diabetes and neuropathy. Diabetes. 59(9): 2152-2159.
  2. Chu S, Bohlen HG. (2004). High concentration of glucose inhibits glomerular endothelial eNOS through a PKC mechanism. Am J Physiol Renal Physiol. 287: F384-F392.
  3. Vincent MA, Montagnani M, Quon MJ. (2003). Molecular and physiologic actions of insulin related to production of nitric oxide in vascular endothelium. Curr Diab Rep. 3: 279-288.
  4. Bajaj S, Khan A. (December 2012). Antioxidants and diabetes. Indian J Endocrinol Metab. 16(suppl 2): S267-S271.
  5. Khansari N, Shakiba Y, Mahmoudi M. (2009). Chronic inflammation and oxidative stress as a major cause of age-related diseases and cancer. Recent patents on inflammation & allergy drug discovery. 3;(1):73-80.
  6. Hui P, Zhou H, Wang Y, et al. (2017). Abnormal glucose metabolism in rheumatoid arthritis. Biomed Res Int. article ID 9670434, 6 pages.
  7. Hammerstad SS, Grock SF, Tomer Y, et al. (2015). Diabetes and hepatitis C: A two-way association. Front Endocrinol (Lausanne). 6:134.
  8. Khovidhunkit W, Kim MS, Grunfeld C, et al. (2004). Effects of infection and inflammation on lipid and lipoprotein metabolism: mechanisms and consequences to the host. J Lipid Res. 2004 Jul; 45(7):1169-96.
  9. Kresser C. How inflammation makes you fat and diabetic (and vice versa). https://chriskresser.com/how-inflammation-makes-you-fat-and-diabetic-and-vice-versa/

*The information posted above is for educational purposes only. Always check with your doctor before initiating any changes in your medical treatment. If you do not, then The Two-Minute Health Fact, Dr. Judson Somerville, nor The Optimal Dose is responsible!


Leave a Reply

Your email address will not be published. Required fields are marked *