Removing the reason for resistance is the most effective remedy for the need to resist that I can think of. If you remove injustice, overcome hate, restore harmonious existence, you eliminate the need for war and resistance is no longer needed. Could this be true for insulin resistance as well?
When it comes to disease, we like to identify a singular cause for a condition to simplify disease eradication. However, with insulin resistance, there are potentially multiple factors associated with it. A person with diabetes may have some factors, while another individual has others. For example, diabetes and obesity often go hand in hand. However, obesity isn’t always present in individuals diagnosed with diabetes. This doesn’t eliminate being overweight as a risk factor. It just means that the individual with a healthy weight has other risk factors present.
Another typical approach to diabetes centers around reducing carbohydrates in the diet. Excess carbs in the diet, however, is not the sole contributor to high blood sugar and therefore typically does not completely solve the problem. Over-nutrition, inflammation, dysbiosis (referring to changes in the community of microbes in the gut, otherwise known as the gastrointestinal microbiota), altered fat metabolism, impaired blood circulation (microvascular perfusion), and toxin accumulation are among other factors found to impact insulin resistance.
Chronic low-grade inflammation is associated with obesity-induced insulin resistance. Our immune cells secrete pro-inflammatory compounds that have been found to lead to insulin resistance. An imbalance between the different kinds of immune cells can tip the scale, resulting in insulin resistance.
Biopsies of excess abdominal fat tissue have revealed that up to 40 percent of fat tissue can be composed of pro-inflammatory white blood cells. Why do white blood cells infiltrate excess fat? It’s as if a special division of the army is being sent in because the body knows this isn’t the way things are supposed to be.
Other immune cells regulate the balance of the divisions of our internal military, keeping inflammation in check and making sure immune function doesn’t get out of hand or become lacking. One of the pro-inflammatory substances these white blood cells produce is Tumour Necrosis Factor alpha (TNF-a), which is elevated in obese fat tissue. When TNF-a is neutralized, insulin sensitivity in obese individuals improves.
Lipids are fat-like substances in the body. Altered ways of processing, storing, and utilizing lipids are seen in insulin resistant states. Excess lipids can be stored in the body in places other than our typical fat stores. It can actually be stored in muscle and the liver. The significance of the accumulation of fat in the liver and in muscle cells is negligible on the scale however. Fatty liver and myocellular fat probably only amount to a few extra pounds at the most, yet it has a huge impact on the insulin sensitivity of those tissues. Fat storage in these parts changes the natural function of the liver and muscles, fostering resistance.
Excess circulating lipids in the blood interferes with insulin signaling as well. Some of these fats, specifically saturated fatty acids, as found in meat and dairy, can be converted by the body into substances that lead to insulin resistance. Some have found that our abundant fat accumulation reduces our ability to burn fat as a fuel source. Not only can lipid accumulation contribute to disease, but it can also be a result of insulin resistance. Studies with rodents have found that increasing the percentage of fat in the diet, irrespective of body weight, results in reducing insulin sensitivity within just a few hours.
Consistently eating a high fat diet has also been observed to promote inflammation and change to the community of bacteria living within the gut (the gastrointestinal microbiota).
The gut microbiota has been identified as a potential contributor to insulin resistance. Just as a resident community in a town affect the environment, so the microbial community within impacts one’s overall health. The community has something to do with inflammation, how fat is processed, and gut health itself, all of which compound insulin resistance. Intestinal permeability refers to the intestine’s role of regulating what enters the body through the gastrointestinal tract. When inflammation is present, permeability can be increased and is referred to as leaky gut.
Some of the substances that can be allowed into the body as a result of this increased permeability are components of bacteria themselves called lipopolysaccharides (LPS). When LPS enters circulation, it activates mechanisms that lead to increased inflammation, and yep, promote insulin resistance. Blood levels of bacterial DNA—that’s right, the DNA of bacteria—are elevated in the blood of individuals with pre-diabetes and are considered by some to be predictive of disease progression into diabetes. How did this come about? Through the gut. Fecal transplanting is the process of taking a sample of bacteria from an individual’s stool and transplanting it into another’s large intestine. While it’s definitely not standard practice for diabetes, it has been found that when a microbiota sample from thin humans was transplanted into an obese individual’s large intestines, insulin sensitivity improved in the obese. When mice were given a high fat diet this sequence of events was carried out. A high fat diet led to intestinal inflammation, resulting in increased intestinal permeability, leading to increased LPS that, in turn, promoted system wide inflammation and resulted in insulin resistance.
Interestingly, the surge of diabetes worldwide correlates with our increasing exposure to environmental contaminants. Some see the association as being so significant that diabetogens is a term coined for contaminants found to disrupt blood sugar control. These include heavy metals, such as arsenic and lead, and persistent organic pollutants (POPs), such as PCPs and plastic derivatives. BPA has been found to promote insulin resistance by disrupting insulin communication with the cell at the receptor site. Heavy metals can promote diabetes, promoting free radicals, resulting in damage to the cells in the pancreas that produces insulin.
As we can see there can be potentially many factors contributing to insulin resistance, which helps us realize that simply eliminating carbs is not the answer for treating diabetes. Addressing the variety of contributors can perhaps result in eliminating the need for resistance. This can be observed in a spiritual context as well. God has approached us “at various times and in various ways” to put an end to our resistance (Hebrews 1:1, NKJV).
- Andrea M. Caricilli and Mario J. A. Saad, “The role of gut microbiota on insulin resistance,” Nutrients, vol. 5, 3 829-51, March 12, 2013, doi:10.3390/nu5030829.
- A. Johnson and J. Olefsky, “The origins and drivers of insulin resistance,” Cell, February 14, 2013, 152(4):673-84.
- Joseph Pizzorno, “Is the Diabetes Epidemic Primarily Due to Toxins?,” Integrative Medicine, Encinitas, Calif., vol. 15, 4, (2016): 8-17.
- Z. Tongzhang et al., “Current Understanding of the Relationship between Metal Exposures and Risk of Type 2 Diabetes,” Curre Res Diabetes & Obes, https://juniperpublishers.com/crdoj/pdf/CRDOJ.MS.ID.555710.pdf.