Insulin resistance is a measurement of the body's cells and tissues to use insulin. If a person is insulin resistant, that is, has a higher level of insulin resistance, then their body does not respond as well to insulin as someone who is insulin sensitive. Thin people and small children are more sensitive to insulin, and a little might go a long way. For example, when first diagnosed with diabetes, my son only needed about a half a unit of insulin when he ate a meal. He was sensitive to insulin, and had low insulin resistance. Someone who is insulin resistant might require 20 units or more of insulin per meal. Insulin resistance is a hallmark of type 2 diabetes. Metabolic syndrome is also known as "insulin resistance syndrome."

While usually associated with type 2 diabetes, a number of studies suggest that increased insulin resistance may also influence the development of type 1 diabetes. For example:

The "Beta Cell Stress" hypothesis (see the hypotheses page) suggests that any phenomenon that induces insulin resistance, and thereby puts extra pressure on the beta cells, should be regarded as a risk factor for type 1 diabetes. When the demand for insulin is great, beta cells may have to work harder to produce adequate insulin. If the immune system is prone to react, increased insulin production could stimulate the autoimmune process (Ludvigsson 2006; Sepa and Ludvigsson 2006). Increasing insulin resistance is likely to be one accelerator of type 1 diabetes, speeding up the process in people who already have compromised beta cells, but probably does not initiate the disease (Gale 2007). 

 

A number of environmental factors may be able to increase insulin resistance, including vitamin D deficiency, infections, increased weight gain, stress, and puberty. Some environmental contaminants can increase insulin resistance in animals, including air pollutants, bisphenol A, some persistent organic pollutants (e.g., PCBs), nitrate/nitrite, and some pesticides. Some contaminants have been associated with increased insulin resistance in humans, including air pollutants, some persistent organic pollutants (including dioxin and PCBs), and phthalates. See the linked pages for more information and sources.

A review discusses the role of endocrine disrupting chemicals in the development of insulin resistance and other related conditions, such as obesity, type 2 diabetes, metabolic syndrome, and points out that these chemicals may also be involved in the development of non-alcoholic fatty liver disease (NAFLD) (Polyzos et al. 2011). 

 

Some authors have proposed that environmental contaminants, including bisphenol A, persistent organic pollutants, heavy metals, and more, affect the functioning of the mitochondria, and thereby induce insulin resistance (Lim et al. 2010).

Increased insulin resistance can probably accelerate the progression of type 1 diabetes in people who already have compromised beta cell function. Based on various hypotheses, anything that can increase insulin resistance may also increase the risk of developing type 1 diabetes. A number of environmental factors, including exposure to many environmental contaminants, can increase insulin resistance in animals, and some have been associated with increased insulin resistance in humans. Exposure to these contaminants, then, could potentially accelerate the development of type 1 diabetes. An accelerated disease process is thought to be one reason for the increasing incidence of type 1 diabetes in younger children. Some contaminants, then, may potentially contribute to increasing incidence of type 1 diabetes in children via inducing insulin resistance. Further studies could determine whether these exposures do indeed increase insulin resistance in people and accelerate the appearance of type 1 diabetes.