Insulin insensitivity, also known as insulin resistance, is a condition in which cells in the body become less responsive to the effects of insulin, resulting in reduced glucose uptake and increased blood sugar levels. Click here to learn more about your master hormone – insulin!

 

In a nutshell, when your cells are nice and sensitive to your insulin, they use it well! That means the insulin is working just as we want it to – to shuttle sugars out of your blood and into your cells where it can be converted into usable energy for you.

 

When this does not happen optimally (it’s a range) it’s called insulin insensitivity. Your cells have become less sensitive to the insulin.

Why is this a problem?

 

Essentially, when the carbs get stored in your muscle cells, they’re used as energy and your body becomes a fat-burning, metabolically optimal machine. If not, it becomes a fat-storing, metabolically deficient machine. Boo 🙁

 

So what causes your cells to become less sensitive to your insulin?

 

Some of the more commonly known factors that can contribute to insulin insensitivity include:

 

Obesity:

Excess body fat, particularly abdominal or visceral fat, has been strongly associated with insulin resistance. Adipose (fat) tissue produces inflammatory substances that impair insulin signaling and then contribute to insulin resistance.

Sedentary lifestyle:

Physical inactivity and a lack of movement in general have been associated with insulin resistance. Exercise is known to improve insulin sensitivity by enhancing glucose uptake into muscles and promoting muscle metabolism.

Genetics:

Like many things, family history and genetic factors can play a role in insulin resistance. In these cases, it’s that much more crucial to implement sound nutrition and lifestyle habits to reduce this risk.

Aging:

Like many things in our bodies, insulin sensitivity also declines with aging. Once again however, sound diet and lifestyle choices can greatly impact the rate of this decline.

 

Some less common factors that can contribute to insulin resistance include:

 

Polycystic ovary syndrome (PCOS):

Numerous studies have demonstrated that insulin resistance is frequently detected in women with PCOS and may play a role in the emergence of metabolic disorders such as type 2 diabetes.

Cushing’s syndrome:

Excess production of cortisol, a hormone associated with stress, is the hallmark of Cushing’s syndrome – a relatively uncommon endocrine disorder. In the long run, this hormonal imbalance can lead to insulin resistance and impaired glucose tolerance.

Medications:

Glucocorticoids, diuretics used for hypertension and edema, statins, and some antipsychotic medications used for the treatment of schizophrenia and bipolar disorder have all been associated with an increased risk of developing insulin resistance, via various pathways in the body.

Menopause:

Estrogen enhances insulin signaling pathways in target tissues, such as adipose tissue, skeletal muscle, and liver. It can also stimulate glucose uptake into cells and promote glycogen synthesis, which helps to lower blood sugar levels and improve insulin sensitivity. Thus, with declining estrogen levels at the onset of menopause, many women experience reduced insulin sensitivity and as a result, increased hunger, weight gain, and/or inability to lose weight.

Snacking:

Believe it or not, grazing – even on good quality whole foods – can contribute to reduced insulin sensitivity, for those who may already be compromised. This is because repeated spikes in blood sugar levels can strain the body’s insulin response, leading to decreased insulin sensitivity over time.

 

Now that you know what it is and what contributes to it happening, you can implement strategies in your life to mitigate it. That’s what we’re all about at BUILD – understanding the science and physiology so that you are empowered to take action for your individual needs, body and goals. Get in touch with us for support!

 

 

 

 

References:

Smeets AJ, Westerterp-Plantenga MS. Acute effects on metabolism and appetite profile of one meal difference in the lower range of meal frequency. Br J Nutr. 2008;99(6):1316-1321. doi:10.1017/S0007114507853374
Mattson MP, Allison DB, Fontana L, et al. Meal frequency and timing in health and disease. Proc Natl Acad Sci U S A. 2014;111(47):16647-16653. doi:10.1073/pnas.1413965111
Adeva-Andany MM, González-Lucán M, Donapetry-García C, Fernández-Fernández C, Ameneiros-Rodríguez E. Insulin resistance is a cardiovascular risk factor in humans. Diabetes Metab Syndr. 2019;13(2):1449-1455. doi:10.1016/j.dsx.2019.02.016
Perreault L, Bergman BC, Hunerdosse DM, Playdon MC, Eckel RH. Updated approaches for assessing insulin sensitivity and resistance in vivo. Methods Mol Biol. 2019;1916:203-229. doi:10.1007/978-1-4939-8994-2_15
DeFronzo, R.A. (2010). Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerosis. Diabetes Care, 14(3), 173-194. doi:10.2337/diacare.14.3.173; Kahn, S.E., Hull, R.L., & Utzschneider, K.M. (2006). Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature, 444(7121), 840-846. doi:10.1038/nature05482
Colberg, S.R., Sigal, R.J., Yardley, J.E., Riddell, M.C., Dunstan, D.W., Dempsey, P.C., . . . Tate, D.F. (2016). Physical activity/exercise and diabetes: A position statement of the American Diabetes Association. Diabetes Care, 39(11), 2065-2079. doi:10.2337/dc16-1728; Haskell, W.L., Lee, I.M., Pate, R.R., Powell, K.E., Blair, S.N., Franklin, B.A., . . . Bauman, A. (2007). Physical activity and public health: Updated recommendation for adults from the American College of Sports Medicine and the American Heart Association. Medicine & Science in Sports & Exercise, 39(8), 1423-1434. doi:10.1249/mss.0b013e3180616b27
References: Chanson, P., Salenave, S., & Ancelle, D. (2008). Cushing’s syndrome. Orphanet Journal of Rare Diseases, 3, 22. doi:10.1186/1750-1172-3-22; Nieman, L.K., Biller, B.M.K., Findling, J.W., Murad, M.H., Newell-Price, J., Savage, M.O., . . . Montori, V.M. (2015). Treatment of Cushing’s syndrome: An Endocrine Society clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism, 100(8), 2807-2831. doi:10.1210/jc.2015-1818
Morley, J.E., & Mooradian, A.D. (1993). Insulin resistance in elderly patients with non-insulin-dependent diabetes mellitus. The American Journal of Medicine.
Florez, J.C. (2003). Clinical review: The genetics of type 2 diabetes: A realistic appraisal in 2003. The Journal of Clinical Endocrinology & Metabolism, 88(8), 3568-3577. doi:10.1210/jc.2003-030342; Lyssenko, V., Almgren, P., Anevski, D., Perfekt, R., Lahti, K., Nissén, M., . . . Groop, L. (2005). Predictors of and longitudinal changes in insulin sensitivity and secretion preceding onset of type 2 diabetes. Diabetes, 54(1), 166-174. doi:10.2337/diabetes.54.1.166
Diamanti-Kandarakis, E., & Dunaif, A. (2012). Insulin resistance and the polycystic ovary syndrome revisited: An update on mechanisms and implications. Endocrine Reviews, 33(6), 981-1030. doi:10.1210/er.2011-1034; Legro, R.S., Arslanian, S.A., Ehrmann, D.A., Hoeger, K.M., Murad, M.H., Pasquali, R., . . . Yildiz, B.O. (2013). Diagnosis and treatment of polycystic ovary syndrome: An Endocrine Society clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism, 98(12), 4565-4592. doi:10.1210/jc.2013-2350

 

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