Insulin Resistance 101: Beating the Sugar Rush
Updated: Jul 17, 2018
It is often said that life is a balancing act, and our bodies are the amazing machines that keep the nutritional, lifestyle and environmental elements we engage with daily in happy equilibrium. All physiological processes, hormones and biological compounds require constant balancing to stave off disease, with blood glucose homeostasis being one of these processes. An important bodily mechanism tasked with safeguarding against insulin resistance, metabolic syndrome and diabetes, glucose homeostasis requires the synergistic action of two hormones: insulin and glucagon.
Both insulin and glucagon are manufactured and released by the pancreas, with insulin exerting its influence when blood glucose levels rise and glucagon taking over when blood glucose levels fall. But what happens when this delicate balance is upset?
The Role of Insulin
Insulin is a glucose-sensitive peptide hormone manufactured and released by beta cells of the pancreas, and whose key roles in the human body are regulating blood glucose levels by ensuring proper uptake of glucose into cells, and maintaining proper metabolism of carbohydrate, protein and fat (Wilcox, 2005). Though carbohydrate-based foods are most rapidly catabolised into sugar in the blood-stream, all food we eat (including fat and protein) is broken down into glucose eventually.
In an ideal world, the presence of glucose in the bloodstream immediately primes the pancreas to manufacture and release insulin, which in turn promotes glucose absorption by body cells. Insulin also primes the liver to store glucose as glycogen until it is required, so that the body doesn't find itself in an energy-deficient state during fasting or food deprivation (Hechtman & Gruner, 2012).
The relationship between insulin and glucose is perhaps best understood by thinking of your body’s cells as the lock and insulin as the key: When insulin unlocks the 'door' to your cells, glucose is transported inside and can be effectively used by cells for energy. Without adequate insulin, cells cannot use glucose for energy, and surplus glucose is instead converted to fat and stored within fat cells and the liver (Qaid & Abdelrahman, 2016). This then leads to weight gain, high cholesterol, and the development of complications such as atherosclerosis and fatty liver disease.
A Loss of Insulin Sensitivity
Insulin resistance is a biological abnormality in which cells lose their sensitivity to insulin and are no longer able to absorb glucose as effectively as before – even if the beta cells of the pancreas are still producing a normal amount of insulin. Because cells begin to lose their responsivity to insulin, the pancreas must then over-compensate by producing a greater amount of insulin to boost cells’ ability to absorb glucose. This is ultimately exhaustive, and the pancreas eventually reaches a point where it is no longer able to produce enough insulin to meet the body’s requirements.
The result is a horrific excess of glucose left floating around unchecked in the bloodstream. Pre-diabetes is the first step in the progression of insulin resistance, and is characterised by fasting glucose levels averaging between 100 and 125 mg/dL, or postprandial glucose levels of 140 to 199 mg/dL (Pizzorno, Murray & Joiner-Bey, 2016). Pre-diabetes is typically characterised by a large waist-to-hip ratio, high blood pressure, high triglyceride levels, and attendant risks for metabolic syndrome and cardiovascular disease (Ndsiang, Rastogi & Vannacci, 2015).
Risk Factors for Insulin Resistance
Insulin resistance is both sneaky and insidious because there are no specific signs and symptoms distinctly associated with the condition - making early detection and management a challenge. In testament, research reports that an alarmingly large number of pre-diabetics go on to develop full-blown diabetes mellitus despite pre-diabetes being easily reversible with the right kind of dietary and lifestyle management (Pizzorno et al., 2016). In fact, most practitioners agree that the only way to know if your cells are losing their sensitivity to insulin is by monitoring your blood glucose levels on a regular basis.
Excess weight remains a constant feature of metabolic disease in general, and research suggests that individuals who are prone to accumulating fat around their abdomen rather than their hips are at a heightened risk for insulin resistance (Ndsiang et. al, 2015). Other studies acknowledge that inflammation caused by excess abdominal adiposity is associated with higher levels of pro-inflammatory markers such as C-reactive protein, interleukin-6, and tumour necrosis factor alpha - all of which decrease insulin signalling and cell responsiveness to insulin (Belkina & Denis, 2010).
Other noteworthy causes of reduced insulin sensitivity include hormonal and metabolic-driven changes during pregnancy, which may cause some women to develop insulin resistance (Catalano, 2010). If uncontrolled, reduced insulin function during pregnancy may develop into gestational diabetes, of which approximately 30 percent of cases lead to pregnancy-induced hypertension which endangers both mother and foetus.
Your risk for insulin resistance also increases if you:
Have a family history of type 1 or type 2 diabetes
Suffer from polycystic ovarian syndrome
Maintain a diet high in trans-saturated fat
Do not engage in regular physical activity
Are overly fond of simple carbohydrates and table sugar
Regularly eat processed foods high in fructose
Take certain drugs such as steroids or growth hormones
Are deficient in essential nutrients such as zinc and chromium
Sleep Deprivation and Cortisol
The relationship between insulin resistance and sleep (or lack thereof) is an interesting one. Sleep is described as a state of "energy conservation and cellular repair", where the body's non-active state results in a decreased demand for glucose to fuel muscle and brain activity (Mesarwi, Polak, Jun & Polotsky, 2013, p. 618). Sleep deprivation, on the other hand, is comparable to a state of physiological stress, and is associated with higher blood levels of cortisol. Like adrenaline, cortisol is a hormone released in response to stress and acts as an insulin antagonist to decrease insulin secretion by pancreatic beta-cells, thereby preventing glucose uptake by cells.
Where insulin promotes cellular absorption of glucose, cortisol reduces it so that circulating glucose can instead be used by muscles as part of the 'fight-or-flight' response, allowing the body to meet the demands of the stressor (fight) or to escape (flight). Though this may seem like a positive thing in the short-term, cortisol produced in response to chronic, long-term stress impairs insulin sensitivity and interferes with lipid metabolism in the long run (Gür, Boz, Müderrisoğlu & Polat, 2015). Disrupted fat metabolism then leads to high circulating blood lipid levels and to fat being stored around the abdomen area. This increase in abdominal adiposity is known as 'central obesity', and is a strong predictor of diabetes, cardiovascular disease and other metabolic complications.
Physical Activity and Insulin Responsivity
The benefits of physical activity are manifold for weight and blood glucose management, with regular exercise being associated with better regulation of leptin and adiponectin, both of which are hormonal markers that predict central obesity (Venkatasamy, Pericherla, Manthuruthil, Mishra & Hanno, 2013). Regular physical activity approximating one hour at least three times a week is reported to have both immediate and long-term benefits for blood glucose regulation, with immediate effects lasting for up to 72 hours post-exercise (Bird & Hawley, 2017). Research reports that moderate-intensity aerobic exercise such as jogging, running or Zumba dancing can boost insulin sensitivity and enhance glucose uptake by approximately 40 percent (Venkatasamy et al., 2013).
Other research reports that like aerobic exercise, resistance activity such as weight-lifting may be similarly beneficial for improving insulin sensitivity by increasing skeletal muscle tone, which in turn stimulates increased glucose uptake via GLUT4 glucose transportation mechanisms (Bird & Hawley, 2017). Increased GLUT4 activity is associated with enhanced storage of glucose as glycogen in skeletal muscle, thereby lowering the burden of circulating glucose in the bloodstream (Richter & Hargreaves, 2013). However, due to skeletal muscle's low acclimatisation to exercise, this adaptive boost in GLUT4 action is most apparent after a period of six to 12 weeks, thus highlighting the need for regular, long-term physical activity (Ren, Semenkovich, Gulve, Gao & Holloszy, 1994).
Nutritional Management for Insulin Resistance
One of the key ways to stave off your risk for insulin resistance is to pay close attention to your diet. Like obesity, heart disease and hypertension, insulin resistance stems from the cumulative influence of age, genes, diet and lifestyle factors. You may not be able to change your age or your genes, but you can certainly change your approach to food, stress, exercise and sleep, thereby circumventing your risk factors for insulin resistance and other metabolic diseases. Research suggests that the following dietary changes may be beneficial for improving insulin function:
1. Choose complex carbohydrates
A completely carb-free diet is not an option, as carbohydrates constitute a very important part of the human diet due to their main substrate (glucose) functioning as the body’s primary source of energy (Smolin & Grosvenor, 2013). However, not all carbohydrates are created equal, with simple carbohydrates being rapidly converted to sugar in the bloodstream and complex carbohydrates being gradually broken down to glucose over a longer period of time. Unlike complex carbohydrates which tend to be abundant in fibre and nutrients, simple carbohydrates such as white bread, sugar, processed foods, cakes and confectionaries are devoid of fibre, phytochemicals, vitamins and other important nutrients required for health and well-being (Murray et al., 2005).
To keep insulin function optimal, favour complex carbohydrates over simple carbohydrates. Eat a variety of fibre-rich whole-grains (brown rice, quinoa, millet, amaranth, kamut), lentils and vegetables alongside quality lean protein. Protein is an important consideration in insulin management as amino acids contained in eggs, meat, fish, dairy and vegetarian protein stimulate insulin production and do not cause rapid spikes in blood glucose levels (Gannon & Nuttall, 2010).
2. Maintain a whole-foods diet
Given that a diet abundant in pre-packaged and processed foods is a common cause of disease, it stands to reason that a diet high in nutrient-rich fresh foods is well-positioned to offer reverse benefits. Processed foods are devoid of myriad nutrients, with research acknowledging that insulin resistance is oftentimes the result of poor dietary intake of essential compounds such as chromium, magnesium, calcium, potassium and zinc. Zinc, in particular, supports insulin action by enhancing signal transduction while alleviating demands for increased insulin manufacture by the pancreas' beta cells (Hechtman & Gruner, 2012). The National Institutes of Health suggests the following foods to help meet your recommended daily intake of the aforementioned vital nutrients:
1 cup broccoli (22mcg chromium)
1 cup spinach (156mg magnesium)
230g Greek yoghurt (415mg calcium)
1 whole avocado (975mg potassium)
100g lean beef (7mg zinc)
3. Say ‘No’ to high-fructose corn syrup
The rise in metabolic disease worldwide is largely attributed to sweeteners such as high-fructose corn syrup, which has been linked to conditions such as insulin resistance, type 2 diabetes, obesity, hyperlipidaemia and cardiovascular disease (Elliot et al., 2002). High-fructose corn syrup is a liquid sweetener produced from corn and a regular ingredient in sodas, baked foods, and all manner of processed and packaged foods (Parker, Salas & Nwosu, 2010). Its widespread use stems from the fact that it is a cheaper alternative to sucrose, and is therefore more cost-effective for mass production purposes.
Fructose’s link to obesity stems from its lipogenic properties, which predispose it to being stored as fat rather than used as energy (Elliot et al., 2002). Additionally, fructose does not favour insulin production by the pancreas’ beta cells, leading to reduced insulin response after high-fructose meals and long-term consequences for weight gain and decreased insulin sensitivity (Elliot et al., 2002). The simple solution is to avoid high-fructose corn syrup at all costs and use healthier sweetening alternatives like jaggery instead. Though all forms of sugar are detrimental to insulin management, sensible consumption of unrefined sweeteners such as jaggery may help satiate sweet cravings without wreaking too much havoc on blood glucose levels.
4. Balance your sodium intake
As with all things in life, balance is crucial, and this holds true for sodium intake as well. Sodium and potassium are the human body's two major electrolytes, and are maintained in homeostatic equilibrium by aldosterone, a mineralocorticoid hormone produced by the adrenal glands. Aldosterone regulates blood pressure via the renin-angiotensin-aldosterone system, and excessively high blood levels of aldosterone have been associated with dangerously low sodium levels - and impaired insulin function. Because insulin function is dependent on this delicate balance between sodium, potassium and aldosterone, both excessive and restricted consumption of sodium has proven detrimental for insulin action (Oh et al., 2006).
While the benefits of a low-sodium diet include reduced blood pressure and protection against cardiovascular and kidney disease, a diet that is excessively low in salt provokes electrolyte imbalances by altering aldosterone concentrations in the body (Oh et al., 2016). This in turn has a knock-on effect on insulin effectiveness and glucose uptake. Because a high sodium intake is associated with displaced potassium balance, adhering to dietary guidelines advocating a daily sodium intake of no more than 2,300mg is important. By managing sodium intake, potassium levels are preserved, which in turn supports insulin receptor efficiency and insulin production by the pancreas' beta-cells (Kumagai et al., 2011).
5. Consider chromium supplementation
An essential trace mineral renowned for its ability to regulate glucose homeostasis, chromium is a vital consideration in metabolic disease treatment for its ability to potentiate insulin. Research reports that chromium supplementation may improve glucose metabolism in individuals with insulin resistance, type 1 and type 2 diabetes, gestational diabetes and diabetes caused by steroid abuse, by increasing insulin’s ability to bind to insulin-specific receptors on cells (Marmett & Nunes, 2016). This enhanced binding affinity then enables glucose to be more effectively transported into the cell, and reduces the risk of hyperglycaemia caused by excess glucose in the blood.
Because not all chromium supplementation is considered equal, it is important to speak to a qualified healthcare professional about which type of supplementation is best suited to your needs. However, supplementation should not be viewed as a means to an end, and is instead recommended alongside supportive dietary and lifestyle changes to safeguard insulin function and to stave off risk factors for metabolic disease while preserving other elements required for physical and mental well-being. Book a consultation with me to discuss the best supplementation, functional foods and lifestyle modification options for optimal blood glucose and diabetes management.
Belkina, A. C., & Denis, G. V. (2010). Obesity genes and insulin resistance. Current Opinion in Endocrinology, Diabetes and Obesity, 17(5), 472-477. doi:10.1097/MED.0b013e32833c5c48
Bird, S. R., & Hawley, J. A. (2017). Update on the effects of physical activity on insulin sensitivity in humans. BMJ Open Sport & Exercise Medicine, 2(1), 1-26. doi:10.1136/bmjsem-2016-000143
Catalano, P. M. (2010). Obesity, insulin resistance and pregnancy outcome. Reproduction, 140(3), 365-371. doi:10.1530/REP-10-0088
Elliot, S. S., Keim, N. I., Stern, J. S., Teff, K., & Havel, P. J. (2002). Fructose, weight gain, and the insulin resistance syndrome. The American Journal of Clinical Nutrition, 76, 911-922. Retrieved from http://ajcn.nutrition.org/content/76/5/911.short
Franz, M. J. (1997). Protein: Metabolism and effect on blood glucose levels. Diabetes Education, 23(6), 643-651. doi:10.1177/014572179702300603
Gannon, M. C., & Nuttall, F. Q. (2010). Amino acid ingestion and glucose metabolism: A review. IUBMB Life, 62(9), 660-668. doi:10.1002/iub.375
Gür, C., Boz, M., Müderrisoğlu, C., & Polat, H. (2015). The relationship between insulin resistance and cortisol levels. Istanbul Medical Journal, 16, 73-76. doi:10.5152/imj.2015.00377
Hechtman, L. & Gruner, T. (2012). In L. Hechtman (Ed.), Clinical naturopathic medicine, pp. 1025-1137. Chatswood, New South Wales: Elsevier Australia.
Kelly, G. S. (2000). Insulin resistance: Lifestyle and nutritional interventions. Alternative Medicine Review, 5(2), 109-132. Retrieved from http://www.altmedrev.com/publications/5/2/109.pdf
Kumagai,E., Adachi, H., Jacobs, D. R., Hirai, Y., Enomoto, M., Fukami, A., Otsuka, M., Kumagae, S., Nanjo, Y., Yoshikawa, K., Esaki, E., Yokoi, K., Ogata, K., Kasahara, A., Tsukagawa, E., Ohbu-Murayama, K., & Imaizumi, T. (2011). Plasma aldosterone levels and development of insulin resistance: Prospective study in a general population. Hypertension, 58, 1043-1048. doi:10.1161/hypertensionaha.111.180521
Marmett, B., & Nunes, R. B. (2016). Effects of chromium picolinate supplementation on control of metabolic variables: A systematic review. Journal of Food and Nutrition Research, 4(10), 633-639. doi:10.12691/jfnr-4-10-1
Mesarwi, O., Polak, J., Jun, J., & Polotsky, V. Y. (2013). Sleep disorders and the development of insulin resistance and obesity. Endocrinology and Metabolism Clinics of North America, 42(3), 617-634. doi:10.1016/j.ecl.2013.05.001
Murray, M., Pizzorno, J., & Pizzorno, L. (2005). The encyclopaedia of healing foods. London, United Kingdom: Piatkus.
National Institutes of Health. (2016). Calcium: Fact sheet for health professionals. Retrieved from https://ods.od.nih.gov/factsheets/Calcium-HealthProfessional/
National Institutes of Health. (2013). Chromium: Fact sheet for health professionals. Retrieved from https://ods.od.nih.gov/factsheets/Chromium-HealthProfessional/
National Institutes of Health. (2016). Magnesium: Fact sheet for health professionals. Retrieved from https://ods.od.nih.gov/factsheets/Magnesium-HealthProfessional/
National Institutes of Health. (2016). Zinc: Fact sheet for health professionals. Retrieved from https://ods.od.nih.gov/factsheets/Zinc-HealthProfessional/
Ndsiang, J. F., Rastogi, S., & Vannacci, A. (2015). Insulin resistance, type 1 and type 2 diabetes, and related complications. Journal of Diabetes Research, Article ID 234135, 1-2. doi:10.1155/2015/234135
Oh, H., Lee, H. Y., Jun, D. W., & Lee, S. M. (2016). Low salt diet and insulin resistance. Clinical Nutrition Research, 5, 1-6. Doi:10.7762/cnr.2016.5.1.1
Parker, K., Salas, M., & Nwosu, V. C. (2010). High fructose corn syrup: Production, uses and public health concerns. Biotechnology and Molecular Biology Review, 5(5), 71-78. Retrieved from www.academicjournals.org/BMBR
Pizzorno, J. E., Murray, M. T., & Joiner-Bey, H. (2016). The clinician's handbook of natural medicine (3rd ed.). St Louis, MI: Elsevier.
Qaid, M. M., & Abdelrahman, M. M. (2016). Role of insulin and other related hormones in energy metabolism: A review. Cogent Food & Agriculture, 2, 1-8. doi:10.1080/23311932.2016.1267691
Ren, J.-M., Semenkovich, C. F., Gulve, E. A., Gao, J., & Holloszy, J. O. (1994). Exercise induces rapid increases in GLUT4 expression, glucose transport capacity, and insulin-stimulated glycogen storage in muscle. The Journal of Biological Chemistry, 260(2), 14396-14403. Retrieved from http://www.jbc.org/content/269/20/14396.full.pdf
Smolin, L. A., & Grosvenor, M. B. (2013). Nutrition: Science and applications (3rd ed). Hoboken, NJ: John Wiley & Sons.
Venkatasamy, V. V., Pericherla, S., Manthuruthil, S., Mishra, S., & Hanno, R. (2013). Effect of physical activity on insulin resistance and oxidative stress in diabetes mellitus. Journal of Clinical & Diagnostic Research, 7(8), 1764-1766. doi:10.7860/JCDR/2013/6518.3306
Wilcox, G. (2005). Insulin and insulin resistance. Clinical Biochemistry Reviews, 26, 19-39. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1204764/