Carbohydrates Explained: Glycemic Index, Insulin and Diabetes

Carbohydrates Explained: Glycemic Index, Insulin and Diabetes

Carbohydrates and their effects on the body can be a contentious, polarizing issue.

Do carbs make you fat?

Do low-carb diets enhance weight-loss?

How important are carbs for energy during workout and recovery?

These are but a few questions you might have heard or asked yourself, so what exactly are carbohydrates, and how do they relate to our overall health?

There are different types of carbohydrates, each with various roles and effects on the body. Starting at their chemical basis, this article will explore the role of carbohydrates in health & disease and some tools you can use to make more conducive to food choices.

Chemical Basics

Glucose is a simple sugar that is the human body’s main source of energy. The most simple form of carbohydrates are monosaccharides, containing one molecule of glucose. Glucose is not the only prevalent monosaccharide, with there also existing fructose and galactose. At the monosaccharide level, the carbohydrates can be used for energy, which is their main purpose in the body.

1. Fructose – fruit sugar
2. Glucose – simple sugar
3. Galactose – simple sugar with a different chemical arrangement

Link two monosaccharides together and it forms a disaccharide, with lactose, maltose, and sucrose being the most prevalent.

1. Sucrose = (Glucose + Fructose)
2. Lactose = (Glucose + Galactose)
3. Maltose = (Glucose + Glucose)

Where monosaccharides and disaccharides are what you might’ve heard commonly referred to as ‘simple carbohydrates’, Polysaccharides are longer chains of monosaccharides ( > 10) or 'complex carbohydrates'. They exist in three main forms: starches, glycogen and cellulose; with the latter being the indigestible part of the plant we know as 'fiber'.

Due to their molecular complexity (with their tougher, fibrous components), the chemical and physical mechanisms in the stomach have a harder time reducing them to their single sugar state of glucose. It therefore takes longer for them to be fully digested and to enter the bloodstream through the small intestine.

Most carbohydrates reach the end of their digestive journey as glucose. They can then be stored within the body as glycogen (the storage form of glucose to be later used for energy), fat, or utilized directly as an energy source.

Glycemic Index

Glycemic Index (GI) measures the speed at which a given food, when eaten in isolation, affects your blood sugar level. Foods are categorized as either low, medium, or high GI, respective to their digestion & assimilation into blood sugar (the concentration of glucose in the blood).

Studies have consistently shown the benefit of adhering to a low glycemic diet in reducing the risk of diabetes, heart disease, and overall health, with one meta-analysis by Brand-Miller and colleagues combining the consensus of 14 studies confirming these effects. 

However, while the Glycemic Index scale of low to high is generally in line with foods good for your health and those less so, it should not be used as the sole indicator for clean nutrition.

Low GI (0-45)
Chickpeas: 28
Kidney beans 24
Apple: 36
Soy milk: 34
Boiled carrots: 39
Fruit yogurt: 41
Chocolate: 40
Lentils: 32

Medium GI (45-59)
Sweet corn: 52
Whole meal pasta: 48
Banana: 51
Rolled oats: 55
Ice cream: 51
Muesli: 57

High GI (60+)
White bread: 75
Boiled pumpkin: 64
French fries: 63
Sweet potato: 63
Boiled potato: 63
Corn Flakes: 81
Honey: 61

We can all appreciate that a diet high in chocolate would not be good for our health, yet chocolate is relatively low on the index. Similarly, sweet potato, a food known for its high vitamin, mineral, and fiber content, is in the High GI category. 

While studies do show the benefits of a low glycemic diet, using your knowledge and intuition regarding limiting junk food and eating quality whole foods, is as always, highly important.

Diabetes: The Role of Carbohydrates and Insulin

There are two types of diabetes (full name ‘Diabetes Miletus’); Type 1 (T1DM) and Type 2 (T2DM). 

Diabetes is, firstly, a disease of either chronically high (hyperglycemia) or chronically low (hypoglycemia) blood glucose.

T1DM occurs when the body’s own immune system attacks and destroys the beta cells of the pancreases, without which insulin cannot be produced, or is produced in a minute amount, causing hypoglycemia. Untreated, prolonged hypoglycemia can result in severe health consequences, such as permanent brain and central nervous system damage with potential for even death. 

Research is ongoing to determine exactly what causes T1DM, but the literature  suggests a large genetic component as well as a possible environmental one.

On the other hand, T2DM is mostly a lifestyle problem of chronic hyperglycemia. Typically seen in obese or overweight populations, the disease is primarily the result of poor lifestyle choices and the dangers associated with the carbohydrate-insulin relationship.

But What Is Insulin?

Insulin is a hormone secreted from the pancreas with its main role being regulation of blood sugar. When the digested carbohydrates enter the blood stream, our blood sugar rises rapidly; this rise being known as ‘hyperglycaemia’. The degree of hyperglycemia is dictated by the food source, with ‘complex’ carbs (polysaccharides) creating a steadier, lower rise due to a slower digestion, and ‘simple carbs’ (di/monosaccharides) inducing a respectively larger rise with their simpler structures. 

This speed of digestion is reflected in the GI of a food. Chronically elevated insulin is known as ‘hyperinsulinemia’. The problem illustrates the body’s inability to cope with repeated excess levels of highly refined carbohydrates, to the point where a vicious cycle ensues. 

Elevated blood glucose requires high levels of insulin to deliver the glucose to the body’s cells. The issue is, in T2DM sufferers these cells are already full from the previous influx of excessive levels of simple, refined carbohydrates. As previously stated, simple carbs cause a considerably larger spike in blood glucose and a larger insulin secretion to deal with it. The already over-filled cells become saturated with sugar and overflow; the effects of which are observed medically as many of the T2DM disorders such as peripheral abscesses and even blindness.

The excess circulating sugar is known as ‘glucotoxicity’ and is responsible for the rotting of the organs and tissues of the body, seen in advanced T2DM sufferers. Furthermore, if the body’s cells are totally overwhelmed by the influx of glucose, insulin seeks another destination for it – the liver. The adult liver weighs roughly only 5 pounds, which is quickly over-whelmed, resulting in the condition ‘fatty liver’. 

Insulin delivers the excess sugar to the liver to be converted into fat, via a process known as ‘denovolipogenisis’. The inevitable overwhelming of this mechanism results in the spilling of converted fat from the liver to around the surrounding organs, as input exceeds output. This fat spillage is known as ‘visceral fat’, which is highly toxic to the body and represents one of the main dangers of T2DM.

Excess simple carbohydrates are the main perpetuator of T2DM, illustrating why low carbohydrate diets have been consistently effective at treating the disease. Truly ending the vicious cycle requires dietary intervention.

Insulin: Health and Performance

Insulin is clearly a very important hormone, with both its importance and potential negative effects to maintain homeostasis; the balance of bodily processes for optimal functioning. Aside from maintaining our blood glucose and fulfilling the crucial task of delivering energy to our cells, Insulin is also important when it comes to exercise performance.

When we exercise, our ‘Insulin sensitivity’ (which refers to how sensitive our cells are to the effects of insulin) is increased. Post exercise, our glucose uptake is elevated up to two hours; which is great for those with T2DM as it enables their insulin resistant body to process glucose more effectively, thereby lessening the cycle of problems. 

In the non-diabetic person, having higher amounts of lean muscle mass is associated with a higher insulin sensitivity, as is having a lower body fat percentage (due to increased levels of insulin resistance being associated with increased levels of visceral fat). 

Being insulin sensitive enables the body to better control, process and store glucose, lessening the risk of the system becoming overwhelmed as the precursor to T2DM. It also reduces your risk of other diseases and health problems, such as cardiovascular disease, thyroid and blood clotting problems. 

Increasing Your Insulin Sensitivity 

One of the best things you can do to improve your insulin sensitivity is cut down on refined, highly processed, high GI carbohydrates that wreak havoc on the glucose-insulin system. 

Ultimately, our ability to optimize the way our body processes carbohydrate is rooted in commonly accepted, healthy lifestyle behaviors. Eating the majority of your carbohydrates from healthier, low processed sources is something we all know we should be doing.

Furthermore, higher insulin sensitivity is just one of the many benefits in engaging in a variety of exercise, and in maintaining an increased level of muscle mass and a low body fat percentage.

Linden Garcia Pepworth is a Sports Nutritionist (BSc Sports Nutrition) and YMCA Accredited Instructor. He is currently working on a review comparing the anabolic differences between plant and animal proteins.

Talbot, K., Wang, H. Y., Kazi, H., Han, L. Y., Bakshi, K. P., Stucky, A., ... & Arvanitakis, Z. (2012). Demonstrated brain insulin resistance in Alzheimer’s disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. The Journal of clinical investigation, 122(4), 1316-1338.
Fujita, S., Rasmussen, B. B., Cadenas, J. G., Grady, J. J., & Volpi, E. (2006). Effect of insulin on human skeletal muscle protein synthesis is modulated by insulin-induced changes in muscle blood flow and amino acid availability. American Journal of Physiology-Endocrinology and Metabolism, 291(4), E745-E754.
Clamp, L. D., Hume, D. J., Lambert, E. V., & Kroff, J. (2017). Enhanced insulin sensitivity in successful, long-term weight loss maintainers compared with matched controls with no weight loss history. Nutrition & diabetes, 7(6), e282-e282.
Borghouts, L. B., & Keizer, H. A. (2000). Exercise and insulin sensitivity: a review. International journal of sports medicine, 21(01), 1-12.
Poehlman, E. T., Dvorak, R. V., DeNino, W. F., Brochu, M., & Ades, P. A. (2000). Effects of resistance training and endurance training on insulin sensitivity in nonobese, young women: a controlled randomized trial. The Journal of Clinical Endocrinology & Metabolism, 85(7), 2463-2468.
Buemann, B., Sørensen, T. I. A., Pedersen, O., Black, E., Holst, C., Toubro, S., ... & Astrup, A. (2005). Lower-body fat mass as an independent marker of insulin sensitivity—the role of adiponectin. International journal of obesity, 29(6), 624-631.
Jenkins, D. J., Wolever, T. M., Taylor, R. H., Barker, H., Fielden, H., Baldwin, J. M., ... & Goff, D. V. (1981). Glycemic index of foods: a physiological basis for carbohydrate exchange. The American journal of clinical nutrition, 34(3), 362-366.
Official GI values - https://www.gisymbol.com/about-glycemic-index/
Brand-Miller, J., Hayne, S., Petocz, P., & Colagiuri, S. (2003). Low–glycemic index diets in the management of diabetes: a meta-analysis of randomized controlled trials. Diabetes care, 26(8), 2261-2267.
American Diabetes Association. (2014). Diagnosis and classification of diabetes mellitus. Diabetes care, 37(Supplement 1), S81-S90.
Cordell, H. J., & Todd, J. A. (1995). Multifactorial inheritance in type 1 diabetes. Trends in Genetics, 11(12), 499-504.
Åkerblom, H. K., & Knip, M. (1998). Putative environmental factors in type 1 diabetes. Diabetes/metabolism reviews, 14(1), 31-68.
Atkinson, M. A., Eisenbarth, G. S., & Michels, A. W. (2014). Type 1 diabetes. The Lancet, 383(9911), 69-82.
Puente, E. C., Silverstein, J., Bree, A. J., Musikantow, D. R., Wozniak, D. F., Maloney, S., ... & Fisher, S. J. (2010). Recurrent moderate hypoglycemia ameliorates brain damage and cognitive dysfunction induced by severe hypoglycemia. Diabetes, 59(4), 1055-1062.
http://pennstatehershey.adam.com/content.aspx?productid=107&pid=33&gid=000090
Krahl, M. E. (1974). Endocrine function of the pancreas. Annual review of physiology, 36(1), 331-360. Seltzer, H. S., Allen, E. W., Herron, A. L., & Brennan, M. T. (1967). Insulin secretion in response to glycemic stimulus: relation of delayed initial release to carbohydrate intolerance in mild diabetes mellitus. The Journal of clinical investigation, 46(3), 323-335.
Modan, M., & Halkin, H. (1991). Hyperinsulinemia or increased sympathetic drive as links for obesity and hypertension. Diabetes care, 14(6), 470-487.
Kawahito, S., Kitahata, H., & Oshita, S. (2009). Problems associated with glucose toxicity: role of hyperglycemia-induced oxidative stress. World journal of gastroenterology: WJG, 15(33), 4137.
Borghouts, L. B., & Keizer, H. A. (2000). Exercise and insulin sensitivity: a review. International journal of sports medicine, 21(01), 1-12.
Srikanthan, P., & Karlamangla, A. S. (2011). Relative muscle mass is inversely associated with insulin resistance and prediabetes. Findings from the third National Health and Nutrition Examination Survey. The Journal of Clinical Endocrinology & Metabolism, 96(9), 2898-2903.
Buemann, B., Sørensen, T. I. A., Pedersen, O., Black, E., Holst, C., Toubro, S., ... & Astrup, A. (2005). Lower-body fat mass as an independent marker of insulin sensitivity—the role of adiponectin. International journal of obesity, 29(6), 624-631.
Goodpaster, B. H., Kelley, D. E., Wing, R. R., Meier, A., & Thaete, F. L. (1999). Effects of weight loss on regional fat distribution and insulin sensitivity in obesity. Diabetes, 48(4), 839-847.
Coyle, E. F., Coggan, A. R., Hemmert, M. K., Lowe, R. C., & Walters, T. J. (1985). Substrate usage during prolonged exercise following a preexercise meal. Journal of Applied Physiology, 59(2), 429-433.
Escobar, K. A., VanDusseldorp, T. A., & Kerksick, C. M. (2016). Carbohydrate intake and resistancebased exercise: are current recommendations reflective of actual need?. British Journal of Nutrition, 116(12), 2053-2065.
Ormsbee, M. J., Bach, C. W., & Baur, D. A. (2014). Pre-exercise nutrition: the role of macronutrients, modified starches and supplements on metabolism and endurance performance. Nutrients, 6(5), 1782-1808.
Murray, B., & Rosenbloom, C. (2018). Fundamentals of glycogen metabolism for coaches and athletes. Nutrition reviews, 76(4), 243-259
Previous article MCT: A Complete Guide to Medium Chain Triglycerides
Next article A Complete, Academic Breakdown of Fat

Comments

avenash samra - July 3, 2020

Awesome article thank you

Leave a comment

Comments must be approved before appearing

* Required fields