09 Mar Sugar Does NOT Cause Insulin Resistance or Diabetes
Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).
Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.
The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.
This is a huge problem, to say the least.
What are Insulin Resistance and Diabetes?
Insulin is one of the regulators of our blood sugar.
When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.
The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.
From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.
Why Would Sugar Cause Insulin Resistance and Diabetes?
Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:
1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.
This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.
In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)
But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.
Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.
However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).
When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.
2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.
Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”
However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.
One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.
But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.
Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.
This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.
It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?
It All Comes Down to Energy
As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.
The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).
Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.
And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).
These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).
In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.
Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”
It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!
With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.
If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!
- Ford, Earl S. “Risks for all-cause mortality, cardiovascular disease, and diabetes associated with the metabolic syndrome: A summary of the evidence.” Diabetes care, 28, no. 7, 2005, pp. 1769–78.
- Centers for Disease Control and Prevention. “New CDC report: More than 100 million Americans have diabetes or prediabetes: Diabetes growth rate steady, adding to healthcare burden.” org 18 Jul. 2017.
- Lau, Cathrine, et al. “Dietary glycemic index, glycemic load, fiber, simple sugars, and insulin resistance: The Inter99 study.” Diabetes care, 28, no. 6, 2005, pp. 1397–403.
- Colditz, G. A., et al. “Diet and risk of clinical diabetes in women.” The American journal of clinical nutrition, 55, no. 5, 1992, pp. 1018–23.
- Janket, Sok-Ja, et al. “A prospective study of sugar intake and risk of type 2 diabetes in women.” Diabetes care, 26, no. 4, 2003, pp. 1008–15.
- Bessesen, Daniel H. “The Role of Carbohydrates in Insulin Resistance.” The Journal of Nutrition, 131, no. 10, 2001, 2782S-2786S. doi:10.1093/jn/131.10.2782S.
- Ruzzin, J., et al. “Consumption of carbohydrate solutions enhances energy intake without increased body weight and impaired insulin action in rat skeletal muscles.” Diabetes & metabolism, 31, no. 2, 2005, pp. 178–88.
- Himsworth, H. P. “Dietetic factors influencing the glucose tolerance and the activity of insulin.” The Journal of Physiology, 81, no. 1, 1934, pp. 29–48. doi:10.1113/jphysiol.1934.sp003113.
- Fukagawa, N. K., et al. “High-carbohydrate, high-fiber diets increase peripheral insulin sensitivity in healthy young and old adults.” The American journal of clinical nutrition, 52, no. 3, 1990, pp. 524–28. doi:10.1093/ajcn/52.3.524.
- Chen, M., et al. “Insulin resistance and beta-cell dysfunction in aging: The importance of dietary carbohydrate.” The Journal of clinical endocrinology and metabolism, 67, no. 5, 1988, pp. 951–57. doi:10.1210/jcem-67-5-951.
- Soop, M., et al. “Preoperative oral carbohydrate treatment attenuates immediate postoperative insulin resistance.” American journal of physiology. Endocrinology and metabolism, 280, no. 4, 2001, E576-83. doi:10.1152/ajpendo.2001.280.4.E576.
- Pérez-Jiménez, F., et al. “A Mediterranean and a high-carbohydrate diet improve glucose metabolism in healthy young persons.” Diabetologia, 44, no. 11, 2001, pp. 2038–43. doi:10.1007/s001250100009.
- Del Prato, S., et al. “Characterization of cellular defects of insulin action in type 2 (non-insulin-dependent) diabetes mellitus.” The Journal of clinical investigation, 91, no. 2, 1993, pp. 484–94. doi:10.1172/JCI116226.
- Simoneau, J. A., and D. E. Kelley. “Altered glycolytic and oxidative capacities of skeletal muscle contribute to insulin resistance in NIDDM.” Journal of applied physiology (Bethesda, Md. : 1985), 83, no. 1, 1997, pp. 166–71. doi:10.1152/jappl.1918.104.22.168.
- Szendroedi, Julia, et al. “Muscle mitochondrial ATP synthesis and glucose transport/phosphorylation in type 2 diabetes.” PLoS medicine, 4, no. 5, 2007, e154. doi:10.1371/journal.pmed.0040154.
- Petersen, Kitt Falk, et al. “Mitochondrial dysfunction in the elderly: Possible role in insulin resistance.” Science (New York, N.Y.), 300, no. 5622, 2003, pp. 1140–42. doi:10.1126/science.1082889.
- Sonksen, P., and J. Sonksen. “Insulin: Understanding its action in health and disease.” British Journal of Anaesthesia, 85, no. 1, 2000, pp. 69–79. doi:10.1093/bja/85.1.69.
- Li, Xiao C., and Jia L. Zhuo. “Current insights and new perspectives on the roles of hyperglucagonemia in non-insulin-dependent type 2 diabetes.” Current hypertension reports, 15, no. 5, 2013, pp. 522–30. doi:10.1007/s11906-013-0383-y.
- Müller, W. A., et al. “Abnormal alpha-cell function in diabetes. Response to carbohydrate and protein ingestion.” The New England journal of medicine, 283, no. 3, 1970, pp. 109–15. doi:10.1056/NEJM197007162830301.
- Rosmond, Roland. “Stress induced disturbances of the HPA axis: A pathway to Type 2 diabetes?” Medical science monitor: international medical journal of experimental and clinical research, 9, no. 2, 2003, RA35-9.