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Diabetes Type 2 and High Fructose Corn Syrup

Written by vikdad1.

The correlation of Type 2 Diabetes to High Fructose Corn Syrup (HFCS) consumption has been analyzed frequently over the last fifteen years. HFCS is an artificial sweetener that, like sucrose (table sugar), contains a mix of glucose and fructose. However, while sucrose contains a 1:1 ratio of fructose and glucose, HFCS is most frequently composed of 55% fructose and 45% glucose, and can range up to 90% fructose composition1. HFCS is found in countless food products, including fruit and dairy products, baked goods, cereals, as well as artificial beverages2. Between the years 1970-1990, HFCS consumption increased between 20-40%, exceeding growth in consumption of any other food product. Soda and juice concentrates account for the majority of HFCS intake: between 1970-1995, HFCS consumption grew from 80 to 132 kcal/day3. In the year 2000, corn syrups accounted for 42% of added sweeteners consumed4.

Effect of High Fructose Corn Syrup on Diabetes Type 2

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HFCS is in most soft drinks.

Amongst several others health issues, HFCS has been implicated in the rise of Type 2 Diabetes (T2D) worldwide. According to World Health Organization, in 2010 around 300 million people were estimated to have T2D, with that number likely to grow to 450 million by 20305. Between 1935-1996, the prevalence of diagnosed T2D climbed by 765%, and it currently estimated that nearly 16 million Americans have T2D, 1/3 of who may not even know6. Paralleling the explosion of Type 2 Diabetes, the consumed sugar calories accounted for high fructose corn syrup has increased from 0 to 66% in the last 30 years7.

Effect of High Fructose Corn Syrup on Type 2 Diabetes Independent of Obesity

Aside from raising T2D incidence through increased obesity risk, HFCS has been implicated in causing T2D through independent metabolic effects. Unlike normal table sugar, the fructose contained in HFCS is not bonded to glucose molecules. Once absorbed, fructose molecules are favorably metabolized by the liver into fats in a process called lipogenesis. These fats are released into the bloodstream, and this can lead to an unhealthy level of lipids in the blood (hypertriglyceridemia). Hypertriglyceridemia has been reported on several occasions to induce insulin resistance, which is the fundamental issue in T2D. Thus, while not completely understood, high-fructose diets may induce T2D (as well as hypertension, and Coronary Artery Disease) by a similar mechanism as high-fat diets8.

Furthermore, because fructose is not bonded to glucose in HFCS, glucose is more rapidly absorbed into the blood stream than it would be when derived from normal table sugar. This rapidly absorbed glucose triggers big spikes in insulin, and dramatic fluctuations in insulin can lead to insulin resistance and T2D7.

Studies on the effect of High Fructose Corn Syrup on Type 2 Diabetes have shown mostly deleterious results. The majority of these studies analyzed sugar-sweetened beverages (soda/juice concentrates) because these food products serve as the largest source of High Fructose Corn Syrup. These studies are presented in the Research Evidence towards the end of this page.

There are several other metabolic issues that High Fructose Corn Syrup is thought to cause, though the science is sparse enough where we will not comment here. Dr. Mark Hyman discusses these HFCS-related syndromes in the Blood Sugar Solution.

Effect of High Fructose Corn Syrup on Type 2 Diabetes via Obesity

In addition to the growing body of evidence linking HFCS to Type 2 Diabetes directly, it is certain that HFCS consumption significantly increases the risk of weight gain/obesity. Obesity has shown an undeniable relationship to Type 2 Diabetes; meta-analysis of several studies has shown that around 80% of T2D sufferers are obese. Thus, it seems that HFCS’s impact on Type 2 Diabetes incidence is at least partially due to an increase in body mass index.

Before reviewing the relevant research, it is helpful to understand the

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Insulin Resistance

mechanisms by which HFCS causes weight gain more so than regular table sugar, and how that relates to an elevated risk of Type 2 Diabetes. Two fundamental reasons were mentioned earlier: first, HFCS is more rapidly absorbed through the intestines because fructose and glucose are not bonded (unlike table sugar). Second, fructose is favorably metabolized into fats by the liver, and as you might assume, this can lead to increased weight gain.

The third reason that HFCS induces weight gain is hormonal. Unlike glucose, fructose does not induce insulin secretion. Insulin serves as a mediator for a second hormone named leptin, a hormone in charge of suppressing hunger. Human’s who have are unable to produce leptin are massively obese13. “Because insulin and leptin act as signals in the regulation of food intake and body weight, (fructose’s failure to induce these hormones) suggests that (high) dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric over-consumption14.“

Several studies have shown SSB consumption, the main source of HFCS, to contribute to significant amounts of weight gain. These studies are presented in the Research Evidence towards the end of this page.

Research Evidence Correlating High Fructose Corn Syrup to Type 2 Diabetes

Studies analyzing HFCS impact independent of obesity

Notable studies are presented here, beginning with a classification of ‘positive, neutral, or no’ correlation of HFCS to T2D:

  • Positive Correlation. A epidemiological study following 91,249 women over an 8 year period found that consumption of ≥1 SSB per day had an 83% greater risk for T2D compared with women who consumed 1 SSB per month or less9. When adjusting for Body Mask Index (BMI), the risk reduced to 41%, suggesting that nearly half the risk caused by excessive SSB consumption is correlated to weight gain.
  • Neutral Correlation. An analysis of >40000 black women over the course of 10 years showed that consumption of ≥2 SSBs per day increased the risk of T2D incidence by 24% when compared to consumption to 1 or less SSB per month10. However, unlike the previous study, when the risk was adjusted with consideration for BMI, the increased risk of T2D incidence was not statistically significant.
  • Positive Correlation. One of the largest studies conducted showed a particular convincing correlation between HFCS and T2D. Over 70000 women were studied over the course of 18 years, and the results showed that consumption of 2-3 SSBs per day increased the risk of T2D by 31% compared to consumption of less than 1 SSB per month. This increased risk includes adjustment for BMI, which makes the result especially convincing11.
  • No Correlation. In contrast, a study of 12204 people with a 9-year follow-up period (both men & women) did not show a significant correlation (9% men, 17% women) between SSB consumption and T2D. One interesting consideration is that, in comparison to the first study listed, participants were heavier by nearly 3 kilograms. Because diabetes risk is partially mediated by weight, it is possible that because the participants were heavier to begin with, additional SSB consumption did not have as large of an impact on T2D risk than it would with a more fit population12.

Studies analyzing HFCS impact via obesity

Notable studies are presented here, beginning with a classification of ‘positive, neutral, or no’ correlation of HFCS to weight gain:

  • Positive Correlation. An epidemiological study following >51,000 women over two 4 year periods found women who increased their soft drink consumption from low (less than 1 per week) to high (1 or more per day) had an average weight gain of 4.45 kg. In comparison, women who had consistently low soft drink consumption had an average weight gain of 0.75 kg over 4 years9.
  • Positive Correlation. The largest prospective of children followed 11,654 children over a 3 year period. The results showed that SSB’s did contribute to weight gain, and that this was likely due to the overall increased caloric intake that occurs during SSB consumption15.
  • Positive Correlation. In an expiremental style study, it was shown that subjects given 2215 kJ of HFCS-sweetened beverages per day for 3 weeks gained significant amounts of weight compared to those subjects given no beverages16.
  • No Correlation. One study of 1345 children showed that soda consumption did not have any significant impact on BMI. However, it may be that the 6-month & 12-month follow up periods used for the study were not long enough to measure BMI increase, especially in children, who tend to have faster metabolisms17.

References

  1. Havel PJ. Dietary Fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Nutr Rev. 2005;63(5):133-157.
  1. Hanover LM, White JS. Manufacturing, composition, and applications of fructose. AM J Clin Nutr. 1993; 58:724S-32S.
  1. Malik VS, Popkin BM, Bray GA, et al. Sugar-sweetened beverages, obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk. Circulation. 2010;121:1356-1364.
  1. Putnam JJ, Allshouse JE. Food consumption, prices and expenditures, 1970-1997. US Department of Agriculture Economic Research Service statistical bulletin no. 965, April. Washington, DC: US Government Printing Office. 1999.

5.Malik VS, Hu FB. Sweeteners and Risk of Obesity and Type 2 Diabetes: The Role of Sugar-Sweetened Beverages. Curr Diab Rep. 2012; 12:195-203.

  1. Gross LS, Li L, Ford ES et al. Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment. Am J Clin Nutr. 2004;79:774-9.
  1. Hyman, Mark. 2012. The Blood Sugar Solution: The ultrahealthy program for losing weight, preventing disease, and feeling great now! New York: Little, Brown and Company.
  1. Ferder L, Ferder MD, Inserra F. The role of high-fructose corn syrup in metabolic syndrome and hypertension. Curr Hypertens Rep. 2010;12:105-112.
  1. Schulze MB, Manson JE, Ludwig DS, et al. Sugar-sweetened beverages, weight gain, and incidence of type 2 diabetes in young and middle-aged women. JAMA. 2004;292(8):927–34.
  1. Palmer JR, Boggs DA, Krishnan S et al.Sugar-sweetened beverages and incidence of type 2 diabetes mellitus in African American women. Arch Intern Med. 2008;168:1487–1492.
  1. Bazzano LA, Li TY, Joshipura KJ, Hu FB. Intake of fruit, vegetables, and fruit juices and risk of diabetes in women. Diabetes Care. 2008;31:1311–1317.
  1. Paynter NP, Yeh HC, Voutilainen S., et al. Coffee and sweetened beverage consumption and the risk of type 2 diabetes mellitus: the atherosclerosis risk in communities study. Am J Epidemiol. 2006;164:1075–1084.
  1. Farooqi IS, Keogh JM, Kamath S, et al. Partial leptin deficiency and human adiposity. Nature. 2001;414:34–5.
  1. Bray GA, Nielsen SJ, Popkin BM. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. AM J Clin Nutr. 2004 Apr;79(4):537-43. Review.
  1. Berkey CS, Rockett HR, Field AE, et al. Sugar added beverages and adolescent weight change. Obes Res 2004;12:778–88.
  1. Tordoff MG, Alleva AM. Effect of drinking soda sweetened with aspartame or high-fructose corn syrup on food intake and body weight. Am J Clin Nutr. 1990;51:963–9.
  1. Newby PK, Peterson KE, Berkey CS et al. Beverage consumption is not associated with changes in weightand body mass index among low-income preschool children in North Dakota. J Am Diet Assoc 2004;104:1086 –94.

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