Fructose and Health Effects Q&A

Transcription

1 Fructose and Health Effects Q&A Fructose is a natural sugar found in many fruits, vegetables, and honey. It is the sweetest of the naturally occurring nutritive (caloric) sweeteners and has many unique functional and nutritional properties that make it a valuable food ingredient. Research has shown that fructose is safe and offers some benefits over other types of sugars. Does consumption of fructose cause obesity? Claims that there is a link between fructose and obesity are based on unproven hypotheses and statistical correlation, not scientific data. There is no evidence to support a unique role for fructose in the global epidemic of obesity. In fact, data has shown that Americans intake of calories from sugar has stayed the same or gone down in the past decade, while the intake of calories from fat has gone up (USDA, 2012; White, 2013). Numerous studies and systematic reviews have found that consumption of fructose does not lead to overweight and obesity (Rippe, 2013; Sievenpiper, 2012; Carden & Carr, 2013; Dolan, 2010; Rizkalla, 2010). A review by Rippe (2013) found that randomized controlled trials, the gold standard for scientific studies, do not support a causal link between weight change and fructose consumption. Another systematic review by Sievenpiper et al. (2012) found that fructose did not cause weight gain when it substituted for other carbohydrates in the diet. The authors concluded that it was likely not the excess fructose intake that lead to weight gain, but rather the intake of excess calories (Sievenpiper et al., 2012). Likewise, a review by Carden & Carr (2013) assessed intake data from the US Department of Agriculture s (USDA) food availability data system and found that excess energy intake was likely a significant contributor to the increase in obesity rates in the US. Further, the authors noted that consumption of fructose has decreased over the past decade while the rate of obesity has continued to increase, suggesting other factors are responsible for the obesity epidemic (Carden & Carr, 2013). A systematic review by Dolan et al. (2010) found no evidence to suggest that fructose ingestion leads to significant changes in body weight. This held true for those consuming fructose at levels up to the 95 th percentile estimates of intake (Dolan et al., 2010). Similarly, a systematic review by Rizkalla (2010) found that moderate to high consumption of fructose (50-100g/day) did not influence body weight. Does consumption of fructose lead to increased blood pressure? Robust scientific data has shown that consumption of fructose does not lead to an increase in blood pressure. A systematic review by Ha et al. (2012) found that isocaloric intake of fructose did not lead to increased blood pressure, and that hypercaloric intake of fructose did not significantly affect mean arterial blood pressure. Likewise, a systematic review of large cohort studies by Forman et al. (2009) found no association between fructose intake and hypertension. A recent review by Rippe (2013) also concluded that the hypothesized association between fructose consumption and increased blood pressure is not supported by other meta-analyses or randomized controlled trials.

2 Does fructose consumption adversely affect hunger cues or satiety hormones? Because fructose is a carbohydrate that provides energy (calories), consumption of it will decrease hunger and help to signal satiety. A comprehensive review by Dolan et al. in 2010 found that fructose consumption did not increase overall food intake. It is unclear if fructose affects hunger and satiety to the same extent as other carbohydrates. In a Moyer and Rodin (1993) study, the authors investigated the potential role of fructose as a hunger suppressant. They found that fructose may be more satiating than other carbohydrates (Moyer & Rodin, 1993). A 2009 review study by Moran found that the results of studies comparing the effect of fructose on satiety to that of other sugars were mixed, with some studies showing differences while others did not. Does fructose lead to dyslipidemia? Research shows that consumption of fructose does not cause dyslipidemia. A systematic review by Sievenpiper et al. (2009) found that isocaloric substitution of fructose for other carbohydrates did not lead to increased circulation of blood lipids. Likewise, a systematic review by Dolan et al. (2010) showed no evidence that the consumption of fructose at normal levels of intake caused biologically relevant changes in triglycerides in overweight or obese individuals. In another review, Dolan et al. (2010) found that fructose consumption at levels approaching 95th percentile estimates of intake did not cause changes in triglyceride levels in healthy weight people. Another systematic review by Wang et al. (2013) found that, when fructose replaced other carbohydrates, it did not lead to a rise in postprandial triglycerides. The authors noted that overall energy intake appeared to be the dominant factor for a possible association between postprandial triglyceride levels and hypercaloric intake of fructose (Wang et al., 2013). A review article by Rippe (2013) also concluded that overall caloric intake might be more to blame than merely fructose when it comes to increased triglyceride levels. Does fructose consumption lead to metabolic syndrome? There is no scientific evidence that fructose causes obesity or metabolic syndrome when consumed in typical amounts. The incidence of metabolic syndrome has risen over the past few decades while Americans intake of calories from sugar has stayed the same or gone down in the past ten years (Rippe, 2013; USDA, 2012; Mozumdar, 2011). There is no evidence to support a unique role for fructose in development of metabolic syndrome. Rather, there is evidence to show that fructose is not implicated in the cause of metabolic syndrome. A review by Tappy et al. (2010) found that replacement of sucrose by high-fructose corn syrup is not likely involved in the prevalence of metabolic diseases as it has the same metabolic effects as sucrose. Further, it is more likely that an increase in caloric consumption and added sugars rather than fructose alone that is associated with an increased risk of metabolic syndrome and related outcomes, such as diabetes and cardiovascular disease (Tappy et al., 2010). Systematic reviews by Sievenpiper et al. have shown that fructose in isocaloric substitution for other carbohydrates does not increase body weight, serum lipids, blood pressure, or insulin levels, all of which are components of metabolic syndrome (Sievenpiper, 2012).

3 Does consumption of fructose cause insulin resistance and diabetes? The consumption of any sugar, including fructose, does not cause diabetes as diabetes is a complex disease brought on by the convergence of many factors. In fact, fructose may beneficial for those trying to control their blood sugar levels. Fructose has a low glycemic index and results in moderate release of insulin to the bloodstream relative to glucose and sucrose. A review article by Bantle et al. (2009) noted that studies in people both with and without diabetes have demonstrated that fructose produces a smaller postprandial rise in plasma glucose and serum insulin than other common carbohydrates. Similarly, a systematic review, by Cozma et al. (2012) found that fructose consumption did not significantly affect fasting insulin or glucose among diabetics. Contrary to concerns that fructose may have adverse metabolic effects, catalytic doses (<10 g/meal) of fructose may decrease the glycemic response to high-glycemic index meals. A meta-analysis by Sievenpiper et al. (2012) found that catalytic doses of fructose significantly reduced glycosylated hemoglobin (HbA1c) (a measure of blood sugar control over a period of several months) and fasting glucose levels without adversely effecting body weight, triglycerides, or insulin levels. A review conducted by Rippe (2013) found that most studies do not support an association between sugar consumption and increased risk of diabetes. Further, stronger studies, including randomized controlled trials and cohort studies, suggest that there is no link (Rippe, 2013). Does fructose cause non-alcoholic fatty liver disease? While it has been postulated that fructose consumption could lead to non-alcoholic fatty liver disease, this is not supported by the totality of the scientific research. Proponents of this theory argue that because fructose may be metabolized by de novo lipogenesis, that fructose could adversely affect the liver. However, de novo lipogenesis is a minor pathway in the overall human energy economy (Rippe & Etherton, 2012; Tappy & Le, 2010). Portion size and overall caloric consumption are more likely causes of non-alcoholic fatty liver disease. A double blind trial by Johnston et al. (2013), found that a high fructose diet did not cause any of the features of non-alcoholic fatty liver disease in participants. They concluded that, any advice on lowfructose diets in NAFLD remains unjustified. A ten week, randomized, prospective, partially blinded, parallel investigation by Bravo et al. (2013) showed that when fructose was consumed as part of the usual diet, there was no promotion of fat storage in the liver. Does fructose lead to increased uric acid production? There is no consistent evidence to show that fructose consumption can lead to elevated serum uric acid levels. While some studies have speculated about a potential association between fructose consumption and elevated serum uric acid levels, those experiments have used extreme diets that do not resemble realworld human exposures; and, thus, have limited relevance. Systematic reviews and meta-analyses on the subject have found that controlled feeding of fructose does not lead to increased uric acid production. A systematic review by Wang et al. (2012) found that, in an isocaloric setting, there was no effect of fructose substitution for other carbohydrates on uric acid concentrations. A review of US National Health

4 and Nutrition Examination Survey (NHANES) results by Sun et al. (2010) found that increased dietary fructose intake was not associated with increased risk of elevated uric acid production. Further, the authors found that those in the highest fructose intake group were more likely to have lower levels of uric acid production (Sun et al., 2010). Does consumption of fructose lead to cognitive decline? There is no evidence that consuming fructose has an unfavorable effect on cognitive abilities. In fact, a study by Miller et al. (2013) found that consuming fructose resulted in comparable cognitive abilities as glucose without raising blood sugar levels as much as glucose. They also found that consumption of fructose produced similar executive functioning as consumption of glucose with a comparable number of anagrams being solved by both groups. The authors concluded that, fructose (a sugar that has little effect on blood glucose levels, does not have reinforcing value post-ingestion, and inhibits cortical responding) can enhance executive control to the same degree as glucose (Miller et al., 2013).

5 References Bantle, J.P. (2009) Dietary Fructose and Metabolic Syndrome and Diabetes. The Journal of Nutrition, 139(6):1263S-1268S. Bravo, S., Lowndes, M.A., Sinnett, S., Fullerton, Z., Rippe, J. Consumption of sucrose and high fructose corn syrup does not increase liver fat or ectopic fat deposition in muscles. Applied Physiology, Nutrition, and Metabolism. 38(999): Carden, T.J. & Carr, T.P. (2013) Food availability of glucose and fat, but not fructose, increased in the US between 1970 and 2009: analysis of the USDA food availability data system. Nutrition Journal, 12(1): 130. Cohen, L., Curhan, G., & Forman, J. (2012) Association of sweetened beverage intake with incident hypertension. Journal of General Internal Medicine, 27(9): Cozma, A.I., Sievenpiper, J.L., de Souza, R.J., Chiavaroli, L., Ha, V., Wang, D.D., Mirrahimi, A., Yu, M.E., Carleton, A.J., Di Buono, M., Jenkins, A.L., Leiter, L.A., Wolever, T.M., Beyene, J., Kendall, C.W., & Jenkins, D.J. (2012) Effect of fructose on glycemic control in diabetes: a systematic review and meta-analysis of controlled feeding trials. Diabetes Care, 35(7): Dolan, L.C., Potter, S.M., & Burdock, G.A. (2010). Evidence-based review on the effect of normal dietary consumption of fructose on development of hyperlipidemia and obesity in healthy, normal weight individuals. Critical Reviews in Food Science and Nutrition, 50(1): Dolan, L.C., Potter, S.M., & Burdock, G.A. (2010) Evidence-Based Review on the Effect of Normal Dietary Consumption of Fructose on Blood Lipids and Body Weight of Overweight and Obese Individuals. Critical Reviews in Food Science and Nutrition, 50:10, Fabbrini, E., Mohammed, B.S., Magkos, F., Korenblat, K.M., Patterson, B.W., & Klein, S. (2008) Alterations in adipose tissue and hepatic lipid kinetics in obese men and women with nonalcoholic fatty liver disease. Gastroenterology, 134: Forman, J.P., Choi, H., & Curhan, G.C. (2009) Fructose and vitamin C intake do no influence risk for developing hypertension. Journal of the American Society of Nephrology, 20: Ha, V., Sievenpiper, J.L., de Souza, R.J., Chiavaroli, L., Wang, D.D., Cozma, A.I., Mirrahimi, A., Yu, M.E., Carleton, A.J., Dibuono, M., Jenkins, A.L., Leiter, L.A., Wolever, T.M., Beyene, J., Kendall, C.W., & Jenkins, D.J. (2012) Effect of fructose on blood pressure: a systematic review and metaanalysis of controlled feeding trials. Hypertension, 59(4): Johnston, R.D., Stephenson, M.C., Crossland, H., Cordon, S.M., Palcidi, E., Cox, E., Taylor, M.A., Aithal, G.P., MacDonald, I.A. (2013) No Difference Between High-Fructose and High-Glucose Diets on Liver Triacylglycerol or Biochemistry in Healthy Overweight Men. Gasteroenterology. 145: Miller, H.C., Bourrasseau, C., & Blampain, J. (2013) Can you enhance executive control without glucose? The effects of fructose on problem solving. Journal of Psychopharmacology, 27(7): Moran, T.H. (2009) Fructose and Satiety. The Journal of Nutrition. 139: 1253S 1256S

6 Moyer, A.E. & Rodin, J. (1993) Fructose and behavior: does fructose influence food intake and macronutrient selection? American Journal of Clinical Nutrition, 58(suppl. 5): 810S-814S. Mozumdar, A. & Liquori, G. (2011) Persistent increase of prevalence of metabolic syndrome among U.S. adults: NHANES III to NHANES Diabetes Care. 34(1): Rippe, J.M. (2013). The metabolic and endocrine response and health implications of consuming sugarsweetened beverages: findings from recent randomized controlled trials. Advances in Nutrition, 4: Rippe, J.M., Kris Etherton, P.M. (2012) Fructose, Sucrose, and High Fructose Corn Syrup: Modern Scientific Findings and Health Implications. Advances in Nutrition. 3: Rizkalla, S.W. (2010) Health implications of fructose consumption: a review of recent data. Nutrition & Metabolism, 7: 82. Sievenpiper, J.L., Carleton, A.J., Chatha, S., Jiang, H.Y., de Souza, R.J., Beyene, J., Kendall, C.W., & Jenkins, D.J. (2009) Heterogeneous effects of fructose on blood lipids in individuals with type 2 diabetes: systematic review and meta-analysis of experimental trials in humans. Diabetes Care, 32(10): Sievenpiper, J.L., de Souza, R.J., Mirrahimi, A., Yu, M.E., Carleton, A.J., Beyene, J., Di Buono, M., Jenkins, A.L., Leiter, L.A., Wolever, T.M., Kendall, C.W., & Jenkins, D.J. (2012) Effect of fructose on body weight in controlled feeding trials: a systematic review and meta-analysis. Annals of Internal Medicine, 156(4): Sievenpiper, J.L. (2012) Fructose: Where Does the Truth Lie? Journal of the American College of Nutrition. 31(3): Sievenpiper, J.L. (2012) Catalytic doses of fructose may benefit glycaemic control without harming cardiometabolic risk factors: a small meta-analysis of randomised controlled feeding trials. British Journal of Nutrition. 108, Sun, S.Z., Flickinger, B.D., Williamson-Hughes, P.S., & Empie, M.W. (2010) Lack of association between dietary fructose and hyperuricemia risk in adults. Nutrition & Metabolism, 7:16. Sunehag, A.L., Toffolo, G., Campioni, M., Bier, D.M., & Haymond, M.W. (2008) Short-term high dietary fructose intake had no effects on insulin sensitivity and secretion or glucose and lipid metabolism in healthy, obese adolescents. Journal of Pediatric Endocrinology & Metabolism, 21: Tappy, L, Lê, K.A. (2013) Metabolic Effects of Fructose and the Worldwide Increase in Obesity. Physiological Reviews. 90: Tappy, L., Lê, K.A., Tran, C., & Paquot, N. (2010) Fructose and metabolic diseases: new findings, new questions. Nutrition, 26(11-12): USDA. (2012) ERS Food Availability (Per Capita) Data System. Available at: Wang, D.D., Sievenpiper, J.L., de Souza, R.J., Chiavaroli, L., Ha, V., Cozma, A.I., Yu, M.E., Carleton, A.J., Di Buono, M., Jenkins, A.L., Leiter, L.A., Wolever, T.M., Beyene, J., Kendall, C.W., &

7 Jenkins, D.J. (2012) The effects of fructose intake on serum uric acid vary among controlled dietary trials. Journal of Nutrition, 142(5): Wang, D.D., Sievenpiper, J.L., de Souza, R.J., Cozma, A.I., Chiavaroli, L., Ha, V., Mirrahimi, A., Carleton, A.J., Di Buono, M., Jenkins, A.J., Leiter, L.L., Wolever, T.M.S., Beyene, J., Kendall, C.W.C., & Jenkins, D.J.A. (2013) Effect of fructose on postprandial triglycerides: a systematic review and meta-analysis of controlled feeding trials. Atherosclerosis, doi: /j.atherosclerosis White, J.S. (2013) Challenging the Fructose Hypothesis: New Perspectives on Fructose Consumption and Metabolism. The Journal of Nutrition. 139: 1219S 1227S.