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Effect of Fructose on Body Weight in Controlled Feeding Trials: A Systematic Review and Meta-analysis

John L. Sievenpiper, MD, PhD; Russell J. de Souza, ScD, RD; Arash Mirrahimi, HBSc; Matthew E. Yu, HBSc; Amanda J. Carleton, MSc; Joseph Beyene, PhD; Laura Chiavaroli, MSc; Marco Di Buono, PhD; Alexandra L. Jenkins, PhD, RD; Lawrence A. Leiter, MD; Thomas M.S. Wolever, MD, PhD; Cyril W.C. Kendall, PhD; and David J.A. Jenkins, MD, PhD, DSc
[+] Article and Author Information

Note: Aspects of this work were presented in abstract form at the 28th Internal Symposium on Diabetes and Nutrition Oslo, Norway, 1–4 July 2010 (70), and the International Diabetes Federation, World Diabetes Congress 2011, Dubai, United Arab Emirates, 4–8 December 2011 (71).

Potential Conflicts of Interest: Dr. Sievenpiper: Grant (money to institution): Canadian Institutes of Health Research, Calorie Control Council; Support for travel to meetings for the study or other purposes: The Coca-Cola Company; Consultancy: Abbott Laboratories, International Life Sciences Institute (ILSI) North America, Archer Daniels Midland; Grants/grants pending (money to institution): The Coca-Cola Company; Travel/accommodations/meeting expenses unrelated to activities listed (money to institution): The Coca-Cola Company, Pulse Canada, Canadian Diabetes Association; Other: Director of BDSK Consulting. Dr. de Souza: Grant: Canadian Institutes of Health Research; Grant (money to institution): Calorie Control Council, Canadian Institutes of Health Research Grants/grants pending (money to institution): The Coca-Cola Company. Dr. Beyene: Grant (money to institution): Canadian Institutes of Health Research, Calorie Control Council; Grants/grants pending (money to institution): The Coca-Cola Company. Ms. Chiavaroli: Other: casual position as a clinical research coordinator at Glycemic Index Laboratories. Dr. A. Jenkins: Grant (money to institution): Canadian Institutes of Health Research; Employment: Part owner and Director of Research at Glycemic Index Laboratories; Grants/grants pending (money to institution): Canadian Diabetes Association; Travel/accommodations/meeting expenses unrelated to activities listed: Canadian Diabetes Association. Dr. Wolever: Grant (money to institution): Canadian Institutes of Health Research. Board membership: Glycemic Index Laboratories; Consultancy: McCain Foods, Temasek Polytechnic; Employment: Glycemic Index Laboratories, Glycaemic Index Testing; Grants/grants pending (money to institution): Canadian Institutes of Health Research, Dairy Farmers of Canada, Canadian Diabetes Association; Payment for lectures including service on speakers bureaus: Northwestern University; Royalties: Phillipa Sandall Publishing Services, CABI Publishers; Travel/accommodations/meetings expenses unrelated to activities listed: Royal Society of London, Glycemic Index Symbol program, CreaNutrition AG, McMaster University, Canadian Society for Nutritional Sciences, National Sports and Conditioning Association, Faculty of Public Health and Nutrition—Autonomous University of Nuevo Leon, Diabetes and Nutrition Study Group of the EASD. Dr. Kendall: Grant (money to institution): Canadian Institutes of Health Research, Calorie Control Council; Grants/grants pending (money to institution): The Coca-Cola Company, Almond Board of California, International Tree Nut Council, Barilla, Solae, Unilever, Saskatchewan Pulse Growers, Pulse Canada; Payment for lectures including service on speakers bureaus: Danone, Almond Board of California, Kellogg, Solae; Travel/accommodations/meeting expenses unrelated to activities listed: International Tree Nut Council, Saskatchewan Pulse Growers, Pulse Canada. Dr. D. Jenkins: Grant (money to institution): Barilla, Solae, Unilever, Haine Celestial, Loblaws Supermarkets, Sanitarium Company, Almond Board of California, Orafti, Canadian Institutes of Health Research, Canadian Foundation for Innovation, Ontario Research Fund, Advanced Foods and Material Network, The International Tree Nut Council Nutrition Research & Education, The Peanut Institute; Consulting fee or honorarium: Solae, Oldways Preservation Trust, Almond Board of California, Kellogg's, Quaker Oats, Procter and Gamble Technical Centre Limited, The Coca-Cola Sugar Advisory Board, Griffin Hospital for the development of the NuVal System, Abbott Laboratories, The Canola and Flax Councils of Canada, Soy Advisory Board of Dean Foods, The California Strawberry Commission, The International Tree Nut Council Nutrition Research & Education, The Peanut Institute, Barilla, Unilever, Haine Celestial, Loblaws Supermarkets; Support for travel to meetings for the study or other purposes: Almond Board of California, The International Tree Nut Council Nutrition Research & Education, The Peanut Institute, Alpro Soy Foundation, Soy Advisory Board of Dean Foods; Board membership: Loblaws Supermarkets, Sanitarium Company, Herbalife International, Nutritional Fundamentals for Health, Pacific Health Laboratories, Metagenics/MetaProteomics, Bayer Consumer Care, The California Strawberry Commission, Orafti, Science Advisory Council Agrifoods and Agriculture, Canadian Agriculture Policy Institute, Soy Advisory Board of Dean Foods, Kellogg's, Quaker Oats, Procter and Gamble Technical Centre Limited, The Coca-Cola Sugar Advisory Board, Griffin Hospital for the development of the NuVal System, Abbott Laboratories, The Canola and Flax Councils of Canada, Pulse Canada, Saskatchewan Pulse Growers; Consultancy: Solae, Oldways Preservation Trust, Almond Board of California, Kellogg's, Quaker Oats, Procter and Gamble Technical Centre Limited, The Coca-Cola Sugar Advisory Board, Griffin Hospital for the development of the NuVal System, Abbott Laboratories, The Canola and Flax Councils of Canada, Soy Advisory Board of Dean Foods, The California Strawberry Commission, The International Tree Nut Council Nutrition Research & Education, The Peanut Institute, Barilla, Unilever, Haine Celestial, Loblaws Supermarkets; Stock/stock options: Pacific Health Laboratories; Other: Spouse (Dr. Alexandra L. Jenkins) is a Director and Partner with Glycemic Index Laboratories, which tests foods for glycemic index used in his studies. Disclosures can also be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M11-1669.

Requests for Single Reprints: David J.A. Jenkins, MD, PhD, DSc, Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, The FitzGerald Building, Room 340, 150 College Street, Toronto, Ontario M5S 3E2, Canada; e-mail, mailto:NutritionProject@smh.ca.

Current Author Addresses: Dr. Sievenpiper: Department of Pathology and Molecular Medicine, Faculty of Health Sciences, McMaster University, HSC-2N22B, 1200 Main Street West, Hamilton, Ontario L8N 3Z5, Canada.

Drs. de Souza and Beyene: Department of Clinical Epidemiology & Biostatistics, Faculty of Health Sciences, McMaster University, 1200 Main Street West, MDCL 3208, Hamilton, Ontario L8N 3Z5, Canada.

Mr. Mirrahimi, Mr. Yu, Ms. Chiavaroli, and Dr. A.L. Jenkins: Risk Factor Modification Centre, St. Michael's Hospital, 61 Queen Street East, #6130, Toronto, Ontario M5C 2T2, Canada.

Ms. Carleton: Undergraduate Medical Education, Faculty of Medicine, University of Toronto Medical Sciences Building, 1 King's College Circle, Room 2111, Toronto, Ontario M5S 1A8, Canada.

Dr. Di Buono: Heart and Stroke Foundation, 2300 Yonge Street, Suite 1300, PO Box 2414, Toronto, Ontario M4P 1E4, Canada.

Dr. Leiter: Division of Endocrinology and Metabolism, St. Michael's Hospital, 61 Queen Street East, #6121, Toronto, Ontario M5C 2T2, Canada.

Drs. Wolever: Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, The FitzGerald Building, Room 434, 150 College Street, Toronto, Ontario M5S 3E2, Canada.

Drs. Kendall and D.J.A. Jenkins: Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, The FitzGerald Building, Room 340, 150 College Street, Toronto, Ontario M5S 3E2, Canada.

Author Contributions: Conception and design: J.L. Sievenpiper, J. Beyene, L.A. Leiter, D.J.A. Jenkins.

Analysis and interpretation of the data: J.L. Sievenpiper, R.J. de Souza, M.E. Yu, J. Beyene, L.A. Leiter, D.J.A. Jenkins.

Drafting of the article: J.L. Sievenpiper.

Critical revision of the article for important intellectual content: J.L. Sievenpiper, R.J. de Souza, A. Mirrahimi, M.E. Yu, A.J. Carleton, J. Beyene, L. Chiavaroli, M. Di Buono, A.L. Jenkins, L.A. Leiter, T.M.S. Wolever, C.W.C. Kendall, D.J.A. Jenkins.

Final approval of the article: J.L. Sievenpiper, R.J. de Souza, A. Mirrahimi, M.E. Yu, A.J. Carleton, J. Beyene, L. Chiavaroli, M. Di Buono, A.L. Jenkins, L.A. Leiter, T.M.S. Wolever, C.W.C. Kendall, D.J.A. Jenkins.

Statistical expertise: R.J. de Souza, J. Beyene.

Obtaining of funding: J.L. Sievenpiper, R.J. de Souza, A. Mirrahimi, A.J. Carleton, J. Beyene, M.D. Di Buono, A.L. Jenkins, L.A. Leiter, T.M.S. Wolever, D.J.A. Jenkins.

Administrative, technical, or logistic support: A. Mirrahimi, L. Chiavaroli, C.W.C. Kendall.

Collection and assembly of data: J.L. Sievenpiper, R.J. de Souza, A. Mirrahimi, M.E. Yu, A.J. Carleton, L. Chiavaroli.


From Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada; Clinical Nutrition and Risk Factor Modification Centre, Division of Endocrinology and Metabolism, and Keenan Research Center of the Li Ka Shing Knowledge Institute, St. Michael's Hospital, Faculty of Medicine and Dalla Lana School of Public Health, University of Toronto, Heart and Stroke Foundation of Ontario, and Research Institute Hospital for Sick Children, Toronto, Ontario, Canada; Harvard School of Public Health, Boston, Massachusetts; and College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.


Ann Intern Med. 2012;156(4):291-304. doi:10.7326/0003-4819-156-4-201202210-00007
Text Size: A A A

Background: The contribution of fructose consumption in Western diets to overweight and obesity in populations remains uncertain.

Purpose: To review the effects of fructose on body weight in controlled feeding trials.

Data Sources: MEDLINE, EMBASE, CINAHL, and the Cochrane Library (through 18 November 2011).

Study Selection: At least 3 reviewers identified controlled feeding trials lasting 7 or more days that compared the effect on body weight of free fructose and nonfructose carbohydrate in diets providing similar calories (isocaloric trials) or of diets supplemented with free fructose to provide excess energy and usual or control diets (hypercaloric trials). Trials evaluating high-fructose corn syrup (42% to 55% free fructose) were excluded.

Data Extraction: The reviewers independently reviewed and extracted relevant data; disagreements were reconciled by consensus. The Heyland Methodological Quality Score was used to assess study quality.

Data Synthesis: Thirty-one isocaloric trials (637 participants) and 10 hypercaloric trials (119 participants) were included; studies tended to be small (<15 participants), short (<12 weeks), and of low quality. Fructose had no overall effect on body weight in isocaloric trials (mean difference, −0.14 kg [95% CI, −0.37 to 0.10 kg] for fructose compared with nonfructose carbohydrate). High doses of fructose in hypercaloric trials (+104 to 250 g/d, +18% to 97% of total daily energy intake) lead to significant increases in weight (mean difference, 0.53 kg [CI, 0.26 to 0.79 kg] with fructose).

Limitations: Most trials had methodological limitations and were of poor quality. The weight-increasing effect of fructose in hypercaloric trials may have been attributable to excess energy rather than fructose itself.

Conclusion: Fructose does not seem to cause weight gain when it is substituted for other carbohydrates in diets providing similar calories. Free fructose at high doses that provided excess calories modestly increased body weight, an effect that may be due to the extra calories rather than the fructose.

Primary Funding Source: Canadian Institutes of Health Research. (ClinicalTrials.gov registration number: NCT01363791)

Figures

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Figure 1. Summary of evidence search and selection.

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Figure 2. Forest plots of isocaloric feeding trials investigating the effect of isocaloric exchange of fructose for carbohydrate on body weight in diabetic, overweight/obese, and normal-weight people.

Four pooled effect estimates (diamonds) are shown: one each for trials in diabetes, overweight/obesity, normal weight, and their combination (total). Paired analyses were applied to all crossover trials (27). Data are expressed as weighted mean differences with 95% CIs, using generic inverse-variance random-effects models. Interstudy heterogeneity was tested by using the Cochran Q statistic (chi-square) at a significance level of P < 0.10. Any CHO = any carbohydrate comparator; HC = high-carbohydrate diet; HD = high dose; LC = low-carbohydrate diet; LD = low dose; T1= trial 1; T2 = trial 2.

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Appendix Figure 1. Subgroup analyses in the isocaloric feeding trials investigating the effect of isocaloric exchange of fructose for carbohydrate on body weight in diabetes, overweight/obese, and normal weight.

Point estimates for each subgroup level (diamonds) are the pooled effect estimates. The dashed line represents the pooled effect estimate for the overall (total) analysis. The residual I2 value indicates the interstudy heterogeneity unexplained by the subgroup. Pairwise between-subgroup mean differences (95% CIs) for comparators were as follows: 0.17 kg (−0.25 to 0.59 kg) (1 vs. 2) to 0.51 kg (−0.08 to 1.11 kg) (1 vs. 3) to 0.44 kg (−0.75 to 1.63 kg) (1 vs. 4) to −0.23 kg (−1.57 to 1.11 kg) (1 vs. 5) to −0.42 kg (−1.57 to 0.73 kg) (1 vs. 6) to 0.34 kg (−0.27 to 0.95 kg) (2 vs. 3) to 0.27 kg (−0.93 to 1.46 kg) (2 vs. 4) to −0.40 kg (−1.75 to 0.95 kg) (2 vs. 5) to −0.59 kg (−1.75 to 0.57 kg) (2 vs. 6) to −0.08 kg (−1.34 to 1.19 kg) (3 vs. 4) to −0.75 kg (−2.16 to 0.67 kg) (3 vs. 5) to −0.93 kg (−2.17 to 0.30 kg) (3 vs. 6) to −0.67 kg (−2.42 to 1.08 kg) (4 vs. 5) to −0.86 kg (−2.45 to 0.75 kg) (4 vs. 6) to and −0.19 kg (−1.91 to 1.53 kg) (5 vs. 6). Any CHO = any carbohydrate comparator; BW = body weight; HFCS = high-fructose corn syrup; MQS = Heyland Methodological Quality Score.

* Statistically significant pairwise subgroup effect modification by meta-regression analyses (P < 0.05).

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Figure 3. Forest plots of hypercaloric feeding trials investigating the effect of a control diet supplemented with 18% to 97% (104 to 250 g/d) excess energy from fructose on body weight in overweight/obese and normal-weight people.

Three pooled effect estimates (diamonds) are shown: one each for trials in overweight/obesity, normal weight, and their combination (total). Paired analyses were applied to all crossover trials (27). Data are expressed as weighted mean differences with 95% CIs, using generic inverse-variance random-effects models. Interstudy heterogeneity was tested by using the Cochran Q statistic (chi-square) at a significance level of P < 0.10. N = normal; ODM2 = offspring of persons with type 2 diabetes mellitus.

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Appendix Figure 2. Subgroup analyses in the hypercaloric feeding trials investigating the effect of a control diet supplemented with 18% to 97% excess energy from fructose on body weight in overweight/obese and normal-weight people.

No subgroup analysis was done by comparator because all trials used diet alone. Point estimates for each subgroup level (diamonds) are the pooled effect estimates. The dashed line represents the pooled effect estimate for the overall (total) analysis. The residual I2 value indicates the interstudy heterogeneity unexplained by the subgroup. Significant subgroup effect modification was assessed by meta-regression analyses (P < 0.05). Any CHO = any carbohydrate comparator; BW = body weight; E = energy; MQS = Heyland Methodological Quality Score.

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Appendix Figure 3. Funnel plots for the effect of fructose on body weight in the isocaloric and hypercaloric feeding trials.

The solid line represents the pooled effect estimate expressed as the weighted mean difference for each analysis. The fitted line corresponds to the best-fit regression of the standard normal deviate of the fructose effect estimate against its precision (Egger test). Dashed lines represent pseudo-95% confidence limits.

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Overweight, and metabolic disorders: need for more clinical trials before blaming (or not) fructose
Posted on February 21, 2012
Luc, Tappy
Department of Physiology, Faculty of Biology and Medicine, University of Lausanne
Conflict of Interest: None Declared

This meta-analysis elegantly demonstrates that fructose consumption will not lead to body weight gain unless energy intake is in excess of energy expenditure . It thus demonstrates that there is nothing extraordinary about fructose and that the laws of thermodynamics remain valid even when it is present in our diet. This apparently trivial observation is nonetheless relevant, given recent statements proposing that fructose is a major cause for metabolic disorders, and calling for immediate litigation to limit fructose intake (1). Such statements stand on several reports showing that high fructose intake causes adverse metabolic effects in animal models and in humans (2), on epidemiological studies showing a relationship between the consumption of caloric sweeteners and metabolic diseases (3), and on basic research reports having identified a variety of mechanisms by which fructose can impair insulin's actions (2). Although the meta-analysis by Sievenpiper et al usefully recalls that fructose per se will not increase body weight irrespective of energy balance, there remain other, important issues which need to be addressed before concluding that it is safe: 1)

The preponderance of evidence still strongly supports a deleterious effect of excessive fructose intake on health
Posted on February 27, 2012
Richard J, Johnson, Chief, Division of Renal Diseases and Hypertension, Miguel A Lanaspa, Carlos Roncal-Jimenez and Laura G Sanchez-Lozada
University of Colorado, Denver
Conflict of Interest: None Declared

The paper by Sievenpiper has the great potential for being misinterpreted to mean that excessive intake of fructose is safe and does not promote long-term weight gain, as such should be interpreted with great caution. For example, one would not expect to see any difference in weight gain for any food if both control and treatment contain the same number of calories. The way fructose increases weight gain is by altering appetite, such that it stimulates increased food intake, by inducing leptin resistance or by direct effects on the brain (1-2). If food intake is forcefully kept equal, however, then how can one expect any difference in weight gain between groups? On the other hand, the hypercaloric studies analyzed in this meta-analysis are flawed, as the median duration of the studies were only 1.5 weeks. How can anyone expect the effects of fructose on weight to manifest in such a short time? The problem is that obesity does not occur overnight, but takes years (3).

One must also consider the metabolic effects of fructose and effects on body composition rather than on body weight. Thus, fructose, and not glucose, stimulates visceral fat accumulation, insulin resistance, with a greater increase in postprandial triglyceridemia and drives nonalcoholic fatty liver disease (4) . We have shown that these types of changes can be induced in animals with fructose or sucrose in the setting where caloric intake is kept equal (4). The paper by Sievenpiper and coworkers unfortunately only addresses weight gain, and hence misses this key aspect about the adverse metabolic effects of fructose. Moreover, this meta- analysis excluded studies in which fructose was administered as HFCS or sucrose, both the largest contributors to added sugar intake (5).

The other aspect of fructose is that not all sources of fructose are the same, and not all people respond the same way to fructose (4). Fructose in fruits tends to be safer because of all of the additional nutrients and antioxidants in fresh (not overripe) fruit. Fructose in sucrose and HFCS is much less safe, and the glucose present in these sugars can accelerate fructose absorption. Likewise, the response to fructose in young healthy people is much less than in older obese subjects. Hence, pooling the studies that contain diabetics, obese, old and young, as well as subjects received fructose in different ways carries the great risk for diluting out any real findings.

Richard J Johnson, M.D. , F.A.C.P(1)

Miguel A Lanaspa, PhD(1)

Carlos Roncal-Jimenez(1)

Laura G Sanchez-Lozada, PhD(2)

From the (1)Division of Renal Diseases and Hypertension, University of Colorado, Denver, and (2) Lab of Renal Physiopathology and Dept of Nephrology, INC Ignacio Chavez, Mexico City, Mexico

References

1.Shapiro A, Mu W, Roncal C, Cheng KY, Johnson RJ, Scarpace PJ. Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding. Am J Physiol Regul Integr Comp Physiol. 2008;295(5):R1370-5.

2.Cha SH, Wolfgang M, Tokutake Y, Chohnan S, Lane MD. Differential effects of central fructose and glucose on hypothalamic malonyl-CoA and food intake. Proc Natl Acad Sci U S A. 2008;105(44):16871-5.

3.Hill JO, Peters JC, Wyatt HR. Using the energy gap to address obesity: A commentary. J Am Diet Assoc. 2009;109:1848-1853.

4.Johnson RJ, Perez-Pozo SE, Sautin YY, et al. Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes? Endocr Rev. 2009;30(1):96-116.

5.Malik VS, Popkin BM, Bray GA, Despres JP, Willett WC, Hu FB. Sugar- sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis. Diabetes Care. 2010;33(11):2477-83.

Conflict of Interest:

RJJ has a patent application on inhibition of fructokinase as a mechanism to treat sugar craving. RJJ also has a lay book, The Sugar Fix: The High-Fructose Fallout That Is Making You Fat and Sick (Rodale and Simon and Schuster, 2008

Response to Johnson et al.
Posted on March 30, 2012
John L, Sievenpiper, MD, PhD, Resident Physician and Adjunct Research Fellow, Russel J. de Souza, ScD, RD, David J.A. Jenkins, MD, PhD, DSc
Departments of Pathology and Molecular Medicine and Clinical Epidemiology and Biostatistics, Faculty
Conflict of Interest: None Declared

We thank Johnson and colleagues for their comments.

Their concern was that people may infer from our data that fructose intake does not promote weight gain. On the contrary, in hypercaloric trials, extreme fructose doses providing excess energy did promote weight gain, despite the short follow-up. Energy, however, appeared to be a more important factor than substrate. The weight gain was similar to that predicted from the excess energy alone. We also found no effect on body weight under the same conditions of excess-energy but where the comparisons were isocalorically matched. The level of energy control was unlikely to play a role in these particular comparisons, as the background diets were largely ad libitum. Even in the isocaloric trials which provided a neutral energy balance, a new subgroup analysis did not reveal a weight-increasing effect of fructose in trials with less strict control of energy (data not shown), a situation where the ability of fructose to stimulate appetite would have been expected to manifest. Appetite effects, however, may be important.

We acknowledge that we did not consider fructose effects beyond body weight. Although fructose increases visceral fat, insulin resistance, triglycerides, blood pressure (BP), uric acid, and nonalcoholic fatty liver in animal models, the experience in humans has been different. We and others have conducted a series of systematic reviews and meta-analyses of controlled feeding trials of the effect of fructose on related endpoints. We found that fructose does not increase lipids [1], BP [2], or uric acid [3] and even improves glycemic control in isocaloric trials [4]. There is, however, a signal for harm under certain conditions. High doses of fructose in excess of the average U.S. intake increase fasting and postprandial triglycerides [1,5]. Hypercaloric fructose also increases uric acid [3].

Differential effects in relation to disease status, type of fructose- containing sugar, and age remain important considerations. We did stratify our primary analyses by categories of diabetes, overweight/obese, and normal weight. The absence of a body weight increasing-effect in the isocaloric trials held across all strata except for overweight/obese, where there was a statistically significant decrease in body weight. We also showed that fructose behaved no differently than high-fructose corn syrup or sucrose in subgroup analyses. A new subgroup analysis revealed no effect modification by age (data not shown).

To address the remaining uncertainties in the data, larger, longer, higher quality trials with clinically important endpoints are needed.

REFERENCES

1. Sievenpiper JL, Carleton AJ, Chatha S, Jiang HY, de Souza RJ, Beyene J, Kendall CW, Jenkins DJ. 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. 2009;32:1930-7

2. Ha V, Sievenpiper JL, de Souza RJ, Chiavaroli L, Wang DD, Cozma AI, Mirrahimi A, Yu ME, Carleton AJ, DiBuono M, Jenkins AL, Leiter LA, Wolever TWS, Beyene J, Kendall CWC, Jenkins DJA. E Effect of Fructose on Blood Pressure: A Meta-Analysis of Controlled Feeding Trials. Hypertension 2012;59:787-95.

3. Wang DD, Sievenpiper JL, de Souza RJ, Chiavaroli L, Ha V, Cozma AI, Mirrahimi A, Yu ME, Carleton AJ, DiBuono M, Jenkins AL, Leiter LA, Wolever TWS, Beyene J, Kendall CWC, Jenkins DJA. Effect of Fructose on Uric Acid: A Meta-Analysis of Controlled Feeding Trials. J Nutr. 2012 Mar 28. [Epub ahead of print]

4. Cozma AI, Sievenpiper JL, de Souza RJ, Chiavaroli L, Ha V, Wang DD, Mirrahimi A, Yu ME, Carleton AJ, DiBuono M, Jenkins AL, Leiter LA, Wolever TWS, Beyene J, Kendall CWC, Jenkins DJA. Effect of Fructose on Glycemic control in Diabetes: A Meta-Analysis of Controlled Feeding Trials, Diabetes Care, in press.

5. Livesey G, Taylor R. Fructose consumption and consequences for glycation, plasma triacylglycerol, and body weight: meta-analyses and meta -regression modelsof intervention studies. Am J Clin Nutr. 2008;88:1419- 37.

Conflict of Interest:

J.L.S. has received consultant fees, travel funding, honoraria, or research support from the Canadian Institutes of Health Research (CIHR), Calorie Control Council, The Coca-Cola Company, Archer Daniels Midland, International Life Sciences Institute (ILSI) North America and Brazil, Abbott Laboratories, and Pulse Canada. R.J.D. is funded by a CIHR Postdoctoral Fellowship Award and has received research support from the CIHR, Calorie Control Council, and The Coca-Cola Company. D.J.A.J. is funded by the Government of Canada through the Canada Research Chair Endowment. D.J.A.J. has received consultant fees, honoraria, travel funding, or research support from or served on the scientific advisory board for the CIHR, the Canadian Foundation for Innovation (CFI), Ontario Research Fund (ORF), and Advanced Foods and Material Network (AFMNet), Calorie Control Council, The Coca Cola Company, Barilla, Solae, Unilever, Hain Celestial, Loblaws Supermarkets, Inc., Sanitarium Company, Herbalife International, Pacific Health Laboratories, Inc., Metagenics/MetaProteomics, Bayer Consumer Care, Oldways Preservation Trust, The International Tree Nut Council Nutrition Research & Education, The Peanut Institute, Procter and Gamble Technical Centre Limited, Griffin Hospital for the development of the NuVal System, Soy Advisory Board of Dean Foods, Alpro Soy Foundation, Nutritional Fundamentals for Health, Pacific Health Laboratories, Kellogg's, Quaker Oats, The Coca-Cola Sugar Advisory Board, Pepsi Company, Agrifoods and Agriculture Canada (AAFC), Canadian Agriculture Policy Institute (CAPI), The Almond Board of California, The California Strawberry Commission, Orafti, the Canola and Flax Councils of Canada, Pulse Canada, the Saskatchewan Pulse Growers, and Abbott Laboratories. D.J.A.J.'s spouse is a Vice-President and Director of Research at Glycemic Index Laboratories.

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