Who knew dear old sugar was this controversial. :shrug:
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J. S White
No unique role for fructose sweeteners in obesity or cardiorenal disease
Am. J. Clinical Nutrition, April 1, 2008; 87(4): 1062 - 1063.
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I wonder if this is the article that has been cited?
Anyway, for anyone interested in this topic, the entire article looks to be free at this link, plus, links to more updated reviews.
http://www.ajcn.org/cgi/content/full/76/5/911American Journal of Clinical Nutrition, Vol. 76, No. 5, 911-922, November 2002
© 2002 American Society for Clinical Nutrition
Special Article
Fructose, weight gain, and the insulin resistance syndrome1,2,3
Sharon S Elliott, Nancy L Keim, Judith S Stern, Karen Teff and Peter J Havel
1 From the Department of Nutrition, University of California, Davis (SSE, JSS, and PJH); the US Department of Agriculture Western Human Nutrition Research Center, Davis, CA (NLK); and the Monell Chemical Senses Institute and the University of Pennsylvania, Philadelphia (KT).
2 Supported by the NIH (DK-50129), the University of California Davis Clinical Nutrition Research Unit (DK-35747), the American Diabetes Association, and the US Department of Agriculture.
Conclusion:
>>A considerable amount of research needs to be done to more completely appreciate the effect of fructose in the American diet. In the meantime, a prudent approach concerning recommendations for dietary fructose would consider the following 2 points. First, added fructose (in the forms of sucrose and HFCS) does not appear to be the optimal choice as a source of carbohydrate in the diet. Small amounts of added fructose are probably benign and may even have some favorable metabolic effects. However, on the basis of the available data regarding the endocrine and metabolic effects of consuming large quantities of fructose and the potential to exacerbate components of the insulin resistance syndrome, it is preferable to primarily consume dietary carbohydrates in the form of glucose (free glucose and starch). This may be particularly important in subjects with existing hyperlipidemia or insulin resistance who could be more susceptible to the adverse metabolic effects of fructose. Second, the concerns raised about the addition of fructose to the diet as sucrose or HFCS should not be extended to naturally occurring fructose from fruit and vegetables. The consumption of fruit and vegetables should continue to be encouraged because of the resulting increased intake of fiber, micronutrients, and antioxidants. In addition, the intake of naturally occurring fructose is low, 15 g/d, and is unlikely to contribute significantly to the untoward metabolic consequences associated with the consumption of large amounts of fructose. Certainly, it would be desirable to have more precise data regarding the current amounts and patterns of fructose consumption. Unfortunately, to our knowledge, no accurate data on fructose consumption more recent than 1977–1978 are available. Although fructose disappearance data show a clear-cut pattern toward increased consumption of fructose, more definitive measurements of intake in different populations require large-scale surveys. In addition, it is important to gain a better understanding of the effects and mechanisms of fructose consumption on metabolic indexes such as insulin sensitivity and lipid metabolism, including triacylglycerol production.<<
Here are newer ones:
American Journal of Clinical Nutrition, Vol. 86, No. 4, 899-906, October 2007
© 2007 American Society for Nutrition
REVIEW ARTICLE
Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease1,2,3
Richard J Johnson, Mark S Segal, Yuri Sautin, Takahiko Nakagawa, Daniel I Feig, Duk-Hee Kang, Michael S Gersch, Steven Benner and Laura G Sánchez-Lozada
1 From the Division of Nephrology and Department of Medicine, University of Florida, Gainesville, FL (RJJ, MSS, YS, TN, and MSG); the Division of Pediatric Nephrology, Texas Children's Hospital, Baylor College of Medicine, Houston, TX (DIF); the Division of Nephrology, Ewha Woman's University College of Medicine, Seoul, Korea (D-HK); the Foundation for Applied Molecular Evolution, Gainesville, FL (SB); and the Instituto Nacional de Cardiologia Ignacio Chavez, Mexico City, Mexico (LGS-L)
Currently, we are experiencing an epidemic of cardiorenal disease characterized by increasing rates of obesity, hypertension, the metabolic syndrome, type 2 diabetes, and kidney disease. Whereas excessive caloric intake and physical inactivity are likely important factors driving the obesity epidemic, it is important to consider additional mechanisms. We revisit an old hypothesis that sugar, particularly excessive fructose intake, has a critical role in the epidemic of cardiorenal disease. We also present evidence that the unique ability of fructose to induce an increase in uric acid may be a major mechanism by which fructose can cause cardiorenal disease. Finally, we suggest that high intakes of fructose in African Americans may explain their greater predisposition to develop cardiorenal disease, and we provide a list of testable predictions to evaluate this hypothesis
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Am J Clin Nutr 89: 1037-1042, 2009. First published February 11, 2009; doi:10.3945/ajcn.2008.27140
American Journal of Clinical Nutrition, doi:10.3945/ajcn.2008.27140
Vol. 89, No. 4, 1037-1042, April 2009
This Article
ORIGINAL RESEARCH COMMUNICATION
Sweetened beverage consumption and risk of coronary heart disease in women
Teresa T Fung1,2,3,4, Vasanti Malik1,2,3,4, Kathryn M Rexrode1,2,3,4, JoAnn E Manson1,2,3,4, Walter C Willett1,2,3,4 and Frank B Hu1,2,3,4
1 From Simmons College, Boston, MA (TTF); the Department of Nutrition, Harvard School of Public Health, Boston, MA (TTF, VM, WCW, and FBH); the Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (KMR, JEM, WCW, and FBH); the Division of Preventive Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (JEM); and the Department of Epidemiology, Harvard School of Public Health, Boston, MA (JEM, WCW and FBH).
2 Partial results of this analysis were presented as a poster at the 2007 American Heart Association Scientific Sessions.
3 Supported by NIH grants HL60712, HL34594, DK58845, and CA87969.
4 Address reprint requests and correspondence to TT Fung, Department of Nutrition, Simmons College, 300 The Fenway, Boston, MA 02115.
Background: Previous studies have linked full-calorie sugar-sweetened beverages (SSBs) with greater weight gain and an increased risk of type 2 diabetes.
Objective: We prospectively examined the association between consumption of SSBs and the risk of coronary heart disease (CHD) in women.
Design: Women (n = 88,520) from the Nurses' Health Study aged 34–59 y, without previously diagnosed coronary heart disease (CHD), stroke, or diabetes in 1980, were followed from 1980 to 2004. Consumption of SSBs was derived from 7 repeated food-frequency questionnaires administered between 1980 and 2002. Relative risks (RRs) for CHD were calculated by using Cox proportional hazards models and adjusted for known cardiovascular disease risk factors.
Results: During 24 y of follow-up, we ascertained 3105 incident cases of CHD (nonfatal myocardial infarction and fatal CHD). After standard and dietary risk factors were adjusted for, the RRs (and 95% CIs) of CHD according to categories of cumulative average of SSB consumption (<1/mo, 1–4/mo, 2–6/wk, 1/d, and 2 servings/d) were 1.0, 0.96 (0.87, 1.06), 1.04 (0.95, 1.14), 1.23 (1.06, 1.43), and 1.35 (1.07, 1.69) (P for trend < 0.001). Additional adjustment for body mass index, energy intake, and incident diabetes attenuated the associations, but they remained significant. Artificially sweetened beverages were not associated with CHD.
Conclusion: Regular consumption of SSBs is associated with a higher risk of CHD in women, even after other unhealthful lifestyle or dietary factors are accounted for.