Calorie Control Council Response to Cox et al

Circulating Concentrations of Monocyte Chemoattractant Protein-1, Plasminogen Activator Inhibitor-1, and Soluble Leukocyte Adhesion Molecule-1 in Overweight/Obese Men and Women Consuming Fructose- or Glucose-Sweetened Beverages for 10 Weeks

Cox CL, Stanhope KL, Schwarz JM, Graham JL, Hatcher B, Griffen SC, Bremer AA, Berglund L, McGahan JP, Keim NL, Havel PJ J Clin Endocrinol Metab. 201

A recent paper by Cox et al. 1 reported that older, overweight/obese adults who consumed fructosesweetened beverages for 10 weeks at 25% of total energy showed increased levels of monocyte chemoattractant protein-1 (MCP-1), plasminogen activator inhibitor-1 (PAI-1) and E-selectin compared with those consuming glucose-sweetened control beverages. The authors concluded fructose may contribute to the development of metabolic syndrome through effects on proinflammatory and prothrombotic mediators. Their conclusion was weakened by an experimental design far removed from typical human sugars consumption patterns and a failure to demonstrate that observed differences between experimental and control subjects were clinically significant.

The experimental design did not reflect real-world sweetener consumption patterns. Fructose and glucose are always consumed together, whether from natural sources like fruits and vegetables, or from added sources like sucrose, high fructose corn syrup, honey and fruit juice concentrates. It would be rare for an individual to consume them separately, as they were tested in this study. And fructose exposure (25% of E) was very high, far exceeding even the 95 th percentile fructose intake estimate (18% of E) for the US population reported by Marriott et al.

Measured differences between sweetener variables MCP-1, PAI-1 and E-selectin reported in Table 1 may have been statistically significant, but baseline and 10-wk values fell well within the ranges reported for apparently normal subjects by suppliers of analytical test kits used in this study. 3-5 Substantial baseline variability seems a more likely cause of the reported disparity than inherent differences in the sugars themselves.

The conclusion by Cox et al. that fructose may contribute to the development of metabolic syndrome through effects on proinflammatory and prothrombotic mediators was not convincing due to their use of an exaggerated experimental design and failure to demonstrate clinical significance.

References
1. Cox CL, Stanhope KL, Schwarz JM, Graham JL, Hatcher B, Griffen SC, Bremer AA, Berglund L, McGahan JP, Keim NL, Havel PJ 2011 Circulating Concentrations of Monocyte Chemoattractant Protein-1, Plasminogen Activator Inhibitor-1, and Soluble Leukocyte Adhesion Molecule-1 in Overweight/Obese Men and Women Consuming Fructose- or Glucose-Sweetened Beverages for 10 Weeks. J Clin Endocrinol Metab
2. Marriott BP, Cole N, Lee E 2009 National estimates of dietary fructose intake increased from 1977 to 2004 in the United States. J Nutr 139:1228S-1235S
3. R&D Systems 2011 Quantikine Human CCL2/MCP-1 ELISA Immunoassay.http://wwwrndsystemscom//product_resultsaspx?c=56&s=13&o=AND&a=0&cj=-1&k=mcp-1 Accessed: 01 November 2011. R&D Systems, Minneapolis, MN
4. R&D Systems 2011 Quantikine Human Serpin E1/PAI-1 ELISA Immunoassay.http://wwwrndsystemscom//product_resultsaspx?c=56&s=13&o=AND&a=0&cj=-1&k=PAI-1 Accessed: 01 November 2011. R&D Systems, Minneapolis, MN
5. eBioscience 2011 Human sE-selectin Instant ELISA.http://www.ebioscience.com/human-seselectin-ce-instant-elisa-kithtm Accessed: 01 November 2011. Bender MedSystems/eBioscience, San Diego, C

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