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THE SCIENCE OF OBESITY Author’s reply to Cottrell Gary Taubes co-founder Nutrition Science Initiative, San Diego, California, USA Cottrell cites a World Sugar Research Organisation report claiming that world consumption of caloric sweeteners (such as sucrose and high fructose corn syrup) has been static for decades. 1 These data are difficult to reconcile with International Sugar Organisation reports that world sugar consumption rose between 2001 and 2011—by an average of 2.2% yearly, nearly twice the population growth rate. 2 Such trends can neither confirm nor refute the hormonal-regulatory defect hypothesis or sugar’s role in obesity. Cottrell assumes incorrectly that caloric sweetener consumption must increase to explain the obesity epidemic. If a threshold effect is at work, then prevalence can increase if sugar consumption is above that threshold. This is another argument for well controlled experiments to establish causality. Cottrell claims that insulin concentrations remain low in healthy people, but the study he cites reports a long term deterioration of insulin sensitivity in this population. 3 The accompanying editorial suggests that it is “the effect of progressive inactivity and middle age spread.” It could also be the effect of a dietary trigger of “progressive inactivity and middle age spread.” 4 Such observations can’t differentiate. Cottrell suggests that the hormonal-regulatory defect hypothesis is incorrect because de novo lipogenesis is low during carbohydrate overfeeding, a common misconception. As the reference Cottrell cites says, body fat stores can be increased “not by conversion of the carbohydrate to fat. Instead, the oxidation of dietary fat [is] suppressed and fat storage thereby increased.” 5 Despite our disagreements, it’s crucial to remember that this discussion is about real people—their health and quality of life. The past 50 years has shown us that we need new information and better science because the conventional wisdom isn’t working. Our friends, families, and neighbours have a spectrum of metabolic disorders; it is incumbent on us to challenge conventional thinking when it is clearly failing. Competing interests: None declared. Full response at www.bmj.com/content/346/bmj.f1050/rr/645317. 1 Cottrell RC. Essay was based on incorrect premises and an unproved assumption. BMJ 2013;346:f3120. 2 International Sugar Organisation. Quarterly Market Outlook. 2011. www.sugaronline.com/ Samples/ISO_QMO.pdf. 3 Tabak AG, Jokela M, Akbaraly TN, Brunner EJ, Kivimäki M, Witte DR. Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study. Lancet 2009;373:2215-21. 4 Matthews DR, Levy JC. Impending type 2 diabetes. Lancet 2009;373:2178-9. 5 Hellerstein MK. No common energy currency: de novo lipogenesis as the road less travelled. Am J Clin Nutr 2001;74:707-8. Cite this as: BMJ 2013;346:f3125 © BMJ Publishing Group Ltd 2013 [email protected] For personal use only: See rights and reprints http://www.bmj.com/permissions Subscribe: http://www.bmj.com/subscribe BMJ 2013;346:f3125 doi: 10.1136/bmj.f3125 (Published 22 May 2013) Page 1 of 1 Letters LETTERS

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THE SCIENCE OF OBESITY

Author’s reply to CottrellGary Taubes co-founder

Nutrition Science Initiative, San Diego, California, USA

Cottrell cites a World Sugar Research Organisation reportclaiming that world consumption of caloric sweeteners (suchas sucrose and high fructose corn syrup) has been static fordecades.1 These data are difficult to reconcile with InternationalSugar Organisation reports that world sugar consumption rosebetween 2001 and 2011—by an average of 2.2% yearly, nearlytwice the population growth rate.2

Such trends can neither confirm nor refute thehormonal-regulatory defect hypothesis or sugar’s role in obesity.Cottrell assumes incorrectly that caloric sweetener consumptionmust increase to explain the obesity epidemic. If a thresholdeffect is at work, then prevalence can increase if sugarconsumption is above that threshold. This is another argumentfor well controlled experiments to establish causality.Cottrell claims that insulin concentrations remain low in healthypeople, but the study he cites reports a long term deteriorationof insulin sensitivity in this population.3 The accompanyingeditorial suggests that it is “the effect of progressive inactivityand middle age spread.” It could also be the effect of a dietarytrigger of “progressive inactivity and middle age spread.”4 Suchobservations can’t differentiate.Cottrell suggests that the hormonal-regulatory defect hypothesisis incorrect because de novo lipogenesis is low duringcarbohydrate overfeeding, a common misconception. As the

reference Cottrell cites says, body fat stores can be increased“not by conversion of the carbohydrate to fat. Instead, theoxidation of dietary fat [is] suppressed and fat storage therebyincreased.”5

Despite our disagreements, it’s crucial to remember that thisdiscussion is about real people—their health and quality of life.The past 50 years has shown us that we need new informationand better science because the conventional wisdom isn’tworking. Our friends, families, and neighbours have a spectrumof metabolic disorders; it is incumbent on us to challengeconventional thinking when it is clearly failing.

Competing interests: None declared.Full response at www.bmj.com/content/346/bmj.f1050/rr/645317.

1 Cottrell RC. Essay was based on incorrect premises and an unproved assumption. BMJ2013;346:f3120.

2 International Sugar Organisation. Quarterly Market Outlook. 2011. www.sugaronline.com/Samples/ISO_QMO.pdf.

3 Tabak AG, Jokela M, Akbaraly TN, Brunner EJ, Kivimäki M, Witte DR. Trajectories ofglycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes:an analysis from the Whitehall II study. Lancet 2009;373:2215-21.

4 Matthews DR, Levy JC. Impending type 2 diabetes. Lancet 2009;373:2178-9.5 Hellerstein MK. No common energy currency: de novo lipogenesis as the road less

travelled. Am J Clin Nutr 2001;74:707-8.

Cite this as: BMJ 2013;346:f3125© BMJ Publishing Group Ltd 2013

[email protected]

For personal use only: See rights and reprints http://www.bmj.com/permissions Subscribe: http://www.bmj.com/subscribe

BMJ 2013;346:f3125 doi: 10.1136/bmj.f3125 (Published 22 May 2013) Page 1 of 1

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