SugarAssociationInc.txt Dear World Health Organization:

The Association, Inc. has prepared comments in response to t he WHO call for comment on the Draft Report entitled "Diet, Nutrit ion and the Prevention of Chronic Diseases." A copy of the commen t document is attached for WHO review and consideration.

The following summary addresses the eight items of information req uested to accompany submitted comments.

Information items 1 - 3 and 8: Provided in the signature file Information items 4 - 6: Available at www.sugar.org/wwa/ Information item 7: Funding is provided solely by the Associatio n members listed at the above URL. For your convenience, The Sugar Association mission statement has been abstracted from the above URL.

The Sugar Association believes that pleasant tasting nutritious food are important in maintaining a healthful diet and a high qual ity of life. We seek to create and maintain an understanding that the benefits of sugar contribute to the flavor and quality of whol esome foods. The Association also seeks to increase appreciation o f the non-food value of sugar. In pursuit of our mission, The Suga r Association is committed to integrity and sound scientific princ iples in all its programs

The Sugar Association educates both consumer and professional au diences about pure, natural sugar. Reliance on sound science has p ositioned the Association as a leader in communicating accurate in formation about the nutritional and functional uses of sugar to co nsumers, professionals and the media.

Thank you for the opportunity to submit the attached commentary.

Respectfully yours,

Charles W. Baker, PhD Vice President Scientific Affairs The Sugar Association, Inc. 1101 15th Street, NW Suite 600 Washington DC 20005-5079

Telephone: 202.785.1122 Extension 12 Facsimile: 202.785.5019 E-Mail: [email protected]

Be Sure It's Sugar: The Natural Sweetener... 15 Calories Per Teaspoon!

Page 1 Draft Report of the WHO/FAO Joint Consultation “Diet, Nutrition and the Prevention of Chronic Disease”

Commentary by The Sugar Association, Inc.

Introduction

The Sugar Association, Inc. [SAI] thanks the World Health Organization for the opportunity to provide comments on the Draft Report. The SAI commentary is confined to policy proposals contained in the Draft Report and Annex 2 of the Draft Report.

SAI is concerned because the policy proposals specified in the Draft Report24 are beyond the purview of the WHO mission25. Additionally, lack of critical analysis of selected Annex 2 documents24 cited to recommend a population target for the intake of “free ” and discounting the complete body of scientific evidence available when Annex 2 was organized and reviewed are readily apparent. Impartiality and integrity require the unequivocal separation of science and politics.

WHO is not to construe submittal of this Commentary as SAI endorsement of any part of this Draft Report, or any of its annexes, conclusions or recommendations, for which no SAI comments were prepared.

Policy Proposals

The expert panel convened to author this Draft Report presumed that mandatory population nutrient goals are required. This postulate is contrary to the foundational standard of the expert WHO/FAO panel convened to formulate22 food-based dietary goals and strategies. Unilateral espousal of this assumption by the present panel does little more than fuel speculation about apparent political bias influencing the wide range of policy proposals contained in the Draft Report. Ultimately, WHO motives and not public health become the issue.

No evidence is cited in the Draft Report in support of the sweeping agriculture and trade recommendations. The simplicity of the diverse policy proposals is certification that the expert panel assembled for this Consultation lacks the expertise required to craft practicable proposals. Such one-dimensional policy proposals weaken not only the credibility of the Draft Report and its expert panel but also tarnish the reputation of WHO. For example, the proposed nutrient target for “” should be removed until supportable by critical, unbiased analysis of the complete body of scientific evidence.

Annex 2 – Weight Gain and

1. Scientific consensus on sugar and weight management

The proposal to limit dietary sugars in Table 3 of Annex 2 of the Draft Report contradicts the conclusions published in two high-profile reports of recent expert consultations. The joint FAO/WHO expert consultation on carbohydrates in human nutrition4 concurred, "There is no evidence of a direct involvement of , other sugars and starch in the etiology of lifestyle- related diseases.” The expert panel on obesity, as stated in WHO Technical Report 894, called attention23 to the evidence that the consumption of sugars leads to “… a subsequent suppression of energy intake by an amount roughly equivalent to the amount provided by the sugars."

A meta-analysis1 of dietary intervention studies corroborates the conclusions of these expert reports. Replacing dietary fat with carbohydrate, without intentional restriction of energy intake, is an effective strategy for achieving weight loss. A recent intervention study16 clearly demonstrates that foods containing sugar, even those considered to be ‘high in sugar,’ can be included among the carbohydrate-rich foods consumed as part of weight-maintaining or weight- reducing diets. These data confirm that people wishing to lose weight, or to prevent weight gain, can include sugar and high-sugar foods in their calorie-controlled eating plans. Advice to singularly shun sugar or sugars-containing foods is not supportable by the totality of the scientific evidence.

Finally, a recent literature review was disregarded. This review13 reaffirms the fact that obesity is a multiple-factor condition and occurs when energy intake exceeds energy requirements, emphasizing that “… the evidence does not single out dietary sugar as a cause.” of obesity.

2. Per Cent Fat in the Diet – secular changes in diet and obesity

The authors of Annex 2 assigned the term of “American Paradox” to describe the inconsistency between the apparent decline in the proportion of fat in the diet and the increased prevalence of obesity. Since only a single study8 was cited, it appears that the Annex 2 authors readily believe that the total food supply carbohydrates and energy increases are due solely to sugar and other carbohydrate sweeteners. Since economic supply data were analyzed by Harnack et al8, this assertion by the Annex 2 authors is pure speculation. Economic data simply reflect the quantity of a product available [(inventory + production) – utilization] during a selected period of time. No matter the food or food ingredient, implying economic supply numbers are equal to nutrient intakes is as fictitious as equating gross salary [availability] and take-home pay [intake].

It is also important to recognize that global food losses are substantial. While there are good estimates9 of U.S. caloric sweetener losses, most U.S. food losses simply are not measured. This gap is particularly important for a food like sugar because of its use as both a tabletop sweetener and a key ingredient in many other foods. Until the weight of all food losses is routinely accounted, the amount of sugar actually eaten defies quantification.

Because little significance is attached to food losses, the theory that consumers selectively under-report the amounts of sugar and sugars-sweetened foods they actually eat can be unilaterally advocated. Thus, actual dietary intake data like those of USDA's Continuing Survey of Food Intakes by Individuals [CSFII] are often discounted, if not ignored entirely. According to the 1994 – 1996 CSFII survey,20 total “added sugars” consumption in the U.S. was 80 grams per person per day. Sugar accounts for no more than 37 grams of this 80-gram total. It appears that the Annex 2 authors overlooked the admonition of Harnack et al8 that “food disappearance data are not useful for estimating absolute intake.”

Besides the deception of inferring economic supply numbers equal human intake, there is a second factual error. This error is the incorrect use of the term sugar to represent all caloric sweeteners. Sugar is only one component of the total sweetener supply tabulated in the United States and elsewhere.

The “American Paradox” is partially explained by the fact that, whereas the relative intake of dietary fat [expressed as % of daily energy] has decreased, actual intakes [expressed as g/day]

2 of dietary fat have been increasing in the 1990s. While below that of the 1977 – 1978 [~83 g/day]18 survey period, dietary fat intake has grown between the 1989 – 1991 [~72 g/day]19 and the 1994 – 1996 [~74 g/day]20 periods in the U.S. Over the 20-year 1977 – 1996 period, reported total daily energy has increased by 176 kilocalories.

The “American Paradox” is more ascribable, however, to the pandemic increase in physical inactivity and sedentary lifestyle. Two recent population studies2,14 reached this same inescapable conclusion. Increased physical inactivity far outweighs any positive effects of dietary adjustment.

Energy Balance

The Annex 2 authors begin the final “Introduction” paragraph by acknowledging that “this review on obesity has not covered the energy expenditure side of the energy balance equation in any depth. Physical activity is at least as important as energy intake in the genesis of weight gain and obesity and there are likely to be many interactions between the two sides of the equation in terms of etiology and prevention.”

The dynamic interaction between diet composition and physical inactivity, while similar on the whole, is sufficiently dissimilar to preclude adoption of a diet-only or physical-activity-only approach to reverse obesity. This fact is exemplified by a recent study17 documenting that high- fat diets are more obesogenic than high-carbohydrate diets at similar levels of physical inactivity. An integrated diet – activity paradigm, i.e. energy balance, is a more effective long- term weight maintenance strategy10 than restricting selected dietary components like the “free sugars” advocated by the Annex 2 authors.

If a single approach were to be adopted to prevent weight gain or weight regain, the body of scientific evidence supports21,26,27 increased daily physical activity as the first strategy. Since an exercise approach has been repeatedly shown to preserve11,15 lean tissue mass, a focus on a diet-only strategy like that proposed by the Annex 2 authors provides little public health value.

3. Sugar in drinks

The manner in which the 1999 Harnack et al study7 was cited by the Annex 2 authors underscores the importance of critical analysis. The inference that the “nearly 200 kcal/day” increase is attributable solely to soft drinks consumed by school-aged [omitted in Annex 2] children is based on citing only what was stated in the study abstract. Analyzing the tabulated data7 would have established that there was a concomitant average increase in dietary fat intake equal to 119 kcal/day by this group of children.

The cited Ludwig study12 has obvious weaknesses beyond its observational design and use of recall questionnaires to measure dietary and physical activity habits. Again, critical analysis of the reported information would have exposed flaws and generated material questions.

1. The proportion of beverage types included in the sugars-sweetened drinks category was undefined. The implication that this category was composed entirely of soda is incorrect.

2. Total daily caloric intake increased by 158 kilocalories during the 19-month study period. Sugars-sweetened drink calories increased somewhere between 16 and 33 kcal/day over this same period. Even if the calories contributed by the sugars-sweetened drinks

3 had been totally due to soda, the failure to determine which dietary components were contributing the remaining 125 – 142 kcal/day is glaring.

3. The 11-year old children gained an average of 21.2 pounds during this 19-month period. The maximum amount that can be attributed to sugars-sweetened drinks category accounts for less than one-tenth [5% to 7%] of the average 21.2-pound weight gain.

Providing context to reported effects becomes critical when a study is designed to test the hypothesis that “a change in consumption of a particular food [sugars-sweetened drinks in this case] directly predicts a change in another measurement [BMI in the present case].” Based on the data reported and the statistics presented12 in the cited article, the practical impact of sugars-sweetened drinks on BMI appears to be small.

4. Ludwig et al12 restricted their analysis to the 37 children who became obese during the course of the study, ignoring an almost equal number [35] who were obese at the beginning of the study but not at the end.

It is readily obvious that Ludwig et al failed to account for the majority of the weight gains they observed during the 19-month study period. Such overly simplified conclusions detract from the real issue that this is a matter of energy balance, not a phenomenon unique to sugars-sweetened drinks or any other food.

5. Although critical for an impartial analysis, the amount of total fluid intake was an unreported variable. This confounder is important because of the difference in age between start and end of the 19-month study. Since neither baseline nor end-of-study total beverage intake amounts were reported, the influence of child maturation on fluid intake is undocumented. It would be instructive to know what proportion of total fluid intake was represented by soda at baseline and at the end of the cited study. It is entirely plausible that the reported12 increase in servings [+0.22] of “sugar-sweetened drinks” simply replaced the observed decrease in servings [-0.20] of “fruit juice.”

It is noteworthy that the observational studies cited by the Annex 2 authors in the “Sugar in foods” section were omitted from the “Sugar in drinks” section. The consistent observation that those whose diets are higher in sugars weigh less than those whose diets are lower in sugars3,5 obviates the supposition that the sugars present in soft drinks are uniquely obesogenic. Gibson6 examined this very issue in UK pre-school children and reported that the overall energy density of these diets was inversely related to consumption. Even when soft drink consumption had been excluded from the analysis, the energy density of these diets continued to decrease as dietary sugars content increased.6

The current body of evidence precludes the conclusions on the role of soft drinks and other sweetened beverages reached by the authors of Annex 2. What limited evidence is available indicates3,6,16 that diets higher in sugars are less energy-dense than lower in sugars.

It is noteworthy that the same factual error repeated throughout Annex 2 is readily apparent in the “drinks” section. Scientific rigor requires use of the generic ‘sugars’ when referencing today’s calorie-containing sweetened beverages.

Conclusion

4 The Annex 2 authors unambiguously state24 [paragraph 3 under “sugar in foods”] that "Overall, the mixed results especially amongst the few available trials does not allow a judgment to be made about the sugar content of food and obesity." This recognition of the lack of rigorous evidence contradicts the proposal to limit the intake of “free sugars.” In fact, unbiased analysis of the total body of science provides little-to-no support for the hypothesis that population limits on sucrose and/or other sugars consumption are required to prevent weight gain.

References

1. Astrup A, Grunwald GK, Melanson EL, Saris WHM and Hill JO. The role of low-fat diets in body weight control: a meta-analysis of ad libitum dietary intervention studies. International Journal of Obesity. 24(12):1545-1552, 2000.

2. Astrup A. The role of dietary fat in the prevention and treatment of obesity. Efficacy and safety of low- fat diets. International Journal of Obesity. 25(Suppl 1):S46-S50, 2001.

3. Bolton-Smith C and Woodward M. Dietary composition and fat to sugar ratios in relation to obesity. International Journal of Obesity 18:820-828, 1994.

4. Food and Agriculture Organization. Carbohydrates in human nutrition. Report of a joint FAO/WHO expert consultation, Rome 14-18 April 1997. FAO Food and Nutrition Paper 66. Rome, 1998.

5. Gibney MJ. Epidemiology of obesity in relation to nutrient intake. International Journal of Obesity 19(suppl 5):S1-S3, 1995.

6. Gibson SA. Associations between energy density and macronutrient composition in the diets of pre- school children: sugars versus starch. International Journal of Obesity and Related Metabolic Disorders. 24(5) 633-638, 2000.

7. Harnack L, Stang J and Storey M. Soft drink consumption among US children and adolescents: Nutritional consequences. Journal of the American Dietetic Association 99(4): 436-441, 1999.

8. Harnack LJ, Jeffrey RW and Boutelle KN. Temporal trends in energy intake in the United States: an ecologic perspective. American Journal of Clinical Nutrition 71(6): 1478-1484, 2000.

9. Kantor LS, Lipton K, Manchester A and Oliveira V. Estimating and addressing America’s food losses. Food Review 20(1): 2-12, 1997.

10. Klem ML, Wing RR, McGuire MT, Seagle HM and Hill JO. A descriptive study of individuals successful at long-term maintenance of substantial weight loss. American Journal of Clinical Nutrition 66(2): 239-246, 1997.

11. Lee CD, Blair SN and Jackson AS. Cardiorespiratory fitness, body composition, and all-cause and cardiovascular disease mortality in men. American Journal of Clinical Nutrition 69(3): 373-380, 1999.

12. Ludwig DS, Peterson KE and Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. The Lancet 357(9255): 505-508, 2001.

13. Mardis AL. Current knowledge of the health effects of sugar intake. Family Economics and Nutrition Review 13(1): 87-91, 2001.

14. Prentice AM and Jebb SA. Obesity in Britain: gluttony or sloth? British Medical Journal 311:1568- 1569, 1995.

5 15. Prentice AM and Jebb SA. Beyond body mass index. Obesity Reviews 2: 141-147, 2001.

16. Saris WHM, Astrup A, Prentice AM, Zunft HJF, Formiguera X, Verboeket-van de Venne WPHG, Raben A, Poppitt SD, Seppelt B, Johnston S, Vasilaras TH and Keogh GF. Randomized controlled trial of changes in dietary carbohydrate/fat ratio and simple vs complex carbohydrates on body weight and blood lipids: the CARMEN study. International Journal of Obesity 24(10): 1310-1318, 2000.

17. Shepard TY, Weil KM, Sharp TA, Grunwald GK, Bell ML, Hill JO and Eckel RH. Occasional physical inactivity combined with a high-fat diet may be important in the development and maintenance of obesity in human subjects. American Journal of Clinical Nutrition 73(4): 703-708, 2001.

18. U.S. Department of Agriculture. Human Nutrition Information Service. Nationwide food consumption survey 1977-78. Report No. I-3. July 1985.

19. U.S. Department of Agriculture. Agricultural Research Service. Food and nutrient intakes by individuals in the United States, 1 Day, 1989-91. National Technical Information Service Accession No. PB-95-272746. September 1995.

20. U.S. Department of Agriculture. Agricultural Research Service. 1994 – 1996 Continuing survey of food intake by individuals and 1994 – 1996 diet and health knowledge survey. Table set 10. December 1999. http://www.barc.usda.gov/bhnrc/foodsurvey/home.htm.

21. Weinsier RL, Hunter GR, Desmond RA, Byrne NM, Zuckerman PA and Darnell BE. Free-living activity energy expenditure in women successful and unsuccessful at maintaining a normal body weight. American Journal of Clinical Nutrition 75(3): 499-504, 2002.

22. World Health Organization. Preparation and use of food-based dietary guidelines. Report of a joint FAO/WHO consultation, Nicosia Cyprus, 1995. WHO Technical Report Series 880. Geneva, 1998.

23. World Health Organization. Obesity: Preventing and managing a global epidemic. Report of a WHO Consultation Geneva, 1999. WHO Technical Report Series 894. Geneva, 2000.

24. World Health Organization. Draft Report of the joint WHO/FAO expert consultation on Diet, Nutrition and the Prevention of Chronic Diseases (Geneva, 28 January – 1 February 2002). http://www.who.int/hpr/nutrition/ExpertConsultationGE.htm.

25. World Health Organization. About WHO – Mission Statement. http://www.who.int/aboutwho/en/ mission.htm.

26. Wyatt HR and Hill JO. Let’s get serious about promoting physical activity. American Journal of Clinical Nutrition 75(3): 449-450, 2002.

27. Yu-Poth S, Zhao G, Etherton T, Naglak M, Jonnalagadda S and Kris-Etherton PM. Effects of the National Cholesterol Education Program’s Step I and Step II dietary intervention programs on cardiovascular disease risk factors: a meta-analysis. American Journal of Clinical Nutrition 69(4): 632- 646, 1999.

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