Calorie Control Council Response to Nothlings et al

Posted by & filed under Uncategorized.

Dietary Glycemic load, added sugars, and carbohydrates as risk factors for pancreatic cancer: the Multiethnic Cohort Study

Nothlings U1,3, Murphy SP1, Wilkens LR1, Henderson BE2, Kolonel LN1. Dietary glycemic load, added sugars, and carbohydrates as risk factors for pancreatic cancer: the Multiethnic Cohort Study. Am J Clin Nutr 2007;86:1495-1501

 

Background
This article is yet another published in AJCN seeking to establish a link between dietary fructose and increased risk for some metabolic perturbation: pancreatic cancer, in this instance. The authors are from the University of Hawaii1 (Honolulu), the University of Southern California2 (Los Angeles) and the German Institute of Human Nutrition Potsdam-Rehbruecke3 (Nuthetal). They are active cancer researchers and appear to be seeking causative factors for pancreatic cancer.

 

Hypothesis
The authors begin with the hypothesis that a high dietary glycemic load (GL) is positively associated with the risk of pancreatic cancer. GL is the product of [the experimentally measured serum glucose response after consumption of a specific food or ingredient (glycemic index, GI)] x [the carbohydrate content of the food or ingredient]. GL is now thought by nutritionists to be a better predictor of serum insulin response than GI alone.

The authors justify their hypothesis by citing previous studies suggesting that glucose metabolism plays a role in the development of pancreatic cancer. In this study, GL and carbohydrate intakes were mathematically derived from the amounts and types of foods consumed by participants as reported in an extensive self-administered questionnaire.

 

Author Conclusions

  1. High sugar intake — fructose intake, specifically — was associated with a greater risk of pancreatic cancer.
    • The purported association between fructose and weight gain is not appropriate, since HFCS has largely supplanted sucrose on a 1-for-1 basis, resulting in no net gain of fructose in the diet relative to other nutrients (9).
    • Pancreatic cancer risk increased with higher intakes of total sugars, fructose and sucrose.
    • The association between fructose and increased pancreatic cancer risk became significant when the highest and lowest fructose consumers were compared.
    • The association between fruit and juice intakes and pancreatic cancer risk was significant.
    • The association between caloric soda intake and pancreatic cancer risk was not significant.
  2. Sucrose (sugar) intake was associated with increased BMI (body mass index) for overweight and obese, but not normal-weight, subjects when the highest and lowest consumers were compared.

Critique

  • It seems rather implausible that fructose, but not added sugars (half fructose), would be associated with increased risk of pancreatic cancer. The solution to this inconsistency may be the unconventional use of terminology by the authors: ‘added sugars’ is here applied to spoonfuls of sugar added to foods, while the term is commonly used in nutrition circles to mean all dietary nutritive sweeteners not intrinsically present in foods and beverages.
  • It seems even more implausible that fruits and juices, but not caloric sodas (half fructose), would be associated with increased risk of pancreatic cancer, since both share similar compositions. The solution to this inconsistency may lie in the amounts consumed: the authors claim that study participants derived more fructose from fruits and juices than from other dietary sources, including caloric soft drinks. Since the data are inexplicably absent, we are forced to accept their explanation. Would the authors advise that the public cut back on fruit consumption? Surely such advice is counterintuitive and ill-considered.
  • Though the authors hypothesize that high dietary GL is associated with the risk of pancreatic cancer, they do not report dietary glucose intakes. This seems a glaring oversight since glucose is accepted to be the most insulinogenic component in the diet and is accordingly given a GI value of 100, the standard against which others compounds are compared. Pure glucose also has the highest GL. By comparison, fructose has a GI of about 20.
    • Since glucose and fructose are equally present and track together in nutritive sweeteners (except pure fructose, pure glucose and corn syrups), fruits/juices and caloric soft drinks, any calculation of fructose intake from dietary questionnaires should yield roughly equivalent intake figures for glucose.
    • When glucose from other dietary sources is added (cereal grains; starch, maltodextrin, corn syrup and glucose ingredients), the intake of glucose is clearly higher than fructose. Forshee et.al. (1) estimated the ratio of fructose-to-glucose at 0.7, a ratio that did not change with the advent of high fructose corn syrup (HFCS).
    • Despite the authors’ conclusion that GL is not associated with increased risk of pancreatic cancer, parallel glucose-fructose tracking must cast doubt on the uniqueness of the conclusion that fructose intake is associated with greater risk of pancreatic cancer — this conclusion can and should be extended to glucose as well.
  • Fructose intakes calculated for participants in the Multiethnic Cohort Study were 4-6% of calories (Table 1, p.1497). These intakes are considerably lower than previous estimates for the general population: Park & Yetley in 1993 estimated fructose intakes at 8% of calories for the whole population (2). More recent estimates have placed fructose intake as high as 12 to nearly 20% of calories. The solution to this inconsistency may also lie with the terminology used: Park & Yetley summed fructose from all dietary sources — both free fructose and that from sucrose — while these authors seem to be reporting free fructose separately from sucrose and added sugars (tabletop). Clearly, Park & Yetley’s approach is the correct one.

In summary, the authors failed to prove the original hypothesis that GL is positively associated with increased risk of pancreatic cancer. They appear to have turned to fructose as an alternative in an effort to salvage a result from their rather disjointed, inconsistent and incomprehensible data.

References
  • Forshee R, Storey M, Allison D, et al. A critical examination of the evidence relating high fructose corn syrup and weight gain. Critical Reviews in Food Science and Nutrition 2007;47:561-582.
  • Park YK, Yetley EA. Intakes and food sources of fructose in the United States. Am J Clin Nutr 1993;58:737S-747S.
  • Centers for Disease Control and Prevention. Overweight and Obesity Trends among Adults. 2007.
  • Sun SZ, Empie MW. Lack of findings for the association between obesity risk and usual sugar-sweetened beverage consumption in adults – A primary analysis of databases of CSFII-1989-1991, CSFII-1994-1998, NHANES III, and combined NHANES 1999-2002. Food Chem Toxicol 2007.
  • Riby JE, Fujisawa T, Kretchmer N. Fructose absorption. Am J Clin Nutr 1993;58:748S-753S.
  • Swanson JE, Laine DC, Thomas W, Bantle JP. Metabolic effects of dietary fructose in healthy subjects. Am J Clin Nutr 1992;55:851-6.
  • Drewnowski A, Bellisle F. Liquid calories, sugar, and body weight. Am J Clin Nutr 2007;85:651-661.
  • Perrigue M, Drewnowski A. Hunger and satiety profiles and energy intakes following the ingestion of soft drinks sweetened with sucrose or high fructose corn syrup (HFCS). Program Abstract #LB433. Experimental Biology. San Francisco, 2006.
  • Hanover LM, White JS. Manufacturing, composition, and applications of fructose. Am J Clin Nutr 1993;58:724S-732S.
  • Havel PJ. Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Nutr Rev 2005;63:133-57.
  • Zuckley L, Rippe JM. The effect of high fructose corn syrup on post-prandial
    lipedemia in normal weight females. Annual Meeting of the Endocrine Society,
    Program Abstract #P2-46, 2007.

The post Calorie Control Council Response to Nothlings et al appeared first on FructoseFacts.

Calorie Control Council Response to Nothlings et al

Posted by & filed under Fructose, Health Professionals, Research Summaries.

Dietary Glycemic load, added sugars, and carbohydrates as risk factors for pancreatic cancer: the Multiethnic Cohort Study

Nothlings U1,3, Murphy SP1, Wilkens LR1, Henderson BE2, Kolonel LN1. Dietary glycemic load, added sugars, and carbohydrates as risk factors for pancreatic cancer: the Multiethnic Cohort Study. Am J Clin Nutr 2007;86:1495-1501

 

Background
This article is yet another published in AJCN seeking to establish a link between dietary fructose and increased risk for some metabolic perturbation: pancreatic cancer, in this instance. The authors are from the University of Hawaii1 (Honolulu), the University of Southern California2 (Los Angeles) and the German Institute of Human Nutrition Potsdam-Rehbruecke3 (Nuthetal). They are active cancer researchers and appear to be seeking causative factors for pancreatic cancer.

 

Hypothesis
The authors begin with the hypothesis that a high dietary glycemic load (GL) is positively associated with the risk of pancreatic cancer. GL is the product of [the experimentally measured serum glucose response after consumption of a specific food or ingredient (glycemic index, GI)] x [the carbohydrate content of the food or ingredient]. GL is now thought by nutritionists to be a better predictor of serum insulin response than GI alone.

The authors justify their hypothesis by citing previous studies suggesting that glucose metabolism plays a role in the development of pancreatic cancer. In this study, GL and carbohydrate intakes were mathematically derived from the amounts and types of foods consumed by participants as reported in an extensive self-administered questionnaire.

 

Author Conclusions

  1. High sugar intake — fructose intake, specifically — was associated with a greater risk of pancreatic cancer.
    • The purported association between fructose and weight gain is not appropriate, since HFCS has largely supplanted sucrose on a 1-for-1 basis, resulting in no net gain of fructose in the diet relative to other nutrients (9).
    • Pancreatic cancer risk increased with higher intakes of total sugars, fructose and sucrose.
    • The association between fructose and increased pancreatic cancer risk became significant when the highest and lowest fructose consumers were compared.
    • The association between fruit and juice intakes and pancreatic cancer risk was significant.
    • The association between caloric soda intake and pancreatic cancer risk was not significant.
  2. Sucrose (sugar) intake was associated with increased BMI (body mass index) for overweight and obese, but not normal-weight, subjects when the highest and lowest consumers were compared.

Critique

  • It seems rather implausible that fructose, but not added sugars (half fructose), would be associated with increased risk of pancreatic cancer. The solution to this inconsistency may be the unconventional use of terminology by the authors: ‘added sugars’ is here applied to spoonfuls of sugar added to foods, while the term is commonly used in nutrition circles to mean all dietary nutritive sweeteners not intrinsically present in foods and beverages.
  • It seems even more implausible that fruits and juices, but not caloric sodas (half fructose), would be associated with increased risk of pancreatic cancer, since both share similar compositions. The solution to this inconsistency may lie in the amounts consumed: the authors claim that study participants derived more fructose from fruits and juices than from other dietary sources, including caloric soft drinks. Since the data are inexplicably absent, we are forced to accept their explanation. Would the authors advise that the public cut back on fruit consumption? Surely such advice is counterintuitive and ill-considered.
  • Though the authors hypothesize that high dietary GL is associated with the risk of pancreatic cancer, they do not report dietary glucose intakes. This seems a glaring oversight since glucose is accepted to be the most insulinogenic component in the diet and is accordingly given a GI value of 100, the standard against which others compounds are compared. Pure glucose also has the highest GL. By comparison, fructose has a GI of about 20.
    • Since glucose and fructose are equally present and track together in nutritive sweeteners (except pure fructose, pure glucose and corn syrups), fruits/juices and caloric soft drinks, any calculation of fructose intake from dietary questionnaires should yield roughly equivalent intake figures for glucose.
    • When glucose from other dietary sources is added (cereal grains; starch, maltodextrin, corn syrup and glucose ingredients), the intake of glucose is clearly higher than fructose. Forshee et.al. (1) estimated the ratio of fructose-to-glucose at 0.7, a ratio that did not change with the advent of high fructose corn syrup (HFCS).
    • Despite the authors’ conclusion that GL is not associated with increased risk of pancreatic cancer, parallel glucose-fructose tracking must cast doubt on the uniqueness of the conclusion that fructose intake is associated with greater risk of pancreatic cancer — this conclusion can and should be extended to glucose as well.
  • Fructose intakes calculated for participants in the Multiethnic Cohort Study were 4-6% of calories (Table 1, p.1497). These intakes are considerably lower than previous estimates for the general population: Park & Yetley in 1993 estimated fructose intakes at 8% of calories for the whole population (2). More recent estimates have placed fructose intake as high as 12 to nearly 20% of calories. The solution to this inconsistency may also lie with the terminology used: Park & Yetley summed fructose from all dietary sources — both free fructose and that from sucrose — while these authors seem to be reporting free fructose separately from sucrose and added sugars (tabletop). Clearly, Park & Yetley’s approach is the correct one.

In summary, the authors failed to prove the original hypothesis that GL is positively associated with increased risk of pancreatic cancer. They appear to have turned to fructose as an alternative in an effort to salvage a result from their rather disjointed, inconsistent and incomprehensible data.

References
  • Forshee R, Storey M, Allison D, et al. A critical examination of the evidence relating high fructose corn syrup and weight gain. Critical Reviews in Food Science and Nutrition 2007;47:561-582.
  • Park YK, Yetley EA. Intakes and food sources of fructose in the United States. Am J Clin Nutr 1993;58:737S-747S.
  • Centers for Disease Control and Prevention. Overweight and Obesity Trends among Adults. 2007.
  • Sun SZ, Empie MW. Lack of findings for the association between obesity risk and usual sugar-sweetened beverage consumption in adults – A primary analysis of databases of CSFII-1989-1991, CSFII-1994-1998, NHANES III, and combined NHANES 1999-2002. Food Chem Toxicol 2007.
  • Riby JE, Fujisawa T, Kretchmer N. Fructose absorption. Am J Clin Nutr 1993;58:748S-753S.
  • Swanson JE, Laine DC, Thomas W, Bantle JP. Metabolic effects of dietary fructose in healthy subjects. Am J Clin Nutr 1992;55:851-6.
  • Drewnowski A, Bellisle F. Liquid calories, sugar, and body weight. Am J Clin Nutr 2007;85:651-661.
  • Perrigue M, Drewnowski A. Hunger and satiety profiles and energy intakes following the ingestion of soft drinks sweetened with sucrose or high fructose corn syrup (HFCS). Program Abstract #LB433. Experimental Biology. San Francisco, 2006.
  • Hanover LM, White JS. Manufacturing, composition, and applications of fructose. Am J Clin Nutr 1993;58:724S-732S.
  • Havel PJ. Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Nutr Rev 2005;63:133-57.
  • Zuckley L, Rippe JM. The effect of high fructose corn syrup on post-prandial
    lipedemia in normal weight females. Annual Meeting of the Endocrine Society,
    Program Abstract #P2-46, 2007.

The post Calorie Control Council Response to Nothlings et al appeared first on FructoseFacts.

Cutting Calories with Splenda

Posted by & filed under Health Professionals, Statements, Sucralose.

ATLANTA (October 4, 2007) — Small changes in the diet may help prevent excessive weight gain among children. A recent study indicates small changes, such as eliminating 100 calories a day from the diet and adding 2,000 steps of physical activity, may help children lose or maintain weight. The study was published in the October 2007 issue of Pediatrics.

Dr. James O. Hill, of the University of Colorado Health Sciences Center, and colleagues evaluated the effectiveness of the America on the Move Foundation’s, “Families on the Move Program,” created to combat rising childhood obesity rates. The families following the “Families on the Move” program were asked to cut 100 calories a day using products such as Splenda brand sweetener (which contains sucralose) and add an extra 2,000 steps.

Researchers examined more than 200 families, all of which had at least one overweight child, between the ages of 7 and 14 years. One hundred eleven families followed the “Families on the Move Program” while 95 of the families self-monitored their usual calorie and activity levels. After six months, researchers found that 43 of the children following the “Families on the Move Program” lost or maintained weight. Half of the children asked to self-monitor reported increases in their body mass index (BMI).

“I think a small change approach is the only way we’re going to get a handle on childhood obesity,” Hill said. Cutting 100 calories from the diet can be done by replacing a full-calorie soda with diet soda, and encouraging children to consume light products such as light yogurt, light lemonade and light orange juice. In order to add 2,000 steps per day, researchers suggest encouraging children to ride bikes and walk to destinations, as well as play outside.

According to the American Obesity Association, more than 45 percent of children are overweight or obese. Although obesity experts have long cited a diet high in calories and fat and decreased physical activity as two factors of childhood obesity, there has been a lack of strategies developed to help combat these issues. Small changes such as cutting 100 calories and adding 2,000 steps per day may help combat the childhood obesity crisis, researchers note.

“A lifestyle approach incorporating light products, such as foods and beverages containing sucralose, and adding physical activity, can help children lose or maintain their weight without drastic changes,” said Beth Hubrich, a registered dietitian and Executive Director of the Calorie Control Council.

Visit www.sucralose.org for more information on Splenda (sucralose).

The post Cutting Calories with Splenda appeared first on Sucralose.

Fructose, but not dextrose, accelerates the progression of chronic kidney disease.

Posted by & filed under Fructose, Health Professionals, Research Summaries.

Calorie Control Council Response

Gersch MS, Mu W, Cirillo P, Reungjui S, Zhang L, Roncal C, Sautin YY, Johnson RJ, Nakagawa T. Fructose, but not dextrose, accelerates the progression of chronic kidney disease. Am J Physiol Renal Physiol. 2007 Oct;293:F1256-61

Background
All authors hold appointments with the Division of Nephrology, Dialysis and Transplantation at the University of Florida; Michael Gersch is also associated with the North Florida/South Georgia Veterans Health System, Gainesville, Florida.

Richard Johnson seems to have staked out a niche in the area of fructose effects on kidney function and related diseases. His recent articles have attempted to implicate dietary fructose in kidney disease, hypertension, obesity, the metabolic syndrome, diabetes, hyperuricemia and cardiovascular disease (1-3). Reference 1, also authored by Johnson, was one of three papers critiqued in a recent Letter to the Editor accepted by theAmerican Journal of Clinical Nutrition (4).

Takahiko Nakagawa is a frequent collaborator with Johnson. The two are also coinventors on patent applications filed by the University of Florida related to the role of fructose in hypertension and the metabolic syndrome. It is clear from this patent activity and References 1 and 3 that Johnson and Nakagawa hope to extend this line of research into commercial applications.

Hypothesis
The authors have adopted the hypothesis of Bray et al (5) that fructose/HFCS are uniquely responsible for the obesity/metabolic syndrome epidemic. They have extended the Bray hypothesis to suggest in this paper that fructose/HFCS are also unique contributors to chronic kidney disease.

 

Justifications
The authors’ justifications for this study are summarized below:

  • Fructose consumption has steadily increased over the past 30 years in parallel to the growth of the obesity/metabolic syndrome epidemic.
  • Over the past 30 years, fructose has become a standard part of the American diet.
  • If we consider the animal and epidemiological data, it is reasonable to hypothesize that fructose consumption in our diet may be among the factors that contribute to the epidemic of the metabolic syndrome and, consequently, to the epidemic of chronic renal disease.
  • Fructose consumption by CKD patients may actually be placing them at an increased risk for progression of their CKD.
  • The 60% fructose diet is the classical model of fructose-induced metabolic syndrome described in the literature. Though it is 4-times the level that many people consume, it is common to use higher-dose treatments in animals to achieve a statistically significant result in a limited time frame.

Experimental Design
Forty-two 150-g male rats were randomized and received a diet of 60% fructose, 60% glucose or standard rat chow control (complex carbohydrates in place of purified sugars). At 6-weeks, all animals received a left nephrectomy and two-thirds right nephrectomy (five-sixths nephrectomy) to model renal insufficiency (failure) —the remnant kidney model. Assigned diets were continued for 11 additional weeks following surgery, after which the study was terminated by animal sacrifice.

Results

  • increased proteinuria (protein excretion), blood urea nitrogen (a renal function measure) and monocyte chemoattractant protein-1 (MCP-1);
  • decreased creatinine clearance;
  • enlarged kidneys and worsened kidney morphology (glomerular sclerosis, tubular atrophy, tubular dilation, cellular infiltration); and
  • higher mortality (3 fructose rats died; all other rats survived to the end of the study).

Author Conclusions

  1. Consumption of a high-fructose diet greatly accelerates progression of chronic kidney disease in the rat remnant kidney model.
  2. It is possible that fructose consumption by clinical patients may be contributing to the development or progression of CKD. Restriction of dietary fructose may slow the progression of CKD in these patients.

Critique

  • In contending that fructose consumption has steadily increased over the past 30 years due to fructose and HFCS use in commercial foods, the authors mislead readers into believing that sweeteners alone have increased. In truth, consumption of total calories has increased 24% in the past 30 years; it is significant that increases in fat and cereal grains have out-paced increases in added sugars consumption over that period.
  • The authors justify their 60% fructose vs. 60% glucose experimental diets (% calories) as acceptable in animal studies in order accelerate the development of disease. However, the fructose variable exposes rats to 7.5-times the level reported by Park & Yetley (6) for the general human population (8% of calories); it is clearly not physiological.
  • Furthermore, no one in the world eats a diet pure in either fructose or glucose to the exclusion of other sugars. We are daily exposed to fructose from fruits and vegetables and nutritive sweeteners (sucrose, HFCS, honey, fruit juice concentrates, crystalline fructose). But the simple sugar most consumed by humans is glucose from sources like cereal grains; food ingredients like starches, maltodextrins, corn syrups and glucose; fruits and vegetables; and nutritive sweeteners.
  • Forshee et al calculated the fructose-to-glucose ratio at 0.78 in the typical diet (7). Despite the authors’ claims to the contrary, this ratio has likely not changed significantly since sucrose became a staple of the American diet over a hundred years ago. It certainly didn’t change with the introduction of HFCS 30 years ago, since HFCS has the same sugars composition as sucrose and largely replaced sucrose in foods and beverages.
  • The authors report upsets in rat kidney physiology and function at grossly elevated fructose concentrations and atypical fructose:glucose ratios. However, they offer no proof that fructose/HFCS adversely affect rats at typical human fructose consumption levels or at the fructose:glucose ratio found in the typical human diet. The results of this study cannot be considered predictive of human dietary outcomes. And it is inappropriate for the authors to extrapolate results from an animal model featuring so extreme a diet to humans.
  • Most importantly, the authors fail to prove their hypothesis that restricting dietary fructose would slow the progression of chronic kidney disease at realistic human fructose exposure levels, or that this is even an important public health issue.
References
  • Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI, Kang DH, Gersch MS, Benner S, Sanchez-Lozada LG. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr. 2007 Oct;86:899-906.
  • Nakagawa T, Hu H, Zharikov S, Tuttle KR, Short RA, Glushakova O, Ouyang X, Feig DI, Block ER, et al. A causal role for uric acid in fructose-induced metabolic syndrome. Am J Physiol Renal Physiol. 2006 March 1, 2006;290:F625-31.
  • Nakagawa T, Tuttle KR, Short RA, Johnson RJ. Hypothesis: fructose-induced hyperuricemia as a casual mechanism for the epidemic of the metabolic syndrome. Nature Clinical Practice. 2005 11 August 2005;1:80-6.
  • White JS. No unique role for fructose sweeteners in obesity or cardiorenal disease. American Journal of Clinical Nutrition. 2008;In press.
  • Bray GA, Nielsen SJ, Popkin BM. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr. 2004 Apr;79:537-43.
  • Park YK, Yetley EA. Intakes and food sources of fructose in the United States. Am J Clin Nutr. 1993 Nov;58:737S-47S.
  • Forshee R, StoreyM, Allison D, Glinsmann W, Hein G, Lineback D, Miller S, Nicklas T, Weaver G, White J. A critical examination of the evidence relating high fructose corn syrup and weight gain. Critical Reviews in Food Science and Nutrition. 2007;47:561-82.

The post Fructose, but not dextrose, accelerates the progression of chronic kidney disease. appeared first on FructoseFacts.

Logging on to CaloriesCount.com Helps One Woman Log Off 60 Pounds for Her Wedding Day – and Keep It Off

Posted by & filed under Media Room.

ATLANTA (September 19, 2007) — A woman’s wedding will last forever through pictures and memories and it is a day when a woman wants to look her best.  But for Sarah in Charlotte, NC, her dream of looking and feeling great on her wedding day seemed out of reach.  In fact, Sarah dreaded shopping for her wedding dress, as she was more than 50 pounds overweight.  After a late night scare with severe acid reflux, Sarah decided to lose the weight and keep it off for good.  She signed up with the online dieting program, CaloriesCount.com, and never looked back.

By logging on to CaloriesCount.com in December of 2005, Sarah was able to shed 57 pounds and went from a size 14-16 to a comfortable size six.  She has kept the weight off for approximately seven months.

Because of her success, Sarah offers simple tips for brides-to-be and anyone who wants to lose weight and keep it off for good:

  • Make lifestyle changes and dump the “on again, off again” dieting mentality. “I knew a ‘diet’ would never work for me.  The idea of controlling portions and watching my caloric intake made a lot of sense to me,” says Sarah.  CaloriesCount.com dietitian Beth Hubrich adds:  “Incorporating simple substitutions into your normal eating regimen can be very effective.  Sugar-free foods and beverages can help people control calories without skimping on taste.  For example, switching from a regular soda to a diet soda can save 150 calories a day, which could lead to a weight loss of 15 pounds a year.
  • Make exercise a priority.  Sarah comments: “You really must exercise.  You must find a way to fit exercise into your day, every day.  Even when you’re finished losing the weight, you still must exercise as it’s important to your health and your long-term success.”  Exercise can be incorporated into even the busiest schedule by breaking it up into ten-minute intervals throughout the day.
  • Find support.  Research indicates that people trying to lose weight have greater success when there is a support group or weight loss buddy to assist during tough times and to share their accomplishments.  Sarah found the support she needed through the support community at CaloriesCount.com.  “We sign in every day and check in with each other, and we have a weekly weigh-in that’s very helpful,” she explains.
  • Beware of naysayers.  Sarah found that as her weight loss progressed some people in her life became jealous or did not understand her commitment to getting healthy.  “It can be very hurtful but you just have to ignore any negativity around you.  It’s important to stay strong and committed.”

Through CaloriesCount.com and a healthy lifestyle approach, Sarah has managed to lower her cholesterol, reduce her heartburn and acid reflux.  She also managed to fit into a size eight wedding dress for her wedding in October of 2006.  “I wanted to look good. And I did!”

owever, she cautions, “Many people want results immediately and if they don’t see them, they give up.  Remember that it took you a long time to get where you are and it will take some time to undo it.”  Sarah and many others have found the long-term weight loss success they were looking for through CaloriesCount.com.  The site is non-commercial, does not contain advertisements of branded products, and membership is available for a low cost.  Also, the CaloriesCount.com approach is to educate and support a healthy lifestyle rather than offer quick weight loss schemes.

Overeating of Low-Energy (Low-Calorie) Foods Among Children is Scientific Speculation

Posted by & filed under Statements.

ATLANTA (August 9, 2007) — A recent study reported in the journal Obesity (“Overeating by Young Obesity-prone and Lean Rats Caused by Tastes Associated With Low Energy Foods”) needs to be considered in the proper scientific context, especially in relation to other previously published research that has reached the opposite conclusion.  The study alleges that consumption of low-calorie foods and beverages by children may lead to increased episodes of overeating.  However, the vast body of scientific literature confirms the safety and benefits of using low-calorie sweeteners and low-calorie products for weight control and weight loss, and does not support the conclusions of the University of Alberta research.  The Council provides the following list of relevant information on childhood obesity and the efficacy and safety of low-calorie sweeteners:

  • With thirty-two percent of U.S. children age 6-19 overweight or at risk of being overweight, taking steps to assure appropriate caloric intake is important. Because products with low-calorie sweeteners (such as yogurt, with the same nutritional value and less than half the calories of a full-calorie yogurt) are lower in calories than their full-calorie counterparts, using products with low-calorie sweeteners together with regular physical activity can help with weight management.
  • Low-calorie sweeteners are not magic bullets and do not make people lose weight.  They are, however, tools that those trying to lose or maintain weight may incorporate as part of an overall healthy lifestyle that includes exercise and a balanced diet.
  • A recent study, presented at the Pediatric Academic Societies Meeting, found that eliminating 100 calories per day from the diet by using products such as sucralose and adding 2,000 steps a day may help children lose or maintain weight.  Researchers examined more than 200 families, all of which had at least one overweight child between the ages 7 to 14 years.  After six months, two out of three of the children following the program lost or maintained weight, while half of the children in the control group increased their body mass index (BMI).
  • The unpublished study conducted by Sharon Fowler et. al. (referenced in the University of Alberta study) is not proof that drinking diet soft drinks causes people to gain weight. The Fowler study is an epidemiological study, which cannot show a direct cause and effect.  Fowler et al. themselves noted that this study raises more questions than answers.  In addition, previous studies have shown that the use of low-calorie products not only aids in facilitating weight loss, but also weight control.
  • The study conducted by Davidson and Swithers referenced in the article is not consistent with the majority of scientific research on this topic.  This study involved a small sample size of 10 rats per group.  Rats especially like the taste of saccharin and it is often used as a reward in rat studies.  Therefore it is not surprising that the rats ate more when fed saccharin sweetened food.
  • According to a recent national survey conducted for the Calorie Control Council, the top reasons for using light products include: staying in better overall health, to reduce calories and to eat or drink healthier foods and beverages.  In addition, 87 percent of adults who use low-calorie, sugar-free foods and beverages say they eat less than or about the same when compared with the full-calorie version (they do not eat more).
  • Previous research has shown that consuming low-calorie foods and beverages not only aids in facilitating weight loss, but also weight control.  Experts agree that achieving and maintaining a healthy weight can help reduce the risk of heart diabetes, diabetes, and other risks associated with obesity.
  • Specifically, the study published in Obesity is contradicted by these other recent studies (references follow):
    • A 2007 study by Bellisle and Drewnowski, published in the European Journal of Clinical Nutrition, evaluated a variety of laboratory, clinical and epidemiological studies regarding low-calorie sweeteners, energy density and satiety.  Dr. Adam Drewnowski, Director, Center for Public Health Nutrition at the University of Washington and co-author of the study, noted, “This review of a variety of studies indicates that low-calorie sweeteners and the products that contain them may assist in weight loss efforts.”
    • Blackburn and his Harvard colleagues investigated whether the addition of aspartame to a multidisciplinary weight control program would improve weight loss and long-term control of body weight in obese women.  One hundred sixty-eight obese women aged 20 to 60 years were studied over a two-year period.  The researchers found that participation in this multidisciplinary weight control program including the use of aspartame-sweetened foods and beverages not only facilitated weight loss, but long-term maintenance of a reduced body weight.
    • Raben and colleagues found that using low-calorie sweeteners aided in the prevention of weight gain. Participants (a total of 41) followed a regular diet supplemented with food and drinks containing either sucrose or low-calorie sweeteners for two and a half months. The researchers found that participants consuming the sucrose sweetened foods and beverages had an increase in caloric energy, while those consuming the low-calorie sweetened foods and beverages showed a statistically significant decrease.  Additionally, those in the sucrose group experienced an increase in weight while the low-calorie sweetener group experienced a decrease in weight.
    • Ludwig and colleagues enrolled 548 ethnically diverse children (ages 7-11 years) and studied them prospectively for 19 months.  They found that diet soft drink consumption was not related to obesity incidence.
    • A 2006 study presented at the Pediatric Academic Societies’ Meeting found that using sucralose or sucralose-sweetened beverages as well as increasing activity helped maintain and lower body mass index for children participating in the Families on the Move Program.
    • A study published in the Journal of Food Science found that people who use reduced-calorie products not only had a better quality diet but also were more likely to consume fewer calories than those who did not use reduced-calorie products.
Resources
American Dietetic Association (2004).  Position of the American Dietetic Association:  Use of Nutritive and Nonnutritive Sweeteners. Journal of the American Dietetic Association.  104(2), 255-275.
Bellisle, F. and Drewnowski, A. (2007).  Intense sweeteners, energy intake and the control of body weight.  European Journal of Clinical Nutrition. 61, 691-700.
Blackburn, G. L., et al. The effect of aspartame as part of a multidisciplinary weight-control program on short- and long-term control of body weight. American Journal of Clinical Nutrition. 1997. Vol. 65. 409-418.
Ludwig, D. S. et el. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. 2001. Vol. 357. 505-508.
Raben, A., et. al. Sucrose Compared with Artificial Sweeteners: Different Effects on Ad Libitum
Food Intake and Body Weight After 10 Weeks of Supplementation in Overweight Subjects.
American Journal of Clinical Nutrition. October 2002. Vol. 76. No. 4. 721-729.
Sigman-Grant, M., and Hsieh, G. (2005) Reported use of reduced sugars foods and beverages reflect high quality diets. Journal of Food Science.  70(1), S42-S46.

Ask an Expert

faq2Do you have questions about low-calorie sweeteners? Want to learn more about maintaining a healthy lifestyle? You asked and we listened. Our resident Registered Dietitians answered the most popular questions about low-calorie sweeteners.

Media Contacts

For media inquiries please reach out to any of the below contacts: