- Email: [email protected]
Causes of obesity
CORRESPONDENCE
colleagues postulated that increased mean arterial pressure and advanced dilution coagulopathy may have aggravated further blood loss in patients immediately fluid resuscitated. Indeed, those patients had lower haemoglobin concentrations and more dilution coagulopathy on admission. However, intraoperative blood loss was similar in the two groups—the difference in mean tranfused packed red cells was only 0·77 units, and patients in the immediate resuscitation group received no more fresh-frozen plasma or units of platelets than the delayed transfusion patients. In addition, length of stay in intensive care was similar for the two groups. Therefore, the different rates of inhospital survival might have resulted from other causes. Burris and colleagues3 showed in an animal model of uncontrolled haemorrhage that improved survival was accompanied by greater blood loss in animals resuscitated to a mean arterial pressure of 80 mm Hg. However, they also noted a significantly lower lactate production compared with no fluid resuscitation or resuscitation to a mean arterial pressure of 40 mm Hg. Although lactate production is only partly altered by volume status, blood lactate concentrations in general are a reliable predictor of survival in critically ill patients.4 Unfortunately, most studies of optimum volume therapy in traumatised patients lack important information such as blood lactate concentrations and arterial acid base status measurements, which makes interpretation of results even more difficult. Finally, in Austria, emergency medicine is provided mostly by anaesthetists trained in airway management and fluid resuscitation. Aggressive volume therapy is started at the trauma scene and continued throughout the perioperative and postoperative period. Among traumatised patients, those with multiple injuries and rupture of the liver exhibit a substantial fluid demand, but are also at special risk of developing severe haemorrhage, which would be increased by dilution coagulopathy and increased arterial pressure. We reviewed data from our computer system for such
Age (years) TISS SAPS Length of stay in intensive care (days)
Operative group (n=6)
Non-operative group (n=15)
35 (16–77) 47 (36–62) 48 (23–71) 10·5 (7·0–40·0)
28 (6–70) 41 (31–58) 30 (2–52) 11·0 (2·0–31·0)
TISS=Therapeutic Intervention Scoring System, SAPS=Acute Physiology Score 11.
Median (range) characteristics and length of stay
THE LANCET • Vol 357 • June 16, 2001
patients who were treated at the scene and taken immediately to the accident and emergency department of Innsbruck University Hospital, 1997–2000. Six (29%) of 21 patients needed an emergency laparotomy, and 15 (71%) were treated without surgery of the liver (table). Thus, the frequency of surgical intervention was within the reported range in the literature.5 The mortality rate of two (10%) of 21 patients was low. We suggest that it is not the fluid supply per se that is harmful for traumatised patients, but the too-late treatment of the complex coagulopathy that occurs earlier now than when whole blood was transfused liberally. *Petra Innerhofer, Gabriele Kühbacher, Wolfgang Schobersberger, Günther Sumann, Walter Hasibeder Department of Anaesthesia and Critical Care Medicine, Leopold-Franzens University, Anichstrasse 35, A-6020 Innsbruck, Austria (e-mail: [email protected]) 1
2
3
4
5
Roberts I, Evans P, Bunn F, Kwan I, Crowhurst E. Is the normalisation of blood pressure in bleeding trauma patients harmful? Lancet 2001; 357: 385–87. Bickell WH, Wall MJ, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med 1994; 331: 1105–09. Burris D, Rhee P, Kaufmann C, et al. Controlled resuscitation for uncontrolled hemorrhagic shock. J Trauma 1999; 46: 216–23. Claridge JA, Traves DC, Shawn JP, et al. Persistent occult hypoperfusion is associated with a significant increase in infection rate and mortality in major trauma patients. J Trauma 2000; 48: 8–15. Boone DC, Federle M, Billiar TR, Udekwu AO, Peitzman AB. Evolution of management of major hepatic trauma: identification of patterns of injury. J Trauma 1995; 39: 344–50.
Authors’ reply Sir—We agree with Anne Sutcliffe and Sandeep Walia that it would be helpful to have valid and reliable information about how much fluid to give inpatients with different patterns of injury. However, we concluded that there is no reliable evidence about how much fluid should be given or what targets should guide resuscitation in any group of trauma patients. We agree that clinical practice in this area should be informed by evidence from randomised controlled trials, but disagree strongly that randomised trials of resuscitation protocols in trauma patients cannot be done and that observational studies are an appropriate alternative. The association between hypotension and poor outcome in observational studies does not imply that attempting to normalise the blood pressure by giving intravenous fluids will improve
outcome. Hypotension implies more severe injury and more severely injured patients are more likely to die. Fluid administration might raise the blood pressure in the short term, but worsen bleeding thus leading to more long-term and severe hypotension. Petra Innerhofer and colleagues point out that the concept of delayed resuscitation is based largely on the randomised trial by Bickell in 598 hypotensive patients with penetrating trauma. In defence of their own policy of aggressive immediate fluid resuscitation in trauma patients, Innderhofer and colleagues cite a case series of 21 patients and selectively cite one out of the forty or so randomised-controlled trials in animal models of uncontrolled haemorrhage, by Burris and colleagues in 61 rats. At the same time they make the observation that coagulopathy is now occurring earlier in their trauma patients. Our concern is that immediate aggressive fluid resuscitation might contribute to the coagulopathy and increase mortality and we are not reassured by Innerhofer’s arguments. *Ian Roberts, Phillip Evans *Public Health Intervention Research Unit, London School of Hygiene and Tropical Medicine, 49–51 Bedford Square, London WC1B 3DP, UK; and Accident and Emergency Department, Leicester Royal Infirmary, Leicester (e-mail: [email protected])
Causes of obesity Sir—As a former scientist with the US National Institute of Environmental Health Sciences, the National Center for Toxicological Research, and the Food and Drug Administration, I am interested in obesity and its causes. The cause of obesity is well recognised to be multifactorial, encompassing genetics, nutrition, and physical activity. Any attempt to link obesity to a single cause or a particular food without consideration of the complexity, is inherently simplistic and does not advance our scientific understanding. David Ludwig and colleagues’ report (Feb 17, p 505)1 on sugar-sweetened drinks and childhood obesity is yet another study that contributes to the reductionist approach. The age at which the students were studied is fraught with difficulties, since gains in height and weight are not uniform. The investigators report 150 children as being obese at baseline and 152 (of 548 total) at follow-up. This net gain of two children arose because 37 new cases of obesity were recorded. I assume that 35 children who were obese at baseline reduced their body-mass index (BMI) during the course of the study. What were the characteristic
1977
CORRESPONDENCE
intakes and physical activities of these 35 children? A key issue is that other studies, such as USDA’s Continuing Survey of Food Intake by Individuals (CSFII analysis2), have shown that higher BMI is associated with higher fat intake, and that high carbohydrate and high sugar intakes are associated with lower BMI. Did Ludwig and colleagues control for fat intake? If the children who gained weight consumed lower-fat diets, that finding would contradict other studies. In an analysis of the CSFII data, workers reported that overweight children consume more total drinks, including sugar-sweetened drinks, milk, cordials, and fruit drinks. However, the slight increase of 0·2 g/day for soft drinks is of little practical importance.3 Therefore, consumption of soft drinks might be an indicator for other dietary changes, rather than a cause of the obesity per se. Furthermore, workers have shown that added sugars have little to no association with the diet quality of individuals older than years, and or with calcium intake among children and adolescents.4 Finally, Ludwig and colleagues state that total energy intake might be a causal factor relating obesity to sugarsweetened drink intake and that energy intake could confound the association if drink consumption is a marker for increased consumption of other foods. Of course consumption is likely to be a marker. Anyone who has children knows, that as children mature, they change many facets of their eating and exercise habits, which is another reason rather Ludwig and colleagues’4 simplistic association between sugarsweetened drinks and childhood obesity is inherently flawed.
importantly, their results are contrary to one of the current views on the biology of appetite control and bodyweight regulation: the glucostatic theory. This theory, first proposed by Mayer2 (from the investigators’ own institution) suggests that glucose may be a powerful inhibitor of food intake. (Sugarsweetened drinks generally contain sucrose, glucose, or fructose). A reduction in food intake is unlikely to lead to obesity, which results only from being in positive energy balance.3 In a series of studies done in Europe and the USA, no association was noted between sugar intake and obesity. 4 Several investigators have suggested an association between fruit juice or sugar-sweetened drink consumption and poor growth in children.5 The fundamental physiological question is, how could excess consumption of sugar-sweetened drinks lead to obesity and undernutrition? A better understanding of this question is critical in our ability to provide evidence-based public-health advice. Until such time, Ludwig and colleagues’ study, despite its importance, perhaps should be treated with circumspection. *Jeya Henry, Janet Warren School of Biological and Molecular Science, Oxford Brookes University, Gipsy Lane, Oxford OX3 OBP, UK 1
2
3
4
Lawrence Fishbein 4320 Ashford Lane, Fairfax, VA 22032, USA 1
2
3
4
Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugarsweetened drinks and childhood obesity: a prospective observational analysis. Lancet 2001; 357: 505–08. US Department of Agriculture 1994–96. Continuing Study of Food Intakes by individuals and 1994–96, diet and health knowledge survey and related materials (CD Rom, 1998). Weaver AR, Storey ML, Woo RY, Clark KF, Forshee RA. Beverage consumption among elementary and high school children. FASEB J 2000; 14: A534. Forshee RA, Storey, ML. The role of added sugars in the diet quality of children and adolescents. J Am Coll Nutr 2001; 20: 1–11.
Sir—David Ludwig and colleagues conclude1 that the association between consumption of sugar-sweetened drinks and obesity might be an oversimplification of a complex and multifactorial phenomenon. More
1978
5
Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugarsweetened drinks and childhood obesity: a prospective, observational analysis. Lancet 2001; 357: 505–08. Mayer J. Glucostatic mechanism of regulation of food intake. N Engl J Med 1953; 249: 13–16. Booth D, Campbell A, Chase A. Temporal bounds of post-ingestive glucose induced satiety in man. Nature 1970; 228: 1104–05. Alexy U, Sichert-Hellert W, Kersting M, Manz F, Schoch G. Fruit juice consumption and the prevalence of obesity and short stature in German preschool children. J Pediatr Gastroenterol Nutr 1999; 29: 343–49. Smith M, Lifshitz F. Excess fruit juice consumption as a contributing factor in nonorganic failure to thrive. Pediatrics 1994; 93: 438–43.
Authors’ reply Sir—We recognise and note in our report that the causes of obesity are multifactorial, as Lawrence Fishbein points out. We attempted to control for the potentially confounding influences of other dietary and lifestyle factors (eg, dietary fat, physical activity, television viewing) in statistical models, by use of standard epidemiological methods for prospective data. However, we do not see why specific causes of complex disease should not be sought. Many studies have linked specific
dietary factors to obesity, including fat, energy density, variety, and socalled fast foods. Indeed, Fishbein refers to some of these studies in his criticism of our work. In view of the high and increasing degree of consumption of sugar-sweetened drinks among US children, we feel that it is appropriate and necessary to assess the relation between these drinks and weight gain. The adolescent period represents a vulnerable time for development of obesity and related complications. Factors that affect bodyweight regulation at this developmental stage are, therefore, of particular publichealth importance. We recognise that large or rapidly growing children will consume more food of all kinds than other children and adjusted statistical models accordingly for total energy consumption as well as baseline anthropometric measures. We excluded individuals who were obese at baseline for estimation of obesity odds ratios, according to standard methods for prospective analyses. Thus, the 9·3% obesity incidence (37 cases) represents individuals who went from non-obese at baseline to obese at follow-up. By contrast, the associations between measures of soft drink consumption and BMI were based on the entire cohort. We did adjust statistical models for percentage energy from fat. We note, however, that there is by no means a consensus on the effects of dietary fat on adiposity.1 Fishbein cites a study showing only a slightly higher degree of soft-drink consumption in obese compared with lean elementary and high-school children. We cannot comment on the strengths or weaknesses of this crosssectional study until it is published in full. By contrast, Harnack and colleagues2 report that the total energy consumption was 10% higher in children drinking about a can of sugar-sweetened drink each day, compared with non-consumers of these beverages. In addition, Mattes did a meta-analysis of studies done over 25 years, and noted that compensation for energy in liquid form is less complete than that for energy in solid form.3 In response to Jeya Henry and Janet Warren, we did not investigate the relation between sucrose consumption and obesity. We did, however, adjust for fruit-juice consumption. Many studies provide a physiological reason why soft drinks may have lower satiating properties than solid foods, such as Rolls and colleagues’ study.4
THE LANCET • Vol 357 • June 16, 2001
colleagues postulated that increased mean arterial pressure and advanced dilution coagulopathy may have aggravated further blood loss in patients immediately fluid resuscitated. Indeed, those patients had lower haemoglobin concentrations and more dilution coagulopathy on admission. However, intraoperative blood loss was similar in the two groups—the difference in mean tranfused packed red cells was only 0·77 units, and patients in the immediate resuscitation group received no more fresh-frozen plasma or units of platelets than the delayed transfusion patients. In addition, length of stay in intensive care was similar for the two groups. Therefore, the different rates of inhospital survival might have resulted from other causes. Burris and colleagues3 showed in an animal model of uncontrolled haemorrhage that improved survival was accompanied by greater blood loss in animals resuscitated to a mean arterial pressure of 80 mm Hg. However, they also noted a significantly lower lactate production compared with no fluid resuscitation or resuscitation to a mean arterial pressure of 40 mm Hg. Although lactate production is only partly altered by volume status, blood lactate concentrations in general are a reliable predictor of survival in critically ill patients.4 Unfortunately, most studies of optimum volume therapy in traumatised patients lack important information such as blood lactate concentrations and arterial acid base status measurements, which makes interpretation of results even more difficult. Finally, in Austria, emergency medicine is provided mostly by anaesthetists trained in airway management and fluid resuscitation. Aggressive volume therapy is started at the trauma scene and continued throughout the perioperative and postoperative period. Among traumatised patients, those with multiple injuries and rupture of the liver exhibit a substantial fluid demand, but are also at special risk of developing severe haemorrhage, which would be increased by dilution coagulopathy and increased arterial pressure. We reviewed data from our computer system for such
Age (years) TISS SAPS Length of stay in intensive care (days)
Operative group (n=6)
Non-operative group (n=15)
35 (16–77) 47 (36–62) 48 (23–71) 10·5 (7·0–40·0)
28 (6–70) 41 (31–58) 30 (2–52) 11·0 (2·0–31·0)
TISS=Therapeutic Intervention Scoring System, SAPS=Acute Physiology Score 11.
Median (range) characteristics and length of stay
THE LANCET • Vol 357 • June 16, 2001
patients who were treated at the scene and taken immediately to the accident and emergency department of Innsbruck University Hospital, 1997–2000. Six (29%) of 21 patients needed an emergency laparotomy, and 15 (71%) were treated without surgery of the liver (table). Thus, the frequency of surgical intervention was within the reported range in the literature.5 The mortality rate of two (10%) of 21 patients was low. We suggest that it is not the fluid supply per se that is harmful for traumatised patients, but the too-late treatment of the complex coagulopathy that occurs earlier now than when whole blood was transfused liberally. *Petra Innerhofer, Gabriele Kühbacher, Wolfgang Schobersberger, Günther Sumann, Walter Hasibeder Department of Anaesthesia and Critical Care Medicine, Leopold-Franzens University, Anichstrasse 35, A-6020 Innsbruck, Austria (e-mail: [email protected]) 1
2
3
4
5
Roberts I, Evans P, Bunn F, Kwan I, Crowhurst E. Is the normalisation of blood pressure in bleeding trauma patients harmful? Lancet 2001; 357: 385–87. Bickell WH, Wall MJ, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med 1994; 331: 1105–09. Burris D, Rhee P, Kaufmann C, et al. Controlled resuscitation for uncontrolled hemorrhagic shock. J Trauma 1999; 46: 216–23. Claridge JA, Traves DC, Shawn JP, et al. Persistent occult hypoperfusion is associated with a significant increase in infection rate and mortality in major trauma patients. J Trauma 2000; 48: 8–15. Boone DC, Federle M, Billiar TR, Udekwu AO, Peitzman AB. Evolution of management of major hepatic trauma: identification of patterns of injury. J Trauma 1995; 39: 344–50.
Authors’ reply Sir—We agree with Anne Sutcliffe and Sandeep Walia that it would be helpful to have valid and reliable information about how much fluid to give inpatients with different patterns of injury. However, we concluded that there is no reliable evidence about how much fluid should be given or what targets should guide resuscitation in any group of trauma patients. We agree that clinical practice in this area should be informed by evidence from randomised controlled trials, but disagree strongly that randomised trials of resuscitation protocols in trauma patients cannot be done and that observational studies are an appropriate alternative. The association between hypotension and poor outcome in observational studies does not imply that attempting to normalise the blood pressure by giving intravenous fluids will improve
outcome. Hypotension implies more severe injury and more severely injured patients are more likely to die. Fluid administration might raise the blood pressure in the short term, but worsen bleeding thus leading to more long-term and severe hypotension. Petra Innerhofer and colleagues point out that the concept of delayed resuscitation is based largely on the randomised trial by Bickell in 598 hypotensive patients with penetrating trauma. In defence of their own policy of aggressive immediate fluid resuscitation in trauma patients, Innderhofer and colleagues cite a case series of 21 patients and selectively cite one out of the forty or so randomised-controlled trials in animal models of uncontrolled haemorrhage, by Burris and colleagues in 61 rats. At the same time they make the observation that coagulopathy is now occurring earlier in their trauma patients. Our concern is that immediate aggressive fluid resuscitation might contribute to the coagulopathy and increase mortality and we are not reassured by Innerhofer’s arguments. *Ian Roberts, Phillip Evans *Public Health Intervention Research Unit, London School of Hygiene and Tropical Medicine, 49–51 Bedford Square, London WC1B 3DP, UK; and Accident and Emergency Department, Leicester Royal Infirmary, Leicester (e-mail: [email protected])
Causes of obesity Sir—As a former scientist with the US National Institute of Environmental Health Sciences, the National Center for Toxicological Research, and the Food and Drug Administration, I am interested in obesity and its causes. The cause of obesity is well recognised to be multifactorial, encompassing genetics, nutrition, and physical activity. Any attempt to link obesity to a single cause or a particular food without consideration of the complexity, is inherently simplistic and does not advance our scientific understanding. David Ludwig and colleagues’ report (Feb 17, p 505)1 on sugar-sweetened drinks and childhood obesity is yet another study that contributes to the reductionist approach. The age at which the students were studied is fraught with difficulties, since gains in height and weight are not uniform. The investigators report 150 children as being obese at baseline and 152 (of 548 total) at follow-up. This net gain of two children arose because 37 new cases of obesity were recorded. I assume that 35 children who were obese at baseline reduced their body-mass index (BMI) during the course of the study. What were the characteristic
1977
CORRESPONDENCE
intakes and physical activities of these 35 children? A key issue is that other studies, such as USDA’s Continuing Survey of Food Intake by Individuals (CSFII analysis2), have shown that higher BMI is associated with higher fat intake, and that high carbohydrate and high sugar intakes are associated with lower BMI. Did Ludwig and colleagues control for fat intake? If the children who gained weight consumed lower-fat diets, that finding would contradict other studies. In an analysis of the CSFII data, workers reported that overweight children consume more total drinks, including sugar-sweetened drinks, milk, cordials, and fruit drinks. However, the slight increase of 0·2 g/day for soft drinks is of little practical importance.3 Therefore, consumption of soft drinks might be an indicator for other dietary changes, rather than a cause of the obesity per se. Furthermore, workers have shown that added sugars have little to no association with the diet quality of individuals older than years, and or with calcium intake among children and adolescents.4 Finally, Ludwig and colleagues state that total energy intake might be a causal factor relating obesity to sugarsweetened drink intake and that energy intake could confound the association if drink consumption is a marker for increased consumption of other foods. Of course consumption is likely to be a marker. Anyone who has children knows, that as children mature, they change many facets of their eating and exercise habits, which is another reason rather Ludwig and colleagues’4 simplistic association between sugarsweetened drinks and childhood obesity is inherently flawed.
importantly, their results are contrary to one of the current views on the biology of appetite control and bodyweight regulation: the glucostatic theory. This theory, first proposed by Mayer2 (from the investigators’ own institution) suggests that glucose may be a powerful inhibitor of food intake. (Sugarsweetened drinks generally contain sucrose, glucose, or fructose). A reduction in food intake is unlikely to lead to obesity, which results only from being in positive energy balance.3 In a series of studies done in Europe and the USA, no association was noted between sugar intake and obesity. 4 Several investigators have suggested an association between fruit juice or sugar-sweetened drink consumption and poor growth in children.5 The fundamental physiological question is, how could excess consumption of sugar-sweetened drinks lead to obesity and undernutrition? A better understanding of this question is critical in our ability to provide evidence-based public-health advice. Until such time, Ludwig and colleagues’ study, despite its importance, perhaps should be treated with circumspection. *Jeya Henry, Janet Warren School of Biological and Molecular Science, Oxford Brookes University, Gipsy Lane, Oxford OX3 OBP, UK 1
2
3
4
Lawrence Fishbein 4320 Ashford Lane, Fairfax, VA 22032, USA 1
2
3
4
Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugarsweetened drinks and childhood obesity: a prospective observational analysis. Lancet 2001; 357: 505–08. US Department of Agriculture 1994–96. Continuing Study of Food Intakes by individuals and 1994–96, diet and health knowledge survey and related materials (CD Rom, 1998). Weaver AR, Storey ML, Woo RY, Clark KF, Forshee RA. Beverage consumption among elementary and high school children. FASEB J 2000; 14: A534. Forshee RA, Storey, ML. The role of added sugars in the diet quality of children and adolescents. J Am Coll Nutr 2001; 20: 1–11.
Sir—David Ludwig and colleagues conclude1 that the association between consumption of sugar-sweetened drinks and obesity might be an oversimplification of a complex and multifactorial phenomenon. More
1978
5
Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugarsweetened drinks and childhood obesity: a prospective, observational analysis. Lancet 2001; 357: 505–08. Mayer J. Glucostatic mechanism of regulation of food intake. N Engl J Med 1953; 249: 13–16. Booth D, Campbell A, Chase A. Temporal bounds of post-ingestive glucose induced satiety in man. Nature 1970; 228: 1104–05. Alexy U, Sichert-Hellert W, Kersting M, Manz F, Schoch G. Fruit juice consumption and the prevalence of obesity and short stature in German preschool children. J Pediatr Gastroenterol Nutr 1999; 29: 343–49. Smith M, Lifshitz F. Excess fruit juice consumption as a contributing factor in nonorganic failure to thrive. Pediatrics 1994; 93: 438–43.
Authors’ reply Sir—We recognise and note in our report that the causes of obesity are multifactorial, as Lawrence Fishbein points out. We attempted to control for the potentially confounding influences of other dietary and lifestyle factors (eg, dietary fat, physical activity, television viewing) in statistical models, by use of standard epidemiological methods for prospective data. However, we do not see why specific causes of complex disease should not be sought. Many studies have linked specific
dietary factors to obesity, including fat, energy density, variety, and socalled fast foods. Indeed, Fishbein refers to some of these studies in his criticism of our work. In view of the high and increasing degree of consumption of sugar-sweetened drinks among US children, we feel that it is appropriate and necessary to assess the relation between these drinks and weight gain. The adolescent period represents a vulnerable time for development of obesity and related complications. Factors that affect bodyweight regulation at this developmental stage are, therefore, of particular publichealth importance. We recognise that large or rapidly growing children will consume more food of all kinds than other children and adjusted statistical models accordingly for total energy consumption as well as baseline anthropometric measures. We excluded individuals who were obese at baseline for estimation of obesity odds ratios, according to standard methods for prospective analyses. Thus, the 9·3% obesity incidence (37 cases) represents individuals who went from non-obese at baseline to obese at follow-up. By contrast, the associations between measures of soft drink consumption and BMI were based on the entire cohort. We did adjust statistical models for percentage energy from fat. We note, however, that there is by no means a consensus on the effects of dietary fat on adiposity.1 Fishbein cites a study showing only a slightly higher degree of soft-drink consumption in obese compared with lean elementary and high-school children. We cannot comment on the strengths or weaknesses of this crosssectional study until it is published in full. By contrast, Harnack and colleagues2 report that the total energy consumption was 10% higher in children drinking about a can of sugar-sweetened drink each day, compared with non-consumers of these beverages. In addition, Mattes did a meta-analysis of studies done over 25 years, and noted that compensation for energy in liquid form is less complete than that for energy in solid form.3 In response to Jeya Henry and Janet Warren, we did not investigate the relation between sucrose consumption and obesity. We did, however, adjust for fruit-juice consumption. Many studies provide a physiological reason why soft drinks may have lower satiating properties than solid foods, such as Rolls and colleagues’ study.4
THE LANCET • Vol 357 • June 16, 2001