Showing papers by "Arne Astrup published in 2000"

Reproducibility, power and validity of visual analogue scales in assessment of appetite sensations in single test meal studies.

Abstract: OBJECTIVE: To examine reproducibility and validity of visual analogue scales (VAS) for measurement of appetite sensations, with and without a diet standardization prior to the test days DESIGN: On two different test days the subjects recorded their appetite sensations before breakfast and every 30 min during the 45 h postprandial period under exactly the same conditions SUBJECTS: 55 healthy men (age 256±06 y, BMI 226±03 kg/m2) MEASUREMENTS: VAS were used to record hunger, satiety, fullness, prospective food consumption, desire to eat something fatty, salty, sweet or savoury, and palatability of the meals Subsequently an ad libitum lunch was served and energy intake was recorded Reproducibility was assessed by the coefficient of repeatability (CR) of fasting, mean 45 h and peak/nadir values RESULTS: CRs (range 20–61 mm) were larger for fasting and peak/nadir values compared with mean 45 h values No parameter seemed to be improved by diet standardization Using a paired design and a study power of 08, a difference of 10 mm on fasting and 5 mm on mean 45 h ratings can be detected with 18 subjects When using desires to eat specific types of food or an unpaired design, more subjects are needed due to considerable variation The best correlations of validity were found between 45 h mean VAS of the appetite parameters and subsequent energy intake (r=±050−053, P<0001) CONCLUSION: VAS scores are reliable for appetite research and do not seem to be influenced by prior diet standardization However, consideration should be given to the specific parameters being measured, their sensitivity and study power

The role of low-fat diets in body weight control: a meta-analysis of ad libitum dietary intervention studies.

Abstract: OBJECTIVES: Low-fat high-carbohydrate diets are recommended to prevent weight gain in normal weight subjects and reduce body weight in overweight and obese. However, their efficacy is controversial. We evaluated the efficacy of ad libitum low-fat diets in reducing body weight in non-diabetic individuals from the results of intervention trials. DESIGN: Studies were identified from a computerized search of the Medline database from January 1966 to July 1999 and other sources. Inclusion criteria were: controlled trials lasting more than 2 months comparing ad libitum low-fat diets as the sole intervention with a control group consuming habitual diet or a medium-fat diet ad libitum. MAIN OUTCOME MEASURES: Differences in changes in dietary fat intake, energy intake and body weight. Weighted mean differences for continuous data and 95% confidence intervals (CIs) were calculated. RESULTS: Two authors independently selected the studies meeting the inclusion criteria and extracted data from 16 trials (duration of 2–12 months) with 19 intervention groups, enrolling 1910 individuals. Fourteen were randomized. Weight loss was not the primary aim in 11 studies. Before the interventions the mean proportions of dietary energy from fat in the studies were 37.7% (95% CI, 36.9–38.5) in the low-fat groups, and 37.4% (36.4–38.4) in the control groups. The low-fat intervention produced a mean fat reduction of 10.2% (8.1–12.3). Low-fat intervention groups showed a greater weight loss than control groups (3.2 kg, 95% confidence interval 1.9–4.5 kg; P<0.0001), and a greater reduction in energy intake (1138 kJ/day, 95% confidence interval 564–1712 kJ/day, P=0.002). Having a body weight 10 kg higher than the average pre-treatment body weight was associated with a 2.6±0.8 kg (P=0.011) greater difference in weight loss. CONCLUSION: A reduction in dietary fat without intentional restriction of energy intake causes weight loss, which is more substantial in heavier subjects.

Redefining type 2 diabetes: 'diabesity' or 'obesity dependent diabetes mellitus'?

Abstract: Type 2 diabetes is considered by diabetes physicians as a complex and heterogeneous disease with a poorly understood aetiology, apart from the fact that there is a strong genetic propensity that becomes overt when exposed to a typical Western lifestyle. Our clinical targets are now moving from controlling the disease to preventing it. Do we need to await more research on the aetiology and pathophysiology before establishing a preventive strategy? No, the pathophysiology may be poorly understood, but there is now solid evidence that type 2 diabetes is a disease of fatness. New, controlled, clinical trials show that as little as 5% weight loss is sufficient to prevent most obese subjects with impaired glucose tolerance developing type 2 diabetes. Since type 2 diabetes is obesity dependent, and obesity is the main aetiogical cause of type 2 diabetes, we propose the term 'diabesity' should be adopted.

Effect of 8 week intake of probiotic milk products on risk factors for cardiovascular diseases

Abstract: Objective: To investigate the effect of a probiotic milk product containing the culture CAUSIDO® and of two alternative products on risk factors for cardiovascular disease in overweight and obese subjects. Design: An 8 week randomized, double-blind, placebo- and compliance-controlled, parallel study. Subjects: Seventy healthy, weight-stable, overweight and obese (25.0

The role of dietary fat in body fatness : evidence from a preliminary meta-analysis of ad libitum low-fat dietary intervention studies

Abstract: The role of high-fat diets in weight gain and obesity has been questioned because of inconsistent reports in the literature concerning the efficacy of ad libitum low-fat diets to reduce body weight. We conducted a meta-analysis of weight loss occurring on ad libitum low-fat diets in intervention trials, and analysed the relationship between initial body weight and weight loss. We selected controlled trials lasting more than 2 months comparing ad libitum low-fat diets with a control group consuming their habitual diet or a medium-fat diet ad libitum published from 1966 to 1998. Data were included from 16 trials with a duration of 2-12 months, involving 1728 individuals. No trials on obese subjects fulfilled the inclusion criteria. The weighted difference in weight loss between intervention and control groups was 2.55 kg (95% CI, 1.5-3.5; P < 0.0001). Weight loss was positively and independently related to pre-treatment body weight (r = 0.52, P < 0.05) and to reduction in the percentage of energy as fat (0.37 kg/%, P < 0.005) in unweighted analysis. Extrapolated to a BMI of about 30 kg/m2 and assuming a 10% reduction in dietary fat, the predicted weight loss would be 4.4 kg (95% CI, 2.0 to -6.8 kg). Because weight loss was not the primary aim in 12 of the 16 studies, it is unlikely that voluntary energy restriction contributed to the weight loss. Although there is no evidence that a high intake of simple sugars contributes to passive overconsumption, carbohydrate foods with a low glycaemic index may be more satiating and exert more beneficial effects on insulin resistance and cardiovascular risk factors. Moreover, an increase in protein content up to 25% of total energy may also contribute to reducing total energy intake. In conclusion, a low-fat diet, high in protein and fibre-rich carbohydrates, mainly from different vegetables, fruits and whole grains, is highly satiating for fewer calories than fatty foods. This diet composition provides good sources of vitamins, minerals, trace elements and fibre, and may have the most beneficial effect on blood lipids and blood-pressure levels. A reduction in dietary fat without restriction of total energy intake prevents weight gain in subjects of normal weight and produces a weight loss in overweight subjects, which is highly relevant for public health.

The effect of a probiotic milk product on plasma cholesterol: a meta-analysis of short-term intervention studies

Abstract: Introduction: Certain fermented dairy milk products may have beneficial effects on plasma cholesterol levels. However, a number of studies have produced conflicting results as to whether dietary supplementation by a probiotic dairy product containing the bacteria culture Causido® reduces plasma cholesterol. Objective: To conduct a meta-analysis of intervention studies to evaluate the effect of the Causido® culture on plasma total cholesterol and low-density lipoprotein (LDL)-cholesterol. The probiotic milk product: The yoghurt product Gaio® is fermented with Causido®, composed of one strain of Enterococcus faecium (human species) with the proposed cholesterol-lowering effect, and two strains of Streptococcus thermophilus. Study inclusion and data extraction: Six studies were identified from a literature search and from the yoghurt producer. All studies met the inclusion criteria. Summary data for plasma concentrations of total cholesterol and LDL-cholesterol were extracted from the original publications or by personal request to the authors. Data from 4–8 weeks of treatment duration was used. Statistical analysis: We performed a traditional meta-analysis where mean differences between intervention and control of the pre–post changes in total cholesterol and LDL-cholesterol were calculated, as well as 95% confidence intervals (CIs). Results: In the six studies included in the meta-analysis, the Gaio® interventions produced changes in total cholesterol above those of the control groups ranging from −0.02 to −1.02 mmol/l and in LDL-cholesterol ranging from −0.02 to −1.15 mmol/l. After inclusion of an open-label study, the meta-analysis of the double-blind studies showed that Gaio® as compared to the control group changed total cholesterol by −0.22 mmol/l (95% CI: −0.35 to −0.08, P<0.01) and LDL-cholesterol by −0.20 mmol/l (95% CI: −0.33 to −0.06, P<0.005). The outcome was essentially the same if all studies were included. Conclusions: The present meta-analysis of controlled short-term intervention studies shows that the fermented yoghurt product produced a 4% decrease in total cholesterol and a 5% decrease in LDL-cholesterol when the open-label study is excluded. To demonstrate sustained effects on blood lipids, long-term studies are required. Sponsorship: MD Foods A/S, Denmark. European Journal of Clinical Nutrition (2000) 54, 856–860

Lessons from obesity management programmes: greater initial weight loss improves long-term maintenance.

Abstract: It is a common belief that weight loss achieved at a slow rate is better preserved than if the weight is lost more rapidly. However, the literature shows that initial weight loss is positively, not negatively, related to long-term weight maintenance. There is evidence from randomised intervention trials to support that a greater initial weight loss induced without changes in lifestyle (e.g. liquid formula diets or anorectic drugs) improves long-term weight maintenance, providing it is followed by a 1-2 years integrated weight maintenance programme consisting of lifestyle interventions involving dietary change, nutritional education, behaviour therapy and increased physical activity. In conclusion, we find evidence to suggest that a greater initial weight loss as the first step of a weight management programme may result in improved sustained weight maintenance.

Effect of obesity and major weight reduction on gastric emptying.

Abstract: BACKGROUND: An enhanced gastric emptying rate might reduce the satiating effect of food and thereby promote obesity. Gastric emptying rate has previously been compared between obese and lean subjects with conflicting outcome. OBJECTIVE: Comparison of gastric emptying rate in lean and obese subjects before and after a major weight reduction. DESIGN: The study was designed as a case–control study comparing obese and lean subjects and a subsequent comparison of obese subjects before and after a dietary induced major weight reduction. METHOD: Gastric emptying rate following a solid test meal was estimated scintigraphically for 3 h using the left anterior oblique projection. SUBJECTS: Nineteen non-diabetic obese (mean BMI=38.7 kg/m2) and 12 lean (mean BMI=23.1 kg/m2) males matched for age and height. All obese subjects were re-examined after a mean weight loss of 18.8 kg (95% CI, 14.4–23.2) achieved by 16 weeks of dietary intervention followed by 8 weeks of weight stability. RESULTS: When comparing obese and lean subjects no differences were seen in overall 3 h emptying rate (30.3% per hour vs 30.5% per hour). However, a trend towards a higher percentage gastric emptying during the initial 30 min was seen in the obese when compared to lean subjects (24.0% vs 17.8% of the test meal; P=0.08). Weight loss was associated with a reduction in percentage gastric emptying during the initial 30 min (from 24.0% to 18.3% of the test-meal; P<0.02), whereas the overall 3 h emptying rate was unaffected (30.3% vs 30.9% per hour). Neither initial or overall emptying rate differed between reduced-obese and lean subjects. CONCLUSION: Overall 3 h gastric emptying rate was similar in obese and normal weight males, and unaffected by a major weight loss. However, percentage gastric emptying during the initial 30 min for a solid meal appeared to be increased in obese males and was normalized after a major weight reduction.

Ad libitum intake of low-fat diets rich in either starchy foods or sucrose: effects on blood lipids, factor VII coagulant activity, and fibrinogen.

Abstract: People are advised to reduce their intake of saturated fat and replace it by carbohydrate to avoid coronary heart disease. It is unknown whether sucrose and starchy foods, two major sources of carbohydrates, have similar effects on cardiovascular risk markers if incorporated as a replacement for saturated fat into diets eaten ad libitum. We served 20 healthy, normal-weight women aged 21 to 52 years three strictly controlled diets ad libitum: FAT, high in total fat (46% of total energy [E%]) and saturated fat (21 E%); STARCH, high in total carbohydrates (59 E%) and low in sucrose (2.5 E%); and SUCROSE, high in total carbohydrates (59 E%) and sucrose (23.2 E%). The diets were eaten in randomized order for a period of 2 weeks. Blood lipids, factor VII coagulant activity (FVIIc), and fibrinogen concentrations were measured with subjects in the fasted state (9:45 AM) and the postabsorptive state (6:00 PM). STARCH was associated with lower total cholesterol (mean difference, 0.34 mmol/L; 95% confidence interval [CI], 0.18 to 0.50), low-density lipoprotein (LDL) cholesterol (0.25 mmol/L; 95% CI, 0.13 to 0.37), fasting triglycerides (0.15 mmol/L; 95% CI, 0.07 to 0.23), nonfasting triglycerides (0.44 mmol/L; 95% CI, 0.30 to 0.58), and nonfasting FVIIc (9.8%; 95% CI, 3.8 to 15.8) than SUCROSE. Compared with FAT, STARCH resulted in a desirable decrease of LDL cholesterol and nonfasting FVIIc. STARCH was also associated with a minor weight loss (0.7 kg) that was not found on the other 2 diets. We conclude that starchy foods with a natural content of dietary fiber can be recommended as substitutes for saturated fat in the dietary prevention of coronary heart disease. According to the present short-term findings in healthy females, substitution with sucrose is not advisable.

Thermogenic drugs as a strategy for treatment of obesity

Abstract: There is accumulating evidence to support the hypothesis that a low-energy-output phenotype is at high risk of weight gain and obesity, irrespective of whether this is owing to a low resting metabolic rate and/or physical inactivity. The low-energy-output phenotype is associated with impaired appetite control, which is improved if energy output is increased. This is the background for pharmacologic stimulation of energy expenditure as a tool to improve the results of obesity management. Targets are the leptin receptors, the sympathetic nervous system and its peripheral beta-adrenoceptors, selective thyroid hormone derivatives, and stimulation of the mitochondrial uncoupling proteins. Currently available compounds such as recombinant leptin, ephedrine/caffeine, and sibutramine possess thermogenic properties owing to their activation of the sympathoadrenal system. Compounds acting selectively on the human beta3-adrenoceptor are still promising tools to achieve a sustained stimulation of lipolysis and energy expenditure, and several are in the pipeline.

Leptin is influenced both by predisposition to obesity and diet composition.

Abstract: OBJECTIVE: (1) To investigate whether plasma leptin concentrations differ between subjects with and without the genetic predisposistion to obesity, and (2) to investigate the effect of dietary manipulations on plasma leptin in these subjects. DESIGN: Fasting and postprandial plasma leptin concentrations were measured before and after 14 days’ ad libitum intake of a fat-rich (FAT), starch-rich (STARCH) or sucrose-rich (SUCROSE) diet. On day 15 ad libitum breakfast and lunch were given and blood sampled regularly until 6 p.m. SUBJECTS: Eight normal-weight, post-obese women and 10 matched controls (body mass index, 23.5±0.5 and 22.9±0.3 kg/m2). MEASUREMENTS: Leptin, glucose, insulin, appetite ratings, dietary intake, body weight and composition. RESULTS: Fasting leptin concentration on day 1 or 15 did not differ between post-obese and controls. However, after meal intake leptin increased in post-obese compared with controls on all three diets. In both groups fasting and postprandial leptin concentrations were greater after SUCROSE compared with FAT and STARCH. CONCLUSION: A larger postprandial leptin concentration was observed in post-obese subjects than in controls. This may be related to greater insulin sensitivity in adipose tissue in the post-obese. Furthermore, increased leptin concentrations were found after a sucrose-rich diet in both groups, possibly related to larger postprandial insulin peaks on this diet. Both contentions should, however, be validated by further studies.

D-tagatose, a stereoisomer of D-fructose, increases blood uric acid concentration.

Abstract: D-Fructose has been found to increase uric acid production by accelerating the degradation of purine nucleotides, probably due to hepatocellular depletion of inorganic phosphate (Pi) by an accumulation of ketohexose-1-phosphate. The hyperuricemic effect of D-tagatose, a stereoisomer of D-fructose, may be greater than that of D-fructose, as the subsequent degradation of D-tagatose-1-phosphate is slower than the degradation of D-fructose-1-phosphate. We tested the effect of 30 g oral D-tagatose versus D-fructose on plasma uric acid and other metabolic parameters in 8 male subjects by a double-blind crossover design. Both the peak concentration and 4-hour area under the curve (AUC) of serum uric acid were significantly higher after D-tagatose compared with either 30 g D-fructose or plain water. The decline in serum Pi concentration was greater at 50 minutes after D-tagatose versus D-fructose. The thermogenic and lactacidemic responses to D-tagatose were blunted compared with D-fructose. D-Tagatose attenuated the glycemic and insulinemic responses to a meal that was consumed 255 minutes after its administration. Moreover, both fructose and D-tagatose increased plasma concentrations of cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1). The metabolic effects of D-tagatose occurred despite its putative poor absorption.

The acute effect of D-tagatose on food intake in human subjects.

Abstract: A double-blind randomized crossover study was performed with nineteen normal-weight men to investigate the effect on subsequent ad libitum food intake of replacing 29 g sucrose with 29 g D-tagatose as sweetener to a breakfast meal. D-Tagatose is a malabsorbed stereoisomer of fructose with potential application as a bulk sweetener. Food intake was measured at lunch offered 4 h after the breakfast meal, during the afternoon with access to abundant snacks, and finally at a supper buffet 9 h after the breakfast. Energy intake at lunch and during the snacking period was similar after ingesting the two sugars, while it was 15% lower after ingesting D-tagatose than with sucrose at supper (P < 0.05). Gastrointestinal factors such as the osmotic effects of unabsorbed D-tagatose causing distension of the gut might have mediated the acute appetite-suppressing effect. The present paper also refers to data from a preceding study in which we observed an increased self-reported energy intake after ingestion of D-tagatose compared with sucrose which, in fact, suggests a relative hyperphagic effect of D-tagatose. However, self-reported food intake may be biased by selective under-reporting and this subsequent study with a more controlled assessment of food intake was therefore conducted. This present study did not support any hyperphagic effect of D-tagatose, but rather suggests that D-tagatose may contribute to a reduced energy intake.

Effects of oral D-tagatose, a stereoisomer of D-fructose, on liver metabolism in man as examined by 31P-magnetic resonance spectroscopy.

Abstract: D-tagatose, which is a stereoisomer of D-fructose, is phosphorylated to D-tagatose-1-phosphate by fructokinase in the liver. Because of a slow degradation rate of D-tagatose-1-phosphate, this substance may accumulate, and ingested D-tagatose may therefore cause a longer lasting reduction in inorganic phosphate (Pi) and adenosine triphosphate (ATP) levels in the liver compared with D-fructose. Similar to what is seen in patients with hereditary fructose intolerance, this may increase purine nucleotide degradation and thereby increase uric acid production. The effect of 30 g D-tagatose or D-fructose administered orally on ketohexose-1-phosphates, ATP, and Pi levels in the liver was studied by 31P-magnetic resonance spectroscopy (PMRS) in 5 young male volunteers. Blood and urine were collected to detect a possible increased uric acid production. A peak at 5.2 ppm assigned as D-tagatose-1-phosphate equivalent to about 1 mmol/L was found in the spectrum within 30 minutes after D-tagatose was administered in all subjects. Concomitantly, ATP was reduced by about 12% (P < .05). Both effects had vanished after 150 minutes. Serum uric acid concentration was increased by 17% 50 minutes after D-tagatose (P < .05) and did not reach baseline level when the experiment was terminated 230 minutes after the load. Although renal fractional extraction of uric acid decreased by approximately 12%, this could not explain the acute hyperuricemic effect of D-tagatose. No changes in 31PMRS spectra or serum uric acid concentration were found after D-fructose. These results suggest that a moderate intake of D-tagatose may affect liver metabolism by phosphate trapping despite the fact that the sugar may only be incompletely absorbed in the gut.

Sugar as a slimming agent

Abstract: Does dietary composition in itself have any importance for weight gain and obesity? Meta-analyses of dietary intervention trials comparing ad libitum normal-fat diets with low-fat diets clearly demonstrate that a reduction in the dietary fat content decreases body fat stores (Bray & Popkin, 1998; Yu-Poth et al. 1999; Astrup et al. 2000). Energy from fat has a weaker satiating power than energy from carbohydrates, and individuals are unconsciously more likely to consume more energy from fat-rich diets than from carbohydrate-rich diets. In addition, there also seems to be important differences in the digestion and metabolism of fat and carbohydrates which may influence energy balance. In order to gain a better understanding of the effects of fat and carbohydrate on energy metabolism, it is necessary to eliminate the effect of appetite regulation and induce overeating in paid experimental subjects. This is a method used by Lammert et al. (2000), who studied the response to overfeeding for 21 d with 5 MJ/d of either a fat-rich or an extremely-carbohydrateand sugar-rich diet. Previous overfeeding studies using extreme carbohydrate-rich lowfat diets have shown that the conversion of the glucose to fat by the de novo lipogenesis does not occur before most of the oxidation of the body is covered by glucose, and the glycogen stores are filled. The conversion of glucose to fat is however energetically a very costly synthesis, and based on the stoichiometry it can be predicted that overfeeding with carbohydrate should result in a 21 % lower fat deposition than overfeeding with an isoenergetic amount of fat (Flatt, 1992). Consequently, it should be less fattening to overeat carbohydrates than fat. This is exactly what Lammert et al. (2000) have tested. However, they do not think that they have revealed any differences between fat and carbohydrate overfeeding, but they overlook the main findings: overfeeding by carbohydrate compared with fat showed a mean net conversion of carbohydrate to fat of 15 ́8 g/d in contrast to 0 g/d on fat overfeeding. This de novo lipogenesis was estimated to account for 40 % of the increase in fat mass about 332 g fat. In addition they found a 30 % higher faecal energy loss equivalent to 8 MJ during the 21 d. These increased energy outputs should be expected to result in a lower fat deposition on the carbohydrate overfeeding and actually they do find a 30 % lower increase in fat mass despite an 18 % higher energy intake during the carbohydrate-overfeeding regimen. The subjects should therefore eat 68 % more energy in order to increase body fat stores by 1 kg on carbohydrate overfeeding than on fat overfeeding (155 MJ/kg v. 42 MJ/kg). This difference was not significant, but the study does not possess the sufficient statistical power to demonstrate a difference of such magnitude. As can also be seen from the study, overfeeding of non-related individuals results in substantial differences in body-fat gain, which can be attributed to genetic variation in the ability (to increase energy expenditure; Bouchard et al. 1990; Levine et al. 1999). When the study was designed, a power calculation would have shown, that a statistically significant difference of 20 % in fat gain would have required at least twice as many subjects. Alternatively a cross-over design or identical twins could have been used. The authors do not comment on this point and one may assume that the lack of significance of the 68 % higher energy cost of fat deposition on the carbohydrate overfeeding is due to a type 2 error. Is it then correct when Lammert et al. (2000) conclude that they do not find any evidence for increased thermogenesis during carbohydrate overfeeding? No, an assessment of the energy balance on the two overfeeding regimens speaks for itself (Fig. 1). The extra energy intake is 5 ́6 MJ/d over 21 d, i.e. 118 MJ, of which 8 ́6 % is lost as faecal energy. Gain of fat mass and fat-free mass can at best explain 34 MJ/kg for 1 ́36 kg, i.e. 46 MJ (Forbes et al. 1986). The additional energetic cost of de novo lipogenesis of 332 g fat can explain an additional 4 MJ, but where is the remaining 118 2 …9‡ 46‡ 4† MJ, i.e. 59 MJ or 50 % of the energy intake during the overfeeding? The authors overlook the possibility of increased thermogenesis (luxury consumption) during day and evening time, when the experimental subjects were awake (Levine et al. 1999). Unfortunately, energy expenditure was only measured at night time. Two alternatives should also be considered:

Reply to R Baschetti

Abstract: intestine per unit time. When sucrose is consumed in such unnatural forms it constitutes a `genetically unknown food' that is largely responsible for the alarmingly high prevalence of diabetes in newly westernised populations, which were virtually free of diabetes prior to the consumption of concentrated sucrose, the greatest novelty of the recently adopted western foods. Westerners, unlike those populations, have achieved passable adaptation to concentrated sugars through millenary natural selection, which accounts for the relatively low prevalence of diabetes in the West. Unfortunately, Raben and Astrup, as a result of their failure to realise the foremost importance of taking into account the form in which sucrose is ingested, do not specify whether sucrose was consumed in the innocuous form of moderately sweetened beverages or in the detrimental form of confectioneries. Considering that insulin sensitivity is in ̄uenced by the form in which sucrose is consumed and that, as Raben and Astrup point out, ` . . . prolonged hyperinsulinaemia has been found to stimulate leptin release', it can be reasonbly suggested that the increased leptin concentrations observed after a sucrose-rich diet are a consequence of the unnatural, highly concentrated forms in which sucrose was probably consumed, not a consequence of the sucrose-rich diet per se. This issue will likely be clari®ed by future studies taking into account the energy density of the forms in which sucrose will be consumed.