PubMed Health⌕ Search

Biomedical subjects

J E Blundell

Publications and source records attributed to J E Blundell.

At least 19 recordsLinked to original sources
PubMed2006

Characterization of obese individuals who claim to detect no relationship between their eating pattern and sensations of hunger or fullness.

OBJECTIVE: To study the phenomenon that obese subjects show considerable individual variability in their reported relationships between eating and sensations of hunger and fullness. DESIGN: A laboratory study of the relationship between eating behaviour traits and the episodic oscillations in sensations of hunger and fullness in response to obligatory, fixed energy breakfast (481 kcal) and lunch (675 kcal) meals. SUBJECTS: Obese subjects were divided into two groups based on their responses to four 'screening' questions associated with their habitual experience of hunger and fullness sensations before and after eating: those who experienced sensations of hunger and fullness related to eating (Related-R; n=20, body mass index (BMI)=42.4 kg/m(2)) and those for whom eating was not related to hunger or fullness sensations (Unrelated - UR; n=19, BMI=41.3 kg/m(2)). In addition, a control, lean group (Control - C; n=14, BMI=22.6 kg/m(2)) who experienced sensations of hunger and fullness related to eating was studied. MEASUREMENTS: The Three-Factor Eating Questionnaire (TFEQ) was used to measure the eating behaviour traits, disinhibition, restraint and hunger. Profiles of subjective appetite sensations were continuously monitored across the day using visual analogue scales. RESULTS: All groups displayed clear meal-related oscillations in subjective sensations of hunger, fullness, desire to eat and prospective consumption. In contrast, the TFEQ disinhibition and hunger scores (but not restraint scores) were significantly different (P<0.05) between the groups ((UR; D=13.5+/-0.5, H=10.0+/-0.5), R (D 7.5+/-0.6, H 6.1+/-0.4), C(D 3.7+/-0.5, H 3.7+/-0.5)). In addition, analysis of the intra-meal changes in subjective appetite sensations revealed that the UR group displayed a smaller meal-induced suppression of hunger and elevation of fullness. CONCLUSION: These data indicate that the reported relationship between eating and hunger/fullness was associated with obese individuals showing high or low disinhibition scores. In addition, the data suggest that the processes underlying disinhibition may be associated with a modulation of the recognition of meal-related satiety sensations.

Adult↗
PubMed2005

Resistance and susceptibility to weight gain: individual variability in response to a high-fat diet.

An obesigenic environment is a potent force for promoting weight gain. However, not all people exposed to such an environment become obese; some remain lean. This means that some people are susceptible to weight gain (in a weight-promoting environment) and others are resistant. Identifying the characteristics of appetite control and food motivation in these two groups could throw light on the causes of weight gain and how this can be either treated or prevented. We have investigated the issue experimentally by identifying people who habitually consume a high-fat diet (greater than 43% fat energy). These individuals have been termed high-fat phenotypes. We have compared individuals, of the same age (mean=37 years old) and gender (male), who have gained weight (BMI=34) or who have remained lean (BMI=22). The susceptible individuals are characterised by a cluster of characteristics including a weak satiety response to fatty meals, a maintained preference for high-fat over low-energy foods in the post-ingestive satiety period, a strong hedonic attraction to palatable foods and to eating, and high scores on the TFEQ factors of Disinhibition and Hunger. The analysis of large databases suggests that this profile of factors contributes to an average daily positive energy balance from food of approximately 0.5 MJ. This profile of characteristics helps to define the symptomatology of a thrifty phenotype.

Appetite↗
PubMed2005

Anorexia and weight loss in male rats 24 h following single dose treatment with orexin-1 receptor antagonist SB-334867.

Acute systemic treatment with the selective orexin-1 receptor antagonist SB-334867 (30 mg/kg, i.p.) has been reported not only to inhibit food intake and to accelerate behavioural satiety in rats, but also to produce a significant loss of bodyweight over the 24 h period post-dosing. The present studies were designed to test the hypothesis that the inhibition of weight gain following acute treatment with SB-334867 is due to a persistent anorectic action of the compound. In Experiment 1, the acute effects of SB-334867 (30 mg/kg, i.p.) on food intake and behaviour in a 1 h test with palatable mash were assessed as a function of injection-test interval. Results confirmed that, when administered 30 min prior to testing, SB-334867 significantly suppressed mash intake and accelerated behavioural satiety. More importantly, significant anorexia and behavioural change were also observed when animals were tested 24 h, but not 48 h, post-dosing. As previously reported, all animals treated with the orexin-1 receptor antagonist lost bodyweight over the 24 h period following acute treatment. The generality of these findings was confirmed in Experiment 2, where acute treatment with SB-334867 (30 mg/kg, i.p.) significantly suppressed home cage chow consumption over the 24 h period post-dosing, an effect also accompanied by a significant loss of bodyweight. The results of Experiment 3 showed that, following i.p. administration of 30 mg/kg, SB-334867 has good CNS penetration, reaches peak plasma and brain concentrations at 30 min, and maintains good exposure over 4 h post-dosing. Overall, current data support the hypothesis that a persistent anorectic action contributes to the significant loss of bodyweight observed 24 h following acute dosing with SB-334867. As the compound is virtually undetectable in plasma or brain beyond 8 h post-dosing, and since nothing is known about potentially active metabolites, we consider the possibility that single dose treatment with SB-334867 results in enduring alterations to the orexin-1 receptor and/or downstream signalling pathways.

Activity Cycles↗
PubMed2005

PYY3-36 as an anti-obesity drug target.

The neuropeptide Y (NPY)/peptide YY (PYY) system has been implicated in the physiology of obesity for several decades. More recently ignited enormous interest in PYY3-36, an endogenous Y2-receptor agonist, as a promising anti-obesity compound. Despite this interest, there have been remarkably few subsequent reports reproducing or extending the initial findings, while at the same time studies finding no anti-obesity effects have surfaced. Out of 41 different rodent studies conducted (in 16 independent labs worldwide), 33 (83%) were unable to reproduce the reported effects and obtained no change or sometimes increased food intake, despite use of the same experimental conditions (i.e. adaptation protocols, routes of drug administration and doses, rodent strains, diets, drug vendors, light cycles, room temperatures). Among studies by authors in the original study, procedural caveats are reported under which positive effects may be obtained. Currently, data speak against a sustained decrease in food intake, body fat, or body weight gain following PYY3-36 administration and make the previously suggested role of the hypothalamic melanocortin system unlikely as is the existence of PYY deficiency in human obesity. We review the studies that are in the public domain which support or challenge PYY3-36 as a potential anti-obesity target.

Animals↗
PubMed2004

Satiety enhancement by selective orexin-1 receptor antagonist SB-334867: influence of test context and profile comparison with CCK-8S.

Acute systemic treatment with the selective orexin-1 (OX1R) antagonist SB-334867 reduces food intake in rats, an effect associated with an acceleration in behavioural satiety and unrelated to gross behavioural disruption, alterations in palatability, or toxicity. However, as enhanced satiety is behaviourally indexed by an earlier-than-normal transition from eating to resting, and since orexin-A has been implicated in mechanisms of arousal, it remains possible that sedation contributes to the anorectic effect of acute OX1R blockade. Previous work has shown that, when treated with SB-334867 (30 mg/kg, i.p.) 30 min before a 1h test with palatable food, rats begin to show appreciable levels of resting 10-15 min earlier than under control conditions (i.e. around 20 min versus 30-35 min into the session). The present results demonstrate that a 20 min increase in the injection-test interval (i.e. 50 min) had no significant impact on the anorectic, behavioural or weight gain effects of SB-334867 in non-deprived male rats. Most importantly, this altered treatment regimen led to a temporal profile of resting virtually identical to that previously observed with the more conventional 30 min injection-test interval. Although parallel studies indicated that the OX1R antagonist accelerated the onset of resting (and suppressed most active behaviours) even in the absence of food, an equianorectic dose of the natural satiety-related signal cholescystokinin octapeptide (CCK-8S; 5 microg/kg, i.p.) also produced very similar behavioural effects regardless of the presence of food. Together with evidence that SB-334867 preserves the structural integrity of natural feeding behaviour, does not induce nausea/illness or alter taste/palatability and fails to influence EEG measures of arousal/sleep, the present findings are consistent with the view that acute OX1R antagonism selectively enhances satiety. However, unlike the immediate short-circuiting of the satiety sequence induced by CCK-8S, the slower response to SB-334867 implies a more indirect mechanism of action.

Analysis of Variance↗
PubMed2004

Physiology: does gut hormone PYY3-36 decrease food intake in rodents?

Batterham et al. report that the gut peptide hormone PYY3-36 decreases food intake and body-weight gain in rodents, a discovery that has been heralded as potentially offering a new therapy for obesity. However, we have been unable to replicate their results. Although the reasons for this discrepancy remain undetermined, an effective anti-obesity drug ultimately must produce its effects across a range of situations. The fact that the findings of Batterham et al. cannot easily be replicated calls into question the potential value of an anti-obesity approach that is based on administration of PYY3-36.

Animals↗
PubMed2004

Differential effects of the selective orexin-1 receptor antagonist SB-334867 and lithium chloride on the behavioural satiety sequence in rats.

Recent studies have shown that acute systemic administration of the selective orexin-1 receptor antagonist SB-334867 significantly reduces food intake in rats. Although this anorectic action of orexin-1 receptor blockade is associated with an acceleration in the transition from eating to resting, it is widely recognised that the behavioural indices of satiety are not dissimilar to those of illness. In this context, Experiment 1 confirmed a significant anorectic effect of 90 (but not 60) mg/kg lithium chloride (LiCl) in male rats presented with palatable mash in the home-cage environment. Experiment 2 employed a continuous monitoring technique to contrast the effects of LiCl (90 mg/kg) and SB-334867 (10 and 30 mg/kg) on food intake and behaviour during a 1-h test with palatable mash. SB-334867 dose-dependently inhibited food intake, with the higher dose producing a comparable degree of appetite suppression (approximately 40%) to that seen with LiCl. Despite equivalent anorectic action, the two compounds produced very different effects on behaviour. LiCl reduced active behaviours (locomotion, rearing, grooming and sniffing), slowed the rate of eating and disrupted the behavioural satiety sequence (BSS). In contrast, SB-334867 (30 mg/kg) decreased the duration of feeding and grooming, and modestly accelerated the transition between eating and resting. Furthermore, whereas LiCl failed to alter posttreatment bodyweight gain, SB-334867 (30 mg/kg) produced a significant weight loss in the 24-h period immediately following injection. Overall, the divergent profiles obtained with equianorectic doses of LiCl and SB-334867 provide convincing evidence for the behavioural selectivity of SB-334867-induced anorexia.

Animals↗
PubMed2004

Effects of a sweet and a nonsweet lunch on short-term appetite: differences in female high and low consumers of sweet/low-energy beverages.

INTRODUCTION: Effects of sweet taste on short-term appetite are still being actively researched. This study investigates the proposal that the effects of sweet tastes on appetite may differ as a result of differing habitual experiences of sweetness with or without energy. METHODS: Effects of sweet tastes on appetite were investigated in habitual high and low consumers of sweet/low-energy beverages. Sweet taste was manipulated in a preload lunch and appetite was subsequently measured using test meal intake and subjective ratings of general and specific appetites. RESULTS: The effects of the sweet and nonsweet lunch on short-term appetite differed significantly in high and low consumers of sweet/low-energy beverages, in subjective ratings of appetite for something sweet [consumer x preload x time interaction F(12,126) = 2.68, P = 0.003] and appetite for something savoury [consumer x preload x time interaction F(12,126) = 3.17, P = 0.001]. Effects in low consumers of sweetness without energy demonstrate close association between taste and energy, whereas effects in high consumers suggest a dissociation between taste and energy in these consumers. DISCUSSION: These findings provide a further indication that the short-term control of appetite varies according to the habitual pattern of dietary intake. The long-term experience of sweetness without energy influences appetite for sweet and savoury tastes.

Appetite↗
PubMed2003

Effects of systematic variation in presatiation and fasting on the behavioural satiety sequence in male rats.

Preclinical research on the neurobiology of appetite regulation is increasingly employing detailed behavioural assessment in addition to measures of food intake. One of the most widely used approaches examines treatment effects on the behavioural satiety sequence (BSS), a concept describing the predictable pattern of behavioural change (feeding-->grooming-->resting) associated with the process of satiation in rats, mice and other mammals. Surprisingly, however, comparatively little published detail is available concerning the impact of more natural appetite modulators on the BSS. In two separate experiments, a continuous monitoring technique was used to calibrate the effects of prefeeding (3, 6 and 9 min) and prior fasting (3, 6 and 12 h) on the microstructure of rat behaviour during a 1 h test with palatable mash. Prefeeding significantly increased eating latencies and reduced both food intake and total duration (but not frequency) of feeding behaviour. The reduction in time spent eating was most evident during the first 15 min of the test when feeding is normally at peak levels. Although behavioural structure was fully preserved in all test conditions, the two larger preloads resulted in shifts to the left (i.e., an acceleration) in the BSS. In contrast, fasting for 6 and 12 h (but not 3 h) increased food intake and duration (but not frequency) of feeding behaviour in the early part of the test. All fasting conditions (including 3 h) produced considerable shifts to the right (i.e., a delay) in the BSS, confirming the greater sensitivity of this measure relative to food intake per se. The potential utility of these reference profiles is discussed in relation to drug-induced changes in food intake and the BSS.

Animals↗
PubMed2003

Palatability, food intake and the behavioural satiety sequence in male rats.

Food intake is influenced not only by nutritional status but also by diverse environmental factors. Indeed, a unique quality of food reward is its strong modulation by palatability cues, such as taste, with animals generally preferring diets that are sweet and avoiding those that are either bitter or sour. As appetite suppressants (including those currently in development) could alter food intake by modifying taste sensitivity and/or palatability, the aim of the present study was to characterise the influence of taste adulteration on the normal structure of feeding behaviour, i.e., the behavioural satiety sequence (BSS). Adult male rats were initially habituated both to the basic test diet (mash) and the test arena. Following stabilisation of basal intake, a continuous monitoring technique was used to profile behaviour in weekly 1-h sessions during which the animals were presented, in counterbalanced order, with the basic diet (control) or one of four taste-adulterated variants (0.015% quinine, 0.04% quinine, 0.2% saccharin, 0.3% saccharin). Food intake was strongly suppressed by the higher quinine concentration but was not significantly altered by any of the other additives. Behavioural analysis revealed that this anorectic-like response to 0.04% quinine-adulterated food was associated with a significant reduction in the peak feeding response, highly atypical intermittent food sampling/digging and the virtual absence of resting behaviour. Importantly, this pattern of behavioural change is readily distinguishable from those seen in response to other manipulations that reduce intake, including selective anorectics, sedatives and psychostimulants. Despite the lack of significant effect on food intake or the duration of feeding behaviour, dietary adulteration with 0.015% quinine (and, to a lesser degree, 0.3% saccharin) produced some effects on behavioural structure/time course consistent with a mild aversive response, i.e., bouts of midsession food sampling and a delay in the transition from eating to resting. Data are discussed in relation to the specific behavioural signature to quinine-induced anorexia and its potential utility in identifying appetite suppressants that may modify intake via changes in taste sensitivity and/or palatability.

Animals↗
PubMed2003

Cross talk between physical activity and appetite control: does physical activity stimulate appetite?

Physical activity has the potential to modulate appetite control by improving the sensitivity of the physiological satiety signalling system, by adjusting macronutrient preferences or food choices and by altering the hedonic response to food. There is evidence for all these actions. Concerning the impact of physical activity on energy balance, there exists a belief that physical activity drives up hunger and increases food intake, thereby rendering it futile as a method of weight control. There is, however, no evidence for such an immediate or automatic effect. Short (1-2 d)-term and medium (7-16 d)-term studies demonstrate that men and women can tolerate substantial negative energy balances of < or = 4 MJ energy cost/d when performing physical activity programmes. Consequently, the immediate effect of taking up exercise is weight loss (although this outcome is sometimes difficult to assess due to changes in body composition or fluid compartmentalization). However, subsequently food intake begins to increase in order to provide compensation for about 30% of the energy expended in activity. This compensation (up to 16 d) is partial and incomplete. Moreover, subjects separate into compensators and non-compensators. The exact nature of these differences in compensation and whether it is actually reflective of non-compliance with protocols is yet to be determined. Some subjects (men and women) performing activity with a cost of < or = 4 MJ/d for 14 d, show no change in daily energy intake. Conversely, it can be demonstrated that when active individuals are forced into a sedentary routine food intake does not decrease to a lower level to match the reduced energy expenditure. Consequently, this situation creates a substantial positive energy balance accompanied by weight gain. The next stage is to further characterize the compensators and non-compensators, and to identify the mechanisms (physiological or behavioural) that are responsible for the rate of compensation and its limits.

Anorexia↗
PubMed2002

Orexins and appetite regulation.

Initial research on the functional significance of two novel hypothalamic neuropeptides, orexin-A and orexin-B, suggested an important role in appetite regulation. Since then, however, these peptides have also been shown to influence a wide range of other physiological and behavioural processes. In this paper, we review the now quite extensive literature on orexins and appetite control, and consider their additional effects within this context. Although the evidence for orexin (particularly orexin-A and the orexin-1 receptor) involvement in many aspects of ingestive physiology and behaviour is incontrovertible, central administration of orexins is also associated with increased EEG arousal and wakefulness, locomotor activity and grooming, sympathetic and HPA activity, and pain thresholds. Since the orexin system is selectively activated by signals indicating severe nutritional depletion, it would be highly adaptive for a hungry animal not only to seek sustenance but also to remain fully alert to dangers in the environment. Crucial evidence indicates that orexin-A increases food intake by delaying the onset of a behaviourally normal satiety sequence. In contrast, a selective orexin-1 receptor antagonist (SB-334867) suppresses food intake and advances the onset of a normal satiety sequence. These data suggest that orexin-1 receptors mediate the episodic signalling of satiety and appear to bridge the transition from eating to resting in the rats' feeding-sleep cycle. The argument is developed that the diverse physiological and behavioural effects of orexins can best be understood in terms of an integrated set of reactions which function to rectify nutritional status without compromising personal survival. Indeed, many of the non-ingestive effects of orexin administration are identical to the cluster of active defences mediated via the lateral and dorsolateral columns of the midbrain periaqueductal gray matter, i.e., somatomotor activation, vigilance, tachycardia, hypertension and non-opioid analgesia. In our view, therefore, the LH orexin system is very well placed to orchestrate the diverse subsystems involved in foraging under potentially dangerous circumstances, i.e., finding and ingesting food without oneself becoming a meal for someone else.

Animals↗
PubMed2002

The effect of graded levels of exercise on energy intake and balance in free-living women.

AIM: We assessed the effect of graded increases in exercised-induced energy expenditure (EE) on appetite, daily energy intake (EI), total daily EE and body weight in six lean women using a within-subject, repeated measures design. METHOD: Subjects were each studied three times during 7 day treatments, corresponding to no-exercise (control; Nex; 0 MJ/day), medium exercise level (Mex; approximately 1.9 MJ/day) and high exercise level (Hex; approximately 3.4 MJ/day), with 2 day maintenance beforehand. Subjects self-weighed ad libitum food intake. EE was assessed by continual heart rate monitoring. During waking hours subjects recorded hourly sensations of hunger and appetite. RESULTS: EE amounted to 9.2, 11.0 and 12.1 MJ/day (F (2, 10)=5.67; P=0.023 (s.e.d.=0.87)) on the Nex, Mex and Hex treatments, respectively. The corresponding values for EI were 8.9, 9.2 and 10.0 MJ/day (F (2, 10)=4.80; P=0.035 (s.e.d.=0.36)). There were very weak treatment effects on hunger. Weight loss was significantly different from zero on the Mex and Hex treatments. CONCLUSION: Markedly increasing EE through exercise produced significant but partial compensations in EI ( approximately 33% of EE due to exercise). Accurate adjustments of El to acute increases in EE are likely to take weeks rather than days.

Adult↗
PubMed2002

Differences in postprandial responses to fat and carbohydrate loads in habitual high and low fat consumers (phenotypes).

The present study investigated metabolic responses to fat and carbohydrate ingestion in lean male individuals consuming an habitual diet high or low in fat. Twelve high-fat phenotypes (HF) and twelve low-fat phenotypes (LF) participated in the study. Energy intake and macronutrient intake variables were assessed using a food frequency questionnaire. Resting (RMR) and postprandial metabolic rate and substrate oxidation (respiratory quotient; RQ) were measured by indirect calorimetry. HF had a significantly higher RMR and higher resting heart rate than LF. These variables remained higher in HF following the macronutrient challenge. In all subjects the carbohydrate load increased metabolic rate and heart rate significantly more than the fat load. Fat oxidation (indicated by a low RQ) was significantly higher in HF than in LF following the fat load; the ability to oxidise a high carbohydrate load did not differ between the groups. Lean male subjects consuming a diet high in fat were associated with increased energy expenditure at rest and a relatively higher fat oxidation in response to a high fat load; these observations may be partly responsible for maintaining energy balance on a high-fat (high-energy) diet. In contrast, a low consumer of fat is associated with relatively lower energy expenditure at rest and lower fat oxidation, which has implications for weight gain if high-fat foods or meals are periodically introduced to the diet.

Adult↗
PubMed2001

Description and evaluation of a Newton-based electronic appetite rating system for temporal tracking of appetite in human subjects.

This study assessed the reliability and validity of a palm-top-based electronic appetite rating system (EARS) in relation to the traditional paper and pen method. Twenty healthy subjects [10 male (M) and 10 female (F)] - mean age M=31 years (S.D.=8), F=27 years (S.D.=5); mean BMI M=24 (S.D.=2), F=21 (S.D.=5) - participated in a 4-day protocol. Measurements were made on days 1 and 4. Subjects were given paper and an EARS to log hourly subjective motivation to eat during waking hours. Food intake and meal times were fixed. Subjects were given a maintenance diet (comprising 40% fat, 47% carbohydrate and 13% protein by energy) calculated at 1.6xResting Metabolic Rate (RMR), as three isoenergetic meals. Bland and Altman's test for bias between two measurement techniques found significant differences between EARS and paper and pen for two of eight responses (hunger and fullness). Regression analysis confirmed that there were no day, sex or order effects between ratings obtained using either technique. For 15 subjects, there was no significant difference between results, with a linear relationship between the two methods that explained most of the variance (r(2) ranged from 62.6 to 98.6). The slope for all subjects was less than 1, which was partly explained by a tendency for bias at the extreme end of results on the EARS technique. These data suggest that the EARS is a useful and reliable technique for real-time data collection in appetite research but that it should not be used interchangeably with paper and pen techniques.

Adult↗
PubMed2001

Control of food intake in the obese.

Food intake (eating) is a form of behavior that is subject to conscious control. In practice, many obese and weight-gaining individuals claim that their eating is out of (their) control. Mechanistic models describe the interplay of biological and environmental forces that control food intake. However, because human food intake is characterized by individuals intervening to adjust their own patterns of behavior, food intake should reflect interactions among biology, environment, and attempted self-imposed control of behavior. In general, humans display a system of weight regulation that is asymmetrical--a reduction in body weight is strongly defended but weight gain is not. The body seems to tolerate a positive energy balance. There is no mechanism that can detect a positive energy balance per se or that can implement a sufficiently strong correction to behavior to maintain body weight in an environment that promotes consumption. The evolutionary process has favored biological traits associated with preferences for high energy density (sweet and/or fatty) energy-yielding foods. The control of food intake in obese or weight-gaining individuals may display various risk factors that favor an increase in energy. These include the preference for high energy-dense over low energy-dense foods, weak postprandial inhibitory signaling, strong hunger traits associated with low leptin levels after weight loss, and the consumption of fatty foods. In addition, many individuals (up to 47% of some samples) display binge eating patterns, whereas approximately 16% show either night eating or nocturnal eating. Because energy expenditure is only loosely coupled to energy intake, sedentariness does not down-regulate food intake.

Appetite Regulation↗
PubMed2001

High-fat and low-fat phenotypes: habitual eating of high- and low-fat foods not related to taste preference for fat.

OBJECTIVE: To characterize taste preferences in habitual high fat (HF) and low fat (LF) phenotypes. DESIGN: Eighteen test solutions to taste for each subject group in a fully repeated 2x6x3 measures design. SETTING: The Human Appetite Research Unit at Leeds University, Psychology Department. SUBJECTS: Eight lean HF (mean percentage fat intake 43.4% daily energy) and eight lean LF (mean percentage fat intake 32.7% daily energy) were recruited from the staff/student population of Leeds University. INTERVENTIONS: All subjects were required to taste 18 solutions based on six levels of fat content and three levels of sucrose content. Subjects rated each solution for fat content, sweetness and pleasantness. RESULTS: HF and LF showed significant effect for the fat content of the solution on the perception of creaminess (P<0.000), and sugar content on the perception of sweetness (P<0.000). HF and LF did not differ in their taste preferences and no preferred level of fat or sweetness was detected in either group. CONCLUSIONS: In young adult males, habitual food selection is not related to taste preference. SPONSORSHIP: This study was supported by the Biotechnology and Biological Sciences Research Council (BBSRC).

Adolescent↗