Terence M. Dovey

Effect of television advertisements for foods on food consumption in children

The impact of television (TV) advertisements (commercials) on childrens eating behaviour and health is of critical interest. In a preliminary study we examined lean, over weight and obese childrens ability to recognise eight food and eight non-food related adverts in a repeated measures design. Their consumption of sweet and savoury, high and low fat snack foods were measured after both sessions. Whilst there was no significant difference in the number of non-food adverts recognised between the lean and obese children, the obese children did recognise significantly more of the food adverts. The ability to recognise the food adverts significantly correlated with the amount of food eaten after exposure to them. The overall snack food intake of the obese and overweight children was significantly higher than the lean children in the control (non-food advert) condition. The consumption of all the food offered increased post food advert with the exception of the low-fat savoury snack. These data demonstrate obese childrens heightened alertness to food related cues. Moreover, exposure to such cues induce increased food intake in all children. As suggested the relationship between TV viewing and childhood obesity appears not merely a matter of excessive sedentary activity. Exposure to food adverts promotes consumption.

Beyond-brand effect of television food advertisements on food choice in children: the effects of weight status

OBJECTIVE To investigate the effect of television food advertising on childrens food intake, specifically whether childhood obesity is related to a greater susceptibility to food promotion. DESIGN The study was a within-subject, counterbalanced design. The children were tested on two occasions separated by two weeks. One condition involved the children viewing food advertisements followed by a cartoon, in the other condition the children viewed non-food adverts followed by the same cartoon. Following the cartoon, their food intake and choice was assessed in a standard paradigm. SETTING The study was conducted in Liverpool, UK. SUBJECTS Fifty-nine children (32 male, 27 female) aged 9-11 years were recruited from a UK school to participate in the study. Thirty-three children were normal-weight (NW), 15 overweight (OW) and 11 obese (OB). RESULTS Exposure to food adverts produced substantial and significant increases in energy intake in all children (P < 0.001). The increase in intake was largest in the obese children (P = 0.04). All children increased their consumption of high-fat and/or sweet energy-dense snacks in response to the adverts (P < 0.001). In the food advert condition, total intake and the intake of these specific snack items correlated with the childrens modified age- and gender-specific body mass index score. CONCLUSIONS These data suggest that obese and overweight children are indeed more responsive to food promotion, which specifically stimulates the intake of energy-dense snacks.

Beyond-brand effect of television (TV) food advertisements/commercials on caloric intake and food choice of 5-7-year-old children.

Food advert exposure has been shown to influence calorie intake and food choice in 9-11 year olds. However, little is known about the effect of food advertisements on feeding behaviour in younger children. Therefore, we conducted a study with 93 children aged 5-7 years, 28 of whom were over weight or obese. The children were exposed to 10 non-food adverts and 10 food adverts in a repeated measures design. Their consumption of sweet and savoury, high and low fat snack foods, and fruit were measured following both sessions. Food advert exposure produced a significant increase in total food intake in young children. The collection of recognition data was incomplete. These data replicate previous findings in that exposure to food adverts increases food intake in all children, but recognition of food adverts is related to body mass index (BMI). Beyond their effects on brand choice, exposure to food advertisements (commercials) promotes over-consumption in younger children.

The Pharmacology of Human Appetite Expression

The discovery of the adiposity signal leptin a decade ago revolutionised our understanding of the hypothalamic mechanisms underpinning the central control of ingestive behaviour. Subsequently, the structure and function of various hypothalamic peptide systems (Neuropeptide Y (NPY), Orexins, Melanocortins, Cocaine and Amphetamine Regulating Transcript (CART), Galanin/Galanin Like Peptides (GALP) and endocannabinoids) have been characterised in detail in rodent models. The therapeutic benefit of targeting these systems remains to be discovered. More is becoming known about the pharmacological potential of peripheral, meal-induced, episodic endogenous peptides. Hormones such as Cholecystokinin (CCK), Gastrin Releasing Peptides (GRP), Glucagon-Like Peptide I (GLP-1) Enterostatin, Amylin, Peptide YY (PYY) and Ghrelin are released prior to, during and/or after a meal, controlling intake and subjective feelings of appetite (hunger and satiety). In addition, there is an expanding body of literature detailing the effects of a wide variety of drugs on human appetite and food intake. Some of these drugs act upon CNS monoamine systems such as Serotonin (5-HT). Dopamine (DA) and Noradrenaline (NA), have long been implicated in appetite regulation. Detailed examination of both the effect of agonising endogenous gut peptide systems and the effect of various monoaminergic drugs on the expression of human appetite can provide a greater understanding of mechanisms underpinning normal appetite regulation. However, such an understanding must be based on knowledge of the effect of the treatment on meal size, eating rate, meal pattern, food choice and the subjective experience of appetite flux (hunger and satiety), and notjust food intake.

Autoradiographic analysis of ghrelin receptors in the rat hypothalamus

Ghrelin exerts potent stimulatory effects on food intake. It is assumed to increase feeding by binding at growth hormone secretagogue receptors (GHS-R), the only sites of action for this gastric hormone identified to date. Initially, the distribution of ghrelin binding sites could only be determined from expression patterns of GHS-R mRNA or the use of immunohistochemical techniques to examine c-fos expression. However, the characterisation of a novel radioligand ([(125)I-his(9)]-ghrelin), has enabled the distribution of GHS-R receptor protein to be directly demonstrated. Here, using quantitative autoradiography, we investigate the distribution and density of ghrelin receptors in the rodent hypothalamus. Specific binding was identified in the appetite-regulating arcuate nucleus, ventromedial hypothalamic nucleus, paraventricular nucleus, dorsomedial hypothalamic nucleus and the lateral hypothalamic area corresponding to the previously reported distribution pattern of GHS-R mRNA. Surprisingly, variations in receptor density were not identified in any of these binding sites upon a change in nutritional status, despite relevant alterations in plasma ghrelin levels being identified. We suggest that this may relate to the paradigm employed to modify nutritional status in the study or could indicate that peripheral ghrelin is unlikely to be the major source of ghrelin that acts in many hypothalamic sites.

When Does Food Refusal Require Professional Intervention

Food refusal can have the potential to lead to nutritional deficiencies, which increases the risk of a variety of communicable and non-communicable diseases. Deciding when food refusal requires professional intervention is complicated by the fact that there is a natural and appropriate stage in a childs development that is characterised by increased levels of rejection of both previously accepted and novel food items. Therefore, choosing to intervene is difficult, which if handled badly can lead to further food refusal and an even more limited diet. Food refusal is often based on individual preferences; however, it can also be defined through pathological behaviours that require psychological intervention. This paper presents and discusses several different types of food refusal behaviours; these are learningdependent, those that are related to a medical complication, selective food refusal, fear-based food refusal and appetiteawareness-autonomy-based food refusal. This paper describes the behaviours and characteristics that are often associated with each; however, emphasis is placed on the possibility that these different types of food refusal can often be co-morbid. The decision to offer professional intervention to the child and their family should be a holistic process based on the level of medical or psychological distress resulting from the food refusal.

Ghrelin restores 'lean-type' hunger and energy expenditure profiles in morbidly obese subjects but has no effect on postgastrectomy subjects

Objective:To examine the effects of ghrelin on appetite and energy expenditure in lean, obese and postgastrectomy subjects.Design:A randomized, double-blind, placebo-controlled study.Patients:Nine lean subjects (mean body mass index (BMI) 23.5±3 kg/m2) and nine morbidly obese subjects (mean BMI 51.4±10 kg/m2) and eight postgastrectomy subjects (mean BMI 22.4±1.0 kg/m2).Interventions:Subjects were infused with either intravenous ghrelin (5 pmol kg−1 min−1) or saline over 270 min. They were given a fixed energy breakfast followed by a free buffet lunch towards the end of the infusion.Main outcome measures:Visual analogue scales were used to record hunger and energy expenditure was measured by indirect calorimetry.Results:Ghrelin increased energy intake at the buffet lunch in lean subjects (a 41% increase, P<0.01) and obese subjects (35% increase, P=0.04) but not in postgastrectomy subjects. Lean subjects showed a characteristic preprandial rise and postprandial fall in hunger scores, which was exaggerated by ghrelin infusion. Obese subjects showed little variation in hunger scores, but a ‘lean-type’ pattern was restored when given exogenous ghrelin. Ghrelin had no effect on resting metabolic rate but did increase respiratory quotient (RQ) in obese subjects. Ghrelin also increased RQ variability over time in all three groups (ANOVA, P<0.001).Conclusions:Hunger scores are abnormal in the obese, perhaps because of impaired ghrelin secretion. The effect of ghrelin in restoring normal hunger profiles in the obese suggests causality, confirming an important role in eating behaviour. Ghrelin also increases RQ in obese humans and increased RQ variability in all groups. This suggests that ghrelin regulates substrate utilization and may promote metabolic flexibility.

The effects of sibutramine on the microstructure of eating behaviour and energy expenditure in obese women

Given the suggestion that many potential anti-obesity drugs may enhance within-meal satiation, few studies have directly measured the effects of any drug on the microstructure of human eating behaviour. The effects of 7 days dosing with sibutramine 10 mg and 15 mg a day on appetite and energy balance were determined in 30 obese women (BMI 34.6 ± 3.3 kg/m2, age 46.0 ± 12.9 years) using a Universal Eating Monitor (UEM) and indirect calorimetry, in a double-blind, placebo-controlled crossover study. At day 7, sibutramine 10 mg and 15 mg reduced food intake by 16.6% and 22.3%, respectively (p < 0.001), compared with placebo. Sibutramine reduced eating rate compared with placebo rather than meal length (10 mg p < 0.05; 15 mg p < 0.001). In addition, sibutramine 10 mg significantly reduced hunger later in the meal (p < 0.05) and sibutramine 15 mg increased fullness early in the meal (p < 0.01), both of which are consistent with enhanced within-meal satiation. Sibutramine had little effect on resting metabolic rate, although 15 mg did significantly reduce respiratory quotient at several time points during the test day. These results provide novel evidence that decreased consumption of a test meal induced by sibutramine is primarily because of reduced eating rate, enhancing the deceleration in cumulative food intake within a meal associated with the development of satiety. Changes in within-meal appetite ratings appear particularly sensitive to drug-induced enhancement of satiation, and may provide key indices for assessing the therapeutic potential of novel anti-obesity drugs.

Metformin prolongs the postprandial fall in plasma ghrelin concentrations in type 2 diabetes

Weight loss is difficult to achieve in type 2 diabetes and many therapies are associated with weight gain, an effect attenuated by metformin. We studied the effects of metformin on energy expenditure, appetite and the regulation of PYY and ghrelin in type 2 diabetes.

Effects of insulin‐induced hypoglycaemia on energy intake and food choice at a subsequent test meal

Hypoglycaemia is assumed to increase food intake, but there is little data on the magnitude or qualitative nature of this effect. We have therefore investigated the effects of insulin‐induced hypoglycaemia on food intake at a test meal.