Please note, this is recovered content from the former website of the New York Obesity Research Center website.


Can We Change Appetitive Traits in Children in Order to Prevent Obesity

Date: June 5, 2008
Speaker’s Name, Affiliation: Susan Carnell, New York Obesity Research Center, St. Luke’s Roosevelt Hospital
Seminar Title: “Appetitive traits in children: measures, causes & consequences”

Dr. Susan Carnell gave a thought provoking summary of her recent studies on the appetitive traits of children. In an environment that is considered highly ‘obesogenic,’ some individuals are able to remain lean, while others cannot. Determining why some children are more susceptible to obesity than others and what proportion of this susceptibility originates from appetitive behaviors can further elucidate the causes and suggest potential treatments for obesity.

role-of-sex-differencesMajor appetitive traits include the following: satiety responsiveness, food cue responsiveness, rewarding value of food, and food preferences. Satiety responsiveness refers to an individual’s responsiveness to internal satiety signals such as gut peptides or gastric distension. Food cue responsiveness refers to the responsivity to external cues (such as the sight or smell of food). The rewarding value of food is the subjective reward experienced when eating liked foods. There is limited evidence that at least some of these traits are related to obesity. Jansen et al. (2003) showed that obese children had poorer caloric compensation (a measure of satiety responsiveness) compared with lean children.

Furthermore, obese children tend to eat faster (Drabman et al., 1979), and those that eat faster tend not to decelerate their eating rate throughout a meal (Barkeling et al., 1992). With respect to food cue responsiveness, Birch and Fisher, 2000, (and Fisher 2007) have shown that obese children show greater “eating in the absence of hunger,” a measure that is similar to the adult measure of disinhibited eating. These obese children eat more palatable, tasty snack foods, even after they have just eaten a meal to reported satiety. fMRI studies also support this, showing that obese children show greater activation in planning and reward centers in response to food cues and no post-meal decrease in food motivation areas.

The first study that Dr. Carnell presented was designed to determine if caloric compensation is associated with obesity in a sample of 150, 4-5 y. old twins from North London. Data revealed a negative association between BMI z-score and level of caloric compensation, such that heavier children showed poorer compensation (Carnell & Wardle, Appetite 2007).

The second study presented by Dr. Carnell was from a sub-sample of the TEDS (Twins Early Development Study) study of 253, 9-11 y. olds. The objective of this study was to assess the association between child eating rate and adiposity. Data were collected through a series of home visits where researchers gave children pre-packed lunch meals and counted the number of bites per minute throughout the meal time. For all children, eating rate decelerated over time, but obese children showed poorer satiety responsiveness overall as indicated by a faster eating rate throughout.

The third study presented by Dr. Carnell contained data from TEDS and PEACHES (Physical Exercise and Appetite in Children Study). A total of 664, 7-12 y. old children were studied, 316 from TEDS and 348 from PEACHES. A modified version of the eating in the absence of hunger measure was used where children were given bags of sweet snacks and puzzle booklets, and intake of the sweet snacks was recorded over 10 minutes. In boys, greater adiposity correlated with increased eating in the absence of hunger (r=0.26 for PEACHES & r=0.40 for TEDS). There was also a significant association for girls in the TEDS sample.

In the fourth study, Dr. Carnell used the CEBQ (Child Eating Behavior Questionnaire). This questionnaire is a parent-report questionnaire that assesses satiety responsiveness, food cue responsiveness, and the enjoyment of food. The scale correlates well with behavioral measures (Carnell & Wardle, 2007). Results showed that satiety responsiveness was negatively correlated with child adiposity (waist circumference and BMI z-score) and enjoyment of food was positively associated with adiposity.

The final portion of the talk discussed the factors that influence children’s appetitive traits, and whether or not these traits can be changed to prevent obesity. Parents may play a powerful role in influencing appetitive traits. For example, Fisher & Birch (1999) have shown that experimentally restricting children’s access to a food-the “forbidden food” effect—increases children’s intake, desire, and selection of that food. In addition, Dr. Carnell also looked at parental feeding styles (eg. restriction, monitoring, pressure to eat, etc). Results showed that children with more restrictive parents had higher levels of food responsiveness, whereas children with parents who reported greater “pressuring” to eat showed greater satiety responsiveness.

Another set of studies discussed the heritability of appetite and adiposity in twins. Results suggested that both waist circumference and BMI z-score have high levels of heritability (h2 = 0.77). Eating rate had a heritability of 0.62, and satiety responsiveness and the enjoyment of food had heritabilities of 0.63 and 0.75, respectively. This study demonstrates that genes are important determinants of appetitive traits, though it is important to stress that environmental factors also play a crucial role, for example by allowing genetically-influenced appetive traits to express themselves.

An important application to this work is to determine if and how appetitive traits in children can be modified to improve eating control. In 2000, Susan Johnson (Johnson, 2000) performed a study where she used a doll with a fullness scale to train children to improve their appetite regulation. Children showed better caloric compensation after this training protocol than before it. In addition, a study using a Mandometer to retrain children’s rate of eating for 617 days showed reductions in BMI across the study.

In sum, individual appetite differences in children are associated with differences in adiposity in cross-sectional studies. Some studies have successfully modified these appetite traits to improve children’s weight status. Future studies should be done to follow children across development to determine the causal influences on appetitive traits and adiposity. Furthermore, biomarkers should be incorporated into these studies to determine mechanisms behind these appetitive traits.


Q. Do twins eat together in your studies?
A. Yes. We did this to try and emulate a natural eating situation.

Q. Some rates of meal paradigms suggest that subjects are actually hungrier at the beginning of the meal, and thus more motivated to eat. Is it possible that this is what you are actually assessing in the relationship you are showing between eating rate and adiposity as a function of child weight status?
A. Yes, that’s a good point. I’m simplifying everything for the talk, but it is very unlikely that each test taps into just one aspect of appetite, and it’s unclear how biologically and conceptually independent each aspect is. For example, eating rate could be picking up on enjoyment of food and food cue responsiveness, not just satiety responsiveness.

Q. Were twins mono- or dizygotic?
A. It was a mixed group of both MZs and DZs.

Q. Were they genotyped, or was this information attained from maternal report?
A. Yes, they were from a much larger cohort study of twins, in which all children were genotyped early in life.

Q. The scale that you are showing (CEBQ Enjoyment of Food by Waist Circumference group in 8-11 y. olds) is a bit expanded. Can you extrapolate to predict the behavior of a single person from that figure?
A. The graphs simply show item mean scores for each scale, ranging from 1-5 – this is why the differences seem small We don’t yet have the data to show whether you can predict an individual child’s behavior from their score.

Q. Are there good scales for measuring dietary restraint in 8-11 y. olds?
A. There are, I think. At least they exist, but I’m not sure how accurate they are.

Q. How did parents report child waist circumference?
A. We gave them an instruction sheet and a tape measure. The correlation between parents’ and researchers’ measures in a sub-sample was 0.92.

Q. You listed food reward in your outline, but you didn’t really go over these data. Is that because you didn’t collect it yourself?
A. Yes, but I did include some slides in the end (portion that was deleted due to time), from Epstein’s group. We tried to repeat some of the findings from Epstein in obese children, but it ended up that the bar pressing was not an arduous task for them to perceive this as work. The children actually enjoyed pushing the bar sometimes.

Q. Did the Epstein study report data from individuals or the mean responses?
A. I believe they reported the mean responses.

Q. You mentioned the Johnson and Fisher study where they trained children to recognize when they were full with the use of dolls. Have you done any work in this area yourselves?
A. In our Eating in the Absence of Hunger study, about half of the kids actually reported that they were still hungry after lunch. We were not sure if we were training the children correctly, or assessing the fullness responses correctly, so we did not pursue this further.

Q. In the Birch and Johnson study, did they have any quantitative data to compare to the hunger/fullness ratings?
A. I don’t think so.
Comment: I don’t know if your paradigm allows it, but one thing that you might want to do is try both a progressive and a fixed ratio when you are trying to measure the amount of work children will do for food.

Q. Did you closely monitor the BMI of mothers and fathers, and how does this relate to children’s BMIs?
A. We have collected self-reports from mothers, and we have some earlier data for fathers, We haven’t got around to analyzing the data on the relationship between parental BMI and child appetite as yet but we expect to find one.

Q. Did you conduct the mandometer study with children? Do you know what age the children were? Is it published data?
A. We did not publish this study. The authors are currently adding these data to a chapter, but as far as I know they have not yet submitted it to a peer reviewed journal. The children were 11-17 years old.

Q. What are you doing next?
A. We have planned a longitudinal twin study beginning right at birth, trying to get at maternal responsiveness to satiety cues and other environmental and genetic determinants of appetite and adiposity.


  • Barkeling B, Ekman S, Rossner S. (1992) Eating behaviour in obese and normal weight 11-year-old children. Int J Obes Relat Metab Disord. 16:355-60.
  • Birch LL, Fisher JO. (2000) Mothers’ child-feeding practices influence daughters’ eating and weight. Am J Clin Nutr. 71:1054-61.
  • Carnell S, Wardle J.(2008) Appetite and adiposity: A behavioral susceptibility theory of obesity. Am J Clin Nutr. In press.
  • Carnell S, Wardle J. (2007) Measuring behavioural susceptibility to obesity: validation of the child eating behaviour questionnaire. Appetite. 48:104-13.
  • Drabman RS, Cordua GD, Hammer D, Jarvie GJ, Horton W. (1979) Developmental trends in eating rates of normal and overweight preschool children. Child Dev. 50:211-6.
  • Fisher JO, Birch LL. (1999) Restricting access to palatable foods affects children’s behavioral response, food selection, and intake. Am J Clin Nutr. 69:1264-72.
  • Fisher, J. O., Cai, G., Jaramillo, S. J., Cole, S. A., Comuzzie, A. G. & Butte, N. F. (2007) Heritability of hyperphagic eating behavior and appetite- related hormones among Hispanic children. Obesity.(Silver.Spring) 15, 1484-1495.
  • Jansen, A., Theunissen, N., Slechten, K., Nederkoorn, C., Boon, B., Mulkens, S. & Roefs, A. (2003) Eat. Behav. 4, 197-209.
  • Johnson SL. (2000) Improving Preschoolers’ self-regulation of energy intake. Pediatrics. 106:1429-35.