‘Health Chatter’: Research Department of Behavioural Science and Health Blog
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    New evidence supports the use of twin studies to explore the effects of nature and nurture on human behaviours in childhood

    By Moritz P Herle, on 5 August 2016

    Written by Moritz Herle, Alison Fildes and Clare Llewellyn

    Over the past century twin studies have been used to explore how nature and nurture influence individual differences in human characteristics (such as personality, intelligence or height). Identical twins share the same genes, while non-identical twins share about half of the same genes; but both types of twins grow up in the same family environment. This means that researchers can compare similarities between identical twins, and similarities between non-identical twins, to get an idea about how much differences between people in characteristics such as height are caused by nature (genes), and nurture (the environment).

    The Health Behaviour Research Centre set up the Gemini twin cohort in 2007.  Gemini is a landmark study of early life growth and behaviour which has been following 2400 British families with twins born in 2007.  Gemini was established to help understand how genes (nature) and the environment (nurture) influence the development of eating behaviours, food preferences and growth in early childhood. Previous studies conducted by the Gemini team have suggested that individual differences in eating behaviours during childhood are strongly influenced by genes.

    Like much research into early child development, these studies have had to rely on parents’ ratings of their children’s eating behaviour. This is because large sample sizes make it difficult to measure behaviours in a laboratory and because young children are unable to report accurately on their own characteristics. Parents of Gemini twins provided information about their children’s behaviour using a widely-used questionnaire called the Child Eating Behaviour Questionnaire (CEBQ).  However, a criticism of twin studies is that parents might be biased by their beliefs about their twins’ zygosity (whether they are identical or non-identical) when rating each of their eating behaviours. For example, parents of identical twins might rate them more similarly simply because they think of them as ‘two peas in a pod’, while parents of non-identical twins might exaggerate the differences between them. Because twin studies are based on the comparison of similarity between identical and non-identical twin pairs, reliable and unbiased parental ratings are crucial.

    We recently published a new study that set out to test if parents are biased by their twins’ zygosity when they rate their eating behaviours. Using the Gemini sample we compared eating behaviour ratings from parents who held a false belief about their twins’ zygosity (i.e. they believed them to be non-identical, when they were in fact identical) to those from parents who held an accurate belief. The only way to conclusively know whether a twin pair is identical is to conduct a genetic test, which compares the DNA of the two siblings. However these genetic tests are not routinely carried out and parents can sometimes be misinformed about their twins’ zygosity. A more thorough account of why these misunderstandings occur has been discussed in a previous study.

    We established whether the Gemini twins were identical or non-identical using a combination of DNA testing and a questionnaire that accurately measures twin similarity. We also asked parents about whether they thought their twins’ were identical or not. Using this information we were able to identify parents who held a false belief about their twins’ zygosity, and those who were right. We found that approximately one third of parents of identical twins falsely believed them to be non-identical when they were about eight months old.

    In order to test if parents’ ratings of their twins’ behaviours are biased by their beliefs about their zygosity, we compared the ratings of parents with false and accurate beliefs about their twins’ zygosity, on a range of eating behaviours during infancy and toddlerhood. If parent ratings were biased then we would expect identical twins whose parents believed them to be non-identical to be rated as less similar than identical twin pairs correctly identified by their parents as identical.

    Interestingly, parents’ reports of their identical twins’ eating behaviours were the same, regardless of whether they had false or accurate beliefs about their twins’ zygosity. In other words, parents rated identical twins as more similarly than non-identical twins on all eating behaviours (in both infancy and toddlerhood), regardless of whether they believed them to be identical or non-identical. This indicates that parents of twins can be relied upon to provide unbiased reports of their young children’s eating behaviour, and that findings from twin studies can be trusted.

     

     

    Article link:

    Herle, M., Fildes, A., van Jaarsveld, C., Rijsdijk, F. & Llewellyn, C. H. (2016). Parental Reports of Infant and Child Eating Behaviors are not Affected by Their Beliefs About Their Twins’ Zygosity. Behavior Genetics. doi: 10.1007/s10519-016-9798-y

    Measuring appetitive traits in adults. What do we know about their relationships to weight.

    By Claudia M E Hunot, on 6 July 2016

    By Claudia Hunot, Alison Fildes and Rebecca Beeken.
    Some people are more likely to put on weight than others, and may find it harder to lose weight. One of the ways in which people differ is in how they respond to food; their ‘appetitive traits’. For example, how full you tend to feel after a meal, how much you want to eat when you see or smell delicious foods, or how fast you eat. These traits are partly influenced by genes, and they explain individual differences in the way we all eat. In the present-day food-filled environment people who are more responsive to food cues (want to eat when they see or smell delicious food), and less sensitive to satiety (take longer to feel full) are more susceptible to over-eat and gain weight.

    For a number of years, appetitive traits have been measured in children using the ‘Child Eating Behaviour Questionnaire’ (CEBQ) and more recently in infancy using the ‘Baby Eating Behaviour Questionnaire’ (BEBQ). These questionnaires measure a number of appetitive traits that can be grouped into two broad categories: food approach and food avoidance traits. Food approach traits, such as ‘food responsiveness’, are associated with a larger appetite or greater interest in food, while food avoidance traits such as ‘satiety responsiveness’ are associated with a smaller appetite and/or a lower interest in food. Research has shown higher scores on food approach traits and lower scores on food avoidance traits are associated with increased weight and weight gain. However, so far most of this research has been carried out in children. Until now no matched questionnaire existed for measuring the same appetitive traits in adults.

    Therefore, in our latest study we developed the ‘Adult Eating Behaviour Questionnaire’ (AEBQ) to measure these appetitive traits in adults. We also wanted to explore whether these traits relate to adult weight, as they do in children. Adult samples were recruited at two time points, one-year apart, from an on-line survey panel. Participants completed the AEBQ and provided their weight and height measurements to calculate BMI. Data from a total of 1662 adults was analysed and showed the 35 item AEBQ to be a reliable questionnaire measuring 8 appetitive traits similar to the CEBQ.

    We also showed that food approach traits such as ‘food responsiveness’, ‘emotional over-eating’ and ‘enjoyment of food’ were positively associated with BMI. This means people with higher scores for these traits were heavier on average. While food avoidance traits including ‘satiety responsiveness’, ‘emotional under-eating’ and ‘slowness in eating’ were negatively associated with BMI. This means people with higher scores for these traits were lighter on average.

    These findings suggest appetitive traits are likely to be important for weight across the life course. The newly developed AEBQ is a reliable instrument, which together with the BEBQ and the CEBQ, could be used to track weight-related appetitive traits from infancy into adulthood. The AEBQ may also help to identify individuals at risk of weight gain and could inform targeted interventions tailored to help people manage their appetitive traits, and in turn control their weight.

    Article link:
    Hunot, C., Fildes, A., Croker, H., Llewellyn, C. H., Wardle, J., & Beeken, R. J. (2016). Appetitive traits and relationships with BMI in adults: Development of the Adult Eating Behaviour Questionnaire. Appetite. http://dx.doi.org/10.1016/j.appet.2016.05.024
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    Why tackling appetite could hold the key to preventing childhood obesity

    By Susanne Meisel, on 19 February 2014

    A heartier appetite is linked to more rapid infant growth and to genetic predisposition to obesity, according to two studies recently published by our researchers in the journal JAMA Pediatrics.

    Although it is clear that some people seem to struggle much more than others to keep a healthy weight, so far it has been less obvious why this is the case.  Researchers from our department have now shown that differences in appetite, and especially lower satiety sensitivity (a reduced urge to eat in response to internal ‘fullness’ signals) and higher food responsiveness (an increased urge to eat in response to the sight or smell of nice food) may hold the key to unhealthy weight gain.

    In the first study, the researchers showed that infants with a heartier appetite grew more rapidly up to age 15 months, potentially putting them at increased risk of obesity.

    Our researchers used data from non-identical, same-sex twins born in the UK in 2007.  As we have previously discussed, twins are a good model to study differences between people because they are born at the same time, and usually grow up in a very similar environment.

    Twin pairs were selected that differed in measures of satiety responsiveness (172 pairs) and food responsiveness (121 pairs) at 3 months, and their growth up to age 15 months was compared. Within pairs, the infant who was more food responsive or less satiety responsive grew faster than their co-twin.

    The more food responsive twin was 654g heavier (1.4lbs) than their co-twin at six months and 991g heavier (2.1lbs) at 15 months. The less satiety responsive twin was 637g heavier (1.4lbs) than their co-twin at six months and 918g heavier (2lbs) at 15 months. 

    This is a considerable weight difference for children of this age, and represents a 10% weight difference. Over time as weight differences increase, these children are at a higher risk of obesity.  Therefore, it might be beneficial to watch out if a child seems to have difficulties filling up, or seems to be somewhat responsive to food cues in the environment.

    However, this first study could not tell whether children with low satiety responsiveness or high food responsiveness would continue to be heavier; nor did it tell about possible underlying genetics. 

    Therefore, the second study was set up to shed more light on how appetite, and especially low satiety responsiveness, acts as one of the mechanisms underlying genetic predisposition to obesity.  For this study, our researchers collaborated with a team from King’s College, London.

    The researchers accessed data from over 2,000 unrelated 10-year-old children born in the UK between 1994 and 1996.  First, the team created a combined genetic risk score (polygenic risk score) for each child.  To do this, they added up the number of higher risk versions of 28 obesity-related genes (each gene has 2 versions, as we all get one version from Mum and one version from Dad). A higher polygenic risk score meant that the child was at higher genetic risk of obesity.

    The researchers then looked at how the children’s genetic risk scores related not only to their satiety responsiveness, but also to their body fatness (measured using body mass index and waist circumference).  

    As expected, they found that children at a higher genetic risk of obesity had higher BMIs (which is a measure of weight status) and a larger waist circumference.  This finding was in line with what we already know about the genetic basis of obesity (see our other blogpost).  But key to our study was showing that they were also less sensitive to satiety. 

    This finding suggests that satiety responsiveness is one of the mechanisms through which ‘obesity genes’ influence body weight.  Therefore, it might indeed be beneficial to teach children with lower satiety sensitivity techniques that might improve their fullness signals when eating.  Advice to parents on encouraging children to eat more slowly, having a ‘no second helpings’ policy, and keeping tempting treats out of sight between meals could help. Knowing that there are genetic influences on appetite might help parents understand and accept that children differ, and that some need more support in learning the boundaries of appropriate eating.

    Likewise, for adults who feel they have difficulty controlling their weight, it might be beneficial to understand that differences in appetite might be one contributing reason.  Techniques that help adults to ‘feel’ the fullness, such as ‘mindful eating’ and portion control may be useful aides in ‘outsmarting’ any biological tendencies to eat too much.

    Article references: JAMA Pediatrics

    van Jaarsveld CM, Boniface D, Llewellyn CH, Wardle J. Appetite and Growth: A Longitudinal Sibling Analysis. JAMA Pediatr. 2014;():. doi:10.1001/jamapediatrics.2013.4951.

     

    Llewellyn CH, Trzaskowski M, van Jaarsveld CM, Plomin R, Wardle J. Satiety Mechanisms in Genetic Risk of Obesity. JAMA Pediatr. 2014;():. doi:10.1001/jamapediatrics.2013.4944.

     

    ”Battling against one’s biology”: Inherited behavioural susceptibility to obesity

    By Susanne Meisel, on 30 March 2012

    As mentioned in one of our previous blog posts, talking about genes in the context of obesity is often not well received.  Those discounting their role in the development of obesity often argue that, because genes have not substantially changed over the past 200 000 years, whereas obesity levels have only been soaring over the past 20 odd years (where it became possible to mass-produce cheap, tasty food in combination with a decreased need for physical activity), obesity must be due to changes in the environment, and not genetics.

    However, using this argument against the heritability of obesity is somewhat flawed, because it ignores that a condition can be dormant over a period of time until the right circumstances bring it to life.  The gardeners among you will know that many plants will adjust their growth according to their surroundings – a plant in a small pot will remain small, whereas a larger pot will allow it to grow.   This, however, does not mean that the plant loses its ability to grow larger in a smaller pot; it merely remains small because its surroundings restrict its growth.  Similarly, genes predisposing to obesity may be present in an environment where little food is available, but without the right ‘medium’ (i.e. food), this is of little consequence.  In the current environment, however, where eating opportunities are plentiful, obesity genes can express their full force.

    If obesity was resulting purely from environmental change, all individuals exposed to this change would become overweight.  Yet, this is not the case. In fact, the proportion of lean people has not substantially changed, but large people are becoming even larger.  This suggests that people respond to the food environment differently.  However, undoubtedly, to gain more weight than is healthy, food must not only be available in sufficient quantities, but one must ingest more of it than necessary.  Therefore, researchers started to look at differences in eating behaviours, such as how much we are drawn to food and how quickly we feel full, to see what is going on.

    Twins can help to untangle the influence of genes and environment on obesity, because identical twins are 100% genetically identical, whereas non-identical twins only share approximately half of their genes (like normal siblings); both, however, grow up in a very similar environment.  This means that researchers can compare identical twins’ resemblance for weight with that of non-identical twins; if genetically identical twins are more similar in a trait than non-identical twins, it is evidence for genes being responsible for the trait.

    Using twins, researchers from our department wanted to see whether genes that influence weight also influence appetite.  If the same genes that influence weight also influence appetite, it suggests that genes influence weight through their effects on appetite – i.e. individuals who inherit more avid appetites might be more susceptible to overeating in the modern food environment, and consequently  more likely to gain excessive weight.  They looked at this in infants, because infants are exclusively milk-fed, which ruled out that other factors such as preference for certain foods would influence the results.   The researchers used questionnaires to ask parents about how fast their twins fed, how easily they got full and how big their appetite was, and related the answers to the babies’ weight.   Because they used a sample of identical and non-identical twins the researchers were able to explore the extent to which appetite is heritable, and the extent to which appetite and weight are caused by the same genes.

    They found that identical twins were not only very similar in weight, but shared many more similarities in appetite than non-identical twins, suggesting a strong genetic basis to both appetite and weight.  In addition, the results  showed that a substantial proportion of the genes that are responsible for weight are also responsible for appetite, in line with the idea that genes influence weight through appetite.  These findings lend evidence to the idea that some of us are more likely to overeat in the current environment because of a larger appetite, which is ultimately driven by genes.

    These discoveries will hopefully contribute to reducing the stigma that surrounds unhealthy weight gain; because it clearly shows that those struggling with weight are in a sense ‘battling against their biology’.  This of course, does not mean that there is nothing that can be done about it; however, acknowledging these differences as real and designing strategies to ‘outsmart’ one’s genes is crucial if the battle is to be fought successfully.

     

    Article reference: http://www.ajcn.org/content/95/3/633.long