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    Remembering Professor Jane Wardle – Part 1 – Understanding the causes of obesity

    By Alice Forster, on 20 December 2015

    On 20th October, we lost the Director of our Health Behaviour Research Centre. Professor Jane Wardle, one of the UK’s leading health psychologists, was an extraordinary woman. She had an apparently insatiable appetite for research and new ideas, and the breadth of her expertise was simply awesome. She nurtured us, her PhD students and staff, to develop into independent researchers and supported us when we had personal difficulties. There was always laughter coming out of her office when she was in meetings and Jane’s door was always open to us. We miss her terribly.

    While much has been written and said about her achievements and how extraordinary she was by Cancer Research UK, in the Guardian, Lancet, BMJ, The Times, The Psychologist and on Radio 4, we wanted to write about the science behind just a few of her contributions to behavioural science in cancer prevention. Over the next few weeks, our blog will do just that, starting with Jane’s work on understanding the causes of obesity written by Dr Clare Llewellyn and Dr Ali Fildes.

    Our understanding of the causes of obesity

    Professor Jane Wardle revolutionized our understanding of the genetic basis of human body weight. She was particularly interested in advancing our understanding of the causes of obesity because obesity is an important risk factor for cancer. In fact, obesity is the most important known avoidable cause of cancer after smoking.

    We have known for many years that weight has a strong genetic basis.  Importantly, Jane established that weight is as heritable now as it was 30 years ago, despite the recent large increases in obesity. This observation has been difficult for researchers to explain given the changes to the food and activity environments that are widely believed to have caused the rising rates of obesity. Researchers were confronted with the question, how can obesity be caused by both genes and the environment at the same time?

    In order to answer this question, Professor Wardle developed the ‘Behavioural Susceptibility Theory’. She proposed that genes could be influencing weight through their effects on appetite.  The key idea was that individuals who inherit a set of genes that make them more responsive to food cues (want to eat when they see, smell or taste delicious food), and less sensitive to satiety (take longer to feel full) are more susceptible to overeat in the current food environment, and become obese.

    In order to test this theory Jane developed a parent-report measure of children’s appetite – the Child Eating Behaviour Questionnaire (CEBQ), and explored the genetic basis of appetite using 10-year-old twins from The Twins Early Development Study (TEDS). Researchers can compare how similar identical twins are, with how similar non-identical twins are, to estimate the importance of genes versus environment for any characteristic, such as appetite.  Using the CEBQ she showed for the very first time that food responsiveness and satiety sensitivity both have a strong genetic basis. She also showed that the FTO gene (the first ‘obesity gene’ to be discovered in 2007), and other obesity genes, appear to be influencing weight through impacting satiety sensitivity.

    After finding out that appetite is already highly heritable by age 10, Jane realized that she needed to go right back to the beginning of life to explore how genes are influencing appetite and weight from birth. She therefore established Gemini – the largest study of twins ever set up to study genetic and environmental influences on weight from birth. The Gemini study includes over 2400 British families with twins born in 2007, and has now been running for over 8 years. Under Jane’s leadership Gemini has become an internationally recognised study that has advanced our understanding of childhood growth. The success of the study can be measured in its numerous publications on a range of topics from appetite, to food preferences, sleep, physical activity and the home environment. Jane loved the Gemini study, and it shone through in every aspect of her work, from discussions about complex genetic analyses to the design of the annual newsletter sent to the many dedicated families who participate. In total, Gemini has trained (and continues to train) 7 PhD students, 5 postdoctoral researchers, and numerous MSc students. The Gemini team miss Jane terribly but are committed to continuing her incredible legacy.

    The Gemini team

    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.