‘Health Chatter’: Research Department of Behavioural Science and Health Blog
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    Family upbringing has no impact on adolescents’ food preferences

    By Alison Fildes, on 11 July 2016

    Written by Andrea Smith, Alison Fildes and Clare Llewellyn

    Understanding the factors behind food likes and dislikes has important implications for politicians and clinicians. Our food preferences strongly influence what we chose to eat, affecting our health in the short- and long-term. Previous studies carried out by our group have shown that aspects of the shared family environment played an important role in shaping young children’s food preferences.  However, the relative influences of genes and the environment on older teenagers’ preferences was previously unknown.

    In a new study published this week in the American Journal of Clinical Nutrition we explored the relative importance of genetic and environmental influences on adolescents’ food preferences using a twin design. The findings revealed that the effects of family upbringing on teenagers’ food preferences seem to disappear as they start to make their own meal choices, to the point where they have no detectable impact by late adolescence. Instead the ‘unique environment’ – aspects of the environment that are not shared by both twins in a pair (e.g. experiences  unique to each twin, such as having different friends) were found to effect food likes and dislikes at this age. Genes were also found to have a moderate impact on food preferences in late adolescence, in keeping with earlier findings from young children.

    The research involved 2,865 twins aged 18-19 years from the Twins Early Development Study (TEDS), a large population based cohort of British twins born in 1994 to 1996. Food preferences were measured using a self-report questionnaire of 62 individual foods which were categorised into six food groups – fruits, vegetables, meat/fish, dairy, starch food and snacks. It is the first study to show how substantial influences of the shared family environment in early childhood are replaced by environmental influences unique to each individual by the time they enter young adulthood. The decreasing influence of the family environment in adolescence has also been observed for other traits, such as body weight.

    The results of this study mean that efforts to improve adolescent nutrition may be best targeted at the wider environment rather than the home, with strategies focused on increasing the availability and lowering the cost of ‘healthier foods’. The substantial influence of the non-shared environment, suggests that food preferences can be successfully shifted towards more healthy choices in late adolescence. Policies that make the healthier food choice, the easier choice for everyone, have potential to achieve substantial public health improvements. In particular, the UK sugar-sweetened beverage levy soon to be introduced is one initiative that has the potential to promote a healthy food and drink environment.

     

    Article link:

    Smith AD, Fildes A, Cooke L, Herle M, Shakeshaft N, Plomin R, and Llewellyn C. Genetic and environmental influences on food preferences in adolescence. American Journal of Clinical Nutrition. First published ahead of print July 6, 2016. doi:10.3945/ajcn.116.133983

    http://ajcn.nutrition.org/content/early/2016/07/05/ajcn.116.133983.full.pdf+html

    Letting your imagination run wild – genetic testing for risk of weight gain

    By Susanne Meisel, on 5 April 2013

    These are exciting times for people working in genetics.  The field has become trendy.  ‘DNA’, ‘genes’ and ‘genetic code’ are no longer specialist terms, but used casually in everyday language. The media love ‘The gene for’ stories  and attributing individual differences to biology and less to environment is becoming commonplace.  I recently read an interview with a singer who explained that she could not imagine being anything else but a singer, because singing ‘was in her DNA’. If this still does not convince you: The pop band ‘Little Mix’ recently released a new song titled ‘DNA’ (http://www.youtube.com/watch?v=D3h-lLj3xv4).

    Why the fascination with genes?  To a degree, it appears to stem from the inherent assumption that our genes can give us insights into ourselves that would otherwise remain inaccessible. Although our DNA is  99.9% identical, this is not interesting – it is all about the tiny bit of difference, the bit which sets us apart and makes us unique.

    Companies have been quick to capitalise on our curiosity of what would be possible once the Human Genome was decoded.  Genetic tests for an array of traits and conditions, including those that are common and driven by lifestyle, such as obesity or heart disease, are already available over the Internet.  So far, we are not sure about the effects of giving this type of information to people. It could be that people will use it to prevent the condition. Alternatively, it could be that they become fatalistic or complacent. I have written in more detail about the current debate in a previous blogpost ( http://tinyurl.com/bve6y2m).  I hope to add some evidence to the debate by looking at the psychological and behavioural consequences of receiving genetic test feedback using obesity as an example for a very common, very complex condition.

    Because we do not know yet how people react to knowing about their genetic susceptibility to weight gain, it would be unwise to give them this information right away.  Instead, we set up an online study where people were asked to imagine their reactions to receiving a ‘higher-risk’ or an ‘average-risk’ genetic test result for weight gain. They were then asked questions on a broad range of feelings and behaviours. We included 2 sets of people, nearly 400 students, who were predominantly of healthy weight and almost as many people from the general public who were or had been overweight.

    Results showed that people in both groups reported to be more motivated to make lifestyle changes after imagining getting a ‘higher’ genetic risk result than after imagining getting an ‘average’ genetic risk result. On average, negative feelings and feelings of fatalism were anticipated to be very low and did not differ between risk scenarios. Those who were already overweight or obese were more likely to think that in comparison with an ‘average’ genetic risk result, receiving a ‘higher’ genetic risk result would offer them an explanation for their weight status.  Finally, people in both groups thought that they would be more likely to seek out information about what their result means in the ‘higher-risk’ than in the ‘average-risk’ scenario.

    These findings are good news, because they suggest that giving people feedback for susceptibility to weight gain is unlikely to have unanticipated negative effects, and may even be motivating.  Furthermore, people who are already overweight may also benefit from genetic feedback.  However, these findings may not hold up once people are actually given genetic test feedback, because they only tell us about what people think they might do – and people find it generally quite difficult to imagine to be negatively affected by an event.  The next step is now to give people ‘real’ genetic feedback for risk of weight gain to discover the effect of this type of information.

     

    Reference:

    Meisel, S. F., Walker, C., & Wardle, J. (2011). Psychological Responses to Genetic Testing for Weight Gain: A Vignette Study. Obesity (Silver Spring); 20 (3).DOI: 10.1038/oby.2011.324

     

    ”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