Written by Andrea Smith, Alison Fildes and Clare Llewellyn

In early childhood, children are gradually introduced to an increasingly varied diet. While some children happily accept new foods and enjoy eating lots of different kinds of foods, many are hesitant. Food avoidant behaviour can be broadly classified into two traits: ‘Food Fussiness’ and ‘Food Neophobia’. Food Fussiness is the tendency to be highly selective about the textures, taste and smell of foods you are willing to eat and is often seen as a consequence of inadequate parenting. However, Food Neophobia – the refusal to try new foods – is often seen as a normal development stage experienced by most young children regardless of the way their parents feed them. Fussy and neophobic eating behaviours typically emerge in toddlerhood and commonly peak between two and six years of age; but for some children these traits persist into later childhood.

Food avoidant behaviour can be both frustrating and worrying for parents; children who eat only a restricted range of foods might miss out on key dietary nutrients essential for healthy development. In particular, fussy eaters tend to reject nutrient-dense foods such as vegetables. Early childhood is also an important period during which food preferences develop; learning to like a range of healthy foods requires the child to try a wide variety of different foods. Researchers have therefore been interested in finding out what shapes food avoidant behaviour in early life. Some research has suggested that children who are breastfed for longer and whose parents use less persuasive feeding practices (e.g. rewarding with food) are less likely to display fussy eating behaviours; suggesting that there are important environmental shapers of this behaviour. On the other hand, Food Neophobia is associated with temperamental traits such as shyness or inhibition; these characteristics have an established genetic influence, indicating that neophobia might also have a strong genetic basis.

In a new study published in the Journal of Child Psychology and Psychiatry we used data from the Gemini twin cohort to investigate the extent to which genes and environmental factors influence children’s food fussiness and food neophobia. Gemini is a large study of 2400 pairs of twins that was set up in 2007 to explore early life growth and behaviour. Twin studies are useful for investigating the relative importance of genetic- and environmental factors on individual differences in traits such as food avoidant behaviours. The current study was based on data from 1,932 families collected when the twins where 16 months old.

We found that both food fussiness and food neophobia have a strong genetic basis, with 46% and 58% of the variation in each trait explained by genetic influences respectively. The shared home environment (which includes factors such as parental feeding practices) was a more important influence on Food Fussiness than Food Neophobia; but overall, these environmental factors were less important than a child’s genetic predisposition towards these behaviours.

The finding that there is substantial genetic influence on fussy eating behaviour in early childhood might be quite a relief for some parents who can often feel judged or guilty about their children’s fussy eating. Understanding that these traits are largely innate might help to deflect this blame.

However, our genes are not our destiny. Establishing the importance of genetic influences on fussy eating behaviours in early childhood does not imply that these behaviours cannot be changed. An effective intervention to overcome food rejection is through repeated exposure to the problem food; the more a child tries a food, the more familiar it becomes and the more they learn to like it. In our group we have developed a tasting game called ‘Tiny Tastes’ to help families introduce foods to reluctant and fussy eaters. This is an avenue through which parents might be able to positively change fussy or neophobic eating behaviours.

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Food fussiness and food neophobia share a common etiology in early childhood

Andrea D. Smith, Moritz Herle, Alison Fildes, Lucy Cooke, Silje Steinsbekk, and Clare H. Llewellyn

Article link: http://onlinelibrary.wiley.com/doi/10.1111/jcpp.12647/epdf

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

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

Finally, the results of my randomized controlled trial are in.

Just to recap, the question I tried to answer was whether knowing that having a gene related to obesity (FTO) would prompt people to take action to prevent weight gain. I tried to answer this using the ‘gold-standard’ method for this kind of question: The randomised controlled trial. I randomly (by chance) assigned over 1,000 students from UCL to one of two groups. One group received a leaflet with seven tips which would help them to prevent weight gain. The leaflet was based on Habit Theory (more about this here). The other group received the same leaflet, plus obesity gene feedback for one gene (FTO) which told them whether they were at ‘higher’ (AT/AA variant) or ‘lower’ (TT variant) genetic risk for weight gain. I found out their genetic risk using DNA from their saliva (they all had to be willing to spit into a tube!).

One month later I sent both groups a questionnaire asking about their intentions to prevent weight gain, and any activities they were engaged in relating to weight gain prevention (e.g. eating slowly, controlling portion size, avoiding snacks, avoiding sweet drinks, exercising). They also completed a measure about their readiness to control their weight based on the stage of change theory.

Although only 279 participants responded to my questionnaire, the study had still sufficient statistical ‘power’ to draw some meaningful conclusions. We statistically controlled for factors which could potentially explain differences between groups; in this case age, gender and BMI.

Earlier studies have shown that genetic feedback can influence behaviour change intentions, regardless of whether the actual result is ‘low’ or ‘high’ risk. This might be because the results give personal feedback, which may itself be motivating. This is why we thought that gene feedback (vs. no feedback) would have an effect on people. And we were right – participants who received genetic feedback in addition to their weight control leaflet were more likely to think about taking some action to prevent weight gain. In particular, people who were already overweight (BMI < 25kg/m2) and received genetic feedback were more likely to report that they had started to do something to prevent weight gain than overweight people who did not receive gene feedback.

We then looked at differences between ‘higher risk’, ‘lower risk’, and ‘no feedback’ groups. Participants who received a ‘higher’ genetic risk result were more likely to report that they were thinking about doing something to control weight gain, or that they had started than people who received ‘no feedback’. There was a small difference between people who had ‘higher’ and ‘lower’ genetic risk results. Importantly, people who got ‘lower risk’ results were just as likely to think about preventing weight gain than those receiving ‘no feedback’. However, when we looked at whether people had actually followed the weight gain prevention behaviours outlined in the leaflet, there was virtually no difference between groups; most people were not following any of the behaviours despite their intentions.

This is the first trial that has had enough participants to show any group differences with some certainty. It also aimed to show effects in a ‘real world’ scenario, with young, healthy people who were largely unaware of their genetic risk. However it also had some very important weaknesses.

We did not assess people’s weight control intentions when they enrolled in the study because it would logistically have been quite challenging, so we couldn’t see if people’s intentions had changed. We also used only one question to make assumptions about their weight control intention. This is not such a good idea, because people sometimes give random answers, and self-report has its own problems – in hindsight it would have been better to use more questions because that allows us to check whether people answer consistently. Another limitation was that we could not have a ‘no treatment’ control group who received neither leaflet nor gene feedback. This was mainly because our study used lots of first year students who all lived in halls together; therefore, there would have been a high chance that people assigned to a ‘control group’ would have read the leaflet anyway. In addition, lots of people did not return the questionnaire. Although we expected this, it limits what we can actually say about how most students would react. People were more likely to enrol in the study if they were not overweight, and were less likely to answer the questionnaire if they were overweight at the start of the study. This means that our results may be different for these students compared to the wider student population, but we don’t know for sure. Lastly, and perhaps most importantly, I only chose to give them feedback on one (albeit well-established) obesity gene – although we know that there are hundreds of genes which influence body weight. This means that it might not be very meaningful for an individual to know whether or not they have just one of these genes – they may have many others. However, I was mainly interested whether gene feedback could ‘in principle’ be used to help people starting to prevent weight gain early, or whether it had any negative effects.

What to make of this? The study showed that FTO feedback can influence weight gain prevention intentions, but has no effect on actual behaviour. Sadly, showing that interventions change intentions but not behaviour is common in behaviour change research. In fact, it is so common that it has a name: The ‘intention-behaviour-gap’. I am sure that most people will be familiar with the concept: You really want to do something (i.e. going to the gym, or cleaning the bathroom), but then, for one reason or another, you fail to follow through with it. In that sense, findings from the study are in good company, since lots of other studies have shown similar things, be it on the effects of genetic test feedback, or on other topics. Unfortunately, researchers are as yet not very good in explaining how to bridge the ‘intention-behaviour-gap’. This is why we thought that genetic test feedback could be a novel way – especially since it is very compelling and rational to assume that once a person knows about their elevated risk for a condition, that they would take steps to prevent it. However, as it is so often the case with human behaviour, it seems that it is not so straightforward. A more optimistic explanation is that participants did not feel the need to act on their results at this point in time – after all, most had a healthy weight – but would keep the results in mind and take action should they gain weight. Since genetic testing for common, complex conditions is still relatively novel, data on the long-term behavioural effects is still lacking.

The good news is that a ‘lower’ risk result did not result in ‘complacency’ – the false assumption that weight gain is not possible with a ‘lower’ FTO gene result. People seem to have a pretty good idea that many genes, and the environment, act together to influence weight gain, so regardless of their result they were motivated to think about preventing weight gain as a consequence of getting feedback.

It will now be important to find out how we can get better at communicating gene results to people, so they may have some impact on behaviour –genomics is undoubtedly here to stay, so this will be an important task for the future.
Article reference: Meisel SF, Beeken RJ., van Jaarsveld CHM., & Wardle J Genetic susceptibility testing and readiness to control weight: results from a randomized controlled trial in university students. Obesity, 23, 2, 305-312. DOI: 10.1002/oby.20958
http://onlinelibrary.wiley.com/doi/10.1002/oby.20958/full

As I have discussed previously, genetic technology is developing at a breath-taking speed. This not only means that scientists gain better insights in the genetic contributors to disease development, but also that this comes at increasingly lower costs.

Genetic testing is not new. In fact, it has been available on the NHS  for many years. However, to be eligible for testing, certain criteria have to be met; commonly, people need to have several affected relatives to qualify for genetic testing on the NHS.

Now, with falling sequencing costs, the question of whether it would be beneficial to offer genetic testing to everyone in the population before conditions manifest becomes ever more pertinent. Proponents of the proposal argue that current approaches based on family history may miss a proportion of individuals because both individuals and healthcare providers have to recognise that there may be an increased risk of disease – this can be challenging if the family is small, or people are not very actively seeking out this information. However, other experts are more cautious and argue that large-scale genetic testing has the potential to cause more harm than good. Regardless, there are many practical, social, legal and ethical questions that have to be sorted out before genetic testing can be applied at a population level.

Currently, in the clinical setting, genetic testing is only performed after thorough genetic counselling. Genetic counselling is defined as ‘a communication process, which aims to help individuals, couples and families understand and adapt to the medical, psychological, familial and reproductive implications of the genetic contribution to specific health conditions’. Genetic counsellors meet with people one-to-one and help them to make a decision whether or not they’d like to have testing. Although research to date has found that people commonly do not react badly to their genetic test results, genetic counselling is thought to play a large role in this because people would have discussed the possibility of an unfavourable result before they got testing. In addition, because people who get genetic tests to date come from high-risk families, they may to have thought a lot about their inherited risk. Therefore, they may be better prepared to cope with an unfavourable genetic test result.

However, if lots of people in a population got genetic testing, the one-on-one model of genetic counselling would be impossible to maintain because it is far too costly and time-intensive. Some experts are concerned that providing access to genetic testing without proper genetic counselling to people who may be largely unaware of their inherited risk would result in a high rate of adverse psychological effects such as worry and anxiety.

In the first study of its kind, our researchers wanted to find out what the effects of population-based genetic testing would be. They chose to look at the effects of returning genetic test results for risk of breast-and ovarian cancer (BRCA 1/2) in the Ashkenazi Jewish population. They picked this population because people of Ashkenazi Jewish descent have a higher chance to get breast-and ovarian cancer than people from other backgrounds and the mutations causing the increased risk are well-defined. People with one of these mutations have a very high chance to get cancer (50%-80% for breast; 20%-40% for ovarian).

Specifically, the researchers wanted to investigate i) whether population-based genetic testing would be able to identify a greater proportion of mutation carriers than the current family history approach, ii) whether people would find testing acceptable, and iii) what the psychological effects (e.g. on anxiety and depression) of genetic testing would be in people which may not necessarily have a strong family history of breast-or ovarian cancer.

Potential participants were recruited in the North London Jewish community. All individuals who registered their interest received genetic counselling before they enrolled into the study, and 1,034 (691 women, 343 men) decided to take part. Participants were randomly (by chance) split into two equally sized groups: In one group, all people would get genetic testing, and in the other, only people who would qualify for genetic testing under current NICE guidelines would get testing. However, this group could access testing after the end of the study if they wanted.

Our researchers asked questions about people’s anxiety levels, depression, and general quality of life before people got genetic counselling (baseline); immediately after study enrolment; and at seven days and three months after people got their genetic test results. The researchers also asked the same questions after one, two and three years after people got their genetic test results, but the results of this bit of the study have yet to be analysed.

In the group where all people were tested for their BRCA status, 13 carriers of a faulty gene were identified vs. 9 in the group which based the testing decision on family history; an increase in detection of 56%. In the family history group, 5 more carriers were detected after the study had finished. This means that current approaches are likely to miss a significant number of people of Ashkenazi Jewish descent who carry faulty BRCA mutations. As for adverse psychological effects, there were no differences between the 2 groups at either 7 days or 3 months after people received their genetic test results. In fact, overall anxiety and uncertainty decreased quite a bit, and positive experience scores increased.

This study is the first to provide evidence that large-scale genetic testing may be beneficial and feasible; at least in certain subgroups of the population. However, in this study, all participants received one-to-one genetic counselling before they enrolled; so it is not possible to say what the effects would have been using a less tailored approach. This might be something that could be investigated in future research. Nonetheless, these results demonstrate that large-scale genetic testing may have real clinical value, and they may spark serious debate about whether the current guidelines should be amended, at least for people of Ashkenazi Jewish descent. After all, identifying BRCA carriers early may save lives.

References:

Manchanda R, Legood R, Burnell M, McGuire A, Raikou M, Loggenberg K et al.: Cost-effectiveness of population screening for BRCA mutations in Ashkenazi Jewish women compared with family history-based testing. J Natl Cancer Inst 2015, 107.

Manchanda R, Loggenberg K, Sanderson S, Burnell M, Wardle J, Gessler S et al.: Population testing for cancer predisposing BRCA1/BRCA2 mutations in the Ashkenazi-Jewish community: A randomized controlled trial. J Natl Cancer Inst 2015, 107

In June 2013 you may have seen headlines about two new drugs that are going to be offered to women who are at an increased risk of breast cancer. These drugs, known as Tamoxifen and Raloxifene, were previously used by women who had been diagnosed with breast cancer as a way of reducing recurrence of the disease. Recent data suggest that these medications may be beneficial for women with a strong family history. As a result, the National Institute for Health and Care Excellence (NICE) has recommended that they be offered to women who meet a certain level of risk based on their family history and other factors.

Taking medications or any other natural, synthetic or biological agent to prevent cancer is known as ‘chemoprevention’. The NICE announcement was particularly exciting because it is the first time they have endorsed a medication for the primary prevention of cancer. While this raises a number of clinical issues, I have recently been given funding from Cancer Research UK to investigate what women think of breast cancer chemoprevention. Women who have been assessed by a specialist and told they are at an increased risk of breast cancer have a number of options, including taking Tamoxifen or Raloxifine. Alternatives include doing nothing, having routine surveillance by mammography or surgical intervention to remove the breasts and/or ovaries. You may have seen newspaper coverage of Angelina Jolie making a similar decision and here is her thoughtful piece on the issue. This decision is challenging, and there is no right or wrong answer. Instead, it must be based on women’s full understanding of the risks and benefits, as well as the values they assign to these factors.

In a joint collaboration between the Health Behaviour Research Centre, and the Centre for Cancer Prevention and funded by Cancer Research UK, I will be recruiting and following a group of women who have been asked to decide between these options. This study (known as the ENGAGE study) will help to identify how women are currently making these decisions, and what can be done to support them during this difficult process. Data from a number of questionnaires will be collected and after 1 year we will report on what decisions women have made and what their experience has been.

Chemoprevention is an exciting new area of research, but understanding the public’s opinion of it is vital if it is to be implemented effectively. So, if you’d like offer an opinion please feel free to leave a comment on our message board or contact me directly via e-mail (samuel.smith@ucl.ac.uk).

Sam (samuel.smith@ucl.ac.uk)

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.

This post really follows my previous one (http://tinyurl.com/d6qo5wl ) about asking people to imagine receiving genetic test feedback for weight gain susceptibility and investigating their anticipated reactions. These types of studies are very valuable when not very much is known about a topic, because they provide us with hints about people’s reactions. However, they can only get us so far.  At some point, we have to take the leap and expose people to the ‘real’ condition we want to test – in this case, whether receiving personal genetic test feedback in addition to generic weight gain prevention advice will motivate people more to prevent unhealthy weight gain than receiving only generic weight gain prevention advice.

This type of question can be best investigated in an experiment involving two groups, one group that receives the ‘intervention’, and one that is the ‘control’ group.  Participants are randomly (by chance) put into either group. We decided to give the ‘control’ group a leaflet with seven memorable tips for weight gain prevention, adapted from a leaflet that has been shown to help people lose weight.  The other group – the ‘intervention’ group – also receives the leaflet, as well as their personal genetic test result for weight gain susceptibility. This means both groups receive exactly the same information, the only difference is that the intervention group will know if they are genetically predisposed to weight gain. This allows us to say whether differences between the groups in their motivation to prevent weight gain are due to receiving the genetic test result.

We decided to use approximately 800 first-year university students in this experiment, because the chance of already being overweight at that age is low, but starting university is linked with weight gain (just think of all the late nights, pizza- and kebab feasts!). One month after the intervention, we will send questionnaires to both groups asking about their motivation to prevent weight gain as well as questions about what they have done if they were trying, and whether they followed any of the tips outlined in the leaflet

This is going to be the first study investigating the effects of genetic testing for weight gain susceptibility and will be completed by September 2013. We hope that our findings contribute to the debate about whether genetic test feedback could be used to help motivate healthy lifestyle behaviours.

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

All animals need it, we go crazy without it, yet, we don’t understand it well – no, I am not talking about love here, but a much less considered, although just as profound, need: The need for sleep.

Sleep is currently a ‘hot topic’ in science, because it appears that it is vital for all other major systems in our brains and bodies to function well – from how we feel , how well our muscles function, how well we concentrate, to the food choices we make.  Moreover, there is growing evidence that shorter sleep is linked with a large number of diseases, such as obesity, heart disease, cancer, lowered function of the immune system and mental health problems.

Although, as a nation overall, we sleep less than ever before, individuals vary substantially in the need for sleep –your partner may be chirpy after 7 hours, whereas you may need more to feel human.  Interestingly, variation occurs even in the same families and among siblings; this raises the question of whether genes play a role in determining how much sleep a person needs, because families usually share a very similar environment.  However, very few large studies have looked at what influences sleep early in life, when sleep is assumed to be mainly governed by the infant’s ‘body clock’.  Twins are especially useful to tease the question of ‘nature’ and ‘nurture’ apart, because twins are either 100% genetically identical; or they share half of their genes, just as ‘normal’ siblings.  Both, however, usually share the same environment, because they are born at the same time.  Our researchers used data from the GEMINI birth cohort, which includes twins from about 2000 families, to take a closer look at the genetic and environmental influences of sleep in young children.

Perhaps surprisingly, the results showed that sleep duration and daytime nap duration were mainly influenced by the environment. Likewise, sleep disturbance was due to environmental influences, although the genetic effect was slightly bigger than for sleep duration.  This was true for both girls and boys.  Although it could be argued that the carer’s schedule determines infants’ sleeping time, it would be expected that they would adjust bed-and nap times according to the infants’ needs.  Unfortunately there was no data available on when the infants actually went to sleep once they were put to bed, so we cannot say for sure how long they actually slept.

This study shows that, as so often, nature and nurture both act together to influence how we behave; in this instance, how much and how well we sleep.  Nonetheless, the study is important, because it shows that being a ‘morning vs. evening’ type person is indeed influenced to an extent by genes and this is apparent already very early in life. However, what is more important, the study clearly shows that the home environment is a crucial factor for providing children with a good night’s sleep. So, it might be wise to practice good ‘sleep hygiene’ (and that is not only true for kids): Remove the TV from the bedroom, have a consistent bedtime routine, put your kids to bed before 9pm if they are under 10 years old, let them fall asleep without anyone present, and limit (soft) drinks containing caffeine.  That will, hopefully, help your kids, and ultimately you, too, to get the well-deserved snooze.

Source

http://pediatrics.aappublications.org/content/early/2012/05/09/peds.2011-1571.abstract