Stigmatisation of obesity remains one of “the last acceptable forms of prejudice”.  People with obesity are widely stereotyped as lazy, weak willed and personally to blame for their weight by the media, employers, educators, health care professionals, and even their friends and family.

Facing discrimination can understandably be very stressful in the moment.  Small experiments have shown that asking people to watch a video that stigmatises obesity, or telling them that their body size and shape are unsuitable to take part in a group activity, increases levels of the stress hormone cortisol in their saliva.

But what wasn’t known until now was whether discrimination has lasting effects on stress levels.  This is important because acute (short-term) stress is a protective, adaptive response whereas chronic stress can have a damaging effect on the body.

In a new study published last week in Obesity we explored the relationship between weight discrimination and chronic stress.  The research involved 563 men and women with obesity (body mass index ≥30) aged 50 years and older taking part in the English Longitudinal Study of Ageing (ELSA), a large population-based cohort of middle-aged and older adults living in England.

Rather than measuring levels of cortisol in saliva, which are sensitive to daily fluctuations and short-term factors such as diet, we analysed cortisol levels in hair.  Measuring hair cortisol is a new technique that gives an indication of average levels of cortisol in the body over several months.  Hair grows at approximately 1 cm per month, so the 1 cm of hair nearest to the scalp represents average exposure to cortisol over the last month.

We found that one in eight people with obesity had experienced discrimination because of their weight, ranging from lack of respect or courtesy to being threatened or harassed.  Among people with severe obesity (BMI ≥40), one in three reported discrimination.

Importantly, our findings revealed that average levels of cortisol in hair were 33% higher in individuals who had experienced weight discrimination than those who had not.  People who experienced more frequent weight discrimination had higher hair cortisol levels than those who faced less regular discrimination.

The results of this study provide evidence that weight discrimination is associated with the experience of stress at a biological level.  Because experiencing high levels of cortisol over a prolonged period can have a substantial impact on health and wellbeing, it is likely that weight discrimination contributes to many of the negative psychological and biological consequences of obesity.  In addition, cortisol is known to increase appetite and fat storage, making people who experience weight discrimination more likely to gain weight.

Article link:

Jackson SE, Kirschbaum C, Steptoe A. Perceived weight discrimination and chronic biochemical stress: A population-based study using cortisol in scalp hair. Obesity. First published ahead of print 14 October 2016. doi:10.1002/oby.21657

http://onlinelibrary.wiley.com/doi/10.1002/oby.21657/full

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

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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In the fifth and final post in our series remembering Professor Jane Wardle and some of the contributions she has made to the field of behavioural science, Dr Becca Beeken writes about Jane’s work on the Ten Top Tips and habits.

Novel approaches to weight management

As part of Jane’s pioneering work on obesity, she developed novel, evidence-based methods for weight control. Jane recognised that there was a real need for weight loss advice for the general public that is easy to communicate, straightforward to follow, and applicable across a variety of lifestyles. She also acknowledged that while most weight management programmes talk about ‘habits’, they often just mean things we do all the time, and it’s usually in the context of breaking bad habits. Jane was one of the first behavioural scientists to explore whether we can teach people to form healthy habits, using habit formation theory.

According to psychological theory, habits are (relatively) automatically triggered actions that are formed through repetition in a consistent context, which makes them more and more automatic. Jane and one of her PhD students, Pippa Lally, asked people to pick a simple healthy behaviour, such as doing 50 sit ups, and then instructed them to repeat it in a consistent context (e.g. after their morning coffee). They showed that as time went on, individuals performed the behaviour more often, and they also reported that it felt more automatic- it was becoming a habit. Based on this study, Jane worked with the charities Cancer Research UK and Weight Concern to develop the Ten Top Tips.

The Ten Top Tips is a simple leaflet, which describes a set of ten simple energy balance behaviours that can be turned into habits. The leaflet explains the habit model and how to repeat the behaviours in a consistent context. Jane believed that this kind of intervention, which requires very little time to explain and is easy to understand, may be beneficial in primary care where time is short and effective advice for weight management is needed. Weight management advice that promotes permanent behaviour change is particularly important, because not only is losing weight very difficult, keeping the weight off is notoriously hard. Jane felt the Ten Top Tips could meet this need through helping people to make small changes that would become automatic over the longer term.

Jane led a large randomised controlled trial in obese adults in primary care (GP practices), across England, comparing weight loss in patients receiving the Ten Top Tips vs. ‘usual care’. This was the first time an intervention explicitly based on habit-formation theory had been delivered in the primary care context, and importantly the first evaluation of a simple weight loss advice leaflet. Jane and her team found that that the Ten Top Tips led to significantly more weight loss over 3 months than usual care, with 16% of patients achieving at least 5% weight loss; twice as many as in the usual care arm (8%). At 2 years over a quarter (27%) of patients who received the Ten Tops Tips had achieved at least 5% weight loss, suggesting patients maintained the changes made to their behaviours in the first few months after receiving the Ten Top Tips; they had become ‘habits’.

Jane’s work on the development and evaluation of the Ten Top Tips represents an important milestone for translational behavioural research. The Ten Top Tips could offer a low cost option for weight management in primary care and it has already been widely disseminated across the UK as part of Cancer Research UK’s Reduce the Risk campaign, which aims to raise the awareness of the avoidable risks of cancer. Her research group are continuing to take this important work forward, with new studies exploring the effectiveness of habit based advice for cancer survivors-‘Heathy Habits for Life’, and adapting the Ten Top Tips for families with overweight children-‘Tips for Tots’.

On 20^th 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.

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

The ‘obesity epidemic’ is a recurring theme within the media. So we might assume that the Great British population is more informed than ever on the topic. However, when our researchers carried out a study among obese adults to find out how they perceived their own weight they uncovered some surprising results.

The researchers looked at data from two surveys, conducted 5 years apart in 2007 and 2012, in which 657 obese persons (established through self-reported height and weight) were asked to select a descriptor for their own body weight. They could choose from the options: very underweight, underweight, about right, overweight, very overweight, obese. The results showed that the proportion of obese adults selecting the term ‘obese’ to describe their body size was very low in both sexes: 13% of women in 2007 and 11% of women in 2012, and less than 10% of men at both time points.

Now, of course the term ‘obese’ goes hand-in-hand with stigmatisation, which might well explain the reluctance to use it. The researchers did take this into consideration and went on to look at whether people were more likely to use the less controversial term ‘very overweight’. However, among women there was actually a decrease in the use of ‘very overweight’ over time and the proportion of obese women describing themselves as either ‘overweight’ or ‘about right’ increased accordingly.

This begs the question: why are people reluctant to use the terms ‘very overweight’ or ‘obese’ when describing themselves? Well, stigma might well play a part. Stigmatisation of those who do not meet society’s ideals for body shape is fuelled by the media and pop culture and may be compounded by representations of obesity in the news media, which often use images of extreme obesity when discussing body weight. This presents a challenge for health professionals whose use of these terms can be perceived as insensitive. It could also be that as a nation we increasingly see obesity as the norm. As we have become ‘bigger’, the social construction of these terms has shifted, so people who fall within these categories feel ‘normal’ when they compare themselves to those around them. This could have some troubling repercussions if it means that people are less likely to try to adjust their health behaviours as a result.

Reinstating ‘normal’ as the ‘norm’ is a challenge and maybe the use of this, and the related weight terminology, needs to be reconsidered altogether. If it is to remain considerable work needs to be done to reduce the stigmatisation that surrounds these terms.

Article reference: Johnson F, Beeken RJ, Croker H, Wardle J:Do weight perceptions among obese adults in Great Britain match clinical definitions? Analysis of cross-sectional surveys from 2007 and 2012. BMJOpen 2014;4:e005561.doi:10.1136/bmjopen-2014-005561

http://bmjopen.bmj.com/content/4/11/e005561.full.pdf

As I have discussed before, the relationship with cancer and weight is complicated. However, it is not only of interest to find out how weight impacts on cancer development, but also what happens to people’s weight once cancer is diagnosed and how this relates to cancer survival. For example, medication to treat cancer might make people more prone to weight gain. This could be problematic for people who are already overweight or obese before they were diagnosed with cancer, because an unhealthy weight has been linked to a higher chance of a cancer coming back. Alternatively, it is possible that a cancer diagnosis acts as a ‘teachable moment’ which may motivate people to change their lifestyle. This may help to avoid the cancer coming back after treatment.

Our researchers looked in two large studies, one with people from the UK, and one from the US, at how BMI changed over time in people diagnosed with cancer; and those who stayed cancer-free. Importantly, they also looked at how weight change differed according to people’s weight status before diagnosis, as emerging evidence has indicated that weight loss may improve the prognosis for cancer survivors who are overweight or obese at the point of diagnosis.

Over a four-year period, there was no difference in weight change between normal weight cancer survivors and normal weight cancer-free individuals in either the UK or the US. However, obese cancer survivors in the UK lost an average of 1.48kg vs. cancer-free obese individuals who lost an average of 0.25kg; and in the US, obese cancer survivors lost an average of 2.35kg in comparison to cancer-free obese participants who gained an average of 0.53kg. These results indicate that being diagnosed with cancer has little impact on weight in individuals who are a healthy weight, but is associated with significant weight loss among those who are obese.

Given that there was very little weight loss in normal weight cancer survivors vs. those who were obese, these results suggests that obese cancer survivors may have made a conscious effort to lose weight and to keep it off. However, it is also possible that people who were obese were diagnosed with cancer at a later stage (I discussed here why this is often the case), and that their weight loss was due to their cancer being more advanced, or treatment having taken a greater toll on the body. Unfortunately, the researchers had no data on the stage at which cancers were diagnosed, or whether the weight loss they observed was intentional, so we cannot say which of these options is true. It is important to do more research to see how weight loss relates to cancer survival to investigate whether keeping a healthy weight after a cancer diagnosis really has benefits for surviving longer.

Given that, on the whole, treatment for cancer is getting better, more and more people will survive cancer. Therefore, it is really important to find out what can be done for cancer survivors to improve their quality of life and to ensure that they remain cancer-free.

Reference:

Jackson SE, Williams K, Steptoe A & Wardle J (2014): The impact of a cancer diagnosis on weight change: findings from prospective, population-based cohorts in the UK and the US, BMC Cancer , 14:926  doi:10.1186/1471-2407-14-926

http://www.biomedcentral.com/1471-2407/14/926/abstract

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

Mentioning genetics in the context of weight is like treading into a minefield; those who are brave enough to approach the topic need to don their hard hats and be prepared to take hits by followers in the ‘eat-less-and-move-more’ camp. Accusations of laziness, lack of willpower, making excuses and just looking for an easy way out are common responses to the genetic argument of obesity.

However, to ignore genetics when talking about obesity is somewhat confusing when considering how keen people are to attribute skinniness to ‘good genes’, ‘fast metabolism’, and ‘being naturally active’. Nobody seems to notice that skinniness and fatness are two sides of the same coin.

As so often in life, the truth lies somewhere in between. While behaviour is certainly not to be ignored when searching for the root cause of the obesity epidemic, neither should the heritability of body weight. Two recent studies from our research group add evidence to the idea that the predisposition to thinness, as well as to overweight, is transmitted across generations. Researchers used data from the Health Survey for England, which included a large sample of families with children aged 2-15 years to see whether thin children were more likely to have thin parents. Of the thousands of families included in the first study, it was shown that thin children were almost twice as likely to have 2 thin parents.  Furthermore, as parents’ weight decreased, children likewise got progressively lighter.

But, what about the reverse side of the coin – parental weight of children who were overweight? Here, exactly the same pattern was found, but it was even more apparent. Children, who had 2 obese or severely obese parents, were approximately 12 times more likely to be overweight and again the likelihood of obesity gradually decreased with decreased parental body weight. In both studies, findings were unrelated to other factors such as age, sex, social status or ethnicity. Interestingly, the mothers’ weight seemed to be more predictive of a child’s than the father’s, but only among those children that were overweight. For thin children, mothers’ and fathers’ genes appeared to contribute equally to being thin.

Two things are important here. Firstly, weight is governed in part by genetic factors; but, and this is the second important conclusion to take away, there are environmental factors involved that influence a child’s weight – otherwise all children would have had parents that fully resembled their weight status. Influences seem to come especially from the mother’s side, which may be, because the foetus receives nutrients from the maternal diet in the womb and after birth when the infant is breast-fed. In addition, maternal environmental influences may be stronger because the mother is usually in charge of food preparation.

Unfortunately, dietary records of participants were not available, so it was not possible to investigate how diets between underweight and overweight children and their parents differed.

Genes do not always act in the same way; their activity is influenced by the environment. This flexibility allowed our species to adapt well to changing environmental conditions, which made it possible to survive and evolve.  Variation is the key. And this is why it is easier for some than for others to (not) have their cake and eat it, too.

References:

Whitaker KL, Jarvis MJ, Boniface D, Wardle J. Inter-generational transmission of thinness. Archives of Pediatrics and Adolescent Medicine. http://archpedi.ama-assn.org/cgi/content/full/165/10/900

Whitaker KL, Jarvis, MJ, Beeken RJ, Boniface D, Wardle J. Comparing maternal and paternal intergenerational transmission of obesity risk in a large population-based sample. American Journal of Clinical Nutrition. 91, 2010, 1560-1567. http://asn-cdn-remembers.s3.amazonaws.com/f8ee4cfad55bd34900cff3371b9a146d.pdf