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

By rmjdafo, on 20 December 2015

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

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

Our understanding of the causes of obesity

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

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

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

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

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

The Gemini team

Parents need more guidance to prevent overeating in ‘at-risk’ toddlers

By ucjthsy, on 17 December 2015

A new study from the HBRC investigating how appetite influences children’s eating patterns has been published in ‘The American Journal of Clinical Nutrition’. The article concludes that reducing toddlers’ portion sizes or number of eating occasions could potentially help to prevent weight gain in later life.

The research has found that how often and how much young children eat seems to be determined by two distinct appetitive traits: 1) ‘food responsiveness’ (the urge to eat in response to the sight, smell or taste of appetising food) and 2) ‘satiety responsiveness’ (sensitivity to internal ‘fullness’ signals). Children who are very responsive to food cues eat more frequently (i.e. more times per day), and children who are less sensitive to internal feelings of fullness consume more calories each time they eat. These eating behaviours may help explain why children who exhibit these appetitive traits are at higher risk of weight gain.

The study used data from 1102 families with twins (2203 children) born in 2007 from the Gemini twin study, a large national birth cohort which focuses on early childhood growth, appetite and the family environment. ‘Food responsiveness’ and ‘satiety responsiveness’ were assessed with the Child Eating Behaviour Questionnaire (CEBQ) when the children were 16 months old; and eating patterns were determined from 3-day diet diaries completed by parents when children were 21 months old. The average eating frequency was 5 times per day (ranging from 1 to 10) and the average amount eaten on each occasion was 180 calories (ranging from 59 to 417 calories per eating occasion).

Previous research has shown that children who are highly food responsive and/or have poor satiety responsiveness tend to be heavier and at greater risk of obesity, but it was not clear why exactly. We know from experimental settings that food responsive children or children with poor satiety responsiveness will eat more when presented with palatable foods such as cookies and crisps. However, this new study is the first to shed light on how children with these traits might overeat in everyday life, and consequently gain weight.

Currently there is little guidance for parents of young children about eating frequency and portion sizes. Parents are commonly told to feed according to their child’s own their appetite as it is generally believed that young children will regulate their own intake. However, this new research suggests some children are less able to regulate their own food intake than others. This means parents may need more tailored advice and information if their young child is at risk of overeating. In addition, assessing eating behaviour in early childhood could help to identify children potentially at risk of obesity later in life.

The research was funded by The Medical Research Council, Cancer Research UK and Nutricia Ltd and the results are published in ‘The American Journal of Clinical Nutrition’.

Syrad, H., Johnson, L., Wardle, J., & Llewellyn, C. H. (2015). Appetitive traits and food intake patterns in early life. The American Journal of Clinical Nutrition. Published Online:16 December 2015.

 

Learning to like vegetables: Starting early

By Alison Fildes, on 10 June 2015

Vegetables are commonly among children’s least liked foods, while sweet-tastes are preferred from the outset. These preferences are reflected in children’s diets with children in the UK and other European countries eating too few vegetables and too many sugary foods. Evidence suggests introducing vegetables early in life may have important implications for future health. It is possible to learn to like foods, such as vegetables, simply by trying them on multiple occasions. Older children (or adults) may need to try a food 14 times or more before they begin to like it but infants are particularly accepting of new tastes. This makes the weaning stage is a key period for learning to like a variety of different foods.

As part of the European HabEat project we conducted an exploratory trial investigating the impact of advising parents to introduce of a variety of single vegetables at the very start of weaning. Pregnant women or mothers with infants less than 6 months old were recruited from healthcare settings in the UK, Greece and Portugal. Mothers and their infants were randomized (allocated by chance) to either an intervention group or a control group, ensuring there were equal numbers of breast-fed and formula-fed infants in each group. Intervention mothers were visited before they started weaning and were given advice on introducing five vegetables (one per day) as their baby’s first foods, repeated over 15 days. After the first 15 days, intervention mothers were told to continue to offer vegetables but also to start introducing other age-appropriate foods such as fruit. Mothers in the control group received standard care, which varied from country to country. For example, UK recommendations are to introduce fruits, vegetables and baby rice or cereal as first foods, but the information provided to mothers is inconsistent and access to advice may vary by region.

Taste tests were conducted one month after the start of weaning. Intervention and control infants were fed unfamiliar vegetable (artichoke) and fruit (peach) purées and a researcher recorded how much of it they ate (g) and how much they appeared to enjoy these foods. When the results for the UK, Greece and Portugal were combined (n=139) the children who took part in the intervention, and ate a variety of vegetables for the first 15 days of weaning, had not eaten significantly more of the unfamiliar vegetable purée than the children from the control group. However in the UK, intervention children ate almost twice as much of the unfamiliar vegetable compared with control children whose parents were not advised to offer vegetables as first foods (32.8g vs. 16.5g). UK mothers and researchers also rated intervention infants’ as liking the vegetable more. Whereas in Portugal and Greece there was no significant effect of the intervention on infants’ intake of or liking for the vegetable. In all three countries, there was no difference between groups in the amount of fruit purée children ate or how much they seemed to like it.

These results may be partly explained by variation in existing weaning practices across Europe. Common first foods given to UK infants include fruits and ‘baby rice’. Vegetables, particularly green or bitter tasting varieties, are offered less frequently. When they are introduced vegetable purées are often combined with fruits such as apple or pear, sweetening the food and potentially masking the vegetable flavour. In contrast vegetables are regularly offered as first foods in Portugal where vegetable soups are a common weaning food. These differences may be reflected in later dietary patterns as Portuguese school-children have some of the highest levels of vegetable intake in Europe.

The findings of this study suggest that repeatedly offering a variety of vegetables to infants at the start of weaning may work to increase vegetable acceptance in countries where vegetables are not already given as first foods. However, we don’t know yet whether this effect will last throughout toddlerhood and into later childhood, so this will need to be explored in future studies.

Reference: Fildes A., Lopes C., Moreira P., Moschonis G., Oliveira A., Mavrogianni C., Manios Y., Beeken R., Wardle J. & Cooke L. (2015). An exploratory trial of parental advice for increasing vegetable acceptance in infancy. British Journal of Nutrition. journals.cambridge.org/bjn/vegetabletrial

Can genetic feedback for risk of obesity prompt people to take action to prevent weight gain?

By Susanne F Meisel, on 16 February 2015

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

More evidence that ‘obese’ is becoming ‘normal’?

By Susanne F Meisel, on 12 January 2015

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

Obese people lose weight following a cancer diagnosis: but is the weight loss intentional?

By Susanne F Meisel, on 9 December 2014

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

To achieve weight loss, fat shaming is not the answer

By Susanne F Meisel, on 11 September 2014

Negative attitudes towards obese individuals therefore remain one of the ‘last socially acceptable forms of prejudice’ . One has only to glance at the ‘comments’ section of media reports discussing obesity to realise that obese people are openly subjected to labelling and stereotyping, and some outright abusive attacks. Unfortunately, stereotypes of the overweight and obese are held across all segments of society, including those working in health and social care .

Despite solid evidence (and frequent discussion on this blog) showing conclusively that whole host of factors contribute to excessive weight gain,currently, responsibility for maintaining a healthy weight rests solely with the individual. Therefore, people may think that stigmatising those who ‘refuse’ to conform to the ‘societal imperative’ is justified . Some may go even further and claim that stigmatising overweight and obese people would encourage them to lose weight. However, when our researchers looked at the scientific literature surrounding stigma and weight loss, there was little evidence showing whether this was actually true.

To find out whether weight and the experience of stigma are related in some way, researchers from our department looked at data from 2,944 UK adults over four years who participated in the English Longitudinal Study of Ageing (ELSA), a study of adults aged 50 or older. Participants are weighed and measured every four years, and asked questions on a range of topics every two years.

To assess stigma, participants were asked how often they encounter five discriminatory situations: ‘In your day-to-day life, how often have any of the following things happened to you: 1) You are treated with less respect or courtesy; 2) you receive poorer service than other people in restaurants and stores; 3) people act as if they think you are not clever; 4) you are threatened or harassed; 5) you receive poorer service or treatment than other people from doctors or hospitals. Responses ranged from ‘never’ to ‘almost every day’. Participants who reported discrimination in any of the situations were asked to indicate the reason(s) they attributed their experience to from a list of options including weight, age, gender, and race. The researchers considered participants who attributed experiences of discrimination to their weight as cases of perceived weight discrimination. Because many participants reported never experiencing discrimination, the researchers divided responses to indicate whether or not respondents had ever experienced discrimination in any domain (never vs. all other options).

Of the 2,944 eligible participants in the study, 5% reported weight discrimination. This ranged from less than 1% of those in the ‘normal weight’ category to 36% of those classified as ‘‘morbidly obese’. Men and women reported similar levels of weight discrimination.

However, those who reported experiencing weight discrimination gained more weight than those who did not over the 4-year period. On average, after taking baseline differences in BMI, gender, age and personal wealth into account, people who reported weight discrimination gained 0.95kg whereas those who did not lost 0.71kg, a difference of 1.66kg.

However, because this study looked only at the relationship of perceived stigma and weight gain, we cannot conclude that stigma caused weight gain – it could also be that weight gain increased perceived stigma, or that a third factor influenced both weight gain and stigma. To conclusively establish whether stigma indeed causes weight gain, we would have to run a controlled experiment with at least two groups of similarly overweight people, where one group is subjected to stigma over a period of time, and the other one is not, and then measure their weight at the end of the study. Of course, such an experiment would be highly unethical, given the damaging effects of stigma on psychological health. Another limitation of this study was that discrimination was assessed two years after the initial weight measurements and two years before the final measurements, although the researchers controlled statistically for this.

However, regardless of its limitations, this study showed that weight discrimination is definitely not associated with weight loss. This means that there was no evidence for the idea that stigmatising overweight and obese individuals would motivate them to lose weight. in many cases, it may even hinder weight loss. Therefore, we should work towards removing prejudice and blame from weight loss advice and should focus on positively supporting those who are trying to lose weight. One way may be to teach active coping strategies and increasing acceptance-based elements into weight loss programmes because this has had some promising effects. Furthermore, we will need to continue highlighting the complex causes of obesity rather than relying on simplistic representations, and increase work to acknowledge and address weight-related stigma, to make the ‘last socially acceptable form of prejudice’ unacceptable.

 

Article link:

Jackson, S. E., Beeken, R. J., & Wardle, J. (2014). Perceived weight discrimination and changes in weight, waist circumference, and weight status. Obesity, n/a.  http://onlinelibrary.wiley.com/doi/10.1002/oby.20891/full

 

The darker side of weight loss – why it is important to pay attention to mood changes when losing weight

By Susanne F Meisel, on 7 August 2014

The increasing prevalence of weight-related diseases have led health organisations world-wide to advise overweight and obese people to lose weight.  Indeed, the notion that weight loss is generally ‘a Good Thing’ for people who are overweight (BMI 25-30) or obese (BMI ≥30) seems to have been taken on board by the wider society.  Rightly or wrongly, magazines are full of stories, tips and tricks on how to achieve the ‘perfect’ weight, and the diet industry’s worth is estimated to be several billion pounds.   In a recent study of over 9000 overweight and obese adults, over 60% reported that they were ‘trying to lose weight’.

Undoubtedly, even losing relatively small amounts of weight (5% of body weight) will reduce the risk of many obesity-related conditions and diseases, most notably, diabetes, heart disease and stroke.  There are also many reports that weight loss has psychological benefits.  Most commonly, people said that they had improved energy levels, and felt less depressed after losing weight.

However, when researchers from our department looked more closely at the evidence for improvements in depression, it became clear that most of these reports came from people in weight loss trials.  Interestingly, mood improvements often occurred before any weight was lost in these studies, and were not related to the actual amount of weight lost.  This suggests that factors other than weight loss per se may have been responsible for the reported mood improvements.  One explanation is that personal contact (which is a central part of most weight loss trials) may have been responsible for people feeling less depressed by providing support during the weight loss process.  Furthermore, it is likely that people who take part in weight loss trials are very different from the ‘average’ weight loser in the population, so we cannot say that findings from trials will also be true for most people in the UK.

When our researchers looked for studies that used big samples that were representative of the population, they found results from only two studies, the Health and Retirement study, and the Health ABC study.  Curiously, both of these reported slight increases in depressive symptoms in people who lost weight.  However, because these studies also included healthy weight people, and did not look at whether people wanted to lose weight, or lost weight because they got ill during the study period or had significant stress in their lives (which is often related to both weight loss and depression) it was difficult to determine what the reason behind this puzzling finding was.

Therefore, our researchers set out to explore the relationship between weight loss and depressed mood in the English Longitudinal Study of Ageing (ELSA), a large cohort, representative of the UK population that has been going on for over 12 years.  The good thing about ELSA is that it includes lots of measures on all sorts of topics, so that it is very unlikely that people take part because they feel strongly about a certain issue, and it weighs and measures all of its participants every four years so does not rely on self-reported data.

For this particular analysis, the researchers decided to only look at overweight and obese people because these are the people who might be advised to lose weight; a sample of 1979 people.  They also used data telling them about participants’ intention to lose weight, their mood (using an established scale for depressive symptoms), any life stressors or illnesses that occurred during the study period, and blood pressure and triglyceride levels (which were used to check that people benefitted physically from weight loss in the expected way).

The results showed that people derived typical physical benefits from weight loss, with blood pressure and blood test results improving over a period of four years.  However, just like in the other two studies, our researchers found that overweight and obese people who lost at least 5% of their body weight (which is recommended) over four years were nearly twice as likely to be depressed than people who were weight stable, even when taking life stress and onset of illness into account.

However, this study was not able to determine cause and effect, so it is impossible to say whether weight loss caused depressed mood, or whether depressed mood caused weight loss or a third factor that was not measured caused both weight loss and depression.  It is important to investigate these findings further in order to establish why these results were observed, and why they differ so greatly from those reported in weight loss trials; especially since there are so few other studies out there at the moment that could hint at an explanation.

People often think that losing weight will make them happier, but these findings suggest that weight loss may not always be a positive experience.  In fact, the psychological ‘costs’ of weight loss might explain why many who do successfully lose weight struggle to keep the weight off in the long term.  However, this is not to say that people should not attempt to lose weight – after all, people in the study got physically healthier.  Rather, it seems important that service providers are mindful of the possibility that weight loss may worsen mood, and to perhaps include an assessment of mood in their weight loss programmes.  It may also be sensible for anyone trying to lose weight to be aware of any on-going mood changes and to seek psychological support from health professionals or even friends and family if they begin to struggle.

Article reference:

Psychological Changes following Weight Loss in Overweight and Obese Adults: A Prospective Cohort Study

Jackson SE, Steptoe A, Beeken RJ, Kivimaki M, Wardle J (2014) Psychological Changes following Weight Loss in Overweight and Obese Adults: A Prospective Cohort Study. PLoS ONE 9(8): e104552. doi: 10.1371/journal.pone.0104552

‘Health and happiness are more important than weight’: Why telling parents that their child is overweight may be ineffective at encouraging behaviour change

By Susanne F Meisel, on 24 March 2014

Childhood obesity is becoming more common.  The latest available statistics show that about 1 in 5 of 4-5year old children (22%), and about 1 in 3 (33%) of 10-11year old children were overweight or obese in the UK .  This puts more and more children at risk of serious, chronic health conditions such as diabetes and heart disease which have traditionally only been observed in adults.  Overweight and very overweight children are also at risk of mental health problems such as depression; sometimes made worse because of weight-related teasing or bullying by their peers.  Preventing more children from becoming overweight, and helping those who already are overweight to prevent further weight gain, or to lose weight, is therefore important. 

However, a huge number of factors contribute to the rising obesity rates in adults and children.  The solution is certainly not simple, and our researchers are working at finding out more about the many different factors that contribute to the current ‘obesity epidemic’. 

Some people think that one factor that plays a part in childhood obesity is that some parents don’t know that their child is overweight and because they don’t know, they don’t do anything about it.  Therefore, it was thought that telling parents that their child is overweight could prompt some action to avoid further weight gain. However, studies so far have shown that telling parents about their child’s weight status has very little effect on behaviour change; although some parents are more likely to agree that their child is overweight after having been informed about it by researchers, many parents do not agree with the feedback or think that their child’s weight puts them at risk of health problems.  In other words, they seem to disregard the information for some reason.

Researchers from our department wanted to better understand why telling parents about their child’s weight status had so little effect; and in fact often resulted in negative reactions. 

They interviewed 52 parents, who received a letter from the National Child Measurement Programme (NCMP), which informed them that their child was overweight or very overweight.  The National Child Measurement Programme was established by the Department of Health in 2005 to monitor national trends in heights, weights and BMIs of children in Reception (aged 4-5 years) and Year 6 (10-11 years) in publicly funded primary schools in England.

The researchers asked questions about parents’ thoughts on the feedback, and whether they agreed with it.

It transpired that in all interviews, parents used a variety of markers, other than weight, to decide whether their child was a healthy weight or at risk of health problems caused by their weight.  The majority of parents felt that their child ate a healthy diet, was physically active, and was not teased or bullied, and therefore they were not concerned about their child’s weight.  Furthermore, many parents did not think their child ‘looked overweight’, often in comparison with the child’s peers. In this context parents also often referred to build (‘big bones’), or to ‘puppy fat’ which they expected their child to lose during puberty. Parents shared the view that ‘health and happiness is more important than weight.’

This means that simply telling some parents that their child is overweight might not be an effective means of raising awareness about potential health problems, because they might not think that weight is a very accurate measure of their child’s health.  Taking a child’s lifestyle into account (diet, physical activity, and emotional health) might be a good way to improve the dialogue with parents about a child’s health. 

Furthermore, because there seems to be an assumption that children will lose any extra weight during puberty, parents may think that overweight is an issue that will correct itself over time.  However, there is plenty of good research showing that overweight children are highly likely to turn into overweight adults; perhaps not least because of differences in appetite, as discussed in our previous blog.  Findings from this study showed us that more work needs to be done to communicate the link between child weight and adult weight better. 

Lastly, because parents compare their own children to others, and weight has overall gone up in the population, they may consider their child ‘normal weight’ when it is, in fact, overweight.  Although there is also the argument that all measures of weight status are somewhat arbitrary and not without their faults, they do give a good indication about where things are headed, particularly for those at the upper end of the range.

Although these findings are from only one study, and interviewed only a small number of parents and may therefore not hold true for a larger number of parents, they nonetheless bring up some points that might be worth thinking about in more detail. No doubt, weight is certainly not the only important marker for a child’s well-being, but given that many overweight children and adults suffer from related physical and mental difficulties, paying attention to a child’s weight is also not insignificant. Because ultimately, parents and health professionals want the same thing: keeping children happy and healthy.

Article Reference:  Syrad H, Falconer C, Cooke L et al. Health and happiness is more important than weight: a qualitative investigation of the views of parents receiving written feedback on their child’s weight as part of the National Child Measurement Programme. J Hum Nutr Diet. 2014;n/a.  http://onlinelibrary.wiley.com/doi/10.1111/jhn.12217/abstract

 

Why tackling appetite could hold the key to preventing childhood obesity

By Susanne F Meisel, on 19 February 2014

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Article references: JAMA Pediatrics

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

 

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