‘Health Chatter’: The Health Behaviour Research Centre Blog

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

Support for flexible sigmoidoscopy (‘flexi-sig’) screening has been one of the most positive developments in cancer screening and prevention in recent years. Landmark publications in the Lancet and the New England Journal of Medicine all reported that less people had bowel cancer found and fewer died from bowel cancer after flexi-sig screening. The publication of these findings even resulted in the UK government introducing flexi-sig screening in the national bowel cancer screening programmes.

However, clinical effectiveness of a medical procedure does not guarantee better public health outcomes. It is one thing to show that screening is effective in combating a disease, but quite another for healthy people to agree to someone – excuse my explicit wording – to stick a tube up their bottoms.

Regrettably, participation in flexi-sig screening pilots has been relatively low compared to breast and cervical screening. Yet, there is hope for improvement. Our latest published study on flexi-sig screening among the general population showed high levels of satisfaction. An overwhelming majority of those who had been screened were glad to have had the test and would recommend it to a friend. As one patient put it: “I was very happy by how easy it all was and how little time the test took. Thank you.” Satisfaction was also uniform across the population: it was unaffected by gender, socioeconomic status and ethnicity. Respondents also reported fewer bowel symptoms following screening.

It is the hope that high satisfaction levels will be maintained in a nation-wide screening programme. If so, the positive experience of early screening participants may help to shift public opinion on embarrassment of rectal examinations and thus help people overcome emotional barriers to screening they may have.

References

Atkin WS, Edwards R, Kralj-Hans I, et al. Once-only flexible sigmoidoscopy screening in prevention of colorectal cancer: A multicentre randomised controlled trial. Lancet 2010;375:1624–3.
Robb K, Power E, Kralj-Hans I, et al. Flexible sigmoidoscopy screening for colorectal cancer: uptake in a population-based pilot programme. J Med Screen 2010;17:75–8.
Robb, K., Lo, S.H., Power, E., Kralj-Hans, I., Edwards, R., Vance, M., von Wagner, C., Atkin, W. & J. Wardle. Patient-reported outcomes following flexible sigmoidoscopy screening for colorectal cancer in a demonstration screening programme in the UK. J Med Screen in press.
Schoen RE, Pinsky PF, Weissfeld JL, et al. Colorectal-cancer incidence and mortality with screening flexible sigmoidoscopy. New Engl J Med 2012;366:2345–57

Type Jade Goody’s name into Google Images and you find an array of pictures from bouncy Big Brother star, through smiling but bald cancer patient, to pain-wracked dying woman.  Jade was diagnosed with cervical cancer in 2008 and died at the age of 27 just a few months later.  Her tragic story received unprecedented media attention and the general public were privy to the intimate details of the last months of her life.  In what has become known as the ‘Jade Effect’, her story had an extraordinary impact on women’s participation in cervical screening – we think about half a million extra women went for screening during the time of her illness.

As psychologists, we were interested in which women were influenced by Jade’s story and why.  To try to understand more about the Jade Effect, we did a survey of 890 women in England – all of them within the age range that are offered screening..  We collected information about women’s age and their social background and we asked them if they’d been affected by Jade’s story in their decisions about cervical screening.  The survey was done about 18 months after Jade’s death, so we asked women to think back over that time period.

The most interesting finding was that younger women were more influenced by Jade, and so were women who had children at a younger age, and who came from more deprived backgrounds.  So why do we think this is?  Well, Jade was 27 when she died, and it’s no secret that she had a hard childhood in Bermondsey – hers was a ‘rags to riches’ story.  She also had children young – in her early 20s.  So it seems possible that the women who were most influenced by her were those who could identify with her.  Perhaps there was a sense of ‘it could have been me’ – and this was the prompt they needed to go for screening.  Suddenly the stakes were raised and the barriers to having a smear test didn’t seem so important.  It’s also possible that some people are more affected by stories than facts.  The blanket media coverage and the emotional story of Jade’s illness probably affected people very differently compared with the kind of factual leaflets that are usually used in screening programmes.  It could be a case of heart vs. head, and perhaps as psychologists and health educators, we need to realise that stories, or ‘narratives’ as they’re sometimes known, can be a good way to get our message across.

Jo Waller (j.waller@ucl.ac.uk)

References

Lancucki L, Sasieni P, Patnick J, Day TJ, Vessey MP.  The impact of Jade Goody’s diagnosis and death on the NHS Cervical Screening Programme.   J Med Screen. 2012 Jun;19(2):89-93. doi: 10.1258/jms.2012.012028. Epub 2012 May 31.

Marlow LA, Sangha A, Patnick J, Waller J.  The Jade Goody Effect: whose cervical screening decisions were influenced by her story?   J Med Screen. 2012 Dec 27. [Epub ahead of print]

The big day has finally arrived. No, I’m not getting married, but our paper has been published. For academic standards, it has short title, namely “The Impact of Media Coverage of the Flexible Sigmoidoscopy Trial on English Colorectal Screening Uptake”. In a nutshell, our study shows that participation in the existing English bowel cancer screening programme rose shortly after and one month after media coverage of a high-quality medical bowel cancer screening trial. Most interestingly, the effect seemed to be particularly strong among those who had previously ignored a screening invitation.

I should add, however, that the trial receiving media publicity used a different screening test from the one used in the programme. Also, we cannot be certain whether the increase observed was due to influences other than increased publicity for bowel cancer. Without those qualifications, my findings would have been much more impressive. Unfortunately, observational research in the real world usually brings practical limitations with it which is why many colleague psychologists prefer laboratory work.

However, it is vital for theories to be tested in the real world. In the case of our recent media impact study, there were competing theories. On the one hand, some argued that the messenger influences the persuasiveness of a message which would result in preaching to the converted. On the other hand, others suggested that awareness is the key factor, thus predicting a larger increase among those not screened so far. Our findings suggest that media coverage of scientific advances in cancer prevention mainly has an awareness raising effect. Efforts to generate positive media attention to cancer prevention and screening should therefore be encouraged. This may not be a surprising conclusion, but it is certainly be a useful one.

References

Lo, S.H., Vart G., Snowball, J., Halloran, S.P., Wardle, J. & C. von Wagner (2012), ‘The impact of media coverage of the Flexible Sigmoidoscopy Trail on English colorectal screening uptake’, Journal of Medical Screening, 19, 83-88.

Have you ever made a New Year’s resolution? If so, you may have been assured – usually by a well-meaning supporter of your attempted transformation – that you only have to stick with your resolution for 21 days for it to become an ingrained habit. The magic number 21 creeps up in many articles about forming a new habit or making a change, but little is known about the origins of the ’21 days’ claim.

Psychologists from our department have devoted extensive time and effort to find out what it takes to form ‘habits’ (which psychologists define as learned actions that are triggered automatically when we encounter the situation in which we’ve repeatedly done those actions).

We know that habits are formed through a process called ‘context-dependent repetition’.  For example, imagine that, each time you get home each evening, you eat a snack. When you first eat the snack upon getting home, a mental link is formed between the context (getting home) and your response to that context (eating a snack). Each time you subsequently snack in response to getting home, this link strengthens, to the point that getting home comes to prompt you to eat a snack automatically, without giving it much prior thought; a habit has formed.

Habits are mentally efficient: the automation of frequent behaviours allows us to conserve the mental resources that we would otherwise use to monitor and control these behaviours, and deploy them on more difficult or novel tasks. Habits are likely to persist over time; because they are automatic and so do not rely on conscious thought, memory or willpower.  This is why there is growing interest, both within and outside of psychology, in the role of ‘habits’ in sustaining our good behaviours.

So where does the magic ’21 days’ figure come from?

We think we have tracked down the source. In the preface to his 1960 book ‘Psycho-cybernetics’, Dr Maxwell Maltz, a plastic surgeon turned psychologist wrote:

‘It usually requires a minimum of about 21 days to effect any perceptible change in a mental image. Following plastic surgery it takes about 21 days for the average patient to get used to his new face. When an arm or leg is amputated the “phantom limb” persists for about 21 days. People must live in a new house for about three weeks before it begins to “seem like home”. These, and many other commonly observed phenomena tend to show that it requires a minimum of about 21 days for an old mental image to dissolve and a new one to jell.’ (pp xiii-xiv)

How anecdotal evidence from plastic surgery patients came to be generalised so broadly is unclear.  One possibility is that the distinction between the term habituation (which refers to ‘getting used’ to something) and habit formation (which refers to the formation of a response elicited automatically by an associated situation) was lost in translation somewhere along the line. Alternatively, Maltz stated elsewhere that:

‘Our self-image and our habits tend to go together. Change one and you will automatically change the other.’ (p108)

Perhaps readers reasoned that, if self-image takes 21 days to change, and self-image changes necessarily lead to changes in habits, then habit formation must take 21 days. Although ‘21 days’ may perhaps apply to adjustment to plastic surgery, it is unfounded as a basis for habit formation. So, if not 21 days, then, how long does it really take to form a habit?

Researchers from our department have done a more rigorous and valid study of habit formation (Lally, van Jaarsveld, Potts, & Wardle, 2010). Participants performed a self-chosen health-promoting dietary or activity behaviour (e.g. drinking a glass of water) in response to a once-daily cue (e.g. after breakfast), and gave daily self-reports of how automatic (i.e. habitual) the behaviour felt. Participants were tracked for 84 days. Automaticity typically developed indistinct pattern: initial repetitions of the behaviour led to quite large increases in automaticity, but these increases then reduced in size the more often the behaviour was repeated, until automaticity plateaued. Assumed that the point, at which automaticity is highest, is also the point when the habit has formed, it took, on average, 66 days for the habit to form. (To clarify: that’s March 6^th for anyone attempting a New Year’s resolution.)

Interestingly, however, there were quite large differences between individuals in how quickly automaticity reached its peak, although everyone repeated their chosen behaviour daily: for one person it took just 18 days, and another did not get there in the 84 days, but was forecast to do so after as long as 254 days.

There was also variation in how strong the habit became: for some people habit strength peaked below the halfway point of the 42-point strength scale and for others it peaked at the very top. It may be that some behaviours are more suited to habit formation – habit strength for simple behaviours (such as drinking a glass of water) peaked quicker than for more complex behaviours (e.g. doing 50 sit-ups) – or that people differ in how quickly they can form habits, and how strong those habits can become.

The bottom line is: stay strong. 21 days is a myth; habit formation typically takes longer than that. The best estimate is 66 days, but it’s unwise to attempt to assign a number to this process. The duration of habit formation is likely to differ depending on who you are and what you are trying to do. As long as you continue doing your new healthy behaviour consistently in a given situation, a habit will form. But you will probably have to persevere beyond January 21^st.

Benjamin Gardner and Susanne Meisel

(www.ucl.ac.uk/hbrc/gardnerb)

References

Lally, P., van Jaarsveld, C. H. M., Potts, H. W. W., & Wardle, J. (2010). How are habits formed: Modelling habit formation in the real world. European Journal of Social Psychology, 40, 998-1009. (http://onlinelibrary.wiley.com/doi/10.1002/ejsp.674/abstract)

Maltz, M. (1960) Psycho-cybernetics. NJ: Prentice-Hall.

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

As mentioned in one of our previous blog posts, talking about genes in the context of obesity is often not well received.  Those discounting their role in the development of obesity often argue that, because genes have not substantially changed over the past 200 000 years, whereas obesity levels have only been soaring over the past 20 odd years (where it became possible to mass-produce cheap, tasty food in combination with a decreased need for physical activity), obesity must be due to changes in the environment, and not genetics.

However, using this argument against the heritability of obesity is somewhat flawed, because it ignores that a condition can be dormant over a period of time until the right circumstances bring it to life.  The gardeners among you will know that many plants will adjust their growth according to their surroundings – a plant in a small pot will remain small, whereas a larger pot will allow it to grow.   This, however, does not mean that the plant loses its ability to grow larger in a smaller pot; it merely remains small because its surroundings restrict its growth.  Similarly, genes predisposing to obesity may be present in an environment where little food is available, but without the right ‘medium’ (i.e. food), this is of little consequence.  In the current environment, however, where eating opportunities are plentiful, obesity genes can express their full force.

If obesity was resulting purely from environmental change, all individuals exposed to this change would become overweight.  Yet, this is not the case. In fact, the proportion of lean people has not substantially changed, but large people are becoming even larger.  This suggests that people respond to the food environment differently.  However, undoubtedly, to gain more weight than is healthy, food must not only be available in sufficient quantities, but one must ingest more of it than necessary.  Therefore, researchers started to look at differences in eating behaviours, such as how much we are drawn to food and how quickly we feel full, to see what is going on.

Twins can help to untangle the influence of genes and environment on obesity, because identical twins are 100% genetically identical, whereas non-identical twins only share approximately half of their genes (like normal siblings); both, however, grow up in a very similar environment.  This means that researchers can compare identical twins’ resemblance for weight with that of non-identical twins; if genetically identical twins are more similar in a trait than non-identical twins, it is evidence for genes being responsible for the trait.

Using twins, researchers from our department wanted to see whether genes that influence weight also influence appetite.  If the same genes that influence weight also influence appetite, it suggests that genes influence weight through their effects on appetite – i.e. individuals who inherit more avid appetites might be more susceptible to overeating in the modern food environment, and consequently  more likely to gain excessive weight.  They looked at this in infants, because infants are exclusively milk-fed, which ruled out that other factors such as preference for certain foods would influence the results.   The researchers used questionnaires to ask parents about how fast their twins fed, how easily they got full and how big their appetite was, and related the answers to the babies’ weight.   Because they used a sample of identical and non-identical twins the researchers were able to explore the extent to which appetite is heritable, and the extent to which appetite and weight are caused by the same genes.

They found that identical twins were not only very similar in weight, but shared many more similarities in appetite than non-identical twins, suggesting a strong genetic basis to both appetite and weight.  In addition, the results  showed that a substantial proportion of the genes that are responsible for weight are also responsible for appetite, in line with the idea that genes influence weight through appetite.  These findings lend evidence to the idea that some of us are more likely to overeat in the current environment because of a larger appetite, which is ultimately driven by genes.

These discoveries will hopefully contribute to reducing the stigma that surrounds unhealthy weight gain; because it clearly shows that those struggling with weight are in a sense ‘battling against their biology’.  This of course, does not mean that there is nothing that can be done about it; however, acknowledging these differences as real and designing strategies to ‘outsmart’ one’s genes is crucial if the battle is to be fought successfully.

Article reference: http://www.ajcn.org/content/95/3/633.long

You don’t need to be Jamie Oliver to figure out what is going on with children’s diets – but his efforts certainly helped to pull the candyfloss from our eyes:  children in England are eating plenty of snacks high in fat, salt and sugar, but only one quarter eats their recommended minimum 5 portions of fruit and vegetables a day.  This can be problematic, because not only could it lead to nutritional deficiencies, but also to disproportionate weight gain.

Unfortunately, it is not the case that children simply ‘outgrow’ their ‘puppy-fat’; the vast majority of overweight children grow into overweight teenagers and potentially obese adults.  This is because people naturally put on about 2 pounds per year as they age (unless they do something about it, of course) – and the higher the ‘starting weight’ is, the higher the chances are that people shift up across the weight spectrum as they get older. Furthermore, people who become overweight or obese early in life are often more severely affected by illnesses linked with an unhealthy weight, such as diabetes, heart disease and some cancers.

This is why it is important to figure out what it is that makes children eat their greens (and all those other healthy fruit and veggies, even if cooking like Jamie isn’t your thing).  It has long been known that many different factors such as inherited taste preferences, family eating habits or the amount of time spent watching TV are important when looking at reasons why children eat (or don’t eat) certain foods; but rarely has research looked at factors related to healthy and unhealthy eating habits at the same time in the same group of families.

In this study, the researchers were interested in the actual foods children in England eat (as opposed to specific nutrients, such as vitamins). The researchers had records of what children and their parents ate from several hundred families, along with information on factors which may influence what they eat.  They decided to look in particular at factors which affected how much fruit, vegetables, unhealthy snacks and sugary drinks children consume; focusing on preschool-aged children – as they are not yet strongly influenced by their peers, and are more dependent on eating what their caregivers provide for them.

Perhaps unsurprisingly, the researchers found that when children liked the taste of fruit and veggies it predicted how much of these they ate.  However, what is more important, they also found that parents’ consumption of either fruit, vegetables, unhealthy snacks or sweetened drinks was a very important indicator of how much children ate of these foods.  This might be not only because caregivers may feed children what they themselves eat, but also because children tend to copy adults’ behaviour – so if mum eats healthily, children will be more likely to want to eat healthily too.  Of course, that is also true for unhealthy eating habits – which is why not having junk foods in the home in the first instance can help.  Because it was mainly mothers who filled out the questionnaires, these results focused only on mothers.

Furthermore, praising children for eating fruit and veggies was a good indicator of how much children ate, and monitoring the unhealthy snacks children eat was linked with them eating less of these and more fruit and vegetables.  The amount of time children spent watching TV was also an indicator of children eating unhealthy snacks and having sweetened drinks, but it had no impact on their consumption of fruit and vegetables.

The research provides a little more evidence on how eating habits are transmitted within a family.  It highlights that different strategies need to be used in order to increase the amount of healthy foods vs. decreasing amounts of unhealthy foods children eat.

So, ultimately, if you want your children to eat their greens, you might not have any choice but to take a bite too and start singing their praises, and if you really want to cut down on their junk intake then get rid of it from within your home and turn off the telly – and at last Jamie will be happy.

http://www.nature.com/ejcn/journal/vaop/ncurrent/full/ejcn2011224a.html

If you thought that the stresses of present-picking, turkey-basting and relative-juggling are to blame for weight gain, you are not alone. A Google search for ‘stress and weight gain’ reveals a staggering 32,000,000 sites dealing with the topic. However, researchers from our research group have shown that the effect of stress on weight gain may not be as large as you may have thought.

The body tries to maintain stability by adapting to a change in the environment, a process called homeostasis. Stress can be defined as any external factor, physical or psychological, which threatens to throw the body out of homeostasis. Whether running from a hungry lion, or suffering stage-fright before a speech, the body’s response will be the same: the stressor (lion or stage-fright) will trigger the so called ‘fight-or-flight-response’, which is marked by increased heartbeat, muscle-tension, sweating, dilation of the pupils and the release of the ‘stress-hormones’ adrenalin and cortisol. This response is extremely useful to mobilise resources, help us get through difficult situations and regain homeostasis. However, when we experience the on-going stresses of modern life, such as money-worries, job stress, or social pressures, we begin to feel the strain. Long-term stressors overwhelm the body’s coping system, deplete resources and ultimately lead to exhaustion. It has been thought that weight gain results from the body trying to restore homeostasis by inducing metabolic changes which promote fat storage on the one hand and behaviour changes on the other, for example making less time to be active or reaching for cookies instead of carrots.

Results from studies investigating this topic are mixed – some have found that stress has an effect on weight gain, and others have not. Researchers from our department decided to look at the effect from all these studies overall. Summarizing results of several studies on the same topic to find out the ‘true’ effect is called meta-analysis. The studies that were included in this meta-analysis had to be conducted over a period of time (because these are more accurate than studies that only look at a single time-point), measure weight objectively, and focus on external stressors such as life events, work-or caregiver stress. Fourteen studies from Europe and the USA met the criteria; each ‘stress category’ (life events, work- or caregiver stress) was analysed separately.

Results of the meta-analysis showed that stress is related to weight gain, although the effects were very small. When the researchers looked at the results in more depth, they saw that studies that went on for longer and were of better quality were more likely to show an effect of stress on weight. They also saw that the effect appeared to be stronger in men. It did not matter whether the stressor was related to life or work. Unfortunately, eating behaviour was not assessed, so the researchers could not tell whether it changed under stress.

Although there are not very many studies that looked at the topic over a period of time, and imprecise measurements of stress were often used, the findings are relatively robust because of the way the studies were combined. Finding a stronger link of stress on weight in men complements other findings which show that men have a stronger fight-or-flight response. Overall, however, it can be seen that the effects of stress on weight are much smaller than often made out in the media. Blaming the relatives for a bulging belly might be convenient, but complex issues like weight gain unfortunately have no simple, or convenient, answer.

Source: http://www.nature.com/oby/journal/v19/n4/full/oby2010241a.html