Just last month, I was chatting to a friend, who happens to be a doctor, about my research. She asked me: “So, really? You would classify obesity as a disease?” I sighed. The kind of sigh that said: I’m not annoyed, just frustrated… how have you completed five years of medical school and not learnt about obesity in the context of disease rather than personal choice? I replied: “Yes of course, it is one of the most complex diseases currently facing the population and modern science”.
As a researcher working in the field of obesity, I often find myself in these types of conversations, arguing against the belief that all individuals who live with obesity are overweight and remain overweight because they are lazy, weak-willed and less disciplined than individuals of a healthy weight.
Sadly, this viewpoint is highly prevalent, even in medical professionals who are in regular contact with patients living with obesity.
Over the last century, obesity has been viewed and addressed by health professionals, policy makers and the general public as a result of how calories are processed. That is, that continuous weight gain in individuals with obesity can be predicted by this simple equation:
CALORIES IN-CALORIES OUT = BODY FAT
There is an intuitive appeal to this theory. ‘Individuals live with obesity because they have eaten too much and exercised too little for too long.’ Simple.
Yes, it is true that diet and exercise are drivers of weight gain, no-one is denying this. But this theory is overly simplistic.
This theory does not explain why we all have that friend who eats a lot, yet never gains weight, or why another person may have a lower calorie intake and put on weight, despite being reasonably active.
The obesity epidemic cannot be down to calories alone.
There is more to this story.
As highlighted in the UK Government’s Foresight Report, weight is influenced by over 100 complex factors which include genetic, environmental, psychological, social, economic and political factors. These interact in varying degrees to promote the development of obesity.
I aim to use this article to highlight some of the factors that have contributed to the obesity epidemic that are rarely given mainstream attention. I will then go on to discuss the robust link between obesity, stigmatisation and it’s mental health consequences.
The food environment
The food environment has changed in ways that promote overeating. Highly caloric and fatty foods are not only affordable but they are also very easily accessible.
High streets are now homes to multiple fast-food outlets. Grimsby in Lincolnshire recently topped the table as Britain’s unhealthiest high street, and the same study found that the number of fast food outlets in the UK increased by 4,000 between 2014 and 2017, with the most deprived areas now occupying five times more than the most affluent areas.
Furthermore, most offices, schools and hospitals have multiple vending machines somewhere on their grounds. These types of highly palatable foods are frequently available in large portions, which contribute to increased daily caloric intake.
In addition, the number of processed food items (foods high in sugar, fat, and salt) available in supermarkets, petrol stations, and corner shops has rapidly increased.
These products are heavily marketed to both adults and, perhaps more dangerously, to children.
Convenient, easy to prep, and cheap, these high calorie products are frequently consumed by millions of families who are struggling to meet the economic and time demands of today’s fast paced lifestyle.
However, even with changes to the food environment, there will be diversity of body weight and size, in the same way that there is a spectrum of height and shoe size.
By linking the food environment to obesity without considering additional influences, the inaccurate assumption that individuals simply gain weight by eating the ‘wrong’ foods, and that thinner people are healthy and less susceptible to ‘junk food’ marketing, will be fueled.
Hormones are chemical messengers that regulate processes in our body.
The hormones leptin and insulin, along with sex hormones, influence our appetite, our metabolism (the rate at which our body burns food for energy), and how body fat is distributed in our bodies.
Leptin is produced by fat cells and then enters our bloodstream. It reduces our appetite by acting on specific parts of the brain to reduce our urge to eat. Because leptin is produced by fat cells, their levels tend to be higher in people with obesity than in people of normal weight.
I know what you’re thinking… surely, if individuals with obesity have higher levels of leptin, then they should have more regulated appetites? But, what research actually finds is that individuals with obesity aren’t as sensitive to the effects of leptin and, as a result, tend not to feel full during and after a meal.
Ongoing research is investigating why leptin’s messages aren’t getting through to the brain in people with obesity.
Another hormone that is important in the development of obesity is Insulin. Commonly discussed in the context of diabetes, Insulin is important for our regulation of carbohydrates and the breakdown of fat after a meal.
Insulin causes glucose (sugar) to move from our bloodstream into our tissues, to make sure that we have enough energy for everyday functioning and to ensure we have normal levels of sugar pumping around our body.
Research suggests that, in individuals with obesity, insulin signals are sometimes lost, which causes higher levels of sugar in the blood. This can lead to development of obesity because the body’s cells cannot access blood sugar for energy, which can lead to an increase in thirst and hunger, as well as feeling drowsy and tired.
Lastly, changes in sex hormone levels of both men and women over the lifespan are associated with changes in body fat distribution. For example, in women, increased testosterone and decreased estrogen contributes to an increase in abdominal fat and may help explain the weight gain commonly experienced during menopause.
Just over a decade ago despite huge efforts, no gene had been clearly associated with body weight and risk of obesity.
In recent years, however, more advanced scientific methods in the field of genetics have succeeded.
The first obesity-susceptibility gene was detected by researchers in 2007 (the FTO gene). A variant in the FTO gene predisposes individuals to type 2 diabetes through an effect on body weight. This genetic variant is thought to contribute to approximately 22% of common obesity in society today.
Exactly how the FTO gene causes obesity is still not entirely clear.
FTO appears to regulate ghrelin, a hormone produced in the gut that alters appetite and food intake. When ghrelin is increased, reduced fullness and increased food intake occur. Different studies have found that FTO is linked to increased intake of fat and protein, increased appetite, reduced fullness, poor food choices and eating habits, and also a loss of control over eating.
Researchers have also found that increased levels of ghrelin occur after diet-induced weight loss, so this may explain why we see such high rates of weight regain after successful diets in this population.
Furthermore, genes can directly cause obesity in disorders such as Prader-Willi syndrome. In Prader-Willi syndrome, certain genes are either missing or not functioning correctly, which changes how the hypothalamus works (a part of the brain that controls thirst and hunger).
Sleep deprivation is typically considered getting less than 7 hours of sleep per night. There are numerous studies which suggest that sleep deprivation can indirectly cause weight gain.
One study recruited 83,377 older adults and followed them over 7 years, concluded that sleep duration of less than 5 hours, compared with 7–8 hours, increased the likelihood of developing obesity by 40%.
This is concerning, given that in 2017, 74% of the UK population got less than 7 hours sleep a night, and 12% got less than 5 hours.
Experimental studies have shown that sleep restriction can influence hormones, like those described in the section above, that regulate the breakdown of food in the body and influence our feelings of hunger and fullness.
Other authors suggest simply that individuals who sleep less have more opportunities to eat food because they are awake for longer, and that short sleepers experience more tiredness which reduces the likelihood of exercising.
These researchers ran a study with 225 study volunteers; for five nights, half of the group had their sleep restricted to just four hours, whilst the other half were free to sleep as long as they wanted.
And what did they find? Sleep restriction is not good for your waistline. Everyone in the restricted sleep group gained weight, on average 1kg over the course of one week.
Drug-induced weight gain
Weight gain is associated with several medications, and the recognition that some of the most widely prescribed classes of drugs can cause significant weight gain supports the hypothesis that drug-induced weight gain may be contributing to the current obesity epidemic.
Certain antipsychotic drugs (such as clozapine, olanzapine, risperidone and quetiapine) are known to cause weight gain. Antidepressants too, such as amitriptyline, mirtazapine and some serotonin reuptake inhibitors (SSRIs), may promote weight gain that cannot be explained solely by the individual not feeling depressed any more.
Furthermore, a common side effect of certain anti-diabetic drugs is weight gain, which is obviously very problematic in clinic as many diabetic patients live with obesity and further weight gain is hence undesirable.
Some individuals are fortunate enough to be able to switch to a different brand of medication if they notice significant weight gain. We see this happen a lot with contraceptives. There are hundreds of different contraceptives available, meaning an individual can try several different ones to find the one that works for their mental and physical health
But what about the individual with bipolar disorder or schizophrenia whose medication has done wonders for curbing their symptoms of psychosis yet has caused them to gain weight? What is more important for that individual? Their mental health or their body size? They should not have to choose.
Obesity, stigma and mental health
Every year there are a substantial number of media articles published that stigmatise and discriminate against people with obesity. These articles are easily accessible and can be read by millions of people.
Recently, the very important medical journal, The Lancet, has published a call for developing collaborative work with the media in order to reduce the weight stigma and discrimination evidenced across society. The call highlighted the following examples from popular UK newspapers:
Individuals with obesity face stereotypical attitudes from employers and disadvantages in hiring, wages, promotions, and job termination. They are also more likely to be prescribed weight loss interventions when presenting with worrying symptoms at their GP, and hence experience delays in alternative interventions because their issues are commonly assumed to be weight-related.
Ironically, weight stigma is also prevalent in anti-obesity campaigns.
The USA’s ‘Strong4Life’ campaign is one such example. Started in 2012 by a hospital in Atlanta, the campaign featured billboard adverts with unflattering photos of visibly unhappy children living with obesity. The adverts were accompanied by warning banners stating messages such as: “Chubby isn’t cute if it leads to type two diabetes”; and “Being fat takes the fun out of being a kid”.
It has been said that the ‘Strong4Life’ adverts were partly modeled on a successful anti-methamphetamine campaign in the states, and the hospital behind the billboards defended the campaign by stating that “it raised awareness of the dangers of obesity”.
Another more recent example is the recent cancer research UK campaign that you may have seen advertised on your local high street. Its focus on weight as a leading cause of cancer is misleading.
Weight is a crude indicator of health and while there is a link between higher weight and cancer, the reasons for this are unclear. Implying that individuals are totally in control of their weight (and therefore cancer) supports a culture of blame and drives marginalisation and inequality of an already stigmatised population.
Not only this, but the evidence is crystal clear that obesity stigma does not motivate individuals with obesity to lose weight.
People with obesity who experience weight-related stigmatisation participate less in physical activity and the stress associated with weight stigma can trigger eating and contribute to further weight gain.
This negative view is contributing to and perpetuating a cycle of weight gain.
Moreover, a recently published study that analysed data on more than 17,000 children born across the UK in 2000–2001 (The Millennium Cohort Study), found that high body weight and poor mental health go hand in hand from early childhood.
The author of the study commented that:
“People think it’s as simple as eating less and exercising more — but it’s much more complex than that”
Unfortunately, largely because of this lack of understanding of the complex web of factors that contribute to causing and maintaining obesity, weight-related stigmatisation (weight stigma) is very common in society.
So where do we go from here?
Journalists reporting obesity-related topics can use balanced and sensitive visual content, depicting non-stigmatising portrayals of individuals with obesity. The European Association for the Study of Obesity has set up an Obesity Image Bank specifically for the media to view and make use of in future articles.
Furthermore, anti-obesity campaigns are likely to be more productive if they focused on respectful care for all bodies, empowering people to make health promoting changes, no matter what their weight.
As a society, if we are to successfully tackle the complex and growing issue of obesity and the mental health problems that come with it, we must move away from viewing weight gain as a personal failure.
Instead, we need to view obesity as a consequence of dealing with a complex condition, and we need to view individual responsibility in the context of uncontrollable factors.
header image source:the women journal