We live in a time where most of us complain about the lack of it. Thus, I often remind myself that our “fast-food culture” is more a time than a food problem.
Now a study by Viral Patel and colleagues, published in OBESITY, takes a detailed look at how US Americans spend their time according to different BMI categories.
The researchers analyse data from over 28,503 observations of individuals aged 22 to 70 from the American Time Use Survey, a continuous cross-sectional survey on time use in the USA.
In a statistical model that adjusted for various sociodemographic, geographic, and temporal characteristics, younger age; female sex; Asian race; higher levels of education; family income >$75 k; self-employment; and residence in the West or Northeast census regions were all associated with a lower BMI relative to reference categories whereas age 50 to 59 years; Black, Hispanic, or “other” race; and not being in the labor force were associated with a higher BMI.
That said, here are the differences in time use associated with higher BMI:
Although there were no substantial differences among BMI categories in time spent sleeping, overweight individuals experienced almost 20 fewer minutes of sleeplessness on weekends/holidays than individuals with normal weight. Furthermore, there was a U-shaped relationship between BMI and sleep duration such that BMI was lowest when sleep duration was approximately 8 h per day and increased as sleep duration became both shorter and longer. Less sleep on weekends and holidays (5 to 7 h) was also associated with higher BMI than 8 to 9 h or sleep.
There were also no major differences between BMI categories and the odds of participating in work or in the amount of time working. However, working 3-4 h on weekends/holidays was associated with the lowest BMI. Individuals with obesity were more likely to be working between 3:30 a.m. and 7:00 a.m. on weekdays than normal-BMI individuals, again perhaps cutting into restful sleep.
Individuals with obesity were less likely to participate in food and drink preparation than individuals with normal weight on weekdays but spent about the same amount of time eating or drinking as the reference category.
Interestingly, individuals with obesity were more likely than individuals with normal weight to participate in health-related self-care, and overweight individuals spent over 1 h more on weekdays than individuals with normal weight on health-related self-care and also spent an additional 15 min (almost double the time) on professional and personal care services.
While individuals with higher BMI were less likely to participate in sports, exercise, and recreation on weekdays and weekends/holidays compared with individuals with normal weight, those who did participate did not differ from individuals with normal weight in the amount of time spent participating. In contrast, overweight individuals were more likely to attend sports/recreation events during the week and spent an additional 47 min (almost 25% more) on this activity than individuals with normal weight.
Overall, there was a positive and generally linear association between time spent viewing television/movies and BMI, with individuals with obesity more likely to watch television almost all hours of the day during the week and weekends.
On weekends/holidays, individuals with obesity were more likely to participate in care for household children and household adults. It was also observed that individuals with obesity spent an additional 15 min on religious and spiritual activities on weekends/holidays, compared with normal-BMI individuals (who spent 116 min).
While these data are of interest and are largely consistent with the emerging data on the role of optimal sleep duration and the detrimental impact of sedentary activities like television viewing on body weight, we must remember that the data are cross-sectional in nature and cannot be interpreted to imply causality (as, unfortunately, the authors do throughout their discussion).
Also, no correction is made for increasing medical, mental, or functional limitations associated with increasing BMI levels, which may well substantially affect time use including sleep, work, participation in sports or work-related activities.
Thus, it is not exactly clear what lessons one can learn regarding possible interventions – it is one thing to describe behaviours – it is an entirely different thing to try and understand why those behaviours occur in the first place.
Thus, unfortunately, findings from these type of studies too often feed into the simplistic and stereotypical “obesity is a choice” narrative, which does little more than promote weight bias and discrimination.
Continuing in my miniseries on reasons why obesity should be considered a disease, I turn to the idea that obesity is largely driven by biology (in which I include psychology, which is also ultimately biology).
This is something people dealing with mental illness discovered a long time ago – depression is “molecules in your brain” – well, so is obesity!
Let me explain.
Humans throughout evolutionary history, like all living creatures, were faced with a dilemma, namely to deal with wide variations in food availability over time (feast vs. famine).
Biologically, this means that they were driven in times of plenty to take up and store as many calories as they could in preparation for bad times – this is how our ancestors survived to this day.
While finding and eating food during times of plenty does not require much work or motivation, finding food during times of famine requires us to go to almost any length and risks to find food. This risk-taking behaviour is biologically ensured by tightly linking food intake to the hedonic reward system, which provides the strong intrinsic motivator to put in the work required to find foods and consume them beyond our immediate needs.
Indeed, it is this link between food and pleasure that explains why we would go to such lengths to further enhance the reward from food by converting raw ingredients into often complex dishes involving hours of toiling in the kitchen. Human culinary creativity knows no limits – all in the service of enhancing pleasure.
Thus, our bodies are perfectly geared towards these activities. When we don’t eat, a complex and powerful neurohormonal response takes over (aka hunger), till the urge becomes overwhelming and forces us to still our appetites by seeking, preparing and consuming foods – the hungrier we get, the more we seek and prepare foods to deliver even greater hedonic reward (fat, sugar, salt, spices).
The tight biological link between eating and the reward system also explains why we so often eat in response to emotions – anxiety, depression, boredom, happiness, fear, loneliness, stress, can all make us eat.
But eating is also engrained into our social behaviour (again largely driven by biology) – as we bond to our mothers through food, we bond to others through eating. Thus, eating has been part of virtually every celebration and social gathering for as long as anyone can remember. Food is celebration, bonding, culture, and identity – all features, the capacity for which, is deeply engrained into our biology.
In fact, our own biology perfectly explains why we have gone to such lengths to create the very environment that we currently live in. Our biology (paired with our species’ limitless creativity and ingenuity) has driven us to conquer famine (at least in most parts of the world) by creating an environment awash in highly palatable foods, nutrient content (and health) be damned!
Thus, even without delving any deeper into the complex genetics, epigenetics, or neuroendocrine biology of eating behaviours, it is not hard to understand why much of today’s obesity epidemic is simply the result of our natural behaviours (biology) acting in an unnatural environment.
So if most of obesity is the result of “normal” biology, how does obesity become a disease?
Because, even “normal” biology becomes a disease, when it affects health.
There are many instances of this.
For example, in the same manner that the biological system responsible for our eating behaviour and energy balance responds to an “abnormal” food environment by promoting excessive weight gain to the point that it can negatively affect our health, other biological systems respond to abnormal environmental cues to affect their respective organ systems to produce illnesses.
Our immune systems designed to differentiate between “good” and “bad”, when underexposed to “good” at critical times in our development (thanks to our modern environments), treat it as “bad”, thereby creating debilitating and even fatal allergic responses to otherwise “harmless” substances like peanuts or strawberries.
Our “normal” glucose homeostasis system, when faced with insulin resistance (resulting from increasingly sedentary life circumstances), provoke hyperinsulinemia with ultimate failure of the beta-cell, resulting in diabetes.
Similarly, our “normal” biological responses to lack of sleep or constant stress, result in a wide range of mental and physical illnesses.
Our “normal” biological responses to drugs and alcohol can result in chronic drug and alcohol addiction.
Our “normal” biological response to cancerogenous substances (including sunlight) can result in cancers.
The list goes on.
Obviously, not everyone responds to the same environment in the same manner – thanks to biological variability (another important reason why our ancestors have made it through the ages).
But, you may argue, if obesity is largely the result of “normal” biology responding to an “abnormal” environment, then isn’t it really the environment that is causing the disease?
That may well be the case, but it doesn’t matter for the definition of disease. Many diseases are the result for the environment interacting with biology and yes, changing the environment could indeed be the best treatment (or even cure) for that disease.
Thus, even if pollution causes asthma and the ultimate “cure” for asthma is to rid the air of pollutants, asthma, while it exists, is still a disease for the person who has it.
All that counts is whether or not the biological condition at hand is affecting your health or not.
The only reason I bring up biology at all, is to counter the argument that obesity is simply stupid people making poor “choices” – one you consider the biology, nothing about obesity is “simple”.
Continuing in my miniseries on objections I have heard against calling obesity a disease, I now address the argument that, doing so “medicalizes a behaviour”.
This argument is of course based on the underlying assumption that the root cause of obesity is a behaviour.
This is perhaps true at the most superficial level of understanding of obesity – yes, there are behaviours that can promote weight gain like eating too much, sedentariness and working shifts.
Note however, that nowhere in the WHO definition of obesity as a “disease that results from excess or abnormal body fat that impairs health”, is there any mention of behaviour whatsoever.
This is because for many people, the relationship between behaviour and weight gain is not at all as straightforward as many think.
Take for example physical activity – although over 95% of Canadians do not meet even the minimum criteria for daily physical activity (a behaviour), only 20% of Canadians have obesity (using the BMI 30 cutoff for the sake of argument).
So if behaviour (not moving enough) is touted as one of the root causes of obesity, why does not 95% of the population have obesity?
The simple answer is that for any given level of physical activity (or rather lack of it), some people gain weight while others don’t.
Similarly, if you believe that eating a lot of junk food (a behaviour) is the root cause of obesity, you will have to explain why not everyone who eats a lot of junk food has obesity and why a lot of people have obesity despite never touching the stuff.
No matter what behaviour you pick, it will never explain all (or even most) of obesity and there will always be plenty of people with those exact same behaviours, who manage to maintain a “normal” weight with no additional effort.
As I have previously outlined in blog posts and articles. “behaviours” leading to obesity, if anything, are no more than a symptom of underlying root causes of energy imbalance that can be related to a wide range of psychological, social and/or biological factors, with the precise cause varying widely from one person to the next.
Thus, equating “behaviour” with “obesity” only happens in the minds of people who fail to see obesity for what it actually is – a complex heterogenous often multifactorial disease characterized by excess or abnormal fat tissue that impairs health.
Thus, all that declaring obesity to be a disease is really doing is “medicalising” obesity (which is of course exactly what medicine needs to do) – it is not “medicalising” a behaviour because obesity is not a “behaviour”.
That is not to say that some pathological behaviours (e.g. binge eating disorder) may lead to weight gain. But most of obesity is attributable to “normal” behaviours in an “abnormal” environment.
And so once again, I would like to remind readers that obesity is not a behaviour (unlike smoking or smoking cessation – which is!) – see here for an explanation of the difference.
To anyone following the “biological” literature on obesity, it should be pretty evident by now that environmental factors can epigenetically modify genes in ways that allow “information” on environmental exposures in parents to be directly transmitted to their offspring.
Now a paper by Peter Huypens and colleagues from the Helmholtz Zentrum München, Germany, published in Nature Genetics, shows that both maternal and paternal exposure to weight gain induced by a high-fat diet in mice can substantially increase the risk for obesity in their offspring.
The key novelty in this study was the fact that the researchers isolated egg and sperm from both male and female mice that had been exposed to high-fat diets (or not) and used these germ cells in various combinations using in-vitro fertilization to create the offspring that were then implanted into surrogate female mice.
In all cases, risk for obesity as well as signs of insulin resistant tracked with both the male and female exposures, pretty much confirming that diets eaten by mothers and fathers can directly influence “genetic” risk for obesity in the next generation.
If transferable to humans (and there is little reason to doubt that this is the case), these findings suggest that a large proportion of the “heritability” of obesity is due to epigenetic modification that transfers risk from one generation to the next.
This means that efforts to prevent childhood obesity need to focus on the parents rather than the kids – kids born to mothers and fathers who have obesity are already born with a substantial higher risk than those born to lean mothers and fathers.
Perhaps our best chances of tackling obesity in the next generation of kids is to focus efforts on younger adults of child-bearing age.
One of the most pervasive problems with quitting cigarettes, is the accompanying weight gain – in fact, post-cessation weight gain is reportedly the number one reason why smokers, especially women, fail to stop smoking or relapse after stopping.
But what exactly happens when you stop smoking?
This is the topic of a comprehensive review article by Kindred Harris and colleagues published in Nature Reviews Endocrinology.
The paper begins by examining the magnitude of weight gain generally experienced after smoking cessation – an amount that can vary considerably between individuals.
As for mechanisms, the authors note that,
“Several theories have been proposed to explain increased food intake after smoking cessation. One theory is that the ability of nicotine to suppress appetite is reversed. Substitution reinforcement, which replaces the rewards of food with the rewards of cigarettes could occur. Nicotine absence increases the rewarding value of food. Reward circuitries in the brain, similar to those activated by smoking, are activated by increased intake of food high in sugar and fat. Furthermore, nicotine withdrawal leads to an elevated reward threshold, which might cause individuals to eat more snacks that are high in carbohydrates and sugars.”
There are also known effects of smoking on impulsive overeating and individuals with binge eating disorder are at risk of even greater weight gain with cessation.
Smoking cessation also has metabolic effects including a drop in metabolic rate that may promote weight gain and new evidence shows that smoking cessation can even change your gut microbiota.
The authors provide evidence that behavioural interventions can prevent much of the cessation weight gain and argue that such programs should be offered with cessation programs.
Finally, it is important to always remember that the health benefits of smoking cessation by far outweigh any health risks from weight gain, which is why fear of weight gain should never stop anyone from quitting.