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”.
It must have been a pretty cheap rubber band, because every few months it would wear out and lose its stretch, so it had to be replaced it with a new band.
Unfortunately, this is not what can be said about the rubber band that I used in my recent TEDx talk to demonstrate what happens when you try to lose weight.
Unlike the cheap band in my pyjamas, the rubber band I used to represent our physiology trying to gain the weight back, never seems to lose its stretch.
No matter how hard or how long we pull, the rubber band keeps wanting to bring our weight back to where we started.
Yes, perhaps for some people, eventually the rubber band may relax (these would certainly be the exceptions) or may be the “muscles” that we use to pull on the band just grow stronger, which makes it seem easier to keep up the pull – but for all we know, in most people, this “rubber band” is of pretty good quality and seems to last forever.
So, how do we take the tension out of the rubber band ?
Well, we do know that people who have bariatric surgery have a much better chance of keeping the weight off in the long-term and we now understand that this has little to do with the “restriction” or the “malabsorbtion” resulting from these procedures but rather from the profound effect that this surgery has on the physiology of weight regain.
Thus, we know that many of the hormonal and neurological changes that happen with bariatric surgery, seem to inhibit the body’s ability to defend its weight and perhaps even appears to trick the body into thinking that its weight is higher than it actually is.
In other words, bariatric surgery helps maintain long-term weight loss by reducing the tension in the rubber band, thus making it far easier for patients to maintain the “pull”.
And that is exactly how we think some of the anti-obesity medications may be working.
For example, daily injections of liraglutide, a GLP-1 analogue approved for obesity treatment, appears to decrease the body’s ability to counteract weight loss by reducing hunger and increasing satiety, thus taking some of the tension out of that band.
Think of it as sprinkling “magic dust” on that rubber band to reduce the tension, which makes it easier for patients to maintain that pull thereby helping them keep the weight off.
Of course, both surgery and liraglutide only reduce the tension as long as you continue using them.
Undo the surgery or come off your anti-obesity meds and the tension in that band comes back as strong as ever.
For readers, who have no idea what I’m talking about, hopefully things will become clearer after you watch my talk by clicking here.
Nevertheless, epidemiologists (and folks in health promotion) appear to like the notion that there is such a weight (at least at the population level), and often define it as the weight (or rather BMI level) where people have the longest life-expectancy.
Readers of this literature may have noticed that the BMI level associated with the lowest mortality has been creeping up.
Case in point, a new study by Shoaib Afzal and colleagues from Denmark, published in JAMA, that looks at the relationship between BMI and mortality in three distinct populations based cohorts.
The cohorts are from the same general population enrolled at different times: the Copenhagen City Heart Study in 1976-1978 (n = 13 704) and 1991-1994 (n = 9482) and the Copenhagen General Population Study in 2003-2013 (n = 97 362). All participants were followed up to November 2014, emigration, or death, whichever came first.
The key finding of this study is that over the various studies, there was a 3.3 unit increase in BMI associated with the lowest mortality when comparing the 1976-1978 cohort with that recruited in 2003-2013.
Thus, The BMI value that was associated with the lowest all-cause mortality was 23.7 in the 1976-1978 cohort, 24.6 in the 1991-1994 cohort, and 27.0 in the 2003-2013 cohort.
Similarly, the corresponding BMI estimates for cardiovascular mortality were 23.2, 24.0, and 26.4, respectively, and for other mortality, 24.1, 26.8, and 27.8, respectively.
At a population level, these shifts are anything but spectacular!
After all, a 3.3 unit increase in BMI for someone who is 5’7″ (1.7 m) is just over 20 lbs (~10 Kg).
In plain language, this means that to have the same life expectancy today, of someone back in the late 70s, you’d actually have to be about 20 lbs heavier.
While I am sure that these data will be welcomed by those who would argue that the whole obesity epidemic thing is overrated, I think that the data are indeed interesting for another reason.
Namely, they should prompt speculation about why heavier people are living longer today than before.
There are two general possible explanations for this:
For one these changes may be the result of a general improvement in health status of Danes related to decreased smoking, increased physical activity or changes in social determinants of health (e.g. work hours).
On the other hand, as the authors argue, this secular trend may be that improved treatment for cardiovascular risk factors or complicating diseases, which has indeed reduced mortality in all weight classes, may have had even greater beneficial effects in people with a higher BMI. Thus, obese individuals may have had a higher selective decrease in mortality.
There is in fact no doubt that medical management of problems directly linked to obesity including diabetes, hypertension and dyslipidemia have dramatically improved over the past decades.
Thus, it appears that the notion of “healthy” weight is a shifting target and that changes in lifestyle and medical management may have more than compensated for an almost 20 lb weight increase in the population.
This is all the more reason that the current BMI cutoffs and weight-centric management of obesity both at a population and individual level may need to be revisited or at least tempered with measures of health that go beyond just numbers on the scale.
Now, a study by Constantin Gasser and colleagues from Melbourne, Australia, in a paper published in the American Journal of Clinical Nutrition, present a systematic review and meta-analysis of confectionary consumption and overweight in kids.
The researchers identified 19 studies fort their systematic review, 11 of which (∼177,260 participants) were included in the meta-analysis.
Overall, odds of excess weight of kids in the highest category of sweets consumption was about 20% less than in the reference category.
This inverse association was true for both chocolate and nonchocolate confectioneries.
Furthermore, in the longitudinal studies and the randomised controlled trial included in the review, no associations were observed between confectionery consumption and overweight, obesity, or obesity-related outcomes.
Thus, based on data from well over 175,000 kids, there appears to be no relationship between sweets consumption and excess weight – if anything, the relationship is the opposite of what one may expect.
As so often, when data don’t fit the “accepted” hypothesis, the authors are also quick to point out that these findings could well be explained by reverse causality (overweight kids avoiding sweets) or underreporting by heavier kids (a polite way of saying that heavier kids may be less honest about their candy consumption).
On the other hand, it may also well be that regular (non-restrictive) sweet consumption actually does in fact make kids less vulnerable to overeating, simply by ruining their appetite (just as grandma always warned you it would – as in, “No sweets before supper!”).
Overall, the findings remind me of a previous study that failed to find any association between sugary pop consumption and body weight in Ontario and PEI kids (if anything skinny kids in PEI drank more pop than those with excess weight).
Whatever the true answer may be, these findings certainly do not support the notion that sweet or chocolate consumption is a key factor in childhood obesity.