In addition to the series of article on long-term outcomes in bariatric surgery, the 2018 special issue of JAMA on obesity, also features several articles discussing the potential role of taxing or otherwise regulating the use of sugar-sweetened beverages (SSB) as a policy measure to address obesity.
In a first article, Jennifer Pomeranz and colleagues discuss whether or not governments can in fact require health warnings on advertisements for sugar-sweetend beverages. The discussion focuses on an injunction issued by the Ninth Circuit Court on the enforcement of San Francisco’s requirement that sugar-sweetened beverage (SSB) advertisements display a health warning statement, finding that this law likely violated the First Amendment rights of advertisers of SSBs.
The background for this court decision was the fact that San Francisco passed a law requiring SSB advertisers to display: “WARNING: Drinking beverages with added sugar(s) contributes to obesity, diabetes, and tooth decay. This is a message from the City and County of San Francisco.”
In its decision, the court felt that the proposed warning label was not scientifically accurate, as it focussed exclusively on “added sugar(s)” rather than sugars overall. It appears that there is no scientific evidence suggesting that “added sugars” are any more (or less) harmful than the “natural” sugar occurring in any other foods or beverages).
However, as the authors argue, warning on SSB may well be warranted as
“In addition to being a major source of added sugar in the US diet, the liquid form of SSBs could enable rapid consumption and digestion without the same satiety cues as solid foods. SSBs also contain no relevant ingredients to provide offsetting health benefits, in comparison with sweetened whole grain cereals, nut bars, yogurt, or other foods with added sugars, which can have healthful components. Furthermore, the associations of SSBs with weight gain, obesity, type 2 diabetes, and heart disease are each stronger and more consistent than for added sugars in solid foods. In addition, compared with other foods containing added sugars, SSBs are the only source for which randomized controlled trials have confirmed the observational link to weight gain.”
Another point of contention identified by the court was related to the fact that the warning stated harm irrespective of quantity and would have been more accurate had it included the term “overconsumption” or at leas the qualifier “may”.
Here, the authors argue that,
“health risks of SSBs increase monotonically. Thus, use of the word “overconsumption” would not be scientifically accurate because there is no clear threshold effect between SSB consumption and harm. Yet, due to potential individual variation in responses, incorporating the word “may” or “can” would be scientifically accurate and are used in alcohol and smokeless tobacco warnings.”
The third objection by the court was related to the proposed size and rectangular border requirements of the warning, which was considered to be “unduly burdensome” – a point that the authors concede could be dealt with by modify formatting requirements by slightly reducing size, permitting “hairline” borders, or using other methods to ensure prominence and conspicuousness.
.In a second article on the issue of SSBs, Lisa Powell and Matthew Maciejewski discuss the case for taxing SSBs, noting they are the largest contributor of added sugar in the US diet, accounting for approximately 6.5% of total daily calories among adults and 7.3% among youth (ages 2-19 years) and approached 8% to 9% of daily calories among minority populations and 9% to 10% among low-income households. In addition consumption of SSBs have been associated with obesity as well as type 2 diabetes, cardiovascular disease, dental caries, and osteoporosis.
As the authors point out, for SSB taxes to be effective, the increased cost of SSBs has to be passed on to the consumer (“pass-through) and the consumer has to respond by decreasing their consumption (“price elasticity”). In places where SSB taxes have been implemented (e.g. Mexico), both effects have been seen, suggesting that an SSB tax can indeed change consumer behaviours.
However, as the authors also note, so far there is little evidence directly demonstrating that such changes have translated into actual health outcomes (for obesity or otherwise).
Nevertheless, the authors feel that an SSB tax can effectively decrease the overall consumption of these beverages and should perhaps be extended even further to include all forms of sugary drinks including 100% fruit juice. For this approach to be broadly acceptable, it would also be important to dedicate any revenue from these taxes to specific educational or public health purposes.
Finally, a third article on this issue by John Cawley deals with an interesting “quasi experimental” pass-through effect of SSB taxes at the Philadelphia International Airport, which happens to straddle the city border, with some terminals in Philadelphia that are subject to the beverage tax (1.5 cents per ounce), and other terminals in Tinicum that are not.
The study included 31 stores: 21 on the taxed side of the airport (Philadelphia) and 10 on the untaxed side (Tinicum).
As the authors found, following the implementation of the SSB tax in Philadelphia, the average price of SSBs increased on both the taxed and untaxed side of the airport (albeit more so on the taxed side). Using only data for taxed stores, the percentage of the tax passed on to consumers was 93%. Overall, however, the price difference between the taxed and untaxed stores was about 0.83 cents per ounce (a 55% relative pass-through rate).
Thus, while the tax did have a significant effect on SSB pricing in Philadelphia, it appears that the non-taxed stores simply went along to increase their profit margins accordingly.
Whether or not these changes in pricing had any impact on actual SSB sales or consumption was not reported.
Together, these studies certainly support the statement by Powell and Maciejewski that
“SSB taxes are likely to remain controversial for some time and policy makers will have a number of issues to consider as they formulate and implement fiscal policies.”
“SSB taxation can only be one approach to what must be a multipronged public health strategy to reduce obesity via improved diets and increased activity. The fact that intake of SSBs has declined over the past decade and the obesity epidemic has continued unabated suggests that reducing SSBs alone is not the sole solution. Adults and youth who frequently consume SSBs are more likely to engage in other unhealthy behaviors (eg, inactivity, greater fast-food consumption), so population-based policies specifically targeting these behaviors need to be designed in concert with SSB taxes. Although SSB consumption remains high in the United States, particularly among vulnerable populations, and taxation is a viable tool for curbing its consumption, the long-run intended and unintended effects of SSB tax policy are yet to be determined. The debate on its merits as an effective tool to improve health outcomes will be greatly informed by rigorous evidence on consumption, sugar intake, and body weight both on average and within vulnerable populations (children, minorities, low-income individuals).”
If there is one thing we know for sure about obesity management, it is the sad fact, that no diet, exercise, medication, not even bariatric surgery, will permanently reset the body’s tendency to defend and regain its body weight to its set point – this generally being the highest weight that has been achieved and maintained for a notable length of time.
Thus, any effective long-term treatment has to offset the complex neurobiology that will eventually doom every weight-loss attempt to “failure” (no, anecdotes don’t count!).
Just how complex and overpowering this biological system that regulates body weight is, is described in a comprehensive review by the undisputed leaders in this field (Michael Schwartz, Randy Seeley, Eric Ravussin, Rudolph Leibel and colleagues) published in Endocrine Reviews. Indeed the paper is nothing less than a “Scientific Statement” from the venerable Endocrine Society, or, in other words, these folks know what they’re talking about when it comes to the science of energy balance.
As the authors remind us,
“In its third year of existence, the Endocrine Society elected Sir Harvey Cushing as President. In his presidential address, he advocated strongly in favor of adopting the scientific method and abandoning empiricism to better inform the diagnosis and treatment of endocrine disease. In doing so, Cushing helped to usher in the modern era of endocrinology and with it, the end of organo-therapy. (In an interesting historical footnote, Cushing’s Energy Homeostasis and the Physiological Control of Body-Fat Stores presidential address was given in , the same year that insulin was discovered.)”
Over 30 pages, backed by almost 350 scientific citations, the authors outline in excruciating detail just how complex the biological system that regulates, defends, and restores body weight actually is. Moreover, this system is not static but rather, is strongly influenced and modulated by environmental and societal factors.
Indeed, after reading this article, it seems that the very notion, that average Jane or Joe could somehow learn to permanently overcome this intricately fine-tuned system (or the societal drivers) with will power alone is almost laughable (hats off to the very few brave and determined individuals, who can actually do this – you have climbed to the top of Mount Everest and decided to camp out there for the foreseeable future – I wish you all the best!).
Thus, the authors are confident that,
“The identification of neuromolecular mechanisms that integrate short-term and long-term control of feeding behavior, such that calorie intake precisely matches energy expenditure over long time intervals, will almost certainly enable better preventive and therapeutic approaches to obesity.”
Sadly, despite all we have learnt about this system, we are still far from fully understanding it. Thus, the canonical molecular/ cellular signaling pathway: LEP → LEPR → POMC, AgRP → PC → MC4R is just one pathway in a complex network of multiple interacting and sometimes redundant pathways that involve virtually every part of the brain.
Also, the effect of environmental factors appears to be far more complex than most people think. Thus,
“During sensitive periods of development, ontogenic processes in both brain and peripheral organs can be modified so as to match anticipated environmental conditions. Although many exposures during development could potentially predispose to obesity in adulthood, we focus here on two that some researchers think contribute to the secular trends in obesity: parental obesity and exposure to endocrine disrupting chemicals (EDCs).”
Throw in the role of gut bugs, infections, and societal factors, and it is easy to see why no simple solution to the obesity epidemic are in sight (let alone a range of effective long-term treatments like we have for most other common chronic diseases).
As for solutions,
“To be viable, theories of obesity pathogenesis must account not only for how excess body fat is acquired, but also for how excess body fat comes to be biologically defended. To date, the preponderance of research has focused on the former. However, we must consider the possibility that some (perhaps even most) mechanisms underlying weight gain are distinct from those responsible for the biological defense of excess fat mass. A key question, therefore, is how the energy homeostasis system comes to defend an elevated level of fat mass (analogous to the defense of elevated blood pressure in patients with hypertension). Answering this question requires an improved understanding of the neuro-molecular elements that underlie a “defended” level of body fat. What are the molecular/neuroanatomic predicates that help establish and defend a “set point” for adiposity? How do these elements regulate feeding behavior and/or energy expenditure, so as to achieve long-term energy balance? By what mechanisms is an apparently higher set point established and defended in individuals who are obese?” [sic]
“Given that recovery of lost weight (the normal, physiological response to weight loss irrespective of one’s starting weight) is the largest single obstacle to effective long-term weight loss, we cannot overstate the importance of a coherent understanding of obesity-associated alterations of the energy homeostasis system.”
There is much work to be done. Whether or not, in this climate of anti- and pseudo-science, funding for such fundamental work will actually be made available, is anyone’s guess.
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.