If there is one article in the 2018 special issue of JAMA on obesity that we could have well done without, it is surely the one by Eve Guth promoting the age-old notion that simply counting calories is a viable and effective means to manage body weight.
As the author suggests:
“It is better for physicians to advise patients to assess and then modify their current eating habits and then reduce their caloric ingestion by counting calories. Counseling patients to do this involves provision of simple handouts detailing the calorie content of common foods, suggested meal plan options, an explanation of a nutrition label, and a list of websites with more detailed information. Patients should be advised that eating about 3500 calories a week in excess of the amount of calories expended results in gaining 1 lb (0.45 kg) of body weight. If a patient reduces caloric ingestion by 500 calories per day for 7 days, she or he would lose about 1 lb of body weight per week, depending on a number of other factors. This is a reasonable and realistic place to start because this approach is easily understood and does not ask a patient to radically change behavior.”
There is so much wrong with this approach, that it is hard to know exactly where to start.
For one, this advise is based on the simplistic assumption that obesity is simply a matter of managing calories to achieve and sustain long-term weight loss.
Not only, do we have ample evidence that these type of approaches rarely result in long-term sustained weight-loss but, more importantly this type of advice comfortably ignores the vast body of scientific literature that tells us that body weight is a tightly regulated physiological variable and that there are a host of complex neuroendocrine responses that will defend our bodies against long-term weight loss – mechanisms that most people (irrespective of whether they have obesity or not) will find it exceedingly hard to overcome with “will-power” alone.
No doubt, caloric “awareness” can be an eye-opener for many patients and there is good evidence that keeping a food journal can positively influence dietary patterns and even reduce “emotional” eating. But the idea that cognitively harnessing “will-power” to count calories (a very “unnatural” behaviour indeed), thereby creating and sustaining a long-term state of caloric deficit is rather optimistic at best.
In fact, legions of people who have been battling obesity all their lives can attest to the fact that encouragement to simply “eat less and move more” (ELMM) as a viable strategy to achieve and sustain significant weight loss is about as effective as reminding people with depression to focus on the brighter side of things and cheer up.
Not to mention the debunked 3500 calorie deficit a week = 1 lb weight loss (week after week after week till a so called “healthy” weight is achieved) myth, which is simply not how bodies work.
Continuing to propagate this antiquated and simplistic idea of what it takes to manage a complex chronic disease like obesity, is exactly what is holding the field back.
There is no reason to assume why more of the same should produce results that are any different from those in the past.
It is time we recognise that restricting caloric intake by willpower alone (irrespective of the dietary strategy) simply does not change the biology of the underlying physiology that effectively defends our bodies against long-term weight loss.
Reading an article like this in 2018 in a reputable journal that promises to “reimagine” obesity is both disappointing and a stark reminder of just how far we have to go to change widely held beliefs that obesity is simply a matter of calories in and calories out – if only life (and human biology) was that simple!
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).”
The assessment of weight history is no doubt a key feature of obesity assessment. Not only can weight history and trajectories provide important insights into obesity related risk but, perhaps more importantly, provide key information on precipitating factors and drivers of excessive weight gain.
Now, in a short article published in MedEdPublish, Robert Kushner discusses how the well-known OPQRST mnemonic for assessing a “chief complaint” can be applied to assess body weight.
In short, OPQRST is a mnemonic for Onset, Precipitating, Quality of Life, Remedy, Setting, and Temporal pattern. Applied to obesity, Kushner provides the following sample questions for each item:
Onset: “When did you first begin to gain weight?” “What did you weight in high school, college, early 20s, 30s, 40s?” “What was your heaviest weight?”
Precipitating: “What life events led to your weight gain, e.g., college, long commute, marriage, divorce, financial loss?” “How much weight did you gain with pregnancy?” “How much weight did you gain when you stopped smoking?” “How much weight did you gain when you started insulin?”
Quality of life: “At what weight did you feel your best?” “What is hard to do at your current weight?”
Remedy: “What have you done or tried in the past to control your weight?” “What is the most successful approach you tried to lose weight?” “What do you attribute the weight loss to?” “What caused you to gain your weight back?”
Setting: “What was going on in your life when you last felt in control of your weight?” “What was going on when you gained your weight?” “What role has stress played in your weight gain?” “How important is social support or having a buddy to help you?”
Temporal pattern: “What is the pattern of your weight gain?” “Did you gradually gain your weight over time, or is it more cyclic (yo-yo)?” “Are there large swings in your weight, and if so, what is the weight change?”
As Kushner notes,
“These features provide a contextual understanding of how and when patients gained weight, what efforts were employed to take control, and the impact of body weight on their health. Furthermore, by using a narrative or autobiographical approach to obtaining the weight history, patients are able to express, in their own words, a life course perspective of the underlying burden, frustration, struggle, stigma or shame associated with trying to manage body weight. Listening should be unconditional and nonjudgmental. By letting patients tell their story, the clinician is also able to assess the patients’ awareness, knowledge, motivation, decision-making, and resiliency regarding weight management. The narrative provides a basis for approaching the patients’ weight holistically, as well as beginning to formulate diagnostic and therapeutic options.”
There is no doubt much to be gained in understanding obesity by allowing patients to tell their own weight stories.
In my talks, I have often joked about how to best keep weight off – just carry around a backpack that contains the lost pounds to fool the body into thinking the weight is still there.
It turns out that what was intended as a joke, may in fact not be all too far from how the body actually regulates body weight.
As readers of these posts are well aware, body weight is tightly controlled by a complex neuroendocrine feedback system that effectively defends the body against weight loss (and somewhat, albeit less efficiently, protects against excessive weight gain).
Countless animal experiments (and human observations) show that following weight loss, more often than not, body weight is regained, generally precisely to the level of initial weight.
With the discovery of leptin in the early 90s, an important afferent part of this feedback system became clear. Loss of fat mass leads to a substantial decrease in leptin levels, which in turn results in increased appetite and decreased metabolic rate, both favouring weight regain and thus, restoration of body weight to initial levels.
Now, an international team of researchers led by John-Olov Jansson from the University of Gothenburg, Sweden, in a paper published in the Proceeding of the National Academy of Science (PNAS), provides compelling evidence for the existence of another afferent signal involved in body weight regulation – one derived from weight-bearing bones.
Prompted by observations that prolonged sedentariness can promote weight gain, independent of physical activity, the researchers hypothesised that,
“…there is a homeostat in the lower extremities regulating body weight with an impact on fat mass. Such a homeostat would (together with leptin) ensure sufficient whole body energy depots but still protect land-living animals from becoming too heavy. A prerequisite for such homeostatic regulation of body weight is that the integration center, which may be in the brain, receives afferent information from a body weight sensor. Thereafter, the integration center may adjust the body weight by acting on an effector.”
In a first series of experiments, the researchers observed that implanting a weight corresponding to about 15% of body weight into rodents (rats and mice), resulted in a rapid “spontaneous” adjustment in body weight so that the combined weight of the animal plus the weight implant corresponded more-or-less to that of control animals.
Within two weeks of implanting the weights, ∼80% of the increased loading was counteracted by reduced biological weight, largely due to reduced white adipose tissue (WAT), accompanied by a corresponding decrease in serum leptin levels. (Interestingly, this weight loss was also accompanied by a substantial improvement in insulin resistance and glucose homeostasis).
The decrease in “biological” body weight was mainly attributable to a reduction in caloric intake with no changes in fat oxidation, energy expenditure or physical activity.
Removal of the implanted weights resulted in rapid weight regain to initial levels, showing that the “weight sensor” was active in both directions.
Experiments showed that this “weight sensing” mechanism was largely independent of the leptin pathway and did not appear to involve grehlin, GLP-1, a-MSH, estrogen receptor-a, or the sympathetic nervous system.
Now for the interesting part: the observed effect of weight loading was not seen in mice depleted specifically of DMP1 osteocytes, demonstrating that the suppression of body weight by loading is dependent on osteocytes.
As the authors note, these findings are consistent with a growing body of data indicating that the skeleton is an endocrine organ that regulates energy and glucose metabolism. Indeed, it is well known that osteocytes can sense dynamic short term high-impact bone loading for local bone adaptation – now it appears, that osteocytes may also play a vital role in sensing overall body weight and signalling this to the brain centres that regulate energy balance and body weight.
Thus, in summary, not only have the authors provided compelling evidence for a “weight-sensing” role for bone osteocytes (presumably through their presence in the long weight-bearing bones of our lower extremities) but also provide a plausible biological explanation for the weight gain and change in fat mass seen with prolonged sedentariness (which literally takes the weight off the bone).
These findings may also finally explain why rats held at increased gravity for extended periods of time (simulated G2) become lean even when their energy intake matches their expenditure.
Perhaps, carrying around a heavy backpack may indeed help with long-term weight loss maintenance after all – who knew?
Hat tip to Jean-Philippe Chaput for alerting me to this article
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.