Why do doctors weigh people? Because, very early in medical school, we are taught that body weight is an important indicator of health.
While one may certainly argue about the value of a single weight measurement at any point in time (especially in adults), there is simply no denying that weight trajectories (changes in body weight – up or down) can provide important (often vital) clinical information.
Let’s begin with the easiest (and least arguable) situations of all – unintentional weight loss.
Among all clinical parameters one could possibly measure, perhaps non should be as alarming as someone losing weight without actively trying. In almost every single instance of “unintentional” weight loss, the underlying problem needs to be found, and more often than not, the diagnosis is probably serious (cancer is just one possibility).
As with any serious condition, the earlier you detect it, the sooner you can do something about it, therefore, the more often you weight someone, the more likely you will detect early “non-intentional” weight loss.
The contrary situation (un-intentional weight gain) is as important. When someone is gaining weight for no good reason, one needs to look for the underlying cause, which can include everything from an endocrine problem to heart failure.
On the other hand, weight stability, is generally a sign that things are probably “under control”, as they should be when energy homeostasis works fine and people are in energy balance.
Perhaps my own obsession with weighing people comes from my work in nephrology, where we obsess about people’s “dry weight” and use weight as a general means to monitor fluid status. The same is true for working with patients who have heart failure.
Note for all of the above, that while a single (random) weight measurement tells you very little (almost nothing) about anybody’s health status, unexplained changes in body weight are one of the most useful and important clinical signs in all of medicine. Obviously, to plot a trajectory, one has to start somewhere, which means that every patient needs to have a “baseline” body weight recorded somewhere in their chart. While this value may not provide any valuable information, the next one may.
This is why every single patient needs to be weighed at least once in a clinical setting.
As you will imagine, both the context and interpretation of serial weight measurements becomes most challenging in the setting of obesity management.
For one, there is no greater challenge than to suspect underlying “un-intentional” weight loss in someone who is actively trying to lose weight. When “suddenly” a weight loss strategy that was providing modest results “starts working” – all alarm bells should go off. Also, if weight loss is much better than “predicted” it is time to take a serious second look at what’s happening. Furthermore, you need to watch out for patients who are doing far better than expected (even after bariatric surgery) – it takes a keen clinical mind to watch out for weight loss that appears “too good to be true” (even if the patient is delighted to see the pounds drop off).
Also, in the obesity management setting, weight stability is an important clinical indicator. In someone at their maximum weight, it tells me that the patient is not actively gaining weight, which by definition means that the patient is in caloric balance – remember, the first sign of “success” in obesity management is when the patient stops gaining weight.
In someone, who has already lost weight (in the context of obesity management), weight stability means that the patient’s efforts are continuing (here weight stability is a means to monitor “control”) – weight regain means that the patient may have to re-engage in weight control efforts or (more often) that something has come up in that person’s life that is “sabotaging” their efforts and may need to be identified and addressed (e.g. lost a job, change in medication, depression, etc.). Again, the earlier you identify a “relapse”, the earlier you can intervene.
Finally, in someone attending an obesity clinic, who continues gaining weight, you can be sure that the underlying cause of weight gain has not yet been fully identified or addressed. In other words, the disease is not “controlled” and continues to “progress”.
Thus, patients must be aware, that asking not to be weighed (usually out of shame or embarrassment) derives their clinician of important and possibly “vital” information about their health status.
Again, while a single weight (or BMI) says very little about a patient’s health, changes in body weight (up or down) is a vital sign that should prompt further clinical investigation and possibly intervention.
None of this has anything to do with the fact that people can very well be healthy over a wide range of body shapes and sizes.
It also does not mean that we should take a “weight-centric” approach to obesity management – all of the usual HAES arguments remain valid, even when you regularly ask your patient to step on the scale.
Recording a weight trajectory should be no more “judgemental” than recording a fever chart in a patient with an infection – everything lies in the context and interpretation of the data.
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.
This morning, I am presenting a plenary talk in Berlin to about 200 colleagues involved in childhood obesity prevention.
The 1-day symposium is hosted by Plattform Ernährung und Bewegung e.V. (Platform for Nutrition and Physical Activity), a German consortium of health professionals as well as public and private stakeholders in public health.
Although, as readers are well aware, I am by no means an expert on childhood obesity, I do believe that what we have learnt about the complex socio-psycho-biology of adult obesity in many ways has important relevance for the prevention and management of childhood obesity.
Not only do important biological factors (e.g. genetics and epigenetics) act on the infant, but, infants and young children are exposed to the very same societal, emotional, and biological factors that promote and sustain adult obesity.
Thus, children do not grow up in isolation from their parents (or the adult environment), nor do other biological rules apply to their physiology.
It should thus be obvious, that any approach focussing on children without impacting or changing the adult environment will have little impact on over all obesity.
This has now been well appreciated in the management of childhood obesity, where most programs now take a “whole-family” approach to addressing the determinants of excess weight gain. In fact, some programs go as far as to focus exclusively on helping parents manage their own weights in the expectation (and there is some data to support this) that this will be the most effective way to prevent obesity in their offspring.
As important as the focus on childhood obesity may be, I would be amiss in not reminding the audience that the overwhelming proportion of adults living with obesity, were normal weight (even skinny!) kids and did not begin gaining excess weight till much later in life. Thus, even if we were somehow (magically?) to completely prevent and abolish childhood obesity, it is not at all clear that this would have a significant impact on reducing the number of adults living with obesity, at least not in the foreseeable future.
Let us also remember that treating childhood obesity is by no means any easier than managing obesity in adults – indeed, one may argue that effectively treating obesity in kids may be even more difficult, given the the most effective tools to managing this chronic disease (e.g. medications, surgery) are not available to those of us involved in pediatric obesity management.
Thus, I certainly do not envy my pediatric colleagues in their struggles to provide meaningful obesity management to their young clients.
I am not sure how my somewhat sobering talk will be received by this public health audience, but then again, I don’t think I was expected to fully toe the line when it comes to exclusively focussing on nutrition and activity (as important as these factors may be) as an effective way to prevent or even manage childhood obesity.
Wow, what a week!
Just back from the 5th Canadian Obesity Summit, there is no doubt that this summit will live long in the minds (and hearts) of the over 500 attendees from across Canada and beyond.
As anyone would have appreciated, the future of obesity research, prevention and practice is alive and kicking in Canada. The over 50 plenary review lectures as well as the over 200 original presentations spanning basic cellular and animal research to health policy and obesity management displayed the gamut and extent of cutting-edge obesity research in Canada.
But, the conference also saw the release of the 2017 Report Card on Access to Obesity Treatment for Adults, which paints a dire picture of treatment access for the over 6,000,000 Canadians living with this chronic disease. The Report Card highlights the virtually non-existant access to multidisciplinary obesity care, medically supervised diets, or prescription drugs for the vast majority of Canadians.
Moreover, the Report Card reveals the shocking inequalities in access to bariatric surgery between provinces. Merely crossing the border from Alberta to Saskatchewan and your chances of bariatric surgery drops from 1 in 300 to 1 in 800 per year (for eligible patients). Sadly, numbers in both provinces are a far cry from access in Quebec (1 in 90), the only province to not get an F in the access to bariatric surgery category.
The presence of patient champions representing the Canadian Obesity Network’s Public Engagement Committee, who bravely told their stories to a spell-bound audience (often moved to tears) at the beginning of each plenary session provided a wake up call to all involved that we are talking about the real lives of real people, who are as deserving of respectful and effective medical care for their chronic disease as Canadians living with any other chronic disease.
Indeed, the clear and virtually unanimous acceptance of obesity as a chronic medical disease at the Summit likely bodes well for Canadians, who can now perhaps hope for better access to obesity care in the foreseeable future.
Thanks again to the Canadian Obesity Network for hosting such a spectacular event (in spectacular settings).
More on some of the topics discussed at the Summit in coming posts.
For an overview of the Summit Program click here
The biguanide metformin is widely used for the treatment of type 2 diabetes. Metformin has also been shown to slow the progression from pre to full-blown type 2 diabetes. Moreover, metformin can reduce weight gain associated with psychotropic medications and polycystic ovary syndrome.
Now, a randomised controlled trial by M P van der Aa and colleagues from the Netherlands, published in Nutrition & Diabetes suggests that long-term treatment with metformin may stabilize body weight and improve body composition in adolescents with obesity and insulin resistance.
The randomised placebo-controlled double-blinded trial included 62 adolescents with obesity aged 10–16 years old with insulin resistance, who received 2000 mg of metformin or placebo daily and physical training twice weekly over 18 months.
Of the 42 participants (mean age 13, mean BMI 30), BMI was stabilised in the metformin group (+0.2 BMI unit), whereas the control group continued to gain weight (+1.2 BMI units).
While there was no significant difference in HOMA-IR, mean fat percentage reduced by 3% compared to no change in the control group.
Thus, the researcher conclude that long-term treatment with metformin in adolescents with obesity and insulin resistance can result in stabilization of BMI and improved body composition compared with placebo.
Given the rather limited effective options for addressing childhood obesity, this rather safe, simple, and inexpensive treatment may at least provide some relief for adolescents struggling with excess weight gain.