The first item on the disease definition modification checklist developed by the Guidelines International Network (G-I-N) Preventing Overdiagnosis Working Group published in JAMA Internal Medicine, pertains to the issue of how a proposed new definition would differ from the existing definition.
As authors are well aware, the current definition that is widely used to define obesity is based on BMI, a simple anthropometric measure calculated from body height and weight – a great measure of size, not such a great measure of health.
In contrast, the proposed definition of obesity, where obesity is defined as the presence of abnormal or excess fat that impairs health, would require the actual assessment and demonstration of the presence of health impairments attributable to a given subject’s body fat.
Thus, while anyone can currently “diagnose” obesity simply by entering height and weight into a BMI calculator and looking up the value on a BMI chart, the new definition would in fact require a full clinical assessment of an individual’s health. Such an assessment would need to look at both mental and physical health as well as overall well-being for issues that may be directly caused (or aggravated by) the presence of abnormal of excess body fat.
This does in fact bring up the issue of how exactly you would define “abnormal” or “excess” body fat and, even more importantly, how you would establish a relationship between body fat and any health impairments in a given individual.
While these issues would clearly need to be worked out, the face value of this approach should be evident in that it focusses on the issue of actual health impairments rather than an arbitrary BMI cut-off, above which everyone would be considered as having obesity.
This of course raises a number of issues around definition precision and accuracy, which is another item on the checklist and will be discussed in a future post.
However, there was also much agreement that the current criteria for diagnosing this disease, based on BMI criteria alone, has important limitations in that it may over-diagnose a significant number of individuals at no or very little imminent risk from their body fat and (even more importantly) under-diagnose a substantial number of individuals, who may well stand to benefit from anti-obesity treatments.
Thus, as my readers are well aware, I have long called for a redefinition of obesity based on the actual presence of health impairments attributable to abnormal or excess body fat.
It is thus timely that JAMA Internal Medicine has just published a seminal article by Jenny Doust and colleagues on behalf of the Guidelines International Network (G-I-N) Preventing Overdiagnosis Working Group, that provides a framework for anyone proposing changes to disease definitions.
Using a 5-step process that included (1) a literature review of issues, (2) a draft outline document, (3) a Delphi process of feedback on the list of issues, (4) a 1-day face-to-face meeting, and (5) further refinement, the group developed an 8-item checklist of items to consider when changing disease definitions.
The checklist specifically deals with the issues of definition changes, number of people affected, trigger, prognostic ability, disease definition precision and accuracy, potential benefits, potential harms, and the balance between potential harms and benefits.
The authors propose that,
“…the checklist be piloted and validated by groups developing new guidelines. We anticipate that the use of the checklist will be a first step to guidance and better documentation of definition changes prior to introducing modified disease definitions.”
No doubt it would be prudent to consider all of the identified aspects in the checklist, when considering changing the definition of obesity from one based simply on BMI to a more clinical definition, based on actual impairments in health.
In coming posts, I will consider each of the proposed checklist items and how they may apply to such a change in the definition of obesity.
Hat tip to Dr. Marcela Flores for drawing my attention to this paper
Following in the footsteps of other organisations like the American and Canadian Medical Associations, the Obesity Society, the Obesity Medical Association, and the Canadian Obesity Network, this month, the World Obesity Federation put out an official position statement on recognising obesity as a chronic relapsing progressive disease.
The position statement, published in Obesity Reviews, outlines the rationale for recognising obesity as a chronic disease and is very much in line with the thinking of the other organisations that have long supported this notion.
In an accompanying commentary, Tim Lobstein, the Director of Policy at the World Obesity Federation notes, that recognising obesity as a disease can have the following important benefits for people living with this disease:
1) A medical diagnosis can act to help people to cope with their weight concerns by reducing their internalized stigma or the belief that their problems are self-inflicted and shameful.
2) A classification of obesity as a disease, or disease process, may help to change both the public and professional discourse about blame for the condition, the latter hopefully encouraging greater empathy with patients and raising the patient’s expectations of unbiased care.
3) Recognition of obesity as a disease may have benefits in countries where health service costs are funded from insurance schemes that limit payments for non-disease conditions or risk factors.
While all of this is great, and I am truly delighted to see the World Obesity Federation come around to this statement, I do feel that the policy statement seems rather tightly locked into the notion that obesity (or at least most of it) is a disease “caused” primarily by eating too much, with the blame placed squarely on the “toxic obesogenic environment”.
Personally, I would rather see obesity as a far more etiologically heterogenous condition, where a wide range of mental, biological and societal factors (e.g. genetics, epigenetics, stress, trauma, lack of sleep, chronic pain, medications, to name a few) can promote weight gain in a given individual.
Although these factors may well operate through an overall increase in caloric consumption (or rather, a net increase in energy balance), they, and not the act of overeating per se must be seen as the underlying “root causes” of obesity.
Thus, I tend to see “overeating” (even if promoted by an obesogenic food environment) as a symptom of the underlying drivers rather than the “root cause”.
Thus, saying that obesity is primarily caused by “overeating” is perhaps similar to saying that depression is primarily caused by “unhappiness”. Readers would probably agree that such a statement regarding the etiology of depression would make little sense, as “unhappiness” is perhaps a symptom but hardly the “cause” of depression, which can be promoted by a wide range of biological, environmental and societal factors, all resulting in the underlying biology that results in the mood disorder.
Similarly, I would say that there are indeed a number of complex socio-psycho-biological factors that underly the biology that ultimately results in overeating and excess weight gain (the food environment clearly being one of these factors).
While this may seem like semantics, I do think that a more differentiated look at the underlying etiology of obesity at the individual level (rather than simply blaming it all on “overeating”), is essential for promoting a more sophisticated view of this complex chronic disease both at the level of the individual and the population.
Thus, for e.g. every plenary session was opened by a brief presentation from a representative of the Canadian Obesity Network’s Public Engagement Committee, which not only illustrated the remarkable diversity of individual “obesity stories” but also set the stage for the scientific and clinical presentations that followed.
Indeed, one of the recurring themes at the Canadian Obesity Summit was, “nothing about us, without us”.
Thus, I was happy to see that the “patient voice” is also gaining increasing attention at the European Congress on Obesity, currently taking place in Porto, Portugal.
In fact, the conference was kicked off by a workshop on weight bias, discrimination, and other issues relevant to people living with obesity, organised by representatives of the EASO patient council, with representatives from across Europe.
How much impact these presentations and role of people living with obesity will have on the overall conference will remain to be seen, but clearly, as in other areas of medicine, the patient voice is certainly become more important as a driver of knowledge and policy – as it should.
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.