In the same manner in that there is not one predisposing factor for the development of obesity, the phenotypic clinical presentation of obesity is likewise extraordinarily heterogenous. (This has some authors speaking of “obesities” rather than “obesity”).
While it is now well established that BMI is a measure of size rather than health, it is perhaps less well recognised how the different types of body fat and their storage in various fat depots and organs can contribute to cardiometabolic disease (location, location, location!).
Now, a comprehensive review by Ian Neeland from the University of Texas Southwestern Medical Center, Dallas, together with my colleagues Paul Poirier and JP Despres from Laval University in Quebec, published in Circulation discusses the cardiovascular and metabolic heterogeneity of obesity.
As the authors point out,
“Although the BMI has been a convenient and simple index to monitor the growth in obesity prevalence at the population level, many metabolic and clinical studies have revealed that obesity, when defined on the basis of the BMI alone, is a remarkably heterogeneous condition. For instance, patients with similar body weight or BMI values have been shown to display markedly different comorbidities and levels of health risk.”
Not only has BMI never emerged as a significant component in risk engines such as the Framingham risk score, there are many individuals with obesity who never develop metabolic complications or heart disease during the course of their life.
The paper offers a good review of what the author describe as adipose dysfunction or “adiposopathy” = “sick fat”. Thus, in some individuals, there is an accumulation of “unhealthy” fat (particularly visceral and ectopic fat), whereas in others, excess fat predominantly consists of “healthy” fat (predominantly in subcutaneous depots such as the hips and thighs).
The authors thus emphasise the importance of measuring fat location with methods ranging from simple anthropometric measures (e.g. waist circumference) to comprehensive imaging techniques (e.g. MRI).
The authors also provide a succinct overview of exactly how this “sick fat” contributes to cardiometabolic risk and briefly touches on the behavioural, medical, and surgical management of patients with obesity and elevated cardiometabolic risk.
I, for one, was also happy to see the inclusion of the Edmonton Obesity Staging System in their reflections on this complex issue.
This paper is certainly suggested reading for anyone interested in the link between obesity and cardiovascular disease.
The 2018 JAMA special issue on obesity also includes a brief paper by Ann Blair Kennedy and colleagues reviewing the debate (which really isn’t much of a debate to anyone who knows the data) on whether it is more important to be fit than to worry about being fat (it is).
As the authors review, there is now ample data showing that cardio-respiratory fitness (CRF) is far more important for the prediction of cardiovascular mortality than the level of fatness (measured as BMI or otherwise).
In fact, once you account for differences in “fitness”, actual BMI levels almost cease to matter in terms of predicting longevity.
Unfortunately, as the authors point out, most studies linking obesity to cardiovascular outcomes (including studies on the so-called obesity “paradox”), fail to properly measure or account for cardiovascular fitness, thereby ignoring the most important confounder of this relationship.
For clinicians (and anyone concerned about their excess weight), it is helpful to remember that while achieving and maintaining a significant weight loss is a difficult (and often futile) undertaking, achieving and maintaining a reasonable degree of cardiorespiratory fitness is possible at virtually any shape or size.
Thus, as the authors point out,
“…in current US society, many people progressively gain weight and lose CRF as they age. Conceivably, maintaining CRF may be more important than preventing the development of obesity. However, for people who are overweight or have mild to moderate obesity, there are effective ways to improve CRF, including exercise and lifestyle interventions and there is general agreement that having low levels of PA is unhealthy. Increasing PA to help keep individuals from becoming unfit can be achieved if patients meet current PA guidelines of 150 minutes of moderate or 75 minutes of vigorous PA per week.”
Clearly, if your primary concern related to your patients’ excess body fat is about their cardiovascular health, you would probably be doing them a far greater service by getting them to improve their cardiorespiratory fitness rather than simply lose a few pounds (and no, exercise is not the best way to lose weight!).
On the other hand, if there are other health issues that are of primary concern (e.g. sleep apnea, osteoarthritis, fatty liver disease, etc.) or the degree of excess fat significantly affects mobility or other aspects of quality of life, then perhaps a frank discussion about available and effective “weight-loss” treatments appears warranted.
Let us not forget that it is never a good idea to simply treat numbers on the scale.
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.
Thus, following weight loss, not only does the body need fewer calories, doing the same amount of physical work uses fewer calories than before (the joke is that, if you ran 5K a day to lose weight, you have to run 10K a day to keep it off).
Now, a study by Maria Fernström and colleagues, published in Obesity Surgery, shows increased mitochondrial efficiency following bariatric surgery.
The researchers performed skeletal muscle biopsies in 11 women before and at 6 months after gastric bypass surgery.
Measurements in isolated mitochondria showed a marked increase in coupled respiration (state 3) and overall mitochondrial capacity (P/O ratio) with a non-significant increase in uncoupled (state 4) respiration.
Thus, at 6 months following gastric bypass surgery, both the mitochondrial capacity for coupled, i.e., ATP-generating, respiration increased as well as the P/O ratio improved.
As the authors note, not only would this increased “fuel efficiency” in part explain the decreased basal metabolism often associated with weight loss but also the propensity for weight regain that often follows weight-loss interventions.
Obviously, due to lack of a control group, this study does not demonstrate that these changes are in any way specific to weight-loss following bariatric surgery.
Also, given that the nadir of weight loss is generally not achieved until about 18 months following surgery, the changes observed in this study may not represent the maximum increase in mitochondrial efficiency to be achieved with further weight loss.
Continuing in my miniseries on why obesity (defined here, as excess or abnormal body fat that affects your health) should be considered a disease, is the simple observation that obesity responds less to lifestyle treatments than most people think.
Yes, the internet abounds with before and after pictures of people who have “conquered” obesity with diet, exercise, or both, but in reality, long-term success in “lifestyle” management of obesity is rare and far between.
Indeed, if the findings from the National Weight Control Registry have taught us anything, it is just how difficult and how much work it takes to lose weight and keep it off.
Even in the context of clinical trials conducted in highly motivated volunteers receiving more support than you would ever be able to reasonably provide in clinical practice, average weight loss at 12 – 24 months is often a modest 3-5%.
Thus, for the vast majority of people living with obesity, “lifestyle” treatment is simply not effective enough – at least not as a sustainable long-term strategy in real life.
While this may seem disappointing to many (especially, to those in the field, who have dedicated their lives to promoting “healthy” lifestyles as the solution to obesity), in reality, this is not very different from the real-life success of “lifestyle” interventions for other “lifestyle” diseases.
Thus, while there is no doubt that diet and exercise are important cornerstones for the management of diabetes or hypertension, most practitioners (and patients) will agree, that very few people with these conditions can be managed by lifestyle interventions alone.
Indeed, I would put to you that without medications, only a tiny proportion of people living with diabetes, hypertension, or dyslipidemia would be able to “control” these conditions simply by changing their lifestyles.
Not because diet and exercise are not effective for these conditions, but because diet and exercise are simply not enough.
The same is true for obesity. It is not that diet and exercise are useless – they absolutely remain a cornerstone of treatment. But, by themselves, they are simply not effective enough to control obesity in the vast majority of people who have it.
This is because, diet and exercise do not alter the biology that drives and sustains obesity. If anything, diet and exercise work against the body’s biology, which is working hard to defend body weight at all costs.
Thus, it is time we accept this reality and recognise that without pharmacological and/or surgical treatments that interfere with this innate biology, we will not be able to control obesity in the majority of patients.
Whether we like it or not, I predict that within a decade, clinical management of obesity will look no different than current management of any other chronic disease. Most patients will require both “lifestyle” and probably a combination of anti-obesity medications to control their obesity.
This does not take away from the importance of diet and exercise – as important as they are, they are simply not enough.
Despite what “lifestyle” enthusiasts will have us believe, diet and exercise are no more important (or effective) for the treatment of obesity, than they are for the treatment of hypertension, diabetes, dyslipidemia, depression, or any other condition that responds to “lifestyle” interventions.
In the end, most patients will require more effective treatments to manage their obesity and all of the comorbidities that come with it. The sooner we develop and make accessible such treatments, the sooner we can really help our patients.