Several years ago, my colleague Raj Padwal and I published a paper in Obesity Reviews, where we outline a rational approach to an aetiological assessment of obesity.
As many readers may not have seen this paper, I will repost several of the key elements we discussed in it. Although some of our thinking has evolved since then, I believe the overall reasoning remain as relevant today, as when we first wrote the paper back in 2010:
Obesity is characterized by the accumulation of excess body fat and can be conceptualized as the physical manifestation of chronic energy excess. Using the analogy of oedema, which is the consequence of positive fluid balance or fluid retention, obesity can be seen as the consequence of positive energy balance or caloric retention. Just as the positive fluid balance of oedema can result from a host of underlying aetiologies including cardiac, hepatic, renal, endocrine, infectious, venous, lymphatic or drug‐related causes, obesity can result from a wide range of aetiologies that promote positive energy balance.
As with oedema, assessment and management of obesity requires an exploration of the root causes and underlying pathologies. To extend the obesity–oedema analogy, addressing all forms of obesity simply with caloric restriction and exercise (‘eat less and move more’) would be akin to addressing all forms of oedema simply with fluid restriction and diuretics. As this narrowly focused approach is not considered standard‐of‐care in managing patients with oedema, why should it be considered as the preferred method of treating obesity?
The classical treatment of obesity, based on increased physical activity and decreased calorie intake, has not been successful. Approximately two‐thirds of the people who lose weight will regain it within 1 year, and almost all of them within 5 years. In our opinion, the lack of efficiency in these therapeutic approaches is likely due to an incomplete understanding of the precise aetiology or aetiologies of obesity and, consequently a failure to address the root causes of energy imbalance.
In this paper, we present a theoretical diagnostic paradigm that provides an aetiological framework for the systematic assessment of obesity and discuss how this framework can enhance our ability to diagnose and manage obesity in clinical practice. The framework considers socio‐cultural, physiological, biomedical, psychological and iatrogenic factors that can determine energy input, metabolism and expenditure.
Comment: In hindsight, I would note that apart from failure to address the underlying pathology and drivers of weight gain, the “failure’ of conventional “eat-less – move-more” approaches to obesity management, relying largely on willpower, primarily fail because these efforts are counteracted by powerful neuroendocrine factors that both defend against continuing weight loss and promote weight regain. At the time we wrote this paper, we had perhaps not given the powerful nature of these effects full consideration. Nevertheless, I still believe that trying to understand exactly why a given person has gained excess weight is a good start to any obesity management endeavour.
More to follow…
Anyone familiar with the issue, would readily agree that the actual surgery involved in bariatric surgery is only a small (but undeniably important) technical piece in what is a rather complex treatment for a rather complex chronic disease.
Clearly, this is not exactly how all bariatric surgeons approach or treat their bariatric patients.
Since 2012, the US has a Metabolic and Bariatric Surgery Accreditation and Quality Improvement Program that designates bariatric surgery centers as Centres of Excellence if they meet specified requirements in 7 core standards that include case volume, commitment to quality, appropriate use of equipment and instruments, critical care support, continuum of care, data collection, and continuous quality improvement.
However, as a recent paper by Andrew Ibrahim and colleagues, published in JAMA Surgery, elaborates, despite these quality criteria, there remains a substantial variability in outcomes across designated Bariatric Centres of Excellence.
Based on their retrospective analysis of claims data from 145 527 patients who underwent bariatric procedures, there was a 17-fold variation (ranging from 0.6% to 10.3%) in rates of serious 30-day complications across accredited bariatric centers nationally and up to 9.5-fold variation across individual states.
As the authors note,
“this finding suggests that participation alone in the Center of Excellence Program did not ensure uniform high-quality care….Given that most bariatric procedures are now performed at accredited centers, wide variation among these centers suggests that accreditation alone does not discriminate enough to guide patients to the best centers for care.”
Moreover, they found that poor performing centres were often located close to better performing centres (regression to the mean?). Interestingly, in contrast to what one may suspect, outcomes overall were not related to case volume (perhaps because in order to be a designated Centre of Excellence, all centres needed to have a minimum number of cases per year).
Rather, the authors discuss that poorer outcomes may be largely attributable to varying technical skills of the surgeons as well as inconsistent adherence to accepted bariatric care pathways.
Finally, the authors argue that there is need to make performance data available to the public, as simply trusting in the “Centre of Excellence” designation by no means guarantees excellent outcomes.
As important as these data may be, it is also important to note that this paper only looked at complications within a 30-day time period following surgery.
As anyone dealing with bariatric patients is well aware, successful outcomes of bariatric surgery(as well as its complications) should be measured in years (if not decades). This is where much of bariatric surgery falls down, as one of the key criteria mentioned above, i.e. “continuum of care” seldom extends beyond the rather brief period of post-surgical discharge. Indeed, in most cases, bariatric patients continue to be prematurely discharged into “the wild” with little ongoing support from health professionals competent in looking after the psychological and medical needs of this population.
None of this takes away from the fact that bariatric surgery is still the most effective long-term treatment for severe obesity – however, clearly there remains substantial room for improvement.
Liraglutide Effects on Upper Gastrointestinal Investigations: Implications Prior to Bariatric Surgery
With the considerable waits that patients in Canada often face prior to bariatric surgery, we generally recommend that patients, who have access to them, try anti-obesity medications while waiting. This not only prevents further wait gain, but also often helps them shed a significant amount of weight prior to surgery.
The GLP-1 analogue liraglutide is now approved for long-term obesity treatment and is generally well tolerated. Nevertheless, we now present a series of patients in Obesity Surgery, who were treated with liraglutide 3.0 mg whilst waiting for bariatric surgery, and showed significant upper GI dismotility that was reversible on discontinuation of liraglutide.
Although, investigations of upper GI motility are by no means part of routine assessment for bariatric surgery, tests may be ordered in patients who present with unclear upper GI symptoms, as the findings may guide the choice of surgical intervention.
In this paper, we present six cases in which patients treated with liraglutie 3.0 mg presented with varying degrees of esophageal and/or gastric dysmotility demonstrated using a variety of investigative procedures including formal gastric emptying scintiography as well as less specific esophageal manometry, and upper endoscopy.
In all cases normal motility was restored on discontinuation of liraglutide and all patients subsequently underwent or are continuing to wait for bariatric surgery.
Based on our observations we discuss that,
“Liraglutide is associated with decreased esophageal peristalsis and gastric emptying. These effects can result in abnormal upper GI investigations, leading to delays, increased testing, and questions of patient candidacy for surgery. If patients on liraglutide are noted to have abnormal esophageal manometry or gastric emptying studies, medication should be discontinued, with repeat studies done to look for reversibility. If this abnormal result is due to drug effect, this should not preclude patients from having bariatric surgery.”
Just how long liraglutide needs to be stopped prior to performing upper GI investigations remains unclear. Furthermore, as the dysmotility often appears to be symptomless and well-tolerated, we do not recommend routine ordering of motility tests in patients treated with liraglutide.
Disclaimer: I have served as a consultant and speaker for Novo Nordisk, the makers of liraglutide.
Obesity medicine, which I define as the medical care of someone living with obesity, should approach patients holistically with the aim of improving their overall health and well-being. Advice to lose weight may or may not be part of obesity management – much can be gained for someone living with obesity by promoting their health behaviours, getting them to feel better about themselves, improving their mental health, and helping them better managing their health issues. Much of this can be achieved with no or very little weight loss.
Thus, we must consider the question of when weight loss would specifically need to be part of the treatment objectives.
In my own practice, I approach this problem by considering the following three questions:
- Is this a problem unrelated to abnormal or excess body weight?
- Is this a problem aggravated by abnormal or excess body weight?
- Is this a problem caused by abnormal or excess body weight?
From what I hear from my patients, the most common mistakes in medical practice fall into the first group – trying to address unrelated issues with weight loss recommendations. There are endless stories of patients going to see their health provider with problems clearly unrelated to their body fat (e.g. a broken arm, a sore throat, the flu, depression, migraines, etc.), who simply get told to lose weight. Indeed, there is evidence to suggest that patients with obesity are less likely to undergo diagnostic testing, most likely based on the assumption that their problems are simply related to their excess weight. This is not only where grave medical errors can be made (late or misdiagnosis), but also where the advice to lose weight is clearly wrong. If the presenting problem has nothing to do with excess weight, then no amount of weight loss will fix it.
The second category deals with issues that are not causally related to abnormal or excess body fat but where the underlying problem either causes more symptoms or is more difficult to treat because of the patient’s size or fat distribution. There are countless medical problems that fall into this category. For e.g. a heart or respiratory problem entirely unrelated to excess weight (e.g. a valvular defect or asthma) can become worse, cause more symptoms, or be much more difficult to treat simply because of the patient’s size. This group also includes issues like neck or joint pain from a trauma (e.g. a motor vehicle or skiing accident), reflux disease (e.g. from a hiatal hernia), urinary incontinence (from multiple child births), etc., etc., etc. – the list is long. Here, although obesity has nothing to do with the underlying problem, weight loss may alleviate the symptoms or at least make them more manageable (they are however unlikely to be fully resolved). These patients present with what may be described as a relative or “secondary” indication for weight loss. Of course, if there are viable treatments options for the primary problem, then this is where the emphasis should be. Weight loss can best be considered as “second-line” treatment. It would be completely unethical to withhold effective treatment for the underlying problem just because of the patient’s size (as in, “no treatment for you until you lose X lbs!”)
Finally, we have the third category of health issues that are directly causally linked to the excess weight – in most cases, the problem did not exist prior to weight gain and losing weight is often likely to completely resolve the problem (unless the patient has already sustained irreversible organ damage). This group of health issues not only includes the vast majority of cases of type 2 diabetes, hypertension, obstructive sleep apnea, fatty liver disease, infertility, etc. but also all of the functional limitations that people may experience simply because of their excess body fat. This is the only category of patients who would be deemed to have a “primary” indication for weight loss. Losing the weight literally solves their problem. Indeed, trying to manage the problem without weight loss is nothing less than “palliative” care. This is not to say that weight loss will always guarantee success even if the underlying problem is directly related to excess weight. For e.g. although there is ample evidence that excess weight is a prime risk factor for gall bladder disease, (rapid) weight loss may actually promote formation of gall stones. Similarly, although intertrigo (skin fold infections) can occur as a direct consequence of excess weight (e.g. chaffing), losing weight may actually make the problem worse by deepening the skin folds. Thus, even in this category, one needs to carefully consider risk-benefit ratios.
Of course, any recommendation to lose weight must take into account the complex nature of obesity in the first place and the fact that long-term weight-loss maintenance will require an approach (behavioural, medical, or even surgical) that takes into account the chronic relapsing nature of this disorder. Simply telling people with obesity to “eat less and move more” is about as medically sound and effective, as simply telling people with depression to “cheer up”.
Both, to avoid grave medical errors and to not insult their patients, I strongly recommend that medical practitioners first approach all their patients with obesity based on the assumption (that their presenting health issues are unrelated to their excess weight) before considering possibilities two (unrelated but aggravated) and three (causal). Advise to lose weight has no role in situation 1, can be considered in situation 2, and is clearly the best course of action for situation 3.
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.