Today’s guest post comes from Christy Turer, MD, Assistant Professor of Pediatrics, Internal Medicine, and Clinical Sciences at University of Texas Southwestern (UTSW) Medical Center, Dallas, Texas, USA.
This week, I saw a 50 year-old female patient with obesity (BMI 44) who desperately needs screening and treatment for obstructive sleep apnea (OSA).
Over the past four years, her heart function (ejection fraction) has declined from >60% to now ~20% with significant pulmonary hypertension, almost certainly related to undiagnosed, untreated OSA based on multiple nightly witnessed apneas.
Although she now sleeps with oxygen, this does nothing for her hypopnea-related, sympathetic overdrive-mediated, cardiac dysfunction.
Without CPAP treatment, her life expectancy is two years or less.
Unfortunately, within the public health system for which I work (county system that offers free or discounted healthcare to poor residents in a metropolitan city, USA), the average wait time for a sleep study is 1-2 years.
To be fair, this patient has had a previous attempt at a sleep study in a sleep lab a couple of years ago. At that time, however, the study was inconclusive, because she could not fall asleep in the sleep lab’s unfamiliar environment.
It is frustrating not being able to help my patients with suspected sleep apnea, especially, when I know that help could be available.
It is high time we had a technological disruption that enables cheap, reliable, in-home OSA assessment for patients.
Christy Turer, MD
Dr Turer is a standing member of the US Food and Drug Administration’s Pediatric Advisory Committee, a consultant to the FDA’s Endocrinologic/Metabolic Drugs Advisory Committee, and Past-Chair of the Obesity Society’s Clinical Management of Obesity Section. She has authored numerous scientific articles and lectured widely on primary-care evaluation and management of overweight/obesity and related metabolic comorbidities across the lifespan. Her comments do not reflect the views of UTSW, FDA, or any of her funding sources.
As readers will be well aware, n terms of health risks, fat is not fat is not fat is not fat.
Rather, whether or not body fat affects health depends very much on the type of body fat and its location.
While there have been ample attempts at trying to describe body fat distribution with simple anthropometric tools like measuring tapes and callipers, these rather crude and antiquated approaches have never established themselves in clinical practice simply because they are cumbersome, inaccurate, and fail to reliably capture the exact anatomical location of body fat. Furthermore, they provide no insights into ectopic fat deposition – i.e. the amount of fat in organs like liver or muscle, a key determinant of metabolic disease.
Recent advances in imaging technology together with sophisticated image recognition now offers a much more compelling insight into fat phenotype.
In this regard, readers may be interested in a live webinar that will be hosted by the Canadian Obesity Network at 12.00 pm Eastern Standard Time on Thu, Nov 23, 2017. The webinar provides an overview of a new technology developed by the Swedish company AMRA, that may have both important research and clinical applications.
The talk features Olof Dahlqvist Leinhard, PhD, Chief Scientific Officer & Co-Founder at AMRA and Ian Neeland, MD, a general cardiologist with special expertise in obesity and cardiovascular disease, as well as noninvasive imaging at the UT Southwestern Medical Center in Dallas, US.
Registration for this seminar is free but seats are limited.
To join the live event register here.
I have recently heard this talk and can only recommend it to anyone interested in obesity research or management.
Next, in my miniseries on arguments I commonly hear against the notion of calling obesity a disease, is that it is “just a risk factor” for other diseases.
This may be true, if you just (wrongly) considered elevated BMI as your definition of obesity, because no doubt, people with higher BMI levels carry a higher risk for obesity related complications including type 2 diabetes, sleep apnea, fatty liver disease, hypertension – just to name a few. (Note that increased risk is not the same as actually having the condition!).
However, when you use the actual WHO definition of obesity, namely, “accumulation of excess or abnormal fat that impairs health”, obesity is no longer just a risk factor – it is now (by definition) impairing your health, which makes it far more than just a risk factor.
So while someone with a BMI of 35 may be at risk of developing obesity (not the same as having it), when their excess fat actually starts impairing their health, it de facto becomes a disease in its own right.
Even then, one might argue that obesity itself is not the disease, rather the complications of obesity are the real disease.
This notion is both right and wrong.
There are many conditions that are both diseases in their own right as well as risk factors for other diseases or complications.
Take type 2 diabetes for instance – it is both a disease in itself but also a risk factor for coronary heart disease or end-stage kidney disease.
Take hypertension – a disease in its own right but also a risk factor for strokes and heart attacks.
Take gastro-oesophageal reflux disease, which is also a risk factor for Barrett’s disease and oesophageal cancer.
Take fatty liver disease, which is also a risk factor for cirrhosis.
Gall bladder stones, which is also a risk factor for pancreatitis.
Multiple sclerosis, which is also a risk factor for neurogenic bladder and pyelonephritis.
The list goes on and on.
So just because obesity is also a risk factor for a wide range of other medical problems, it does not make obesity any less of a disease in its own right.
When excess or abnormal body fat affects health – it’s a disease. When it doesn’t, it’s at best a risk factor.
That, is perhaps a subtle but important distinction.
Continuing in my mini series on the pros and cons of considering obesity a chronic disease, I would like to now discuss the perhaps most illogical argument against recognising obesity as a disease that I often hear, “Calling obesity a disease will reduce our efforts at prevention”.
This argument makes virtually no sense at all, as I cannot think of a single “preventable” disease, where calling it a “disease” would have reduced or thwarted prevention efforts.
Whether the aim is to prevent heart disease (dietary recommendations, fitness, smoking cessation), cancers (physical activity, healthy diets, smoking cessation, sunlight exposure), infectious diseases (vaccinations, food safety, hand washing, condom use), road accidents (helmets, seat belts, speed limits), in no instance has calling something a “disease” ever stopped us from doing the utmost for prevention (although more can always be done).
Rather, if you truly embrace the concept that obesity, once established, becomes a life-long problem for which we have no cure (the very definition of “chronic disease”), we should be doubling or even quadrupling our efforts at prevention.
After all, who would want to be stuck with a chronic disease, if it can indeed be prevented?
Governments, NGOs and individuals should be even more enthusiastic about preventing a “real” disease than simply modifying a “risk factor” (which sounds a lot less threatening).
Indeed, if I was working in population health, I’d be all for emphasizing just how terrible and devastating the disease of obesity actually is – all the more reason to double down on efforts to do what it takes to prevent it.
In fact, considering obesity a “real disease” would put all the folks working hard to prevent obesity right up there on par with those working to prevent “real” diseases like cancer, HIV/AIDS, or Alzheimer’s disease.
Thus, the argument that calling obesity a “disease” would somehow distract from efforts to prevent it makes absolutely no sense at all.
New Orleans, LA
Continuing in my mini series on arguments that I often hear against considering obesity a chronic disease, I turn to another common argument, “Obesity cannot be a disease because it is preventable and modifiable.”
That may well be the case (although, we must admit that we are doing a remarkably poor job of either preventing or modifying it), but so what?
There are 100s of diseases that are both preventable and modifiable – and yet no one would argue that they should not be considered diseases.
In fact, virtually all “lifestyle” diseases (by definition) are preventable and modifiable. Take for instance strokes and heart disease – most strokes and the vast majority of heart attacks are both preventable and modifiable (once they occur). So are diabetes, osteoarthritis, obstructive lung disease and many forms of cancer, not to mention the many infectious diseases that are both preventable and modifiable.
There are even a number of in-born genetic diseases that may be preventable or modifiable (e.g. phenylketonuria).
Thus, the fact that a disease can be prevented or modified (once it occurs) says nothing about whether something qualifies as a disease or not.
That said, as recently pointed out by Ted Kyle, for all practical purposes, obesity is proving pretty hard to modify and even harder to prevent in real life. It may therefore be more accurate (and honest) to say that obesity is “theoretically” preventable and modifiable – while we await large-scale real-life examples demonstrating that this is in fact the case, and not just limited to relatively rare exceptions like the 1990’s catastrophic economic crisis in Cuba.
Let’s remind ourselves that there is a vast difference between “efficacy” and “effectiveness” of proposed measures to “prevent” and “modify” obesity.
But even if we did have ample proof that obesity can indeed be prevented or modified by most people, it still says nothing that would speak against recognising excess or abnormal body fat that affects your health as a disease.