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.
Today’s guest post comes from Tasuku Terada, a postdoctoral research fellow with the Bariatric Care and Rehabilitation Research Group (BCRRG), a multidisciplinary research collaboration, focused on improving the care and rehabilitation outcomes of patients with obesity. Dr. Terada is an Exercise Physiologist and 2015 Canadian Obesity Network, Obesity Research Bootcamp alumni. His research interests include the role of exercise in counteracting chronic health conditions associated with obesity.
Obesity is a risk factor for cardiovascular disease, and referrals for coronary artery bypass graft surgery (CABG) have increased in patients with severe obesity (body mass index: BMI ≥40 kg/m2).
In our recent study published in the Journal of American Heart Association, using data from the Alberta Provincial Project for Outcome Assessment in Coronary Heart Disease (APPROACH) registry, we show that patients with severe obesity were 53% more likely to have complications within 30 days of surgery and had threefold higher risk of infection compared to patients without obesity.
In addition, the median hospital stay was one day longer in patients with severe obesity compared to patients without obesity. In patients with severe obesity, those who had diabetes and experienced infection stayed 3.2 times longer days in hospital compared to patients without either condition.
Taken together, these results highlight a need for attentive care in bypass patients with severe obesity. Strategies to minimize the risks of infection and efforts to ensure good glucose control for patients with diabetes may also be important for better patient care quality and to reduce the length of hospital stay.
This type of information should be useful to caregivers and lead to prevention or preparation for possible adverse outcomes.
This study was supported by a Partnerships for Research and Innovation in the Health System (PRIHS) award from Alberta Innovates – Health Solutions (AIHS).
Nevertheless, epidemiologists (and folks in health promotion) appear to like the notion that there is such a weight (at least at the population level), and often define it as the weight (or rather BMI level) where people have the longest life-expectancy.
Readers of this literature may have noticed that the BMI level associated with the lowest mortality has been creeping up.
Case in point, a new study by Shoaib Afzal and colleagues from Denmark, published in JAMA, that looks at the relationship between BMI and mortality in three distinct populations based cohorts.
The cohorts are from the same general population enrolled at different times: the Copenhagen City Heart Study in 1976-1978 (n = 13 704) and 1991-1994 (n = 9482) and the Copenhagen General Population Study in 2003-2013 (n = 97 362). All participants were followed up to November 2014, emigration, or death, whichever came first.
The key finding of this study is that over the various studies, there was a 3.3 unit increase in BMI associated with the lowest mortality when comparing the 1976-1978 cohort with that recruited in 2003-2013.
Thus, The BMI value that was associated with the lowest all-cause mortality was 23.7 in the 1976-1978 cohort, 24.6 in the 1991-1994 cohort, and 27.0 in the 2003-2013 cohort.
Similarly, the corresponding BMI estimates for cardiovascular mortality were 23.2, 24.0, and 26.4, respectively, and for other mortality, 24.1, 26.8, and 27.8, respectively.
At a population level, these shifts are anything but spectacular!
After all, a 3.3 unit increase in BMI for someone who is 5’7″ (1.7 m) is just over 20 lbs (~10 Kg).
In plain language, this means that to have the same life expectancy today, of someone back in the late 70s, you’d actually have to be about 20 lbs heavier.
While I am sure that these data will be welcomed by those who would argue that the whole obesity epidemic thing is overrated, I think that the data are indeed interesting for another reason.
Namely, they should prompt speculation about why heavier people are living longer today than before.
There are two general possible explanations for this:
For one these changes may be the result of a general improvement in health status of Danes related to decreased smoking, increased physical activity or changes in social determinants of health (e.g. work hours).
On the other hand, as the authors argue, this secular trend may be that improved treatment for cardiovascular risk factors or complicating diseases, which has indeed reduced mortality in all weight classes, may have had even greater beneficial effects in people with a higher BMI. Thus, obese individuals may have had a higher selective decrease in mortality.
There is in fact no doubt that medical management of problems directly linked to obesity including diabetes, hypertension and dyslipidemia have dramatically improved over the past decades.
Thus, it appears that the notion of “healthy” weight is a shifting target and that changes in lifestyle and medical management may have more than compensated for an almost 20 lb weight increase in the population.
This is all the more reason that the current BMI cutoffs and weight-centric management of obesity both at a population and individual level may need to be revisited or at least tempered with measures of health that go beyond just numbers on the scale.