It seems that every year someone else comes up with a diet that can supposedly conquer obesity and all others health problems of civilization.
In almost every case, the diet is based on some “new” insight into how our bodies function, or how our ancestors (read – hunters gatherers (never mind that they only lived to be 35) ate, or how modern foods are killing us (never mind that the average person has never lived longer than ever before), or how (insert remote population here) lives today with no chronic disease.
Throw in some scientific terms like “ketogenic”, “guten”, “anti-oxidant”, “fructose”, or “insulin”, add some level of restriction and unusual foods, and (most importantly) get celebrity endorsement and “testemonials” and you have a best-seller (and a successful speaking career) ready to go.
The problem is that, no matter what the “scientific” (sounding) theories suggest, there is little evidence that the enthusiastic promises of any of these hold up under the cold light of scientific study.
Therefore, I am not the least surprised that the same holds true for the much hyped “alternative-day fasting diet”, which supposedly is best for us, because it mimics how our pre-historic ancestors apparently made it to the ripe age of 35 without obesity and heart attacks.
Thus, a year-long randomised controlled study by John Trepanowski and colleagues, published in JAMA Internal Medicine, shows that alternate day fasting is evidently no better in producing superior adherence, weight loss, weight maintenance, or cardioprotection compared to good old daily calorie restriction (which also produces modest long-term results at best).
In fact, the alternate day fasting group had significantly more dropouts than both the daily calorie restriction and control group (38% vs. 29% and 26% respectively). Mean weight loss was virtually identical between both intervention groups (~6 Kg).
Purists of course will instantly critisize that the study did not actually test alternative-day fasting, as more people dropped out and most of the participants who stayed in that group actually ate more than prescribed on fast days, and less than prescribed on feast days – but that is exactly the point of this kind of study – to test whether the proposed diet works in “real life”, because no one in “real life” can ever be expected to be perfectly compliant with any diet. In fact, again, as this study shows, the more “restrictive” the diet (and, yes, starving yourself every other day is “restrictive”), the greater the dropout rate.
Unfortunately, what counts in real life is not what people should be doing, but what people actually do. The question really is not whether or not alternate-day fasting is better for someone trying to lose weight but rather, whether or not “recommending” someone follows an alternate-day fasting plan (and them trying to follow it the best they can) is better for them. The clear answer from this study is “no”.
So why are all diets the same (in that virtually all of them provide a rather modest degree of long-term weight loss)?
My guess is that no diet (or behaviour for that matter) has the capability of fundamentally changing the body’s biology that acts to protect and restore body fat in the long-term. Irrespective of whether a diet leads to weight loss in the short term and irrespective of how it does so (or how slow or fast), ultimately no diet manages to “reset” the body-weight set point to a lower level, that would biologically “stabilize” weight loss in the long-term.
Thus, the amount of long-term weight loss that can be achieved by dieting is always in the same (rather modest) ballpark and it is often only a matter of time before the biology wins out and put all the weight back on.
Clearly, I am not holding my breath for the next diet that comes along that promises to be better than everything we’ve had before.
My advice to patients is, do what works for you, but do not expect miracles – just find the diet you can happily live on and stick to it.
Continuing in my miniseries on arguments that support calling obesity a disease, is the simple fact that, once established, it behaves like a chronic disease.
Thus, once people have accumulated excess or abnormal adipose tissue that affects their health, there is no known way of reversing the process to the point that this condition would be considered “cured”.
By “cured”, I mean that there is a treatment for obesity, which can be stopped without the problem reappearing. For e.g. we can cure an ear infection – a short course of antibiotics and the infection will resolve to perhaps never reappear. We can also cure many forms of cancer, where surgery or a bout of chemotherapy removes the tumour forever. Those conditions we can “cure” – obesity we cannot!
For all practical purposes, obesity behaves exactly like every other chronic disease – yes, we can modify the course or even ameliorate the condition with the help of behavioural, medical or surgical treatments to the point that it may no longer pose a health threat, but it is at best in “remission” – when the treatment stops, the weight comes back – sometimes with a vengeance.
And yes, behavioural treatments are treatments, because the behaviours we are talking about that lead to ‘remission’ are far more intense than the behaviours that non-obese people have to adopt to not gain weight in the first place.
This is how I explained this to someone, who recently told me that about five years ago he had lost a substantial amount of weight (over 50 pounds) simply by watching what he eats and maintaining a regular exercise program. He argued that he had “conquered” his obesity and would now consider himself “cured”.
I explained to him, that I would at best consider him in “remission”, because his biology is still that of someone living with obesity.
And this is how I would prove my point.
Imagine he and I tried to put on 50 pounds in the next 6 weeks – I would face a real upward battle and may not be able to put on that weight at all – he, in contrast, would have absolutely no problem putting the weight back on.
In fact, if he were to simply live the way I do, eating the amount of food I do, those 50 lbs would be back before he knows it.
His body is just waiting to put the weight back on whereas my biology will actually make it difficult for me simply put that weight on.
This is because his “set-point”, even 5 years after losing the weight, is still 50 lbs higher than my “set-point”, which is around my current weight (the heaviest I have ever been).
Whereas, he is currently working hard against his set-point, by doing what he is doing (watching what he eats, following a strict exercise routine), I would be working against my set-point by having to force myself to eat substantially more than my body needs or wants.
That is the difference! By virtue of having had 50 lb heavier, his biology has been permanently altered in that it now defends a weight that is substantially higher than mine.
His post-weight loss biology is very different from mine, although we are currently at about the same weight.
This is what I mean by saying he is in “remission”, thanks to his ongoing behavioural therapy.
Today, we understand much of this biology. We understand what happens when people try to lose weight and how hard the body fights to resist weight loss and to put the weight back on.
This is why, for all practical purposes, obesity behaves just like every other chronic disease and requires ongoing treatment to control – no one is ever “cured” of their obesity.
Not even people who have bariatric surgery – reverse the surgery and before you know it, the weight is back.
So, if for all practical purposes, obesity behaves like a chronic disease, why not just call a spade a spade?
For an illustration on why obesity acts like a chronic disease watch this short TEDx talk
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.
In my miniseries on arguments that I often hear against calling obesity a chronic disease, I now turn to the objection that declaring obesity a disease would reduce or even abolish personal responsibility.
The argument being, that the term “disease” carries the connotation of being inevitable and will thus reduce motivation in patients to do anything about it.
This is complete nonsense!
When has calling something a disease ever taken away an individuals “responsibility” to do what they can to avoid or ameliorate it?
Take for example type 2 diabetes – a very avoidable and modifiable condition. Calling diabetes a disease does not mean that the individual can do nothing to prevent it or that, once it occurs, the patient can do nothing to change the course of the disease – of course they can and should and often do!
Or take people with a high risk of heart disease or lung disease or bone and joint disease or even cancer – in no instance do we expect less of patients to do their part in helping manage these conditions just because we call them “diseases”.
There is even a term for this – it is called “self-management” – a key principle of chronic disease management.
The course of almost every chronic disease can be changed by whether or not patients change their diet, follow their exercise program, monitor their symptoms, take their medications, come in for their visits – all a matter of “responsibility” if you so wish.
So just how exactly would calling obesity a disease take away from any of this?
Frankly, I cannot help but sense that people who use this argument most often, are erring on the side of “shame and blame” and probably still see obesity largely as a matter of personal “choice” rather than the complex multifactorial problem that it actually is.
Indeed, the opponents often appear “morally” opposed to the very notion of accepting obesity as a disease, as it now gives people the “excuse” to not do anything about it. Sorry, but this whole line of arguing reeks of nothing less than weight bias and discrimination.
As far as I can tell, calling something a disease often leads to exactly the opposite response – when obesity happens (and it can happen to anyone), it places a tremendous mental, physical and social burden on the people who get it – no matter what you call it.
People living with obesity have no greater or lesser “responsibility” of contributing to the self-management of their disease, than people living with hypertension, diabetes, depression, heart disease, or cancer – people living with any disease should be doing what they can – why would obesity be any different?
New Orleans, LA
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).