In my experience, patients presenting with obesity tend to fall into three categories, each of which requires a distinct management approach.
They are 1) Active Gainers, 2) Weight Stable, and 3) Post-Weight Loss.
Active Gainers are patients currently at their lifetime maximum and continuing to gain significant amounts of weight – i.e. more than the usual 0.5 to 1 lb/year. Patients in this category require immediate attention – if nothing happens, their weight will most likely just continue to increase. The good news is that in almost every patient in this category, there is an identifiable reason for the ongoing weight gain – this can be psychosocial (e.g. depression, binge-eating disorder, etc.), due to a medical comorbidity (arthritis, chronic pain, etc.) or medications (e.g. atypical antipsychotics, hypoglycemic agents, etc.). From a management perspective, the sooner we identify and address the underlying problem, the sooner we can slow or even halt the rate of weight gain – in this patient – gaining less weight than before is the first sign of success. There is really no point trying to embark on losing weight as long as the underlying problem driving the weight gain has not been addressed, as this is likely to make sustained weight loss even more unlikely that it already is..
Weight Stable patients are those that present with excess weight but are relatively weight stable. Even though they may be at their lifetime maximum, they have been pretty much the same weight (perhaps a few lbs up or down but nothing drastic) for several years (sometimes even decades). By definition, a patient who is weight stable is in caloric balance, and thus, by definition is not eating too much. In fact, these patients are eating the exact number of calories needed to sustain their bodies, which is why they are weight stable. (Remember, even if you are weight-stable eating 4000 Cal a day, you are technically not “overeating”.) These patients of course have experienced significant weight gain in the past (historical weight gain), but whatever it was that caused them to gain weight is no longer an active problem (e.g. pregnancy, past depression, etc) – and therefore, probably doesn’t need to addressed (although, I always find it of interest to find out what caused the weight gain in the first place). With these patients, we can determine whether or not their weight is affecting their health, and if it is, we can jump right into discussing treatment options (behavioural, medical and/or surgical).
The third group of patients, Post-Weight Loss, are those who are not at their lifetime maximum, or in other words, have already lost weight (by whatever means). These patients generally present either because they want to lose even more weight (Doctor, my diet has stopped working! = “weight-loss plateau“), or are experiencing weight regain (Active Regainers). In case of the patients experiencing a “weight-loss plateau”, one needs to determine if there is in fact any medical indication for further weight loss – many of these patients may already be at their “Best Weight”. If there is indeed a medical indication for further weight loss, it generally means adding therapeutic options that may include anti-obesity medications and/or surgery. (In my experience, patients who have been maintaining a significant amount of weight loss on their own, generally leave little room for further behavioural intervention). On the other hand, there are the post-weight loss patients who are actively regaining weight. These tend to fall into two groups – the first one are those, who have lost a significant amount of weight with a strategy that is in fact unsustainable (e.g. a very low-calorie diet, an excessive exercise program, or whatever else desperate patients will try just to drop their weight). As the strategy they were on is not one that they can sustain (for good reasons), some weight regain is inevitable and the best we can do is to offer a weight management strategy that is sustainable in the long run (and may include medication or surgery) . The other group of Active Regainers, are those that were on a more-or-less sustainable management plan (behavioural, medical or surgical) and have for some reason “fallen off”. Here one needs to determine what exactly they have stopped doing (e.g. no longer keeping their food journal, stopped their anti-obesity medications, etc.) or what additional weight-gain promoting change has occurred that has thrown them off (again, reasons can be psychosocial or medical). Here one needs to determine if the patient can in fact go back to doing what was “working”, which may require addressing the new problem that has arisen or add additional therapeutic options (e.g. medications or surgery).
Thus, as each type of patient needs a somewhat different assessment and management strategy, I find this approach to thinking about each patient most helpful.
Comments are very much appreciated.
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.
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.
The biguanide metformin is widely used for the treatment of type 2 diabetes. Metformin has also been shown to slow the progression from pre to full-blown type 2 diabetes. Moreover, metformin can reduce weight gain associated with psychotropic medications and polycystic ovary syndrome.
Now, a randomised controlled trial by M P van der Aa and colleagues from the Netherlands, published in Nutrition & Diabetes suggests that long-term treatment with metformin may stabilize body weight and improve body composition in adolescents with obesity and insulin resistance.
The randomised placebo-controlled double-blinded trial included 62 adolescents with obesity aged 10–16 years old with insulin resistance, who received 2000 mg of metformin or placebo daily and physical training twice weekly over 18 months.
Of the 42 participants (mean age 13, mean BMI 30), BMI was stabilised in the metformin group (+0.2 BMI unit), whereas the control group continued to gain weight (+1.2 BMI units).
While there was no significant difference in HOMA-IR, mean fat percentage reduced by 3% compared to no change in the control group.
Thus, the researcher conclude that long-term treatment with metformin in adolescents with obesity and insulin resistance can result in stabilization of BMI and improved body composition compared with placebo.
Given the rather limited effective options for addressing childhood obesity, this rather safe, simple, and inexpensive treatment may at least provide some relief for adolescents struggling with excess weight gain.
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