It must have been a pretty cheap rubber band, because every few months it would wear out and lose its stretch, so it had to be replaced it with a new band.
Unfortunately, this is not what can be said about the rubber band that I used in my recent TEDx talk to demonstrate what happens when you try to lose weight.
Unlike the cheap band in my pyjamas, the rubber band I used to represent our physiology trying to gain the weight back, never seems to lose its stretch.
No matter how hard or how long we pull, the rubber band keeps wanting to bring our weight back to where we started.
Yes, perhaps for some people, eventually the rubber band may relax (these would certainly be the exceptions) or may be the “muscles” that we use to pull on the band just grow stronger, which makes it seem easier to keep up the pull – but for all we know, in most people, this “rubber band” is of pretty good quality and seems to last forever.
So, how do we take the tension out of the rubber band ?
Well, we do know that people who have bariatric surgery have a much better chance of keeping the weight off in the long-term and we now understand that this has little to do with the “restriction” or the “malabsorbtion” resulting from these procedures but rather from the profound effect that this surgery has on the physiology of weight regain.
Thus, we know that many of the hormonal and neurological changes that happen with bariatric surgery, seem to inhibit the body’s ability to defend its weight and perhaps even appears to trick the body into thinking that its weight is higher than it actually is.
In other words, bariatric surgery helps maintain long-term weight loss by reducing the tension in the rubber band, thus making it far easier for patients to maintain the “pull”.
And that is exactly how we think some of the anti-obesity medications may be working.
For example, daily injections of liraglutide, a GLP-1 analogue approved for obesity treatment, appears to decrease the body’s ability to counteract weight loss by reducing hunger and increasing satiety, thus taking some of the tension out of that band.
Think of it as sprinkling “magic dust” on that rubber band to reduce the tension, which makes it easier for patients to maintain that pull thereby helping them keep the weight off.
Of course, both surgery and liraglutide only reduce the tension as long as you continue using them.
Undo the surgery or come off your anti-obesity meds and the tension in that band comes back as strong as ever.
For readers, who have no idea what I’m talking about, hopefully things will become clearer after you watch my talk by clicking here.
The last time I checked, my TEDx talk “How To Lose 50 Pounds And Keep Them Off“, had over 3,500 views on its first day!
While that is far from going “viral”, I do admit that it’s a lot more than I expected.
Although the overwhelming response and comments were positive, some viewers appeared frankly disappointed, not to say frustrated by the notion that obesity, once established, behaves like a chronic disease.
This may in part be due to the fact that, despite all evidence to the contrary, many people continue to believe (as suggested by the diet, fitness and weight-loss industry) that “permanent” weight loss is within anyone’s reach (it isn’t) and reaching your “dream weight” means winning the battle (it doesn’t).
But, I also believe that some of the frustration that comes with seeing obesity as a chronic disease for which we have no cure (which happens to be the definition of “chronic disease”), stems from the notion that living with a “disease” is terrifying and hopeless (it isn’t!).
In fact, most of what we deal with in our health care systems are “chronic diseases” – the exceptions being largely limited to accidents, acute infections and some cancers – these we can “cure”, by which I mean that we treat them for a given period of time after which they ceases to exist and the patient can be considered “cured”.
Unfortunately, as important as these “cures” may be, they constitute a rather small proportion of what goes on in the health care system. It is fair to say that for the vast majority of medical conditions, we may have treatments, but most certainly no “cures”.
However, this is not as depressing as it may seem. Indeed, it is one of the great achievements of modern medicine that we have turned diseases that would have been fatal in the not too-distant past (e.g. type 1 diabetes, coronary artery disease, HIV/AIDs, breast cancer), into conditions where, with proper treatments, most patients can enjoy decades of meaningful and productive life, despite living with their “chronic” disease.
Not that the treatments are always easy or cheap or well tolerated – but, when applied and adhered to properly, they generally do their job of allowing patients to go about their lives in a fairly acceptable manner.
So the idea that living with a chronic disease is all doom and gloom is certainly not true – ask anyone living with well-controlled diabetes, hypertension, coronary artery disease or even cancer.
Compared to a lot of these conditions, people living with obesity may well be a lot better off.
For one, while even with the best treatment many chronic diseases tend to get worse over time (take for e.g. chronic kidney disease with progressive loss of kidney function), stopping obesity form progressing (i.e. stopping further weight gain) is actually very achievable. In fact, as shown by the “placebo” groups in most obesity trials, even minimal intervention can help stabilize weight and prevent further weight gain – thus, while you may continue living with obesity, at least we can do a fairly good job of preventing it from getting worse.
Secondly, we have ample evidence that many of the health consequences associated with excess weight will improve with very little or even no weight loss through appropriate interventions that focus on improving mood, self-esteem, sleep, diet and physical activity. We know that with these interventions many people living with obesity will feel a lot healthier and better about themselves – which in the end should really be the principal goal of treating obesity in the first place.
Thirdly, there is hope on the horizon as both medical and surgical treatments for obesity are steadily getting better. Take for example bariatric surgery, which has gone from not too long being a highly invasive procedure ridden with often catastrophic complications in the days of open surgery, to a minimally invasive procedure with surprisingly minor risks and complications (in appropriate hands) with well-documented and often remarkable long-term benefits for health and well-being (not to say that there isn’t further room for improvement).
On the medical front, the last few years have seen the approval of several new obesity drugs, which have been rigorously tested for safety and efficacy in thousands of volunteers in randomised controlled trials. While these drugs may not be for everyone and come with a price tag (that varies from drug-to-drug and country-to-country), they do raise optimism that one day, medical treatment of obesity will be no more (or less) routine than treating diabetes, hypertension or any of the other many chronic diseases where long-term medical treatment is well established.
So, the notion that just because obesity is a chronic disease somehow means that all hope is lost, is simply nonsense.
Yes, the idea of thinking of of obesity as a “disease” may not sit well with everyone, especially with the minority of people, who happen to meet the BMI criteria for obesity but appear in perfect health – I do understand that for this minority, we do need a better definition of obesity that is not based on BMI and the Edmonton Obesity Staging System is certainly a start.
But for the vast majority of people with obesity (Stage 1-4), who do experience (or will experience) the health consequences of obesity, we can certainly do a better job of serving them, by looking at their obesity as a chronic disease rather than a “problem” that can be easily “fixed” by simply telling them to “eat less and move more”.
We know a lot about managing chronic diseases – we do this all the time.
It is now time to apply that knowledge to the benefit our patients living with obesity.
They deserve no less.
In March, I had the privilege of being invited by the organisers of TEDx UAlberta to present a talk on obesity.
This talk is now online – please take a look and join the discussion on facebook
If clicking on the image does not work for you, click on this link for YouTube
Obesity caused by disruption of the hypothalamic centres that control body weight are among the most challenging forms of obesity to treat. Patients often experience relentless appetite with loss of satiety resulting in often dramatic weight gain. Causes can range from physical trauma to tumors that impact on the functioning of the hypothalamus.
Now, a study by Jefferson Lormenick and colleagues from Vanderbilt University, Nashville, Tennessee, published in OBESITY, describes the use of the GLP-1 analogue exenatide for weight loss in individuals with hypothalamic obesity.
The baseline weight of the 10 participants (7 female) was about 140 kg.
Overall, 8 individuals completed the 52 weeks of study.
Although the average weight loss of the entire group was not significant, 6 of the 8 participants, who did complete the 52 weeks of treatment, did lose about 6 kg.
While these results may sound disappointing, even this modest degree of weight loss in some patients, given the complexity of hypothalamic obesity, is remarkable, especially as participants were not offered any additional diet or lifestyle modification during the study.
It is also worth noting that untreated participants continued to gain weight over the study period.
As for the limitations of the study the authors also note that,
“Medication adherence was moderate and it is possible that long-acting GLP1RA could have better efficacy. HO is a heterogeneous disorder and better understanding of each patient’s hypothalamic damage may identify patients with improved responsiveness to GLP1RAs. The majority of our patients developed HO in childhood and longstanding obesity may be more refractory to treatment.”
Clearly, the use of GLP-1 analogues deserve further study for use in this patient population.
Liraglutide, a GLP-1 analogue now available for the treatment of obesity (as Saxenda) in North America, works by reducing appetite and increasing satiety, thus making it easier to lose weight and keep it off (with continuing treatment).
Now, a study by Olivia Farr and colleagues, in a paper published in Diabetologia not only present data showing the presence of GLP-1 receptors in human cortex, hypothalamus and medulla, but also provide functional evidence for altered brain response to food cues.
After documenting the presence of GLP-1 receptor in human brains using immunohistochemistry, the researchers conducted a randomised controlled placebo-controlled, double-blind, crossover trial in 18 individuals with type 2 diabetes who were treated with placebo and liraglutide for a total of 17 days each (0.6 mg for 7 days, 1.2 mg for 7 days, and 1.8 mg for 3 days).
Using functional MRI neuroimaging studies, the researchers found that liraglutide remarkably decreased activation of the parietal cortex in response to highly desirable (vs less desirable) food images.
They also observed decreased activation in the insula and putamen, areas involved in the reward system.
Furthermore, using neurocognitive testing, the researchers showed that increased ratings of hunger and appetite correlated with increased brain activation in response to highly desirable food cues while on liraglutide.
In contrast, ratings of nausea (a well-known side effect of liraglutide) correlated with decreased brain activation.
As the authors note,
“Our data point to a central mechanism contributing to, or underlying, the effects of liraglutide on metabolism and weight loss.”
These findings no doubt match the reports from my own patients of experiencing less interest in highly palatable foods and finding it much easier to pass up on foods that they would have otherwise found hard to resist.
Clearly, as we learn more about brain function in eating behaviour, we are thankfully moving towards treatments that are clearly proving to be far more effective than just telling patients to “simply eat less” (which I have often likened to telling people with depression to “simply cheer up”).
Disclaimer: I have received honoraria for speaking and consulting from Novo Nordisk, the maker of liraglutide