Continuing in my miniseries on why obesity (defined here, as excess or abnormal body fat that affects your health) should be considered a disease, is the simple observation that obesity responds less to lifestyle treatments than most people think.
Yes, the internet abounds with before and after pictures of people who have “conquered” obesity with diet, exercise, or both, but in reality, long-term success in “lifestyle” management of obesity is rare and far between.
Indeed, if the findings from the National Weight Control Registry have taught us anything, it is just how difficult and how much work it takes to lose weight and keep it off.
Even in the context of clinical trials conducted in highly motivated volunteers receiving more support than you would ever be able to reasonably provide in clinical practice, average weight loss at 12 – 24 months is often a modest 3-5%.
Thus, for the vast majority of people living with obesity, “lifestyle” treatment is simply not effective enough – at least not as a sustainable long-term strategy in real life.
While this may seem disappointing to many (especially, to those in the field, who have dedicated their lives to promoting “healthy” lifestyles as the solution to obesity), in reality, this is not very different from the real-life success of “lifestyle” interventions for other “lifestyle” diseases.
Thus, while there is no doubt that diet and exercise are important cornerstones for the management of diabetes or hypertension, most practitioners (and patients) will agree, that very few people with these conditions can be managed by lifestyle interventions alone.
Indeed, I would put to you that without medications, only a tiny proportion of people living with diabetes, hypertension, or dyslipidemia would be able to “control” these conditions simply by changing their lifestyles.
Not because diet and exercise are not effective for these conditions, but because diet and exercise are simply not enough.
The same is true for obesity. It is not that diet and exercise are useless – they absolutely remain a cornerstone of treatment. But, by themselves, they are simply not effective enough to control obesity in the vast majority of people who have it.
This is because, diet and exercise do not alter the biology that drives and sustains obesity. If anything, diet and exercise work against the body’s biology, which is working hard to defend body weight at all costs.
Thus, it is time we accept this reality and recognise that without pharmacological and/or surgical treatments that interfere with this innate biology, we will not be able to control obesity in the majority of patients.
Whether we like it or not, I predict that within a decade, clinical management of obesity will look no different than current management of any other chronic disease. Most patients will require both “lifestyle” and probably a combination of anti-obesity medications to control their obesity.
This does not take away from the importance of diet and exercise – as important as they are, they are simply not enough.
Despite what “lifestyle” enthusiasts will have us believe, diet and exercise are no more important (or effective) for the treatment of obesity, than they are for the treatment of hypertension, diabetes, dyslipidemia, depression, or any other condition that responds to “lifestyle” interventions.
In the end, most patients will require more effective treatments to manage their obesity and all of the comorbidities that come with it. The sooner we develop and make accessible such treatments, the sooner we can really help our patients.
This, according to a study by Ruth Brown and colleagues from Toronto’s York University, published in Medicine and Science in Sports and Exercise.
The study included 58 adult men and women of either normal weight (NW) or overweight (OW), who reported either attempting (WL) or not attempting weight loss (noWL)
Following 25 mins of exercise on a treadmill at either a moderate (60% HRmax) or a vigorous intensity (75% HRmax), participants were asked to estimated the number of calories they expended through exercise and create a meal that they believed to be calorically equivalent to the amount of calories they had just burnt.
Both the moderate and intense exercise groups were on average spectacularly wrong in their estimates.
In contrast, the active weight loss (WL) groups appeared to do far better at estimating energy consumption than the non-WL groups.
As an example, following vigorous exercise, the OW-noWL overestimated energy expenditure by 72%, and overestimated the calories in their food by 37%.
Although the WL groups did better, all groups showed a wide range of over and underestimation (-280 kcal to +702 kcal).
These findings show that while most people tend to over or underestimate caloric expenditure with exercise, overweight adults who are not attempting weight loss may be even more off the mark than others.
The most obvious solution would be to use some kind of monitor that does a better job of predicting calories consumed that just guessing.
That is of course, if overcompensating is not your goal (as in people who actually gain weight when they begin exercising).
For those interested in staying in energy balance, perhaps simply stepping on the scale regularly during the week should be enough.
For those interested in losing weight, they may need to be reminded that exercise (alone) is actually a pretty inefficient way to lose weight, so the calories burnt during exercise probably don’t matter all that much for weight management (despite all other benefits of exercise – its the calories you eat or drink that count).
Yesterday, I attended the inaugural networking event of the Canadian Obesity Network’s Toronto Chapter. Judging by the enthusiasm of the almost 100 folks who came out to this event, this chapter appears off to a great start.
As expected for any CON event, the participants came from virtually every walk of interest in obesity – from professional to personal – research, prevention, clinic, policy, industry, NGOs.
Hopefully, we will see similar activities and chapters starting across Canada in the coming months – the success off this event shows that there is a dire need for local networking to address local issues related to obesity prevention and management.
For more information on the Toronto Chapter (CON-YYZ) click here.
For more information on how to start a CON chapter in your city click here.
In my conversations with skinny runners, they often cannot stop telling me how much satisfaction and enjoyment they get from their “runner’s high”. No wonder, they so often seem “addicted” to their runs (or other workouts).
In contrast, a “runner’s high” seldom comes up when any of my patients living with obesity talk about their exercise experiences (yes, many people with obesity exercise regularly).
Now, work by Maria Fernandes and colleagues from the University of Montreal, published in Cell Metabolism, reports findings in rats, which, if applicable to humans, may provide a biological explanation for this observation.
Building on previous studies showing that leptin modulates multiple components of brain reward circuitry, particularly in dopamine (DA) neurons of the ventral tegmental area (VTA), an area of the brain allegedly responsible for the “runner’s high”.
Using an elegant set of experiments, the researchers showed that leptin markedly reduces mice’s willingness to work for access to a running wheel or show other signs of seeking out exercise-induced reward.
In contrast, mice with a deletion of the signal transducer and activator of transcription-3 (STAT3), involved in leptin signalling in dopamine neurons of the VTA, showed greater interest in voluntary running.
In other words, STAT3 deletion increased the rewarding effects of running whereas intra-VTA leptin blocked it in a STAT3-dependent manner.
Together these findings strongly suggest that leptin influences the motivational effects of running via LepR-STAT3 modulation of dopamine tone.
Or, in other words, higher levels of leptin (as seen in people living with obesity) directly inhibit the rewarding nature of running, making it less likely to experience a runner’s high, than in someone with low leptin levels (as seen in people with low fat mass).
As to why this may be the case, the authors offer the following explanation:
“We speculate that in conditions of restricted food availability the mesolimbic DA system engages motivational processes concerned with obtaining food and more readily responds to leptin to decrease appetitive physical activity. On the other hand, during fed states, the actions of leptin may be biased toward hypothalamic processes that could increase physical activity as a means to maintain energy homeostasis.”
“While heightened physical activity during food restriction seems paradoxical to the maintenance of energy reserves, it is considered an expression of increased food acquisition behaviors. The capacity for endurance running in cursorial mammals is considered to enable food attainment when it is distant or requires pursuit. Correspondingly, the runner’s high may have evolved to encourage stamina and thereby increase the probability of return on this energetic investment.”
As the authors note, this line of reasoning is supported by the recent observation that exercise addiction in men is associated with low, fat-adjusted leptin levels.
In light of these findings, I also wonder if the “increase in energy levels”, which is rather consistently reported by my patients when they lose weight, may simply be reflective of their often dramatic reduction in leptin levels.
The amygdala is a part of the so-called limbic system that performs a primary role in the processing of memory, decision-making, and emotional reactions. The amygdala has also been implicated in a variety of mental health problems including anxiety, binge drinking and post-traumatic stress syndrome.
A study by Xu and colleagues, published in the Journal of Clinical Investigation now shows that in mice, activity of the estrogen receptor–α (ERα) in the medial amygdala may have a profound influence on the development of obesity – an effect, which appears to me largely mediated through effects on physical activity.
Building on previous work showing that ERα activity in the brain prevents obesity in both males and female rats, the researchers used a series of complex experiments to demonstrate that specific deletion of the ERα gene from SIM1 neurons, which are highly expressed in the medial amygdala, cause a marked decrease in physical activity and weight gain in both male and female mice fed with regular chow, without any increase in food intake. In addition, this deletion caused increased susceptibility to diet-induced obesity in males but not in females.
Deletion of the ERα receptor also blunted the body weight-lowering effects of a glucagon-like peptide-1-estrogen (GLP-1-estrogen) conjugate.
In contrast, over-expression or stimulation of SIM1 neurons increased physical activity in mice and protected them from diet-induced obesity.
These findings point to a novel mechanism of neuronal control of physical activity, which in turn appears to have important effects on the susceptibility to weight gain.