Unfortunately, all current treatments fail to “cure” obesity, as they fail to reset the set point to what would be considered “normal weight”. This makes ongoing treatment (be it behavioural, medical, or surgical) inevitable.
For all we know, any attempt at creating and sustaining weight loss regularly activates complex neurohormonal responses that serve to promote weight regain.
The only treatment, which may prove to be an exception is bariatric surgery (although this also only works as long as the surgery is in place – reverse the surgery, and the weight comes back).
Now, a paper by Hans Rudi Berthoud and colleagues, published in the International Journal of Obesity takes an in depth look at if and how gastric bypass surgery changes the body weight set point.
The paper reviews the data in support of the notion that surgery physiologically reprograms the body weight defense mechanism.
Thus, behavioural studies in animal models have shown that the defended body weight is indeed lowered after RYGB and sleeve gastrectomy.
For example, after surgeries, rodents return to their preferred lower body weight if over- or underfed for a period of time, and the ability to drastically increase food intake during the anabolic phase strongly argues against the physical restriction hypothesis.
Furthermore, these authors have also demonstrated that the defense of fat mass is less efficient (whereas defense of lean mass remains intact) after surgery.
However, as they point out,
“…the underlying mechanisms remain obscure. Although the mechanism involves central leptin and melanocortin signaling pathways, other peripheral signals such as gut hormones and their neural effector pathways likely contribute.”
Trying to elucidate the exact underlying mechanisms will hopefully not just improve our understanding of how bariatric surgery works, but also hopefully ultimately lead to the development of novel medical treatments that specifically target the body weight set point and its defence.
Childhood obesity is a grave concern and so far community based interventions to prevent it have been rare and far between, with little evidence that any changes (however meagre) are in fact sustainable over time and will actually lead to a reduction in adult obesity.
Thus, the Australian team of Steven Allander and colleagues must be commended on embarking on what I believe will be the first cluster randomized trial in ten communities in the Great South Coast Region of Victoria, Australia to test whether it is possible to: (1) strengthen community action for childhood obesity prevention, and (2) measure the impact of increased action on risk factors for childhood obesity.
According to the trial design published in the International Journal of Environmental Research in Public Health, the WHO STOPS intervention will involve a facilitated community engagement process that: creates an agreed systems map of childhood obesity causes for a community; identifies intervention opportunities through leveraging the dynamic aspects of the system; and, converts these understandings into community-built, systems-oriented action plans.
Ten communities will be randomized (1:1) to intervention or control in year one and all communities will be included by year three.
The primary outcome is childhood obesity prevalence among grade two (ages 7–8 y), grade four (9–10 y) and grade six (11–12 y) students measured using established community-led monitoring system (69% school and 93% student participation rate in government and independent schools).
An additional group of 13 external communities from other regions of Victoria with no specific interventions will provide an external comparison.
All of this makes sense and is highly commendable.
What is shockingly lacking however – at least I see no mention of this in the published study design – is the inclusion of an explicit focus on what such community interventions aimed at reducing childhood obesity, will do to self-esteem and body image of the kids involved and weight bias in the communities overall.
Indeed, I see no mention of anyone with an explicit expertise in weight bias or kids mental health on the panel of researchers involved in this study.
This is concerning, as we now understand well that body image concerns and both implicit and explicit weight bias begin in kindergarten-age kids and must acknowledge that the “moral panic” created around childhood obesity has been accused of further promoting eating disorders, body image issues and weight bias.
Thus, we have here the unique opportunity to study the potential harm that could be done by school “surveillance” programs that assess body weight in kids or by the well-meant education on “healthy activity and healthy eating” that may teach kids that obesity is simply a result of making poor choices and not moving enough (rather than a complex biopsychosocial chronic disease, that is highly resistant to lasting effects of time-limited interventions).
I would sincerely appeal to the researchers involved to amend their study protocol to include changes in weight bias, unhealthy weight obsessions, body image issues, and eating disorders both at the level of the kids and the community overall, to ensure that the well-meant interventions do not inadvertently replace one problem with another – as always, the Devil of public health interventions lies in the unintended consequences.
In fact, if I was on the ethics committee tasked with approving this study, I would insist that an in-depth assessment plan for the potential harm of this intervention be in place before commencement of any study related activities in the relevant communities.
If the overall goal of the WHO STOPS intervention is to have a healthier generation of kids, nothing is more important than fully understanding the potential impact of this intervention on mental health and social attitudes towards kids and adults living with obesity.
Yesterday, I posted on a study suggesting that people at high risk of obstructive sleep apnea may have a harder time losing weight that people without sleep apnea.
This prompted a reader to send me a link to a study by Luciano Drager and colleagues, published in Thorax, that presents a meta-analysis of randomised controlled trials on the effect of CPAP treatment on body weight.
The authors found 25 randomised controlled trials (RCTs) enrolling over 3000 patients with OSA ranging from 1 to 48 months in duration.
Paradoxically, they report that overall CPAP is associated with a 0.5 kg weight gain compared with control therapy.
Whether this weight gain is clinically relevant or not, the key finding is that (perhaps contrary to popular belief – including my own), the data does not support the idea that commencement of CPAP treatment for sleep apnea leads to weight loss.
As for the reasons for weight gain, an accompanying editorial by Sanjay Patel has this to offer,
“The reduction in leptin levels associated with CPAP therapy may result in increased hunger if the degree of leptin resistance does not change. Another explanation is that CPAP leads to reduced energy expenditure during sleep, as work of breathing is reduced due both to a patent upper airway as well as lung volumes rising to a more efficient point on the pressure–volume curve. Removal of the anorectic effects of hypoxia also may play an important role.”
It is also not exactly clear where the additional weight goes.
“A number of trials have demonstrated no substantial impact of CPAP on visceral fat volume, although the imaging methods used may not be sensitive enough to exclude the small magnitude of weight gain observed. Improvements in growth hormone and insulin-like growth factor 1 signalling with CPAP might result in increased muscle mass.13 Further studies are clearly needed to determine whether CPAP-induced weight gain represents increases in fat, lean body or water compartments.”
As for the potential health effects of the weight gain,
“The impact of 0.5 kg weight gain on health outcomes is fairly minimal and so should not change decision making regarding the use of CPAP in symptomatic OSA. However, it does give one pause regarding the use of CPAP in asymptomatic OSA where a cardiovascular benefit of CPAP has yet to be definitively established and makes more urgent the need for RCTs adequately powered to assess meaningful outcomes in this population.”
Clearly, the relationship between sleep apnea and body weight is a fair bit more complex than I would have thought.
Also, whether or not treating sleep apnea actually makes it easier for patients to lose weight (if they get adequate obesity treatment) remains to be seen.
Given that untreated sleep apnea negatively affects restorative sleep, which in turn affects both metabolism and appetite, it may well be that sleep apnea is an important barrier to weight loss.
This is exactly what is suggested in a recent study by Whited and colleagues, published in Health Psychology.
The researchers conducted a secondary analysis of a 12 month randomized trial comparing 2 weight loss interventions consisting of dietary counseling for adults with obesity and metabolic syndrome.
Subjects who screened positive for high risk of sleep apnea using the STOP questionnaire (about 50% of the 175 participants), lost less weight (1.2% vs. 4.2%) and were less likely to lose 5% or greater (24% vs. 75%) than participants without risk for sleep apnea.
Thus, the authors conclude that,
“…an OSA screening indicating high risk identifies individuals who will struggle to lose weight when participating in a weight loss intervention, despite equal attendance at treatment sessions and study assessments. Findings of this study suggest that OSA is a significant barrier to weight loss.”
Whether or not treating sleep apnea makes weight loss any easier, the authors have this to offer:
“Although we found that participants reporting current OSA treatment had greater weight loss (6.5% vs. 0.6%), the small sample of individuals receiving OSA treatment (n = 24) precluded statistical comparison.”
“OSA screening as a standard component of weight loss interventions has a high potential for usefulness, as identified individuals can be targeted for more intense or comprehensive treatment. The benefits of OSA treatment as a standard part of weight loss interventions among individuals with obesity and metabolic syndrome has yet to be determined, and future research must include examination of adherence to both OSA and weight loss intervention components.”
However, there is no easy way to measure fitness short of standardized exercise testing, both cumbersome and unpractical in a clinical setting.
Now, a paper by Joshua Denham and Priscilla Presetes, published in Frontiers in Genetics, suggests that muscle-enriched microRNAs (miRNAs) measured in whole blood may provide a sensitive blood test for physical fitness.
MiRNAs are genetically conserved, small (18–25 nucleotides), non-coding RNA molecules that post-transcriptionally control gene expression by either promoting mRNA degradation or down-regulating translation. There are over 2,500 known human mature miRNAs and each one can have hundreds of mRNA targets, making them powerful regulators of gene expression.
miRNAs are sensitive to the internal and external environments and it is therefore likely that circulating miRNAs isolated from the peripheral vasculature could serve as biomarkers of disease (and health).
In their study, the researchers examined the effect of long-term strenuous aerobic exercise training and a single bout of maximal aerobic exercise on five muscle-enriched miRNAs implicated in exercise adaptations (miR-1, miR-133a, miR-181a, miR-486, and miR-494).
They also determined linear correlations between miRNAs, resting heart rate, and maximum oxygen uptake in endurance athletes compared to non athletes.
Specific miRNAs were increased in athletes compared to non-athletes and there was a positive correlations between miRNA abundance and O2 max and resting heart rate.
Thus, the authors suggest that muscle-enriched miRNAs isolated from whole blood are regulated by acute and long-term aerobic exercise training and could serve as biomarkers of cardiorespiratory fitness.
Whether this would ever make it into a simple blood test for fitness remains to be seen.
Now, a paper by Ari Schechter and colleagues from Columbia University, NY, published in Physiology and Behaviour, publish data from a small ‘pilot study’ suggesting that treating obesity with CPAP may reduce calorie intake, at least in some individuals.
The researchers examined ad libitum energy intake in four adult males with overweight or obesity, who had been diagnosed with sleep apnea but had not yet initiated CPAP.
After participants began using CPAP at their titrated setting (active) at home each night for 2 mo, they were invited to participate in this study for two days in an in patient setting.
On the first inpatient day, participants were fed a controlled weight maintenance diet with fixed meal times and participants were asked to use CPAP at their prescribed setting during the scheduled in-lab sleep episode (23:00–7:00).
Ad libitum energy intake was measured throughout the waking period on laboratory day 2, whereby all meals were presented in excess. Participants were instructed to eat until they felt comfortably full.
After a 1-mo washout, participants crossed over into the sham phase. Participants were provided with the sham CPAP devices, and instructed to use the CPAP at the titrated level for 2 mo. This was followed by the second laboratory period (repeat of first phase). After the second phase, participants were debriefed and instructed to return to active CPAP.
Mean total ad libitum EI including fixed meals and free snacks was 3744 ± 511 kcal in the active and 4030 ± 228 kcal in the sham CPAP setting. Three of the four participants increased their total daily EI during sham vs. active, whereas one participant showed a decrease.
While these findings are far from conclusive, they do point to the possibility that ongoing treatment of sleep apnea may influence appetite in a way that serves to reduce energy intake.
This is perhaps not all that surprising given that there is increasing recognition of the importance of restorative sleep on appetite and food intake.
I look forward to seeing more definitive studies exploring this interesting issue.
I would also be interested in hearing is anyone else has experience changes in appetite with starting CPAP treatment for sleep apnea.
Now, the International Federation for the Surgery of Obesity and Metabolic Disorders (IFSO), has published a new Position Statement on indications for surgery for obesity and weight-related diseases, published in Obesity Surgery.
Recommendations are graded based on the strength of the current evidence.
Recommendations with the highest strength of evidence include the following:
- Surgery for obesity and weight-related diseases is a codified discipline that has proven to be effective in the treatment of obesity resulting in long-term weight loss, improvement in or resolution of comorbidities, and the lengthening of life expectancy. (Level of evidence 1, grade of recommendation A)
- Surgery for obesity and weight-related diseases is a safe and effective therapeutic option for the management of T2DM in patients with obesity. Along with optimal medical treatment and lifestyle adjustment, it has been demon- strated that surgery for obesity and weight-related diseases can achieve a better glycemic control, lower glyco- sylated hemoglobin, and reduction of diabetes medications than optimal medical and lifestyle treatment alone. (Level of evidence 1, grade of recommendation A)
- Surgery for obesity and weight-related diseases demonstrated an excellent short- and midterm risk/benefit ratio in patients with class I obesity (BMI 30–35 kg/m2) suffering from T2DM and/or other comorbidities.
(Level of evidence 1, grade of recommendation A)
- Obesity, and visceral obesity in particular, is a major modifiable risk factor for cardiovascular diseases (CVD). Weight loss induced by surgery has been shown to reduce CVD risk, with the most relevant reductions in risk ob- served in the group of patients having the higher CVD risk before surgery. These patients obtain the most significant metabolic improvements thereafter. (Level of evidence 1, grade of recommendation A)
- Weight loss induced by surgery for obesity and weight- related diseases is associated to a reduction in the inci- dence of major cardiovascular events in patients with obesity, including myocardial infarction and stroke. Event reductions are more relevant in patients with a high cardiovascular risk before surgery. (Level of evidence 1, grade of recommendation A)
- Surgery for obesity and weight-related diseases may result in resolution/improvement of obstructive sleep apnea syndrome (OSAS). (Level of evidence 1, grade of recommendation A)
- In patients undergoing surgery for obesity and weight- related diseases, weight loss results in a substantial im- provement in pain and a reduction of disability derived from joint disease. (Level of evidence 1, grade of recommendation A)
- Surgery for obesity and weight-related diseases has proven to be effective in determining the overall improvement of the quality of life of patients suffering from obesity. (Level of evidence 1, grade of recommendation A)
- The improvement in the quality of life of the patient with obesity treated by surgery for obesity and weight-related diseases is independent from the type of performed procedure. (Level of evidence 1, grade of recommendation A)
- Surgery for obesity and weight-related diseases is effective in patients with class I obesity (BMI 30–35 kg/m2) and comorbidity. (Level of evidence 1, grade of recommendation A)
In addition, there are numerous recommendations, for which the evidence is perhaps less robust but nevertheless promising.
These recommendations cover a wide range of health issues including gastroesophageal reflux disease (GERD), hepatobiliary diseases, mental health, endocrinopathies and fertility, cancer and organ transplantation, pseudotumor cerebri, chronic inflammation, urinary tract and renal function, functional status, and quality of life.
I was particularly pleased to see the statement include recommendations regarding the limitations of BMI and an extensive discussion of the Edmonton Obesity Staging System as a potential guide to better defining indications for surgery.
Behavioural interventions (generally aimed at reducing caloric intake and/or increasing expenditure) are notoriously unsuccessful as a strategy for sustainable weight loss in the vast majority of people (at any weight).
For the few, who do succeed (and the word “succeed” is used here rather loosely), it takes nothing short of constant (daily) diligence and ongoing determination to make it work – any reduction in effort is immediately “punished” by weight regain – even after years of successful weight-loss maintenance.
Yet, the scientific literature abounds with study after study after study with one behavioural strategy (diets are behaviours!) after the next to try and achieve the almost impossible – sustainable weight loss.
The simple reason why behavioural measures fail is because they are up against a powerful array of neuroendocrine defences that our bodies can harness to effectively sabotage our efforts.
Any time we try to wander off into negative energy balance, our bodies instantly respond with opposing increases in appetite and reduction in energy expenditure to defend and restore energy stores.
That is simply the reality of human (=animal) physiology.
However, this does not mean that behavioural interventions in obesity management are useless.
Indeed, if behaviours are causing weight gain, then changing those behaviours is in fact the first step in addressing ongoing weight gain.
So, if drinking two litres of sugary pop a day or eating most of your food out of boxes is contributing to your weight gain, then changing your diet can stop the gain.
If sitting at your desk (or on your couch) all day is contributing to your weight gain, then increasing your activity levels can stop the gain.
The critical part of the preceding two sentences is “stop the gain”.
When you identify and address the cause of weight gain, you do not automatically get weight loss – you do, however, stop the gain.
If not having breakfast contributes to your overeating (as it may well do in some individuals), then having breakfast may help you stop the gain – it does not necessarily mean that having breakfast will get you weight loss.
Thus, while I expect to see better weight control with regular breakfasts in someone who is actively gaining weight, I do not expect to see weight loss in someone who is weight stable (even if they just eat once a day).
Similarly, if binge eating disorder is contributing to ongoing weight gain, then successful treatment of that disorder should prevent further weight gain – it does not automatically reverse the process and lower your body weight.
Yes, there are behaviours that can make maintenance of weight loss more manageable – like regular weighing, keeping a food diary, managing hunger, mindfulness, etc. but by themselves, these behaviours will rarely result in significant sustainable weight loss in most people.
Can healthy behaviours improve health at any weight – of course they can!
Can healthy behaviours limit further weight gain – of course they can!
Can healthy behaviours result in significant sustainable weight loss – in some people perhaps?
Let us stop overselling behavioural interventions as a “treatment” for obesity, when in real-life, they are supportive at best.
That doesn’t make behavioural interventions any less valuable – patients can sure use all the support they can get.