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.
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.
Exposure to endocrine disrupters in humans included our diets, personal care products, antimicrobial soaps, household or agricultural pesticides, and cleaning products.
Now, the Endocrine Society has produced its second Scientific Statement on environmental endocrine-disrupting chemicals (EDC-2), published in Endocrine Reviews. (a summary appears in JAMA Internal Medicine)
The major EDC classes reviewed were industrial chemicals (polychlorinated biphenyls [PCBs], dioxins), pesticides, plastics and plasticizers (bisphenol A [BPA] and phthalates), perfluorinated compounds, and flame retardants.
As for the relationship between ECDs and obesity, the authors summarize:
“In animals, several EDCs now referred to as obesogens and diabetogens were associated with obesity and DM2, respectively, with results dependent on the chemical, dosage, and age of exposure. The evidence is strongest for tributyltin, persistent organic pollutants (POPs), pesticides, and BPA. Some EDCs exert actions on adipogenesis, or on pancreatic β- and α-cells. Developmental EDC exposures also led to insulin resistance and hyperinsulinemia and were associated with alterations in serum adiponectin and leptin. Although the mechanisms varied, they included effects mediated via the aryl hydrocarbon receptor, peroxisome proliferator-activated receptor γ (PPARγ), and estrogen receptors (ERs). Furthermore, limited evidence suggests that the hypothalamic control of energy balance may be perturbed. Cross-sectional epidemiological data showed associations between EDCs, obesity, and/or DM2, although causality cannot be inferred. Less is known about EDCs and cardiovascular disease, but emerging work suggests that this merits further research.”
I have little doubt that both exposure and susceptibly varies widely between individuals, however there are currently no tests that would allow us to discern the contribution of ECDs to obesity in a given individual.
Thus, while the magnitude of the contribution of ECDs to any given person’s weight problem may be hard to diagnose and even harder to manage, the findings do remind us that the environmental drivers of obesity may well go beyond just our foodscape and sedentariness.
Free access to the Executive Summary of the Statement is available here
Every two years the Canadian Obesity Network holds its National Obesity Summit – the only national obesity meeting in Canada covering all aspects of obesity – from basic and population science to prevention and health promotion to clinical management and health policy.
Anyone who has been to one of the past four Summits has experienced the cross-disciplinary networking and breaking down of silos (the Network takes networking very seriously).
Of all the scientific meetings I go to around the world, none has quite the informal and personal feel of the Canadian Obesity Summit – despite all differences in interests and backgrounds, everyone who attends is part of the same community – working on different pieces of the puzzle that only makes sense when it all fits together in the end.
The 5th Canadian Obesity Summit will be held at the Banff Springs Hotel in Banff National Park, a UNESCO World Heritage Site, located in the heart of the Canadian Rockies (which in itself should make it worth attending the summit), April 25-29, 2017.
Yesterday, the call went out for abstracts and workshops – the latter an opportunity for a wide range of special interest groups to meet and discuss their findings (the last Summit featured over 20 separate workshops – perhaps a tad too many, which is why the program committee will be far more selective this time around).
So here is what the program committee is looking for:
- Basic science – cellular, molecular, physiological or neuronal related aspects of obesity
- Epidemiology – epidemiological techniques/methods to address obesity related questions in populations studies
- Prevention of obesity and health promotion interventions – research targeting different populations, settings, and intervention levels (e.g. community-based, school, workplace, health systems, and policy)
- Weight bias and weight-based discrimination – including prevalence studies as well as interventions to reduce weight bias and weight-based discrimination; both qualitative and quantitative studies
- Pregnancy and maternal health – studies across clinical, health services and population health themes
- Childhood and adolescent obesity – research conducted with children and or adolescents and reports on the correlates, causes and consequences of pediatric obesity as well as interventions for treatment and prevention.
- Obesity in adults and older adults – prevalence studies and interventions to address obesity in these populations
- Health services and policy research – reaserch addressing issues related to obesity management services which idenitfy the most effective ways to organize, manage, finance, and deliver high quality are, reduce medical errors or improve patient safety
- Bariatric surgery – issues that are relevant to metabolic or weight loss surgery
- Clinical management – clinical management of overweight and obesity across the life span (infants through to older adults) including interventions for prevention and treatment of obesity and weight-related comorbidities
- Rehabilitation – investigations that explore opportunities for engagement in meaningful and health-building occupations for people with obesity
- Diversity – studies that are relevant to diverse or underrepresented populations
- eHealth/mHealth – research that incorporates social media, internet and/or mobile devices in prevention and treatment
- Cancer – research relevant to obesity and cancer
…..and of course anything else related to obesity.
Deadline for submission is October 24, 2016
To submit an abstract or workshop – click here
For more information on the 5th Canadian Obesity Summit – click here
For sponsorship opportunities – click here
Looking forward to seeing you in Banff next year!
It is now well established that the almost non-existant rates of long-term weight loss are not because of lack of will power or lack of motivation. Rather, they are firmly embedded in human (and animal) physiology, that is designed to defend body weight at all costs through complex neuroendocrine homeostatic mechanisms that will eventually wear out even the staunchest dieter.
But just how strong is the physiological drive to defend and regain lost body weight? Or even more specifically, how much does an increase in appetite counteract weight loss?
This is the topic of a paper by David Polidori and colleagues, prepublished on bioRxiv*.
The researchers use data from a 52-week trial of canagliflozin, a sodium glucose co-transporter (SGLT2) inhibitor leads to a urinary glucose loss of approximately 90 g/day throughout the duration of treatment.
This amounts to a net daily energy loss of ~360 kcal/day that occurs without directly altering central pathways controlling energy intake and without the patients being directly aware of the energy deficit.
Based on the observed changes in body weight over time, the researchers used a validated mathematical method to calculate changes in daily energy intake using principles from engineering control theory.
The complex mathematical formula takes into account a wide range of parameters including changes in the energy expenditure rate and density of fat and fat-free mass, energy cost of fat and protein turnover, dietary and adaptive thermogenesis as well as changes in physical activity (no change in physical activity was assumed in this study).
Subjects in the treatment arm showed the typical initial weight loss (of about 5 Kg) followed by the maintenance of a weight-loss plateau throughout the remainder of the study, a pattern which, in light of a continuing daily energy loss of about 360 kcal is consistent with a proportional feedback control system that serves to limit the amount of weight loss and creates a drive towards weight regain (think of this as the tension that counteracts a steady pull on a rubber band).
Based on their calculations, the amount of daily increase in caloric intake required to maintain the weight loss plateau (rather than continuing to lose weight), was in the order of about 100 Kg/day per Kg weight loss. This is substantially more than the reduction in metabolic rate generally seen with weight loss (of about 10-20% of body weight) is only about 30 kcal/day per Kg weight loss).
When applying these finding to the typical weight-loss curve seen in the usual commercial weight loss programs (an initial weight loss followed by gradual weight regain), the researchers show that the difference between the homeostatic drive to eat and the actual energy intake, a quantitative index of the ongoing effort to sustain the intervention in the face of the continuing biological signals to overeat, requires that subjects have to demonstrate a persistent effort to avoid overeating above baseline during the intervention even when the average energy intake returns to near baseline levels.
“…homeostatic feedback control of energy intake is likely a primary reason why it is so difficult to achieve large sustained weight losses in patients with obesity. Rather, weight regain is typical in the absence of heroic and vigilant efforts to maintain behavior changes in the face of an omnipresent obesogenic environment. Unfortunately, there is no evidence that the energy intake feedback control system resets or relaxes with prolonged maintenance of lost weight – an effect similar to the long-term persistent suppression of energy expenditure in weight-reduced humans. Therefore, the effort associated with a weight loss intervention persists until either body weight is fully regained or energy intake increases above baseline to match the homeostatic drive to eat.”