Continuing in my miniseries on arguments in favour of calling obesity (defined as excess or abnormal fat tissue that impairs health) a disease, I turn to the perhaps most important reason of all – access to care.
Currently, few health care systems feel obliged to provide individuals presenting with obesity treatment for their condition (beyond a few words of caution and simplistic advise to simply eat less and move more).
Most health plans do not cover treatments for obesity, arguing that this is simply a lifestyle issue.
In some countries (e.g. Germany), health insurance and health benefit plans are expressly forbidden by law to cover medical treatments for obesity.
Although long established as the only evidence-based effective long-term treatment for severe obesity, many jurisdictions continue to woefully underprovide access to bariatric surgery, with currently less than 4 out of 1,000 eligible patients receiving surgery per year in Canada.
Pretty much all of this can be blamed on one issue alone – the notion that obesity is simply a matter or personal choice and can be remediated by simple lifestyle change.
Declaring obesity a disease can potentially change all of this.
As a disease in its own right, health care systems can no longer refuse to provide treatments for this condition.
In the same manner that no health system or insurance plan can refuse to cover treatments for diabetes or hypertension, no health system or insurance plan should be able to deny coverage for treatments for obesity.
As a chronic disease, obesity care must now be firmly integrated into chronic disease management programs, in the same manner that these programs provide services to patients with other chronic diseases.
How long will it take before this becomes accepted practice and funding for obesity treatments rises to the level of funding currently available for treating other chronic diseases?
That, is anyone’s guess, but no doubt, declaring obesity a disease finally puts patients living with this condition on an equal footing with patients living with any other chronic disease.
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.
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.
As this year’s Congress President, together with World Obesity Federation President Dr. Walmir Coutinho, it will be our pleasure to welcome delegates from around the world to what I am certain will be a most exciting and memorable event in one of the world’s most beautiful and livable cities.
The program committee, under the excellent leadership of Dr. Paul Trayhurn, has assembled a broad and stimulating program featuring the latest in obesity research ranging from basic science to prevention and management.
I can also attest to the fact that the committed staff both at the World Obesity Federation and the Canadian Obesity Network have put in countless hours to ensure that delegates have a smooth and stimulating conference.
The scientific program is divided into six tracks:
Track 1: From genes to cells
- For example: genetics, metagenomics, epigenetics, regulation of mRNA and non–coding RNA, inflammation, lipids, mitochondria and cellular organelles, stem cells, signal transduction, white, brite and brown adipocytes
Track 2: From cells to integrative biology
- For example: neurobiology, appetite and feeding, energy balance, thermogenesis, inflammation and immunity, adipokines, hormones, circadian rhythms, crosstalk, nutrient sensing, signal transduction, tissue plasticity, fetal programming, metabolism, gut microbiome
Track 3: Determinants, assessments and consequences
- For example: assessment and measurement issues, nutrition, physical activity, modifiable risk behaviours, sleep, DoHAD, gut microbiome, Healthy obese, gender differences, biomarkers, body composition, fat distribution, diabetes, cancer, NAFLD, OSA, cardiovascular disease, osteoarthritis, mental health, stigma
Track 4: Clinical management
- For example: diet, exercise, behaviour therapies, psychology, sleep, VLEDs, pharmacotherapy, multidisciplinary therapy, bariatric surgery, new devices, e-technology, biomarkers, cost effectiveness, health services delivery, equity, personalised medicine
Track 5: Populations and population health
- For example: equity, pre natal and early nutrition, epidemiology, inequalities, marketing, workplace, school, role of industry, social determinants, population assessments, regional and ethnic differences, built environment, food environment, economics
Track 6: Actions, interventions and policies
- For example: health promotion, primary prevention, interventions in different settings, health systems and services, e-technology, marketing, economics (pricing, taxation, distribution, subsidy), environmental issues, government actions, stakeholder and industry issues, ethical issues
I look forward to welcoming my friends and colleagues from around the world to what will be a very busy couple of days.
For more information on the International Congress on Obesity click here
For more information on the World Obesity Federation click here
For more information on the Canadian Obesity Network click here
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