Today is officially World Obesity. As pointed out in the 252-page OECD report on “The Heavy Burden of Obesity: The Economics of Prevention”, Canada, like most OECD countries is not doing a great job at it (nor are others!). This leaves us with the fact that there are currently well over 6 million Canadian adults and children living with what the World Obesity Federation (and the Canadian Medical Association) calls a complex chronic disease.
So what is obesity and what does obesity care look like from the perspective of Canadians living with obesity (PwO), health care providers (HCPs), and employers? This is the topic of the Canadian ACTION Study, released today by Obesity Canada.
Conducted as a nationally representative survey, the ACTION study reveals that although people living with obesity, health care providers, and employers all agree that obesity is a significant health problem (on par with heart disease, diabetes, or even cancer), their views vastly differ when it comes to what to do about it.
Responses to the survey also suggest that people with obesity, health care providers and employers don’t fully understand the complexity of obesity, and believe that, contrary to current research findings, diet and exercise are sufficient approaches to managing it.
Based on the findings of the report, Obesity Canada makes the following recommendations:
For People Living with Obesity:
- Learn evidence about obesity causes and treatments and understand that obesity management is a lifelong process that requires medical intervention.
- Find health professionals who have been trained in obesity management.
- Self-advocate for support and access to treatments and supports with Obesity Canada’s online resources.
For Health Care Providers:
- Understand recent research supporting obesity’s complex etiology and heterogeneity.
- Learn more about current evidence-based approaches to treating obesity (see Obesity Canada website).
- Treat obesity as a chronic disease using available treatments (new Clinical Practice Guidelines available in 2020).
- Include obesity in the training program curricula for health professionals.
- Treat obesity as a chronic disease and move obesity out of the lifestyle category in bene ts plans.
- Offer meaningful obesity services/coverage that move beyond healthy eating and exercise programs.
This week I am speaking at the LATAM Obesity Summit in Santaigo, Chile, where I again had occasion to hearing my Canadian colleague Michael Vallis (Halifax), speak about behavioural change.
In his talk, he discussed an important strategy in counselling patients, whch he referred to as the “limbic dump”. As readers will know, the limbic system is responsible for holding our emotions – anxiety, fear, apprehension, disappointment, frustration, but also, joy, optimism, anticipation, motivation.
In a classical doctor-patient encounter, the doctor generally focusses on analysing the problem (making the diagnosis) and giving advice (providing treatment) – both are functions that largely rely on the cognitive or “logical” part of our brains. The general idea is that, the doctor will provide rational information and advice to the patient, and the rational part of the patient’s brain will take in this advice and “follow instructions”.
Unfortunately, in most situations, this “rational” approach is overriden by the limbic or “emotional” part of the patient’s brain, which is far too busy dealing with feelings (shame, fear, anxiety, disappointment, frustration, etc.) to take in the “rational” information that is being provided.
This is where the “limbic dump” comes in. As Vallis points out, before getting into the “rational” part of any encounter, it is far more useful to begin by allowing the patient to first “dump” their concerns (or successes) on the table. Once these are out in the open, have been duly acknowledged, and discussed, the conversation can move on to the more “logical” transactional part of the encounter. Now, after the “limbic dump” you actually have a patient who is able to listen to what you have to say.
Of course, all experienced clinicians probably already know this. I, for one, generally start any patient encounter with an open ended question as to how the patient is feeling about how things are going. This gives them the opportunity to “dump” their feelings on the table – positive or negative. Only after acknowledging these (sometimes prompting them for details), do we move on to the more objective part of the encounter (I’m a big believer in motivational interviewing, so generally, I let my patients do most of the talking).
Now, thanks to Vallis, I have an explanation and term for what I have been doing all along – long-live the “limbic dump”.
For the past 10 years, I have had the rather exclusive privilege of being on the External Advisory Board (which I have chaired for the past five years) of the Integrated Research and Treatment Center (IFB) AdiposityDiseases, a multi-million Euro a joint research and clinical center of the University and the University Hospital Leipzig – sponsored by the German Federal Ministry of Education and Research. This funding period has now come to term (although obesity research will remain alive and kicking in Leipzig) and the 2nd International Symposium on Obesity Mechanisms, marks an important celebration of this milestone.
The three-day symposium, at which I will be presenting the Key Note Lecture, is held in collaboration with the DFG-funded SFB1052 and focuses on central obesity mechanisms, brain periphery crosstalk, adipose tissue heterogeneity, adipokines, and the clinical consequences of obesity.
The findings and publications emanating from this research consortium over the past decade are far too numerous to mention in this post (publications appeared in the New England Journal of Medicine, The Lancet, Cell, Nature, Nature Medicine, and other top international journals).
As Matthias Blüher remarked in his opening address, many of these findings are now finding their way into translational research, including the testing of novel anti-obesity compounds and behavioural interventions based on findings from neuroimaging studies.
I, for one, have very much enjoyed being associated with these important efforts here in Leipzig and look forward to continuing involvement in the exciting work that continues to advance our understanding of this complex chronic disease.
This morning, I spoke at the German Diabetes Congress in Berlin on the issue of whether or not metabolic surgery offers a cure (or just remission) in patients with type 2 diabetes.
I also had the pleasure of attending the Hans Langerhans Award Lecture, the highest distinction awarded by the German Diabetes Society, given by my colleague Matthias Tschöp, who is also the Director of the Helmholtz Centre for Diabetes Research in Munich.
Tschöp focussed his acceptance speech on his ground-breaking work on polyagonists, i.e. molecules that can co-stimulate two or more peptide receptors (e.g. for GLP-1, GIP, and glucagon).
Tschöp began his presentation by declaring that we could almost completely reverse the global epidemic of type 2 diabetes, if only we had more effective treatments for obesity.
As we now know, appetite and energy regulation is tightly controlled by a host of neuroendocrine signals, which act on the central nervous system as part of a complex homeostatic system that acts to sustain and defend body weight.
Based on these findings, Tschöp’s work has pursued the notion that effective obesity treatments require targeting of the homeostatic centres in the brain. As we have learnt from the extensive research on bariatric surgery, there are a number of signal molecules released by the gut (incretins) that directly affect central mechanism of appetite and satiety.
However, given the complexity and redundancy of the system, just targeting one of these molecules may not be effective enough to counteract the powerful mechanisms that defend against long-term weight loss. This insight, led Tschöp to pursue the idea that developing single synthetic molecules, that could simultaneously stimulate several distinct but synergistic pathways, may prove to be more effective than targeting a single molecular target.
This idea, ultimately led to the development of molecules that simultaneously act as dual co-agonists (e.g. for GLP-1 and glucagon or for GLP-1 and GIP ) or even tri-co-agonists (e.g. for GLP-1, GIP, and glucagon). These co-agonists appear to have potent metabolic and anti-obesity effects both in animal models and in early human studies. Indeed, this approach is now being actively pursued by a number of pharmaceutical companies hoping for more effective anti-obesity medications.
While these studies are currently underway, they certainly hold great promise for the future of medical treatments for obesity and diabetes.
Congratulations to Matthias Tschöp and his team for this most well-deserved award.
p.s. As an aside, I will have the pleasure of playing guitar with the “Sugar Daddies”, featuring Matthias Tschöp on drums (along with other prominent German diabetes researchers) at the Diabetes Gala Evening this evening.
Given that our efforts to stop the childhood obesity have so far yet to show any signs of success and that treatment efforts of kids already struggling with excess weight have been sketchy at best, there is unfortunately a growing number of adolescents living with severe obesity, for who we have very little choice but to consider bariatric surgery.
As drastic as surgery may seem, it is important to recognise that for adolescents weighing in at 250 lbs or more, waiting and hoping for obesity to spontaneously resolve, while these kids miss out on opportunities ranging from education to social relationships (never mind the bullying and discrimination), is hardly an acceptable option.
Thus, a study by Thomas Inge and colleagues published in the New England Journal of Medicine, showing that 5-year outcomes of adolescents undergoing bariatric surgery are as positive as in (most) adults, is heartening.
The study looks at 5-year outcomes in 161 adolescent patients enrolled from 2006 through 2012) and a cohort of adults (396 patients enrolled from 2006 through 2009) undergoing Roux-en Y gastric bypass surgery.
Overall, the extent of weight loss 5 years after surgery in the adolescents (-26%) was similar to that in adults (-29%). Adolescents were significantly more likely than adults to have remission of type 2 diabetes (86% vs. 53%) and of hypertension (68% vs. 41%).
Three adolescents (1.9%) and seven adults (1.8%) died in the 5 years after surgery. In the adolescent cohort, one death was attributed to suspected sepsis in a patient with type 1 diabetes who had multiple complications after a hypoglycemic episode 3 years after surgery, and features of the other two deaths in adolescents, both of which occurred 4 years after surgery, were consistent with overdose (acute combined drug toxicity). Among the adults, three died of early complications of surgery, one died of colon cancer, one of suicide, and the cause of death in the two remaining cases was unclear.
Adolescents experienced a greater rate of abdominal reoperations than the adults (19 vs. 10 reoperations per 500 person-years). As a possible explanation for this, the authors offer: “…closer monitoring for complications in adolescent patients and the potential for a lower threshold to reoperate for suspected complications in younger patients, which would lead to the capture of more events.” Nutritional deficiencies were slightly more common in adolescents compared to adults, which the authors attribute to less compliance with recommended nutritional supplements.
While 5-years of follow up may not seem particularly long, it is important to note that this occurs at a critical stage of development for adolescents and can potentially change the life-trajectories of these kids. Nevertheless, decisions to proceed with bariatric surgery in adolescents should be made on a case-by-case basis, carefully weighing the pros and cons for each case.
Regular readers will be well aware of the limitations of applying BMI to obesity diagnosis – after all, BMI is a measure of size, not health. If there is one thing we have learnt, it is that good health is possible over a wide range of shapes and sizes and that using a static measure like BMI, will mean overdiagnosing obesity in people who have no relevant impairment in health and underdiagnosing obesity in people who would in fact stand to gain from obesity treatments.
As I have noted before, in a medical context, obesity should be defined as, “the presence of excess or abnormal fat tissue that impairs health“. In clinical practice this would mean asking the question (irrespective of BMI), “does this patient have a health impairment that is likely to get better with obesity treatment?” If yes, the patient most likely has obesity and should be offered obesity treatment. If not, the patient does not have obesity and will be unlikely to benefit from obesity treatment.
This approach would identify both the “high-BMI” individuals with medical issues likely to get better with obesity treatment, as well as the “normal-BMI” individual, who may stand to benefit from obesity management.
Not only will this “common-sense” approach to diagnosing obesity identify individuals over the entire BMI range, who would potentially benefit from obesity treatments, but will also help set specific targets for assessing the success of treatment.
Thus, if the presenting problem is hypertension (say in a patient with a BMI of 24 with clear signs of increased belly fat – but skinny arms and legs), then the goal of obesity treatment would be to lower blood pressure, rather than to simply reduce body weight. Similarly, a patient with a BMI of 24 with type 2 diabetes would likely benefit from obesity management in terms of better diabetes control. If, in these patients, effective obesity treatment (as measured by weight loss) does not lead to better hypertension or diabetes control, then their health issues are probably not related to their body fat, meaning that they probably don’t have obesity.
Thus, the obesity diagnosis and management algorithm would look something as follows:
Does the patient have any impairments in health likely to improve with obesity treatment? (list impairment/s)
if no, patient does not have obesity and does not need any obesity intervention (irrespective of BMI).
If yes, offer obesity treatment to see if this improves the health issues.
If health condition improves, continue obesity management.
If health condition does not improve, reconsider the obesity diagnosis (problem may be entirely unrelated to body fat). discontinue obesity treatment.
Basically, BMI, or for that matter body weight, does not have to enter the equation. The only thing that matters, is whether or not the presenting health problem actually responds to obesity treatment or not.
Fortunately, we have a long list of health issues that we know will improve with obesity treatment (e.g. hypertension, type 2 diabetes, sleep apnea, psoriasis, musculoskeletal pain, knee osteoarthritis, PCOS, etc. etc.), thus making clinical assessment of whether or not someone may have obesity relatively straightforward. Considering obesity treatments to better manage these conditions makes a lot of sense. On the other hand, treating obesity simply to lower body weight (without any measurable health benefits) does not.
As any clinician knows, changes in appetite are an important part of taking a good medical history. While loss of appetite is generally a warning sign that your patient may be seriously ill (sometimes, loss of appetite is the first sign of an illness – physical or mental), an increase in appetite may likewise indicate a serious problem.
In order to assess whether the reported change in appetite is clinically relevant, it is important to follow any appetite question with a “weight change” question. Thus, if a patient reports loss of appetite, an obvious follow-up question would be to ask whether the patient has lost weight. In contrast, if the patient reports an increase in appetite, it is only fair to ask if this has been associated with weight gain. In fact, even if the patient says that their appetite has not changed, it would be fair to ask if their weight has been stable.
While some patients (and clinicians) may be wary of bringing up the issue of weight, no patient in my experience has ever objected to being asked about their appetite. In addition, no patient has ever objected to being asked a weight question after first being asked about their appetite.
Thus, in my experience, the easiest way to start a conversation about body weight, is to begin by asking about appetite.
A typical conversation could run as follows:
Clinician, “So have you notice any change in appetite?“
Patient, “Funny you should ask, yes, I seem to be particularly hungry after dinner, I often have to eat a sandwich before I go to bed“
Clinician: “So have you noticed any change in your weight?“
Patient: “Well, I think I may have gained a few pounds since I last saw you“
Clinician: “Is that something that concerns you, something you’d like to talk about?“
Obviously, the tone of this conversation needs to be completely non-judgemental and if the patient is not interested or willing to talk about this issue, we can always park this discussion for later.
In any case, if you’ve ever wondered how to start a discussion about body weight with a patient, try first talking about appetite. As a mnemonic, I call this the A&W (Appetite & Weight) approach to discussing body weight.
Can Exercise-Induced Modulation of the Tumor Physiologic Microenvironment Improve Antitumor Immunity?
Both obesity and sedentariness have been linked to increased risk for a wide range of cancers. While there is some evidence that weight loss (e.g. through bariatric surgery) can reduce the incidence of and deaths from malignancies, the role of exercise on cancer morbidity and mortality is less clear. Although a growing body of literature suggests that increased physical activity can reduce the mental and physical stress of living with cancer, its role in directly influencing the malignant process is less clear.
Now, a paper by Xiaojie Zhang and colleagues, published in Cancer Research, discusses the many ways in which exercise may potentially promote the body’s ability to fight cancer by modulating the tumor microenviroment.
As the authors point out, “Preclinical and human studies suggest that exercise elicits mobilization of leukocytes into circulation (also known as “exercise-induced leukocytosis”), especially cytotoxic T cells and natural killer cells. However, the tumor physiologic microenvironment presents a significant barrier for these cells to enter the tumor and, once there, properly function.“
Among the mechanisms by which exercise can alter immunological response to tumors, the authors include positive changes to the tumor microvasculature as well as the tumor microenviroment including decreased hypoxia, hypoglucosis, lactosis, and reduced pH. For each of these potential mechanisms (that are likely to work in concert), the authors discuss current evidence from animal models that would support these potentially beneficial effects of exercise.
While we have yet to see a definitive controlled study on the long-tem benefits of exercise treatments on cancer survival (and not just rehabilitation and well-being), the authors make a strong case that such studies are perhaps long overdue. In addition, “Rigorous studies that elucidate the link between exercise and immune cell function in the tumor microenvironment and in the periphery will also serve as a guide of how to implement exercise in the context of immunotherapies that harness the immune system against cancer. ”