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
Much of the research on the contribution of screen time, sedentariness, food consumption and other factors comes from cross-sectional or longitudinal studies, where researchers essentially describe correlations and statistical “effect sizes”.
To be at all meaningful, analyses in such studies need to be adjusted for known (or at least likely) confounders (or at least the confounders that happen to available).
No matter how you turn and wind the data, such studies by definition cannot prove causality or (even less likely) predict the outcome of actual intervention studies.
Nevertheless, such studies can be helpful in generating hypotheses.
Thus, for example, I read with interest the recent paper by Lei Shang and colleagues from the University of Laval, Quebec, Canada, published in Preventive Medicine Reports.
The researchers looked at cross-sectional data on 630 Canadian children aged 8-10 years with at least one obese biological parent.
While the overall median daily screen time was about 2.2 hours, longer screen time was associated with higher intake of energy (74 kcal) and lower intake of vegetables & fruit (- 0.3 serving/1000 kcal).
This unhealthy “effect” of screen time on diet appeared even stronger among children with overweight.
Thus, there is no doubt that the study shows that,
“Screen time is associated with less desirable food choices, particularly in overweight children.”
The question of course remains whether or not this relationship is actual causal or in other words, does watching more television lead to an unhealthier diet (I am guessing no one assumes that eating an unhealthier diet leads to more TV watching).
Unfortunately, this is not a question that can be answered by this type of research.
Nor, is this type of research likely to predict whether or not reducing screen time will get the kids to eat better.
Indeed, it doesn’t take a lot of imagination to come up with other explanations for these findings that would not require any assumption of a causal link between eating behaviours and television watching.
For one, TV watching could simply be a surrogate measure for parenting style – perhaps parents that let their kids watch a lot of TV are also less concerned about the food they eat.
And, for all we know, reducing TV time may (e.g. by cutting the kids off from TV – or cutting the parents off from a convenient babysitter) in the end make the kids eating behaviours even worse.
Who knows – that’s exactly the point – who knows?
To be fair, the authors are entirely aware of the limitations of such studies:
“This study was cross-sectional, so no causal inference could be made and the possible mechanism is not clear. Although our data collection strictly followed the detailed manual procedure to guarantee the quality control (QUALITY Cohort Technical Documents, 2011), potential bias and errors may still exist in those self-reported questionnaires. A number of potential confounding factors have been adjusted in the regression models, but the results may still be confounded by other known and unknown factors.”
So, while the findings may well fit into the “narrative” of sedentariness -> unhealthy diets -> obesity, we must remain cautious in not overinterpreting findings from these type of studies or jumping to conclusions regarding policies or other interventions.
As I explained to the audience, while I do not disregard or trivialize the potential conflict of interest that may come from financial interests (e.g. such as holding a patent or industry funding), we need to also be aware of other powerful conflicts that range from a simple desire to advance one’s personal career (e.g. get tenure, publish in a high-impact journal) to ideological conflicts (e.g. as in spinning research findings to support dearly held world-views or hypotheses).
Whereas disclosing financial conflicts is relatively straightforward (and now pretty much the norm), disclosing other conflicts is more challenging.
Just how devastating ideological conflicts can be to the scientific discourse is perhaps best illustrated by the recent publication by Chritopher Ramsden and colleagues in the British Medical Journal on their analysis of recovered data from the Minnesota Coronary Experiment (MCE).
Conducted back in 1968-73, the MCE was not only the largest (n=9570) but also the most rigorously executed randomized controlled dietary trial of cholesterol lowering by replacement of saturated fat with vegetable oil rich in linoleic acid.
The MCE, conducted in one nursing home and six mental health hospitals in Minnesota (apparently an accepted practice back then), is the only dietary study to-date to fully rely on postmortem assessment of coronary, aortic, and cerebrovascular atherosclerosis grade and infarct status and the only one to test the clinical effects of increasing linoleic acid in large prespecified subgroups of women and older adults.
The trial was initiated by Ancel Keys, a fervent supporter of the idea that atherosclerosis was directly related to dietary saturated fat intake and a champion of replacing dietary fats with vegetable oils rich in linoleic acid.
Importantly, this line of thinking was the driver behind the low-fat recommendations that found their way dietary recommendations and ultimately the low-fat craze that characterized much of second half of the last century.
Although completed in 1973, the findings from this study were never published – until now, when Ramsden and colleagues not only managed to recover the original data but also to conduct the analyses according to hypotheses prespecified by original investigators.
As has been suspected by some for a long time, the results turn out to be devastating for the idea that reducing saturated fat intake or switching to vegetable oils can help prevent heart attacks.
According to the present analysis, although the intervention group experienced a significant reduction in serum cholesterol, there was no demonstrable mortality benefit for the intervention group in the full randomized cohort or for any prespecified subgroup nor for the incidence of coronary atherosclerosis or myocardial infarcts.
Contrary to expectations, there was in fact a 22% higher risk of death for each 30 mg/dL (0.78 mmol/L) reduction in serum cholesterol.
As the authors point out, these findings are in line with the overall findings from five other (albeit smaller) randomized controlled trials in about 10,000 individuals, in whom dietary cholesterol lowering interventions through the use of vegetable oils rich in linoleic acid showed no evidence of benefit on mortality from coronary heart disease or all cause mortality.
As to why these results (that could well have changed decades of dietary recommendations) were never made public, the authors have this to offer,
“In the case of the MCE, the crude study results were clearly at odds with prevailing beliefs….There would have been little or no scientific or clinical trial literature at the time to support findings that were so contrary to prevailing beliefs and public policy.”
“It is interesting to speculate whether complete publication of randomized controlled trial results might have altered key policy decisions promoting replacement of saturated fat with linoleic acid rich oils (such as the 1977 McGovern report and National Cholesterol Education Program (1984-85)) or contributed to a shift in research priorities.”
How much was the fact that the findings were never published influenced by the investigators’ strong “beliefs” in the benefits of reducing saturated fat intake and their “ideological” interest in promoting linoleic-acid rich vegetable oils?
We may never know.
No doubt, Ancel Keys and colleagues would have realised that making these findings public would have done severe damage to their “pet hypothesis”.
Here is an important learning for anyone involved in dietary research or in the business of making dietary recommendations,
“Thus, although the story of the traditional diet-heart hypothesis did not unfold as predicted, the foods that we eat likely play critical roles in the pathogenesis of many diseases. Given the complexity of biological systems and limitations of our research methods, however, current understanding of the biochemical and clinical effects of foods is rudimentary. The history of the traditional diet-heart hypothesis suggests that nutrition research could be improved by not overemphasizing intermediate biomarkers; cautious interpretation of non-randomized studies; and ensuring timely and complete publication of all randomized controlled trials. Given the limitations of current evidence, the best approach might be one of humility, highlighting limitations of current knowledge and setting a high bar for advising intakes beyond what can be provided by natural diets.”
When “ideological conflicts” creep into science it can be far more damaging to science in the long run than any financial conflicts simply because the former is far less evident than the latter.
When someone has “no financial conflicts to declare” I often ask my self, “what are the authors really hiding?”
Some faithful readers may remotely recall that back in 2010, I travelled to Whitehorse in the Yukon to help set up a bariatric specialty clinic modelled on our Edmonton program.
Background for this initiative was the fact that we were receiving a number of referrals from the Yukon for patients who had to travel at great cost to Edmonton for consultations and surgery, with little to no follow up in Whitehorse. (A one-way trip from Whitehorse to Edmonton is 1995 km or 1240 miles).
Since my initial help in starting this program, the Whitehorse obesity specialty clinic, appropriately called the Whitehorse Klondyke Medical Clinic (run by Isabelle Gagnon, a family doctor, who has now dedicated much of her practice to bariatric care) has looked after a rather large number of patients with severe obesity.
My surgical colleague, Daniel Birch now regularly travels up to Whitehorse to see patients ready for surgery. These patients are then operated on in Edmonton, but all of the follow-up care in provided locally in Whitehorse.
Now, Angela Chan and colleagues publish paper in the American Journal of Surgery, which compares outcomes in the Yukon clinic to results in similar patients here in the Edmonton program.
The paper compares data from chart reviews of 20 patients at each site as well as patient/provider satisfaction measures assessed by questionnaires.
The Whitehorse cohort consisted of post-operative patients who reside in Yukon territory, who fly to Edmonton for their surgery only, but attend all pre and post-operative appointments locally at the Whitehorse Clinic.
Overall, both the outcomes and satisfaction between the two centres were very much comparable, with the only significant difference being a slightly more frequent follow-up in the Yukon.
Funnily enough, patients from the Yukon with access to local pre- and post-operative care were in fact happier with the ease and comfort of attending the clinic than the patients in Edmonton, who travel considerable distances from all over Alberta to the Edmonton program (on average 655 km or 407 miles).
Thus, it is indeed good to see that the initiative I helped kick off back in 2010 is now flourishing with patient outcomes as good (if not better) at a much lower cost and greater convenience to patients than before.
Last week’s global obesity report published in The Lancet is accompanied by a thoughtful editorial comment by George Davy Smith from the School of Social and Community Medicine, Bristol, UK, who takes a rather realistic view of our attempts to reverse the epidemic.
As Smith points out,
“Prevention of the global increase in obesity is proving hard — partly for physiological reasons. With respect to calorie intake, weight change is a buffered and self-limiting process. Increased voluntary physical activity leads to compensatory decreases in other components of energy expenditure, resulting in little net benefit. In this respect, human beings are no different to other primates, and genetically informed studies suggest that the association between BMI and physical activity is generated to a large extent by higher BMI leading to lower voluntary physical activity, rather than vice versa.
Many proposals exist for comprehensive sets of advisory and legislative policies aimed at tackling obesity. Such presentations greatly outnumber interventions that have robust evidential support. Evaluations that use methods that allow for reasonable causal inference have been applied to several of these approaches with generally disappointing results, yet they have had little influence on the flow or content of the many “calls to action” on global obesity.”
Indeed, only time will tell if and when population approaches to obesity prevention will bear fruit.
As for our ability to reduce the health consequences of excess weight, Smith notes that,
“Many health consequences of high BMI are unlikely to be directly related to the increased weight itself, rather they are mediated by the adverse metabolic and physiological consequences of increased BMI, including higher blood pressure, adverse lipid profiles, and other metabolic consequences.
These links can be broken, particularly pharmacologically, which is now being done on a mass scale globally (although unevenly). These interventions will attenuate the anticipated morbidity and mortality sequelae of high BMI. However, some of the health effects—and many of the adverse economic consequences—of obesity will not be alleviated in this way.”
There are of course numerous complications of excess body weight, including sleep apnea, osteoarthritis, or urinary incontinence, for which we have no good medical treatments – all of these issues will likely be best mitigated by treating obesity itself.