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.
Now, a study by Constantin Gasser and colleagues from Melbourne, Australia, in a paper published in the American Journal of Clinical Nutrition, present a systematic review and meta-analysis of confectionary consumption and overweight in kids.
The researchers identified 19 studies fort their systematic review, 11 of which (∼177,260 participants) were included in the meta-analysis.
Overall, odds of excess weight of kids in the highest category of sweets consumption was about 20% less than in the reference category.
This inverse association was true for both chocolate and nonchocolate confectioneries.
Furthermore, in the longitudinal studies and the randomised controlled trial included in the review, no associations were observed between confectionery consumption and overweight, obesity, or obesity-related outcomes.
Thus, based on data from well over 175,000 kids, there appears to be no relationship between sweets consumption and excess weight – if anything, the relationship is the opposite of what one may expect.
As so often, when data don’t fit the “accepted” hypothesis, the authors are also quick to point out that these findings could well be explained by reverse causality (overweight kids avoiding sweets) or underreporting by heavier kids (a polite way of saying that heavier kids may be less honest about their candy consumption).
On the other hand, it may also well be that regular (non-restrictive) sweet consumption actually does in fact make kids less vulnerable to overeating, simply by ruining their appetite (just as grandma always warned you it would – as in, “No sweets before supper!”).
Overall, the findings remind me of a previous study that failed to find any association between sugary pop consumption and body weight in Ontario and PEI kids (if anything skinny kids in PEI drank more pop than those with excess weight).
Whatever the true answer may be, these findings certainly do not support the notion that sweet or chocolate consumption is a key factor in childhood obesity.
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?”
Given the highly rewarding nature of food, picking a favourite food over. almost anything else appears the natural choice. Thus food reinforcement is generally established at an early age and tends to continue throughout life.
Now, Kai Ling Kong and colleagues, in a paper published in OBESITY, test the hypothesis that conditioning infants as young as 9-16 months to an cognitively stimulating alternative reinforcer may reduce the appeal of food as the default goto reward.
The researchers studied 27 infants, who were found to have rather high food reinforcing ratios at baseline, half of who were randomised to 6 weeks of a program that provided them with a rich variety of music and playful activities, which encouraged infants and parents to participate at their own level in singing, moving, listening, or exploring musical instruments. Participating parents and infants attended weekly, 45-min classes as a group for 6 weeks and parents were encouraged to listen and sing together with their infants at home during everyday home activities such as bath time, meal time, and bed time using the CD and instructional song book provided by the program.
“Our findings provide initial evidence that alternatives to food may be cultivated at a young age to alter the reinforcing value of food in children who are strongly motivated to eat…..Interventions targeting non-food behavior may be a new and promising avenue for the prevention of obesity in infants.“