It must have been a pretty cheap rubber band, because every few months it would wear out and lose its stretch, so it had to be replaced it with a new band.
Unfortunately, this is not what can be said about the rubber band that I used in my recent TEDx talk to demonstrate what happens when you try to lose weight.
Unlike the cheap band in my pyjamas, the rubber band I used to represent our physiology trying to gain the weight back, never seems to lose its stretch.
No matter how hard or how long we pull, the rubber band keeps wanting to bring our weight back to where we started.
Yes, perhaps for some people, eventually the rubber band may relax (these would certainly be the exceptions) or may be the “muscles” that we use to pull on the band just grow stronger, which makes it seem easier to keep up the pull – but for all we know, in most people, this “rubber band” is of pretty good quality and seems to last forever.
So, how do we take the tension out of the rubber band ?
Well, we do know that people who have bariatric surgery have a much better chance of keeping the weight off in the long-term and we now understand that this has little to do with the “restriction” or the “malabsorbtion” resulting from these procedures but rather from the profound effect that this surgery has on the physiology of weight regain.
Thus, we know that many of the hormonal and neurological changes that happen with bariatric surgery, seem to inhibit the body’s ability to defend its weight and perhaps even appears to trick the body into thinking that its weight is higher than it actually is.
In other words, bariatric surgery helps maintain long-term weight loss by reducing the tension in the rubber band, thus making it far easier for patients to maintain the “pull”.
And that is exactly how we think some of the anti-obesity medications may be working.
For example, daily injections of liraglutide, a GLP-1 analogue approved for obesity treatment, appears to decrease the body’s ability to counteract weight loss by reducing hunger and increasing satiety, thus taking some of the tension out of that band.
Think of it as sprinkling “magic dust” on that rubber band to reduce the tension, which makes it easier for patients to maintain that pull thereby helping them keep the weight off.
Of course, both surgery and liraglutide only reduce the tension as long as you continue using them.
Undo the surgery or come off your anti-obesity meds and the tension in that band comes back as strong as ever.
For readers, who have no idea what I’m talking about, hopefully things will become clearer after you watch my talk by clicking 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.
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
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?”