This week, Participaction released the 2015 report card on activity in Canadian kids (a yearly exercise formerly undertaken by Healthy Active Kids), and its message is simple – send your kids outside to play!
This is how Participaction defines the protection paradox:
“We may be so focused on trying to intervene in our children’s lifestyles to make sure they’re healthy, safe and happy, that we are having the opposite effect….We overprotect kids to keep them safe, but keeping them close and keeping them indoors may set them up to be less resilient and more likely to develop chronic diseases in the long run.”
And it works best when you send the kids out alone – here is what research shows:
- Grade 5 and 6 students who are often or always allowed to go out and explore unsupervised get 20% more heart- pumping activity than those who are always supervised.
- 3- to 5-year-old kids are less likely to be active on playgrounds that are designed to be “safer,” because many kids equate less challenging with boring.
- Children and youth are less likely to engage in higher levels of physical activity if a parent or supervising adult is present.
Safe is boring – who would have guessed?
And here’s even more research to support this idea:
- Kids with ready access to unsupervised outdoor play have better-developed motor skills, social behaviour, independence and conflict resolution skills.
- Adventure playgrounds and loose parts playgrounds, which support some exposure to “risky” elements, lead to an increase in physical activity and decrease in sedentary behaviours.
“We need to consider the possibility that rules and regulations designed to prevent injuries and reduce perceived liability consequences have become excessive, to the extent that they actually limit rather than promote children’s physical activity and health. Adults need to get out of the way and let kids play.”
Time to set your kids free!
However, it turns out that perhaps one of the most powerful predictors of mortality is a simple and inexpensive assessment of grip strength – something rarely assessed in clinical practice.
Now, a study by Darryl Leung and colleagues, in a paper published in The Lancet, reports that grip strength does just that.
The paper presents data from the Prospective Urban-Rural Epidemiology (PURE) study, a large, longitudinal population study done in 17 countries of varying incomes and sociocultural settings involving nearly 150,000 individuals.
During a median follow-up of 4·0 years, grip strength (as a simple measure of muscular strength) was found to be inversely associated with all-cause mortality (hazard ratio per 5 kg reduction in grip strength 1·16), cardiovascular mortality (1·17), non-cardiovascular mortality (1·17), myocardial infarction (1·07), and stroke (1·09).
In fact, grip strength was a stronger predictor of all-cause and cardiovascular mortality than systolic blood pressure.
In contrast, grip strength was not associated with diabetes, hospital admission for pneumonia or COPD, injury from fall, or fracture.
Interestingly, the association between grip strength and cardiovascular mortality is not new – however, the association with all-cause mortality and the consistency of this findings across populations and economic strata is remarkable.
Obviously, these findings beg the question whether increasing grip strength (or rather muscular strength in general) through resistance training and adequate protein intake will lower mortality – a question that would take a rather large randomised controlled study to answer.
Till then, it is prudent to remember that association does not prove causation – it would thus be premature to conclude that your weak handshake is killing you.
And finally, to conclude this week’s discussion of evidence to support the notion that weight cycling predicts weight (fat) gain especially in normal weight individuals, I turn back to the paper by Dulloo and colleagues published in Obesity Reviews, which quotes these interesting findings in US Rangers:
“…U.S. Army Ranger School where about 12% of weight loss was observed following 8–9 weeks of training in a multi-stressor environment that includes energy deficit. Nindl et al. reported that at week 5 in the post-training recovery phase, body weight had overshot by 5 kg, reflected primarily in large gains in fat mass, and that all the 10 subjects in that study had higher fat mass than before weight lost. Similarly, in another 8 weeks of U.S. Army Ranger training course that consisted of four repeated cycles of restricted energy intake and refeeding, Friedl et al. showed that more weight was regained than was lost after 5 weeks of recovery following training cessation, with substantial fat overshooting (∼4 kg on average) representing an absolute increase of 40% in body fat compared with pre-training levels. From the data obtained in a parallel group of subjects, they showed that hyperphagia peaked at ∼4 weeks post-training, thereby suggesting that hyperphagia was likely persisting over the last week of refeeding, during which body fat had already exceeded baseline levels.”
Obviously, association (even in a prospective cohort) does not prove causality or, for that matter, provide insights into the physiological mechanisms underlying this observation.
All we can conclude, is that these observations in US Rangers (and the other studies cited in Dulloo’s article) are consistent with the notion that weight loss in normal weight individuals can be followed by significant weight gain, often overshooting initial weight.
Incidentally, these findings are also consistent with observational studies in women recovering from anorexia nervosa, famine, cancer survivors and other situations resulting in significant weight loss in normal weight individuals.
Certainly enough evidence to consider a work of caution against “recreational” weight loss, especially in individuals of normal weight.
Dulloo AG, Jacquet J, Montani JP, & Schutz Y (2015). How dieting makes the lean fatter: from a perspective of body composition autoregulation through adipostats and proteinstats awaiting discovery. Obesity reviews : an official journal of the International Association for the Study of Obesity, 16 Suppl 1, 25-35 PMID: 25614201
My recent reading of the paper by Dulloo and colleagues on post-dieting weight gain in non-obese individuals, reminded me of my clinical observation that a surprisingly large proportion of patients I see in our bariatric clinic report a history of competitive sports.
When I have previously discussed this observation with colleagues, the answer I often get is that this weight gain is simply due to the fact that active athletes are used to eating a lot, which they continue to do after their activity levels decline, thus resulting in weight gain – a theory, I don’t quite buy largely because it appears far too simplistic (and I have yet to see any evidence to support it).
Rather, if the phenomenon of weight-cycling induced weight gain is real, one would assume that not all athletes are at risk, but rather that this phenomenon would be limited to athletes in disciplines where weight cycling (e.g. to meet certain weight criteria), often referred to as “weight cutting”, is part of the culture of that sport. Examples of such sports include wrestling, boxing, and weight lifting.
It turns out that this very issue has been studied by Saarni and colleagues, who, in a paper published in the International Journal of Obesity, report their findings on a large national cohort of 1838 male elite athletes who had represented Finland in major international sport competitions in 1920-1965.
This cohort included 370 men engaged in sports in which weight-related performance classes are associated with weight cycling (boxers, weight lifters and wrestlers) and 834 matched control men with no background in athletics.
Over the 20+ years of follow-up, the weight-cycling gained a whooping 5.2 BMI units from age 20 years to their maximum mean weight (at around age 60) conpared to only 3.3 BMI units in non-weight-cycling athletes or just 4.4. BMI units in the non-athletic controls.
Indeed, weight-cycling athletes were about three times as likely to develop obesity (defined as a BMI > 30), than their non-weight cycling colleagues or controls.
This enhanced risk of developing obesity in weight-cycling athletes remained significant even after correction for a number of potential confounders including health habits (smoking, alcohol use, use of high-fat milk or physical activity) or weight at age 20 years.
While this paper does not prove causality, or for that matter, provide any insights into possible biological mechanisms that would promote weight gain, it is certainly consistent with the hypothesis that repeated cycles of weight loss and regain in people who start out with a normal weight (in this case elite athletes) strongly predicts subsequent weight gain and the development of obesity.
Or, as the authors put it,
“The weight cycling behavior of the former athletes engaged in power sports at a young age resembles that of young dieters who lose weight temporarily and soon regain it. The present observations concerning the enhanced weight gain of these athletes raise the concern that the repeated cycles of weight loss and regain caused by dieting at a young age could similarly affect weight in the long term.”
Saarni SE, Rissanen A, Sarna S, Koskenvuo M, & Kaprio J (2006). Weight cycling of athletes and subsequent weight gain in middleage. International journal of obesity (2005), 30 (11), 1639-44 PMID: 16568134
This year’s prestigious Fredrich Wassermann Award of the European Association for the Study of Obesity presented at the 22nd European Congress on Obesity goes to Helsinki’s Aila Rissanen, Europe’s grande dame of obesity research.
I have personally known Aila for as lo as I have been involved in obesity and there is much in her work and approach to obesity that has stimulated my own thoughts on this issue.
In her acceptance address, Aila chose to focus on her work in BMI-discordant twins (among the many topics she has worked on) due to the remarkable insights into the “natre-nurture” discussion that this model offers.
Indeed, it is extremely rare to find genetically identical twins, who differ in body weight (demonstarting just how highly heritable body weight actually is). Thus, body weight in identical twins is remarkably homogeneous not only because of the heritability of weight per se but also due to heritability of weight gain.
Cining the work of her wildly successful trainee Kirsi Pietilainen, Aila described the efforts it took to identify just 30 obesity discordant (weight difference of >10 Kg) identical twins from well over 500 identical twin pairs.
These discordant twin pairs have now been extensively phenotyped with every imaginable laboratory test, measurement and tissue biopsies.
The most consistent difference between the discordant twins appears to be a greater level of physical activity in the leaner twin, which appears to precede the onset of weight gain. In addition to voluntary physical exertion, there also appears to be a significant difference in fidgeting between the twins.
Compared to their co-twins, the obese twins had greater pro-inflammatory lipid profiles, lower antioxident activity and higher pro-coagulation markers. The reasons for these differences remains unclear.
Finally, Aila provided a brief overview of some of the exciting work that is now going on to further study the differences between these genetically identical but obesity disparate twins – metabolomics, lipidomics, epigenomics and even bacteriomics.
Although any of this has yet to translate to better obesity prevention or management, you never know where these fundamental insights into human biology may lead you.
For know, this is certainly a space I intend to watch.
Prague, Czech Republic