Yesterday, I attended the inaugural networking event of the Canadian Obesity Network’s Toronto Chapter. Judging by the enthusiasm of the almost 100 folks who came out to this event, this chapter appears off to a great start.
As expected for any CON event, the participants came from virtually every walk of interest in obesity – from professional to personal – research, prevention, clinic, policy, industry, NGOs.
Hopefully, we will see similar activities and chapters starting across Canada in the coming months – the success off this event shows that there is a dire need for local networking to address local issues related to obesity prevention and management.
For more information on the Toronto Chapter (CON-YYZ) click here.
For more information on how to start a CON chapter in your city click here.
In my conversations with skinny runners, they often cannot stop telling me how much satisfaction and enjoyment they get from their “runner’s high”. No wonder, they so often seem “addicted” to their runs (or other workouts).
In contrast, a “runner’s high” seldom comes up when any of my patients living with obesity talk about their exercise experiences (yes, many people with obesity exercise regularly).
Now, work by Maria Fernandes and colleagues from the University of Montreal, published in Cell Metabolism, reports findings in rats, which, if applicable to humans, may provide a biological explanation for this observation.
Building on previous studies showing that leptin modulates multiple components of brain reward circuitry, particularly in dopamine (DA) neurons of the ventral tegmental area (VTA), an area of the brain allegedly responsible for the “runner’s high”.
Using an elegant set of experiments, the researchers showed that leptin markedly reduces mice’s willingness to work for access to a running wheel or show other signs of seeking out exercise-induced reward.
In contrast, mice with a deletion of the signal transducer and activator of transcription-3 (STAT3), involved in leptin signalling in dopamine neurons of the VTA, showed greater interest in voluntary running.
In other words, STAT3 deletion increased the rewarding effects of running whereas intra-VTA leptin blocked it in a STAT3-dependent manner.
Together these findings strongly suggest that leptin influences the motivational effects of running via LepR-STAT3 modulation of dopamine tone.
Or, in other words, higher levels of leptin (as seen in people living with obesity) directly inhibit the rewarding nature of running, making it less likely to experience a runner’s high, than in someone with low leptin levels (as seen in people with low fat mass).
As to why this may be the case, the authors offer the following explanation:
“We speculate that in conditions of restricted food availability the mesolimbic DA system engages motivational processes concerned with obtaining food and more readily responds to leptin to decrease appetitive physical activity. On the other hand, during fed states, the actions of leptin may be biased toward hypothalamic processes that could increase physical activity as a means to maintain energy homeostasis.”
“While heightened physical activity during food restriction seems paradoxical to the maintenance of energy reserves, it is considered an expression of increased food acquisition behaviors. The capacity for endurance running in cursorial mammals is considered to enable food attainment when it is distant or requires pursuit. Correspondingly, the runner’s high may have evolved to encourage stamina and thereby increase the probability of return on this energetic investment.”
As the authors note, this line of reasoning is supported by the recent observation that exercise addiction in men is associated with low, fat-adjusted leptin levels.
In light of these findings, I also wonder if the “increase in energy levels”, which is rather consistently reported by my patients when they lose weight, may simply be reflective of their often dramatic reduction in leptin levels.
The amygdala is a part of the so-called limbic system that performs a primary role in the processing of memory, decision-making, and emotional reactions. The amygdala has also been implicated in a variety of mental health problems including anxiety, binge drinking and post-traumatic stress syndrome.
A study by Xu and colleagues, published in the Journal of Clinical Investigation now shows that in mice, activity of the estrogen receptor–α (ERα) in the medial amygdala may have a profound influence on the development of obesity – an effect, which appears to me largely mediated through effects on physical activity.
Building on previous work showing that ERα activity in the brain prevents obesity in both males and female rats, the researchers used a series of complex experiments to demonstrate that specific deletion of the ERα gene from SIM1 neurons, which are highly expressed in the medial amygdala, cause a marked decrease in physical activity and weight gain in both male and female mice fed with regular chow, without any increase in food intake. In addition, this deletion caused increased susceptibility to diet-induced obesity in males but not in females.
Deletion of the ERα receptor also blunted the body weight-lowering effects of a glucagon-like peptide-1-estrogen (GLP-1-estrogen) conjugate.
In contrast, over-expression or stimulation of SIM1 neurons increased physical activity in mice and protected them from diet-induced obesity.
These findings point to a novel mechanism of neuronal control of physical activity, which in turn appears to have important effects on the susceptibility to weight gain.
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.