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.
In the same week that we learned about the devastating metabolic effects of the weight loss induced by hours-long exhausting workouts in participants in the “Biggest Loser”, a paper byJenna Gillen and colleagues from McMaster University, Hamilton, Canada, published in PLOS One, shows that all it takes is one minute of vigorous all out exercise to significantly improve your health.
Unbelievable as it sounds, the rather rigorous randomised controlled 12-week trial in 27 sedentary men showed just that.
The researchers divided the participants into three groups: three weekly sessions of sprint interval training (SIT) involving a total of 1 minute of intense exercise within a 10-minute time commitment (n = 9), three weekly sessions of traditional moderate-intensity continuous training (MICT) involving 50 minutes of continuous exercise per session (n = 10) or no training controls (n = 6).
SIT involved 3×20-second ‘all-out’ cycle sprints (~500W) interspersed with 2 minutes of cycling at 50W, whereas MICT involved 45 minutes of continuous cycling at ~70% maximal heart rate (~110W). Both protocols involved a 2-minute warm-up and 3-minute cool-down at 50W.
Peak oxygen uptake increased by around 20% in both exercise groups as did insulin sensitivity as assessed by an intravenous glucose tolerance test.
Participants in both exercise groups also lost about 2% of body fat.
Furthermore, metabolic and mitochondrial function (as measured in muscle biopsies) improved similarly in both exercise groups.
Thus, the researchers conclude that
“12 weeks of brief intense interval exercise improved indices of cardiometabolic health to the same extent as traditional endurance training in sedentary men, despite a five-fold lower exercise volume and time commitment.”
This is not just news for people who find it hard to make the time for exercise (e.g. due to work or family commitments).
It is also of interest to anyone just trying to get fitter without wanting to invest hours in the gym.
The key however, is the term “all-out” – the 60 sec bout of exercise has to be at virtually maximum capacity, which may increase the risk of injury in some individuals and can hardly be described as “pleasant”.
As for the implications for my patients, who often present with considerable amount of excess weight and thus, every movement (e.g. just walking up a flight of stairs) often appears to happen at near maximum exercise capacity (no surprise given the tremendous weight that they are lifting and carrying), I can only speculate, of what these bouts of activity may have on their metabolic health.
Whatever the case, this study certainly corroborates the notion that one does not have to spend hours in the gym to improve one’s health.
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
This is once again demonstrated in a fascinating series of experiments by Stefano Guidotti and colleagues from the University of Groningen, The Netherlands, in a paper published in Physiology and Behaviour.
The researchers performed their experiments in mice that were selectively bred over 50 generations to voluntarily spend hours in running wheels. Interestingly, the female “runner” mice remain resistant to becoming obese as adults when exposed to a high-fat diet even when they don’t have access to a running wheel.
Thus, these mice are resistant to developing obesity whether they run or just sit around.
What the researchers now show is that this “resistance” to gaining excess weight (bred over generations) can be fully cancelled out simply by exposing the mice to a high-fat diet for a couple of days shortly after birth.
With this exposure, these mice (and even their offspring) are suddenly no longer resistant to weight gain later in life and in fact gain as much weight on high-calories diets as normal mice.
Even more interestingly, the short term perinatal exposure to the high-energy diet does not cancel out their love for running. When given a wheel, they continue running just as much as before but even this no longer prevents them from gaining weight.
Thus it appears that exposure to a high-energy diet during the perinatal period can have profound effects on the risk of developing adult obesity even in animals bred to be obesity resistant – and, the love for running, does not appear to protect against weight gain.
Or, as the authors put it,
“..resistance to high-energy diet-induce obesity in adult female mice from lines selectively bred over ~ 50 generations for increased wheel running behavior was blocked by additional perinatal high-energy diet exposure in only one cycle of breeding. An explanation for this effect is that potential allelic variants underlying the trait of diet-induced obesity proneness were not eliminated but rather silenced by the selection protocol, and switched on again by perinatal high-energy diet exposure by epigenetic mechanisms”
Moreover, this effect of perinatal high-energy diet exposure and its “reversal effect” on obesity resistance can be passed on to the next generation.
Reason enough to wonder just how much the rather dramatic changes in perinatal feeding of infants over the last few decades may be contributing to the obesity epidemic.
This, however, does not mean that genetic risk is not modifiable.
Thus, a paper by Carlos Celis-Morales and colleagues, published in OBESITY, suggests that physical activity may attenuate some of the weight gain attributable to the FTO gene, one of the more common obesity risk alleles.
Their study includes data from 1,280 participants in the European Food4Me trial.
Overall, the FTO (rs9939609) genotype was associated with a higher body weight of about 1 Kg per risk allele, 0.5 Kg/m2 higher BMI, and 1.1 cm greater waist circumference.
While these “effects” were higher among inactive individuals (BMI by 1.06 kg/m2 per allele and waist circumference by 2.7 cm per allele), they were lower in individuals with moderate to high physical activity (BMI by 0.16 kg/me and Waist circumference by 0.5 cm).
Thus, it appears that increased physical activity may attenuate (but not fully prevent) the effect of FTO genotype on BMI and WC.
Exactly how clinically relevant these findings are and whether they would have any effect at all on public health messages or individual counselling, where increased physical activity is likely to be recommended irrespective of any “genetic markers” (or at least should be) is pretty doubtful.
Currently, we have yet to await any practical consequences of genotyping individuals for obesity “risk” alleles.