In March, I had the privilege of being invited by the organisers of TEDx UAlberta to present a talk on obesity.
This talk is now online – please take a look and join the discussion on facebook
If clicking on the image does not work for you, click on this link for YouTube
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
To anyone following the “biological” literature on obesity, it should be pretty evident by now that environmental factors can epigenetically modify genes in ways that allow “information” on environmental exposures in parents to be directly transmitted to their offspring.
Now a paper by Peter Huypens and colleagues from the Helmholtz Zentrum München, Germany, published in Nature Genetics, shows that both maternal and paternal exposure to weight gain induced by a high-fat diet in mice can substantially increase the risk for obesity in their offspring.
The key novelty in this study was the fact that the researchers isolated egg and sperm from both male and female mice that had been exposed to high-fat diets (or not) and used these germ cells in various combinations using in-vitro fertilization to create the offspring that were then implanted into surrogate female mice.
In all cases, risk for obesity as well as signs of insulin resistant tracked with both the male and female exposures, pretty much confirming that diets eaten by mothers and fathers can directly influence “genetic” risk for obesity in the next generation.
If transferable to humans (and there is little reason to doubt that this is the case), these findings suggest that a large proportion of the “heritability” of obesity is due to epigenetic modification that transfers risk from one generation to the next.
This means that efforts to prevent childhood obesity need to focus on the parents rather than the kids – kids born to mothers and fathers who have obesity are already born with a substantial higher risk than those born to lean mothers and fathers.
Perhaps our best chances of tackling obesity in the next generation of kids is to focus efforts on younger adults of child-bearing age.
One of the most pervasive problems with quitting cigarettes, is the accompanying weight gain – in fact, post-cessation weight gain is reportedly the number one reason why smokers, especially women, fail to stop smoking or relapse after stopping.
But what exactly happens when you stop smoking?
This is the topic of a comprehensive review article by Kindred Harris and colleagues published in Nature Reviews Endocrinology.
The paper begins by examining the magnitude of weight gain generally experienced after smoking cessation – an amount that can vary considerably between individuals.
As for mechanisms, the authors note that,
“Several theories have been proposed to explain increased food intake after smoking cessation. One theory is that the ability of nicotine to suppress appetite is reversed. Substitution reinforcement, which replaces the rewards of food with the rewards of cigarettes could occur. Nicotine absence increases the rewarding value of food. Reward circuitries in the brain, similar to those activated by smoking, are activated by increased intake of food high in sugar and fat. Furthermore, nicotine withdrawal leads to an elevated reward threshold, which might cause individuals to eat more snacks that are high in carbohydrates and sugars.”
There are also known effects of smoking on impulsive overeating and individuals with binge eating disorder are at risk of even greater weight gain with cessation.
Smoking cessation also has metabolic effects including a drop in metabolic rate that may promote weight gain and new evidence shows that smoking cessation can even change your gut microbiota.
The authors provide evidence that behavioural interventions can prevent much of the cessation weight gain and argue that such programs should be offered with cessation programs.
Finally, it is important to always remember that the health benefits of smoking cessation by far outweigh any health risks from weight gain, which is why fear of weight gain should never stop anyone from quitting.