As readers are well aware, the crux of the obesity problem is that the body tends to defend it’s highest body weight. This is why anytime you try to lose weight, the complex neuroendocrine kick in to try to “sabotage” your efforts and seemingly won’t rest till the weight is regained.
So why does bariatric surgery work? Why do people who undergo bariatric surgery not simply eat back the extra calories required regain all of the weight they lost in the first year after surgery?
One of the notions is that the surgery itself makes it hard to overeat (restriction) or works by interfering with digestion (malabsorption) – but there is now increasing evidence that neither of these mechanisms appear to be the real reason surgery is so successful.
Now, a study by Zheng Hao and colleagues from Baton Rouge, LA, published in OBESITY, provides evidence to support the idea that gastric bypass surgery may produce favourable long-term outcomes by reprogramming the way that they body regulates its weight.
The studies (performed in mice), show that after Roux-en-Y gastric bypass surgery, the animals begin to regulate body weight at a level that is lower than before surgery.
What was most surprising in these experiments, was that mice which were starved down to a rather low weight before surgery, actually regained weight after surgery (albeit to a weight that is still well below where they would have been before the experiment) and that this weight gain was mainly due to an increase in lean-body mass.
This response is very different from animals (or humans) regaining weight after dietary caloric restriction, where most of the weight gain is due to an increase in fat mass.
Thus, it seems that the neuroendocrine alterations that happen with surgery, trigger mechanisms that appear to defend against a higher level of body fat, while remaining sensitive to the defense of lean mass.
How exactly this works remains unclear but the hope is that by better understanding the molecular and physiological mechanisms underlying this reprogramming we may be able to develop medications that will mimic the effects of surgery.
The past two days, I’ve been at a young investigator’s meeting convened by the Canadian Institutes of Health Research Institute for Nutrition, Metabolism and Diabetes, in Kelowna, BC.
This annual event brings together promising and emerging young investigators working in the fields of metabolic, renal and digestive disease from across Canada.
The talks by experienced faculty are given on topics ranging from grant writing, finding a good mentor and building partnerships (my topic), to the importance of not forgetting about work-life balance.
There is no doubt that every year, the research environment for funding becomes yet more competitive. Thus, it is always refreshing to see the enthusiasm, passion and enthusiasm with which young researchers approach the many research questions that desperately need answers.
Finding better ways to prevent and treat obesity are certainly among the top issues on the list, and it was therefore not surprising to see several of the research projects presented by the young attendees focusing on various aspects of obesity.
I found attending this event particularly rewarding as this was a reunion with several past “bootcampers” (attendees of the Canadian Obesity Network’s annual Obesity Research Summer School), who, I am happy to say, have progressed nicely into junior faculty and new investigator positions.
Congratulations to the organisers and all who had the privilege of attending.
Now a paper by Argyro Syngelaki and colleagues from the UK, published in the New England Journal of Medicine, suggests that the anti-diabetes drug metformin may limit weight gain in pregnant non-diabetic women with obesity and also reduce the incidence of pre-eclampsia.
The researchers randomised 450 pregnant women with a BMI greater than 35 and no diabetes to either metformin (3 g/day) or placebo from weeks 12-18 weeks of gestation till delivery in a double-blind fashion.
Among the 400 women who completed the study, those on metformin gained about 2 Kg less weight than the placebo group.
There was also an almost 75% decrease in the risk of developing preeclampsia.
Despite these effects, metformin did not significantly reduce the incidence of large-for-gestational-age babies or other adverse neonatal outcomes.
While these findings may be somewhat disappointing with regard to outcomes in the offspring, the reduction in pre-eclampsia is impressive and, if confirmed, could well be an interesting use of this compound in high-risk pregnancies.
It is now widely recommended that addressing childhood obesity requires a whole-family approach with a focus on educating and helping parents provide a healthier environment for their children. This has sometimes resulted in the slogan, “treat the parents”.
But just how effective is this approach?
Now a study by Gisela Nyberg and colleagues from the Karolinska Institute in Stockholm, Sweden, published in the International Journal of Behaviour, Nutrition and Physical Activity, suggests that even this strategy may not be quite as effective as one would hope.
The study was designed to study the effectiveness of a universal parental support programme to promote health behaviours and prevent overweight and obesity in 6-year-old children in disadvantaged areas in Stockholm.
The cluster-randomised controlled trial involved 31 school classes with 378 six-year-old children. The 6 month interventions were 1) Health information for parents, 2) Motivational Interviewing with parents and 3) Teacher-led classroom activities with children.
Overall, while there was some effect of the intervention on eating behaviour, there was no overall impact on physical activity levels.
There was also no change in BMI for the whole group, although there was small drop in BMI in kids at the higher range of the BMI spectrum, which disappeared at 5-months post-intervention.
The authors grasp at the fact that the effects of the intervention were short-lived to recommend that the programme needs to be prolonged and/or intensified in order to obtain stronger and sustainable effects.
Just how much longer or how much more intense the intervention would need to be is unclear.
These findings certainly reflect the real-life problem that we currently have no universally effective approach to dealing with childhood obesity (with parents or without).
Sadly, no one has yet demonstrated that any type of intervention for childhood obesity, whether individual, family, shool or community based, despite occasional short-term improvements in health behaviours and body weight, ultimately translates into fewer adults with obesity.
Perhaps, the best time to intervene to prevent childhood obesity is even before the kids are born.
Now a study by Crump and colleagues published in JAMA Intern Medicine suggests that some of this risk may be mitigated by increased physical fitness.
The cohort study involving over 1.5 million Swedish young men in Sweden, who underwent standardized aerobic capacity, muscular strength, and BMI measurements obtained at a military conscription examination and were followed for up to 40 years.
Almost 100,000 men went on to develop hypertension, whereby both high BMI and low aerobic capacity (but not muscular strength) were associated with increased risk of hypertension, independent of family history or socioeconomic factors.
A combination of high BMI (overweight or obese vs normal) and low aerobic capacity (lowest vs highest tertile) was associated with the highest risk of hypertension.
The association with aerobic fitness was apparent at every level of BMI.
Form this study the authors conclude that high BMI and low aerobic capacity in late adolescence are associated with higher risk of hypertension in adulthood.
Although one must also be cautious in assuming causality with regard to associations found in such studies, the observations are certainly compatible with the notion that increased cardiorespiratory fitness may well mitigate some of the impact of increased BMI on hypertension risk.