Anyone dealing with pediatric obesity knows that there is now an increasing number of massively obese kids for whom behavioural and/or medical weight management will simply not cut it. It is therefore no surprise that an increasing number of kids and their families are now looking to surgeons for help.

To address this demand, Toronto’s Hospital for Sick Children last week announced the creation of a centre for pediatric and adolescent bariatric surgery (see report on CTV).

While to some readers this may seem shocking, extreme, drastic, and will likely provoke much head shaking amongst people who simply do not get that calling for more prevention efforts will be of no benefit to these kids, the reported outcomes for pediatric obesity surgery (at least in the short term) are actually quite good.

Thus, Ai Xuan Holterman and colleagues from Rush University, Chicago, IL, recently reported their experience with bariatric surgery in morbidly obese adolescents in the Journal of Pediatric Surgery.

This looked at the more than one year outcomes in twenty 14-17 year olds undergoing plaparoscopic adjustable gastric banding (LAGB). BMI at baseline was around 50 and was associated with hypertension (45%), dyslipidemia (80%), insulin resistance (90%), metabolic syndrome (95%), and biopsy-proven nonalcoholic steatohepatitis (88%).

At mean follow-up of 26 months, mean excess weight loss was around 30% and the metabolic syndrome was resolved in 63% and 82% of the patients at 12 and 18 months, respectively. Hypertension normalized in all patients, along with improvement in lipid abnormalities and quality of life scores.

LABG is relatively safe with few perioperative complications. Nevertheless, long-term complications including band slippage, erosions, and other problems remain a concern. Furthermore, LABG patients have to follow stringent dietary regimens to be successful. Despite these reservations, LABG certainly currently appears to be the procedure of choice both because it is theoretically reversible and has such low perioperative complication rates.

While we of course all wish that there was no need to reach for such drastic treatments in kids, the reality is that an increasing number of severely obese adolescents and kids will no doubt benefit and will get a real chance at regaining control over their weight and lives.

I predict that Toronto’s Sick Kids is very unlikely to remain the only place in Canada that performs pediatric bariatric surgery for long.

AMS
Edmonton, Alberta

Obesity is often described as a state of low grade inflammation. Activated macrophages (white blood cells) in adipose tissue play an important role in this inflammatory response by secreting a number of pro-inflammatory molecules (cytokines) that can promote the development of insulin resistance and other complications of obesity.

Previous studies have shown that the “glitazone” class of antidiabetic agents can suppress inflammatory macrophage activation and can also increase the expression of an DGAT1 (triacylglycerol (TG) synthesis enzyme acyl CoA:diacylglycerol acyltransferase 1), an enzyme that makes it easier for fat cells and macrophages to store excess fat.

Now a paper by Suneil Koliwad and colleagues from the Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, CA, published in this weeks’ issue of the Journal of Clinical Investigation, provides further evidence that increasing activity of DGAT1 in adipocytes and macrophages may protect animals from the pro-inflammatory effects of obesity.

The researchers found that although mice overexpressing DGAT1 in both macrophages and adipocytes were more prone to weight gain, they did not show signs of the inflammatory response commonly seen with diet-induced obesity.

Through a series of experiments, the researchers were able to establish that DGAT1 is indeed necessary to protect against this inflammatory response, thereby raising the question of wether stimulation of this enzyme may also protect against the complications of obesity in humans.

Thus, although this research may not lead to new ways of preventing or reducing obesity, it may open new avenues for attenuating some of the health consequences related to excess weight.

AMS
Copenhagen, Denmark

While there is no doubt that our current obesogenic environment is the major driver of the obesity epidemic there is also no doubt that these environmental factors don’t affect everyone to the same degree. Indeed, there is now largely consensus amongst experts that the question of who will get obese and who won’t, given that we are all more or less exposed to the same environmental pressures, is largely determined by our genetic make up (yes, genes also influence behaviour!).

This is even more true for those individuals who make up the rapidly growing group of people with severe obesity - anyone, who believes that you can get to weighing over 350 lbs or more simply by making wrong “choices” probably also still believes in Santa Claus and can’t wait for the Easter Bunny.

Yesterday, the journal Nature reported another study that shows how genetic mutations can markedly increase the risk for severe obesity.

In this large multicentre study headed by my friend and colleague Philippe Froguel, the investigators found a highly penetrant form of obesity, initially observed in 31 subjects who were heterozygous for deletions of a surprisingly large area of chromosome 16 (593 kilobases at 16p11.2) and who also presented with some cognitive deficits.

Subsequently, they identified 19 similar deletions in genome wide association data in 16,053 individuals from eight European cohorts. None of these deletions were found in healthy non-obese controls and were estimated to account for 0.7% of the morbid obesity cases in the dataset.

Interestingly, the parents of some of these index cases also had this deletion and were likewise obese. The cases with the deletion tended to be born with a normal weight but then became overweight at childhood and severely obese as adults.

Unfortunately, this large stretch of chromosome 16 contains many different genes (as many as 30) and it is not clear from these studies exactly which or how these missing genes contribute to the severe obesity phenotype.

Nevertheless, given that this is neither the first genetic defect to be associated with severe obesity nor likely to be the last one of what is believed to be a relatively large number of genetic mutations that have yet to be found, this report should come as a strong warning to anyone who believes that severe obesity is solely a self-inflicted condition resulting purely from poor “choices”.

AMS
Copenhagen, Denmark

I have previously blogged about how obesity accelerates pubertal development in young girls, with all of the complex psychosocial sequelae that can make life for these girls quite difficult.

Interestingly, as now described in a paper by Joyce Lee and colleagues published in the latest issue of the Archives of Pediatric and Adolescent Medicine, exactly the opposite is seen in boys, where excess weight is associated with delayed pubertal development.

Thus, in the longitudinal prospective National Institute of Child Health and Human Development Study of Early Child Care and Youth Development, boys in the highest BMI trajectory had 2.6-fold greater risk of being prepubertal at age 11.5 than boys in the lowest BMI trajectory.

This means that as a consequence of the childhood obesity epidemic, the already apparent fact that boys tend to “grow up” much later than girls, is further amplified.

As a father of three adult daughters, I can well recall how years ago my teenage girls simply could never understand how their male classmates could only be so “childish” and refuse to grow up. Thanks to the childhood obesity epidemic, that gender gap is now widening even more.

I’d certainly love to hear from parents on how this issue appears to be affecting our kids today.

AMS
Edmonton, Alberta

Although excess weight is well known to substantially increase the risk for heart disease, we and others have consistently reported that obese patients with heart failure actually live longer than those who are normal weight or skinny.

This obesity “paradox” obviously begs the question of whether or not weight loss is something that you would actually recommend to someone who is obese and has heart failure - if being obese when you have heart failure, wouldn’t losing weight make things worse?

Believe or not, there are almost no studies addressing the impact of intentional weight loss on heart function. The few available studies are largely limited to small series of patients who underwent bariatric surgery, where weight loss does show marked improvements in heart function.

But can similar effects be achieved with dietary weight loss?

This is exactly the question that will be addressed by a study to be performed in collaboration with researchers at the Mazankowski Alberta Heart Institute. The study will include twenty severely obese individuals with heart failure, who will undergo intentional weight loss using a standardized low calorie diet (OPTIFAST 900). Their cardiac function and other parameters will be carefully measured and will hopefully show significant improvements in hemodynamic function and exercise capacity.

The study is funded with a $250,000 grant provided by the Alberta University Hospital Foundation and is due to be completed within three years (if not sooner).

To watch a video on this study as reported on CTV News click here or to read more about the background on CBC News click here.

AMS
Edmonton, Alberta