As I discuss in an editorial published this week in CMAJ, annual access to bariatric surgery (2012-13) per 1,000 individuals living with a BMI >= 35 kg/m2 (2007-2010 prevalence) in Canada is around 5.4, however, this number ranges from as high as 9.6 in Quebec to as low as 1.1 in Nova Scotia – an almost 10-fold difference (bariatric surgery is not available in Prince Edward Island or the Territories).
To catch up with the current rate of surgery in Quebec, Alberta would need to perform an additional 813 procedures a year, while BC would need an additional 805 and Nova Scotia an additional 463 per year.
Overall, bringing the rate of surgery across Canada to the current rate in Quebec, would require an additional 5,129 surgeries per year.
However,, even bringing the rate of bariatric surgery across Canada to the current rate in Quebec may not be enough to significantly reduce the burden of severe obesity across Canada.
This, must not be an argument against further increasing access to surgery – there is no doubt that the vast majority of the 1000s, who currently do manage to get surgery benefit significantly from this intervention.
While it is important to acknowledge that obesity competes for scarce resources in strapped health care systems and that choices must be made about what services/treatments to provide, we must remember that bariatric surgery is currently the only effective long-term treatment for people living with severe obesity.
Despite all the risks inherent in any surgical procedure, and the fact that the occasional patient may struggle to lose weight or end up putting it back on, surgery currently remains the best treatment we have.
Nevertheless, as I point out in the editorial,
“Even as provinces work to increase access to bariatric surgery, other aspects of bariatric care cannot be ignored. For one, efforts at secondary prevention, to reduce and limit weight gain in individuals already carrying excess weight must be increased. Given the over 6 million Canadian adults and children living with obesity, these services must be provided at the primary care level rather than at specialized centres. Secondly, these services need to apply the established tenets of chronic disease management to obesity, which include patient education, self-management and ongoing follow-up and support. These principles are embedded in the 5As of Obesity Management framework developed by the Canadian Obesity Network. Thirdly, education on the complex etiology and evidence-based management of obesity needs to be integrated into every level of professional education for physicians and allied health professionals.”
As increasingly safe and effective medical treatments for obesity become available, these must be made accessible to patients who stand to benefit from such treatments.
In the meantime, the least we can expect from provincial health systems is that patients who need bariatric surgery have the same level of access across the country.
This, according to a study by Ruth Brown and colleagues from Toronto’s York University, published in Medicine and Science in Sports and Exercise.
The study included 58 adult men and women of either normal weight (NW) or overweight (OW), who reported either attempting (WL) or not attempting weight loss (noWL)
Following 25 mins of exercise on a treadmill at either a moderate (60% HRmax) or a vigorous intensity (75% HRmax), participants were asked to estimated the number of calories they expended through exercise and create a meal that they believed to be calorically equivalent to the amount of calories they had just burnt.
Both the moderate and intense exercise groups were on average spectacularly wrong in their estimates.
In contrast, the active weight loss (WL) groups appeared to do far better at estimating energy consumption than the non-WL groups.
As an example, following vigorous exercise, the OW-noWL overestimated energy expenditure by 72%, and overestimated the calories in their food by 37%.
Although the WL groups did better, all groups showed a wide range of over and underestimation (-280 kcal to +702 kcal).
These findings show that while most people tend to over or underestimate caloric expenditure with exercise, overweight adults who are not attempting weight loss may be even more off the mark than others.
The most obvious solution would be to use some kind of monitor that does a better job of predicting calories consumed that just guessing.
That is of course, if overcompensating is not your goal (as in people who actually gain weight when they begin exercising).
For those interested in staying in energy balance, perhaps simply stepping on the scale regularly during the week should be enough.
For those interested in losing weight, they may need to be reminded that exercise (alone) is actually a pretty inefficient way to lose weight, so the calories burnt during exercise probably don’t matter all that much for weight management (despite all other benefits of exercise – its the calories you eat or drink that count).
Now a study by Robert Eckel and colleagues, published in Current Biology, illustrates how sleep deprivation and timing of meals can markedly alter insulin sensitivity.
Studies were conducted in 16 healthy young adults (8w) with normal BMI. Following a week of 9-hr-per-night sleep schedules, subjects were studied in a crossover counterbalanced design with 9-hr-per-night adequate sleep (9-hr) and 5-hr-per-night short sleep duration (5-hr) conditions lasting 5 days each, to simulate a 5-day work week. Sleep was restricted by delaying bedtime and advancing wake time by 2 hr each.
Energy balanced diets continued during baseline, whereas food intake was ad libitum during scheduled wakefulness of 5- and 9-hr conditions.
Overall, the simulated 5-day work week of 5-hr-per-night sleep together with an ad libitum diet resulted in a 20% decrease in oral and intravenous insulin sensitivity, which was compensated for by increased insulin secretion..
These changes persisted for up to 5 days after restoring 9-hr sleep opportunities.
The authors also showed that shifting circadian rhythm resulted in morning wakefulness and eating during the biological night, a factor that may promote weight gain over time.
Neuroimaging studies have implicated the left dorsolateral prefrontal cortex (LDLPFC), an area of the brain that plays an important role in the organization and planning of behavior including goal-oriented regulation of eating behavior and food choice, has been implicated in obesity.
Now Marci Gluck and colleagues, present a proof of concept study published in OBESITY, suggesting that effects of cathodal transcranial direct current stimulation (tDCS)aimed at the LDLPFC may reduce energy intake and promote weight loss in individuals with obesity.
The randomised sham-controlled study was conducted in 9 (3m, 6f) healthy volunteers with obesity, who were admitted as inpatients for 9 days to a metabolic ward.
In a first study, following 5 days of a weight-maintaining diet, participants received cathodal or sham tDCS (2 mA, 40 min) on three consecutive mornings and then ate ad libitum from a computerized vending machine, which recorded energy intake.
In a second study participants repeated the 1st study, maintaining original assignment to active (this time anodal) and sham.
In both studies, each stimulation session consisted of 40 min of anodal tDCS delivered with a neuroConn® DC-STIMULATOR device, at a constant current of 2 mA (with a 30-second ramp at on- and offset) using two 5 × 5 cm sponge electrodes soaked in a sterile 0.9% sodium chloride solution.
Participants who received active tDCS consumed about 700 fewer total kilocalories per day during anodal versus cathodal stimulation. This reduction in caloric intake was mainly a result of reduced fat and pop consumption.
In contrast, sham stimulation had no effect on energy intake.
As may be expected in this short term study, not much happened to body weight.
Regarding the mechanisms the authors speculate that,
“Our results, in combination with previous work, point to a role for the LDLPFC in energy intake and body weight regulation. However, the mechanisms that mediate this association are not clear. Capacity for self-control in reward-related decision-making tasks depends critically on the activity of the DLPFC, a region that is activated in response to cues that induce food craving…. Thus, anodal tDCS over the LDLPFC could have reduced food intake by simultaneously suppressing food cravings and facilitating choices requiring delayed gratification.”
As the authors optimistically conclude,
“In this proof of principle clinical trial, participants with obesity receiving anodal versus cathodal tDCS to the LDLPFC tended to have lower ad libitum energy intake, less fat and soda intake, and significant differences in weight change. “
Obviously, it will take longer term studies as well as further exploration of the type of patient who may benefit from this type of treatment, before we can judge whether this type of treatment (which appears to be otherwise safe) can play a role in obesity management.
Yesterday, I posted about the interesting study by Madjd and colleagues suggesting that drinking water may be better for weight loss than drinking diet beverages.
But what exactly is the evidence that low-calorie sweeteners (of which there are many) may actually have non-caloric effects on energy intake or body weight?
The authors assessed both animal and human studies involving the consumption of low-calorie sweeteners in conjunction with an ad libitum diet.
In 62 of 90 animal studies exposure to low-calorie sweeteners did not affect or decreased body weight. Of 28 studies that did report increased body weight, 19 compared compared low-calorie sweeteners with glucose exposure using a specific ‘learning’ paradigm.
In humans, 12 prospective cohort studies found inconsistent associations between the use of low-energy sweeteners and body mass index, with overall minimal effects at best.
A meta-analysis of short-term randomized controlled trials (involving 129 comparisons) showed reduced total energy intake for low-calorie sweetener versus sugar-sweetened food or beverage consumption before an ad libitum meal (about −94 kcal per day), with no difference versus water (−2 kcal per day).
These findings were consistent with energy intake observations in sustained intervention randomized controlled trials (10 comparisons), a meta-analysis of which (with study durations ranging from 4 weeks to 40 months) showed that consumption of low-calorie sweeteners versus sugar led to relatively reduced body weight (nine comparisons), and a similar relative reduction in body weight compared to water (three comparisons).
Thus, contrary to what is often stated in popular media or even by some experts, there is little if any evidence either from animal or human studies that the use low-caloric sweeteners has any measurable impact on energy intake (other than reducing total caloric intake) or body weight.
Thus, the authors conclude that
“Overall, the balance of evidence indicates that use of low-energy sweeteners in place of sugar, in children and adults, leads to reduced energy intake and body weight, and possibly also when compared with water.”
Obviously, even this analysis is not going to silence the sceptics, who will continue to claim that somehow low-calorie sweeteners are still messing up your energy intake or metabolism.
However, it may be fair to conclude that if indeed such effects exist, their magnitude is likely marginally and of doubtful clinical significance.
I will continue recommending that my patients do their best to replace sugar with non-caloric sweeteners if giving up their liking for sweet foods or beverages is not an option.