Last week at the 8th Annual Obesity Symposium hosted by the European Surgery Institute in Norderstedt, one of the case presentations included an individual with type 1 diabetes (no insulin production), who had gained weight and subsequently also developed increasing insulin resistance, the hallmark of type 2 diabetes.
In my discussion, I referred to this as 1+2 diabetes, or in other words, type 3 diabetes.
Unfortunately, it turns out that the term type 3 diabetes has already been proposed as the type of neuronal insulin resistance found in patients with Alzheimer’s disease.
As discussed in a paper by Suzanne de la Monte and Jack Wands published in the Journal of Diabetes Science and Technology,
“Referring to Alzheimer’s disease as Type 3 diabetes (T3DM) is justified, because the fundamental molecular and biochemical abnormalities overlap with T1DM and T2DM rather than mimic the effects of either one.”
These findings have considerable implications for our understanding of Alzheimer’s disease as a largely neuroendocrine disorder, which may in part be amenable to treatment with drugs normally used to treat type 1 and/or type 2 diabetes.
In retrospect, I believe, whoever came up with the term type 3 diabetes for Alzheimer’s disease, should perhaps have called it type 4 diabetes, given that the 1+2 diabetes is now increasingly common (and well studied) in patients with type 1 diabetes, who go on to develop type 2 diabetes (which, as discussed at the symposium responds quite well to bariatric or “metabolic” surgery).
- Does Liraglutide Mimic The Vascular Benefits Of Gastric Bypass Surgery?
- Re-Do Bariatric Surgery
- Active Video Games Do Not Promote Negative Energy Balance
- Exercise Reduces Cravings For Sugar?
- Free Online Courses For Obesity Management
Have a great Sunday! (or what is left of it)
On the last day of the 8th Annual Obesity Symposium here in Norderstedt, Germany, Marco Bueter from the University of Zurich presented a fascinating series of studies (just published in Circulation), demonstrating the “weight-independent” benefits of gastric bypass surgery on endothelial function (using an animal model).
Besides showing that 8 days after bypass surgery rats with diet-induced obesity had higher plasma levels of bile acids and GLP-1, that were associated with improved endothelium-dependent relaxation, not seen in sham-operated weight matched controls, but also that these effects could be prevented by blocking GLP-1 receptors with exendin 9-39.
In contrast, similar effects to those seen on vascular function in bypass rats were seen in sham-operated rats treated for 8 days with the GLP-1 analogue, liraglutide, or as the authors describe it,
“liraglutide restored NO bioavailability and improved endothelium-dependent relaxations and HDL endothelium-protective properties, mimicking the effects of RYGB”
Together these studies suggest that GLP-1 may well play an important causal role in the improved vascular function seen in patients undergoing gastric bypass surgery.
These findings are all the more interesting as liraglutide has now been approved for obesity treatment in the USA, Canada and Europe.
While these data are certainly not enough to describe liraglutide as “surgery in a pen”, they are indeed promising in terms of potential benefits of this treatment that may well be weight independent.
All the more reason to anticipate the outcome of the ongoing LEADER trial, which is currently evaluating the effect of liraglutide treatment on cardiovascular outcomes in patients with type 2 diabetes.
Disclaimer: I have served as a paid consultant and speaker for Novo Nordisk, the maker of liraglutide.
As was pointed out, even in the best hands, 10 to 20% of patients undergoing bariatric surgery will “fail”, often prompting surgeons to reoperate.
As I write this post, I am watching live “re-do” surgery on a patient who had an open Mason vertical-banded gastroplasty in 1987 (remining us that bariatric surgery has been around far longer than many people think).
Listening to the surgeon (Dr. Bruno Dillemans, Bruges, Belgium) commenting on the operation, it is apparent (even to a non-surgeon like myself), that this kind of surgery can be most challenging.
With the vast increase in the number of patients undergoing bariatric surgery worldwide, it is easy to see that bariatric “re-do” surgery will pose a significant challenge down the road.
Over the past few months, I have been working with mdBriefCase, a major provider of free online accredited continuing medical education, to produce interactive modules for obesity management.
The modules are aimed at practitioners working in primary care and pharmacists and align closely with the Canadian Obesity Network’s 5As of Obesity Management framework.
The accredited course (Mainpro M1 and MOC Section 1 or 3 credits) is available free of charge to all Canadian Health Professionals.
To access the course for physicians and allied health practitioners on mdBriefCase – click here
To access the course for pharmacists on rxBriefCase – click here
Unfortunately, judging by a randomised-controlled trial by Aidon Gribbon and colleagues from the University of Ottawa, published in the American Journal of Clinical Nutrition, this remains but a dream.
For this study, 26 male adolescents were randomised to three 1-hour sessions of rest, seated video game and an active video game. This was each followed by an ad libitum lunch. The researchers also asked the subjects to complete dietary records for another 3 days
Energy expenditure was measured by using portable indirect calorimetry throughout each experimental condition, and an accelerometer was used to assess the subsequent 3-d period.
Although energy expenditure (as measured by indirect calorimetry) was significantly higher during the active game, there was no significant differences in energy balance at 24hrs or 3 days after the end of the game (no surprise here).
Thus, while the researchers did not see any change in appetite or food intake after the active game, they also found no difference in energy balance after 24 hrs.
Thus, the energy expended during the game was apparently fully compensated for, suggesting that active gaming may have a rather modest (if any) effect on energy balance.
As to exactly how this compensation happens – the researchers attribute this to the:
“compensatory adaptation in spontaneous physical activity occurs subsequent to playing Kinect, resulting in no significant differences in net energy expenditure over the course of 24 h. This compensation in PAEE after engaging in AVGs is consistent with results from exercise trials that showed that individuals tend to compensate for physical activity interventions by decreasing subsequent spontaneous physical activity levels”
On a positive note, the authors also did not see an expected increase in caloric intake after the games.
Whether or not active video gaming over time may lead to different effects remains to be seen.
I have long postulated that the benefits of exercise in weight management have little to do with burning calories. Rather, I am pretty sure that when people lose weight with exercise, they do so because of the impact that exercise may have on their food intake (I call it exercising to ruin your appetite!).
Thus, I am happy to acknowledge my affirmation bias in paosting about the recent study by Larissa Ledochowski and colleagues from the University of Innsbruck, Austria, published in PLOS One on the outcome of a randomised controlled trial of brisk walking on cravings for sugary snacks.
The study was conducted in 47 overweight volunteers who reported habitually consuming a fair share of sugary snacks. Following 3 days of “chocolate abstinence” subjects were randomised (using a within-subject design) to a 15-min brisk walk or passive control.
On each occasion, subjects were then stressed using the Stroop color–word interference task after which they reported their urges for sugary snacks using the State Food Craving Questionnaire [FCQ-S] adapted for sugary snacks.
Compared to the control situation, brisk walking resulted in a significant and relevant reduction in the urge for sugary snacks and attenuated the increase in sugar-cravings under trigger conditions (stress).
Although the authors are careful about not over-interpreting their findings from this acute study (that did not actually measure sugary-snack intake), they do make the following speculation regarding clinical relevance,
“This study adds to the increasing evidence that physical activity can somehow help to regulate the urge to consume snack food. It may be easy for overweight people to fit in short bouts of low-moderate intensity physical activity, instead of being sedentary, to elevate affective activation and valence and reduce high energy food cravings which may be triggered by stress and the presence of snack foods.”
While I am certain that more intense exercise may well trigger a hunger response, it appears that even a short bout of brisk walking may help dispel those cravings for sugary snacks (let me know if you have experienced this).
Regular readers will recall that for the past 9 years, I have spent 10 days each summer at the Canadian Obesity Network’s 9-day obesity training camp for students and new professionals (post-docs, residents, etc). This year’s camp will again be held in the attractive setting of the Canadian Rockies.
The Camp is a unique research training activity designed to help trainees advance their careers and continuing engagement in the obesity field and promotes a better understanding of the multi-disciplinary aspects of obesity.
The curriculum covers all aspects of obesity ranging from epidemiology and public health to cell biology, energy, regulation, clinical management. The program has a strong practical component that allows participants to integrate the learnings into their research and/or practice. Opportunities for formal and informal interactions between participants and senior faculty are a key factor in determining the success of the camp.
One of the most important outcomes of this activity is the establishment of a community of young researchers and practitioners that can respond to the growing obesity epidemic in Canada and around the world. A formal social networking analysis of Boot Camp graduates indicates that the boot camp supports the advancement of trainees’career and contributes to ongoing engagement in the obesity field.
The Obesity Boot Camp consists of nine days of intensive teaching and networking, offered to Canadian and international young obesity researchers and new professionals. Young professionals include individuals in their last year, or within five years of, completing their MSc/PhD training. The program is also open to health practitioners and/or clinician scientists such as physicians, dietitians, and exercise specialists.
Participants must submit a completed registration form, a letter of recommendation from their supervisor, a copy of their curriculum vitae and a single-spaced page summary of their research interests or area of practice, and a brief explanation of what they hope to get out of the boot camp.
Cost: $2500 (includes shared accommodation, syllabus, full program, meals, breaks and select social events).
Space is limited. Click here to see the most recent boot camp announcement