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 for 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).
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).
Now, Mary Boggiano and colleagues from the University of Birmingham, Alabama, in a paper published in Appetite, report that using tasty foods as a coping strategy is associated with weight gain.
The study administered the Palatable Eating Motives Scale (PEMS), which assesses eating for coping motives (e.g., to forget about problems, reduce negative feelings), to 192 college students, who were reexamined after two years (with a few measures in between).
Not too surprisingly, PEMS scores predict changes in BMI over two years.
On a positive note, however, the researchers found that PEMS scores (i.e. using food for coping) can change over time and a reduction in PEMS scores was also associated with a lesser weight gain. In overweight subjects, a reduction in PEMS scores was even associated with modest weight loss.
Thus, the authors suggest that interventions aimed specifically at reducing palatable food intake for coping reasons, should help prevent obesity if this motive-type is identified prior to significant weight gain.
That there are no easy solutions to obesity and managing your weight is challenging at the best of times. But trying to find manage it without understanding even the basics of how your body works to defend its weight is hopeless at best.
A sort paper by Christopher Ochner and colleagues, published in The Lancet Diabetes and Endocrinology, succinctly describes the challenges, and appeals to clinicians (and decision makers) to take this problem seriously (instead of trivialising it as a simple “lifestyle” issue).
“Many clinicians are not adequately aware of the reasons that individuals with obesity struggle to achieve and maintain weight loss, and this poor awareness precludes the provision of effective intervention.”
As readers of these pages are well aware,
“Irrespective of starting weight, caloric restriction triggers several biological adaptations designed to prevent starvation. These adaptations might be potent enough to undermine the long-term effectiveness of lifestyle modification in most individuals with obesity, particularly in an environment that promotes energy overconsumption.”
But is is not just about the body’s defense mechanisms.
“Additional biological adaptations occur with the development of obesity and these function to preserve, or even increase, an individual’s highest sustained lifetime bodyweight. For example, preadipocyte proliferation occurs, increasing fat storage capacity. In addition, habituation to rewarding neural dopamine signalling develops with the chronic overconsumption of palatable foods, leading to a perceived reward deficit and compensatory increases in consumption.”
“…improved lifestyle choices might be sufficient for lasting reductions in bodyweight prior to sustained obesity. Once obesity is established, however, bodyweight seems to become biologically stamped in and defended. Therefore, the mere recommendation to avoid calorically dense foods might be no more effective for the typical patient seeking weight reduction than would be a recommendation to avoid sharp objects for someone bleeding profusely.”
As the authors point out,
“…there is now good evident that these biological adaptations often persist indefinitely, even when a person re-attains a healthy BMI via behaviourally induced weight loss….Thus, we suggest that few individuals ever truly recover from obesity; individuals who formerly had obesity but are able to re-attain a healthy bodyweight via diet and exercise still have ‘obesity in remission’ and are biologically very different from individuals of the same age, sex, and bodyweight who never had obesity.”
To overcome these biological adaptations it is not enough to appeal or rely on will-power alone to sustain long-term weight loss. Rather, treatments need to address these biological adaptations and homeostatic mechanisms, which is exactly what anti-obesity drugs or surgery does.
Thus, the authors have the following advice for clinicians:
“Specifically, clinicians should be proactive in addressing obesity prevention with patients who are overweight and, for those who already have sustained obesity, clinicians should implement a multimodal treatment approach that includes biologically based interventions such as pharmacotherapy and surgery when appropriate.”
“We urge individuals in the medical and scientific community to seek a better understanding of the biological factors that maintain obesity and to approach it as a disease that cannot be reliably prevented or cured with current frontline methods.”
For all my Canadian readers (and any international readers planning to attend), here just a quick reminder that the deadline for early bird discount registration for the upcoming 4th Canadian Obesity Summit in Toronto, April 28 – May 2, ends March 3rd.
To anyone who has been at a previous Canadian Summit, attending is certainly a “no-brainer” – for anyone, who hasn’t been, check out these workshops that are only part of the 5-day scientific program – there are also countless plenary sessions and poster presentations – check out the full program here.
To register – click here.