Last week, an article in the New York Times with the title “The Obesity-Hunger Paradox“, addressed the issue of food insecurity - or how, not knowing when or where your next meal will come from, can make you overeat - thus promoting obesity.

Interestingly, this month’s issue of OBESITY uses an animal model to illustrate a similar point.

In this study by Xingshenk Li and colleagues from the University of Alabama, one set of mice was first allowed free access to food for six weeks and was then mildly calorie restricted (5%) over three more weeks during which the animals were provided access to food only once a day. In a second experiment mice were either mildly calorie restricted or had free access to food.

Interestingly, one of the big changes in feeding behaviours with calorie restriction was overeating, where the mice ate almost four times the amount of food in a two hour period, than when they had free access to food.

Importantly, despite the overall calorie restriction, the researchers found no change in body weights - rather, the calorie-restricted mice appeared to become fatter, exchanging fat for lean tissue. They also showed a significant reduction in energy expenditure.

The researchers interpret their evidence as supporting the notion that the gorging behaviour in response to food “uncertainity” alters energy partitioning resulting in more effective triglyceride production and fat storage. This altered metabolism may in part be due to the hormonal changes resulting from the “stress” of calorie restriction.

Clearly, these findings should be of interest to those of us who wonder about the long-term effects of caloric restriction, meal skipping, and binge eating.

The study may also explain why chronic (especially intermittent) dieting can be counterproductive and in some individuals paradoxically increase fat stores.

Certainly the study should remind us that any restriction of food intake (whether voluntary or involuntary) can profoundly change our “feeding” behaviour and change the way our bodies handle calories.

The next time you wonder why you or your patients are not losing weight despite restricting calories, remember that there is apparently no end to the tricks our body will come up with to protect its weight.

AMS
Edmonton, Alberta

Dr. Hei Sook Sul

Yesterday, I had the pleasure of listening to Hei Sook Sul (picture) from the University of California, Berkeley, who spoke at the Alberta Diabetes Institute here in Edmonton (host Dennis Vance).

Sul’s group, which works on better understanding the molecular mechanisms underlying the synthesis of fatty acids, recently identified DNA-PK, a protein kinase that plays a role in DNA repair, as a possible key factor in the activation of fatty acid synthase (FAS), the enzyme that helps convert dietary carbohydrates to fat.

In a paper, recently published in the journal Cell, Sul’s group showed that feeding high-carb diets to mice with a disabled DNA-PK gene resulted in lower levels of body fat than in their normal counterparts. This was evidently due to their inability to convert carbs to fats, a key step when excess calories from carbs need to be stored for future use.

As always, one must be careful in jumping from findings in mice to humans, and although DNA-PK may well seem an attractive pharmacological target to prevent fat accumulation in people who eat high-carb diets, it is important not to forget that this enzyme also plays an important role in DNA repair, a possible critical factor in preventing cells from mutating into cancer cells.

Nevertheless, the elucidation of this important metabolic step - the conversion of dietary carbs to fat - is certainly a major breakthrough in our understanding of how the body metabolizes carbohydrates and definitely provides fascinating new insights into the complex workings of nutritional biology.

AMS
Edmonton, Alberta

In medical school I learnt that we have four senses of taste: sweet, sour, salty, and bitter.

Several years ago a fifth sense, umami, was officially added to this list. Umami is stimulated by glutamate (as in MSG) and apparently allows us to taste protein (as in meat, sea food, or cheese).

Now, Jessica Stewart and colleagues from Deakin University in Australia show that a sixth sense, i.e. the ability to orally “sense” the fat content of foods may explain differences in fat preferences (British Journal of Nutrition).

Indeed, previous studies in animals have suggested that oral hypersensitivity to fatty acids (the building blocks of fat) are associated with decreased fat intake and body weight.

In the current study, the investigators first examined the taste thresholds for different types of fatty acids (olate, linolate, and laurate) in 31 normal weight subjects and classified them as hypo- or hypersensitive. Subjects also completed a fat ranking task using custard containing varying amounts (0, 2, 6 and 10 %) of fat.

Hypersensitive subjects reported lower energy and fat intakes, had an increased ability to rank the custards based on fat content and also had a lower BMI levels.

These data suggest that the increased ability to detect nutritional fat may result in lower energy and fat intake, which in turn may result in lower body weights.

Obviously, the idea here is that people who are less sensitive to fat are likely to need more fat in their foods to get that same level of enjoyment as people with more sensitive fat receptors. Because of fat’s high caloric content, this means that they may in the end also end up with more calories, and thus, weight gain.

I can think of a number of interesting questions that these findings may prompt:

1) Is the increased ability to taste fat genetic or are changes in fat-sensitivity determined by habitual fat intake (gustatory plasticity)?

2) Does weight loss affect people’s ability to taste fat (resulting in them searching out fattier foods when on a diet)?

3) Does going on a low fat-diet increase fat sensitivity thereby allowing people to get the same pleasure out of low-fat foods?

4) Can we develop artificial compounds that can stimulate the fat receptors thereby mimicking a higher fat content of foods (like we do with artificial sweeteners)?

Lots of interesting questions, which may not only explain why some people derive more pleasure from fatty foods than others but also open new possibilities for the food industry to manipulate the taste of foods (hopefully to our benefit).

I’d love to hear from my readers regarding their thoughts on “tasting” fat.

AMS
Edmonton, Alberta

There is no doubt that dietitians are the health professionals most often looked to for advise on weight management.

It may therefore come as a surprise to many readers that although dietitians have vast knowledge about healthy eating and the dietary management of a wide range of diseases like diabetes, kidney disease, celiac disease and many others, most dietitians interestingly do not have specific training in treating obesity (the same can sadly be also said for the vast majority of doctors, nurses, exercise physiologists, or any other health profession you can think of).

No one is more acutely aware of this lack of expertise than the dietitians themselves, especially as they are so often called upon for dietary advise by people trying to manage their weight.

As anyone working in this field quickly recognizes (and regular readers of these pages will know this by now), eating or ingestive behaviour is only one part of the energy balance equation and even there, the many socio-psycho-biological factors that determine caloric intake are anything but simple.

I am therefore particularly pleased that the Dietitians of Canada have partnered with the Canadian Obesity Network to co-host the first pan-Canadian Learning Retreat on the Principles & Practice of Interdisciplinary Obesity Management for Dietitians, that is currently being held in Winnipeg.

The aim of the retreat is of course not to teach dietitians about counseling clients on healthy eating or even about nutritive approaches to weight losst. Rather, the retreat focusses on all of the other topics that dietitians need to know about in order to fully understand and appreciate the many factors that are essential for effective obesity management.

It is therefore not surprising that there is a lot of room on the program for the discussion of topics like weight bias, psychosocial factors, mental health, neurobiology of hunger and satiety, exercise physiology, body composition, and of course medical and surgical management of obesity.

Judging by the enthusiasm of the attendees, it appears that such a learning opportunity has been long overdue and I am certainly hopeful that events like this will help ensure that patients struggling with excess weight will have an increasing number of dietitians to turn to, who have been specifically trained in obesity management.

AMS
Winnipeg, Manitoba

Reader of these pages are by now probably quite familiar with the complexity of ingestive behaviour and the importance of understanding brain function in relationship to food intake.

A study, published in this month’s issue of Obesity, illustrates how differences in brain function between obese and non-obese people can explain important differences in response to food.

In this study, Laura Martin and colleagues from the Kansas Medical Center, used functional magnetic resonance imaging (fMRI) to examine changes in brain activity in obese and normal weight adults while they viewed food and nonfood images in premeal and postmeal states.

Both in the premeal and postmeal state, obese participants showed showed increased activation in the anterior cingulate cortex (ACC) and the medial prefrontal cortex (MPFC), regions of the brain responsible for the reward response and impulsiveness, respectively.

In addition, activation of the ACC was associated with decreased levels of self-reported disinhibition while MPFC activation was associated with increased self-reported hunger amongst obese participants.

These findings clearly suggest that brain function associated with food motivation differs in obese and non-obese adults and may well explain the different susceptibilities to weight gain and variability in response to diet interventions.

Given the emerging science on brain plasticity, it is certainly of interest whether or not these differences in brain function are acquired or are indeed innate. Whatever the case, we need to understand and acknowledge that our brains respond differently to the same food stimuli which easily explains why some people may find it much harder to resist overeating in our current obesogenic environment than others.

As I have said before, the obesity epidemic is simply the natural response to our unnatural environment.

AMS
Edmonton, Alberta