I have previously noted that the real problem with fast food is not so much the ‘food’ but rather the ‘fast’ - i.e. the fact, that it is designed to be eaten quickly.

I also, earlier this year, blogged about novel approaches like the MandoMeter or the SMART device to help people slow down their eating to better control their weights.

it turns out that the speed of eating may in fact be one of the earliest predictors of obesity, even in 4-year old kids.

Thus, in a study by Robert Berkowitz and colleagues from the University of Pennsylvania, published in the latest issue of OBESITY, rapid eating (higher number of mouthfuls per minute) of a single laboratory testmeal was a remarkably strong predictor of subsequent weight gain in kids.

At 4 years of age, 32 children of overweight mothers and 29 children of normal weight mothers were given a test meal in a controlled laboratory setting. Mouthfuls of food per min at this single meal not only predicted changes in BMI from 4 to 6 years but also changes in sum of skinfolds and total body fat.

As the authors note, rapid eating could well be an innate (genetic?) trait related to food reward and it will be interesting to see if slow eating can be taught and if this would reduce the risk for weight gain. Of course you can always trick your 4-year old into eating slow by providing slow foods that take longer to eat. 

In the meantime, if your 4-year old prefers to play with her food and takes forever to finish, you can at least comfort yourself with the notion that she is probably not in danger of having to worry about excess weight any time soon.

AMS
Toronto, Ontario

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

Regular readers of these pages are well aware of the close link between addictions and some forms of overeating. This topic is now nicely addressed in a commentary by Valerie Taylor (McMaster, Hamilton), Claire Curtis and Caroline Davis (both York University, in this week’s edition of CMAJ.

As they discuss,

“The concept of food addiction, which more accurately may reflect addiction to specific components of food, can be described in much the same way as other addictive behaviours. Both food and drugs induce tolerance over time, whereby increasing amounts are needed to reach and maintain intoxication or satiety. In addition, withdrawal symptoms, such as distress and dysphoria, often occur upon discontinuation of the drug or during dieting. There is also a high incidence of relapse with both types of behaviour.“

To further support their arguments, they cite the many imaging studies showing that specific areas of the reward or mesolimbic system, such as the caudate nucleus, the hippocampus and the insula, are activated both by drugs and by food.

Thus, the easy accessibility of highly palatable foods together with our innate preferences for such foods, can increase the likelihood that vulnerable people will “misuse” food, in much the same way that addicts misuse other drugs to blunt negative emotional states, such as depression, anxiety, loneliness, boredom, anger orinterpersonal conflict.

While the concept of addiction should not negate the role of free will and personal choice, it does provide a rationale for the including addiction screens as a routine part of assessment for obesity. It may also help explain the success of lifestyle programs that incorporate pharmacotherapy or behavioural strategies specifically designed to address the addictive component of this illness.

Thus, as pointed out by Taylor and colleagues, there is not only considerable overlap among the medications shown to interfere with food and drug abuse in animal models, but the many behavioural interventions developed for managing addictions (motivational interviewing, cognitive behavioural therapy and 12-step programs), are increasingly recognised as also being helpful in managing obesity.

Health professionals and decision makers charged with tackling the obesity epidemic would do well to familiarise themselves with the science of addictions and utilize learnings from addiction management in their counseling of patients presenting with excess 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