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

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

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