In Obesity Variety is Bad

Humans are omnivores and apparently our hunter-gatherer ancestors ate an extraordinary range of plant and animal foods.

The advent of culinary skills and use of spices and seasonings further enhanced the variety, taste, flavour, appearance, texture and consistency of foods.

Today, the apparently limitless choice of foods in our supermarkets, restaurants and homes is a sure sign of the importance we place on variety and variation when it comes to eating.

When trying to manage your weight, however, variety may be your downfall.

This at least is the gist of a recent study by Ramona Guerrieri and colleagues from the Department of Experimental Psychology, Maastricht University, in The Netherlands, who examined the interaction between impulsivity and a varied food environment and its influence on on food intake and overweight, published in the International Journal of Obesity.

The study is based on two observations:

1) Our current food environment offers a large variety of cheap and easily available sweet and fatty foods

and

2) Impulsive people may be reward sensitive and are generally less successful at inhibiting prepotent responses (i.e. a response that is or has been previously associated with positive reinforcement)

Using a rather complicated experimental design masquerading as a taste test, Guerrieri and colleagues studied 78 healthy primary school children (age: 8-10 years) regarding two aspects of impulsivity: reward sensitivity and deficient response inhibition.

The kids were studied in two groups: one was offered rather monotonous foods; the other was offered foods varied in colour, form, taste and texture.

As expected, reward sensitivity interacted with variety. In the "monotony group" there was no difference in food intake between the less and more reward-sensitive children (183 kcal+/-23 s.d. versus 180 kcal+/-21 s.d.).

However, in the "variety group" the more reward-sensitive children ate almost 70% more calories than the less reward-sensitive children (237 kcal+/-30 s.d. versus 141 kcal+/-19 s.d.).

While reward sensitivity in itself was not linked to overweight, deficient response inhibition (a measure of impulsivity) was.

Clearly, the kids with poor impulse control were handicapped when it came to dealing with variety.

Why is this important?

What the data suggest is that kids (and adults?) who have poor impulse control are more likely to overeat when faced with variety. Therefore, the incredible variety and choices of food that we have available to us, may indeed be a major factor in the problem of overeating.

As blogged previously, attention deficit disorders (ADD) are surprisingly common in obese children and adults - in our currently environment, this increased impulsivity may be an important factor contributing to their weight gain.

If your problem is impulse control - the less choices you give yourself the better.

AMS
Edmonton, Alberta

Why Hunger Makes You Eat Crap

The best recipe for poor food choices and weight gain is to only eat when you are hungry.

This is best done by skipping meals and allowing yourself to get so hungry that you will end up eating anything edible, no matter how bad for you.

Obviously, if you are hungry and have the choice, last night's leftover pizza will prevail over carrot sticks.

So why is it more difficult to make healthy food choices when you are hungry?

Because healthy foods are seldom your favorite foods and usually not the ones that trigger your reward centres and make you feel happy and content.

Hey wait a minute! Did you not in a previous blog entry remember me making the distinction between hunger (homeostatic) eating and appetitive (hedonic) eating?

Well, it turns out the two systems are more closely linked than we may have thought - at least according to a new paper by Saima Malik and colleagues from McGill University, Montreal, Canada, just out in CELL METABOLISM.

Malik and colleagues infused the "hunger-hormone" ghrelin into volunteers and used functional MRI to look at what parts of the brain were activated in response to pictures of junk foods or scenery (controls).

It turns out that not only did ghrelin (as expected) increase the sensation of hunger, but it also increased brain activity in the amygdala, orbitofrontal cortex, anterior insula, and striatum which form part of the mesolimbic reward system involved in addictive behaviours.

This finding is new, because so far ghrelin was largely associated with the homeostatic system - i.e. the system that is more concerned with ensuring energy balance rather than the hedonic system - i.e. the system that is more about the reward you get from eating foods you like.

When you think about it, this finding sure makes sense. After all if you are hungry (and have a choice) you may as well eat the foods that you enjoy.

Unfortunately in today's world that may also mean that you are more likely to chose energy-dense foods that make you feel good, which in turn makes you eat too much - a sure recipe for weight gain.

So while in clinical practice it may make sense to distinguish between homeostatic and hedonic hyperphagia, it is important to remember that biologically the systems are linked and ingestive behaviour may well display characteristics of both systems at a given meal.

It is indeed a fine line between biological need and addiction.

AMS
Edmonton, Alberta

Does Obesity Surgery Convert "Bingers" to "Grazers"?

Classical Binge Eating Disorder (as defined by DSM-IV) is found in around 20-40% of severely obese patients presenting at bariatric centres (including ours). Numerous studies have shown that patients with BED can achieve significant weight loss, resolution of comorbidities and improvement in quality of life with obesity surgery and therefore should not generally be denied surgery.

Nevertheless, many centres (including ours) are reluctant to operate on patients with active BED fearing poorer outcomes and greater distress. It turns out that we really don't know much about how bariatric surgery affects eating patterns in patients with BED.

This question was now addressed by Susan Colles and colleagues from Monash University in Melbourne in a study published in the March issue of OBESITY. Colles and colleagues planned to study eating behaviours in 180 patients before and 12 months following laparoscopic adjustable gastric banding (LABG). Of these, 6 did not receive surgery, 1 died of a myocardial infarct and 44 (25% of eligible subjects) did not return for the 12-month survey (more on this later).

While only 14% of patients had BED at baseline, 31% were described as "uncontrolled eaters", 40% had night eating syndrome (NES) and 26% were "grazers".

Although all groups, including the "bingers" lost similar amounts of weight and BED reduced to 3% in this group, patients with preoperative BED were most likely to develop uncontrolled eating or grazing. Patients who reported uncontrolled eating or grazing after surgery tended to lose less weight and reported greater psychological distress.

Interestingly, the authors report that the 12-month non-responders were more likely to have had presurgical BED, have lost less weight and attended less clinic appointments. This may be due to patients with these behaviours feeling more ashamed about their "loss of control" and therefore avoiding follow-up visits.

This study highlights the risk of preoperative "bingers" to become "uncontrolled eaters" or "grazers" resulting in psychological distress and poorer weight outcomes. As these patients are more likely to drop out of follow-up they may also be at increased long-term risk of nutritional deficiencies and other long-term complications of bariatric surgery.

In an accompanying paper in the same issue of OBESITY, Colles and colleagues describe how "loss of control" may be at the root of the significant psychological distress of patients with BED resulting in their greater likelihood of seeking out bariatric surgery as a means to control their eating behaviour. This may well in part explain the high prevalence of BED in patients presenting in bariatric clinics.

Clearly, we need to learn more about how to pre-screen patients for potentially poor outcomes and how best to monitor post-surgical patients for the development of aberrant eating behaviours.

Given that BED, once diagnosed, is actually quite responsive to psychological treatments resulting in a remarkably high rate of resolution, I wonder about the rational for operating on patients with active BED - after all weight loss should not be the only parameter by which results of obesity surgery are measured.

AMS
Edmonton, Alberta

Deconstructing Ingestive Behaviour

As someone with an interest in ingestive biology, I continue to be amazed by the complexity of eating behaviour.

Three commonly recognized eating behaviour constructs are "disinhibition", "cognitive restraint" (rigid or flexible) and "hunger" (internal or external).

Of these only "disinhibition" has been consistently shown to be strongly associated with adult weight gain.

There are actually three forms of disinhibition:

1) habitual disinhibition: the tendency to overeat in daily life

2) emotional disinhibition: the tendency to overeat in response to emotional states like anxiety or depression

3) situational disinhibition: the tendency to overeat in response to specific situations, e.g. social occasions

A recent study by Nicholas Hays and Susan Roberts from the University of Arkansas, published in OBESITY, examined the relationship between 20 year weight gain and eating behaviour subscales using the Eating Inventory (also often referred to as the Three-Factor Eating Questionnaire) in 535 women aged 55-65 years.

While "habitual" disinhibition showed the strongest association with weight gain, "emotional" disihibition showed only a modest association, while "situational" disinhibition was largely unrelated to weight gain. Flexible restraint significantly attenuated the effect of habitual disinhibition on weight gain.

As acknowledged by the authors, this study has several limitations including the fact that the weight data are self-reported and retrospective and that the participants' ingestive behaviour may have changed over time.

Nevertheless, if true, the paper raises a significant issue in terms of the focus of dietary counseling.

Thus far, dietary counseling has often tended to focus on situational disinhibition (e.g. dealing with eating on social occasions, in restaurants, etc.) or emotional disinhibition (e.g. coping strategies to avoid emotional eating). According to the findings of this paper, it would be far more appropriate to focus attention on reducing habitual overeating i.e. eating in "everyday" situations.

Strategies shown to help reduce habitual disinhibition include cognitive behavioural therapy, reducing variety and treatment with sibutramine.

It may be time for studies to expressly target habitual disinhibition in individuals who display this ingestive behaviour.

Obviously, this does not mean that for some people "emotional" or too frequent "situational" disinhibition cannot also significantly contribute to their weight gain.

Once again - one size is unlikely to fit all - but, providing the right dietary counseling requires making the right "diagnosis",

AMS