Arya M. Sharma, MD

Traditionally, dietary counseling has focused largely on client education and prescriptive approaches to promoting better ‘choices’.

Based on the limited success that such approaches have had on changing long-term dietary habits, a rather provocative article by Bradley Applehaus and colleagues from the Rush University Medical Centre, Chicago, Il, published in a recent issue of the Journal of the American Dietetic Association, argues that it is perhaps now time to discard the notion of ‘choice’ in favor of a strategy based on a deeper understanding of the complex interaction between neurobehavioural processes and environmental determinants of overeating.

As the authors discuss, both counselors and clients frequently attribute obesity largely to poor ‘personal choices’ and studies have shown that dietitians rank ‘lack of willpower’ as far more important to the development of obesity than genetic or other biological factors. This is not only contrary to our current understanding of the complex neurobiology of ingestive behaviour but also only serves to stigmatise and frustrate patients, who in turn blame their own ‘failures’ on lack of motivation or personal ‘failings’.

“The term personal choice implies that human behavior derives from conscious, volitional decisions, and connotes that human beings have free will to decide between alternative courses of action independent of biological and environmental forces. An implication of this definition of personal choice is that individuals can be considered causally, financially, and morally responsible for their behavior”

“In contrast to the notion of personal choice, some argue that human behavior is explained by neurobiological processes and their interaction with environmental stimuli. Supporting this deterministic model of personal choice are studies demonstrating that future actions can be predicted by brain activation patterns up to 10 seconds before individuals become aware of having made a decision, behavior is strongly influenced by processes outside of conscious awareness, and individuals can be led to believe that they have caused actions outside of their control.”

Thus, the authors propose that rather than making adoption of a ‘healthy’ diet a matter of choice, dietetic practitioners may better serve their clients by basing their counseling strategies on the emerging understanding of neurobehavioural drivers of eating behaviours, particularly, on the issues of food reward, inhibitory control, and time discounting.

Whereas the concept of ‘food reward’ involving the brain’s complex mesolimbic reward circuitry (as in addictions) is readily evident, as is the complex neurobiology of the prefrontal cortex that determines motivation, impulsivity and inhibitory self-regulation, time discounting refers to the increased value of immediate (short-term) rewards compared to deferred (long-term) benefits routinely demonstrated in psychological testing and deeply ingrained in human behaviour.

Recognising and fully acknowledging how the brain’s neural circuitry that underlies these behaviours interacts with (and is thus ultimately responsive to) environmental situations and cues can perhaps provide a far more realistic and effective counseling strategy.

In their paper, the authors provide several specific examples of how such an approach may work.

For e.g., the tendency for the brain’s reward circuitry to drive the intake of highly palatable foods can be thwarted by eliminating such foods from the personal foodscape and avoiding temptation and exposure to such foods by sticking to grocery lists or online grocery shopping.

Similarly, inhibitory control can be made easier by avoiding situations that challenge (e.g. buffets) or weaken (e.g. stress) inhibitory control.

The tendency to discount time can be countered by focussing on short-term (immediate) rather than long-term (health) goals.

Many of these strategies may seem familiar to present recommendations, however, the context and manner in which these strategies are presented to and discussed with the client would be vastly different.

Thus, rather than making these behaviours a matter of ‘personal choice’ the counseling goal would be to have clients fully understand how their own genetic predispostiion and neurobiology drives them to these behaviours and how they have to adopt these ‘unnatural’ and ‘difficult’ strategies to overcome their ‘nature’.

As the authors point out:

“the model explains eating behaviors that promote obesity without invoking character flaws (eg, lack of willpower). By emphasizing genetically-influenced neurobiological processes that confer vulnerability to overeating in a toxic food environment, the model enables dietetics practitioners to more effectively address obesity without promoting stigma.”

In terms of the counseling process, the authors suggest that this approach

“…acknowledges that patients are working against potent genetic vulnerabilities and a toxic food environment, and normalizes patients’ (and dietetics practitioners’) frustration with failed attempts at weight control.”

and that

“…patients can better control their weight through strategies focused on the interaction between the brain and the environment. For the majority of dietetics practitioners, this second message constitutes a shift in strategy from urging patients to make the tough choices required for weight control to helping patients minimize the number of tough choices they encounter.”

While it remains to be seen whether or not such a shift in strategy will indeed produce better outcomes, I do appreciate the fact that this paper makes a serious attempt at recognising just how effectively biology drives eating behaviour and that the simplistic concepts of ‘personal choice’ and ‘will power’ are clearly not the most effective strategies to counter the toxic food environment that most of us are exposed to.

To use an analogy that I have used before, recognising that someone has a hypersensitive bronchial system that predisposes them to asthma should lead them to avoiding and eliminating air-borne pollutants in their immediate environment rather than simply trying to breathe less.

AMS
Edmonton, Alberta

Hat tip to Annette for pointing me to this article.

Appelhans BM, Whited MC, Schneider KL, & Pagoto SL (2011). Time to abandon the notion of personal choice in dietary counseling for obesity? Journal of the American Dietetic Association, 111 (8), 1130-6 PMID: 21802557

A couple of weeks ago, at the SCOPE Summer School, I had the pleasure of meeting and listening to Carel Le Roux, a bariatric physician from London’s Imperial College, on the many complex ways in which bariatric surgery appears to affect gut hormones and eating behaviour.

In his talk, he also presented the results of a fascinating study, that he recently published in the American Journal of Physiology.

Based on the observations, that I alluded to in yesterday’s post, namely, that bariatric surgery appears to very much change the appetite and food preferences of patients, Le Roux and colleagues examined how gastric bypass affects intake of and preference for high fat food in an experimental (rats) study and within a trial setting (humans).

Le Roux and colleagues noted that gastric bypass surgery in rats not only reduced total fat and caloric intake but, interestingly, increased their preference for standard low fat chow compared to more palatable high-fat chow (preferred by the sham-operated rats).

In addition, compared to sham-operated rats, gastric bypass rats displayed much lower preferences for Intralipid® (a fat emulsion) concentrations above 0.5% in an ascending concentration series (0.005%, 0.01%, 0.05%, 0.1%, 0.5%, 1%, 5%).

Furthermore, an oral gavage of 1 ml corn oil after saccharin ingestion in gastric bypass rats induced a conditioned taste aversion.

Thus, gastric bypass surgery in these rats evidently reduced their liking for (and in fact appeared to invoke an aversion to) high-fat chow, suggesting that changes in fat preference may contribute to long-term maintained weight loss after gastric bypass.

Interestingly, the authors also noted that their patients with successful gastric bypass surgery consumed considerably less fat in their diet than patients, who had undergone gastric banding.

Regular readers may recall my recent post on how complex neuronally mediated changes in the gut endocannabinoid system may make it difficult to eat just one French Fry. Similarly, the authors speculated that gut hormones like GLP-1, which appear to be consistently elevated following gastric bypass (but not gastric banding) may also have important effects on appetite and desire to eat highly-palatable energy dense foods.

Clearly, there is still much to be learnt about how exactly (different kinds of) bariatric surgery affect appetite and food intake - clearly the simplistic notion of ‘restriction’ and/or ‘malabsorbtion’ are just that - ’simplistic’.

AMS
Edmonton, Alberta

Le Roux CW, Bueter M, Theis N, Werling M, Ashrafian H, Löwenstein C, Athanasiou T, Bloom SR, Spector AC, Olbers T, & Lutz TA (2011). Gastric bypass reduces fat intake and preference. American journal of physiology. Regulatory, integrative and comparative physiology PMID: 21734019

Loyal readers may recall a previous post on how the incredible diversity of food choices may be an important but underestimated contributor to the obesity epidemic. Particularly in children, variety has been shown to promote overeating, especially, when variety is provided in a setting that encourages ‘mindless’ eating.

In most cultures, traditional foods eaten every day, were often simple and repetitive (e.g. pretty much the same meat and potatoes, or the same old pasta dish everyday), which was exactly, why you went to the extents of preparing special meals with lots of different dishes on those special occasions (which were rare and far apart).

In contrast, our daily diets today are highly variable with seemingly unlimited choices (e.g. five different salad dressings to chose from or endless combinations even at fast food restaurants - just think of the wide range of offerings at a food court).

Previous studies have shown that most people, when confronted with choice, will eat more than ‘normal’ - even if simply out of curiosity (the Bootcampers will know exactly what I am talking about).

So does making your diet more ‘boring’ help reduce caloric intake?

This question was addressed by Leonard Epstein and colleagues from the Universities of Buffalo and Vermont in a paper just published in the American Journal of Clinical Nutrition.

The researchers randomised 16 obese and 16 non-obese women to a macaroni and cheese meal presented 5 times, either daily for 1 wk or once per week for 5 wk in a carefully controlled experimental setting.

In both obese and nonobese women, daily presentation of the marcaroni-cheese meal resulted in faster habituation, decreased ‘liking’ and eating about 100 fewer calories per meal than did once-weekly presentation of the macaroni-cheese meal.

Thus, making food ‘boring’ by presenting the same meal everyday will reduce ‘liking’ and caloric intake - but it is unclear how much ‘variability’ can be allowed to elicit this effect:

“Will someone show long-term habituation to consecutive meals of cheese pizza, pepperoni pizza, and mushroom pizza? Likewise, would people show long-term habituation if they consumed macaroni and cheese and risotto with the same cheese sauce, because of the representations of the cheese sauce? It is likely that the level of habituation is based on generalization of characteristics of food across meals, but research is needed to identify what similarities across foods are adequate to produce long-term habituation.”

As the authors point out, this experiment may point a way to rather simple dietary intervention strategies:

“Long-term habituation has many implications. Increasing food variety is a reliable way to increase energy intake within a meal, and increased variety in the diet is associated with greater body weight and poor choice of foods. Reducing variety may be an important component of interventions for obesity. Habituation may provide a mechanism for the effects of variety on energy intake, such that within-session habituation during a meal can lead to reduced intakes with reduced variety of foods. The long-term habituation reported here may be a mechanism for the effects of variety across (as opposed to within) meals. Thus, promoting long-term habituation by repeatedly serving the same food over days would lead to reduced energy intake over time. Such an intervention may be much simpler than the complex self-regulation approaches that are the basis for much of the current obesity therapy, which often meet with limited long-term success.”

I can think of a number of interesting experiments to see if this also works for highly palatable foods like snacks and desserts.

I wonder for just how long would one have to eat daily servings of chocolate or chips before someone gets tired enough of these foods to cut back?

I am certainly curious about whether any of my readers have used this strategy and found it helpful?

What are your favourite ‘most-boring’ foods?

AMS
Toronto, Ontario

Epstein LH, Carr KA, Cavanaugh MD, Paluch RA, & Bouton ME (2011). Long-term habituation to food in obese and nonobese women. The American journal of clinical nutrition, 94 (2), 371-6 PMID: 21593492

Have you ever wondered why it is almost impossible to only eat one potatoe chip or French fry?

Regular readers may recall a previous post on the discovery that we have specific oral sensory receptors that allow us to sense the ‘fattiness’ of food - a function that makes a lot of sense, given that dietary fat provides the densest source of caloric intake.

Now, Nicholas DiPatrizio and colleagues from the University of California, Irvine, have discovered that these oral dietary fat sensors activate a powerful ‘addiction-type’ mechanism in your gut that serves to promote further fat intake - their study is published in a recent issue of the Proceedings of the US National Academy of Science.

For their studies, the researchers used a well established ’sham feeding’ model in the rat, where liquid diets eaten by the animal can be drained from the stomach via a chronically implanted gastric cannula, thereby preventing them from reaching the small intestines.

Using this model, the researchers showed that ’sham feeding’ of a high-fat diet resulted in the potent activation of endocannabinoids in the early part of the small intestine by altering enzymatic activities that control endocannabinoid metabolism. The endocannbinoids (cannabis-like compounds produced in the body) are well known to play an important role in regulating ‘rewarding’ feeding behaviours.

This effect was abolished by surgical transection of the vagus nerve showing that the stimulation of these changes in the gut is driven through a centrally mediated neuronal pathway.

Furthermore, the local application of cannabinoid type 1 receptors blockers (e.g. rimonabant) in the small gut, reduced increased sham fat ingestion.

In other words, this study shows that oral sensing of fat sends a signal to the brain, which in turn sends a signal to the gut leading to formation of endocannabinoids, which in turn re-enforce fat eating.

This is probably why, just eating one piece of fatty food (say one potatoe chip or French fry) is so hard - simply eating one makes you want to continue eating till the whole bag or plate is empty.

Unfortunately, the drug rimonabant, used to effectively block this effect in this study, is no longer available for obesity management (it was withdrawn due to its negative impact on mood), but it may well be that other CB-1 inhibitors that do not enter the brain may prove to be effective to reduce fat intake.

Or, in the words of the authors:

“Our findings identify the gut endocannabinoid system as a critical component of the positive feedback mechanism that drives fat intake and suggest that therapeutic strategies aimed at restraining small intestinal endocannabinoid activity might help to selectively reduce the overeating of fatty foods.”

In the meantime using strategies based on limiting portion size, e.g. asking for a small serving of fries or transferring a small portion of chips into a separate bowl, while leaving the full bag in the pantry, may be the best strategy to thwart this mechanism.

AMS
Duchesnay, Quebec

Dipatrizio NV, Astarita G, Schwartz G, Li X, & Piomelli D (2011). Endocannabinoid signal in the gut controls dietary fat intake. Proceedings of the National Academy of Sciences of the United States of America PMID: 21730161

I always get nervous when anyone proclaims that the cause or solution to the obesity epidemic is any one factor.

As regular readers will appreciate, obesity is complex, heterogeneous and diverse. There are 100s of factors that can promote weight gain or make weight loss difficult and different factors are more or less important in different individuals - no diet, no exercise program, no psychological counseling, no medication, no surgery will ever be found that works for everyone.

That said, there may well be some factors that are more important than others, when it comes to issues like population exposure - even factors that have small individual effects, can have large population effects, simply because they affect so many people.

This does not mean that such factors are the most important or even the most powerful drivers of obesity in a given individual - in fact, in a given individual, this same factor may play absolutely no role - either because this individual is not exposed to this risk factor or because this person is genetically or biologically ‘resistant’ to this factor.

One of the factors that often comes up in obesity discussions is the role of fructose. While, I doubt that fructose (or any one factor) can explain all of the obesity problem (or provide a simple solution), there is some fascinating science about how fructose could possibly play a role.

This complex science (epidemiology, history, biochemistry, policies, politics, etc.) of fructose is comprehensively discussed in this fascinating and captivating 90 minute(!) presentation by Robert Lustig, Professor of Pediatrics in the Division of Endocrinology at the University of California, San Francisco.

Amazingly, this very scientific and rather lengthy video went ‘viral’ on YouTube and has been viewed almost 1.5 million times since it was originally posted back in 2009.

So grab a non-fructose-sweetened beverage, head to my blog page, and sit back as Lustig takes you through a lot of very interesting science (some of this may be too complex for some readers, but you’ll still get the picture).

By no means, am I as convinced as Lustig about fructose being the root of all ‘evil’, but this video certainly is highly educational and, if nothing else, reminds us of how complex human biology actually is.

AMS
Edmonton, Alberta