Arya M. Sharma, MD

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

One of my favourite sayings to patients asking me about bariatric surgery is, “If you think surgery is a quick fix - don’t do it”.

That said, one of the consistent messages I hear from patients, who have undergone successful surgery, is about how it appears to affect their appetite, cravings and response to food.

This is particularly impressive, when you hear patients tell you how their previous obsession and desire to eat (many liken this to a addiction) before surgery, has been replaced with a surprising disinterest, not to say, indifference to foods that they previously found most tempting and rewarding.

This anecdotal report from post-surgical patients may well have a sound biological basis, according to a study by Christopher Ochner and colleagues from St. Luke’s Roosevelt Hospital, New York, NY, published in a recent issue of the Annals of Surgery.

The researchers used functional magnetic resonance imaging (fMRI) and verbal rating scales to assess brain activation and desire to eat in response to high- and low-calorie food cues in 10 female patients 1-month pre- and post-Roux-en-Y bypass surgery.

Following surgery, there was a distinct decrease in the activation of key areas of the brain known to be involved in the mesolimbic reward pathways in response to high-caloric highly palatable food cues (pepperoni pizza, fudge sundae).

These changes in brain imaging were mirrored by the participant’s subjectively reduced desire to eat in response to these cues, suggesting that the surgery may have resulted in substantial changed in the neuronal response mechanisms to such cues.

Thus, this study provides further evidence that bariatric surgery owes its success to neuronal (and hormonal?) mechanisms that go beyond simplistic notions of ‘restriction’ or ‘malabsorbtion’.

Indeed, as the authors point out, these findings are in stark contrast to previous findings in patients losing similar amounts of weight without surgery, who regularly report an increase rather than a decrease in their appetite and desire for highly palatable foods.

Clearly, as the researchers conclude, elucidation of exactly how gastric bypass surgery affects the brain’s reward system, may point to novel pharmacological targets that could lead to new medications that may ultimately reduce (or completely abolish?) the need for obesity surgery.

I would certainly be curious to hear from my readers how, in their experience, bariatric surgery affected their (or their patients’) appetite and cravings for highly palatable foods.

AMS
Edmonton, Alberta

Ochner CN, Kwok Y, Conceição E, Pantazatos SP, Puma LM, Carnell S, Teixeira J, Hirsch J, & Geliebter A (2011). Selective reduction in neural responses to high calorie foods following gastric bypass surgery. Annals of surgery, 253 (3), 502-7 PMID: 21169809

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

Regular readers will recall my recent posts on the notion that the benefits of regular exercise on body weight are largely mediated by the positive impact on caloric intake rather than by the number of calories burnt.

This notion is based on the idea that exercise modulates eating behaviour by reducing stress, improving mood, and perhaps, even by reducing the ‘reward’ response of palatable foods.

The latter assumption, is supported by a recent stud by Maciej Buchowski and colleagues from Vanderbilt University, Nashville, Tennessee, published in PLoS.

The study was conducted in 12 sedentary or minimally active non-treatment seeking cannabis-dependent adults, who attended 10 supervised 30-min treadmill exercise sessions standardized using heart rate (HR) monitoring (60-70% HR reserve) over 2 weeks.

Self-reported drug use reduced from about 6 joints per day to less than 3 joints a day during the exercise intervention and remained at 4 joints per day 2 weeks after the end of the study.

Average Marijuana Craving Questionnaire factor scores for the pre- and post-exercise craving assessments were also markedly reduced for compulsivity, emotionality, expectancy, and purposefulness.

As the authors discuss:

“Consistent with the changes in cannabis use reported by participants, subjective cravings elicited by cannabis cues were also significantly reduced by exercise, suggesting the possibility that the potential therapeutic effect of exercise may be mediated via brain mechanisms responsible for cue-induced craving.

These same brain mechanisms have been invoked in behavioral addictions involving non-drug rewards, as is observed in overeating and obesity, problematic hypersexuality, and pathological gambling. Analogously, it has been reported that exercise activates some of the same reward pathways as are activated by addictive drugs. For instance, acute bouts of exercise increase central dopamine concentrations and chronic exercise leads to sustained increases in dopamine concentrations and compensatory alterations in dopamine binding proteins in brain regions relevant to reward.”

Thus, the findings from this rather small study provides the basis for conducting a much larger and longer-term study on the use of exercise as a treatment for marijuana addiction.

On the other hand, given important role of the brain’s reward circuitry for food in take, it may not be expected if such a study also demonstrates a positive effect on overconsumption of highly palatable foods.

AMS
Dushesnay, Quebec

Buchowski MS, Meade NN, Charboneau E, Park S, Dietrich MS, Cowan RL, & Martin PR (2011). Aerobic exercise training reduces cannabis craving and use in non-treatment seeking cannabis-dependent adults. PloS one, 6 (3) PMID: 21408154

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