Monday, February 17, 2014

Why Hunger Lets You Smell Through Doors

sharma-obesity-olfactionWhy does hunger make our noses more sensitive to the smell of food?

This riveting scientific enigma has now been solved thanks to the tireless work of Edgar Soria-Gómez and Luigi Bellocchio (together with a distinguished team of European colleagues), the results of which are now revealed in Nature Neuroscience.

As casual observers may not be all that surprised to learn, it turns out that the mechanisms involves the exact same system implicated in “the munchies” (Yes, those munchies).

Using pharmacological and genetic experiments in mice, the researchers showed that stimulation of cannabinoid type-1 receptors in the main olfactory bulb (the smell centre) promotes the animals’ ability to smell food when hungry (and eat it).

The fact that hunger draws our focus to smelling out foods of course makes a lot of sense – now at least we know how this works.

How else would you make it back to camp just in time for dinner?

Edmonton, AB

ResearchBlogging.orgSoria-Gómez E, Bellocchio L, Reguero L, Lepousez G, Martin C, Bendahmane M, Ruehle S, Remmers F, Desprez T, Matias I, Wiesner T, Cannich A, Nissant A, Wadleigh A, Pape HC, Chiarlone AP, Quarta C, Verrier D, Vincent P, Massa F, Lutz B, Guzmán M, Gurden H, Ferreira G, Lledo PM, Grandes P, & Marsicano G (2014). The endocannabinoid system controls food intake via olfactory processes. Nature neuroscience PMID: 24509429

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Monday, July 30, 2012

Alcohol, Sleep Deprivation and TV Watching Drive Overeating

Regular readers are well aware that I am more interested in the ‘whys’ of why people eat than in the ‘whats’ of what they eat.

Now a paper by Colin Chapman and colleagues from Upsalla University, Sweden, published in the American Journal of Nutrition, looks at the key lifestyle drivers of overeating, with a particular focus on TV watching, sleep deprivation and alcohol consumption as studied in controlled laboratory settings with healthy volunteers.

Their search of the literature yielded 8 television studies, 5 sleep studies, and 10 alcohol studies.

All three of these factors had significant effects on food intake in the laboratory setting with alcohol having the strongest effect, followed by sleep deprivation and TV viewing.

With regards to the possible mechanisms on how these behaviours affect food intake, the authors have the following to offer:

Alcohol consumption:

“Alcohol is known to induce alterations in circulating ghrelin, a peptide implicated in food reward. In addition, alcohol affects g-aminobutyric acid and opioid systems. The alteration of g-aminobutyric acid signaling in reward centers of the brain stimulates appetite, and opioid signaling has been implicated in regulating the orosensory reward components of eating. These pharmacologic findings are consistent with human studies that showed a greater increase in hunger during the early phase of a test meal after an alcohol preload compared with an energymatched carbohydrate preload. This mimics the pattern of response shown when the palatability of food is enhanced through flavor manipulation.”

Sleep Deprivation:

“There is similar evidence that links sleep deprivation to an increase in the hedonic value of food. Sleep loss causes a constellation of metabolic and endocrine changes, including an increase in circulating ghrelin. Interestingly, recent studies on sleep deprivation have found that it increases overall brain response to palatable food image. In particular, short sleep increased activation in brain areas involved in reward processing, such as the putamen, nucleus accumbens, thalamus, insula, and anterior cingulate cortex. This strongly suggests that sleep deprivation, like alcohol, leads to deregulation of reward system activation in response to food.”

TV Watching:

“Several of the studies included in the meta-analysis found that the effect of television viewing on food intake was most pronounced with high-calorie foods, which suggests that television viewing alters the saliency of food reward. Epidemiologic studies have shown a similar trend, in that those who watch more television tend to snack more while watching and to consume more energy-dense snacks. Additional evidence suggests that watching images of palatable food increases plasma ghrelin concentrations.”

The implications of all of this, when seen in the context of habitual reinforcement and perpetuation of such behaviours are worth noting:

“With regard to the lifestyle factors analyzed, all three, when experienced habitually, should strengthen memory traces that trigger reward expectancy to food cues: that is, when presented with rewarding food or food cues, people who often suffer from sleep deprivation or who often watch television or drink alcohol while eating are more likely to experience a greater reward response as a result. In addition, both alcohol and television likely become their own conditioned cues for those who consume food in conjunction with these factors.”

The authors are optimistic that addressing these factors early on (especially in kids and young adults) may be important measures to reduce the risk of obesity. Thus, they cite evidence that curbing alcohol consumption, increasing sleep time and reducing TV viewing may all lead to decreased accumulation of body fat.

Based on these findings I guess it is time to lay off the night cap, turn off the TV and go to bed.

Edmonton, Alberta

p.s. Hat tip to Carlene for pointing me to this article.

p.p.s. Maintaining this blog costs both time and money – if you have enjoyed these posts, please consider making a small donation to the upkeep of this site by visiting my website by clicking here.

ResearchBlogging.orgChapman CD, Benedict C, Brooks SJ, & Schiöth HB (2012). Lifestyle determinants of the drive to eat: a meta-analysis. The American journal of clinical nutrition PMID: 22836029


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Wednesday, March 28, 2012

ISORAM Day 2: Eating With Your Brain, Taste Alterations, Glucose Transport, and Dietary Fibre

Day 2 of the 2nd International School on Obesity Research and Management (ISORAM) was kicked off by Bill Colmers (Edmonton), who provided a succinct review of the neurohormonal regulation of energy homeostasis and its importance for survival. While there was no evolutionary pressure to not exceed the minimum needs, biology favoured the ability to opportunistically store excess energy and defend body weight. While the former is the job of the hedonic system (thus, promoting weight gain), the latter is the job of the homeostatic system (thus, promoting weight regain).

Andres Thalheimer (Wuerzburg, Germany) discusses how olfactory sense and taste may change following bariatric surgery. While anecdotally, patients undergoing surgery often report changes in appetite and response to food stimuli, whether or not these changes are accompanied by changes in gustation or olfaction are less clear. In their own studies, they found a slightly lower olfaction threshold in patients following sleeve gastrectomy but not following Roux-en-Y gastric bypass. However, these preliminary data are far from conclusive and there is a need for significantly more work in this area.

Christian Jurowich (Wuerzburg) presented novel findings on changes in intestinal glucose transport in animal models of bariatric surgery in diabetic rodents. His work focussed on the Na+-D-glucose Cotransporter SGLT1, a pivotal mechanism for intestinal glucose absorption and glucose-dependent incretin secretion and shows how adaptation of this transporter may affect glucose transport and incretin secretion post surgery.

Michael Lyon (Vancouver) reviewed the many biological functions of dietary fibre on a wide range of health conditions ranging from ischemic heart disease, stroke atherosclerosis, type 2 diabetes, overweight and obesity, insulin resistance, hypertension, dyslipidemia, as well as gastrointestinal disorders such as diverticulosis, irritable bowel disease, colon cancer, and cholelithiasis. The physiological effects of fiber relate to the physical properties of volume, viscosity and water holding capacity that the fiber imparts to food leading to important influences over the energy density of food. Beyond these physical properties, fiber directly impacts a complex array of microbiological, biochemical and neurohormonal effects directly through modification of the kinetics of digestion and through its metabolism into constituents such as short chain fatty acids which are both energy substrates and important enteroendocrine ligands. Of particular interest to clinicians is the important role dietary fiber plays in glucoregulation, appetite, and satiety.

Other talks on day 2 of ISORAM included a session on the psychosocial aspects of bariatric care, including a talk by Birgit Wagner (Leipzig) on the complex issue of suicidality, depression, and anxiety disorder particularly in adolescents with severe obesity, a discussion of the many psychological and social issues relevant to the management of childhood obesity and family interventions, and a talk by Almut Rudolph (Lepizig) on the need for pre and post-surgical psychosocial support and interventions in patients undergoing bariatric surgery.

Another talk deserving special mention was a presentation by Tina Ullrich (Edmonton/Leipzig) on some of the mechanisms involved in the development of endothelial dysfunction in childhood obesity – a topic of interest given the early impact that obesity can have on cardiovascular function, thus setting the stage for future complications.

Lake Louise, Alberta

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Wednesday, January 18, 2012

How The Hedonic System Ratchets Up Your Weight

Earlier this week, Bill Colmers and I gave the inaugural Centennial Lecture for our Faculty of Medicine and Dentistry in anticipation of the upcoming 100 year anniversary of the University of Alberta medical school.

In this talk, we discussed why it is so difficult to keep weight off. I presented the clinical problem, and Colmers, the neuroscientist, presented an overview of how the brain affects eating behaviour and regulates body weight.

I was particularly impressed by how Colmers described the respective roles of the hedonic and homeostatic systems in human evolution.

While the hedonic (pleasure seeking) system evolved to help our hunter-gatherer ancestors seek out and take advantage of any highly palatable energy dense foods they happened to come upon, the homeostatic system evolved to protect from wasting away those extra calories that they did ingest.

Thus, according to Colmers, the hedonic system’s job was to make it hard to resist, in fact, make our ancestors to often go to considerable lengths to searching out those rare palatable energy dense foods and then to eat as much of them as possible, whether they were actually hungry or not. They could of course always store those extra calories as fat tissue for later use – a tremendous survival advantage.

In contrast, the job of the homeostatic system was to ‘defend’ those stored calories – in fact, it is designed to regard any accumulation of fat stores as the ‘new normal’ and from then on make sure that this increased level of fatness was maintained (or regained) ever after.

Indeed, the homeostatic system is ‘designed’ to readjust its set point of body weight – after all it has to do this starting from birth as body weight continues to increase as the baby grows into a toddler that grows into a kid and ultimately into an adult.

Unfortunately, the mechanisms that allow the set point to reset to ‘defend’ a progressively higher body weight – generally works in only one direction – after all that is all that is required by nature, where people do not naturally ‘shrink’.

Colmers used the analogy of a ratchet to describe how the homeostatic system is designed to defend ever increasing body weights without having the ability to reset itself to a lower body weight even if the person now wants to lose weight.

Once set to a higher weight (e.g. resulting from ‘overindulgence’ driven by the hedonic system or other factors that may promote weight gain), the homeostatic system uses a wide range of mechanisms affecting hunger, satiety, appetite, metabolic rate, etc. to ‘defend’ this weight from then on.

A very helpful analogy I thought, nicely explaining why evolution has given us the mechanisms to gain weight but not to lose it.

Edmonton, Alberta

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Wednesday, August 10, 2011

Is It Time To Abandon The Notion Of Personal Choice In Dietary Counseling?

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.

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

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