Monday, April 14, 2014

Can Video Games Make You Eat Too Much?

sharma-obesity-videogame-pacmanGenerally, TV viewing and playing video games are blamed for weight gain because of their sedentary nature (as opposed to more active recreational activities).

However, as has been argued before, the key impact of TV viewing and video gaming on body weight may well lie in their effect on food intake.

An elegant randomised controlled trial by Jason Gan and colleagues, published in APPETITE shows that vide0 gaming can lead to an increased intake of foods, particularly sweets.

The study involved 72 overweight/obese adult males, divided into three equal groups, randomised either to one hour of (i) watching TV; or playing (ii) a non-violent video game; or (iii) a violent video game.

This was followed by a 25 minute rest period with free access to a selection of sweet and savoury snacks/drinks. D

Heart rate, blood pressure, and stress measured by visual analogue scale (VAS)) were all significantly higher when playing video games compared to watching TV.

This increase in stress levels was associated with a 170 higher caloric intake and a preference for sweets and fatty foods in the video game group compared to the TV watchers.

In addition, the violent video games led to even higher stress levels with an even stronger preference for sweet foods.

Thus, the authors conclude that, compared to TV viewing, playing video games (especially violent ones) is associated with a stress response, and increased calorie intake.

This phenomenon may well confound previous findings that show associations between playing video games and weight gain, leading to the assumption that it is the sedentariness of video gaming that promotes weight gain, when it fact it may well be the associated impact on snacking.

@DrSharma
Edmonton, AB

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Friday, April 11, 2014

Does Eating More Protein Help Keep The Pounds Off?

sharma-obesity-diogeneslogoAs a regular reader, you may remember the DIOGENES trial, which studied the impact of different levels of protein intake on sustaining a weight-loss induced by eight weeks of a low-calorie formula diet (800 Kcal resulting in an average weight loss of about 11 Kg).

The original paper showed that individuals on a high-protein diet (providing 12 % more energy from protein that the low-protein diet) were about half as likely to discontinue the 26 week trial than those on a low-protein intake.

Now, a new paper from DIOGENES, published in the International Journal of Obesity, reports on the weight outcomes in participants, who were followed for up to 12 months in two of the participating centres (n=256).

The five ad libitum diets (no caloric restrictions) that followed the low-calorie diet (resulting in an average weight loss of about 11 Kg) were:

1) a low-protein and low-glycemic index diet,

2) a low-protein and high-glycemic-index diet,

3) a high-protein and low-glycemic-index diet,

4) a high-protein and high-glycemic-index diet,

5) a control diet.

While average weight regain over the 12-months was about 4 Kg (of the 11 Kg lost initially), the subjects on the high-protein diets kept off almost twice as much weight as those on the low-protien diets (glycemic index did not appear to make any significant difference).

Thus, the authors conclude that following a higher-protein ad libitum diet improves weight loss maintenance in overweight and obese adults over 12 months.

Clinicians may wish to stress the importance of maintaining a high-normal protein intake to clients trying to avoid regaining pounds that they have lost.

@DrSharma
Edmonton, AB

 

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Friday, March 7, 2014

Leipzig Forging Its Way As Leaders in Obesity Research

Seal Faculty of Medicine, University of Leipzig, GermanyThis week, for the 5th consecutive year, I have had the privilege of participating in an extensive review of the obesity research program at the University of Leipzig.

I believe that it is fair to say, that starting from scratch, this centre has certainly shown a most remarkable growth and advancement in both fundamental and clinical aspects of obesity research.

It is indeed an honour to have had the opportunity to help evaluate and guide this world-class research program over the past five years.

It is particularly heartwarming to see how much emphasis this program has placed on supporting the career development of the next generation of obesity researchers in Germany.

As the program goes into the renewal phase for hopefully acquiring funding for the next five years, here is a link to past posts on their achievements.

@DrSharma
Leipzig, Germany

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Wednesday, February 26, 2014

Why The Energy Balance Equation Results In Flawed Approaches To Obesity Prevention And Management

1st law of thermodynamics obesityAllow me to start not with the first law of thermodynamics (energy cannot be created or destroyed) but rather, the second law of thermodynamics, according to which entropy (best thought off as a measure of disorder), in any closed system, increases till it ultimately reaches thermodynamic equilibrium (or a state of complete disorder).

As some of us may recall from basic biology, the very definition of “life”, which tends to move from a state of lesser organisation to a state of higher organisation, is that it appears to defy the second law of thermodynamics (this is often referred to as “Schroedinger’s Paradox”).

In actual fact, we can easily argue that the second law does not apply to living organisms at all because living organisms are not closed systems and life’s complex processes continuously feed on its interactions with the environment.

Yet, when we consider the first law of thermodynamics and how it applies to obesity, we seem to forget the fact that we are again dealing with a complex living organism.

Thus, in what has been referred to as the “Folk Theory of Obesity”, we simply consider weight to be a variable that is entirely dependent on the difference between energy input and energy output (or “calories in” and “calories out”). And in our arithmetical thinking, we consider “energy in” and “energy out” as simple “modifiable” or “independent” variables, which if we can change, will result in any desired body weight.

In fact, our entire “eat-less-move-more” approach to obesity is based on this concept – the central idea being, that if I can effectively move “energy in” and “energy out” in the desired directions, I can achieve whatever weight I want.

This notion is fundamentally flawed, for one simple reason: it assumes that weight is the “dependent” variable in this equation.

However, as pointed out in a delightful essay by Shamil Chandaria in my new book “Controversies in Obesity“, there is absolutely no reason to assume that weight is indeed the “dependent” or “passive” player in this equation.

Indeed, everything we know about human physiology points to the fact that it is as much (if not more) body weight itself that determines energy intake and output as vice versa.

Generally speaking, heavier people tend to eat more because they have a stronger drive to eat and/or need more calories to function – in other words, body weight itself may very much determine energy intake and output (and not just the other way around).

Similarly, losing weight tends to increase hunger and reduce energy expenditure – or in other words, changes in body weight can very much determine changes in energy intake and expenditure (and not just the other way around).

Thus, the idea that we can control our body weight by simply controlling our energy intake and output, flies in the face of the ample evidence that it is ultimately our physiology (in turn largely dependent on our body weight) that controls our energy intake and output.

Thus, to paraphrase Chandaria’s key argument, it is not so much about what “energy in” and “energy out” does to our body weight – it is more about what our body weight does to “energy in” and “energy out”.

Once we at least accept that this equation is a two-way street, rather strongly biased towards body weight (or rather “preservation of body weight”) as the key determinant of “energy in” and “energy out”, we need to ask a whole different set of questions to find solutions to the problem.

No longer do we restrict our focus to the exogenous factors that determine “calories in” or “calories out” (e.g. our food or build environments) or see these as the primary targets for decreasing caloric intake or increasing caloric output.

Rather we shift our focus to the physiological (and psychological) factors (often dependent on our body weights) that ultimately dictate how much we “choose” to eat or expend in physical activity.

Chandaria’s essay goes on to discuss the many “derangements” of physiology that we know exist in obese individuals (and probably already exist in those at risk for obesity), including leptin resistance, impaired secretion of incretins like GLP-1, insulin resistance, alterations in the hypothalamic-pituitary-adrenal (HPA axis), and sympathetic activity. (Any keen student of human physiology or psychology should have no problem further extending this list.)

In Chandaria’s view, it is these physiological (and psychological) processes that ultimately determine whether or not someone is prone to weight gain or ultimately gains weight.

In fact, the only factor that determines why two individuals living in the same (obesogenic) environment will differ in body weights (even when every known social determinant of health is exactly equal), is because of their individual physiologies (and psychologies) which ultimately determine their very own individual levels of “energy in” and “energy out” (and how their bodies respond to it).

Readers may be well aware that in tightly controlled feeding studies, the same absolute amount of extra calories can result in very different amounts of weight gain.

Similarly, the exact same amount of caloric deficit will result in widely different amounts of weight loss.

Ignoring this basic fact of human nature distracts or, at the very least, severely limits us from finding effective solutions to the problem.

This “physiological” view of the first law of thermodynamics should lead us away from simply focussing on the supposedly “exogenous” variables (“energy-in” and “energy-out”) but rather draw our attention to better understanding and addressing the biological (and psychological) factors that promote weight gain.

This would substantially change the aims and goals of our recommendations.

Thus, for e.g., rather than aiming exercise recommendations primarily at burning more calories, these should perhaps be better aimed at improving insulin sensitivity and combating stress. Thus, rather than counting how many calories were burnt on the treadmill, the focus should be on what that dose of exercise actually did to lower my insulin or stress levels.

Indeed, we may discover that there is a rather poor relationship between the amount of calories burnt with exercise and the physiological or psychological goal we are trying to achieve. While more exercise may well help burn more calories (which I can eat back in a bite or two), it may do little to further improve insulin resistance or combat stress thus leaving my weight exactly where it is.

Similarly, rather than trying to restrict caloric intake, dietary recommendations would be based on how they affect human physiology (e.g. gut hormones, reward circuitry or even gut bugs) or mood (e.g. dopamine or serotonin levels).

In other words, fix the physiology (or psychology) and “calories in” and “calories out” will hopefully fix themselves.

Given that our past efforts primarily focussing on the “energy in” and “energy out” part of the equation have led nowhere, it is perhaps time to focus our attention and efforts elsewhere.

Or, as I often say in my talks, “We’re not talking physics here – we”re talking physiology – that’s biology messing with physics”.

We cannot mess with the physics but we sure can mess with the biology.

@DrSharma
Edmonton, AB

Shamil A. Chandaria: The Emerging Paradigm Shift in Understanding the Causes of Obesity. In Controversies in Obesity. Eds: Haslam DW, Sharma AM, Le Roux CW. Springer 2014

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Tuesday, February 25, 2014

Can Portion Sizes Really Drive Weight Gain?

out_to_lunchEven a casual visitor to North America will unlikely have missed the humongous portion sizes (enough to feed a small family) routinely served up at chain restaurants (and most other places).

Indeed, in any “folksy” discussion of what drives obesity, portion sizes are sure to be on the plate.

In addition, cutting portion sizes is one of the most common pieces of advise given to anyone trying to lose weight.

But how important are portion sizes in promoting weight gain?

This is where a new randomized controlled trial designed to test this hypothesis in free living individuals may provide some answers.

In this study, just published in OBESITY, Simone French and colleagues from the US and UK randomly assigned 233 volunteers (mean BMI ~30) to one of three lunch size groups (400 kcal, 800 kcal, and 1,600 kcal) or to a no-free lunch control group for 6 months.

The study was “disguised” as an intervention to test the “feasibility of providing box lunches to employees at a large metropolitan medical complex.

The free box-lunches were provided Monday to Friday. Fifteen different box lunch menus were created and menus were implemented on a 3-week repeating cycle. However, the conditions were on different cycles, so that participants assigned to different conditions could not directly compare their lunch box items on any given day. The same size box was used in all three conditions. Only water was served as a beverage.

As one may expect, people with the 800 and 1600 kcal lunches ate more that those with the 400 kcal lunches both at lunch and as total daily energy.

Interestingly however, while those on the 1600 kcal managed to gain about 2 pounds over the 6 months, there was no weight change in those eating fewer calories.

Incidentally, the individuals in the control group also gained about 2 pounds suggesting that the 1600 kcal was closer to what these folks were generally served as their “usual” meals.

Thus the authors rightly conclude that weekday exposure for 6 months to a 1,600 kcal lunch can cause significant increases in total energy intake and a weight gain.

On the other hand, the study also shows that simply limiting the size of lunch may not result in the significant weight loss that people may hope for.

I would interpret the overall findings as supporting the notion that our body’s homeostatic systems are much better in preventing weight loss than in defending against weight gain. Thus, while it takes a hefty 1600 kcal free lunch to drive weight gain, our bodies appear quite competent in regulating our body weights when served free lunches in the 400-800 kcal range.

On a side note, all box-lunch recipients increased their intake of fruits and vegetables compared to the control group – clearly showing (as noted in a recent previous post) that simply eating more fruits and veggies alone is not a viable recipe for weight loss (or even preventing weight gain).

So will efforts to reduce portion sizes (of weekday lunches) pay off in terms of preventing weight gain? Probably.

Will efforts to reduce portion sizes (of weekday lunches) help reduce obesity? Probably not.

@DrSharma
Edmonton, AB

ResearchBlogging.orgFrench SA, Mitchell NR, Wolfson J, Harnack LJ, Jeffery RW, Gerlach AF, Blundell JE, & Pentel PR (2014). Portion size effects on weight gain in a free living setting. Obesity (Silver Spring, Md.) PMID: 24510841

 

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In The News

Diabetics in most need of bariatric surgery, university study finds

Oct. 18, 2013 – Ottawa Citizen: "Encouraging more men to consider bariatric surgery is also important, since it's the best treatment and can stop diabetic patients from needing insulin, said Dr. Arya Sharma, chair in obesity research and management at the University of Alberta." Read article

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