Arya M. Sharma, MD

Regular readers of these pages may be well aware that there are considerable variations in how individuals respond to changes in their diets and activity levels. Some people lose weight on some diets, others don’t - some people eat less food when they exercise, others eat more.

The same applies to almost any variable that has been measured - people simply respond differently to different interventions - diet, lifestyle, medications, or even surgery.

One of the key determinants of how individuals respond, is certainly genetic. Thus, for example, a considerable body of evidence supports the notion that the response of cardiovascular risk factors like blood pressure, lipids, insulin resistance, etc. to exercise are highly heritable - in other words, some people experience significant improvements - others, performing the same amount of exercise, don’t.

So far, however, exactly which genes (let alone which variants of these genes) could determine this variability in response is largely unclear.

Nevertheless, researchers working in genetics (and the many companies involved in developing genetic tests), justify their considerable efforts with the promise of ‘personalised’ medicine, which would allow to predict disease risk and thereby allow people to adopt behaviours that could mitigate such risk (although so far there is virtually no evidence that telling people that they are at higher genetic risk for anything has any impact on their behaviours - in fact, some folks may rather take a fatalistic approach and simply decide to continue eating, drinking, and being merry).

The reason why we should probably not be holding our breath in anticipation of a genetic test that will predict who will benefit most (or least) from exercise is now outlined in an article by Jim Hagberg from the University of Maryland, published in the latest issue of the Journal of Applied Physiology.

Thus, although there is some evidence supporting “possible” candidate genes that may affect responses to exercise training - APO E and CETP for plasma lipoprotein-lipid profiles, eNOS, ACE, EDN1, and GNB3 for blood pressure, PPARG for type 2 diabetes phenotypes, and FTO and BAR genes for obesity-related phenotypes - there is one very significant barrier to advances in this field.

This limitation relates to the fact, that one would need to generate vast amounts of data from exercise interventions studies - an undertaking that may be both unfundable and unfeasible.

The need for such large sample sizes is becoming more and more evident, as attempts to find genes for diabetes, obesity or blood pressure, despite utilizing populations of 10,000 to 250,000 subjects, have found few genes that have largely minor effects - too small to have any clinical utility in predicting these conditions with any reasonable sensitivity or specificity.

As the impact of individual genes on exercise responses are likely to be of similar magnitudes, one would need to perform exercise studies in 10s of thousands of individuals to have any hope of ever finding the genetic determinants of exercise response.

This does not mean that genetics is not an important determinant of exercise response - it just means that finding the genes responsible for differences in responses is a virtually hopeless undertaking.

The same is likely true for other attempts at finding genes to predict individual responses to ‘lifestyle’ interventions.

It may well be that ‘personalised’ medicine in the future will largely be no different from ‘personalised’ medicine today, consisting namely of listening to your patients relating their personal concerns or problems and using your best judgement, your interpretation of clinical evidence (where available) and your (hopefully extensive) clinical experience to advise them the best you can.

When you think about it, it seems quite funny how the use of the term ‘personalised’ medicine in the context of genetic testing, if it ever becomes a reality, will actually result in a further ‘depersonalisation’ of medicine - sounds a lot like Orwelian Douplespeak to me.

AMS
Edmonton, Alberta

Hagberg JM (2011). Do Genetic Variations Alter the Effects of Exercise Training on Cardiovascular Disease and Can We Identify the Candidate Variants Now or In the Future? Journal of applied physiology (Bethesda, Md. : 1985) PMID: 21565989

Yesterday, readers may have observed a live debate organised by the CON-Student and New Professional (SNP) group at the University of Ottawa.

I, unfortunately missed it, but I know that the debaters were meant to debate the issue of whether diet or exercise is more important in preventing and managing obesity.

In the diet corner the CON-SNPSs had the CON members Dr. Yoni Freedhoff, Ottawa family doctor and Canada’s food ‘watch dog’ of Weighty-Matters fame; In the exercise corner they had Dr. Bob Ross, Professor of Kinesiology at Queen’s University, Kingston, Ontario, well known for his extensive work on exercise and visceral obesity.

Knowing both the passion and the immense knowledge base of both contestants, this is definitely a debate I will go back and watch.

But even without having seen the debate or having heard exactly what the discussants had to say, here are my own two cents on this whole topic: while both healthy diets and exercise are important to maintain good health, I always cringe, when these two topics are so directly linked to discussions on obesity and here is why:

Healthy eating and increased physical activity are recommendable for 100s of conditions that I can think of - everything from cancers to dementia, not to mention diabetes, heart disease, osteoporosis and almost every other chronic condition out there.

So, if promoting healthy diets and physical activity is as useful for preventing or managing any of these 100s of conditions, why focus any discussion on diet and exercise on obesity?

Thus, although eating healthier and exercising more reduces the risk or impact of countless health conditions, why is it only, when we talk about obesity, that diet and exercise suddenly become the central (and often only) topic of discussion?

Not only will readers recall my reservations about the limited efficacy of ‘Eat-Less-Move-More” (ELMM) approaches to weight management but also the fact that eating and activity are both behaviours that are driven by everything from genetics, psychosocial circumstances, cormorbidities, or medications.

In general, no diet or exercise plan that I have ever seen, really addresses the root causes of unhealthy diets or inactivity - they are just ‘prescriptions’ (and sometimes ‘gimmicks’) that seek to address, what I would call ’symptoms’ of what’s really going on. Or, as I’ve said before, they address the “what” but not the “why” of these behaviours (which is probably why ELMM approaches tend to fail).

But there is another negative aspect of turning every discussion about obesity prevention or management into a discussion about healthy eating and exercise and that is the simple fact that such discussions (and recommendations) do little more than reinforce the widespread stereotypes of obesity being a condition solely attributable to unhealthy eating and lack of exercise (although this is by no means true) and that by simply eating healthy and exercising, anyone can achieve an ‘ideal’ weight (whatever that may be).

Not only is this a gross oversimplification of the actual etiological diversity and complexity of obesity but it also turns, what I see as a complex heterogeneous psycho-social-biomedical condition, into a simple issue of eating right and moving more, thereby squarely placing the ‘blame’ on the people, who already carry this burden (no one I have ever met is obese by ‘choice’ although many may have given up the struggle for good reasons of their own).

Thus, it may perhaps be time to completely cut all links between finding solutions to the obesity epidemic from any discussions about healthy eating and excercising.

Not because healthy eating and exercising are not as important for people with excess weight as they are for people of normal weight or people with 100s of other health conditions - but exactly for this reason! There is absolutely nothing ’special’ that I can see about diet and exercise being any more important to prevent and manage obesity than for generally improving health and managing all those other conditions.

I therefore propose that we completely dissociate the discussion about improving population health by improving diet and physical activity from the necessary discussion about how we will tackle the obesity epidemic.

Linking diet and exercise exclusively to obesity (as if it were that simple) is a distraction to finding real solutions and will not solve the problem; if it increases weight bias and stigma, things can only get worse.

So, while I very much commend the efforts that the Ottawa CON-SNP groups went to in order to set up this debate (especially given the immensely busy schedules of both debaters) and very much look forward to eventually getting around to watching the recording of the debate (in which I am sure good points will be made on both sides) perhaps future debates will focus more on the ‘whys’ and less on the ‘whats’ of the obesity epidemic.

The debate will be posted on Obesity Panacea.

AMS
Regina, Saskatchewan

Regular readers will recall a recent post asking whether the reason that some people lose weight with exercise is that it helps them reduce their caloric intake (e.g. by improving mood, reducing stress, improving self-esteem, promoting sleep, etc.).

I also noted that, if this was indeed the reason behind any ‘exercise-related’ weight loss, then it probably does not matter how many calories were actually burnt as long as the amount of exercise was enough to positively influence ingestive behaviour.

A recent article, published by Jean-Philippe Chaput (Ottawa) and colleagues in the American Journal of Clinical Nutrition, now suggests that the notion that sedentariness and playing video games contributes to obesity because of reduced caloric expenditure is also flawed - the real reason some kids (and adults) gain weight playing video games is more likely due to increased caloric intake.

In their study, the researchers used a randomized crossover design to examine the effect of playing a video game for an hour (vs. just sitting around) in 22 healthy, normal-weight, male adolescents, on spontaneous food intake, energy expenditure, stress markers, appetite sensations, and profiles of appetite-related hormones.

Markers of mental stress including heart rate, systolic and diastolic blood pressures, sympathetic tone, and mental workload were significantly higher during the video game play condition than during the resting condition and energy expenditure was also modestly higher during the video game.

More importantly, however, spontaneous caloric intake after the video game exceeded that measured after rest resulting in a daily energy surplus of 163 kcal compared to resting for an hour.

The increase in food intake associated with video game play was observed without increased sensations of hunger and was not compensated for during the rest of the day.

Thus, this study strongly suggests that the reason kids (and adults?) may gain weight when playing video games is not because they are not burning calories but because they are eating more.

Although this study looked at videogames, it may be fair to assume that any form of inactivity that increases mental stress (work, play, or watching a hockey game) can translate into increased caloric intake.

This makes a lot of sense as in the vast majority of cases, weight gain has more to do with excessive caloric intake than with reduced caloric expenditure (although there are certainly important exceptions to this rule).

Based on this and previous studies, I believe it is fair to conclude that neither weight gain with increased screen time nor weight loss with exercise has anything to do with the burning of calories. Both effects are far more likely to affect weight because of their impact on caloric intake.

This is probably why reducing screen time and increasing physical activity should be part of dietary counseling for weight management.

AMS
Toronto, Ontario

Chaput JP, Visby T, Nyby S, Klingenberg L, Gregersen NT, Tremblay A, Astrup A, & Sjödin A (2011). Video game playing increases food intake in adolescents: a randomized crossover study. The American journal of clinical nutrition PMID: 21490141

Regular readers will recall a recent post on the issue of recommending weight loss in older individuals with obesity.

Now Dennis Villareal and colleagues from the Washington University School of Medicine, St. Louis, Missouri, in a paper published in the New England Journal of Medicine, examined the effect of weight loss, exercise, or both on physical function in obese older adults.

In this 1-year, randomized, controlled trial, 107 adults who were 65 years of age or older and obese were randomly assigned to a control group, a weight-management (diet) group, an exercise group, or a weight-management-plus-exercise (diet-exercise) group. A total of 93 participants (87%) completed the study.

The Physical Performance Test score, increased more in the diet-exercise group (21%) than in the diet group (12%) or the exercise group (15%) compared to scores in the control group (1%).

Perhaps surprisingly, the peak oxygen consumption (a measure of fitness) improved more in the diet-exercise group (17%) than in the diet group (10%) or the exercise group (8%).

The Functional Status Score, increased more in the diet-exercise group than in the diet or exercise groups.

Body weight decreased by 10% in the diet group and by 9% in the diet-exercise group, but did not decrease in the exercise group or the control group.

Lean body mass and bone mineral density at the hip decreased less in the diet-exercise group than in the diet group.

Strength, balance, and gait improved consistently in the diet-exercise group.

Adverse events included a small number of exercise-associated musculoskeletal injuries.

The authors conclude that a combination of weight loss and exercise provides greater improvement in physical function than either intervention alone in obese older individuals.

It is perhaps also worth noting that health status and physical functioning improved in all intervention groups compared to doing nothing (controls).

This study certainly lends support to the notion that a combination of diet and exercise may be best to improve both health and physical function in older individuals with excess weight.

AMS
Edmonton, Alberta

Hat Tip to Carla for drawing my attention to this study

Villareal DT, Chode S, Parimi N, Sinacore DR, Hilton T, Armamento-Villareal R, Napoli N, Qualls C, & Shah K (2011). Weight loss, exercise, or both and physical function in obese older adults. The New England journal of medicine, 364 (13), 1218-29 PMID: 21449785

Regular readers may recall a previous post calling for treating the parents to tackle childhood obesity. Indeed, there is little evidence that trying to address childhood obesity without involving the whole family is likely to have any success.

Thus, it may not be all that surprising that Clare Collins and colleagues from the University of Newcastle, NSW, Australia, in a randomised controlled study just published in PEDIATRICS, find that targeting the parents’ diets appears far more likely to affect the weight of their overweight offspring than trying to getting the kids to be more active.

This study included 165 overweight prepubertal children (68 boys, aged 5.5-9.9 years) who were randomised to either a child-centered physical-activity program to either a child-centered physical-activity program, a parent-centered dietary-modification program, or both in an assessor-blinded 6-month intervention.

All group interventions weekly 2-hour face-to-face session for 10 weeks that included homework activities followed by a relapse-prevention program that reviewed short- to medium-term goals set by parents, by telephone, monthly for 3 months.

The diet program, which was delivered exclusively to the parents, focused on goal setting, problem solving, role modeling, and positive reinforcement.

The activity program, consisted of weekly face-to-face sessions aimed to improve child fundamental movement-skill proficiency, with parents participating in the first session and being encouraged to complete the homework activities weekly with their child.

The combined intervention consisted of both the dietary intervention for the parents and the activity intervention for the kids.

At 24 months after the start of the intervention, BMI z scores showed the greatest reduction in the parent-centred diet-modification group (-0.35), followed by the activity and diet group: -0.24, and the activity-only group -0.19.

Thus, the greatest effects were achieved through inclusion of a parent-centered diet program, indicating the importance of targeting parents within treatment. In fact the authors even suggest the possibility that exclusively targeting parents diet may be a viable option for treating obese prepubertal children.

“The implication for health service providers, and parents who seek effective treatment options, is that parental involvement is essential for program effectiveness. In addition, parents can participate in intervention programs that will benefit their child without their child being required to participate.”

In any case, it is probably safe to say that (perhaps contrary to popular belief) programs that exclusively focus on trying to address childhood obesity by getting kids to be more active are probably the least effective strategies.

In contrast, leaving the kids alone and focussing on the parents, may be best, unless of course one has the resources and capacity to do both.

AMS
Edmonton, Alberta

Collins CE, Okely AD, Morgan PJ, Jones RA, Burrows TL, Cliff DP, Colyvas K, Warren JM, Steele JR, & Baur LA (2011). Parent Diet Modification, Child Activity, or Both in Obese Children: An RCT. Pediatrics PMID: 21444600