Arya M. Sharma, MD

One of the major concerns around the childhood obesity epidemic is that early onset obesity may be associated with greater health risks when these kids grow into obese adults compared to individuals who only become obese as adults.

This hypothesis was recently tested in a study Markus Juonala (Finland) and colleagues in a study published last month in the New England Journal of Medicine.

The researchers examined data from four prospective cohort studies that measured childhood and adult BMI with a mean length of follow-up was 23 years.

Data were compared between four groups:

Group 1: nonobese kids who grew into nonobese adults(n=4742)
Group 2: obese kids who grew into nonobese adults (n=274)
Group 3: obese kids who grew into obese adults (n=500)
Group 4: nonobese kids who grew into obese adults (n=812)

All analyses were adjusted for age, sex, height, length of follow-up, and their respective cohorts.

The not so good new is that when childhood obesity persists into adulthood (Group 3), the risk is markedly higher than in Group 1 (never obese) - unfortunately, this is what happens to most of obese kids as 82% of them grew into obese adults.

The good news, however, is that there was absolutely no difference in the cardiovascular risk factors (diabetes, hypertension, dyslipidemia, or intima-media thickess) between Group 1 (never obese) and Group 2 (only obese as kids but not as adults) - this suggests that any increased risk associated with being an obese kid can be virtually completely reversed if they manage to grow into nonobese adults.

Unfortunately, the health risks associated with adult-onset obesity (Group 4) were exactly as bad as with childhood-onset obesity. In other words, even if you managed to get through childhood with normal weight - gaining weight as an adult put you at the same risk as if you’d been obese all your life.

These findings certainly provide important nuances to the discussions about where obesity prevention and treatment resources should be focussed.

Obviously, if you can prevent or treat childhood obesity, thereby reducing the number of obese adults, you would substantially lower risk. But this may be easier said than done, as so far, we are not exactly sure that ’successful’ obesity treatment in childhood actually prevents adult obesity (we certainly hope it does but no one has yet shown this to be the case). In fact, in this study, two out of three obese adults were nonobese as kids!

On the other hand, even if you get through childhood with normal weight only to go on and become an obese adult, you may as well have been obese all your life. This finding suggests that potential benefits of treating adult obesity may not depend on whether or not you were an obese kid or not. Incidentally, we are also not sure that treatment success in adulthood is any different between childhood-onset and adult-onset obesity.

I am also very much intrigued by the finding that growing into a nonobese adult essentially reverses all of the risk (and damage?) that may have incurred from childhood obesity. This is in someway reminiscent of how the risks of tobacco smoking are now known to be largely reversed within a few years of smoking cessation.

So, on the one hand, it looks like it may never be too late (even as an adult) to lose the excess weight (at least if you do have weight-related risk factors - EOSS 1+).

On the other hand, any cardiometabolic benefits of preventing or treating childhood obesity will only be relevant to population health if this actually prevents or reduces the burden of obesity in adulthood - simply ‘delaying’ the onset of obesity into adulthood by focussing most of our efforts on kids (as suggested recently by Canada’s Health Ministers), may have less benefit than some of us may suspect.

I look forward to hopefully lively discussion on this issue.

AMS
Edmonton, Alberta

p.s. Registration for the International School on Obesity Research and Management (ISORAM 2012, Lake Louise March 25-30 is now open - click here to register).

Juonala M, Magnussen CG, Berenson GS, Venn A, Burns TL, Sabin MA, Srinivasan SR, Daniels SR, Davis PH, Chen W, Sun C, Cheung M, Viikari JS, Dwyer T, & Raitakari OT (2011). Childhood adiposity, adult adiposity, and cardiovascular risk factors. The New England journal of medicine, 365 (20), 1876-85 PMID: 22087679

Today’s post is another excerpt from “Best Weight: A Practical Guide to Office-Based Weight Management“, recently published by the Canadian Obesity Network.

This guide is meant for health professionals dealing with obese clients and is NOT a self-management tool or weight-loss program. However, I assume that even general readers may find some of this material of interest.

CARDIOVASCULAR AND/OR RESPIRATORY DISEASES

Patients with chronic cardiopulmonary disease (angina, heart failure, chronic obstructive pulmonary disease [COPD] and reactive airways disease) are often inactive and may be unable to follow recommendations to increase physical activity. Combining cardiopulmonary rehabilitation and exercise training may therefore help patients increase their daily energy expenditure and improve quality of life.

Weight gain and central adiposity independently contribute to increased risk for hypertension, dysglycemia, dyslipidemia, left-ventricular heart disease, ventricular dysfunction, coronary heart disease, congestive heart failure, arrhythmias, peripheral artery disease, deep vein thrombosis, pulmonary embolism, stroke, and sudden death. Consequently, impaired cardiovascular function is common in obese patients. Symptomatic cardio-pulmonary disease affects a patient’s lifestyle, and treatment may both dramatically improve their quality of life and motivate them to undertake lifestyle changes.

© Copyright 2010 by Dr. Arya M. Sharma and Dr. Yoni Freedhoff. All rights reserved.

The opinions in this book are those of the authors and do not represent those of the Canadian Obesity Network.

Members of the Canadian Obesity Network can download Best Weight for free.

Best Weight is also available at Amazon and Barnes & Nobles (part of the proceeds from all sales go to support the Canadian Obesity Network)

If you have already read Best Weight, please take a few minutes to leave a review on the Amazon or Barnes & Nobles website.

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

Regular readers of these pages will recall my previous posts on the Edmonton Obesity Staging System (EOSS), which uses a 5 point ordinal scale (0 to 4) to rate how sick patients are rather than just how big they are.

This morning, I am presenting this concept and some preliminary data that we have on this system at the 4th International Congress on Prediabetes and the Metabolic Syndrome, in Madrid Spain.

This conference focuses on various aspects of preventing and treating the ‘cardiometabolic’ risk factors that I blogged about earlier this week.

While this is clearly important, EOSS considers not just the ‘cardiometabolic’ risk or consequences of excess weight but also the mental and functional problems that these patients may encounter.

Thus, EOSS provides a far more ‘holistic’ understanding of the potential impact of excess weight on an individuals health and functioning - a concept that goes well beyond simply treating numbers on a scale.

Readers may wish to refer to a previous post EOSS for more information.

AMS
Madrid, Spain

Sharma AM, & Kushner RF (2009). A proposed clinical staging system for obesity. International journal of obesity (2005), 33 (3), 289-95 PMID: 19188927

The term ‘cardiometabolic’ has recently crept into the medical literature as a designation for the common constellation of risk factors that promote atherogenic cardiovascular disease and/or the development of type 2 diabetes.

A position paper by the Canadian Cardiometabolic Risk Working Group, under the leadership of Lawrence Leiter (Toronto), just published in the Canadian Journal of Cardiology, addresses the concepts of ‘cardiometabolic risk’, ‘metabolic syndrome’, and ‘risk stratification’, what these terms mean, and how they can best be used to improve our understanding of cardiovascular disease treatment and prevention.

The authors propose ‘global cardiometabolic risk’ as an umbrella term for a comprehensive list of existing and emerging factors (including abdominal obesity) that predict cardiovascular disease and/or type 2 diabetes.

The paper presents practical strategies to identify and reduce cardiometabolic risk in multiethnic patient populations, based on an extensive review of data on emerging cardiovascular risk factors and Canadian guideline recommendations.

Health behaviour interventions (weight loss, physical activity, diet, smoking cessation) and pharmacotherapy in appropriate patients are essential to reduce cardiometabolic risk and are best delivered by a multidisciplinary approach.

In the context of obesity, readers will recall that, while important, ‘cardiometabolic’ risk touches on only one of the four ‘Ms’ (metabolic) relevant to the assessment and management of individuals with excess weight - the other three ‘Ms’ (mental, mechanical, and monetary health), all of which can affect patients even in the absence of metabolic problems, may be as important for the quality-of-life, functioning and overall health of overweight and obese individuals.

Perhaps similar working groups will now be convened to address the global ‘mental’, ‘mechanical’ and ‘monetary’ (=socioeconomic) risk factors associated with excess weight.

Indeed, it may well be that in overweight and obese patients with significant ‘mental’, ‘mechanical’ and/or ‘monetary’ health problems, simply focussing all efforts on improving ‘metabolic’ health may prove daunting if not futile.

AMS
Edmonton, Alberta

Cardiometabolic Risk Working Group: Executive Committee, Leiter LA, Fitchett DH, Gilbert RE, Gupta M, Mancini GB, McFarlane PA, Ross R, Teoh H, Verma S, Anand S, Camelon K, Chow CM, Cox JL, Després JP, Genest J, Harris SB, Lau DC, Lewanczuk R, Liu PP, Lonn EM, McPherson R, Poirier P, Qaadri S, Rabasa-Lhoret R, Rabkin SW, Sharma AM, Steele AW, Stone JA, Tardif JC, Tobe S, & Ur E (2011). Cardiometabolic risk in Canada: a detailed analysis and position paper by the cardiometabolic risk working group. The Canadian journal of cardiology, 27 (2) PMID: 21459257