Obesity Classification: Time to Move Beyond BMI?

Current definitions of obesity based on BMI and waist circumference (WC), while widely accepted, are hardly helpful in counseling individual patients. Readers of my blog are probably quite familiar with my views on this.

As most clinicians will readily agree, when dealing with indiviual patients, both measures lack sensitivity and specificity with regard to identifying the presence or risk of obesity-related risk factors, comorbidities, psychopathology, global functioning or quality of life.

In fact recent epidemiological studies emphasize that good health including low morbidity and mortality is possible over a wide range of BMI. Thus, basing the decision on who to treat and who to leave well alone solely on measures of weight or size is neither sensible nor does justice to the complexity of the relationship between excess body fat and its impact on health and well-being. The well-established obesity-chronic disease paradox makes decisions on who to treat and who not to treat even more uncertain.

Telling healthy large people who have no apparent comorbidities, functional limitations or reduced well-being to lose weight may be counterproductive in that it can introduce and reinforce dissatisfaction with body image, foster frustrations and despair (given the poor long-term success of weight loss attempts) and lead to unhealthy behaviours focusing on weight loss (e.g. excessive exercise or dieting) rather than on healthy lifestyles (which are possible at almost any weight).

Thus, for practical purposes, it is important to move beyond defining who needs obesity treatment simply based on BMI and/or WC to a more clinically meaningful system.

Indeed, what we direly need is a classification of obesity that is clinically relevant in that it helps identify patients who have or are at high-risk of obesity-related complications and are most likely to benefit from treatment.

In this context, it may be worthwhile to look at the systems of classification and staging used for other disease states.

Oncologists have long used the TNM system to classify the extent of cancer spread. This system has established itself for the classification and staging of the vast majority of cancers not only because it is clinically meaningful in that it reflects extent of disease, indicates prognosis and allows evaluation of treatment response but also facilitates surveillance and research.

Psychiatrists and other mental health workers now routinely report on their patients using the five axes set out in the DSM-IV, each of which refers to a different domain of information that help the clinician plan treatment and predict outcome. The five axes are:

Axis I Clinical Disorders (all mental disorders except Personality Disorders and Mental Retardation)

Axis II Personality Disorders and Mental Retardation

Axis III General Medical Conditions (must be connected to a Mental Disorder)

Axis IV Psychosocial and Environmental Problems (for example limited social support network)

Axis V Global Assessment of Functioning (Psychological, social and job-related functions are evaluated on a continuum between mental health and extreme mental disorder)

While these systems are by no means simple or easy for the layman to understand, they are clinically useful and provide a standardized framework within which it is possible to describe the extent and impact of disease in a way that all clinicians, researchers and payors will understand.

Contrast these systems to the rather simplistic obesity classification, where knowing that a given person has Class II obesity (BMI 35-39.9) tells you virtually nothing about that person's health or well being. Furthermore, it provides no meaningful guide in determining outcomes: e.g. someone who weighs 120 Kg with a BMI of 39 (Class 2 obesity) despite losing 10 Kg (8% weight loss) still has Class II obesity (BMI 36). This classification neither tells us what (if any) comorbities were actually present or whether (or not) these actually got better.

Now I am no expert on disease classification and realise the large amount of work and consensus meetings that go into developing these classification systems. But I am a clinician, who regularly sees patients and would be happy to see even the simplest form of staging that provides a meaningful framework.

The simplest classification I can think of would be to use a staging system similar to the following:

Stage 0: no apparent obesity-related risk factors (blood pressure, lipids, glucose, etc.), physical symptoms, psychopathology, functional limitations, or impairment of well-being

Stage 1: presence of obesity-related sub-clinical risk factors (elevated blood pressure, impaired fasting glucose, fatty liver, etc.), mild physical symptoms (dyspnea on moderate exertion, occasional aches and pains, etc.), mild psychopathology, mild functional limitations or mild impairment of well-being

Stage 2: presence of established obesity-related chronic disease like hypertension, type 2 diabetes, sleep apnea, osteoarthritis, reflux disease, polycystic ovary syndrome, depression, anxiety disorder, moderate limitations in activities of daily living and/or well being.

Stage 3: established end-organ damage like myocardial infarction, diabetic complications, severe osteoarthritis, significant psychopathology, significant functional limitations and impairment of well-being

Stage 4: severe (end-stage?) disabilities from obesity-related chronic disease, severe disabling psychopathology, severe functional limitations and severe impairment of well-being

Thus for e.g. a 24 year-old physically active female with a BMI of 32 with no measurable risk factors, functional limitations or self-esteem issues would have Class I, Stage 0 Obesity - benefits of treatment will be marginal or non-existent.

A 32 year-old male with BMI of 36 with hypertension and sleep apnea would have Class III, Stage 2 Obesity - definite indication for obesity treatment.

A 45 year-old female with BMI of 54 who is in a wheel chair because of severe gonarthritis with severe hypoventilaltion would have Class III, Stage 4 Obesity - will require aggressive obesity treatment unless deemed palliative.

But this may not be the only conceivable system. In fact, given the significant importance of psychopathology, personality traits, physical disease, psychosocial and enviromental factors as well as global functioning, I wonder if an approach similar to the axes in DSM-IV may be best. Of course, one could easily envision combinations of both systems, e.g. applying staging to Axis III disorders.

Obviously any such system would need careful definitions and perhaps a complex manual of diagnostics and classifications similar to DSM-IV - but at least we would have a way to assess, describe, treat, monitor and research obesity in a way that goes beyond the relatively meaningless anthropometry-based classification, which is nothing short of useless in clinical practice.

I can see why health authorities, professional organisations and even clinicians may be reluctant to devise a more complex classification of obesity - all I can say is that the present classification does not provide a meaningful framework in which to make clinical decisions or evaluate outcomes. There is certainly a need for a more complex system to guide practice (and research).

More often than not in clinical medicine - simple is simply wrong!

AMS
Edmonton, Alberta

Counseling the Community Health Councils on Obesity

Last evening I gave a presentation to members of the Strathcona County Community Health Council (CHC). The CHCs are advisory bodies appointed by the Capital Health Board, to provide community perspectives that support Board business planning and strategic direction.

Council members are volunteers with strong community linkages. Most have been involved with local groups or organizations where they receive community input on various health issues.

Input from CHCs helps the Board to update its business plan and meet the health needs of people in the Capital Health region.

Thus, informing the CHC members about the importance of the Weight Wise program and its relevance to improving the health of their communities is of utmost importance.

As anticipated, the interest in Weight Wise was keen. Not only were they interested in learning about my vision for the program but also in the challenges and possible solutions to the obesity crisis.

I emphasized that Weight Wise is in fact not a single program but rather a whole suite of programs and initiatives addressing both obesity prevention and treatments in the Capital Health Region and beyond.

I spoke about the unique opportunities here in Edmonton, where we can indeed create a seamless obesity program that provides services across the continuum of care.

I spoke to the need of providing obesity care to the over 250,000 people in the region already clinically obese and the over 25,000 with severe obesity.

I also spoke about the many excellent researchers here at the University of Alberta already working on important issues relevant to obesity prevention and care.

My guess is that my presentation was well received - indeed, I hope it was.

It will take all the support we can get to create a climate in which spending money on obesity prevention and treatments is not the exception but rather the rule.

AMS

Orient Express

Yesterday we held another Orientation Forum for patients who have been referred to the Adult Weight Wise Program. Some have been waiting over a year for an appointment. Many are desperate for help. The average BMI of the 30 or so folks who attended the Forum was in the mid 40s - most have obesity-related comorbidities - clear indications for treatment.

So what did we orient them about?

Well, for one that obesity is a chronic disease and if they really want to deal with their weight problem, it will mean long-term if not lifelong treatment.

There are many factors contributing to weight gain and no treatment is going to work for everyone. Some may do well by simply making important changes to their lifestyles, some may need more intensive behavioural treatments, some may need medications, some may require surgery.

For some, the best they can realistically hope for is to stabilize their weight - i.e. stop gaining more weight every year.

For others, treatments may be more effective achieving 5, 10, 15 or even 20% weight loss that they may be able to keep off in the long term - but only if treatment continues. Stopping treatment will lead to relapse, or weight regain.

Tough words - tough decisions. No hope for cure, but certainly treatments that work and can effectively help manage weight and relieve comorbidities, i.e. if they stick with it.

No quick fixes, no magic pills, no miracle surgery and most of all - no false promises!

But also no blame, no pointing the finger, no sermons, no patronizing.

Just empathy and sound medical advice - the best we can offer!

AMS

How Far Will You Travel for Obesity Treatment?

One consequence of the rapid increase in obesity is that the vast majority of Canadians cannot rely on local facilities or expertise for obesity treatments. As a result, patients often have to travel long distances or even across borders to seek obesity treatments.

For example, our program has over 300 patients from other provinces awaiting assessment and hoping for treatment.

This throws up a number of logistical but also practical issues: how do you provide cross-border management for a chronic disease?

It is one thing to fly across the country to consult an expert for a diagnosis of a rare condition or a one-time specialized procedure. But what do you do for a common condition that requires on-going lifelong management? How do you provide education, counseling, monitoring and support across 1000s of kilometers?

Sure there are telephones, internet and telehealth but this does not entirely replace the need to actually see and examine a patient face-to-face.

Remember, obesity is a complex and heterogeneous condition - patients may require 10s of visits with a whole array of health professionals to determine the best treatment plan. Successful obesity management requires continued intervention and monitoring to keep the patient in remission. Early signs of relapse need to be recognized and dealt with to prevent weight regain. Surgical patients need band readjustments, dietary counseling and psychological support.

Much of this is theoretically possible across distances with modern communication technologies but in reality often impractical and inefficient.

On the other hand, how do you refuse to see patients who are clearly in dire straits for whom no local help is available or forthcoming any time soon?

Frankly, I see no alternative to rapidly ramping up obesity care across Canada - this will take both time and resources but most of all a change in attitude: ignoring obesity is no longer an option - limiting efforts to prevention is not helping the millions already struggling with this condition.

AMS

Why Weight-Loss Challenges Send the Wrong Message

There appears to be a rather widespread notion out there that introducing a bit of competition into the affair may spurn people on to try and lose those "extra" pounds.

In fact, a quick google search on the term "weight-loss challenge" reveals an amazing array of challenges from voyeuristic and sadistic TV shows like the "Biggest Loser" to well-meant workplace wellness initiatives or fund raisers. I am sorry to admit that I recently even became aware of a weight-loss challenge within my own hospital - well intended, but useless in the fight against obesity.

So what's wrong with this idea? Isn't competition a great motivator?

Sure it is - and people will do anything to win a competition - including crazy stuff like starve themselves, exercise till they drop or even (God forbid) pop diet pills, diuretics or laxatives just to win.

All of this is in direct contradiction to a fundamental principle of obesity management: you do not do things to lose weight that you are unlikely to continue doing to keep the weight off.

Most people seem to think that if only they could lose some weight, they will somehow be able maintain that lower body weight in the long-term with less effort.

The reality unfortunately is (and most dieters have experienced this over and over again) that no matter what diet or exercise routine you chose, no matter how slow or fast you lose the weight, no matter how long you keep the weight off - the minute you relax your efforts, the weight simply comes back.

As I have blogged before: obesity is a chronic disease for which we have no cure - only treatments! When you stop the treatment the weight (and any related problem) simply comes back.

By now you will already have figured out the problem with these challenges - unless you are very modest and reasonable about your weight-loss target and are carefully making changes that you can reasonably sustain forever, you are simply setting yourself up for failure.

If you are indeed modest and reasonable - you've already lost the competition to all the crazy folks who'll do anything just to win.

My advise to anyone with a weight problem - the next time you see an invitation to a weight-loss challenge - simply ignore it!

If you really think you will benefit from obesity treatment - seek help from a trained and accredited health professional with experience in weight management - let's put an end to weight cycling!

AMS

Obesity: It's all in Your Cells?

Yesterday I blogged about a remarkable Finnish twin study, in which the investigators went to the considerable trouble of finding monozygotic twin pairs who showed marked differences in body weight. The biggest predictor of weight gain in these genetically identical but weight-discordant co-twins was a markedly lower physical activity level, which in turn, declined even further as the obese co-twins packed on the pounds.

Assuming that this was not just a bunch of "lazy" co-twins, I wondered about what biological factors could possibly be causing these co-twins to be less physically activity. The answer to this question may lie in the results of another study by the same investigators in the same set of twins published in the open access journal PLoS Medicine.

In this study, Kirsi Pietiläinen and colleagues compared the genetic expression profiles in fat cells and macrophages between the obese and non-obese co-twins. Because, by design, the twins were genetically identical, they were able to normalise expression patterns for differences in genetic background, gender and age - thereby cutting through the considerable noise generally associated with expression studies.

In short, the authors found that the fat tissue from the obese co-twins showed a significant up-regulation of inflammatory pathways, significantly reduced mitochondrial DNA copy number, and disturbed mitochondrial energy metabolism—statistically most significantly, the decreased catabolism of branched-chain amino acids (BCAA). These impairments correlated with critical clinical measures of obesity including liver fat accumulation, reduced whole-body insulin sensitivity, hyperinsulinemia, hypoadiponectinemia and adipocyte hypertrophy.

In one individual, who the investigators were able to study before and after an additional weight gain of around 11 Kg over 3 years, mtDNA copy number was further reduced while serum BCAA concentrations and inflammatory activity increased even further.

Although the authors acknowledge that correlations do not prove causality, it is clear from the tone of their discussion that they believe that the metabolic derangements and low mtDNA copy count are a consequence of the obesity and are thus amenable to treatment by diet and exercise (the "politically correct" conclusion).

This is where I wonder if not the reverse may be true. I am no expert on mitochondrial biology, but I would assume that a key consequences of a reduction in mtDNA copy number is a decreased maximal capacity for oxidative phosphorylation, i.e., utilization of fat for energy production.

Assuming for a moment that these findings are also present in skeletal muscle, it would not be hard to imagine that these individuals are likely to find exercise more difficult and tiring than their co-twins with a normal mitochondrial population - less exercise means further weight gain and further decline in mitochondrial function - a nice little vicious cycle, if I ever saw one.

It is hard for me to image that in all 14 obese co-twins lack of physical activity alone was able to bring about the reduced mtDNA copy number, increased inflammation and reduced BCAA metabolism - somehow I find it easier to imagine that it was rather a malfunction in their mitochondria which significantly affected their ability to be (and enjoy being) physically active in the first place.

But of course, this is a chicken-or-egg question that cannot be resolved by the present study.

So the obvious questions now are: Can these co-twins be "rescued" by prescribing higher activity levels? How much activity will be needed to reverse these changes? And most importantly, will these co-twins stick with this prescription?

It's probably hard to enjoy exercise when there's a problem with your fuel cell.

AMS

Activity Determines Discordant Obesity in One-Egg Twins

So for Easter I wanted a posting with "Egg" in the title. What better paper to choose than the recent publication by Kirsi Pietiläinen and colleagues from Helsinki University published in last month's OBESITY?

In this remarkable study, Pietiläinen and colleagues went to the considerable effort of screening 1,870 young adult twin pairs to find 658 monozygotic (MZ) pairs, of whom only 14 (!) pairs reported a BMI difference of at least 4 kg/m2, with one twin being non-obese (BMI approximately 25 kg/m2) and the other obese (BMI approximately 30 kg/m2).

This effort alone shows how rare it is to find MZ twins that are discordant for weight, clear evidence for the well-known fact that body weight is one of the most heritable complex traits found in man, in fact, only marginally less heritable than height.

Nevertheless, the investigators were able to further characterize at least 10 of the 14 BMI-discordant twin pairs and readily identified the difference in physical activity as the key determinant of the discordance. Virtually all of the co-twins who ultimately became obese reported having been less physically active in adolescence than their non-obese co-twins. Furthermore, as they grew heavier, the obese co-twins' physical activity levels declined even further as did their self-perceived physical fitness. Based on accelerometer recordings, the obese co-twins had less than half the daily activity of their non-obese co-twins

In contrast, in the weight-concordant reference MZ twin pairs, physical activity patterns and fitness changed little during adolescence and were similar in the co-twins.

Thus, this paper appears to suggest that even in genetically identical individuals, large amounts of physical activity (or lack thereof) can "override" the genetic determinants of BMI.

What the paper, however, fails to tell us is why in these rare instances (only 14 out of 658 or 2% of MZ pairs) the obese co-twins were less active than their non-obese counterparts.

Why, as discussed in a previous posting on this blog, if the disposition to be physically active is such an 'innate" trait, did these 14 co-twins behave so differently from their siblings? Was it lack of interest, competing hobbies, sibling rivalry, injury?

Or was it epigenetics - i.e. post-conceptional modification of DNA that may involve paramutations, bookmarking, imprinting, gene silencing, X chromosome inactivation, position effects, reprogramming, transvection or maternal (intrauterine) effects - all of which could impact character traits or behaviour in later life?

So, while the paper shows that even in genetically identical individuals the heritability of BMI can be overridden by marked differences in physical activity, it does not provide the answer to whether or not this level of activity can be cognitively induced or, rather, happens as a result of rare quirks of nature.

Clearly, there are a few more eggs to crack before we fully understand why some people "chose" to be physically active and others don't.

Happy Easter!

AMS