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

Is Obesity a Question of Choice?

This is the title of a Canadian Institutes of Health Research (CIHR) Marketing & Communications and the Institute of Nutrition, Metabolism and Diabetes (INMD) 2008 Journalist Workshop being held in Toronto.

Speakers include INMD Director Diane Finegood, Angelo Tremblay, JP Despres, Gillian Booth, Kim Raine, Hertzel Gerstein, Mark Tremblay and JP Chanoine (all of whom are prominent Canadian Obesity Network members), very much reflecting the wide range of issues relevant to obesity.

I had the privilege of delivering the Keynote Lecture at the dinner event in which I focused on why I believe that patients with obesity deserve treatment like patients with any other chronic disease of our times. Even if we do not know how to cure obesity, we certainly have treatments that work and know the significant benefits that treatment can have on morbidity and quality of life.

As expected, this notion led to an interesting and extensive discussion with the usual challenges including not least the question why people with obesity cannot simply pull themselves together and make "healthy choices" to overcome their problem.

Well, of course that was the whole point of the symposium - to explain how complex the psychosocial and biological determinants of obesity actually are and why it is that individuals have such a hard time controlling their weight.

I emphasized all the usual points, well known to readers of my blog:

1) Weight is tightly controlled and cognition-driven changes in energy intake or output are immediately countered by the body's natural ability to restore energy stores making long-term weight-loss maintenance a life-long struggle

2) For obesity treatments to work (irrespective of whether they are behavioral, pharmacological and/or surgical) they have to be continued indefinitely to avoid relapse

3) Lack of adequate access to obesity treatments within the health care system is largely a reflection of the continuing bias that obesity is a self-inflicted condition that can be controlled by will-power alone

4) Because obesity is a remarkably heterogeneous condition, no single treatment fits all

5) The vast majority of health professionals are not trained to deal with this condition (which is why for example the University of Guelph and Humber College in Ontario have now decided to offer a course specifically for fitness professionals wishing to work in this area).

Lot's of great questions and note taking - curious to see what the media will do with all this information in the next few weeks.

AMS

Obesity Paradox also Holds in Denmark

Regular readers of this blog will have noted previous entries on the "paradoxical" reverse epidemiology of obesity and cardiovascular mortality, where risk is apparently higher in underweight compared to normal weight, overweight or even mildly obese individuals (for e.g. of previous blog entries on this click here, here or here).

Now a new Danish study by Jawdat Abdull and colleagues published in the European Heart Journal that looks at pooled data from 5 large registries with over 21,500 consecutive high-risk patients with myocardial infarction or heart failure finds essentially the same story:

After a follow-up of 10.4 years, compared with normal weight individuals (BMI 18.5-24.9) all-cause mortality was higher in underweight (BMI < 18.5) but not in overweight (BMI 25.0-29.9) or class I obese (BMI 30-34.9) individuals. Only with class II obesity (BMI 35-39.9) and higher was there a significantly increased risk for myocardial infarction and increased death risk.

This finding is very much in line with the mounting evidence that moderate overweight and mild obesity does not automatically translate into higher cardiovascular mortality in high-risk individuals with established heart disease.

As argued before, given that increased weight is a well-established risk factor for high blood pressure, diabetes, and other risk factors for cardiovascular disease, the reasons for this rather consistent "paradoxical" relationship are not clear.

Possible explanations include the idea that being underweight is a sign of general ill health and that thin people may be less able to cope with life-threatening illnesses like a heart attack at least compared to people with some extra "nutritional reserve". Of course there are a couple of more sophisticated theories out there that to me appear highly speculative (which is why I will not mention them today).

Nevertheless, in light of this "paradox", we may have to look beyond reducing cardiovascular morbidity and mortality to justify aggressive treatments of overweight and class I obesity with established cardiovascular disease - perhaps the aim of obesity treatment in high-risk individuals should simply be to prevent further weight gain rather than to reduce it?

I guess it would take intervention trials to find out - thankfully, these are already well underway.

AMS

Alberta: No Country for (Fat) Old Men

Last Saturday, apart from participating in the Super Size Me event, I also spoke at the 2nd Annual Endocrine Day for Family Physicians, organized by our division of endocrinology.

At this meeting Donald Morrish from our division presented a neat little update on Androgen Deficiency in the Aging Male (ADAM). This is what happens when guys' testosterone levels drop to below 10 mmol/L with age.

Typical symptoms include sexual dysfunction (decreased libido and erection problems), osteoporosis, gynecomastia and infertility often accompanied by fatigue and low-energy levels.

What makes this issue interesting to the bariatrician is the fact that male hypogonadism is also associated with loss of lean body mass and accumulation of abdominal fat.

Indeed, there is ample evidence to support the idea that testosterone substitution in hypogonadic men will increase muscle strength and decrease visceral fat. Without substitution, trying to lose weight, build muscle or finding the energy to exercise may be impossible.

Importantly, while these benefits have been shown for replacement doses, there is no proven benefit of using supra-physiological or "pharmacological" doses of testosterone.

Similarly, while replacing low levels of testosterone is probably without risk, the use of testosterone in males with normal testosterone levels is potentially problematic.

Unfortunately, the diagnosis of male hypogonadism is not straightforward. The most commonly used assay for testorsterone measures total testosterone, i.e. both free (active) testosterone and that bound to sex homone-binding globulin (SHBG). The latter, however, is commonly decreased in obesity, resulting in a falsely low level of total testosterone.

So to really know if someone with obesity who also has low total testosterone levels truly has hypogonadism, one has to order the more expensive bioavailable or free testosterone.

This test, at least in Alberta, is not covered by the public health system and will cost the poor fellow around $45 - by no means a trivial sum.

Furthermore, once you decide to substitute testosterone (of which the most convenient gel form is also not covered by Alberta Blue Cross), you again have to monitor the free-testosterone levels at regular intervals - overall a venture that may cost around $1500 a year - definitely not cheap.

I guess Alberta is no Country for Fat Old Men.

AMS

The Faster the Food - the Greater the Risk?

This weekend, I was invited to participate in a panel discussion following a public viewing of the documentary Super Size Me.

The event was part of the University of Alberta's Centenary Celebrations and was co-hosted by the Faculty of Medicine and Dentistry's Arts & Humanities in Health & Medicine program and the Edmonton Public Library in their film series called "Good Medicine".

As a panelist, I had the opportunity to see the film again and to reflect on what the film is actually about.

Of course, given that the film shows how Morgan Spurlock super sizes himself by eating nothing but McDonald's for 30 days, this film can easily be interpreted to simply show how bad fast food is for you.

While there is no question that given its high content of fat, sugar and salt, fast food is certainly not the most nutritious food, to me, this is not what the film actually proves.

In fact, when you think about it, Morgan could have splurged on 5000 KCal a day of even the most nutritious and expensive foods for 30 days and probably have gained as much weight and felt as sick in the end. Yes, you can gain weight on healthy foods!

Even the most pricey restaurants, do not necessarily design their meals to be healthy and balanced and I am probably not the only one who has eaten over 2500 KCal in food and wine at a single meal even in restaurants featuring celebrity chefs - no shortage of fat, sugar and salt in those foods either.

So eating at McDonald's was just a cheaper way to make this film - no doubt, had Morgan eaten all his meals at a 3-star restaurant, he would have needed a much larger budget for his film. In other words - this was just a "cheap" shot at McDonald's.

Don't get me wrong - there is nothing healthy about McDonald's or most of the food you can get at any fast food chain. But the film does not prove this.

What the film does show though, is that eating 5000 KCal a day can lead to weight gain and make you feel pretty sick. What the film also shows is that this is quite easy to do on fast food. Part of this is because the food is so cheap (=affordable). But another important reason why it is so easy to overeat is because the food is designed to be eaten fast.

I have previously blogged about the notion that the problem with fast food is more the "fast" than the "food" (see my post No Time to be Thin). It is indeed very hard to significantly overeat on "slow" food. This is because, when you eat slow, you will be quite full long before you have managed to tuck away 2000 KCal at a single meal. In fact, the bulkier and greater the volume of the food (i.e. the lower the caloric density), the harder it is to eat 2000 KCal at a single meal.

In the film Morgan also criticizes McDonald's for offering to super size your order (which they have since stopped doing). This, however, is also not so different from what happens in any restaurant, where the servers are trained to offer an appetizer, salad, dessert and more wine if you don't remember to order these extra calories yourself. They will also be happy to "super size" your steak order by offering to add a lobster tail or extra cream or cheese on you baked potato.

So here is what I think the film does show:

a) eating 5000 KCal a day leads to weight gain, which in turn is likely to make you sick

b) McDonald's (and no doubt other fast food restaurants) make it easy and affordable for you to do so

c) McDonald's (and virtually every other restaurant I know of) wants you to eat more and will try any trick in the book to get you to do so

How do we deal with this - for one, we could begin by posting calories on ALL menus - hopefully a disincentive to overeating, no matter how fast or slow the food.

AMS

Opening Eyes to Obesity Management

Yesterday I had the privilege of speaking to around 400 dietitians (and other health professionals) at Capital Health's 12th Annual Regional Nutrition and Food Services symposium.

After my presentation, many of the attendees came up to personally thank me for such an "eye opening" take on obesity.

This of course is surprising, given that you'd think that, if anyone, dietitians would be the ones with the greatest knowledge and understanding of the issues around obesity management.

So I asked the folks who came up to me about what exactly they found so "eye opening".

The answers were pretty much the issues that I have so often blogged about:

- The problems with clinically defining exactly what obesity is and who really needs treatment (no, BMI is not the best criterium!).

- The fact that obesity is a chronic disease that requires life-long treatment - a condition for which we have no cure (with a few rare exceptions).

- The rather limited long-term success of lifestyle (3-5% sustained weight loss), pharmacological (5-15% sustained weight loss) and even surgical (20-30% sustained weight loss) treatments (and even these results only if you continue the treatments!).

- The fact that while maintaining energy balance appears simple (energy in must equal energy out), energy regulation is highly complex.

- The concept that pharmacotherapy and surgery are not a "substitute" for lifestyle change but in fact only work when patients really do make substantial changes to their lifestyle (click here for a previous entry on this topic).

So, to readers of my blog, nothing really new or enlightening - yet, "eye opening" to many in the audience.

I guess we have a long way to go before all health professionals (especially physcians!) understand these basic concepts of obesity management.

If only I could speak to 400 health professionals everyday!

AMS

To Lose 40 lbs in 40 Days Click Here!

Regular readers of my blog will have noticed that I recently added a tiny little world map to my blog page showing how many visitors from around the world now visit my blog. Those of you, who only subscribe to my blog by e-mail or in a reader, may not have seen this. You have to actually go to my blog to check it out (to visit my blog click here).

Clicking on the world map takes you to a site called ClustrMaps, where you will see a larger and more detailed version of the map. In this view, you will also see several "weight-loss" ads peddling everything from Chinese herbs to bariatric surgery.

I have no control over these ads and neither has ClustrMaps. They are automatically provided by Google Ads on the assumption that readers of my blog are probably interested in weight loss. Every time you click on one of these ads, Google and ClustrMaps earn a couple of cents from the advertisers (I, unfortunately, get nothing).

Any reader of my blog will of course quickly realise that the majority of claims made in these ads are entirely ridiculous and have little to do with obesity management. People will apparently spend money on anything!

If you are tempted to click on these ads and end up buying any of these products or services, I can only say "you have been warned!".

If you click on the ads out of sheer curiosity about what the weight-loss industry has to offer - you will be putting their money into the coffers of Google and ClustrMaps - I don't mind either: as far as I know Google is trying hard "Not to be Evil" and ClustrMaps deserves it for coming up with this neat little tool, which I think looks great on my Blog.

AMS

Deconstructing Ingestive Behaviour

As someone with an interest in ingestive biology, I continue to be amazed by the complexity of eating behaviour.

Three commonly recognized eating behaviour constructs are "disinhibition", "cognitive restraint" (rigid or flexible) and "hunger" (internal or external).

Of these only "disinhibition" has been consistently shown to be strongly associated with adult weight gain.

There are actually three forms of disinhibition:

1) habitual disinhibition: the tendency to overeat in daily life

2) emotional disinhibition: the tendency to overeat in response to emotional states like anxiety or depression

3) situational disinhibition: the tendency to overeat in response to specific situations, e.g. social occasions

A recent study by Nicholas Hays and Susan Roberts from the University of Arkansas, published in OBESITY, examined the relationship between 20 year weight gain and eating behaviour subscales using the Eating Inventory (also often referred to as the Three-Factor Eating Questionnaire) in 535 women aged 55-65 years.

While "habitual" disinhibition showed the strongest association with weight gain, "emotional" disihibition showed only a modest association, while "situational" disinhibition was largely unrelated to weight gain. Flexible restraint significantly attenuated the effect of habitual disinhibition on weight gain.

As acknowledged by the authors, this study has several limitations including the fact that the weight data are self-reported and retrospective and that the participants' ingestive behaviour may have changed over time.

Nevertheless, if true, the paper raises a significant issue in terms of the focus of dietary counseling.

Thus far, dietary counseling has often tended to focus on situational disinhibition (e.g. dealing with eating on social occasions, in restaurants, etc.) or emotional disinhibition (e.g. coping strategies to avoid emotional eating). According to the findings of this paper, it would be far more appropriate to focus attention on reducing habitual overeating i.e. eating in "everyday" situations.

Strategies shown to help reduce habitual disinhibition include cognitive behavioural therapy, reducing variety and treatment with sibutramine.

It may be time for studies to expressly target habitual disinhibition in individuals who display this ingestive behaviour.

Obviously, this does not mean that for some people "emotional" or too frequent "situational" disinhibition cannot also significantly contribute to their weight gain.

Once again - one size is unlikely to fit all - but, providing the right dietary counseling requires making the right "diagnosis",

AMS

Obese Folks: on Your Feet!

One of the most common accusations faced by people with weight problems is that they are simply lazy and just lack the motivation to be active (the other one is that they simply eat too much!).

It turns out that some obese people may in fact be less active than lean individuals. For e.g., a recent study by Darcy Johannsen and colleagues from Iowa State University published in OBESITY, used state-of-the-art activity monitoring technology (IDEAA) to examine in detail the activity patterns of 20 free-living lean and obese women over 14 days. Total energy expenditure was measured using doubly labeled water, body composition was measured using dual energy X-ray absorptiometry.

The main finding was that even after correction for increased body mass, obese women on average expended around 300 KCal less in physical activity per day than their lean counterparts. Overall, obese women sat 2.5 hrs more each day and stood 2 hrs less than the lean women. They also spent only half the time being physically active compared to lean women.

This finding is not new. Previous studies have noted that obese individuals spend less time on their feet and expend less energy through non-exercise thermogenesis (fidgeting). Importantly, intervention studies have shown that this is not corrected by weight loss - rather, the tendency to be less active appears to be innate, i.e. not due to the excess weight.

Well, as usual, Johannson and colleagues conclude their paper with the profound insight that if only obese women adopted the activity pattern of lean women, they wouldn't be obese - and that is where the logic breaks down.

In fact, this is very much like saying that, "if only depressed people could be less sad and, like "normal" people, show more interest in things, they'd be so less depressed".

The issue is not whether or not obese people move less - the question is why they do so. If the tendency to be less physically active and spend less time on their feet is innate - i.e. a character trait that is determined largely by genetics, then trying to get someone with this trait to be more physically active is likely to be difficult.

Perhaps one way of thinking about this is to reverse the argument. If, for a moment, we assumed that being lean was really the problem, then we'd have to teach lean people to really try to sit down more and to focus on being less active, so that they could gain weight. Anyone who believes that it would probably be difficult to teach lean people to sit still, to stop fidgeting and to simply be less active, should realise that for exactly the same reasons it may be unreasonable to expect the opposite of people with excess weight.

Not to say it is impossible - but in both cases it would take a special focus, a lot of resolve and perhaps constant reminding as it goes against their "natural" disposition.

While in today's obesogenic environment the natural disposition to fidget and rush around works to the advantage of lean people, the natural disposition to sit down and not rush around (indeed a "sensible" behaviour in a calorically frugal environment) is a handicap.

Again, the results of such studies should not be interpreted in the sense of: "Aha, so now we know what is "wrong" with people who have obesity - they are indeed lazy!". Rather they should be interpreted in the sense of: "Aha, so that is why people with obesity have such a hard time keeping their weight off - they are simply "programmed" against a senseless waste of energy".

This of course is not an excuse to do nothing - it just means that we must appreciate the extra effort that is required.

In other words, when lean people run around - that's just their nature, they can't help it - it's not because they are extra smart or better people. In fact, now that we have seen this research we should realise that when people who have obesity run around (even a little) this is certainly highly commendable, as we now know that they have to consciously make this extra effort despite their innate tendency to preserve energy.

Creating an environment that fosters time on your feet will serve everyone - the lean people will love it (or not care), those with weight problems will benefit without having to make a conscious effort. Time for more stand-up meetings?

AMS

Out on a Binge

Anyone running an obesity clinic is well aware of the surprisingly large number of patients who have Binge Eating Disorder (BED). Some reports put the number at around 30% of patients with severe obesity who seek help for their weight.

But you have to ask the right questions to make the diagnosis:

Do you ever, especially when you are alone and are not even really hungry, rapidly eat vast amounts of food that is not really a proper meal (e.g. a bag of chips followed by a box of cookies followed by a loaf of bread followed by all the cheese you can find followed by a bag of nuts followed by a pot of ice cream followed by..........you get the picture!) till you get uncomfortably full (or run out of food) and then end up feeling quite disgusted about yourself for having done it again but have no idea why you are doing this or how to stop yourself from doing it again?

If this behaviour occurs at least a couple of times a week over at least six months, this patient probably has BED, a well described eating disorder listed in the appendix of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV).

To me, the most important differential diagnosis is overeating because of true hunger (homeostatic hyperphagia) or as part of a planned social event (e.g. a birthday, a festival, a special treat, etc.).

Typically homeostatic hyperphagia occurs when you have not eaten enough during the day and your body craves calories so that when you finally allow yourself (or find the time) to eat, you end up eating the wrong things too fast till you vastly overshoot your actual caloric requirements. Also, overeating at social events, especially when there is plenty of great-tasting food (and alcohol), i.e. "pigging out at the buffet" - does not mean you have binge eating disorder.

The key differences are that the patient with BED is not eating because of any "need for calories" or physical hunger, is not eating as part of a regular meal or social event, and ends up feeling quite troubled and disgusted at the lack of control (unlike the "hedonic overeater" who truly enjoys splurging on tasty foods and actually feels quite happy and content after a large scrumptious meal).

Diagnosing BED (which, despite popular belief, occurs as commonly in men as in women!) is essential, as this condition is actually made worse by dieting and patients usually have long-standing histories of weight cycling (usually with the help of commercial weight loss programs). Given that patients have little control over their behaviour, recidivism of weight gain is extraordinarily high and long-term maintenance of weight loss is virtually impossible without addressing the pscychopthology specific to this condition.

Fortunately, BED is highly responsive to psychotherapy (e.g. cognitive behavioural therapy, group interpersonal therapy, etc.) with various investigators reporting upto 95% reduction in the frequency of binge-eating episodes with almost 80% of patients becoming completely free from binging. Pharmacotherapy also appears to provide some relief.

The bottom line is: "true" BED is common and needs to be treated as a separate and distinct psychiatric disorder before hoping to make any progress in weight management.

Luckily this is possible.

AMS

Sifting Through Obesity Research

There is no doubt, obesity research is hot!

With over 100 new obesity publications appearing in the literature every month, it is impossible to keep up.

This is where the Canadian Obesity Network's OBESITY+ service comes in.

Based on McMaster University’s Health Information Research Unit's unique secondary peer rating system, OBESITY+ provides access to the current best evidence about the causes, course, diagnosis, prevention, treatment, and economics of obesity and its related mental, metabolic and mechanical complications.

Every week, the best evidence relevant for clinical practice in the fields of medicine, nursing, dietetics, and rehabilitation is identified from over 130 premier clinical journals with a focus on or strength in obesity.

All citations are pre-rated for quality by research staff, then rated for clinical relevance and interest by at least 3 members of a worldwide panel of practising health professionals with an interest in obesity.

The service includes a searchable database of the best evidence from the health care literature and features a customizable email alerting system.

Only the best research makes it through the rigorous review process - reducing "noise" by 98%

A related service Pre-OBESITY+ provides a broader overview for researchers - this service is less rigorous about the methodological criteria and therefore also includes studies that may not be ready for prime time, but are nevertheless of interest.

And best of all - both services are absolutely free to subscribers.

Click here to sign up for OBESITY+ (for health professionals)

Click here to sign up for Pre-OBESITY+ (for researchers)

AMS

Googling Guggul for Weight Loss

Guggul, or rather guggulsterone, is the active ingredient in an age-old Indian Ayurvedic remedy derived from the gum resin of the guggul tree (Commiphora mukul), which has been shown to lower lipid and cholesterol levels. Claims have also been made regarding its usefulness as an antiobesity drug, although the data on this is far from consistent.

A recent paper by Yang and colleagues from the University of Georgia, published in a recent issue of OBESITY, demonstrates that guggelsterone in fact does substantially inhibit adipogenic differentiation of cultured 3T3-L1 cells (a widely used in vitro model of fat cells). In this model, guggulsterone also promotes lipolysis as well as induces apoptosis of fat cells, albeit at higher concentrations. (link to abstract)

Together, these findings appear to provide a biological mechanism to support the anti-obesity health claims for this compound.

However, this does not mean that we now have a new natural "solution" to the obesity problem (although, as a brief excursion to Google confirms, guggul is already widely promoted and available for exactly that).

Here are my reservations:

1) Fat cells are the safest place to store excess calories. Limiting the growth or destroying fat cells, without also targeting the state of caloric excess raises the issue of where those extra calories should go. Because they are in excess of what the body needs, they are not simply "burnt off". Rather, the body now has to store them somewhere else, i.e. in non-fat tissue (for e.g. liver, muscle, etc.) - also referred to as "ectopic" fat deposition. There is now ample evidence that it is in fact this ectopic fat that causes the metabolic problems (e.g. diabetes) that are often associated with obesity. So if guggul prevents the formation of fat cells or destroys them (by apoptosis) the big question is: what happens with all the excess energy? If this now ends up in the form of fat stores in other organs like your liver or muscle, you are more likely to cause harm rather than reap any benefits.

2) Obviously, extrapolating from an in vitro finding to clinical benefits in patients is a long shot. While the data on guggul's clinical antilipid effects appears well-documented, I am not convinced of any weight-loss effects thus far. Destroying fat cells, to me does not necessarily translate into weight loss unless the extra calories stored in those cells are actually burnt. For that guggul would either have to promote burning of calories, for which to my knowledge there is no indication. Alternatively, guggul would have to also reduce energy intake for which I have also seen no evidence.

The bottom line is that, despite this elegant laboratory work demonstrating biological action of guggelsterone in vivo, health claims should be based on demonstration of clinically significant health benefits in rigorously conducted clinical trials. As the issue in obesity treatment is not short-term weight loss but rather long-term weight-loss maintenance, these studies would have to be long enough (i.e. 12 months or longer).

Is this going to stop people from selling and buying guggul because of its now "proven ability to destroy fat cells"?

Not likely.

Will I be recommending guggulsterone as obesity treatment to my patients?

Definitely not!

AMS

Replacing Meals Beats Skipping Them

One of the basic principles in weight management is not to let yourself get hungry.

This is based on the simple rationale that when you are hungry, your hypothalamus "kicks in", essentially overriding any "sensible" choices you may have intended to make.

For one, when you are hungry you are more likely to eat energy-dense foods.

But hunger also makes you eat faster, in turn making you more likely to overshoot your actual caloric requirements before satiety sets in. I have previously referred to this as ""homeostatic hyperphagia"".

Skipping meals is perhaps the most common reason for people to get hungry. The meals most likely to be skipped are breakfast and lunch, resulting in the evening "binge".

If the reason for skipping breakfast and lunch is lack of time and an irregular hectic schedule, commercial meal replacements can come in handy. The convenience of quickly drinking a shake or eating a bar is hard to beat.

Sure, a proper balanced meal prepared with fresh wholesome ingredients enjoyed in a relaxing setting would be best, but the reality is that that is rarely the reality.

Therefore, I would rather see my patients eating a meal replacement than skipping a meal. Meal replacements also promote portion control. Not least, meal replacements are cheap - costing as little as a couple of dollars per meal.

Because I have seen this strategy work over and over again, I was not at all surprised by the results of a recent randomised-controlled trial from John Hopkins (Baltimore), where a diet using portion-controlled meal replacements yielded significantly greater initial weight loss and less regain after 1 year of maintenance than a standard, self-selected, food-based diet in patients with type 2 diabetes (click here for abstract).

Obviously, this is not a strategy for people who "hate" meal replacements. And, like any weight-management strategy, it only works as long as you stick with it.

But for those who embrace it, using meal replacements to replace meals that they'd otherwise skip may prove a viable long-term strategy to regain control of their hypothalamus and their diet.

AMS

Are Obese People Fit to Parent?

Yesterday's headline in the Toronto Star was about a case where an Ontario family court judgment cited obesity as a reason for removing a child from the parental home, after determining the mother was contributing to her child's weight gain and was oblivious to the required medical regime. The article cites other cases where obesity was a factor in rulings regarding parenting and foster care. (Click here to read the article)

The question is: can parents, who are actively contributing to their child's excessive weight gain or are not doing enough to ensure a healthy eucaloric diet, be accused of chid abuse or neglect?

My take on this is that the situation is probably no different from other circumstances, where parents are endagering the health of their children by exposing them to potential health risks (e.g. passive smoking, not using a child seat, etc.).

Obviously the rulings will have to depend on the extent of the actual risk. Clearly, there is a substantial difference between feeding your otherwise healthy active child the occasional French fry versus letting your child with a peanut allergy enjoy a couple of nuts.

I do not envy the folks, who have to make these rulings and are called upon to decide where the limit is of what is acceptable parental discretion and what constitutes abuse or neglect.

In the end however, there is no special case for obesity - it needs to be treated like any other condition based on the actual risk to the child and on the extent to which the parental behaviour is deemed a significant contributor.

Tough call - I am glad that it is not mine to make.

AMS

Is Obesity Critical in Critical Care?

Although obesity is now well-recognized as a risk factor for the development of many chronic diseases, its role in acute situations is less clear.

So while one might assume that severe obesity in critical ill patients is a predictor of poor outcomes, this hypothesis was not confirmed in a recent meta-analysis of studies comparing outcomes in obese (BMI > 30 kg/m2) critically ill patients in intensive care settings published by Akinnusi and colleagues from the University of Buffalo School of Medicine in the January issue of Critical Care Medicine (for Abstract click here).

Fourteen studies with 15,347 obese patients met inclusion criteria. Surprisingly, obesity was not associated with an increased risk of intensive care unit mortality, albeit duration of mechanical ventilation and intensive care unit length of stay were statistically but not remarkably longer in the obese group.

Interestingly, in a subgroup analysis, an improved survival was observed in obese patients with body mass index ranging between 30 and 39.9 compared with nonobese patients (relative risk, 0.86; 95% Cl, 0.81-0.91; p < .001). This latter finding is reminiscent of the "obesity survival paradox" alluded to in previous blogs.

Clearly, obesity is not a significant risk factor for poor survival outcomes in critical care. Whether or not this also applies to the subset of extremely obese patients that are now increasingly seen in hospital settings remains to be seen.

AMS