Most textbooks on obesity will tell you that assessing someone for obesity should start with a careful exploration of weight history, eating habits and lifestyle.

I disagree!

For reasons that I will outline below, I believe that the proper assessment of patients presenting with excess weight should first focus on the four “M”s or the mnemonic “M”, “M”, “M”, & “M”.

As I presented yesterday in a talk on obesity assessment at the American Heart Association Meeting in Orlando, obesity is not only a remarkably heterogeneous condition resulting from a wide range of environmental, psychosocial and biomedical causes, successful weight management is also remarkably difficult and tenuous even in the most motivated and determined of patients.

The primary goal of assessment therefore should first strive to identify the possible causes and circumstances leading to excess weight gain, determine to what extent that excess weight is affecting health and systematically look for barriers that will make weight management difficult, if not impossible.

Each of the four “M”s explores a domain that is potentially relevant to all of the above questions.

The first “M” stands for “Mental Health”. Not only can common mental health problems often lead to weight gain (e.g. depression, addictions, attention deficit, abuse, PTSD, sleep disorders, emotional eating, etc.), but when present (as is often the case), they can make weight management most challenging. In addition, excess weight can directly affect mental health by promoting poor self-esteem, depression and social anxiety disorder. Thus, devising a weight management plan always requires a good understanding of a patient’s mental health status, if only to determine that there are indeed no major mental health causes or consequences of weight gain nor significant mental health barriers that will make weight management difficult, if not impossible.

The second “M” is a reminder to look for the many “Mechanical” causes or complications of excess weight. These can present in the form of back pain or osteoarthritis, sleep apnea, reflux disease, urinary incontinence, and many other problems associated with excess weight. When present, these issues can not only promote or exacerbate weight gain but can also pose important barriers to weight management – clearly someone with plantar fasciitis is unlikely to walk the recommended 10,000 steps.

The third “M” should prompt us to look for the wide range of “Metabolic” complications of excess weight. These not only include diabetes, dyslipidemia or gout, but also hypertension (a problem of sodium metabolism), fatty liver and gall-bladder disease, polycystic ovary syndrome, and some forms of cancer. Often the presence of these conditions or the treatments we use to control them can contribute to further weight gain rather than help solve the problem.

The fourth “M” stands for “Money”, a not unimportant factor that can affect weight gain (healthy eating is expensive) or pose an important barrier to weight management (weight management costs time and money).

Only after a complete understanding of the four “M”s can a clinician hope to fully appreciate the likely causes and consequences of obesity and the potential barriers to its treatment in a given patient.

Only after we have fully explored the four “M”s does it make sense to delve further into issues related to energy balance, i.e. ingestive behaviour, energy metabolism and physical activity in order to devise a sensible and effective management plan.

As I have argued before, simply assessing and describing a behaviour is not a diagnosis - understanding the root cause of that behaviour is.

AMS
Toronto, Ontario

Some readers may recall earlier studies on the increased risk for dementia associated with increased body weight.

A new study, by Cyrus Raji and colleagues from the Universities of California and Pittsburgh, just published in Human Brain Mapping, finds a significant decrease in brain volume in overweight and obese elderly individuals despite largely normal cognitive function.

The researchers used sophisticated morphometric methods to examine grey and white matter volume differences in MRI scans from 94 elderly subjects who remained cognitively normal for at least 5 years after their scan.

After correcting for various covariates including age, gender, race as well as fasting plasma insulin levels and and Type 2 Diabetes Mellitus increased BMI was associated with with atrophy in frontal, temporal, and subcortical brain regions.

Specifically, in individuals with a BMI >/= 30, atrophy was found in the frontal lobes, anterior cingulate gyrus, hippocampus, and thalamus compared with individuals with a normal BMI (18.5-25). These parts of the brain are particularly important for planning and for memory.

Whether or not subjects actually had clinically relevant defects in brain function was not examined in this study. Furthermore, this cross-sectional study does not provide any causal or mechanistic insights into this relationship.

Obviously, whether or not these findings of brain atrophy can be prevented by weight loss also remains to be seen.

Thus, while this paper is sure to get wide publicity in the media, the clinical relevance and implications of these findings remain obscure. Nevertheless, even subtle deficits in planning and memory, if present in elderly individuals with obesity, can potentially affect their ability to plan meals or follow complicated diet plans - something that may (if confirmed in other studies) have to be considered in counseling such patients.

AMS
Edmonton, Alberta

While I am taking a brief break from clinics and other obligations (including daily blog posts), I will be reposting past articles, which I still believe to be relevant but may have escaped the attention of the 100s of new readers who have signed up in the past months.

The following was first posted on 08/19/08

Many readers of this blog are familiar with the ongoing (endless?) discussion about whether or not obesity is a risk factor, a disease, a condition, or simply an extreme of the normal “bell curve” of body weights. Today, I want to throw in another term into this discussion. In fact, the more I think about it, the more I am convinced that we should look at obesity as a clinical sign - not unlike edema.

In the same manner that edema reflects the excess accumulation of fluid, obesity reflects the excess accumulation of body fat. As edema is a clinical sign of a perturbation of fluid homeostasis, excess fat accumulation is indicative of a perturbation in energy balance.

In a patient with edema, we can of course opt to simply provide symptomatic treatment by restricting salt and water intake, but my guess is that most experienced clinicians will likely make an effort to understand whether the fluid retention is a result of abnormal cardiac function, renal failure, venous or lymphatic stasis, vasodilatory drugs or a list of other possible causes of fluid retention.

Similarly, in a patient with excess body fat, we can simply prescribe “symptomatic treatment” by restricting food intake or increasing activity, or we can make an effort to truly understand the factors that are causing the patient to overeat or “undermove” (apologies for coining this term, but I kind of think it conveys the point). Obviously, whether or not the overeating is a result of peer pressure, hunger (meal skipping), depression, binge-eating, olanzapine, sugar-addiction, MC-4 receptor defect, or a craniopharyngeoma may well influence the choice of treatments.

Similarly, whether or not the “undermoving” results from lack of time, unsafe neighbourhoods, obstructive sleep apnea, anxiety disorders, depression, back pain, fibromyalgia, plantar fasciitis, vital exhaustion or quadroplegia will (hopefully) help determine the most appropriate and effective management strategy.

The idea that all people with excess body fat should simply eat less and move more is not unlike the notion that all people with edema should simply restrict their fluid intake and cut the salt.

If obesity is simply a “sign”, then “overeating” and “undermoving” are just symptoms!

The differential diagnosis of overeating and undermoving is complex and can involve sociocultural, psychological, medical and iatrogenic causes.

Let’s get more sophisticated in our diagnostics - hopefully our ability to address the underlying causes will follow.

AMS
Edmonton, Alberta

While I am taking a brief break from clinics and other obligations (including daily blog posts), I will be reposting past articles, which I still believe to be relevant but may have escaped the attention of the 100s of new readers who have signed up in the past months.

The following was first posted on 30/03/08 (the Edmonton Obesity Staging System suggested in this original post, is now published in the International Journal of Obesity. Also note the foresight expressed in this post in light of Margaret Wente’s thought-provoking comment published in yesterday’s Globe and Mail - as this “classic” blog post demonstrates, we were well over a year ahead of Margaret in our thinking about what constitutes obesity and who needs treatment - good to see the mainstream media catch up!).

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

Fatty liver disease, which can in some case progress to fibrosis and cirrhosis, is an increasingly recognized complication of obesity. Currently, characterization of fatty liver disease is dependent on a liver biopsy.

In a paper appearing this month in GUT, Trak-Smayra and colleagues from the Centre de recherche Biomédical Bichat Beaujon, Paris, France, used SELDI-TOF ProteinChip profiling to detect fatty liver disease in eighty obese non-alcoholic patient candidates for bariatric surgery and who were devoid of hepatitis B and C infection. Proteomic profiles were compared to liver tissue samples.

Three peaks were detected in the proteomic profile (double charged ions of alpha- and beta-haemoglobin subunits), the intensity of which significantly increased according to the severity of the liver lesions and returned to normal after bariatric surgery.

These findings suggest that novel blood tests may be helpful in identifying and characterizing the extent of fatty liver disease in obese patients.

AMS
Edmonton, Alberta