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Tuesday, April 29, 2008

Waist Loss Trumps Weight Loss

Yesterday, I had the pleasure of listening to Robert (Bob) Ross from Queen's University, Kingston, Ontario, speaking at the 77th European Congress on Atherosclerosis, Istanbul. Turkey.

Here are his key messages:

1) Exercise helps reduce visceral fat even if you don't lose much weight. Walking as little as 60 mins a weeks can have an effect - of course, the more the better

2) Measuring waist circumference can detect changes in abdominal fat even when overall weight does not change

3) People who are exercising to lose weight may lose their motivation if they solely focus on weight and fail to recognize the "other" health benefits of exercise

Anyone who has heard Bob speak, knows that he is a most eloquent and persuasive speaker.

Very much enjoyed his talk.

Great work Bob!

Istanbul, Turkey

Monday, April 28, 2008

Obesity and Atherosclerosis

The next couple of days I will be at the 77th European Atherosclerosis Society Congress in Istanbul, Turkey.

Given the importance of obesity (particularly visceral fat deposition) as a risk factor for atherosclerosis, it is not surprising that there are several talks on various aspects of obesity including its pathophysiology and management at this meeting.

My own talk on Tuesday morning will be on the role of "ectopic" fat on cardiovascular risk.

Generally speaking, ectopic fat is fat that accumulates in depots other than just underneath your skin and includes fat deposits in the gut, liver, muscle and other organs.

Always important to remember that not all fat is bad and that not everyone with a couple of extra pounds of fat tissue is at risk for heart disease.

When it comes to fat and heart disease, the "where" appears to be far more important than the "how much"!

Istanbul, Turkey

Friday, April 25, 2008

Does Maternal Obesity Promote ADHD?

Regular readers of my blog know about the risk of increased pre-pregnancy weight and pregnancy-induced weight gain for mother and child.

Readers may also recall my posting on the potential importance of recognizing attention deficit disorder (ADD) as a common and important barrier to obesity treatment.

This month, a new study by Alina Rodriguez and colleagues from the University of Upsalla, Sweden, published in the International Journal of Obesity, may help bring it all together.

Rodriguez and colleagues examined whether pregnancy weight (pre-pregnancy body mass index (BMI) and/or weight gain) is related to core symptoms of attention deficit hyperactivity disorder (ADHD) in school-age offspring.

They analyzed data from three separate prospective pregnancy cohorts from Sweden, Denmark and Finland within the Nordic Network on ADHD. Maternal pregnancy and delivery data were collected prospectively. Teachers rated inattention and hyperactivity symptoms 12 556 school-aged offspring in relationship to maternal weight measures.

While gestational weight gain was unrelated to ADHD rate, the researchers found significant associations between pre-pregnancy overweight or obesity and a high ADHD symptom score in offspring, ORs ranged between 1.4 and 1.9 fold higher despite adjustment for gestational age, birth weight, weight gain, pregnancy smoking, maternal age, maternal education, child gender, family structure and cohort country of origin.

Children of women who were both overweight and gained a large amount of weight during gestation had a 2-fold risk of ADHD symptoms compared to normal-weight women.

Although the authors carefully note that associations do not prove causality, they do point out that if future studies prove causality, then we may need to add ADHD to the list of deleterious outcomes related to maternal overweight and obesity in the prenatal period.

It would certainly explain why ADHD is so common in patients battling overweight and obesity.

Edmonton, Alberta

Thursday, April 24, 2008

Will a Urine Test Predict Obesity?

Urine analysis has long played an important role in diagnosing disease. As most of you may know, the term diabetes mellitus actually refers to the honey-like sweetness of the excessive urine produced by patients with this disorder.

Now Elaine Holmes and colleagues from the Imperial College London, UK, take urine diagnostics to new heights in a recent paper published in Nature.

Holmes and colleagues used a large-scale exploratory analytical approach, based on (1)H NMR spectroscopy, to anlayse the metabolic spectra from two 24-hour urine specimens for each of 4,630 participants from the INTERMAP epidemiological study, involving 17 population samples aged 40-59 in China, Japan, UK and USA.

The metabolic phenotypes are the products of interactions among a variety of factors-dietary, other lifestyle/environmental, gut microbial and genetics.

They were able to show that urinary metabolite excretion patterns for East Asian and western population samples, with contrasting diets, diet-related major risk factors, and coronary heart disease/stroke rates, are significantly differentiated, as are Chinese/Japanese metabolic phenotypes, and subgroups with differences in dietary vegetable/animal protein and blood pressure.

The authors go on to speculate that mean 24-hour urinary excretion of various metabolites, may not only reflect diet and gut microbial activities, but may also help discover novel biomarkers related to cardiovascular disease risk factors including obesity.

Can't wait to see how long it will take before I see a urinal replacing my bathroom scale.

Edmonton, Alberta

Wednesday, April 23, 2008

Anatomy Lesson

Nothing on obesity today (actually moving house, so not a lot of time this week).

But here's a link to a fascinating series of pictures for anyone with an interest in human anatomy.

Remember, all of this is normally hidden under a layer of subcutaneous fat (you can still see it in some of the preparations).

None of the dramatics of von Hagen's Bodyworlds.

Just true to life - and humbling,

Edmonton, Alberta
p.s. Hat Tip to Michael Dwyer of CIHR for suggesting this site

Tuesday, April 22, 2008

Does Surviving Cancer Lead to Weight Gain?

Yesterday's big news was the study by Kerry Courneya, professor and Canada Research Chair in Physical Activity and Cancer at the University of Alberta, published in CANCER.

I am not going to repeat the findings or the data here because this was nicely summarized by Sharon Kirkey from Canwest News Service in the Edmonton Journal.

The bottom line is that cancer survivors are apparently not exercising more or eating healthier than everyone else, and are therefore at least as, if not even more, likely to develop obesity than the average Canadian.

This is particularly true for survivors of breast and colon cancer, which are particularly likely to recur with lack of physical activity, unhealthy eating and weight gain.

The dramatic impact of weight on cancer risk is perhaps best demonstrated by the observation that obesity surgery, which on average reduces body weight by 25%, results in an almost 60% reduction in cancer mortality! (see Adams et al. for an example of such a study).

I guess it just goes to show that cancer survivors are no less susceptible to the consequences of our obesogenic environment, which certainly does not make weight control easy, even at the best of times.

That is of course, unless there is something special about surviving cancer that makes you more likely to gain weight - an interesting hypothesis pursued by other researchers here at the University of Alberta.

I can think of a number of reasons why surviving cancer could predispose to weight gain: "catch-up" fat, depression, "post-traumatic" stress, anxiety, susbtance abuse, "overfeeding", immobility, medications, and perhaps a few others.

Whatever the reasons, it looks like we may now need intervention programs to specifically address weight gain and obesity in cancer survivors?

For one, educating cancer survivors about the links between excess weight and cancer would be a start.

My sense is that most people still don't fully appreciate the close link between obesity and cancer - all the more reason to promote healthy eating and active living for all.

Obesity prevention (and treatment?) may well turn out to be the most effective cancer prevention strategy (short of smoking cessation) - looks like a whole new field for bariatric health professionals?

I guess we'd call them Bariatric Oncologists?

Edmonton, Alberta

Monday, April 21, 2008

Interprofessional Approach to Obesity

Obesity is a complex and heterogeneous chronic condition that significantly affects many aspects of the mental, physical and economic well-being of Canadians.

The federally-funded Canadian Obesity Network with well over 2700 member, represents a wide range of obesity researchers, health professionals, policy makers and other stakeholders from across Canada and around the world.

How do these members see the role of interprofessional practice in dealing with obesity? This was the subject of a pilot survey conducted by Shelly Russell-Mayhew and colleagues from the University of Calgary at an obesity conference organized by the Obesity Network held in Kananaskis, Alberta, in May 2006.

The survey on interprofessional attitudes and relationships was conducted using semi-structured individual interviews with CON members attending the conference using established qualitative methodology. The researchers analysed the‘‘Who?, What?, When?, Where?, Why?, and How?’’ framework of interprofessional practice and obesity.

The results of the study just appeared in the March issue of the Journal of Interprofessional Care.

While the study makes interesting reading, the bottom line is relatively straightforward:

Both obesity prevention and treatment cannot be approached in silos. No single profession has all the expertise necessary to counter this epidemic.

Interprofessional collaborations and interactions will be key to the solutions.

I was particularly pleased to see that the interviewees consistently felt that the Canadian Obesity Network is strategically positioned to foster this interprofessional dialogue and to ensure that all relevant professions and stakeholders benefit and translate the rapidly emerging research in this field into effective prevention and treatment strategies.

In the meantime, the Canadian Obesity Network continues to evolve into a well-recognized and respected entity in the Canadian public health and healthcare landscape.

Membership is open to anyone with a professional interest in obesity by registering at

Edmonton, Alberta

Friday, April 18, 2008

Does Belly Fat Beget Belly Fat?

Obesity is a chronic disease and it seems that the heavier you get, the easier it is to put on even more weight.

I can think of many reasons why this may happen: less activity as you get heavier, more "emotional" eating, poorer sleep, to just name a few.

But here is a new idea: fat cells themselves may produce a substance that helps you grow even more fat cells.

This may indeed be the case, according to a study by Kaiping Yang and colleagues from the University of Western Ontario, London, Ontario published last month in the FASEB Journal.

The study was about Neuropeptide Y (NPY), a potent stimulator of hunger. Yang and colleagues not only found that in mouse and rat models of obesity, visceral fat cells can produce NPY, but also that NPY can promote the proliferation of adipocyte precursor cells via the Y1 receptor.

In fact NPY levels in visceral fat tissue were 6-fold higher in an early-life programmed rat model of increased visceral adiposity, but also more than 2-fold higher in visceral fat tissue of obese Zucker rats.

It turns out that at least in rodents, belly fat itself may be a risk factor for even more belly fat.

Would not surprise me if the same was true for humans.

An interesting question is whether or not the NPY made by fat cells can actually enter the brain to stimulate hunger, and thus, cause the animals (and humans?) to eat more - thereby creating a true vicious cycle.

Certainly an intriguing (although somewhat depressing) hypothesis.

Edmonton, Alberta

Thursday, April 17, 2008

Back Surgery Does Not Cure Obesity

Immobility, due to pain or otherwise, is certainly a major contributor to weight gain. Pain is indeed often presented by overweight and obese patients as a factor limiting their ability to lose weight.

Given the widely-held (but false!) belief that exercise is the most effective way to lose weight, the general expectation of both patients and health professionals is probably that restoring mobility by relieving pain will enable patients to be more physically active and thereby lose weight.

But is this actually the case?

This issue was recently addressed by Ryan Garcia and colleagues from the Department of Orthopaedic Surgery, Case Western Reserve University, Cleveland, OH in a study just out in the Journal of Bone and Joint Surgery.

Garcia and colleagues examined weight changes in 63 overweight and obese patients with neurogenic claudication who experienced substantial pain relief after lumbar decompression surgery for spinal stenosis. Although Zurich Claudication Questionnaire (ZCQ) Symptom Severity and Physical Function scores significantly improved by a mean of 56.4% and 53.0%, respectively, body weight and BMI significantly increased by 2.48 kg and 0.83 kg/m(2), respectively.

Overall, an average 34 months after surgery, 35% of the patients had actually gained at least 5% of their preoperative body weight while only 6% of the patients weighed at least 5% less than before their operation. The vast majority (59%) remained within 5% of their preoperative body weight.

This study, consistent with several previous studies on joint surgery, nicely documents that increased mobility after pain-alleviating surgery does not necessarily translate into weight loss - in fact, most people will either continue to gain weight or simply stay the same.

Obviously, this should not be an argument against alleviating pain in obese patients - no one deserves to live with pain. It just goes to show that increased mobility alone is not likely to substantially lower body weight - at best, it may prevent further weight gain (difficult enough even at the best of times).

This is probably something patients should be counseled about to not raise any false expectations.

On the other hand, it is important to note that this was not a weight-loss study. This means, that patients were not expressly counseled for weight loss or offered obesity treatments.

The question therefore remains whether or not improving mobility in patients by alleviating pain would improve efficacy of obesity management strategies (which I believe it would).

That is obviously a study that remains to be done.

Edmonton, Alberta

Wednesday, April 16, 2008

Time to Limit Weight Gain in Pregnancy?

Regular readers of my blog will have noticed several previous postings on the issue of maternal obesity and health risk for mother and infant.

This issue seems to be developing into a really "hot topic", at least judging from the flurry of articles in the most recent alerts from CON/McMaster University's OBESITY+ services.

The first was a nested case-control study comparing 251 mothers who developed gestational diabetes to matched normal controls, both selected from a multiethnic cohort of 14,235 women. In this study, Monique Heddersen and colleagues from Kaiser Permanente, Oakland, CA, demonstrated that women who gained significant amount of weight in the five years preceding their pregnancy, had a 2.5-fold higher risk of GDM compared to women with stable weight. Gestational diabetes has been linked to increased birth weights and later risk of obesity in the offspring (American Journal of Obstetrics and Gynecology, April 2008).

In the same issue of AJOG, Holly Hull from Columbia University, New York, NY, compared body weight and composition (air-displacement plethysmography) in 33 neonates born to mothers with a normal pregravid BMI to 39 neonates born to overweight/obese mothers with normal glucose tolerance. Babies born to normal BMI mothers had significantly less total and relative fat and more fat-free mass than babies born to overweight/obese mothers. Although preliminary, the authors interpret these data to suggest (and I agree) that the antecedents of future disease risk (eg, cardiovascular disease, diabetes, and obesity) occur early in life.

So what, if anything, can we do about this?

That question was addressed by Wolff and colleagues from the University of Copenhagen, who performed a randomized controlled trial in 50 obese mothers (pre-pregnancy BMI around 35) with or without restriction of gestational weight gain to 6-7 kg by ten 1-h dietary consultations. Not only did the women in the intervention group successfully limit their energy intake to restrict gestational weight gain to 6.6 kg (vs. a gain of 13.3 kg in the control group) but this was associated with a significantly reduced fasting glucose and insulin levels in the intervention group with no apparent harm to the babies. Thus, restriction of gestational weight gain in obese women is achievable and reduces the deterioration in the glucose metabolism. (International Journal of Obesity, March 2008)

Together these studies clearly support the importance of addressing obesity in mothers before and during pregnancy - an intervention that will hopefully prove beneficial to both mother and child.

So while weight management should probably soon become part of routine prenatal care, I do wonder how long it will take before we start seeing a whole new wave of "weight-loss-in-pregnancy" products and services from the ever vigilant and enterprising weight-loss industry.

Hopefully not too soon!

Edmonton, Alberta

Tuesday, April 15, 2008

Stop Walking to Gain Belly Fat

As regular readers of my blog know, I love walking (at least when I have to!).

To find out how important walking actually is to help control your weight, apparently all you need to do is stop.

This was exactly what Rasmus Olsen and colleagues from the University of Copenhagen convinced 18 healthy male subjects to do. Participants were instructed to reduce daily steps by using elevators instead of stairs and riding in cars instead of walking or bicycling while maintaining their habitual food intake (JAMA, March 19).

The first set of eight men decreased their pedometer recorded daily steps from a mean value of 6,203 to 1,394 over 22 days. The second set of ten men decreased their mean daily steps from 10,501 to 1,344 over 2 weeks.

While body weight was not reported for the first eight men, they had a marked rise in insulin area-under-the-curve (AUC) following the glucose tolerance test (interpreted as reduced insulin sensitivity).

But even more interestingly, in the second group, although BMI DECREASED(!) from 22.1 to 21.8, intra-abdominal (visceral) fat INCREASED by 7% (as measured by MRI). Lean body mass (as measured by DEXA) decreased by 1.2 Kg while both the insulin and triglyceride response to the tolerance tests were adversely affected.

Not bad for just two weeks of not walking! And these were healthy lean young men to start with - my guess is that the effects in older overweight folks would be even more dramatic.

So why spend money at McDonalds? Just walking less will "supersize" your abdomen as nicely.

Edmonton, Alberta

Monday, April 14, 2008

ICD-10 Classification of Obesity: Can Someone Please Explain?

The International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10) is a widely-used coding of diseases and signs, symptoms, abnormal findings, complaints, social circumstances and external causes of injury or diseases, as classified by the World Health Organization (WHO).

Classification for obesity can be found in Chapter IV (Endocrine, nutritional and metabolic diseases) under the subsection Obesity and Other Hyperalimentation (Codes E66.0 to E66.9).

These are defined as follows:

E66.0 Obesity due to excess calories

E66.1 Drug-induced obesity

E66.2 Extreme obesity with alveolar hypoventilation (Pickwickian syndrome)

E66.8 Other obesity (Morbid obesity)

E66.9 Obesity, unspecified (Simple obesity NOS)

Here is why I do not understand this classification:

Well firstly, as far as I know, every form of weight gain requires an imbalance between energy intake and output. This means that all forms of obesity result from “excess” calories – i.e, if you define “excess” as exceeding caloric expenditure. Code E66.0 would therefore apply to all patients with obesity.

Weight gain in E66.1, which refers to drug-induced obesity, is of course also related to caloric “excess” – whether this results from hyperphagia (e.g. clozapine) or reduced metabolic rate (e.g. beta-blockers). When do you decide that someone is gaining weight solely because of a medication? More often than not there are other predisposing factors (e.g. sedentariness, depression, etc.).

Why the “coders” decided to make a special case for the rather rare alveolar hypoventilation (E66.2) but ignored all other major complications of severe obesity (e.g. heart failure, sleep apnea, osteoarthrits, etc.), at least to me, makes no sense.

But things get even more confusing!

E66.8 refers to “other obesity” – does this mean obesity not caused by caloric excess? Then none of my patients would ever qualify for this code. Or does E66.8 apply only to “morbid obesity” – which is not a WHO definition, unless they actually mean Class III obesity – then what about Class II obesity in case of a patient who is “morbid” because he has type 2 diabetes? Would this person qualify?

To fully add to the confusion, you can also choose code E66.9, i.e. “unspecified” or “simple” obesity – again, do they mean not resulting from caloric excess? Or do they perhaps mean patients with no complications? Or does ”simple” refer to cases where the cause is not “complicated” (as in, "this fellow “simply” eats too much")?

Overall, to me this classification makes no sense whatsoever. It is neither consistently based on etiology nor is it clinically meaningful in any sense of the word.

Take for example the case of someone with a BMI of 42 due to “simple” overeating who gains another 40 lbs after starting on clozapine resulting in numerous complications including alveolar hypoventilation. Would this patient’s obesity have to be classified as E66.0, E66.1; E66.2 or E66.8? Or, would this “simply” be E66.9. Or perhaps all of the above?

None of this makes any sense to me!

If there is anyone out there who can help me interpret these codes and show me how to use them to classify my patients in a way that would be clinically relevant, I’d be more than grateful.

In the meantime, I will continue using my own classification of obesity (which we now internally refer to as the “Edmonton Obesity Classification”). Although this system is not meant to provide insights into etiology, at least it allows me to clinically grade the amount of weight and to stage the extent of disease in every patient.

Edmonton, Alberta

Friday, April 11, 2008

Employees' Obesity Costs Employers

This week, The US Conference Board released a report called "Weights and Measures: What Employers Should Know about Obesity" on the financial and ethical questions surrounding whether, and how, US companies should address the obesity epidemic.

Apparently employees' obesity-related health problems cost US companies an estimated $45 Billion each year in medical coverage and absenteeism - more than smoking or problem drinking.

Given the high costs of obesity, the report estimates the return on investment for employee wellness programs from zero to $5 per $1 invested. ROI aside, these programs may give companies an edge in recruiting and retaining desirable employees. The report also looks at the issue of awarding employees cash and prizes for weight loss rather than devoting resources to long-term wellness programs.

Interestingly the report also discusses the benefits of paying for employees' obesity surgeries. Apparently 9% of the US workforce would be eligible for such surgery, but because people often change jobs (e.g. in the retail industry), employers may not always recoup the full costs of supporting obesity surgery in their employees.

One big concern of course is how employers can address this issue without seeming intrusive or discriminatory. It is recommended that companies should involve employees in planning health initiatives, rather than working from the top-down, and should make sure personal privacy is protected.

While this report focuses on the US, and for obvious reasons cannot directly be transferred to the Canadian situation with its more or less universal health coverage, it is unlikely that obesity, at least with regard to absenteeism and early disability, is any less expensive to Canadian employers.

While preventive "wellness initiatives" may work for the 3/4 of the workforce, which does not yet have obesity, how do you provide effective obesity treatments to the employees who already have the problem?

Allow me to offer a few pointers:

1) Inform employees about evidence-based treatment options for this condition.

2) Encourage employees to seek treatments for obesity like they would seek treatments for any other chronic disease (e.g. diabetes, hypertension, etc.).

3) Supplement costs for evidence-based obesity treatments (including behavioural interventions, special diets, medications and surgery) as prescribed by qualified health professionals.

As I have blogged before - we may not have a cure for obesity - but we sure have treatments that work!

Edmonton, Alberta

Thursday, April 10, 2008

Recognising Barriers Key to Obesity Management?

Most people fail to keep off any weight they lose.

This may in part be attributable to the substantial barriers that undermine long-term obesity management strategies.

In a paper I wrote with my colleagues Marina Mauro, Valerie Taylor and Sean Whartan just out in the European Journal of Internal Medicine, we highlight the importance of recognizing and addressing these barriers before embarking on obesity treatments.

Common barriers include lack of recognition of obesity as a chronic condition, low socioeconomic status, time constraints, intimate saboteurs, and a wide range of comorbidities including mental health, sleep, chronic pain, musculoskeletal, cardiovascular, respiratory, digestive and endocrine disorders.

Furthermore, medications used to treat some of these disorders may further undermine weight-loss efforts and promote weight regain.

Unfortunately, lack of specific obesity training of health professionals, attitudes and beliefs as well as coverage and availability of obesity treatments can likewise pose important barriers.

Health professionals need to take care to identify, acknowledge and, if possible, address these barriers in order to increase patient success as well as compliance and adherence with treatments.

Failure to do so may further promote the sense of failure, low self esteem and low self efficacy already common among individuals struggling with excess weight.

I have little doubt that addressing treatment barriers can save resources and increase the prospect of long-term success.

Identifying and discussing barriers with patients has to be a routine part of obesity care.

Edmonton, Alberta

Wednesday, April 9, 2008

Preventing Weight Gain is the First Step in Obesity Management

Overweight is the result of normal-weight people gaining weight.

Obesity is the result of overweight people gaining more weight.

Severe obesity is the result of people with obesity gaining even more weight.

The first step, common to both obesity prevention and treatment, is to stop further weight gain.

In fact, simply preventing weight gain at any weight may be preferable to losing weight just to gain it back. The more often you lose weight and gain it back, perhaps, the worse the consequences.

At least that is the message of a recent paper by Anne Claire Vergnaud and colleagues from the Centre de Recherche en Nutrition Humaine Ile-de-France, Bobigny, France, who studied the relationship between weight fluctuations and the risk for metabolic syndrome (International Journal of Obesity).

Metabolic syndrome status was assessed at baseline (1994/1995) and at the end of follow-up (2001/2002) in 3553 middle-aged subjects. Weight fluctuations were estimated with four weight measures during follow-up. Risk for developing metabolic syndrome was highest in the tertile with the greatest weight fluctuations, independent of whether these subjects gained weight overall or not. Of course, subjects who only gained weight (with no recorded losses) also had a higher risk than individuals whose weight did not change at all.

As in several previous studies on this issue (cited in the paper), it appears that losing and regaining weight (weight fluctuation) is worse than not losing weight at all.

Obviously, these findings have important implications for both public health messaging and clinical management. Although in both cases we propagate and promote "weight-loss" messages, the reality is that very few people who lose weight keep it off. This is true both for self-directed attempts as well as commercial weight-loss programs.

Sadly, even with clinical treatments (including obesity surgery), a substantial proportion of patients fail to keep the weight off, but indeed, success is greater the more intense the treatment and follow-up.

Given this poor success of weight-loss attempts, I cannot but wonder whether recommending weight loss to anyone who is overweight or obese is as beneficial as it is made out to be. This would be particularly true for people with what I prefer to call Stage 0 obesity.

Perhaps, with the exception of treatments with well-documented long-term outcomes, most people are best served with preventing further weight gain (difficult enough) rather than losing weight only to gain it back.

Clearly, the onus is on weight management programs, whether behavioural, medical or surgical, to document their long-term success in weight-loss maintenance.

Programs associated with a high rate of relapse probably do more harm than good.

Individuals with a high chance of relapse should not be subjected to weight-loss attempts without ongoing medical care and close follow-up.

While we await further research on this subject, we perhaps need to be a bit less casual about simply advising everyone with a "higher-than-normal" BMI to lose weight.

Edmonton, Alberta

Tuesday, April 8, 2008

Weighing in on In-Car Traffic Injuries

Given the increase in average body size (and weight), it is not surprising that the automotive safety community is questioning the impact of obesity on the performance and assessment of occupant protection systems.

This issue was recently addressed by David Viano and colleagues, who work at ProBiomechanics LLC, a Michigan firm specializing in occupant kinematics and injury causation, published last month in Traffic Injury Prevention.

The authors investigated the relationship between fatality and serious injury risks for front-seat occupants by body mass index (BMI) using a matched-pair analysis. They also developed a simple model for the change in injury risk with obesity which includes the normal mass (m) and stiffness (k) of the body resisting compression during a blunt impact. For a given impact severity, the risk of injury was assumed proportional to compression. Energy balance was used to determine injury risks with increasing mass.

Data for 1993-1004 was analyzed from the National Automotive Sampling System Crashworthiness Data Set (NASS-CDS), an ongoing study of more than 5,000 accidents each year, in which trained investigators look at wrecked vehicles, read through police reports, and talk to accident victims. Occupant injury was divided into normal and obese categories. A matched-pair analysis was carried out. Driver and front-right passenger fatalities or serious injuries (MAIS 3+) were analyzed in the same crash to determine the effect of obesity.

Based on the model, an obese occupant (BMI = 30-35 kg/m2) has 54-61% higher risk of injury than a normal BMI occupant (22 kg/m2). Matched pairs showed that obese drivers have a 97% higher risk of fatality and 17% higher risk of serious injury than normal BMI drivers. Obese passengers have a 32% higher fatality risk and a 40% higher risk than normal passengers. Obese female drivers have a 119% higher risk than normal BMI female drivers and young obese drivers have a 20% higher serious injury risk than young normal drivers.

These data add to several prior publications highlighting the increased risk for overweight and obese drivers and passengers in automobiles.

Viano and colleagues also estimated how much extra ballast the family of Hybrid III crash test dummies would need to represent an obese or morbidly obese occupant. According to these assessments, the smallest crash test dummies need proportionately more ballast to represent an obese or morbidly obese occupant in the evaluation of safety systems. The 5% female Hybrid III (BMI = 20.4) and needs 22 kg of ballast to represent an obese and 44.8 kg to represent a morbidly obese female, while the 95% male needs only 1.7 and 36.5 kg, respectively.

The authors conclude that

"Obesity influences the risk of serious and fatal injury in motor vehicle crashes. The effect is greatest on obese female drivers and young drivers. Since some of the risk difference is related to lower seatbelt wearing rates, the comfort and use of seatbelt extenders should be examined to improve wearing rates by obese occupants. Also, crash testing with ballasted dummies to represent obese and morbidly obese occupants may lead to refined safety systems for this growing segment of the population."
As also noted recently by Ben Zarzaur and Stephen Marshall, Surgeons at the University of Tennessee Health Science Center, Memphis, in The Journal of Trauma, the combination of obesity and not using a seat belt is particularly deadly.

Most importantly, David Schlundt and colleagues from Vanderbilt University just reported in OBESITY based on data from the 2002 Behavioral Risk Factor Surveillance System Survey, that seatbelt use declines as BMI increases, with approximately 55 percent of extremely obese individuals say that they do not use a seatbelt.

Consequence of these finding for counseling our obese patients: buy cars where seatbelts fit your size or buy seatbelt extenders AND USE THEM!

Sounds like a class-action waiting to happen!

Edmonton, Alberta

Monday, April 7, 2008

Supersizing Pregnancy Care: the Dawn of Bariatric Obstetrics?

Last week's issue of the New England Journal of Medicine features an article by Susan Chu and colleagues from the US Centers for Disease Control and Prevention (Atlanta, GA) on the impact of obesity on health care during pregnancy.

Dr. Chu and colleagues examined 13,442 pregnancies (2000-2004) according to pre-pregnancy BMI. After appropriate corrections for confounders, hospital stay for delivery was significantly greater by approximately a full day among women with obesity than in normal weight women. Most of the increase in length of stay associated with higher BMI was related to increased rates of cesarean delivery and obesity-related high-risk conditions.

A higher-than-normal BMI was also associated with significantly more prenatal fetal tests, obstetrical ultrasonographic examinations, dispensed medications, telephone calls to obstetrics, and prenatal visits with physicians. Thus clearly, obesity during pregnancy is associated with increased use of health care services.

Obesity in pregnancy is not a topic that is discussed much in the media. I first became aware of the magnitude of this problem, when I was approached by the obstetrics folks from the McMaster University Hospital (Hamilton, Ontario) who found themselves looking after an increasing number of severely obese expecting mothers. This contact led to the initiation of a working group on bariatric nursing that devised protocols for looking after large and very large mothers.

I further realised the importance of this issue when I heard about the apparently close link between maternal obesity and the risk for both the mother and infant and the fact that obesity during pregnancy may set up the infant for future obesity through epigenetic programming. As I have blogged before, limiting weight gain during pregnancy in overweight and obese mothers may be a first step towards preventing childhood obesity.

Given that there are around 13,000 babies born in the Capital Health Region every year, about 10% of these to mothers with pre-pregnancy BMI>30, the finding of Dr. Chu et al., if translated to our region, could mean as many as 1,500 or so extra days in hospital for new mothers, much of this due to obesity-related risk. Obviously more screening tests, more frequent prenatal visits and more medications would add to the costs.

Clearly, the issue of increasing weights and weight gain in women of child-bearing age is a public health issue whose consequences and impact have yet to be fully appreciated.

As these issues affect both mothers and infants, it would not be a bad place to focus prevention measures for best impact.

Edmonton, Alberta

Friday, April 4, 2008

Carrying the TORCH for Obesity

Yesterday, I presented a seminar on the challenges of obesity management to the trainees of the TORCH (TomorrOw's Research Cardiovascular Health professionals) program.

TORCH is an integrated program at the Universities of Alberta and Calgary with the mission to prepare Canada's next generation of transdisciplinary cardiovascular health research leaders. TORCH trainees come from diverse areas ranging from basic sciences to medicine and surgery.

The TORCH Program was born from an initiative by the Canadian Institutes of Health Research (CIHR) to encourage transdisciplinary, integrative health research and to build capacity of the Canadian health research community through the development of researchers and the provision of sustained support for scientific careers in health research.

While it was evident from some of the questions that prior knowledge on obesity varied considerably amongst the participants, this was easily made up for by their interest and enthusiasm for the topic.

Clearly, the next generation of cardiovascular health researchers will benefit from greater insights into the psychosocial and biomedical causes and consequences of obesity.

I am grateful to Gary Lopaschuk (Program Director) and his colleagues for the opportunity to speak to these leaders of tomorrow.

Edmonton, Alberta

Thursday, April 3, 2008

Rimonabant for CAD - it's Not Just About the Heart

The heart is an important organ. Heart disease kills millions every year. Abdominal obesity is an important risk factor for heart disease. Medical treatments for obesity should help reduce cardiovascular risk.

Not surprisingly, several large studies are examining the effect of anti-obesity drugs, both old (e.g. sibutramine) and new (e.g. rimonabant), on cardiovascular morbidity and mortality.

This week, one such study reported on its results. STRADIVARIUS, a double-blind randomized controlled trial with over 800 patients conducted at 112 centres in North America, Europe and Australia was designed to determine whether treatment with 20 mg of the CB-1 antagonist rimonabant (an anti-obesity drug now available in many countries but not in Canada or the US) would reduce progression of coronary artery disease (CAD) in patients with abdominal obesity and the metabolic syndrome. Progression of CAD was measured by intravascular ultrasound (IVUS) before and after 12 to 18 months of treatment.

On average, patients on rimonabant lost 4.5 Kg and as many cms off their waistlines. HDL cholesterol, triglycerides and HbA1c levels (in patients with diabetes) improved as expected. Although the primary endpoint (change in percent atheroma volume) was not different between rimonabant and placebo, other measures of atherosclerosis appeared to change favourably. Rimonabant was well tolerated although (as expected) there were more psychiatric and gastrointestinal side effects and discontinuations in the rimonabant group.

So why, with the significant reduction in weight and risk factors were the results not more positive? The authors speculate that this may have been because patients were already receiving effective treatment for CAD (e.g. 80% of patients were on statins). Therefore showing incremental benefits of adding rimonabant would have been difficult.

The real question to ask, however, is whether or not influencing heart disease is indeed the best and most important use of an anti-obesity drug. We already have a multitude of effective medications to reduce the progression of heart disease. When used according to current guidelines, these agents can indeed markedly reduce the risk of cardiovascular disease (obviously, this risk will never be zero, no matter how good the treatment).

So is reduction in heart disease really the great "unmet need" when it comes to obesity treatment? As a bariatrician, I would say NO!

Yes, while preventing heart disease (or its progression) is perhaps one benefit of treating obesity, I can think of many other benefits that are relevant to patients battling obesity-related comorbidities for which we currently have no effective medical treatments.

My short list would include sleep apnea, osteoarthritis, hepatic steatosis, polycystic ovary syndrome, infertility, pseudo tumor cerebri and many more. Sure, these conditions may not sound as dramatic as heart disease and may be less likely to kill you, but for the people who have these problems, these conditions are very real, distressing and affecting their quality of life. If obesity treatments can help alleviate these conditions, perhaps even just limit exacerbation by helping curb further weight gain, a lot would be won.

Remember, obesity is a chronic disease with virtually 100% rezidivism. It significantly affects many aspects of mental, physical and socioeconomic health. Effective treatments for obesity are required irrespective of whether or not they also help reduce heart disease.

Unfortunately, pharma companies, regulators and payors appear obsessed with the cardiometabolic consequences of obesity and fail to see the urgent need for treating obesity-related comorbidities beyond heart disease.

So, while the results of STRADIVARIUS are nice, I'd be far more interested in whether or not rimonabant reduces obesity-related comorbidities for which we have no alternative treatments - at least that's where I'd put my research money if I had any say in the matter.

Edmonton, Alberta

Wednesday, April 2, 2008

The Real Cost of Obesity May Not be in Health Care

When you follow the current public discussion on the consequences of obesity, the focus is most often on the potential costs for health care. This is not surprising, given that obesity is directly linked to a wide range of chronic diseases including hypertension, type 2 diabetes, sleep apnea, osteoarthritis and many forms of cancer.

But health risk are not the only cost of obesity. Even a cursory glance at the patients presenting in our clinic immediately makes it evident that a disproportionate number are on short or long-term disability, not working to their full potential or simply unemployed. If you take into consideration that the average age of patients in our clinic is in the lower 40s, it immediately becomes evident that there are economic losses to society here that go well beyond the simple costs of health care.

Numerous studies have in fact documented that obesity may have important economic consequences for individuals - and thus society.

This was once again demonstrated in the largest study on this issue to date. Nina Karnehed and colleagues from the Karolinska Institute in Stockholm examined social mobility in over 750,000 men born between 1951 and 1965. Subjects were studied at age 10 and again at age 30.

Men who were obese at age 18 were almost 30% less likely to be upwardly mobile (achieve a higher socioeconomic status than their fathers) and 30% more likely to be downwardly mobile (achieve a lower socioeconomic status than their fathers) compared to normal weight men. This finding was independent of childhood socioeconomic index (SEI), IQ or education, suggesting that societal factors (e.g. bias and discrimination) may be responsible.

This difference is substantial. Downward social mobility means less income and lower SEI with all its consequences. These costs to society may be far greater than any costs to health care.

I am no economist, but I don't find it difficult to imagine that when a substantial proportion of the population (currently 25% of all adults) are at risk of not realizing their full economic potential this could mean a huge loss for the overall economy.

Thus, apparently obesity not only affects mental or physical health but also socioeconomic health - an important consequence of the obesity epidemic that I have not heard much about in the media or elsewhere.

Perhaps the increased health care costs of obesity are the least of our worries.

Edmonton, Alberta

Tuesday, April 1, 2008

Does Obesity Surgery Convert "Bingers" to "Grazers"?

Classical Binge Eating Disorder (as defined by DSM-IV) is found in around 20-40% of severely obese patients presenting at bariatric centres (including ours). Numerous studies have shown that patients with BED can achieve significant weight loss, resolution of comorbidities and improvement in quality of life with obesity surgery and therefore should not generally be denied surgery.

Nevertheless, many centres (including ours) are reluctant to operate on patients with active BED fearing poorer outcomes and greater distress. It turns out that we really don't know much about how bariatric surgery affects eating patterns in patients with BED.

This question was now addressed by Susan Colles and colleagues from Monash University in Melbourne in a study published in the March issue of OBESITY. Colles and colleagues planned to study eating behaviours in 180 patients before and 12 months following laparoscopic adjustable gastric banding (LABG). Of these, 6 did not receive surgery, 1 died of a myocardial infarct and 44 (25% of eligible subjects) did not return for the 12-month survey (more on this later).

While only 14% of patients had BED at baseline, 31% were described as "uncontrolled eaters", 40% had night eating syndrome (NES) and 26% were "grazers".

Although all groups, including the "bingers" lost similar amounts of weight and BED reduced to 3% in this group, patients with preoperative BED were most likely to develop uncontrolled eating or grazing. Patients who reported uncontrolled eating or grazing after surgery tended to lose less weight and reported greater psychological distress.

Interestingly, the authors report that the 12-month non-responders were more likely to have had presurgical BED, have lost less weight and attended less clinic appointments. This may be due to patients with these behaviours feeling more ashamed about their "loss of control" and therefore avoiding follow-up visits.

This study highlights the risk of preoperative "bingers" to become "uncontrolled eaters" or "grazers" resulting in psychological distress and poorer weight outcomes. As these patients are more likely to drop out of follow-up they may also be at increased long-term risk of nutritional deficiencies and other long-term complications of bariatric surgery.

In an accompanying paper in the same issue of OBESITY, Colles and colleagues describe how "loss of control" may be at the root of the significant psychological distress of patients with BED resulting in their greater likelihood of seeking out bariatric surgery as a means to control their eating behaviour. This may well in part explain the high prevalence of BED in patients presenting in bariatric clinics.

Clearly, we need to learn more about how to pre-screen patients for potentially poor outcomes and how best to monitor post-surgical patients for the development of aberrant eating behaviours.

Given that BED, once diagnosed, is actually quite responsive to psychological treatments resulting in a remarkably high rate of resolution, I wonder about the rational for operating on patients with active BED - after all weight loss should not be the only parameter by which results of obesity surgery are measured.

Edmonton, Alberta