Dr. Sharma's Obesity Notes

Few events are likely to command your attention as urgently as a sudden interruption of blood flow to your heart muscle.

Fortunately, thanks to the miracle of modern cardiac revascularization, you may well find yourself amongst the many, who today survive this “heart-wrenching” event – a situation which often precipitates remarkably intense longings for lifestyle change.

Indeed, at no time (other than January 1), would you meet anyone more determined to swear off their cigarettes, convert to the solemn teachings of Canada’s Food Guide and embrace the rejuvenating powers of exercise – an only fitting response to celebrate this new lease on life.

This is why many modern health systems dedicate a significant amount of personnel and resources to the exploitation of this life-changing moment with the laudable goal of “re-habilitating” the fortunate survivor to a life of healthier habits.

But, you may ask, is even such a dramatic event enough to prompt lasting betterment in the victims? And, will those, who have brought this upon themselves through their supposedly unholy practice of gluttony and sloth, really manage to turn things around?

This burning question has now been thoroughly examined by Billie-Jean Martin (a former Obesity Network Bootcamper) and colleagues from the University of Calgary, in a paper published in OBESITY.

Happily enough, almost 4,000 participants, studied one year after their participation in a 12-week rehabilitation program (which invoked the dedicated services of exercise physiologists, nurses, registered dieticians, social workers and clinical psychologists), did indeed experience a small but measurable improvement in aerobic fitness – a parameter known to forecast survival.

Sadly, however, not everyone benefitted equally. Despite enthusiastic participation in the program, obese patients (who also happened to start off on a poorer footing in terms of exercise capacity) showed a lesser sustained improvement in peak estimated metabolic equivalents (a sciency measure of aerobic fitness) than their less corpulent counterparts.

Prejudiced readers should, however, not jump to the conclusion that the obese participants were perhaps less enthusiastic or committed to this enterprise.

Indeed, during the 12 week intervention, the obese group increased their weekly mins at the prescribed exercise heart rate by 40 mins (from 123 to 163), whereas their leaner peers merely managed to add a measly 10 mins to their routine (from 153 to 164). Clearly, the obese participants were not shying away from the extra effort – if anything, they were working substantially harder (relatively speaking) than their leaner colleagues.

Notably, at one year, BOTH groups had regressed in their enthusiasm to slightly BELOW their baseline weekly mins of exercise heart rates; the obese group fell back to 121 mins, while the normal weight group fell back to 150 mins.

Thus, to be fair, NEITHER group managed to sustain the recommended 160+ mins of weekly exercise heart rate at 12 months.

It would seem that neither the “life-changing” occurrence of clogged coronaries nor 12 weeks of the dedicated services of an inter-disciplinary team of healthcare professionals, appears to be all that life-changing after all.

Would a 16 week program, a 24 week program, or perhaps even a 52 week program have lead to better results?

My gut tells me that any “time-limited” behavioural-change program will always produce “time-limited” behavioural change.

Apparently, the situation for cardiac rehab appears no better than the story for weight loss – when “treatment” stops, the lifestyle/weight comes back.

Incidentally, the Albertan actors in this story are no better or worse than the rest of Canada.

According to a recent report from Statistics Canada, three in four smokers with respiratory disease do not quit smoking; most people with diabetes or heart disease will not become more physically active and virtually no one diagnosed with cancer, heart disease, diabetes or stroke will increase their intake of fruit and vegetables.

Nonetheless, I am told, cardiac rehab efforts have demonstrated benefits in a host of modifiable cardiovascular risk factors, at least during and perhaps for a few months following the intervention.

However, the durability of these efforts certainly leave substantial room for improvement across the full spectrum of body shapes and sizes.

AMS
Edmonton, AB

Martin BJ, Aggarwal SG, Stone JA, Hauer T, Austford LD, Knudtson M, & Arena R (2012). Obesity negatively impacts aerobic capacity improvements both acutely and 1-year following cardiac rehabilitation. Obesity (Silver Spring, Md.), 20 (12), 2377-83 PMID: 22627915

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Regular readers will note my past interest in hypertension, especially with regard to managing this condition in people with excess weight.

A paper by Michael Weber and Colleagues, now presents an analysis of the relationship between body size and hypertension treatments on cardiovascular event rates, in a paper published in The Lancet.

The paper consists of a prespecified analysis of the ACCOMPLISH (Avoiding Cardiovascular Events through Combination Therapy in Patients Living with Systolic Hypertension) trial, that compared the effect of single-pill combinations of either benazepril and hydrochlorothiazide or benazepril and amlodipine on hard cardiovascular outcomes.

Based on BMI, the full ACCOMPLISH cohort was stratified into obese (n=5709), overweight (n=4157), or normal weight (n=1616) categories.

In patients allocated benazepril and hydrochlorothiazide, the primary endpoint (per 1000 patient-years) was 30·7 in normal weight, 21·9 in overweight, and 18·2 in obese patients.

In contrast, there were no differences in outcomes between the BMI groups in those allocated benazepril and amlodipine(18·2, 16·9, and 16·5, respectively).

From these findings the authors conclude that.

“..thiazide-based treatment may give less cardiovascular protection in normal weight than obese patients, but amlodipine-based therapy is equally effective across BMI subgroups and thus offers superior cardiovascular protection in non-obese hypertension.”

Given the known differences in physiology, where obesity related hypertension is largely mediated by volume expansion and sodium retention, these findings may not be all that surprising.

Clearly, including a diuretic in the treatment regimen for obesity related hypertension makes a lot of sense – now we have the outcome data suggesting that such a regimen also reduces hard outcomes.

AMS
Calgary, Alberta

Hat tip to Scott Kahan for alerting me to this study.

Last week, the US National Institutes of Health (NIH) announced the discontinuation of the intensive diet and lifestyle interventions in the Look AHEAD (Action for Health in Diabetes) study.

This study, now in its eleventh year, was designed to compare the effects of an intensive diet and lifestyle program designed to promote and sustain weight loss versus ‘usual care’ on the prevention of heart attacks, strokes and cardiovascular deaths in individuals with long-standing type 2 diabetes.

The study was conducted at 16 centers across the United States included 5,145 people who were 45 to 76 years old when they enrolled in the study. Sixty percent of participants were women.

Participants in the intervention group lost more than 8% of their initial body weight after one year of intervention and maintained an average weight loss of nearly 5 percent at four years.

This reduction in body weight was accompanied by significant improvements in glycemic control and numerous other health benefits (e.g. decreased sleep apnea, improved mobility and quality of life).

However, given a remarkably low incidence of ‘hard’ endpoints in both the interventions and control groups, it became evident the the study would stand little chance of demonstrating superiority of the lifestyle intervention in terms of preventing cardiovascular complications.

These results are perhaps not all that surprising, given that recent pharmacological studies in patients with type 2 diabetes have also failed to show a significant reduction in cardiovascular deaths.

Moreover, readers may be aware that even with the substantially greater reduction in body weigh with bariatric surgery, the Swedish Obesity Surgery study, took over 13 years to demonstrate a barely significant reduction in myocardial infarcts (but not deaths!) in patients with type 2 diabetes.

In hindsight, hoping for a greater impact with diet and exercise than even that seen with bariatric surgery would seem rather optimistic (to be fair, the surgical data were not available at the time this study was planned).

Nevertheless, according to the recommendations of the Data Monitoring Board, the study should be continued (without the intervention) to determine the long-term outcomes in the participants.

While the results of this study are certainly disappointing to the researchers involved, they do provide important lessons for designing future trials of obesity treatments in patients with type 2 diabetes.

Not only may future studies have to enrol a substantially greater number of participants but such studies may also need to substantially enrich the study population with higher risk individuals to increase event rates (i.e. EOSS Stage 3 rather than just EOSS Stage 2 patients).

Obviously, the wild card here is whether or not ANY amount of weight loss will suffice to reduce mortality in a population that already has well-established heart disease (remember the obesity paradox).

Thus, whether or not weight loss (through lifestyle interventions or otherwise) will save lives in individuals with established type 2 diabetes may well, in the end, be a question, to which we will never quite know the answer.

AMS
Chicago, IL

photo credit: Môsieur J. [version 7.1.2] via photopin cc

In 2005, while still at McMaster University, I had the privilege of being involved in a publication that is now, by any standard, already a ‘classic’ in the field of obesity.

The paper, published in Lancet, compares BMI (as a measure of obesity) to wasit-to-hip ration (as a measure of fat distribution) as a predictor of myocardial infarction in 27,000 participants from 52 countries.

In this standardised case-control study (INTERHEART), with 12,461 cases and 14,637 controls, we found that although BMI showed a modest and graded association with myocardial infarction (OR 1.44), this relationship was was substantially reduced after adjustment for waist-to-hip ratio (1.12), and non-significant after adjustment for other risk factors (0.98).

In contrast, we found that for waist-to-hip ratio, the odds ratios for every successive quintile were significantly greater than that of the previous one (2nd quintile: 1.15; 3rd quintile: 1.39; 4th quintile: 1.90; and 5th quintiles: 2.52 [adjusted for age, sex, region, and smoking]).

In fact, both waist (adjusted OR 1.77) and hip (0.73) circumferences were highly significant after adjustment for BMI.

Finally, the population-attributable risks of myocardial infarction for increased waist-to-hip ratio in the top two quintiles was 24.3% compared with only 7.7% for the top two quintiles of BMI.

For anyone still believing that BMI is even a weak indicator of cardiovascular risk, this study should have long dispelled any such notions – increased BMI (alone) is simply not a good measure of cardiovascular risk – period!

Despite this, BMI continues to appear in guidelines, continues to be used as indications for treatments (e.g. bariatric surgery), and continues to be the basis for predictions on the health impact of the obesity epidemic.

Some people just take longer to learn than others.

Not surprisingly, this paper has so far been cited well over 1300 times.

AMS
Edmonton, Alberta

Dr. Gianluca Iacobellis

In this paper we reviewed the growing evidence that epicardial fat is a metabolically active organ that generates various bioactive molecules, which could well affect cardiac function.

We speculated that, although relatively small, this ‘visceral’ fat depot is a rich source of free fatty acids and a number of bioactive molecules, such as adiponectin, resistin and inflammatory cytokines, which could affect the coronary artery response.

We also noted that epicardial fat mass might reflect intra-abdominal visceral fat and proposed that echocardiographic assessment of this tissue could serve as a reliable marker of visceral adiposity.

Furthermore, epicardial adipose tissue is clinically related to left ventricular mass and other features of the metabolic syndrome, such as concentrations of LDL cholesterol, fasting insulin and adiponectin, and arterial blood pressure.

Thus, we suggested that echocardiographic assessment of epicardial fat could serve as a simple and practical tool for cardiovascular risk stratification in clinical practice and research.

While assessment of epicardial fat is not yet part of routine clinical assessment, since we published this paper, interest in this tissue has grown substantially and new research on the function of this tissue are now a recurring topic of interest at cardiovascular conferences around the world.

AMS
Edmonton, Alberta