Arya M. Sharma, MD

Reader may recall that the H1N1 flu outbreak in 2009 was particularly deadly to obese individuals.

This increased severity and fatality of H1N1 infections in obese patients became apparent early during the spring outbreak of the epidemic and prompted the Public Health Agency of Canada to recommend that individuals with severe obesity should be included amongst those to be given first access to the H1N1 influenza vaccine.

A paper by Chris Kaposy from Memorial University of Newfoundland, published in VACCINE, suggests that this PHAC recommendation was largely ignored by the provinces, who bear the responsibility for health care delivery in Canada.

In fact, only one province (Manitoba) followed the PHAC recommendations and considered all people under 65 with severe obesity eligible for H1N1 influenza vaccination on October 26 2009 – early in the vaccination campaign.

Alberta, Nova Scotia, and Saskatchewan, did list individuals with severe obesity, but placed narrow age restrictions on those who were given early access.

New Brunswick and Ontario listed severe obesity as a sequencing category late in the vaccination campaign (as late as November 2009).

In British Columbia, Newfoundland and Labrador, Prince Edward Island, and Quebec, obesity (or ’severe’ obesity) was never specifically listed as a chronic health condition that qualified one for early access to the H1N1 influenza vaccine. In fact, it appears that ‘obesity’ was specifically removed from the list of eligible chronic conditions that warranted early access.

The author provides at least two pieces of evidence that weight bias may have played a role in the provinces’ decisions:

“First of all, consider that in every single province the H1N1 influenza vaccine was available to pregnant women over 20 weeks gestation very early in the mass vaccination campaign. In most provinces, the vaccine was available to this group from late October 2009 onward. Clearly there was a pan-Canadian commitment during the H1N1 influenza pandemic to offer early vaccine access to pregnant women – who were also listed in the PHAC categories as a vulnerable group. Every Canadian province could have similarly chosen to vaccinate people with severe obesity early in the campaign, but they did not.”

Secondly, the delay in access cannot be explained by scarcity of vaccine - in fact, in each of the four provinces (British Columbia, Newfoundland and Labrador, Prince Edward Island, and Quebec) that never listed people with severe obesity as eligible for early vaccination, school children were vaccinated early – prior to the availability of the vaccine to the general public despite the fact that the PHAC guidelines did not list school children as a vulnerable group and computer modelling did not support the priority use of vaccination in school children ahead of high-risk individuals.

Thus, this commentary argues, Canadian provinces demonstrated an ambiguous commitment to the early vaccination of people who were severely obese, despite clear and strong early evidence that individuals with severe obesity presented an especially vulnerable group and despite clear and timely recommendations by the federal public health agency to consider severely obese individuals for priority access.

Given that H1N1 influenza ultimately did result in significant number of fatalities (especially amongst people with severe obesity), I wonder if public outrage would have been greater had any other group of ‘vulnerable’ individuals been as overtly ‘overlooked’.

AMS
Edmonton, Alberta

Kaposy C (2011). The influence of the stigma of obesity on H1N1 influenza vaccine sequencing in Canada in 2009. Vaccine PMID: 22041304

A recent report commissioned by Alberta Health Services estimates that in 2005, the total direct and indirect costs of illnesses attributable to obesity in Alberta were $1.27 billion.

This represents 28.0% of the total direct and indirect costs attributable to obesity for 22 specific health conditions and 5.6% of the total direct and indirect costs for all health conditions in Alberta.

Coronary heart disease ($307.1 million) had the highest direct and indirect costs attributable to overweight and obese BMI status; osteoarthritis ($167.7 million), type 2 diabetes ($161.5 million), hypertension ($125.5 million), and the 14 cancer sites ($117.5 million) had the highest obesity-attributable costs after coronary heart disease. Among the 14 cancer sites, colorectal cancer ($31.6 million), postmenopausal breast cancer ($14.5 million), and leukemia ($11.0 million) had the highest costs attributable to overweight and obesity in Alberta.

While the direct health care cost attributable to overweight and obesity was $630.1 million, or 49.5% of the total cost of overweight and obesity, the indirect cost was $643.8 million including $63.1 million in short-term disability costs, $209.6 million in long-term disability costs, and $371.1 million in premature mortality costs.

As the report notes, these costs are conservative as the analysis did not include the costs for:

• Private out-of-pocket costs such as those paid for private caregivers, illness-related aids, and home modifications not reimbursed by governmental agencies;
• Costs associated with reduced production during work hours (presenteeism) as a result of a health problem;
• The value of time lost from work
• The value of lost leisure time of family members or friends who care for the patient;
• Intangible costs that involve pain and suffering borne by patients and their families.

The report also did not assess the cost of obesity in youth under age 15 or in the Aboriginal population living on reserves.

Although the report did not analyses how much of these costs could be reduced or avoided by providing effective obesity treatments, it is very likely (based on other estimates) that the savings could be substantial.

As I have said before, no health care system can afford not to tackle obesity.

AMS
Edmonton, Alberta

The Summary of The Cost of Obesity in Alberta Report is available here

Yesterday, as widely reported in national media, Statistics Canada and the US National Center for Health Statistics released a study that directly compares the prevalence of obesity among adults in Canada to the number in the US.

The good news is that the prevalence of obesity among adults in Canada is lower than it is in the US (24.1% of adults in Canada vs. 34.4% in the US).

The bad news is that during the past two decades, in both Canada and the US, the rates of adult obesity have been increasing at roughly the same rates (about 10% points overall) with small, but perhaps interesting, variations across age groups - in men the greatest increase was among those aged 60 to 74; among women, the increase was highest among those aged 20 to 39.

The latter figure is particularly alarming because, with all of the accumulating data on epigenetic programming, where maternal obesity is literally transferred to her offspring via actual modification of their genetic code, we are in for an ever burgeoning epidemic of childhood obesity - one that is unlikely to be stopped by taxing pop or reintroducing 20 mins of daily phys-ed into school curricula.

As blogged before, we should now be seriously talking about actually providing obesity treatments to those already struggling with excess weight - perhaps starting with providing treatments for young moms and dads and those with severe obesity, who need it most.

Once obesity is established, simply preventing further weight gain can be seen as success. Without treatment, the currently over 6,000,000 obese Canadians will simply continue gaining weight, with all of its economic and health consequences.

Note that the solution for many may not be weight loss -after all, if simply losing weight were the solution, then this problem would not exist - I have yet to meet an overweight or obese person, who has never lost weight.

What Canadians need is access to weight management in the same manner as they would seek and receive management for their diabetes, their hypertension, their asthma, their depression, or any other chronic condition that affects their health.

Currently such weight management resources in our healthcare systems are beginning to emerge but remain rare and hard to find amongst the deafening cacophony of the commercial weight-loss industry.

This is exactly where the Canadian Obesity Awareness and Control initiative for Health (COACH) comes in - providing Canadians struggling with excess weight with reliable and un-biased information on obesity management and pointing them to credible weight management resources in their healthcare systems and communities.

The time for COACH is now - not once we have caught up with our friends south of the border. If anything, this report should remind us that without immediate action, Canada may well soon be where the US is today.

If you have not already done so - please show your support for COACH and help spread the message by clicking here.

AMS
Edmonton, Alberta

Simple but Completely Wrong Depiction of Energy Balance

According to the laws of physics when [calories in] exceed [calories out] people gain weight.

Unfortunately, when you actually deal with people (read: biological systems), this simple law is anything but simple. This is because, thanks to complex biological feedback mechanisms, designed by nature to keep us alive and thriving, changing caloric intake in turn affects caloric expenditure and vice-versa.

Let me illustrate this important difference between physics and biology with a few analogies:

Consistently putting less fuel in your car will never make your car “learn” to run the same distance on less fuel, but our bodies actually quite readily and effectively adapt to eating less food by simply burning fewer calories (ultimately resulting in the most frustrating “weight-loss plateau”).

Regularly overfilling your gas tank will never make your car “learn” to burn more fuel, whereas eating too much actually does increase energy expenditure (we sweat, we get restless, we fidget).

Over or underfueling your car will never eventually lead to a bigger or smaller car, whereas this is exactly what happens to us, a fact that leads to a further complication: larger bodies (like bigger cars) need more fuel.

When you now consider that all of these biological reponses to changes in [calories in] and [calories out] vary considerably between individuals (due to genetics, age, sex, hormones, medications, etc.), you end up with a situation where trying to precisely predict weight changes by simply calculating [calories in] and [calories out] becomes more or less like forecasting next week’s weather - sometimes surprisingly accurate but, perhaps as often, completely off the mark.

This is probably why population studies have such a hard time figuring out why exactly we are all getting bigger.

As recently blogged, the recent Canadian Health Measurements Survey certainly does not convince me that overweight and obese people are any less physically active than non-obese Canadians - ALL Canadians seem to be inactive, period!

Now it turns out that overweight and obese people may actually not be simply “overeating” either.

At least not according to a study just published in the American Journal of Nutrition that reports on changes in energy intake in normal-weight, overweight, and obese individuals between 1971-2006.

In this study, Gregory Austin and colleagues from the University of Colorado Denver, compared carbohydrate, fat, protein, and total energy intake in adults aged 20-74 y from the first NHANES (NHANES I, 1971-1975; n = 13,106) to data from NHANES 2005-2006 (n = 4381).

While the prevalence of obesity increased from 11.9% to 33.4% in men and from 16.6% to 36.5% in women, there were rather modest changes in percentage of energy from carbohydrates (44.0% vs. 48.7%), fat (36.6% vs. 33.7%), or protein (16.5% vs. 15.7%). Importantly, these trends were identical across normal-weight, overweight, and obese groups, therefore it is hard to really blame the massive change in obesity rates simply on these rather modest changes in relative macronutrient intake.

But now comes the surprise: compared with NHANES I, normal-weight men consumed an additional 247 kcal per day, overweight men consumed an additional 165 kcal, and obese men consumed an additional 225 kcal in NHANES 2005–2006. In other words, ALL men were eating more - the normal-weight men in fact increased their caloric intake slightly more than the obese men!

In women, the results were not quite the same, in that normal weight women consumed an additional 183 kcal, overweight women consumed an additional 304 kcal, and obese women consumed an additional 341 kcal.

But once again, let us remember that larger people actually need more calories because they tend to have higher caloric expenditures (like bigger cars needing more fuel), so really it is not fair to simply compare the number of calories without adjusting these for higher requirements. Once you do such adjustments, the difference in increased calorie intake in obese women does not appear all that much greater anymore.

In their paper the authors go on to discuss the potential importance of the relative changes in carbohydrate, fat, and protein intake between the two surveys, but as these trends did not differ between the normal, overweight, and obese groups, I will not get into their arguments here.

The whole surprising point here is that it is actually by no means straightforward to deduce from these data that obese people are obese because they “overeat” compared to their non-obese peers. If anything, the thin guys are the ones who are actually “overeating” (and getting away with it).

So if obesity is not because of overeating or undermoving, why the heck are so many people so much heavier today than ever before?

Either our assessments of caloric intake (and expenditure) are simply completely off because of “underreporting” or other methodological problems - but in that case, this entire exercise of trying to figure out caloric intake and expenditure as a cause of the obesity epidemic is worthless.

What I believe this data actually shows is that we are seeing the population effect of the same changes in energy intake (and expenditure) affecting some people more than others.

Thus, readers will recall the recent post that heavier kids appear to be far more “sensitive” to obesogenic factors than thin kids - the “naturally” thin kids are just lucky and get away with their crappy lifestyles, while the poor “naturally” heavier kids pack on the pounds by doing exactly what the thin kids are doing (namely eating too much and sitting around all day).

Similarly, it seems that while EVERYONE is eating more calories now than they were back in 1971, “naturally” thin people somehow manage to stay thin, while “calorie-sensitive” folks get heavier.

Thus, the laws of physics which would tell us that obese people gain weight because they simply eat more and move less don’t quite tell us why thin people can eat more and move less and still stay thin.

So if the obesity epidemic is not simply due to people becoming obese because they’re eating more and moving less (than thin people), then the solution is probably not in simply having them eat less and move more - which, incidentally, is probably why “eat-less-move-more” (ELMM) so seldom works.

Somedays I wish life were simpler.

AMS
Edmonton, Alberta

Austin GL, Ogden LG, & Hill JO (2011). Trends in carbohydrate, fat, and protein intakes and association with energy intake in normal-weight, overweight, and obese individuals: 1971-2006. The American journal of clinical nutrition PMID: 21310830

On most days, our obesity clinic could easily be confused with an orthopedic clinic given the sheer number of patients who present with severe pains in their backs, knees, hips, and ankles - often to the point of immobility.

It turns out (perhaps not surprisingly) that today, obesity and knee osteoarthritis are among the most frequent chronic conditions affecting Americans aged 50 to 84 years - my guess is that these conditions are no less frequent among Canadians.

Given the high prevalence of both obesity and knee osteoarthritis and their very significant impact on quality of life, Losina and a team of researchers from Harvard, Boston University, Chapel Hill, Yale and the University of Sydney undertook the rather momentous task of estimating the impact of these conditions on morbidity and mortality in older Americans. Their results were now published in the Annals of Internal Medicine.

The researchers based their analyses on U.S. Census and national obesity data with estimated prevalence of symptomatic knee osteoarthritis, whereby they assigned the US population aged 50 to 84 years to four subpopulations: nonobese without knee osteoarthritis (reference group), nonobese with knee osteoarthritis, obese without knee osteoarthritis, and obese with knee osteoarthritis.

They then used a computer simulation model (The Osteoarthritis Policy Model) to estimate quality-adjusted life-year losses due to knee osteoarthritis and obesity and to determine health benefits of reducing obesity prevalence to levels observed a decade ago.

It turns out that the estimated total losses of per-person quality-adjusted life-years ranged from around 2 years in nonobese persons with knee osteoarthritis to about 3.5 years for persons affected by both conditions. Although these numbers may not sound shocking, they actually represent 10% to 25% of the remaining quality-adjusted survival of persons aged 50 to 84 years.

When calculated for the entire US population in that age range, this amounts to a staggering 86 million quality-adjusted lost to these conditions.

The researchers also calculate that reversing obesity prevalence to levels seen 10 years ago would avert just over 110,000 total knee replacements - so reducing obesity (even to where it was just 10 years ago) could indeed save a substantial number of knees.

What the paper of course does not disclose is how exactly such a reversal in obesity rates could possibly be achieved.

Clearly, the impact of weight loss on knee (and other) pain that we see in our clinic is often dramatic, but achieving weight loss for someone who is already immobilised by knee (or other) pain is definitely a challenge.

I’d certainly love to hear from my readers on how knee (or other) pain has affected their weight and whether or not they have experienced improvement in their knee (or other) pain with weight loss.

AMS
Edmonton, Alberta

Losina E, Walensky RP, Reichmann WM, Holt HL, Gerlovin H, Solomon DH, Jordan JM, Hunter DJ, Suter LG, Weinstein AM, Paltiel AD, & Katz JN (2011). Impact of obesity and knee osteoarthritis on morbidity and mortality in older americans. Annals of internal medicine, 154 (4), 217-26 PMID: 21320937