This Month’s edition of Canadian Family Physician, the official journal of the College of Family Physicians of Canada, features a debate on whether or not family doctors should stop telling their patients to lose weight.

On the Pro side, we have Jana Havrankova, an endocrinologist at Clinique familiale Saint-Lambert in Quebec, notes that keeping weight off is anything but simple.

“The few patients who manage to lose weight and keep it off achieve something truly remarkable. From a public health standpoint, however, the treatment of obesity is a failure.“

Thus, rather than trying to treat obesity, Havrankova places her bets on prevention:

“Efforts at prevention involve some degree of telling people what to do, and some people will criticize this. Screening and monitoring excess weight from early childhood, ensuring that physical activity is part of the curriculum right up to university, creating neighbourhoods that encourage people to get out and walk, and teaching people how to prepare healthy meals are just a few suggestions.”

In the Contra corner we have Dominique Garrel, a specialist in endocrinology and metabolism and Full Professor in the Department of Nutrition at Université de Montréal, Quebec.

Not only does Garrel argue that obesity must be treated, but also that the treatment of obesity can be simple and effective. However, treatment needs to focus on health and not on weight loss.

“Treat the patient, not his weight. Telling an obese patient to lose weight is about as effective as telling an asthmatic patient to breathe better! Care consists of assessing the risks of excess weight to a patient’s health. The Edmonton Obesity Staging System recently proposed by Kuk et al [sic] is an interesting tool designed for this point of view. This system includes recommendations for each level of intervention, ranging from simply recommending that the patient maintains his weight, to recommending bariatric surgery.”

He also points out the importance of recognising and treating comorbidities as these may often represent roadblocks to weight management, to set reasonable (read ‘modest’) objectives for weight loss, and inform the patient of the tools at his disposal for losing weight (as well as warn them against unhealthy weight loss efforts).

In an accompanying editorial, Roger Ladouceur, Associate Scientific Editor of CFP, notes the following:

“Why, then, do we tell our patients to lose weight? Why do we repeat, “You should lose weight”? What’s with that? Somewhat sadistic, don’t you think? Do we do this as a way of shifting the guilt and transferring the responsibility of the therapeutic failure?”

In fact, Ladouceur concludes with the rather profound statement that:

“All things considered, shouldn’t we put a stop to this preoccupation with our patients’ weight and simply encourage them to develop healthy lifestyle habits, to adopt a balanced diet, to practise on a regular basis any form of exercise that they enjoy, even if it is simply walking? Instead of repeating “You should lose weight,” shouldn’t we help them to become more comfortable with themselves?”

Although this statement may not at all sound ‘profound’ to regular readers of these pages, such an ‘insight’ printed in the ‘house journal’ of the CFPC, which goes out to every family doctor in Canada, represents a major step forward in our thinking about obesity - if anything, it certainly moves right into the mainstream of what the Canadian Obesity Network’s experts and Family Practice Group has been saying all along (and is about to promote with a nationwide program due to be released in the next few days).

Not only am I happy to see promotion of the Edmonton Obesity Staging System, but am also particularly pleased to see that both sides (and the editorial) are seeing health as being more than just numbers on the scale.

Neither suggests we ignore obesity or that it does not confer health risks - but they do suggest that it is time to radically rethink the traditional “lose weight and you’ll be fine” approach based on the simplistic notion of “eat-less move-more”.

Incidentally, this debate and editorial accompanies another article in this edition of CFP with the title: “The Downside of Weight Loss” - more on this paper in tomorrow’s post.

AMS
Grand Prairie, Alberta

Hat tip to the Canadian Obesity Network’s Primary Practice Working Group member Dr. Shahebina Walji, Calgary, for alerting me to these articles.

Bariatric surgery can profoundly affect how the body absorbs medications - this issue, however, remains largely understudied.

In a paper, just published in the Journal of Antimicrobial Chemotherapy, we examine the effect of gastric bypass surgery, a procedure that circumvents the upper gut on the bioavailability (absorption) of azithromycin, a widely used treatment for community-acquired infections.

We performed single-dose pharmacokinetic studies in 14 female post-gastric bypass patients and 14 sex- and body mass index (BMI)-matched controls (mean age 44 years and BMI 36.4).

Azithromycin concentrations, following the administration of two 250 mg tablets were about 30% lower in gastric bypass patients compared with controls.

This finding suggests that there may be a substantial risk for treatment failure with this antibiotic in and clinicians should consider dose modification and/or closer clinical monitoring of gastric bypass patients receiving azithromycin.

AMS
Calgary, Alberta

Padwal RS, Ben-Eltriki M, Wang X, Langkaas LA, Sharma AM, Birch DW, Karmali S, & Brocks DR (2012). Effect of gastric bypass surgery on azithromycin oral bioavailability. The Journal of antimicrobial chemotherapy PMID: 22577100

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Relative Size Illusion

Regular readers may recall previous posts on the widespread reporting of weight loss in surgical studies as ‘excess weight loss’ - a meaningless number based on outdated concepts of ‘ideal weight’. In fact, not only is there is little correlation between the amount of weight lost and improvements in post-surgical morbidity and mortality but there is nothing to suggest that using this measure does anything more than amplify the numbers - after all a rather remarkable 60% EWL is little more than 20% of initial weight - but of course 60% sounds so much better.

I was therefore happy to see that last week, at the FDA hearing on obesity devices, according to Close Concerns:

“There was nearly unanimous support for using percentage of total body weight rather than percentage of excess weight loss as a study endpoint. Panelists cited the “significant flaws” in excess weight loss, especially the challenge of applying it to individuals with lower BMIs. In contrast, many believed that using percentage of total body weight loss provided a more valid metric for people at both high and low BMIs.”

Hopefully, surgeons and surgical device makers will take note and comply with what I am hoping the FDA will from now on like to see in all future submissions - strict reporting of percentage of ‘total weight loss’ rather than the confusing, arbitrary, and scientifically unsound use of ‘excess weight loss’, which I fear the surgeons may find hard to abandon.

AMS
Brooks, Alberta

As not everyone may have a chance during the week to read every post, here’s a roundup of last week’s posts:

• Removing the Cause of Weight Gain Does Not Mean Weight Loss
• Why Stopping Weight Gain is More Important Than Losing Weight
• Institute of Medicine Big on BMI, Eat Less and Move More
• Challenges in the Medical Management of Severe Obesity
• European Joint Statement on Obesity and Hypertension

Have a great Sunday! (or what is left of it)

AMS
Edmonton, Alberta

Given our interest in the renin angiotensin system (RAS) in adipose tissue, in the early 2000s, my lab back in Berlin was studying the effect of how this system affects the growth and differentiation of cultured human fat cells.

Other laboratories had suggested that angiotensin II (Ang II) plays a role in the differentiation of preadipocytes into mature adipocytes in mouse cell lines. We wanted to explore if the same was true for human cells

So we performed a series of experiments, in which we isolated preadipocytes from human adipose tissue and exposed them to angiotensinogen (AGT), Ang II, or angiotensin receptor antagonists in the differentiation medium. We found that the expression of the RAS genes AGT, renin, angiotensin-converting enzyme, and Ang II type 1 receptor increased during adipogenesis.

To our surprise, we also found that stimulation of the Ang II type 1 receptor by Ang II reduced adipose conversion, whereas blockade of this receptor markedly enhanced adipogenesis.

Assuming that the angiotensinogen formed by mature adipocytes may perhaps directly affect preadipocyte differentiation, we performed co-culture experiments, where we were able to show that mature adipocytes were indeed able to inhibit preadipocyte differentiation, an effect that was almost entirely abolished by blockade of the Ang II type 1 receptor.

In our paper, published in DIABETES, we not only interpreted these findings as indicative of a functional role of the RAS in the differentiation of human adipose tissue but also postulated that a paracrine negative-feedback loop, which inhibits further recruitment of preadipocytes by maturing adipocytes may be an important mechanisms in regulating adipose tissue growth and expansion.

These findings subsequently prompted us (and several other laboratories) to further explore the role of this system in adipose tissue, including studies in animal models and humans.

According to Google Scholar, this paper has been cited 242 times.

AMS
Lyon, France

Prof. Dr. med. Jens Jordan, Institut für Klinische Pharmakologie, Medizinische Hochschule Hannover, Germany

As regular reader may recall, this week I am attending the 19th European Congress on Obesity, where, this morning, I spoke in a joint session of the European Association for the Study of Obesity (EASO) and the European Society of Hypertension (ESH).

Interestingly enough, today also saw the online release of a Joint statement of EASO and ESH on obesity and difficult to treat arterial hypertension in the Journal of Hypertension.

As discussed by Jens Jordan, lead author of this statement (and a close collaborator from my time back in Berlin), obese individuals are not only more prone to arterial hypertension, and despite requiring more antihypertensive medications, have an increased risk of treatment-resistant arterial hypertension.

However, it is also important that there is considerable inter-individual variability in the relationship between excess weight and hypertension - many obese people are normotensive or have uncomplicated mild hypertension. These differences may perhaps be related to genetic mechanisms, as having a positive family history of hypertension is certainly an important risk factor.

Although, weight loss is often recommended as a means to lower blood pressure, current hypertension guidelines fail to provide evidence-based guidance on how to institute (or maintain) weight loss.

Furthermore, there is emerging evidence that perhaps the influences of weight loss on blood pressure may be overestimated.

Thus, although hypertension generally decreases following bariatric surgery, many patients tend to experience subsequent increases in their blood pressure and will generally again require antihypertensive medications a few years after surgery.

Jordan also pointed out that data from large-scale studies with hard clinical endpoints on antihypertensive medications specifically addressing obese patients are lacking and the morbidity from the growing population of severely obese patients is poorly recognized or addressed.

Although renin-angiotensin system inhibitors are widely considered to be the most appropriate drugs for antihypertensive treatment of obese patients, most will likely require two or more antihypertensive drugs.

It also remains unclear how best to combine weight loss strategies and antihypertensive treatment to achieve an optimal clinical outcome.

This state of affairs is not very different from that of over a decade ago, where I already deplored the lack of specific studies and/or guidelines on the management of hypertension in obese patients.

Perhaps, this joint statement, which is not only an important indication that these two organisations are talking, may help drive initiatives that will ultimately help improve obesity related hypertension management.

AMS
Lyon, France

Jordan J, Yumuk V, Schlaich M, Nilsson PM, Zahorska-Markiewicz B, Grassi G, Schmieder RE, Engeli S, & Finer N (2012). Joint statement of the European Association for the Study of Obesity and the European Society of Hypertension: obesity and difficult to treat arterial hypertension. Journal of hypertension, 30 (6), 1047-1055 PMID: 22573071

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I am currently attending the 19th European Congress on Obesity, here in Lyon, France, where yesterday, I spoke on the medical management of severe obesity.

Rather than repeating my take on this, I would prefer to quote the following passage from today’s Close Concerns newletter, that covers my talk (and the rest of the session).

After characterizing the increasing prevalence of severe obesity (BMI >40 kg/m2), the burdens it places on patients and the healthcare system, and the challenges of its management, Dr. Sharma discussed potential lifestyle and pharmacologic for consideration for the treatment of severe obesity. He mentioned that medically supervised low-calorie diets could in rare cases be an option for long-term weight management for highly motivated patients with severe obesity, while pharmacologic agents in development are slowly getting to the point where they could be efficacious enough to move the needle.

Dr. Sharma noted that conservative management (using a combination of intensive lifestyle, medication, and a low-calorie diet) could help approximately 20-30% of individuals to achieve and sustain clinically meaningful weight loss in a clinical setting.

• Obesity places numerous burdens on patients, spanning the four M’s: metabolic, monetary, mental, and mechanical. Dr. Sharma noted that in his practice, severely obese patients who are referred for bariatric surgery undoubtedly face these burdens – 75% suffer from depression, approximately one-third experience mechanical problems (e.g., osteoarthritis, sleep apnea), a large percentage has cardiometabolic issues (e.g., diabetes and/or hypertension), and approximately one-fifth are on long-term disability or unemployed (even though it is a relatively young population; average age of 44 years).

• Dr. Sharma highlighted the burdens that severe obesity places on the healthcare system. Dr. Sharma noted that severe obesity decreases post-acute rehabilitation efficiency, increases hospital lengths of stay, and increases hospital costs. Specifically, at the Glenrose Rehabilitation Hospital in Canada, rehabilitation length of stay was on average 56 days for severely obese individuals compared to non severely obese individuals, and rehabilitation costs averaged $115,000 versus $44,000. These stem from the fact that severely obese patients waited on average 43 days to transfer to another facility, whereas other patients waited zero days on average.

• He emphasized that while bariatric surgery is the most effective option for the treatment of severe obesity, it is by no means a population-level solution for two reasons: 1) many do not want to undergo surgery, are ineligible to do so, or do not have access; and 2) if all individuals with severe obesity wanted surgery, the current healthcare system wouldn’t have nearly enough capacity to perform all those procedures. Dr. Sharma noted that currently an approximate 2.5% of the population in Canada is severely obese; the current surgical capacity in the country could only service 1/600 of the potential demand per year (Padwal and Sharma, CMAJ 2009). As such, for practical reasons, clinicians have to think about other ways to manage severely obese patients.

• Dr. Sharma stated that we need to stop thinking about obesity as a single condition; rather, “we need to start thinking of obesity as obesities” – heterogeneous, complex disorders of multiple etiologies characterized by excess body fat. Drawing an analogy to the treatment of cancer, Dr. Sharma noted that the treatment of obesity should depend on the type and stage of disease.

• He emphasized that BMI alone is not an adequate marker of cardiovascular risk; rather, one must also look at comorbidities. In the Edmonton Obesity Staging System (EOSS), the clinical staging system Dr. Sharma developed along with Dr. Kushner, patients are categorized from Stage 0 to Stage 4, based on their medical, mental, and functional health, with Stage 0 patients having no sign of obesity-related risk factors, psychological symptoms, or functional limitations, and Stage 4 patients experiencing end-stage disease. Dr. Sharma noted that the EOSS is a good predictor of mortality – applying the EOSS to NHANES III (1988-1994) data, there was a nice separation of mortality curves, whereas things were not as differentiated when using BMI as the criterion (Padwal et al., CMAJ 2011). He suggested that by using BMI cutoffs as a basis of treatment, clinicians run the risk of overtreating healthy but obese patients and undertreating overweight but metabolically unhealthy patients.

• Dr. Sharma stated that in rare cases, medically supervised low-calorie diets (LCD) could be an option for long-term weight management for highly motivated patients with severe obesity. That is, very few people will want to go on a long-term LCD and be able to tolerate doing so. He noted that at his clinic, eight patients started on low-calorie diets and were kept on them as long as they wanted to stay on them; one has been on an LCD for four years, while others have been on an LCD for three years. They’ve lost on average between 20-40% of their initial body weight, reversed their diabetes, and decreased the use of their blood pressure medications. Several of his patients stated that they plan to be on LCDs for the rest of their lives.

• He noted that pharmacologic options are slowly entering the 10% weight-loss range, which is the amount of weight loss he thinks is needed to move the needle. Dr. Sharma suggested that this 10% weight loss might be achievable with liraglutide, and that phentermine/topiramate brought about between a 12-14% weight loss (“getting into the gastric banding territory”) for severely obese patients on the high dose of phentermine/topiramate in the EQUIP trial (Allison et al., Obesity 2011).

Questions and Answers

Q: I disagree with the analogy you draw in the title of your article, “Bariatric Medicine Without Surgery Is Like Nephrology Without Dialysis.” Dialysis is treatment for end-stage kidney disease. If we applied surgery to patients with end-stage obesity, probably Stage 3 or Stage 4 in your Edmonton Obesity Staging Scale, we would probably do more harm than benefit.

A: Thank you for that remark. This editorial is five years old. I would not write it again, as I agree with you. I used to view surgery as a last resort, but I no longer think that. If you have a patient who needs to lose at minimum 15% body weight, the first thing you should discuss is bariatric surgery. Bariatric surgery is not the last option for these patients; it should always be the first option. If the patient does not want surgery, then we discuss other options. I think that is a change that has happened in the past five years.

Q: You mentioned that patients are using liraglutide for their obesity. What dose are you using in your practice?

A: The data that I showed you was data that is published in The Lancet. In our practice, we use liraglutide in obese patients who present with diabetes, as part of treatment for their diabetes. As you know, even those treated at the 1.8 mg dose will lose weight. We’ll have to wait until the SCALE study completes to find out more.

AMS
Lyon, France

This week, the US Institute of Medicine released an impressive 500-page thome called “Accelerating Progress in Obesity Prevention: Solving the Weight of the Nation“.

The report extensively reviews population and policy issues relevant to obesity prevention.

However, it also includes a brief chapter on obesity treatment and access in health care systems.

The following are some of the key recommendations from this section pertaining to health care:

Goal: Expand the role of health care providers, insurers, and employers in obesity prevention.

Recommendation 4: Health care and health service providers, employers, and insurers should increase the support structure for achieving better population health and obesity prevention.

Strategy 4-1: Provide standardized care and advocate for healthy community environments. All health care providers should adopt standards of practice (evidence-based or consensus guidelines) for prevention, screening, diagnosis, and treatment of overweight and obesity to help children, adolescents, and adults achieve and maintain a healthy weight, avoid obesity-related complications, and reduce the psychosocial consequences of obesity. Health care providers also should advocate, on behalf of their patients, for improved physical activity and diet opportunities in their patients’ communities.

Potential actions include

• health care providers’ standards of practice including routine screening of body mass index (BMI), counseling, and behavioral interventions for children, adolescents, and adults to improve physical activity behaviors and dietary choices;

• medical schools, nursing schools, physician assistant schools, and other relevant health professional training programs (including continuing education programs), including instruction in prevention, screening, diagnosis, and treatment of overweight and obesity in children, adolescents, and adults; and

• health care providers serving as role models for their patients and providing leadership for obesity prevention efforts in their communities by advocating for institutional (e.g., child care, school, and worksite), community, and state-level strategies that can improve physical activity and nutrition resources for their patients and their communities.

Strategy 4-2: Ensure coverage of, access to, and incentives for routine obesity prevention, screening, diagnosis, and treatment. Insurers (both public and private) should ensure that health insurance coverage and access provisions address obesity prevention, screening, diagnosis, and treatment.

Potential actions include

• insurers, including self-insured organizations and employers, considering the inclusion of incentives in individual and family health plans for maintaining healthy lifestyles;

• insurers considering (1) benefit designs and programs that promote obesity screening and prevention and (2) innovative approaches to reimbursing for routine screening and obesity prevention services (including preconception counseling) in clinical practice and for monitoring the performance of these services in relation to obesity prevention; and

• insurers taking full advantage of obesity-related provisions in health care reform legislation.

While all of this is well intended - it is really much of the same with little new insights for the practitioner.

As readers of these pages are well aware, if recording people’s BMIs and counselling them on eating less and moving more only worked, we’d probably have solved the obesity problem by now.

I may have missed it (have yet to work my way through all of the 500 pages) but I certainly did not see much that would actually help practitioners address and manage the ‘root causes’ of obesity - which, are not simply eating too much and not moving enough!

Nowhere do I see the authors address the importance of mental health, stress, time, genetics, medications, and countless other issues relevant for weight gain and its management. Nor do I see much on the urgent need for medications or the role for surgery. Entirely missing is a recommendation to address bias and discrimination in health care settings (this would have been my #1 recommendation for the entire document!) or in simply accommodating those with obesity so that they can even access proper health care in a professional, sensitive, and caring environment.

Like I said, I may have missed these passages - if yes, I apologise - if they are actually missing, this report is unlikely to change much in obesity management.

AMS
Lyon, France

Yesterday, I posted on the notion that simply removing the cause of weight gain does not directly translate into weight loss.

In fact, I have previously posted on the idea that the first sign of success in weight management is the prevention of further weight gain.

For those of us in clinical practice, this idea raises several important questions:

1) Is everyone at risk of weight gain?

2) Does is matter when or how fast this weight is gained?

3) Is there a sub group of individuals in whom prevention of weight gain may be more important than in others?

This is where, in a discussion with my former student Tobias Pischon (now Professor for Molecular Epidemiology at the Max-Delbrueck Centre in Berlin), he pointed me to a study by Anja Schienkiewitz and colleagues from the German Institute of Human Nutrition Potsdam-Rehbrücke, published in the American Journal of Clinical Nutrition back in 2006.

The study examined the relationship between the history of weight gain and risk of type 2 diabetes in 7720 men and 10,371 women from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam Study with information on weight history.

In both men and women, weight gain during the ages 25 and 40 was a far greater risk factor for developing type 2 diabetes than weight gain between the ages 40 and 55.

While this is an important observation, I was far more interested in the data on the temporal patterns of weight gain in this population.

The researchers divided the patients into those who were weight stable (less than 1 point increase in BMI) and those, who experienced moderate (a 1-4 point increase in BMI) or severe (a greater than 4 point BMI increase) between the ages of 25-40, 40-55, or both.

Interestingly enough, only about 15% of men and women remained weight stable over the 30 years of observation!

Of those, who experienced moderate (~50%) or severe (~12%) weight gain between age 25-40, about 30% remained weight stable, while 40% continued to experience moderate and 30% experienced more severe weight gain over the next 15 years.

Similarly, of those individuals, who experienced severe weight gain between age 25-40, about 30% continued to experience moderate weight again, while about 35% continued to experience severe weight gain.

Not surprisingly, the latter group - those with severe weight gain both between ages 25-40 and 40-55, were at an almost 20-fold higher risk of diabetes than those who stayed weight stable over the entire 30 years - their total weight gain between age 25-55 was almost 15 BMI points.

Those who had moderate or severe weight gain between ages 25-40 but managed to not gain weight between ages 40-55 had only about half the diabetes risk of the continuous gainers.

Most interestingly, however, those who were weight stable between 25-40 but experienced moderate or severe weight gain between 40-55 had less than 10% the risk of the continuous gainers.

Several lessons are evident from this:

At least when it comes to diabetes, weight gain in early adulthood, particularly when this weight gain continues into middle-age, is of far greater significance than gaining weight after the age of 40, even if this later weight gain is quite severe.

Thus, it is evident that weight management strategies are perhaps best targeted at younger adults, particularly with the aim of preventing continuing weight gain into middle age.

In a tightly strapped health care system, one would perhaps want to identify younger adults between the ages of 25-40 with rapid weight gain (about 12% of the total population) as the majority of these will continue gaining considerable weight as they get older - this ‘highest risk’ group makes up about 6% of the total population.

In contrast, it may make far less sense to target weight gain in those who are weight stable (even if obese) or those who are only gaining moderate amounts of weight, especially later in life.

This is of critical importance when thinking about health care systems: while it may be neither feasible nor affordable to address obesity in the entire population, identifying and better managing those at the highest risk, namely, those who are experiencing considerable weight gain in early adulthood, and especially those, in whom this weight gain continues into later years, may be both feasible and affordable.

This is probably the group where simply stopping weight gain may be more important than getting everyone, especially those who are weight stable or have gained weight only after the age of 40, to lose weight.

AMS
Lyon, France

One of the most common misconceptions about obesity management is that identifying and addressing a potential contributor to weight gain should automatically translate into weight loss - it does not!

As I pointed out in a recent post, when you identify and address the cause of weight gain - weight gain stops, and that’s usually it!

That many of us fail to recognize this rather simple principle, is again illustrated by a paper by Penner and colleagues published in the Journal of Joint and Bone Surgery, which found that successful ankle reconstruction surgery does not decrease BMI in overweight and obese patients.

According to their findings, the 145 patients with excess weight who underwent successful ankle replacement or ankle fusion, despite significant improvements in Ankle Osteoarthritis Scale (AOS) scores and increased physical activity scores, pretty much maintained their preoperative BMI levels at six months and one, two, and five years.

Based on these findings, the authors conclude that:

“Pain and disability are significantly reduced in overweight and obese patients after successful ankle replacement or fusion. Despite this, the mean BMI remains unchanged after the surgery, indicating that weight loss does not commonly occur following successful ankle reconstruction in this patient population. Obesity is likely attributable to factors other than limited mobility caused by ankle arthritis.”

Obviously, the authors assumed that if limited mobility caused weight gain, then increasing mobility should reduce it - that, however, is not what happens.

Rather, what they found, is exactly what I would expect - with regain of their mobility, patients stopped gaining weight - and that’s all.

Without a targeted obesity treatment strategy, there is indeed no reason to expect that these patients would now begin losing weight simply because their activity levels may now be somewhat higher than before. The few extra calories that they may perhaps now burn as a result of being more physically active would easily be compensated by an increased intake or other biological mechanisms that are there to ‘defend’ their current weight.

Thus, the observation that successful ankle surgery did not result in ’spontaneous’ weight loss neither disproves nor proves that pain or disability may have contributed to weight gain in the first place - it probably did in some and probably did not in others.

Interestingly enough, I believe that this study also bears an important lesson for those attempting to address obesity at a societal level - even if we did know what exactly is driving the obesity epidemic - removing this cause does not necessarily mean everyone gets thinner - it just means that things may hopefully not get worse.

AMS
Berlin, Germany

Penner MJ, Pakzad H, Younger A, & Wing KJ (2012). Mean BMI of Overweight and Obese Patients Does Not Decrease After Successful Ankle Reconstruction. The Journal of bone and joint surgery. American volume, 94 (9) PMID: 22552679

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