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Brave New World —

January 13, 2012

This week we’ve covered the Strong4Life story from several critical angles: why the billboard campaign is wrong, why their “it’s for the parents” claim is BS, why their foundational research is bunk, how they are enabling bullies, why their censorship policy is hypocritical, and, finally, how they profit from the very companies they claim are contributing to childhood obesity.

Criticism is great, but criticism is easy. To transform criticism into change you need two additional components: solutions and action.

We’ve outlined, and will continue to outline, a clear plan of action. But supporters of Strong4Life have complained that we have not offered any alternative solutions.

Not true, but today I will outline a specific solution to solve the childhood obesity crisis.

Are you ready for it?There is no solution.

Let me repeat that for those who can’t believe what they’ve just read.

There is no solution to the childhood obesity crisis.

Primarily, because there is no childhood obesity crisis.

Did you just crap your pants in outrage a bit? Good. Now, before I explain what the real “crisis” is and how we solve it, let me explain why I do not believe there is a childhood obesity crisis.

First of all, groups like Strong4Life want you to believe that childhood obesity is a runaway train, picking off more and more children every year.

The fact is that childhood obesity rates plateaued*, along with the obesity rates of women, in 1999, according to data from the NHANES study released in 2008. NHANES is the only study of national obesity trends that actually weighs and measures its subjects, making it significantly more reliable than telephone surveys, such as the one used in the flawed “F as in Fat” report from the Robert Wood Johnson Foundation.

So, obesity rates aren’t out of control. They are stable, which is what we want at the very least, right? But if you’d rather have skyrocketing obesity rates among children,  there is one sure fire way to do that: tell the parents of fat children make their kids thin.

Because I’ve got news for you: the only way to make fat kids thinner (albeit temporarily) is to impose caloric restriction on a child. Simply feeding a fat child healthy foods will not necessarily make him thinner. It is only by feeding a fat kid those healthy foods in limited and controlled quantities that parents get the kind of weight loss results that would make “obese” child “normal.”

When you restrict the caloric consumption of anyone, but particularly a child, their bodies will respond metabolically to the perceived famine by slowing your metabolism and clinging to every calorie you consume. Whatever temporary weight loss you see will only be sustainable with the kind of continued dietary oversight that has been implicated in the explosion of eating disorders among our nations children.

The most noticeable change has taken place among children under age 12, where eating disorders have increased 119% between 1999 and 2006. The problem is so severe that the American Academy of Pediatrics urged doctors to be cautious in executing anti-obesity policies:

When counseling families on preventing obesity, pediatricians should focus on healthy eating and building self-esteem while still addressing weight concerns. Care needs to be taken not to inadvertently enable excessive dieting, compulsive exercise, or other potentially unhealthy weight-management strategies.

For those fortunate children who don’t develop an eating disorder from weight loss practices, the most frequent consequence of weight loss is that the dieting child’s weight will return to its original level. Just ask any fatty about their childhood experiences of Weight Watchers or Jenny Craig or Deal-A-Meal.

Parents who want their child to lose weight will frequently attempt multiple strategies for reducing their child’s size. If watching calories doesn’t work, they try Slim Fast, and if Slim Fast doesn’t work, they try vegetarianism. Each time, the child may lose 5 or 10 pounds, then slowly regain it. The child will be blamed for the failure to maintain the loss, the parent will be blamed for the fat child, and the public health campaign will post billboards shaming all of them for their inability to snatch thinness from the jaws of obesity.

And although some of these children may escape the insidious grasp of an eating disorder, others have just begun a lifelong habit that is clinically proven to have serious metabolic consequences: weight cycling.**

The science of weight cycling is in its infancy, but most researchers agree that weight cycling presents a health risk because it is significantly correlated with insulin resistance, chronic inflammation, type 2 diabetes, hypertension, muscle wasting, major weight gain, abdominal fat and all-cause mortality.

All of these correlations are still poorly understood, but anti-obesity activists, such as Walter Willett, have fought hard to show that weight cycling isn’t dangerous, so people should keep trying to lose weight. Their “proof” is that when you control for overall BMI, many of these risk factors disappear. Yet, Willett’s own research admits that severe weight cyclers have overall higher weights.

From the American Journal of Epidemiology:

Despite the repeated weight losses, severe weight cyclers gained more weight between 1989 and 1993 than mild weight cyclers, who gained more weight than non-weight cylcers (mean change 15.6 lbs. vs. 9.1 lb.s vs. 6.9 lbs.).

And from the Archives of Internal Medicine:

Weight cycling was positively associated with BMI at baseline. Approximately 40% of the noncyclers between 1972 and 1992 were overweight or obese compared with 74% of the mild cyclers and 87% of the severe cyclers.

So, Willett tries to separate the fact that weight cycling obviously leads to higher weights, but that it’s the higher weights caused by weight cycling, NOT the weight cycling itself, that exacerbates all of the health issues outlined above.

But the one health issue which I did not mention, and that few researchers would disagree with, is that weight cycling is definitely a contributor to cardiovascular disease. The only problem is that nobody can figure out exactly why weight cycling causes cardiovascular damage.

One paper I recently read, however, offers a plausible theory that is worth considering. It’s called the Repeated Overshoot Theory, and the gist is that when a dieter begins to regain the weight they have lost (and the vast majority will regain the weight they have lost) it will lead to fluctuations in blood pressure, heart rate, sympathetic activity, blood glucose and lipids. This “overshoot” of metabolic indicators, when repeated upon subsequent weight cycles, can stress the cardiovascular system and lead to long-term cardiovascular damage.

By starting a child on a weight loss regimen, you are setting him or her up for a lifetime of repeated overshoots.

And the only people who deny that the vast majority of weight loss attempts result in regaining the weight, and often weighing more than your starting weight, are people who have not read the extensive body of literature on the subject and people who stand to profit from each weight loss attempt you undertake.

But don’t take my word for it. There’s a doctor in Canada who I greatly respect, though don’t always agree with, whose name is Arya Sharma, and his credentials are unquestionable:

Dr. Arya M. Sharma, MD/PhD, FRCPC is Professor of Medicine & Chair in Obesity Research and Management at the University of Alberta, Edmonton, Canada. He is also the Medical Director of Alberta Health Services Edmonton Region’s interdisciplinary Weight Wise Program and the Clinical Co-Chair of the Alberta Health Services Obesity Initiative.

Dr. Sharma is also the founder and Scientific Director of the Canadian Obesity Network, a network of over 6000 obesity researchers, health professionals and other stakeholders.

He is also the Past-President of the Canadian Association of Bariatric Physicians and Surgeons.

Although Dr. Sharma blogs about obesity and health issues, he is not some snot-nosed kid, like myself. He is a bariatric physician, working only with obese patients, and he has been advocating for against weight loss and has written extensively about the dangers of weight cycling.

Dr. Sharma promotes an approach to health and nutrition known as Health at Every Size®, and so do I. You can read the details of HAES in a great book by Dr. Linda Bacon, available in paperback for $10 or on Kindle for $1.79.

The main principles of HAES are simple: eat healthy foods, move your body in an enjoyable way, and let your body respond to these healthy lifestyle changes without worrying about weight loss. The evidence behind this approach is building and support for HAES by nutritionists and physicians is growing.

The mainstream medical community already accepts that a modest weight loss of 5-10% of your original starting weight is enough to create a profoundly positive impact on your health. Hell, even Jenny Craig’s own research admits to this 5-10% figure:

As discussed in Wing et al. [ed. note: read the study referred to here], seemingly small reductions in body weight or BMI can have a significant impact on the proportion of the population categorized as overweight or obese. Further, small amounts of weight loss can have a significant impact on health, as demonstrated in the Diabetes Prevention Program, which found that 1 kg of weight loss is associated with a reduction in risk of diabetes of 16%

Of course, they cite this research to defend their disappointing average weight loss results of 13% of starting weight after one year with ~88% of clients dropping out by then… but still.

Weight loss advocates insist that the weight loss is responsible for the improved health, but HAES proponents point out that it is the lifestyle changes, regardless of whether weight is lost, that causes health improvements.

Whether it is the modest weight loss or the lifestyle change itself that is responsible for the health improvements is up for debate, as explained in this excerpt from a position statement by the American Diabetes Association explains:

Several studies have demonstrated the potential for moderate, sustained weight loss to substantially reduce the risk for type 2 diabetes, regardless of whether weight loss was achieved by lifestyle changes alone or with adjunctive therapies such as medication or bariatricsurgery (see energy balance section) (1). Moreover, both moderate-intensity and vigorous exercise can improve insulin sensitivity, independent of weight loss, and reduce risk for type 2 diabetes (1).

What we do know is that making positive lifestyle changes can have a great impact on your health, regardless of whether you end up looking thin or not. As a 5’6″, 265 pound guy, a 5-10% weight loss would still make me between 239  and 252 pounds. My BMI would go from 41.5 (morbidly obese) to between 37.4 and 39.5, on the cusp of morbid obesity.

But since I’m already doing strength training and using the elliptical, as well as getting a diverse, healthy diet, you don’t know how much weight I have already lost, and, quite frankly, it doesn’t matter.

And it does not matter if our children are fat either. If you want to have a health crisis to freak out over, let me give you one… I propose that our nation’s children do face a health crisis: an Insulin Resistance Crisis.

It’s not nearly as catchy as the Childhood Obesity Crisis®, but it is a better marker of disease risk than obesity.

As I pointed out in this post (and directly to Strong4Life), insulin resistance is the disease they want to prevent, not obesity. Insulin resistance can be caused by an energy dense diet (the kind of fast food, Western diet that is blamed for obesity) and sedentary lifestyle. Insulin resistance affects children of ALL SIZES, not just fat kids.

The reason is that insulin resistance affects us all differently, based on our genetic makeup. Some people gain weight due to insulin resistance, while others develop type 2 diabetes without weight gain. Still others can experience high blood pressure or high cholesterol. And the unluckiest among us can develop all of these symptoms and more.

But obesity is just that: a possible symptom. Not all obese people are insulin resistant. Nearly 75% of obese people will never be diabetic. And using BMI to gauge a person’s health is essentially useless. A better, but more invasive, measurement is body fat percentage (%BF), but even using those metrics, body fat only correlates with insulin resistance half the time, according to one of the few studies on pediatric body fat and insulin resistance (PDF):

Based on these results it could be concluded that adiposity accounts for 55% of the variability in insulin sensitivity in normal children. Previous studies in pediatrics have used body mass index… However, BMI is not a sensitive indicator of body composition, especially during puberty. In our study the correlation between BMI and %BF is only 0.

Thin kids who are sedentary and eat too much energy-dense food are just as much at risk for insulin resistance, and its many consequences, as fat kids who are sedentary and eat too much energy-dense food. So, a campaign that focuses on obesity, rather than lifestyle choices, will give those thin, sedentary kids a free pass, potentially setting them up for a lifetime of complacency-related health problems.

The perfect model for this kind of lifestyle-based approach to healthcare is outlined in nutritionist Ellyn Satter’s “Your Child’s Weight: Helping Without Harming.” Ms. Satter provides additional research on how our weight-loss focused approach to health may contribute to the very problem that Strong4Life is trying to prevent: obesity.

Satter’s approach teaches parents how to help their children learn to normalize their relationship with food through what is essentially HAES for kids. Satter provides multiple examples of extremely large children (some in the 400 to 500 pound range) who she has helped to normalize their relationship with food through nutrition, and emotional, counseling, which subsequently led to weight loss.

If your child makes lifestyle changes, he or she may lose weight, but that isn’t the goal. The goal is health, and weight loss may, or may not, be a consequence.

But regardless, Satter’s approach is infinitely more compassionate and sustainable than Strong4Life’s approach, which in the case of a 500 pound 16-year-old resulted in gastric sleeving:

Why not explore these non-surgical, non-weight-loss-centered approaches? Why not focus on giving parents the tools and resources they need to make healthy choices for their family?

This post did not even touch on the social determinants of health, a globally-recognized (except in the United States) contributor to metabolic disorders, which I did not even touch on. But this graphic of the US Toil Index (which charts how hard families have to work to make the house payment), gives a taste of what parents have been facing since the 1970s, when obesity rates began to climb:

Elizabeth Warren’s “The Two-Income Trap” also outlines how time and money have become precious resources, which has created the vacuum for energy-dense convenience foods to take a load off an already stressed population.

I could write about that extensively, but I’ll save that for another 2,500-word diatribe.

The point I’ve been trying to make is that childhood obesity is not the problem; our lifestyle choices, as well as our ability to choose healthy lifestyle choices without dying from stress, is the problem. Fat kids are not the problem; sedentary lifestyles and energy-dense foods are the problem.

In attempting to “cure” one of the symptoms of insulin resistance, Strong4Life has essentially waged a health campaign that would, in analogical terms, be like fighting the scourge of tobacco use by waging a War on Yellow Teeth, when, in some cases, yellow teeth can be a completely normal genetic inheritance. Posting billboards of people with yellow teeth unfairly suggests that all people with yellow teeth are smokers.

Likewise, preaching against fat people as the “problem” that needs fixing will necessarily target fat people who eat healthy but are genetically predisposed to being fat. And for those genetics deniers, we are only now scratching the surface of genetic obesity and learning that there are hundreds, if not thousands, of genetic contributors to a person’s body weight.

So, stop focusing on fat kids. Stop focusing on fat. Promote healthy lifestyles for PEOPLE OF ALL SIZES and we maybe we can start addressing the real health problems that this country faces.

And if you agree, then keep contacting CHOA and the Surgeon General’s office. I have put all of the relevant contact information on the side of the site where it will stay.

Next week we will begin focusing on CHOA’s many corporate sponsors, as well as targeting other healthcare professionals to speak out against this heartless shame campaign. We will not stop until every last Strong4Life billboard comes down and every television commercial ends.

*There is an exception to the childhood obesity plateau. Boys between the ages of 6 and 19 (~15% of the male population), who were in the 97th percentile, did experience an increase. This is a relatively small portion of the population and the increase was described as “a slight but statistically significant increase in obesity.”
**Weight cycling is defined in various ways by various researchers in terms of how much weight loss and how many times is considered “moderate” or “severe” weight cycling. Generally speaking, a weight loss and regain of approximately 20 pounds in adults is considered one weight cycle, no matter how long that 20 pound loss is maintained. Most research seems to suggest that three or more of these cycles is the definition of “severe.” You must read each study to know exactly what is being defined.

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10 Comments leave one →
  1. January 13, 2012 1:01 pm

    Wow — I think you just wrote the outline for a really great book. Maybe a follow-up to Campos: “The Childhood Obesity Myth”

    • January 13, 2012 1:34 pm

      Thank you, Pattie. I really wanted to talk about the social determinants at length, but I got caught up in the red herring of childhood obesity. But, really, the social determinants is an even more important conversation we should be having.

      Peace,
      Shannon

      • January 13, 2012 2:32 pm

        WRITE THAT BOOK, ASAP.

        Not a request. Not even joking. Get going, Shannon. We’ll hold the fort while you hunker down and get to work.

        • January 13, 2012 2:34 pm

          Thanks Jen. I actually have finished two chapters and have been editing on the train. After I finish this I’m going to start looking for representation. We’ll see what happens. 🙂

          Peace,
          Shannon

  2. vesta44 permalink
    January 13, 2012 2:00 pm

    Did you see this article in the news about the 21-hour work week? I’m thinking this would be a huge contribution to the social determinants of ending this so-called “crisis” – cut down the hours for people who are over-worked and don’t have time to spend with their families and cook meals, and give hours to people who need jobs so they can feed their families and put roofs over their heads. It’s a huge sea change, but I think it’s one that’s needed if people are going to have happy, stress-free lives.

    • January 13, 2012 2:22 pm

      I heard a fascinating interview with the authors of that study on the BBC World News the other night, and meant to mention it in the post I meant to write on the social determinants of health. I wish I had a clip of it because it was that study author versus some capitalist douchebag who whined his opinion the entire time.

      Of course, this could lead to European-style socialism. *GASP*

      Peace,
      Shannon

  3. January 20, 2012 5:22 pm

    I think stress is raising all the obesity levels, cortisol etc.

    Far more then food.

    And STRESS is part of the insulin resistance picture. If you learn about Cushings and Pseudo Cushings, that is a part of the health puzzle being ignored here too in why everyone is gaining so much. Please read. STRESS is a BIG PART OF THIS PUZZLE…

    http://fivehundredpoundpeeps.blogspot.com/2010/08/is-stress-making-everyone-fat.html

    I am old enough to remember life 30 years back and life was far more carefree.

    I do think that people are getting fatter, I am not sure whether to call it an epidemic. I have weighed over 450lbs on up since 1998, and can tell you for a fact I see far more people in my weight category then I used to. We are rarer then the norm of course but I see more people in my boat then ever before.

    • January 20, 2012 9:37 pm

      500pp,
      Obesity rates in general have leveled off (the newest NHANES just came out too), but the greatest shift, percentage-wise (though the numbers are still around 0.42% of the population) has been in the number of people with a BMI over 50. I wonder if what you’re noticing is people of your size who are feeling more comfortable going out in public since there’s an “epidemic” and they aren’t the only ones, ya know?

      But I definitely agree that stress is a seriously ignored component of metabolic disorders, even though the research on the relationship between stress and metabolic disorders is widespread. They choose to ignore it.

      Peace,
      Shannon

  4. Robert Wright permalink
    March 19, 2012 1:30 pm

    You state that “energy dense foods” may be the cause of insulin resistance. A lot of current research has found that it may simply be refined carbohydrates (starchy foods, white flour foods, and sugars) that are the cause of insulin resistance, not simply energy dense foods. The most energy dense nutrient, fat (9 calories/gram versus 4 for carb and protein) appears to be protective against metabolic syndrome, at least in randomized controlled trials comparing a low-carb, high fat (ab libitum=eat as much as you want) diet to a low-fat, calorie-restricted diet (the traditional fail diet that’s been advocated for 40 years to curb obesity and CHD but may have caused both).

    See references below:

    Dyson PA, et al.(Dec. 2007). “A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic and non-diabetic subjects.” Diabetic Medicine;24(12). Pgs. 1430-5. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/17971178 .

    Krebs NF, et al. (August, 2010). “Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese Adolescents.” Journal of Pediatrics Vol. 157, pgs. 252-8. Retrieved from: http://www.jpeds.com/article/S0022-3476(10)00120-4/abstract .

    Brehm BJ, et al. (2003). “A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women. The Journal of Clinical Endocrinology and Metabolism , Vol. 88, pgs.1617–1623. Retrieved from: http://jcem.endojournals.org/content/88/4/1617.long.

    Samaha FF, et al. (2003). “A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity.” The New England Journal of Medicine, Vol. 348, pgs. 2074–81. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa022637.

    Sondike SB, et al. (March 2003). “Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents.” The Journal of Pediatrics. Vol. 142(3), pgs. 253–8. Retrieved from: http://www.jpeds.com/article/S0022-3476(02)40206-5/abstract.

    Aude YW, et al. (2004). “The National Cholesterol Education Program Diet vs a Diet Lower in Carbohydrates and Higher in Protein and Monounsaturated Fat. A Randomized Trial.” Archives of Internal Medicine, Pgs. 164:2141–2146. Retrieved from: http://archinte.ama-assn.org/cgi/content/full/164/19/2141.

    Volek JS, et al. (2004). “Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women.” Nutrition & Metabolism, Vol. 1, pg. 13. Retrieved from: http://www.nutritionandmetabolism.com/content/1/1/13.

    Yancy WS Jr, et al. (2004). “A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia. A Randomized, Controlled Trial.” Archives of Internal Medicine, pgs. 140:769–777. Retrieved from: http://www.annals.org/content/140/10/769.long

    Nichols-Richardsson SM, et al. “Perceived Hunger Is Lower and Weight Loss Is Greater in Overweight Premenopausal Women Consuming a Low-Carbohydrate/High- Protein vs High-Carbohydrate/Low-Fat Diet.” Journal of the American Dietetic Association, Vol. 105, pgs. 1433–1437. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed?term=Perceived%20Hunger%20Is%20Lower%20and%20Weight%20Loss%20Is%20Greater%20in%20Overweight%20Premenopausal

    Gardner CD, et al. (2007). “Comparison of the Atkins, Zone, Ornish, and learn Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The a to z Weight Loss Study: A Randomized Trial.” Journal of the American Medical Association, Vol. 297, pgs. 969–977. Retrieved from: http://jama.ama-assn.org/content/297/9/969.long

    Shai I, et al. (2008). “Weight loss with a low-carbohydrate, mediterranean, or low-fat diet.” The New England Journal of Medicine, Vol. 359(3), pgs. 229–41. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa0708681.

    Summer SS, et al. (Mar 31, 2011). “Adiponectin Changes in Relation to the Macronutrient Composition of a Weight-Loss Diet.” Obesity (Silver Spring). [Epub ahead of print] Retrieved from: http://www.nature.com/oby/journal/v19/n11/full/oby201160a.html.

    Daly ME, et al. (Jan 23, 2006). “Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes–a randomized controlled trial.” Diabetic Medicine, Vol. 23(1), pgs. 15–20. Retrieved from: http://onlinelibrary.wiley.com/doi/10.1111/j.1464-5491.2005.01760.x/abstract;jsessionid=F2FCA81A7A0BD31D425BCDD7291C4D9E.d03t01?systemMessage=Wiley+Online+Library+will+be+disrupted+2+July+from+10-12+BST+for+monthly+maintenance.

    Westman EC, et al. (2008). “The effect of a low-carbohydrate, ketogenic diet versus a low- glycemic index diet on glycemic control in type 2 diabetes mellitus.” Nutritional Metabolism (Lond.), Vol. 19, pgs. 5-36. Retrieved from: http://www.nutritionandmetabolism.com/content/5/1/36.

    • March 19, 2012 3:15 pm

      Robert,
      Clearly you’re well-versed in low-carb ideology, and I’ve read quite a bit on the issue as well. I’ve read “Good Carbs, Bad Carbs” and quite a few studies of both low-fat and low-carb diets, and I am not convinced that either approach is the silver bullet we’re looking for in terms of insulin resistance or obesity. Long-term studies show that adherence to either a low-fat or low-carb lifestyle does not lead to significant weight loss (for example, this study you cited), nor do long-term studies suggest that low-carb or low-fat improves insulin resistance in the short-term, but in the long-term it does not.

      Personally, I don’t believe it’s either carbs or fat, but overall dietary quality. I’m not about to recommend the low-carb lifestyle because I have read some disturbing studies on the effects LC has on flow-mediated vasodilation, an indicator of cardiovascular damage. There simply isn’t enough evidence out there to support LC (or LF for that matter) as a healthy diet. As such, I’m not going to tell people that fat and protein are harmless in the quantities that LC advocates.

      If you want to talk strictly research, then vegetarian diets fare the best in terms of long-term health. But we have to find a middle ground because most people are not capable of, let alone interested in, the vegetarian lifestyle.

      Only two of the studies you’ve listed were for longer than 1 year, and both found comparable weight loss between LF (or Mediterranean) and LC, and neither result was impressive. I’m not looking for short-term fixes for insulin resistance, but real, sustainable results.

      Peace,
      Shannon

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