Notice I selected a picture of an obese person that didn't involve inaccurate stereotypes of them eating crappy food or being lazy.

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Over the past year or so a few fitness professionals (many of whom I respect) have written blog posts on how to train people with obesity.  As someone who is very familiar with this area, I figured I’d chime in with my own thoughts to add to the discussion and information about training this specific population for those who are interested in my take on the subject.

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As some of my readers know, I do some work for one of the very few government funded bariatric medical programs in my province providing evidence based (i.e., research backed) treatment for patients with obesity.  In our clinic we see hundreds of patients per year with weights ranging from 250 to 700 pounds.  My main role is to oversee the design and implementation of the exercise component of the program to get everyone exercising regardless of their physical, emotional, psychological, and economic limitations.  Combining that with my ongoing experience in the private sector in training people for fat loss (both online and in person), I feel that I’m in a good place to share my views on the topic.

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Definitions, Categorization, Etc.

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Before we can really talk about obesity though, we’ll need to clear up some definitions and lay down a foundation of understanding about how it is categorized.

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In short, obesity is defined and categorized primarily based on something called the Body Mass Index (BMI) which is essentially a height-weight scale.  In a publication in the early 1970′s it  scale was created as a proxy to determine body fatness in relation to height and weight, but more recent evidence suggests that this isn’t exactly true.  I’ll get into that in a bit, but for now you should know that BMI is the most widely used tool for the categorization of obesity in a medical setting.

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If you want to determine your BMI you can go HERE and use the calculator to let you know where you’re at.

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Categorization Based on BMI

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Under 18.5  -  Underweight

18.5 – 25  – Normal Weight

25 – 30  -  Overweight

30 – 35  -  Class I Obesity

35 – 40  -  Class II Obesity

Over 40  -  Class III Obesity

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Although this is the accepted World Health Organization categorization for obesity, it is pretty arbitrary and the divisions between most of the categories have no scientific explanation.  And since their are regional differences in “normal” body weights,  some places have different categorizations for obesity.  For example, the Japanese categorize anyone with a BMI of 23 as overweight and anyone with a BMI of 25 as obese.

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Of course, any astute fitness minded person will also note that BMI is limited in that it is not able to determine actual muscle and fat weight so someone who works out regularly and has a higher muscle mass might be categorized as obese while actually being quite lean.  In fact, the reverse can actually true as well which means that people with a “normal” body weight might actually carry an excess amount of body fat.  These are the people that we might call ”skinny-fat”, but are clinically defined as having normal weight obesity.

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Although I’m not sure this is universally agreed upon, having a body fat above 20% for males and 30% for females would make you obese regardless of your BMI.  And all of this leaves out the fact that where that fat is distributed may have an effect on cardiac health (i.e., fat around the waist = bad, fat around the hips = good) so you may be in danger regardless of whether or not you actually have a lot of fat.

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The Staging System

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So thus far we’ve talked about categorization of obesity based on weight and to some degree we’ve talked about body fat percentage without mentioning the methods used to measure body fat which is a different post entirely (Short version: Your home bathroom scale that measures body fat probably sucks).  However, to train people with obesity it is important not to just know how much they weigh, but the degree to which obesity is actually impacting their health, movement, etc.  To determine this it is helpful to determine the “stage” of obesity using something called the Edmonton Obesity Staging System (EOSS).  While I could type it all out for you, I’ll just swipe it from the site of Dr. Arya Sharma who is one of the creators of the system.

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STAGE 0: Patient has no apparent obesity-related risk factors (e.g., blood pressure, serum lipids, fasting glucose, etc. within normal range), no physical symptoms, no psychopathology, no functional limitations and/or impairment of well being.

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STAGE 1: Patient has obesity-related subclinical risk factor(s) (e.g., borderline hypertension, impaired fasting glucose, elevated liver enzymes, etc.), mild physical symptoms (e.g., dyspnea on moderate exertion, occasional aches and pains, fatigue, etc.), mild psychopathology, mild functional limitations and/or mild impairment of well being.

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STAGE 2: Patient has established obesity-related chronic disease(s) (e.g., hypertension, type 2 diabetes, sleep apnea, osteoarthritis, reflux disease, polycystic ovary syndrome, anxiety disorder, etc.), moderate limitations in activities of daily living and/or well being.

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STAGE 3: Patient has established end-organ damage such as myocardial infarction, heart failure, diabetic complications, incapacitating osteoarthritis, significant psychopathology, significant functional limitation(s) and/or impairment of well being.

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STAGE 4: Patient has severe (potentially end-stage) disability/ies from obesity-related chronic diseases, severe disabling psychopathology, severe functional limitation(s) and/or severe impairment of well being.

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Looking at the list above, you might discover that as a client you have a person who is actually has Class III obesity, but is a stage zero and has no related health or mobility problems.  This could be a guy who was a lineman on his college football team, maybe he’s actually still fairly active, and he’s not sick.  This guy might thrive with hard training and a slowly integrated nutritional program.

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Training this guy might be different than working with someone with class I obesity that is a stage 3 and has disabling arthritis making it difficult to move let alone hit up some heavy squats.  This person would obviously require a drastically different program which is why I get worried when I see generalized recommendations for training obese folks.

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And if YOU are an “offseason” bodybuilder or you just train regularly and don’t have a solid nutrition program you might have gotten off easy before with the old mantra that “BMI doesn’t take into account my muscle mass so I’m not really obese”, but now you know that if your body fat is breaking 20% (or 30% for women) you ARE obese.  And you might actually be a class 1 or 2 on the staging system too.  You know that heartburn you’ve been getting and the slightly elevated blood pressure that you’re not paying attention to?  Those are potentially obesity related issues.

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So if you wonder why I spend so much time talking about obesity on my blog it isn’t because I’m talking about someone who is vastly overweight.  In my experience, most people who see themselves as having “only a few extra pounds” are actually clinically obese…and this includes those who exercise regularly and even fitness professionals themselves (we are not immune).

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Now that we’ve covered the basics and some definitions, in my next couple posts I’ll come back and drop some information about how I would go about training someone with different classes and stages of obesity.

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Check out Part II of the series HERE.

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PS:  If this post helped you or you think it would benefit others please share it.

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PPS:  Please feel free to join me on Facebook and Twitter.

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A while back I was very fortunate to connect with a very bright guy named Chi Chiu and recently began having a discussion with him about Gary Taubes new book Why We Get Fat.  I meant to get around to purchasing and reviewing the book myself, but given Chi’s passion for the topic (and the fact that he’s an evidence based uber genius) I asked him to do a guest blog about it.  I have to say…he certainly didn’t disappoint.  If you’re thinking about purchasing or have already read Why We Get Fat, you need to read this!

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Take it away Chi!

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This is not your typical review, because at the time of writing it, I do not own the book nor have I read it. It would have been easy for me to simply buy the book, read it, and write you a review, but I chose not to. Instead I’ll let Gary Taubes himself, try to convince me, to buy his book.

Gary Who?

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Gary Taubes is a science writer who has a Masters in applied physics and one in journalism. He has written numerous articles, but became an overnight sensation with the most controversial article of 2002 in the New York Times, ‘What If It’s All a Big Fat Lie” in which the role of (saturated) fat as a cause of cardiovascular disease was questioned. A bestseller “Good Calories, Bad Calories” followed. Taubes has won several awards during his career and recently he published “Why We Get Fat and What to Do About It.”

Where to start?

Most coaches get annoyed when they get advice from people who have no real world experience. I don’t care that Gary Taubes is a writer-only, and is not in the trenches with us. I’ll judge him solely on the information he provides.  He recently started a new blog to promote his book and there are numerous podcasts and YouTube interviews available, so you can get a general sense of what the major concepts in his book are and whether it is worth spending your hard-earned money on.

My first impression of Taubes is that of a reasonable man, posing reasonable questions.  He does not defy the energy balance and he seems to be genuinely annoyed by the failure of the widely promoted low-fat dogma combined with exercise approach to combat obesity. So let’s see what else he’s got to say.
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The Significant 20 kcal

His first post on his blog is about the significant 20 kcal per day. It’s a thought experiment on how eating one or two bites (20 kcal) too many can lead to 2 pounds of excess fat a year and 40 pounds in a period of 20 years (365 x 20 kcal x 20 years / 3500). So when you overshoot only 1 energy percent of your energy requirement, obesity will be inevitable.

With only such a small margin, it would be impossible to maintain a stable weight for longer periods. He argues that the body does not have such an accurate bookkeeping system and that therefore the laws of thermodynamics, while true, cannot explain why we do or do not get fat.

The 20 kcal per day thought experiment is actually a classic one, with many variations found in textbooks. He uses it to ridicule the counting calories approach as a means to maintain or lose weight. In a podcast Taubes jokes that the laws of physics only make sense, when you apply math skills of an eighth grader. And although it’s amusing, that doesn’t necessarily make it true.

Whether the body has an accurate enough bookkeeping system or not, is actually irrelevant. Thermodynamics controls this process all by itself, because weight change is self-limiting. Those extra two bites lead to more mass, which needs to be maintained and carried around. This comes at an energy expense and quickly leads to energy equilibrium. The other way around is that losing weight will lead to less mass and lower resting metabolism. These natural restrictions create a bandwidth and explain perfectly why a set point can be reached without high precision bookkeeping (Katan MB 2010).

This is a well-known fact and physiologists have developed mathematical models that accurately predict the required energy surplus to gain a certain amount of mass during a specific period. According to one of those models, a woman in her twenties with a BMI of 23 needs an excess of 370 kcal per day to get to a BMI of 29 in a period of 30 years (Katan MB 2010), a far cry from the 20 kcal Taubes suggests. 

In the same post he devotes at least a dozen paragraphs on why thermodynamics does not explain why we get fat, while ridiculing experts in the process. He uses a restaurant analogy to show that the laws of physics will only tell you that a restaurant is crowded because more people went in then there went out.

Well, the restaurant analogy therefore tells you quite accurately why people get fat and even what to do. Hire a door bitch!

[Note from Mark : A door bitch is a person who stands outside of a bar or club alongside the bouncers and chooses which people beautiful people to let in and which to keep out.  Don’t worry…I had to look it up too]

Of course it doesn’t tell you why people want to get into the restaurant in the first place and he ridicules the experts for not knowing the answer. In my experience, authorities that tell you that they do not know the answer are usually the real experts. Unlike the dime a dozen wannabe gurus whom seem to have all the answers. Taubes also claims to have the answer which I will cover in the next section.

Although the laws of thermodynamics don’t tell you the complete story, they give you the boundaries. You cannot create something (mass) from nothing and the calories in / calories out concept is therefore not useless. After reading this post I was wondering whether this was representative for his book. The fact that he mentions that there is a whole chapter on the significant 20 kcal per day, suggests that the book must be filled with incorrect assumptions and useless over bloated analogies.

Why Diets Work, When They Do

While I found the first post somewhat amusing, the second blog post made me wonder whether I was actually wasting my time. The main concept of his post boils down to the following assumptions. 

1. Carbs are bad and make you fat

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2. Restricting calories is restricting carbs

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3. Weight loss through calorie restriction is carb restriction and any weight loss success may therefore be solely attributed to carb restriction. 

He covers a couple diet intervention studies and accuses the authors for not controlling the relevant variables, because they only control calories instead of carbs. The authors of the study actually only set out to control one single variable and that’s (the adherence to) the diet. Nothing wrong with that and for the most part they succeeded nicely. Adherence to the diet is the deciding factor, because it simply makes you eat less.

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Taubes then goes on that the hypothesis of carb restriction as a causal factor for weight loss, has never been tested and that therefore all results of the covered studies are unreliable. He needs more than 3800 words for this rant and fails to mention one of dozens metabolic ward studies (Grey N 1971, Kinsell LW 1964, Krehl WA 1976) that already refuted his unfounded assumption. No significant difference in weight loss has ever been established in studies designed to compare a low-carb with isocaloric high carb diet. The authors of the covered studies did not control the carb variable, because they already knew that particular answer. It would have been as useful as testing whether hot water is indeed warmer than cold water.

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Taubes articles and the increasingly popular paleo diet have fuelled the low-carb interest. They seem to inspire each other and Taubes does mention hunter-gatherer tribes more than once in his interviews. The general idea seems to be that hunter-gatherers eat low-carb.

Taubes mentions in a PODcast that Eskimo’s don’t eat carbs at all, while demonstrating great athleticism. This is a common misconception. I actually own a ‘carbs gone wild’ edition of an Inuit cookbook with no less than 240 pages exclusively with plant based recipes. That’s a whole lot of pages for a non-carb population. It comes as no surprise, that a study found that the Inuit actually have a daily carb intake of 127 grams  (Bang HO 1980). Taubes was of 20 times with the calories in/calories out calculation, but with the Eskimo’s he manages to miss the mark by 127 times. The 127 gram carbs may still be considered low-carb, but the Inuit are not living fossils nor are they representative for all hunter-gatherer tribes. The dietary pattern of the Kitava Indians for example, consists of around 70% carbs and yet obesity, diabetes, heart-disease and exercise for that matter, are non-existent in that tribe (Lindeberg S 1994). Paleo is not low-carb per se and carbs are not the causal factor for all western diseases.

It’s All Insulin, Bro!

In his third blog Taubes cites a couple of biochemistry books. The basic premise boils down to the following.

1. Insulin stimulates fat cells to accumulate fat while inhibiting fat mobilization

2. Chronic high insulin levels lead to insulin resistance and less uptake by the muscles and more uptake by the fat cells

3. Carbs lead to a high insulin response, which leads to B, which leads to A, which leads to why we get fat

He then goes to say that this insulin resistance is the underlying defect of obesity, diabetes and heart disease. Notice that he states ‘the’, not one of them or a risk factor, but the defect. He also states ‘underlying’, not contributing, not shared, not correlated, but he suggests it’s the causal factor. We get fat because we become insulin resistant, seems to be his main message.

This does not explain why more than 25 percent of obese persons are not insulin resistant (Stefan N 2008, Wildman RP 2008). The statement that it is the underlying defect, is at least an exaggeration, but that does not mean that insulin resistance may not be one of the causal factors.

Taubes mentions a lot of rodent studies, because human studies on the subject do not exist, for good reasons. To study it, you need to shut down the insulin receptors, but then you’ll die within days, which is an inconvenience. The fact that there is not enough time to get you obese, is of course the major obstacle. The next best thing is to shut down the liver insulin receptors and that’s what researchers have done with the so-called “knock-out mice”.

Having no receptors will of course lead to 100% local insulin resistance, which progressed into systemic insulin resistance with these mice. This was an interesting finding, but even more interesting was the fact that the mice did not get obese (Cohen SE 2007, Michaels MD 2000). So the little evidence that actually exists on the topic, suggests that insulin resistance is not the causal factor of obesity. 

If the insulin hypothesis is the heart of his book, it’s flawed. Not to mention all the nitpicking I can do on the claims he makes on insulin physiology, but it would take multiple posts to debunk all of them, like carbs being the sole driver of insulin response or his rather incomplete picture on how fats get stored and oxidized, etc. I can only add that I find it shocking, how many of his ideas seem to be based on conflicted or even refuted theories.

Saturated Fat, Can You Handle Me Baby?

The last part of his third blog post and the main topic on his fourth is the diet-heart hypothesis. He refutes the idea that saturated fat (SFA) causes heart disease and I have to agree with him. A recent review (Mozaffarian D 2010) containing intervention studies, suggests that saturated fat increases coronary events, but they were mostly JADAD level 2 studies. In other words they were poorly controlled. If you have no idea what that means, may I suggest purchasing Mark’s product How to Read Fitness Research.

In the same year another publication (Ramsden CE 2010) showed no causal relation between SFA intake and coronary incidents. The authors were rigorous in obtaining missing data and shed new light on well-known studies. They also suggest that coronary incidents increase when you replace SFA with omega-6 oil. A practice that is actively promoted for deep frying and may get people killed.

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An invitation-only symposium last year in Denmark, lead to a recent consensus statement  (Astrup A 2011) shedding even more doubt on the contributing role of SFA in coronary disease. Even Dr. Daniel Steinberg, a world-renowned cholesterol specialist with over 400 published articles, states in his book that he does not support the diet-heart connection.

What to Do About It…according to Taubes

The subtitle of Taubes book is ‘What to do about it’ and that seems obvious. Stay off the carbs, don’t worry about the increase of dietary fat and the obesity epidemic will soon be over.

I counsel ‘how to lose the love handles’ clients, elite athletes, and bodybuilders (two of whom happen to be national champions) so I know a thing or two about weight loss. I have been involved in various nationwide multicenter lifestyle programs for obesity, diabetes, COPD, pregnancy, kids, low back pain, and RSI.

In most cases I co-developed the programs with experts, trained the practitioners and collected the data. In a 2-year multicenter (n=80) obesity program I’ve seen the results of thousands of obesity clients. I’ve seen the effect on weight, on physical, emotional and social functioning. I’ve seen the joy, the pain, the envy, the relapses and the recoveries. I’ve collected data through SF-12 surveys, the MHI-5, diaries, HRV measurements, weight scales and other health related tools. So, I know a thing or two about obesity.

I was shocked by the McKinsey report (2011) on the ‘real’ cost of obesity, which estimates a stellar sum of 450 billion dollar annually in the US alone. I find that hard to believe, because I found the report very limited. We have no idea what causes the obesity epidemic or whether it’s even bad for your health. There is no mention of the obesity paradox, a phenomenon where obese people are healthier and live longer than their slimmer counterparts.

So what about the unnecessary costs of overtreatment of obesity? No mention of confounding variables either. Most studies are from the United States, where the income gaps are huge. We know that low income is correlated with obesity, but most studies have not corrected the relationship of social economic status (SES) on disease endpoints. This is not a minor issue, knowing that in the US around 50 million (!) people lack health insurance (during any period of time).

So do poor obese people die from fat accumulation or from insufficient, but unrelated treatment? Or do poor obese people eat more cheap calorie dense food, deep fried in so-called heart-healthy omega-6 oil, which may get them fat and killed at the same time?

We also know stress kills and obese people have a lot to stress about like negative self-image issues, ridiculing, and even discrimination. On top of that, most of them weight cycle their whole lives, adding more to the stress, while increasing inflammation, which seems to be an integral part of weight cycling.

So what is it, that makes the obese sick? Is it fat accumulation, is it excess omega-6, is it lack of health-insurance, is it a negative self-image, an increase of inflammation, discrimination and therefore the McKinsey report itself? The interventions to heal the obese may actually contribute to the sickness, the increased mortality and therefore to the cost of obesity.

Obesity is not a simple problem that can be solved by buying a book, based on some serious flawed theories. If you think you are actually helping your obese clients with a low-carb diet and high intensity interval training, you may in fact have shortened their lives by a couple of years. Working with the obese requires specific knowledge and commitment, so if your program is an overweight XXL version of the program you have for your non-obese clients, please quit and give your clients a refund!

Not Your 23 Dollar Bill

From a hypothesis point of view, I’ve seen nothing novel in Taubes vision in Why We Get Fat. fat. Anyone who has some notion on alternative nutritional views will notice the familiar concepts. And of course some of it has merit, but some of it is out of context or even downright wrong.

If you already bought the book, or were sold on the concept, don’t feel bad about it. It’s like accepting counterfeit money. Nobody will blame you for it. It’s not like you accepted a 23 dollar bill and Taubes book is not as obvious as a 23 dollar bill. It looks like real money, it feels real money. it may even smell like real money, but that doesn’t make it real.

Then there is the ethical question. If it can pass for real, because people do tend to lose weight when following a low carb diet, what would be the harm in embracing the book? The same holds true for counterfeit money. If it looks real and you can pay with it, why should you stop using it?

There are actual several reasons. First of all is that someone gets hurt further down the line, because it will come out eventually. This will reflect badly upon you, which is of course your problem. But mind that it will reflect badly on our profession as well, which concerns us all.

The second reason is that we make progress, because we have rational in-depth theories that we turn into great experiments with outcomes we learn from.  Storytelling without conclusive evidence however, has kept us in the dark ages for centuries.

Do you really want to return to medieval ages where science had no place and babies died for what we now consider trivial reasons? I don’t think so!

Conclusion

Believing is accepting without proof, which is not a bad thing by itself, if you’re open to non-supporting evidence. Taubes selective citations and inappropriate examples suggest that he is more than just a believer, he seems to be a radicalist, ridiculing anyone opposing him. Judging Taubes own blog posts and interviews, I can only conclude that his book is unreliable. It’s not all bad, but if you cannot separate the good from the bad information, it will make you unreliable.

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The many flaws in his hypothesis make it impossible to answer the question of why we get fat. The subtitle ‘and what to do about it’ offers no real solution and does not take into account the complexity of (treating) obesity. This is the reason why I did not buy this book and will not recommend it to anyone else.

References

• Astrup A (2011), Dyerberg J, Elwood P, Hermansen K, Hu FB, Jakobsen MU, Kok FJ, Krauss RM, Lecerf JM, Legrand P, Nestel P, Risérus U, Sanders T, Sinclair A, Stender S, Tholstrup T, Willett WC. The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010? Am J Clin Nutr. 2011 Apr;93(4):684-8. Epub 2011 Jan 26.
• Bang HO (1980), Dyerberg J, Sinclair HM. The composition of the Eskimo food in north western Greenland. Am J Clin Nutr. 1980 Dec;33(12):2657-61.
• Cohen SE (2007), Kokkotou E, Biddinger SB, Kondo T, Gebhardt R, Kratzsch J, Mantzoros CS, Kahn CR. High circulating leptin receptors with normal leptin sensitivity in liver-specific insulin receptor knock-out (LIRKO) mice. J Biol Chem. 2007 Aug 10;282(32):23672-8. Epub 2007 Jun 7.
• Grey N (1971), Kipnis DM. Effect of diet composition on the hyperinsulinemia of obesity. New England Journal of Medicine, Oct 7, 1971; 285 (15): 827-831.
• Katan MB (2010), Ludwig DS. Extra Calories Cause Weight Gain — But How Much? JAMA, January 6, 2010—Vol 303, No. 1
• Kinsell LW, et al. Calories do count. Metabolism, Mar, 1964; 13: 195-204.
• Krehl WA (1967), et al. Some Metabolic Changes Induced by Low Carbohydrate Diets. American Journal of Clinical Nutrition, Feb, 1967; 20: 139-148
• Lindeberg S (1994), Nilsson-Ehle P, Terént A, Vessby B, Scherstén B. Cardiovascular risk factors in a Melanesian population apparently free from stroke and ischaemic heart disease: the Kitava study. J Intern Med. 1994 Sep;236(3):331-40.
• McKinsey Quarterly (2011) The real cost of obesity, January 2011
• Michael MD (2000), Kulkarni RN, Postic C, Previs SF, Shulman GI, Magnuson MA, Kahn CR. Loss of insulin signaling in hepatocytes leads to severe insulin resistance and progressive hepatic dysfunction. Mol Cell. 2000 Jul;6(1):87-97.
• Mozaffarian D (2010), Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010 Mar 23;7(3):e1000252.
• Ramsden CE (2010), Hibbelna JR, Majchrzaka SF, Davisa JM. N-6 Fatty acid-specific and mixed polyunsaturate dietary interventions have different effects on CHD risk: a meta-analysis of randomised controlled trials. British Journal of Nutrition (2010), 104: 1586-1600
• Taubes G Blog post 1 to 4 on www.garytaubes.com

Chi L. Chiu has a master’s degree in nutrition, one in health sciences and is currently a grad student psychology. He is the owner of Chivo personal training, Chivo physical therapy, Chivo sports performance and Chivo Continuous Professional Development center for lifestyle professionals. He is a member on various government en non-government funded advisory boards and works with clients on a daily basis.

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PS: Leave a comment below and let me know what you think.  Agree?  Disagree?

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PPS: No…he doesn’t have a blog.  I’m trying to push him into it…trust me.

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I figured I’d start out today with a quote from Dr. Arya Sharma’s because I think everyone trying to lose weight or help others lose weight should be reading his blog.

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“Public health discussion on preventing obesity that focus on eating less and moving more may do little more than perpetuate the already widespread stereotype that people, who are obese, carry that excess weight simply because they eat too much and don’t exercise enough.

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This is not a ‘healthy’ public discussion to have – as it calls on governments to intensify the ‘blame and shame’ game (adding a punitive touch when it comes to taxing and banning) rather than addressing the real underlying problems, which is that as a society we no longer have time to eat, have jobs that force us into sedentariness, make unhealthy food cheaper than healthy options, build cities that discourage active transportation, and create a latch-key generation of kids that cannot come home to a simple home-cooked meal eaten by the whole family seated at the table (with the television off).”

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I can’t even tell you how much I agree with that a statement.  If you are a fitness professional yourself, you need to think about how this statement relates to your practice and even your thoughts about weight management.

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And speaking about thoughts on weight management (see how I did that little seque there?) my question for all my readers who are fitness professionals is CAN WE HELP PEOPLE THAT WE ARE BIASED AGAINST?

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Despite trying to help people, many of us our equally as guilty of biases against people obesity as the general public (and even obese people themselves).  Today I thought it would be interesting to share a little resource I’ve discovered from the Yale Rudd Center to help you determine how weight bias is impacting YOUR beliefs. 

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You can check it out HERE.

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Simply fill out the ATOP (Attitudes Toward Obese Persons) and BAOP (Beliefs About Obese Persons) questionnaires and use the scoring sheets on the site to see how you did.  If you’ve got time, you can even do some of the other tests on the site.

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I think you might be surprised to find out what your real perceptions are.  I certainly was when I did these tests over two years ago and it changed my entire philosophy towards dealing with obese people for weight loss.  In short, I think helping people with weight loss first starts with the perceptions of those in a position to help.  If you think it is all their fault and are playing the blame game like everyone else, do you think they’re really going to listen?

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Take the tests and let me know how you make out in the comments below.

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Today I want to switch gears and share a reader question that I’ve received and a snippet of my answer.  But first, a little background.

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Within the body there are two main types of adipose (fat) tissue.  White adipose tissue is probably what you’re most familiar with as this is what you’ll be spending most of your time and effort trying to lose when you’re on a fat loss plan.  Brown adipose tissue (BAT) or brown fat, on the other hand, is actually metabolically active fat and can contribute to thermogenisis and calorie burning due to the large number of mitochondria within the cells.  Some have actually proposed that new weight loss drugs will be able to target brown adipose tissue to increase calorie output and increase weight loss as a result.

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Which leads me to our reader question…

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I think it’s great that we find out as much about our physiology as possible, but then using this just to give fat people drugs to raise their BAT content, so they can eat as before or even more is quite perverse.  What about dieting?! This is a great dilemma of our society today.  Always trying to find the easy way out (i.e. pharmaceuticals) instead of just trying hard enough by dieting (and exercising).  What do you think about this?

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And my answer…

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In terms of obesity management, there are still many unknowns, but one thing we do know is that diet and exercise typically only prove useful in the short term as many people (over 95%) will regain some or all of the weight lost in the long term.  So just saying “exercise more and eat less” is not an effective strategy for weight management in this group.  They don’t fail because they don’t understand WHAT to do.  It is more about application.  Further, this underscores the need for a greater focus on the cognitive and behavioural strategies for weight loss which is the focus of much research and practice right now.

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However, we also know that previous anti-obesity drugs can not only help morbidly obese patients lose 5-10% of their body weight (not a lot, but the amount required to improve health markers dramatically) and keep it off with greater success.  In the wake of drugs like Merida being pulled from the market (due largely to use on contraindicated patients) and other drugs like Contrave and Qnexa getting rejected by the FDA, there is only one anti-obesity drug on the market right now.  That drug (called Xenical) is a fat blocker and it is not really well tolerated as it can lead to loose stools and a bad sneeze could totally ruin your day.

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How is it that we have drugs for Diabetes, depression, hypertension, anxiety, and almost any other problem under the sun, but we can’t treat obesity???  Isn’t this THE single biggest epidemic causing many of the conditions above?  (Hint: Part of the reason is weight bias and discrimination where we think obesity it solely the fault of the afflicted.  This stereotype needs to change.)

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Now I am not saying that we should medicate INSTEAD of behavioural treatment, dietary counselling, and exercise, but I think that medication in conjunction would go a long way to making weight loss more sustainable and improve the health of these people.  To take it further, the previous classes of drugs for obesity that act like stimulants will probably never survive the FDA panels.  New classes like GLP1 Agonists are coming, but drugs for BAT might just save lives.

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And I don’t think these should be for the general population who want to lose a few pounds, but I have no problem treating people for obesity with these drugs.  After all, the very best drugs have only resulted in just over 5% weight loss anyway.  While this is great for obesity treatment and health, most people wouldn’t even bother.

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Which, of course, leads to the question…if we can’t create drugs that safely produce more than 5% weight loss, what makes people think there are supplements that can do more?

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So that’s my perspective.  What do you think?  Agree?  Disagree?  Let me have it in the comments section below.

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Yesterday I posted a link to an article that talked about many of the psychosocial elements that play into the success or failure of a weight loss program with obese clients. 

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In the comments below, another Canadian fitness professional named Kyle Grieve asked what I think is a very important question:

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“For people in the fitness industry, how will we ever be able to treat the physiological, psychological, or sociological issues they have?  It’s way out of my scope of practice.”

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To me, rather than being a limitation, perhaps this is an opportunity for those fitness professionals working with obese clients to add another approach to their paradigm.  Many private fitness studios have physiotherapists and massage therapists to with with things that are beyond the scope of most strength coaches and trainers.  Why not add a social worker to the team and offer counselling as well?

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The studios that do this would invariably set themselves miles apart from those that don’t and, as I said before, I think this is going to be the future of weight management.  Dealing with client nutrition and training is going to be futile in the long run unless you deal with their barriers in the first place.

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From a business standpoint (because you can’t run a business without making money) it is another service that can be billed for.   Since group classes often work well in this regard, the cost to clients could be low and the facility owner could make a tidy profit.  This is a win for the client and the owner of the facility. 

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The other point to be taken home is that those not trained to deal with the psychosocial elements in weight management should step back and leave it to those who are or refer out for such counselling to run parallel to their training/nutrition efforts.  If a client got injured you’d refer out right?  Why not here?

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And finally, I’ll state again that I think that addressing barriers to fat loss should not only be limited to morbidly obese clients, but to anyone who needs a lifestyle change whether pursuing fat loss or muscle gain.  If you think about it, do your clients struggle because they don’t know what to eat or how to train (they should if they’re paying you) or is it because they’re “just not getting it done” for some reason?  If this is the case (and it will be for most people) then this is where extra attention needs to be spent.

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More time hammering home the importance of good nutrition and not missing workouts alone isn’t going to do the trick.  After all, if that worked the number of overweight people in North America wouldn’t be nearly so high would it?

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PS: Don’t forget to leave me a comments on THIS POST to score your free copy of Nick Tumminello’s Strength Training for Fat Loss DVD which I’ll do a draw for tomorrow morning.  Go get it!

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PPS: If this post strikes a chord with you, please consider sharing it.  This is most certainly a topic that I’m very passionate about.