Doogie Howser, M.D. —
Trigger warning for weight loss science talk.
Once again, a reply to a comment has become a post unto itself. This time, I’m responding to a certain Dr. Peter, who has posted comments here and here and here. Oh, and who could forget this fun chunk of condescension.
Seeing as how I’m still waiting for the “medical team” of Children’s Healthcare of Atlanta to respond to our evidence-based alternative to Strong4Life’s Shame and Salvation campaign, I think it’s fair to see you, Dr. Peter, as a proxy for CHOA and the traditional weight-based view of health.
You have a few advantages over me. You’re clearly qualified to comment on the subject of obesity and health, while I am not. You have years and years of medical training and an advanced degree, while I have my GED. I’ve only been doing this for two years, while you’ve been in practice for who knows how many years. Your opinion certainly holds more water than mine.
And I say this with all sincerity: I have the utmost respect for the medical profession and the people who serve our communities in the service of human health and welfare. I’ve seen first-hand how dedicated and selfless our doctors, nurses and medical professionals are across the board, and I am nothing but grateful for your service.
That being said, some of you are just plain wrong on the subject of obesity, health and weight loss.
And you don’t have to believe me. Why would you? You’re in the trenches every day trying to help people improve their health and their lives. You are on the front line in the War on Obesity. I get it.
But the thing is, I didn’t make this shit up. I didn’t just wake up one day and say, “Hey Shannon, let’s start a medical revolution that will put you at odds with mainstream medical opinions!” Everything I’ve learned about obesity, health and weight loss is from the work of other equally dedicated doctors who have studied this subject much more intensely than you have, I assure you.
Like Dr. Stephen Blair who has run what may be one of the most exhaustive studies on fitness with tens of thousands of patients for multiple decades at one of the most respected fitness organizations, The Cooper Institute (although he recently left Cooper for the University of South Carolina’s Arnold School of Public Health). Blair’s research unequivocally finds that cardiorespiratory health is by far the best indicator of metabolic health, not BMI and not weight loss.
And while we’re on the subject of weight loss, even the CDC says that a 5-10% weight loss will have a profoundly positive impact on your health.
For example, if you weigh 200 pounds, a 5 percent weight loss equals 10 pounds, bringing your weight down to 190 pounds. While this weight may still be in the “overweight” or “obese” range, this modest weight loss can decrease your risk factors for chronic diseases related to obesity.
So, I’m curious about this comment, when you say, “We advise a 200 calorie deficit per day… A pound of human fat is about 3600 so this is moderate weight loss.”
Let’s assume your patient is compliant (and your attitude on the compliance is not surprising considering the tendency among medical professionals to assume non-compliance by their obese patients (PDF), which is why fat patients stay away from doctors… fat patients tell their doctors that they are sticking to the diet and because the diet has failed, the doctor labels them non-compliant, rather than trying to understand why weight loss doesn’t work), and he adheres strictly to a 200 calorie deficit.
In fact, let’s use me as your theoretical patient. I’m 5’7″, 265 pounds. Let’s say I make this change permanently. Approximately how much weight do you believe that I would lose as a result of this reduced calorie diet after one year, two years, five years? I agree that a 200 calorie deficit is not much. In fact, it sounds rather low in terms of weight loss. I’ve done one of those classes where they check your metabolic rate and recommend a caloric level for your desired body weight, and I put in a modest goal of 250 pounds and they recommended a 500 calorie deficit. So, in terms of weight loss only, I’m just curious what you think a 200 calorie deficit is going to do for a person.
Also, I’m curious if you can find a single, decent-sized, well-controlled study that demonstrates that weight loss of greater than 10% can be achieved by more than, let’s say, 25% of the population for longer than two years. And those are generous figures. Unless we’re talking Very Low Calorie Diets of 800 and below, or bariatric surgery, then two years is when the backslide begins to creep into the data. And if you can find one study meeting these criteria, I can give you 20 that show exactly the kind of failure rates I’m describing.
My understanding of weight loss failure comes straight from Dr. Jeffrey Friedman, the man who discovered the hormone leptin in 1994, and whose lecture series at the Howard Hughes Medical Institute in 1994 can transform even the staunchest cynic into a skeptic like me. Because of the response that leptin and ghrelin have to even modest caloric deficits, sustained weight loss becomes an uphill battle of increasing difficulty.
Finally, I’d like to know how familiar you are with the research on weight cycling and the strong correlation with cardiovascular disease and major weight gain, and I’m leaving out the mixed studies on abdominal obesity, hypertension, hyperlipidemia, type 2 diabetes, and any other “obesity-related” disease you can think of. But the cardiovascular correlation is the most disturbing by far, and fairly well-established and accepted in the literature. Even Dr. Walter Willett has a hard time spinning the results of his own research into saying that weight cycling isn’t a big deal.
Between 1993 and 1999, we documented 418 new cases of type 2 diabetes that were confirmed by supplementary questionnaire. The crude incidence rate was 313 cases per 100,000 person-years. As expected, BMI in 1993 had a strong association with the risk of developing diabetes. Compared with women with a BMI <22 kg/m2, those who were overweight, but not obese (BMI 25 to 29.9 kg/m2), were approximately eight times [risk ratio (RR) = 8.29; 95% confidence interval (CI), 4.14 to 16.62] more likely to develop diabetes. Women who were obese class I (BMI 30 to 34.9 kg/m2) were 29 times more likely and those who were obese class II (BMI 35 kg/m2) were 84 times more likely to be diagnosed with type 2 diabetes. Weight cyclers were significantly heavier than noncyclers; therefore, when BMI was not controlled for in the statistical model, weight-cycling status in 1993 seemed to be a strong risk factor for developing diabetes (mild cyclers: RR = 2.57, severe cyclers: RR = 5.56). After adjustment for BMI, however, neither mild (RR = 1.07; 95% CI, 0.87 to 1.32) nor severe (RR = 1.46; 95% CI, 0.98 to 2.17) weight cycling predicted diabetes. Further adjusting the model for physical activity, inactivity, and dietary intake further attenuated the severe-cycling effect. Adjusting for total activity instead of vigorous activity did not materially change the results (data not shown). Both BMI and recent weight gain (data not shown) predicted the development of diabetes; therefore, adjusting the model for recent weight change further attenuated the effect of severe weight cycling. [emphasis mine]
But that doesn’t stop Willett et. al. from trying. It’s right there in Willett’s own work: severe weight cyclers are significantly heavier than non-cyclers; severe cyclers have twice the incidence of a recent weight gain of more than 15 pounds; and BMI and recent weight gain predicted the development of type 2 diabetes. And somehow, in the midst of all of this information, the authors have the temerity to say, “But this has nothing to do with weight cycling.”
You cannot disentangle the effects of weight cycling (weight gain and high BMI) from the diseases correlated with those effects. It’s like there’s this mental block with anti-obesity advocates that make them completely unable to accept that weight loss, as a medical prescription, is more complicated than the dual, flawed axioms of “calories in/calories out” and “3,500 calories in a pound.” Although these assumptions may be roughly true when someone puts on weight, the research does not support these theories regarding weight loss.
And advising a patient to “keep trying” a prescription that fails the vast majority of the time in the vast majority of patients, all the while ignoring evidence that the prescription is not only a failure, but may even contribute to cardio-metabolic damage… well, that’s borderline malpractice.
Now, as to the information in this comment, which is the one that I’ve pondered the most. In particular, your questions about Insulin Resistance (IR).
Once again, I’m essentially ignorant on my own. I’m not a medical person, I’m a creative person. But I’m intelligent enough to understand the medical basis for my beliefs, as well as your own, based on all of the books and research I have read. By relying on the experience and education of others, I’ve been able to educate myself on these subjects, most recently in a conversation with a friend who is both a nurse practitioner and diabetes educator.
When I asked her about the correlation between obesity and IR, she initially agreed with you that in her 20 years, she has never seen a thin person with IR (although the research you cited certainly found a small risk factor for those in the normal BMI). But it’s more complicated than just reaching a cutoff point and suddenly you’re IR.
Not all people who are obese are insulin resistant. There are other causes of obesity such as thyroid disorders, leptin deficiencies, etc. Also you can be diabetic and not IR. Some have more of an insulin production problem rather than an insulin usage problem. You can have hypertension and hyperlipidemia and not be insulin resistant. There are other causes of all of these. But when you are IR, it generally causes you to have hypertesnion, hyperlipidemia, obesity and eventually diabetes.
Our inheritance determines where your IR range is. You inherit a range and can go up and down based on the environment and choices. In other words if you choose to follow a healthy diet, exercise regularly, sleep well, be happy, not depressed… you will be less IR and if you do the opposite you will be more IR. But not everyone gets the same effect with the same activity or starts at the same place due to genetics. If you have “uncontrolled IR” ( you are more IR ) you are more likely to have everything that goes along with it. But you can be extremely IR and not have diabetes as long as the pancreas can produce a lot of insulin. Some people who are overweight, but do not have hypertension, hyperlipidemia, or diabetes (are usually not IR) but then do not have the bad effects of being overweight. The ones that are IR usually have all the above, but as long as we control the sugar, BP, cholesterol, they spend their children’s inheritance. So it is not the fat that gets them, it is the effects of the IR.
We had a lengthy phone conversation last night where she gave me an example of her boyfriend, who is thin and frequently asserts his own right living as the cause of his thinness. Yet he drinks sugar-sweetened beverages and other sweet treats and, as a result, has high blood pressure and high cholesterol. But because his genetic inheritance gave him an IR range on the lower end, he would not technically qualify as IR.
So, let’s say his IR range is from 1-5, but because of his lifestyle choices, his IR level is around 5, which is bad for his particular range. Then you take someone who has a genetic IR range of 5-10, but this person is eating healthy and exercising, so her IR level is also around 5. She is doing the best she can within her given range and will reap the benefits of living a healthy lifestyle, while he may appear healthy, but his lifestyle habits are causing metabolic damage nonetheless.
In short, this nurse practitioner and diabetes educator agreed that IR is the problem and obesity is a red herring. Everyone can benefit from improving their insulin sensitivity, and focusing so many resources on obesity is a waste of time and money.
As far as the other research you presented, you claim that “NHANES clearly DOES demonstrate that obesity prevalence has increased over the last two decades” and you cite this study as proof. First of all, NHANES is an awesome research project led by Dr. Katherine Flegal, an epidemiologist and Distinguished Consultant with the CDC’s National Center for Health Statistics, who shattered the dubious research which said that obesity causes 400,000 or 365,000 deaths per year.
The study you cited does indeed say that obesity rates increased over the past two decades… problem is, your study was publish in 2002 and gave results for 1999-2000. For some reason, you’ve completely ignored the 2010 study published by Flegal et. al., which covers adolescent obesity trends for 2007-2008. These results showed no significant increases, except among the heaviest boys:
Among 6- through 19-year-old boys, however, there was a significant linear trend at the highest BMI cut point (BMI for age ≥97th percentile) but not at the lower cut points, nor was there a significant trend in the younger age groups. The categorical analysis of survey period suggests that among 6- through 19-year-old boys the difference is only significant between the 2 time periods 1999-2000 and 2007-2008, so it not possible to tell if the 2007-2008 estimate is the continuation of a trend or not.
And while we should be investigating this trend and how to ensure the health of these heavier boys, the fact that every other category has remained level is worth keeping at the forefront of our minds while we are discussing whether stigmatization is an appropriate response to a leveled “epidemic.”
You can continue to point to studies like this one that show a correlation between BMI and all-cause mortality, but as Dr. Blair told me in an interview, if these studies do not control for cardio-respiratory fitness, then they are bunk. Too many confounders contribute to obesity and poor health, such as poverty, education, genetic susceptibility to IR, and the social determinants of health. Simply pointing to a correlation does not impress me much.
This 1998 study in the Journal of the American Medical Association looked at the influence of socioeconomic status in relation to four behavior risk factors draws a telling conclusion:
Our results suggest that despite the presence of significant socioeconomic differentials in health behaviors, these differences account for only a modest proportion of social inequalities in overall mortality. Thus, public health policies and interventions that exclusively focus on individual risk behaviors have limited potential for reducing socioeconomic disparities in mortality. While reducing the prevalence of behavioral risk factors is an important and critical public health goal, socioeconomic differentials in mortality are due to a wider array of factors and, therefore, would persist even with improved health behaviors. Increasing health promotion and disease prevention efforts among the disadvantaged is not a “magic policy bullet” for reducing persistent socioeconomic disparities in mortality. [emphasis mine]
And simply focusing on obesity, rather than behavior, makes even less sense within the framework of our understanding of the effects of SES on health. If three-fourths of fat people will never be diabetic, then why treat all fat people like they’re a donut away from an amputation?
There is an alternative to your highly flawed approach to healthcare, Dr. Peter, and it is Health At Every Size®, and when we say that it’s an “evidence-based alternative,” we don’t just mean that our claims of disease prevalence are based on clinical evidence (as you have done), we mean that the success of our prescription is also found in the literature.
Now, I have just provided you a 2,600 word response to your challenge of our beliefs. I’ve done so multiple times for several people. I do so by citing my sources and providing ample evidence that the approach I advocate is both effective and sustainable. When you, or CHOA, can do the same for your beliefs by providing evidence that weight loss works for more than two years, then I might start taking you seriously.
Until then, you’re just another medical professional mired in magical thinking and unfounded axioms.