No, It's Not the Sugar – Bittman and MotherJones have overinterpreted another study

Diet seems to be all over the New York Times this week, with an oversell of the benefits of the Mediterranean diet, and now Mark Bittman, everyone’s favorite food scold, declaring sugar is the culprit for rising diabetes. His article is based on this interesting new article in PLoS One and begins with this wildly-inaccurate summary:

Sugar is indeed toxic. It may not be the only problem with the Standard American Diet, but it’s fast becoming clear that it’s the major one.
A study published in the Feb. 27 issue of the journal PLoS One links increased consumption of sugar with increased rates of diabetes by examining the data on sugar availability and the rate of diabetes in 175 countries over the past decade. And after accounting for many other factors, the researchers found that increased sugar in a population’s food supply was linked to higher diabetes rates independent of rates of obesity.
In other words, according to this study, obesity doesn’t cause diabetes: sugar does.

No! Not even close. I hate to repeat his misstatement, because I’d hate to reinforce this as a new myth, but it’s critical to see his full mistake here. This is a wildly inaccurate summary of the authors’ findings, and one they don’t even endorse in their discussion. Bittman has actually just said “obesity doesn’t cause diabetes”, and now has proven himself a deluded fool.
Let’s talk about this paper. This is what is called an “ecological study”, which means it studies populations as a whole, rather than individual patients. Using data from the United Nations Food and Agricultural Organization, the International Diabetes Federation, and various economic indicators from the World Bank, the authors compared populations of whole countries, in particular the prevalence of diabetes correlated to other factors such as GDP, urbanization, age, obesity, and availability of certain varieties of food like sugar, meat, fibers, cereals and oil. Using the rise, or fall, of diabetes prevalence over the last decade in various countries, they correlated this increase with increasing availability of sugar, obesity, urbanization, aging populations etc., and found a few interesting things. For one, increases in GDP, overweight and obesity, tracked significantly with increasing diabetes prevalence. But interestingly, when those factors were controlled for, increasing availability of sugar also tracked linearly with increasing diabetes prevalence, and the longer the duration of the exposure, the worse it got.
However, this does not mean that “obesity doesn’t cause” diabetes, if anything, it’s further support for the exact opposite. While a correlative study can’t be a “smoking gun” for anything, the data in this paper supports increasing modernization/GDP, obesity, and sugar availability are all correlated with higher diabetes prevalence. Even if the sugar relationship is causal, which is no guarantee, the increase in sugar availability could only explain 1/4 of the increase in diabetes prevalence. Obesity is still the main cause of diabetes, which can be demonstrated on an individual level by increases in weight resulting in loss of glycemic control, and subsequent weight loss results in return of euglycemia. In particular, the results of studies of bariatric surgery, in both restrictive and bypass procedures, weight loss is accompanied by improvement in diabetes. The attempts of toxin paranoids like Bittman to reclassify sugar as a diabetes-causing agent, and to dismiss obesity as a cause, are highly premature.
Mother Jones, has a slightly more balanced read, but it still oversells the results.

This is a correlation, of course, and correlation does not always equal causation. On the other hand, it’s an exceptionally strong correlation.

Well, that’s another overstatement. Want to see a picture?

Article Source: The Relationship of Sugar to Population-Level Diabetes Prevalence: An Econometric Analysis of Repeated Cross-Sectional Data
Basu S, Yoffe P, Hills N, Lustig RH (2013) The Relationship of Sugar to Population-Level Diabetes Prevalence: An Econometric Analysis of Repeated Cross-Sectional Data. PLoS ONE 8(2): e57873. doi:10.1371/journal.pone.0057873
Figure 2. Adjusted association of sugar availability (kcal/person/day) with diabetes prevalence (% adults 20–79 years old).

I wonder what the R-squared is on that line fit. Now, consider a comparison with obesity rates by diabetes prevalence:
Figure 1. Relationship between obesity and diabetes prevalence rates worldwide.
Obesity prevalence is defined as the percentage of the population aged 15 to 100 years old with body mass index greater than or equal to 30 kg/meters squared, from the World Health Organization Global Infobase 2012 edition. Diabetes prevalence is defined as the percentage of the population aged 20 to 79 years old with diabetes, from the International Diabetes Federation Diabetes Atlas 2011 edition. Three-letter codes are ISO standard codes for country names.

Hmm, they didn’t fit a line here, but I can bet the fit would be better. Diabetes strongly correlates with BMI, this has been shown time and again using national survey data like NHANES or SHIELD. And before people start whining about BMI as an imperfect measure of obesity, it is perfectly appropriate for studies at a population level, and other metrics such as waist size, hip/waist ratios etc., all show the same thing. Diabetes risk increases linearly with BMI, with as many as 30% of people with BMI > 40 having diabetes, and further, we know from cohort and interventional studies that weight loss results in decreased diabetes. Much of this data is correlative as well (with the exception of the weight-loss studies), and the study that would prove this for certain – dividing people into diets providing excess fat, vs sugar, vs mixed calories, vs controls, with resultant measurement of diabetes rates, would be unethical. Either way, declaring sugar the enemy is both incomplete, and premature. While this paper provides interesting correlative evidence for increased sugar availability increasing diabetes prevalence, it is still subject to risk of confounding errors, it is correlative, and the link does not explain away other known causes of type II diabetes such as obesity. It is a warning however, and we should dedicate more study towards determining if sugar consumption (rather than mere availability) is an independent risk factor for type II diabetes.
Bittman has wildly overstated the case made by this article. He should retract his claims, and the title and false claims should be corrected by the editors. This is a terrible misrepresentation of what this study shows.

Two great obesity articles from the NYT and what they mean for you

A few weeks ago Tara Parker Pope wrote The Fat Trap for the NYT and once I read it I started sending it to other doctors I know. It is a great summary on the current knowledge of why we get fat, and more importantly for those of us that already are tipping the scales, why is it so damn hard to take that weight back off. (I’ll discuss Young, Obese and Getting Weight Loss Surgery nearer the end)

Beginning in 2009, he and his team recruited 50 obese men and women. The men weighed an average of 233 pounds; the women weighed about 200 pounds. Although some people dropped out of the study, most of the patients stuck with the extreme low-calorie diet, which consisted of special shakes called Optifast and two cups of low-starch vegetables, totaling just 500 to 550 calories a day for eight weeks. Ten weeks in, the dieters lost an average of 30 pounds.
At that point, the 34 patients who remained stopped dieting and began working to maintain the new lower weight. Nutritionists counseled them in person and by phone, promoting regular exercise and urging them to eat more vegetables and less fat. But despite the effort, they slowly began to put on weight. After a year, the patients already had regained an average of 11 of the pounds they struggled so hard to lose. They also reported feeling far more hungry and preoccupied with food than before they lost the weight.

Who among us can’t identify with that story? If you can’t you’ve been thin all your life and can go suck an egg. But for those that have carried extra pounds it’s part of the yo-yo routine of dieting. But why is this? Were we permanently programmed for a preset weight and will feel as though were starving below it? If this is the case, why is obesity increasing now, in the last 20 years? The answer suggested is more subtle, but the fascinating thing is, your body’s set weight might be a real thing. It’s just not programmed from birth.
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Obesity – A new study and what it means to be a “healthy weight”

ResearchBlogging.orgIn response to the conversation on “Obesity, Evolution and Delayed Gratification” on the main page and Razib’s coverage of a fascinating new study on the relationship to the lactase gene and obesity, I thought now would be a good time to write about an important new study that helps define the boundaries of what normal and healthy weights are in humans.

This study, entitled Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies is a whopper of a meta-analysis. That is, a study that increases the power of other similar studies by combining their results so that, in this case, data from hundreds of thousands of patients can be aggregated. Meta-analyses have their flaws, and I criticize them frequently when poorly-done or poor-quality studies end up being averaged-in with the results of better-designed studies, but this one is large enough and thorough enough that its results should not be dismissed.

What this study describes is the mortality, and causes of mortality, one observes when one sorts people by body mass index. Body mass index also has it’s flaws but it is a useful, if imperfect method of describing one’s relative contribution of body fat to their total mass. It is calculated by taking and individual’s body weight in kilograms and dividing by the square of their height in meters. “Normal” is defined between 18.5-25, overweight is 25-30, and obese is greater than 30. These numbers do not describe all people well, and you may be an exception to these predictions. This usually occurs if you have a large amount of muscle mass relative to your height, so Arnold Schwarzenegger would be obese according to these scales. However, most people are not Arnold Schwarzenegger and the scale fits, it’s better not to let the perfect spoil the good. One must also remember that it would be unethical to design a study in which we prospectively made people overweight or obese, since we suspect that will cause poor health, so this is necessarily a correlative study of BMI and health. But this information combined with what we know about mechanisms of cardiovascular disease, diabetes, etc., makes a lot of sense, and I believe in the context of the literature we can make a safe assumption the effects we see are causal.

Overall what the study suggests is that the current 18.5-25 recommended BMI is probably about right, BMI of 25-30 marginally increases morbidity and mortality, and BMIs much greater than 30 significantly shorten one’s life. The reason I like this study is that they have aggregated such a huge data set, they demonstrate a clear dose-response curve between obesity and mortality, and they’ve done a better job than most in teasing out the relationship between health, weight, smoking and other co-morbidities at all BMIs.

Let’s take a look at some of the data.
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Obesity and health—a quick primer

Still coughing and tired, so here’s another one I’m migrating from the old blog. –PalMD

Blogging on Peer-Reviewed ResearchThere has been much talk in the media over the last few years about the “obesity epidemic” in the U.S. This has led to a bit of a backlash among a small but vocal group of critics who don’t believe the evidence linking obesity and poor health. The reasons for their disbelief are not all that clear to me, given the overwhelming amount of evidence linking obesity with both serious health conditions such as diabetes and heart disease, and adverse outcomes, such as premature death. When their arguments are examined in detail, most of these critics appear to be classic denialists, rather than honest skeptics. So let’s examine a small slice of the obesity pie.

When citing scientific research to back up an assertion, it is important to make sure you are not “cherry-picking” studies that support your point of view, and that you are not “quote-mining” the literature, taking statements out of context to change their original meaning. These are tactics commonly used by denialists. The way we interpret scientific literature in medicine is to examine as many studies as possible for quality, methods, and conclusions. We make decisions based on the overall picture, not on any single study. For example, if an overwhelming number of good-quality studies support the idea that smoking causes heart disease, but a couple of small studies do not support this conclusion, this does not mean that smoking does not cause heart disease.
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Obesity Crankery in the Washington Post

Why the Washington Post decided to devote space to libertarian crankery from the Pacific Research Institute, I’ll never know, but today’s op-ed from Sally Pipes on the evils of governmental interference in diet is a bit much.

The way I see it, obesity cranks recycle 3 arguments over and over. It usually goes: (1) BMIs don’t fit everyone (2) the stupid government has arbitrarily changed the definition of overweight to make more people fat and (3) exercise is all that matters anyway and overweight doesn’t hurt you.

First, we have BMI’s are inaccurate:

The standard metric for this measurement is a person’s body-mass index, or BMI — the ratio of one’s height to one’s weight. But at best, BMI is a rough tool that does not take into account an individual’s body type. A six-foot-two athlete who weighs 210 pounds would be classified as “obese” according to BMI charts — despite his 32-inch waistline, 17-inch biceps and his less than 6 percent actual body fat.

If you believe the BMI tables, most of the best players in the NBA and NFL are “overweight,” including superstar athletes Kobe Bryant and Tom Brady.

Many Hollywood heartthrobs also qualify as fatties — Brad Pitt, Matt Damon, Tom Cruise and George Clooney, to name a few.

Once you read this you know you’re going to see the standard idiotic attacks on science from someone defending the food industry or obesity itself. Why is BMI used? It is a indirect measure of adiposity. It is not perfect, and sadly, there is no perfect way to measure and track total body fat easily. BMI is an approximation, but on average a pretty good one.

Now, the obesity cranks love to throw out this red herring, usually it’s Arnold Schwarzenegger, but whatever. Is anyone really confused by this? Certainly I doubt that professional athletes and body builders are losing sleep because their BMIs aren’t ideal. BMI is an indicator for the average schmo and not professional athletes and body builders. No one is confused about this, and if anything it hurts their case as it suggests overweight statistics are being brought down by healthy athletic people. No one thinks the BMI is perfect, but until we develop a better indirect measure of adiposity that can be easily tracked in individuals (or an easy direct measure) we shouldn’t let the perfect ruin the good.

Next, this endless refrain from people who are full of it:

What’s more, the acceptable BMI continues to be ratcheted downward — transforming those who were considered perfectly healthy yesterday into “overweight” and “obese” today.

Before 1998, a “healthy” BMI was anything less than 27. Then, suddenly, the government changed the “healthy” number to anything less than 25. Overnight, more than 25 million people who were previously considered to be a healthy or normal weight were reclassified as overweight. Looked at another way, the government artificially manufactured an obesity crisis by moving the BMI goal posts.

The Govmint! The Govmint! It’s a conspiracy! For one her first statement is completely incorrect. Obesity has always been > 30, and still the number of obese has been increasing based on this threshold. Therefore it would be very difficult to manufacture an obesity crisis by keeping the BMI threshold for obesity the same!

Further, the “government” said anything less than 27 was healthy? Whom do you mean? The NIH? Or the CDC? Which “government” are you talking about? One group of government researchers convinced the government researchers in the CDC in 1998 to stop using 27 as a measurement of overweight so they would fit with everyone else who had always used 25. It’s no great conspiracy, they were sick of the definition being different across different evil government groups. Further this only changed the definition of overweight from the CDC, not obesity nor the definition for overweight being > 25 that many other gov’mint researchers had used for a long time.

Now, the third nonsense argument – that exercise is all that matters and overweight isn’t that bad – I’m not even going to go into extensively as I’ve harped on it so much already. Remember, it’s about primary vs. secondary prevention. Overweight and obesity get you by giving you diabetes, hypertension, and dyslipidemia. These conditions, however, can be largely controlled with drugs which will largely abrogate overweight/obesity’s effects on mortality. The goal though is primary prevention – preventing the co-morbidities in the from occurring at all. This is superior to secondary prevention – prevention of increased mortality through pharmaceuticals. The irony is the cranks are using the success of medicine at preventing harm from obesity to criticize medicine for trying to keep us healthy in the first place!

Instead I’ll just jump to a paragraph I found so cranky, I almost plotzed:

While we may not always like the choices others might make, it is essential that we all have the freedom to choose for ourselves. Once we accept the idea that the Nanny State should step in when it’s “for our own good,” we’ve taken a very big step down the road to something like the scene painted in George Orwell’s “1984” — when citizens wake each day to mandatory exercise classes on the Telescreen.

Holy persecution batman, I think we have ourselves a crank! That was pretty fast – usually I have to read more than one article from someone before they so perfectly fulfill the crank criteria. Pipes, however, has managed in record speed. Considering this is coming from the libertarians I guess I shouldn’t be surprised. But damn! That was some high-speed crankery.

What is most tragic about this article, however, is that she takes a study with an important holiday message about obesity, and only mentions it in passing, rather than describing its very relevant message to all of you eaters out there. She mentions in her first sentence, “it should come as no surprise that the average American gains about one pound between Thanksgiving and New Year’s, according to the National Institutes of Health. That pound a year really adds up over the decades.”

It really does add up, because the study showed that not only do you gain a pound a year over the holidays (and about 10% of people gain 5 pounds!), you don’t lose that weight throughout the year. The result is that for many people weight gain occurs in discrete steps of over-consumption rather than steady accumulation. It used to be the harvest feast was followed by a winter lull in food availability – no more. You get stuck with that extra turkey for life. There’s a holiday message of joy, and a suggestion for a New Year resolution. Aim low, and try to get rid of those pounds you just added. In the long run, it might make a big difference. Primary prevention people. Get on it!

Obesity Crankery Part II

Orac alerted me, based on my recent obesity writings, of a new crank obesity attack on science.

This latest is in the form of a rebuttal to Morgan Spurlock’s excellent film Supersize me. Comedian Tom Naughton, who has all the charisma of a wet sponge, is making his own documentary Fathead: You’ve been fed a load of bologna. Here’s the trailer:

Aside from the shoddy production, noncharismatic host, and general crankery, I guess it’s not so bad. But I am growing concerned about the continual assault on what little good nutritional data is out there, and the misleading tactics of those defending food that is responsible for obesity and poor cardiovascular health.
Continue reading “Obesity Crankery Part II”

Obesity Crankery – A growing problem

Recently, it seems there has been a backlash against medicine and the current knowledge of the relationship between diet, weight and overall health. I don’t actually believe this is directly the fault of scientists or doctors, who react to the trashy mainstream reporting of science with little more than the occasional raised eyebrow. However, many people in response to all these silly health pronouncements, which seemingly come from on high but really are from press coverage of often minor reports in the medical literature, have lost their trust in what science has to offer as a solution to what Michael Pollan refers to as “the Omnivore’s Dilemma”. That is, what should we be eating?

The result of this confusion is a mixture of distrust, cynicism, and receptivity to crankery and lies about diet. After all, if science ostensibly can’t keep their message straight, who knows what to believe?

The fact is, science knows many things about the relationship between diet, obesity, and health with great confidence and it hasn’t changed nearly so much as the popular press would have you believe. The failure to state clear messages about nutrition is a reflection on the haphazard way in which nutritional health is reported, the often confusing nature of epidemiologic science, and the various parties that are interested in cashing in the confusion by promoting their own nonsensical ideas about diet.

Take, for example, Sandy Szwarc. Sandy doesn’t believe obesity or any food choices are actually bad for you. To help spread this nonsense she dismisses valid sources of information like WebMD (which has quite good information) based on the rather silly conspiracy that they have designed their entire website and health enterprise around misleading people into using their products – especially weight-loss products. Because, you know, it’s impossible for a corporation to offer free health advice as a public service without conspiring to grab you buy the ankles and shake the money from your pockets. But it doesn’t end there. We see rest of the standard denialist tactics of course!

Case in point, in a recent article she makes the astonishing assertion that her mortal enemy – bariatric or gastric-bypass surgeons – have admitted that obesity makes you healthier!

Today brought another unbelievable example of ad-hoc reasoning, as well as a remarkable admission that the war on obesity is without scientific merit. It appeared in a paper published in the journal for the American Society for Bariatric Surgery (now calling itself the American Society for Metabolic and Bariatric Surgery), which is edited by the Society’s president, Dr. Harvey Sugerman, M.D. FACS.

The article, “Do current body mass index criteria for obesity surgery reflect cardiovascular risk?” was “work presented at the 2005 American Society for Bariatric Surgery Meeting in poster form.” The authors, led by Edward H. Livingston M.D. at the University of Texas Southwestern School of Medicine, reported that the conventional risk factors for cardiovascular disease “decreased with increasing degrees of obesity.”

Yes, you read that correctly, decreased.

“Therefore,” the authors argued …

“the criteria for obesity surgery should be changed to lower BMIs than are currently used.”

Now, boys and girls, what is the very first thing you do when a suspected denialist feeds you some nonsense in quotes? Check the source! Always, always, always, check the source. Let’s expand those six words that Sandy lifted out of the abstract and see what else the authors had to say:

Continue reading “Obesity Crankery – A growing problem”

Obesity and Overweight – what do these new studies really mean?

Blogging on Peer-Reviewed ResearchMultiple news sources have been covering this recent article in JAMA (1) which provides epidemiological evidence that being overweight (but not obese) may decrease the risk of some illnesses, while not increasing one’s overall mortality from cardiovascular disease.

Given that we’ve talked about overweight and obesity recently on the blog, I think it’s worthwhile to go over these findings in context, and discuss what this paper, and related ones in the literature, actually mean in terms of our health.

Sorry, the news is not all good, you don’t want to start putting on the pounds, and the analysis so far in the MSM has been pretty shoddy.
Continue reading “Obesity and Overweight – what do these new studies really mean?”

Obesity – Primary vs. Secondary prevention

I will never forget the very first patient history I ever took. Part of medical school training is they send you onto the wards to gather patient histories and physicals so you learn to gather information effectively as a clinician. My first patient history was on a woman about 35 years old on the orthopedics ward, who was a triple-amputee. She had her legs removed below the thigh, and one arm amputated below the elbow. The cause was imminently preventable. She had type II diabetes that was poorly controlled. She was obese, weighing about 180 lbs despite the removal of large parts of her body. A common problem with diabetics is that they are susceptible to infection in their bones. Diabetics have have poor pain perception from diabetic neuropathy and poor blood supply, the result is that cuts on their extremities go unnoticed, heal poorly, and ultimately result in infection that frequently goes into the bone. The result, osteomyelitis, is persistent infection of the bones from these infections, and, if antibiotics are ineffective, the only treatment is to surgery to remove the infected tissue and often amputation. Such was the case with my patient. She was poor, from Appalachia, had inadequate control of her diabetes, and as a result lost multiple limbs from infection (she was hospitalized for yet another infected bone).

The major reason for the increase in Type II diabetes rates is obesity and lack of exercise. Disturbingly, younger and younger people are presenting with diseases often only seen with age, like type II diabetes and gout. This is unquestionably due to increasing rates of obesity in the US population. Thus, it is with dismay, that I read Sandy Szwarc’s blog Junkfood science, that seems to exist for the sole purpose of denying the health risks of obesity and of being overweight. Sandy, who is on CEI’s staff, routinely writes about obesity as a health-scare, that is not harmful as doctors and health scientists suggest.

To illustrate the problems with her analysis, let’s go through one of her more recent posts on the Obesity Paradox – the apparent decrease in mortality in studies of the obese.
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