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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Abdominal adiposity and risk of death, or “belly fat’ll kill ya'”

Last week’s New England Journal of Medicine gave us some remarkable news, via the JUPITER Trial, adding additional evidence to the pile of articles on the cardioprotective effects of statins. This article is getting lots of press, which is great, but I’d hate to see this week’s edition of the Journal get lost. Specifically, there’s a huge population-based study on obesity and mortality. We’ve explored previously the dangers of obesity, and we’ve been fought the whole way by various denialists.

Earlier studies have shown associations between excess body weight (as measured by body mass index (BMI)) and death, but this study did a few things differently. The latest study in the Journal, titled “General and Abdominal Adiposity and Risk of Death in Europe”, takes a look at a larger data set, and takes a closer look at different measures of obesity.

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Eating can be bad for your health. Oh, and don’t forget the phages.

Sure, we have obesity problems in this country, but we also have more direct food safety problems. Summer has brought with it news of the bungled tomato-Salmonella affair, and now, from the Midwest, contaminated beef.

One of our local supermarket chains has been forced to recall hamburger meat because of over a dozen cases of E. coli-related disease. These cases have occurred over a wide area, and the bacteria are genetically linked, indicating a likely common source.
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Mike Adams – Hysterical Luddite of the Natural Food Movement

Sometimes I just can’t get too angry about some particularly insane rant from a denialist. In this case, HIV/AIDS denialist, scientific medicine denialist and all-around crank Mike Adams rants about the prospect of food sterilization by irradiation:

Let’s be blunt about this: The corporations running this country (which also run the U.S. government) want the U.S. food supply to be dead. They don’t want foods to be used as medicines, and they sure don’t want the natural medicines found in foods competing with their own patented pharmaceutical medicines (that just happen to earn them a whole lot more money than any food ever did).

The FDA, for its part, has for many decades conducted its natural medicine censorship campaign, whose only purpose is to deny the People access to accurate information about the healing properties of natural medicines found in foods and herbs.

I believe we must keep our food supply fresh and alive. (Sounds kinda obvious, huh?) And if there’s a little extra bacteria on the spinach, it’s nothing that a healthy body can’t handle anyway. Take some probiotics and avoid antibiotics, and you’ll be just fine. E. Coli is really only a threat to the health of individuals who have had their immune systems (or intestinal flora) destroyed by pharmaceuticals in the first place. There’s nothing wrong with some living organisms in your milk, on your almonds or on your spinach. Wash your food, get plenty of sunlight and avoid using antibiotics.

The human body is NOT a sterile environment. To try to make our food supply sterile is insane, and anyone who supports the irradiation of the food supply is, in my opinion, supporting a policy of genocide against the American people. To destroy the vitality of the food supply is a criminal act of such immense evil that it stands alongside the worst crimes ever committed against humanity.

You see, it’s not enough for them to poison our water (fluoride), poison our children (vaccines) and lie to us about the sun (skin cancer scare stories). Now they want to destroy our foods… and thereby take away any natural medicine options that might actually keep people healthy and free. Remember: A diseased population is an enslaved population.

Now go eat your Big Mac, drink your Pepsi and don’t ask too many questions.

Wow, talk about some paranoia, conspiracism, denialism, and crankery all rolled into one! I mean we’ve got fluoride paranoia, anti-vaccination denialism, germ theory denialism, skin cancer denialism (a new one!), combined with a completely inane fear about irradiation of food.

I’ll just mention one thing that has elluded our hysterical little health ranger. Irradiation does not “kill” your food. In fact, if a cell is living a “lethal” dose of radiation doesn’t necessarily make the cell keel over and die. All it does is cause enough DNA damage so that cells can no longer reproduce. The bacteria are still there, which is different than sterilization by washing or autoclaving, they’re just incapable of reproduction, and guess what? Strawberries aren’t particularly mitotically active after they’ve grown and ripened. I have cells in my lab called feeder cells – fibroblasts irradiated so they can no longer divide – that are used to maintain embryonic stem cells in a pluripotent state that stay alive for weeks in culture. Irradiation of humans, for instance, is only lethal when cells that are susceptible to irradiation, like GI and marrow cells, are killed. Maybe too subtle a point for Adams, but I digress.

This is such a wonderful rant and I can’t get angry over it because it just demonstrates how completely insane this particular denialist is. He doesn’t understand electromagnetic radiation and even has a piece up from a colleague on the the evils of microwaving (read cooking your food). The microwave is an evil Nazi invention that is responsible for everything from obesity to erectile dysfunction! Food irradiation is the greatest crime ever committed in history! The government wants to kill us all using clean cooked food!

It’s denialism that comes pre-debunked, I love it.

I love bacon

Blogging on Peer-Reviewed ResearchA reader, who happens to write one of the best-named blogs on teh tubes, pointed me toward an article I never would have seen. This parallels a news story we had here in the States late last year. So, since the story is getting press overseas (albeit late), it’s time to dust off the old post and update it a bit.

The story repeats the finding that processed meats increase the risk of colon cancer. This news comes from a large report published by the World Cancer Research Fund, which looks at data surrounding diet and cancer. It states that there is no safe level of processed meat consumption when it comes to colorectal cancer risk. It’s going to take a long time to parse through all the data, but since I love my processed meat, I’ll start there, and once again, my scientist colleagues will please forgive me for oversimplifying.

First, this is a huge report, pooling tons of data. One of the most important conclusions is regarding obesity and cancer risk, but that will have to wait until later.

Per USAToday, “every 1.7 ounces of processed meat consumed a day increases the risk of colorectal cancer by 21%.” Per the Daily Mail, “[e]ating just one sausage a day raises your cancer risk by 20 per cent.” What does that mean? “Risk” is a complicated concept in medicine. It is easy to draw overbroad conclusions from bits of data. When risk is measured, it is rarely intuitive–small percentages can indicate large increases in risk, large numbers can refer to small increases in risk–it depends quite a bit on the base line incidence and prevalence of the disease. A 50% increase in a disease sounds big, but in the right situation it can be big or small. For example, if your “usual” risk of disease A is 2/100, then a 50% increase makes your risk 4 in 100, meaning out of 100 people, 2 more get the disease then they would without the extra risk. If the “usual” risk is 10/100, then a 50% increase means 5 more people get the disease.

I hope you haven’t given up on me here. Keep reading…trust me…

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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.
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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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