Today, the World Health Organization's International Agency for Research on Cancer published a statement in The Lancet detailing its position on the carcinogenicity of processed and red meat (1).  The statement, resulting from a meeting of 22 scientists from 10 countries, concluded that processed meat is a group 1 carcinogen, meaning that it is "definitely carcinogenic to humans".  They also judged that red meat is a group 2A carcinogen, meaning that it probably causes cancer but the evidence isn't as strong.  They're mostly referring to the links between processed and red meat and digestive tract cancer, particularly cancers of the colon and rectum.

These statements were met with a media frenzy, and the expected furor from the meat industry.  The most surprising thing, for me, is that anyone would be surprised by the IARC's statement.
We like explanations that are simple, easy to understand, and explain everything.  One example of this is the idea that eating carbohydrate, or sugar, is the primary cause of obesity.  This lets us point our finger at something concrete and change our behavior accordingly.  And it's true enough that it has practical value.  But the world around us often turns out to be more complex than we'd like it to be.

The CDC recently released its latest data on the prevalence of obesity in the US, spanning the years 2013-2014 (1).  These data come from its periodic National Health and Nutrition Examination Surveys (NHANES).  Contrary to what many of us had hoped for after a slight decline in obesity in the last survey, the prevalence has once again increased.  Today, roughly 38 percent of US adults have obesity.  As a nation, we're continuing to gain fat, which is extremely concerning.
In the last post, we saw that carbohydrate and particularly sugar intake have been declining in the US since 1999, even as our obesity rate has continued to climb.

In this post, let's look at another putative driver of obesity: our fat intake, and especially our intake of added fats like seed oils, butter, and olive oil.  Like the graphs in the last post, the data underlying the following graphs come from USDA food disappearance records (not self-reported), and NHANES survey data (1, 2).  Also like the last post, the graph of total fat intake is not adjusted for waste (non-eaten food), while the graph of added fat intake is*.  As a consequence, the figures for total carbohydrate and total fat intake are higher than actual intakes, but still good for illustrating trends.
Obesity involves changes in the function of brain regions that regulate body fatness and blood glucose, particularly a region called the hypothalamus.  My colleagues and I previously showed that obesity is associated with inflammation and injury of the hypothalamus in rodent models, and we also presented preliminary evidence that the same might be true in humans.  In our latest paper, we confirm this association, and show that hypothalamic injury is also associated with a marker of insulin resistance, independently of BMI.
I've put off writing this post for many years because I know it will be controversial.  But we're a few days from Christmas, and I also know this post will be a wonderful gift for some people.

Chronic or intermittent pain, often located in the back, neck, and/or buttocks, is a major driver of personal suffering and reduced productivity in the US and other affluent nations.  While pain can obviously have a variety of structural causes, such as sprained ankles or bruising, garden-variety back pain usually doesn't.  I've come to believe that such pain is usually psychosomatic in nature-- in other words, caused by the brain but resulting in physical signs and symptoms in the body.  It's widely accepted that a person's mental state can affect pain perception, but this idea goes further.  Pain isn't just exacerbated by a person's mental state; it's often entirely caused by it.
David Ludwig, MD, recently published a new book titled Always Hungry? Conquer cravings, retrain your fat cells, and lose weight permanently.  The book is getting widespread media coverage.  Ludwig is a professor of pediatrics at the Harvard Medical School and a professor of nutrition at the Harvard School of Public Health.  He's a pediatric endocrinologist, but his primary focus is research, particularly the impact of nutrition on hunger, calorie expenditure, and body weight.  Although I sometimes disagree with how he interprets evidence, he has made significant and useful contributions to the scientific literature in these areas, and I also support his efforts to find policy solutions to curb the intake of sweetened beverages and other junk foods.  In the grand scheme of things, he's an ally in the fight to improve the American diet.

Ludwig has written several high-profile op-ed pieces in recent years, both in the popular press and in scientific journals (1, 2).  He argues that our understanding of eating behavior and obesity may be all wrong, and that our focus on calories may be leading us away from the true cause of obesity: hormonal imbalance.  And the primary culprit is insulin.  You might recognize this idea, because it's similar to the one that science journalist Gary Taubes developed in his book Good Calories, Bad Calories.
Dr. David Ludwig, MD, recently published a response to my critique of the carbohydrate-insulin-obesity hypothesis.  This is good because he defends the idea in more detail than I've encountered in other written works.  In fact, his piece is the most scientifically persuasive defense of the idea I can recall.

Before we dig in, I want to emphasize that this is science, not tribal warfare.  The goal is to arrive at the best answer, rather than to win an argument.  I'm proceeding in good faith, based on my belief that Ludwig and I are both serious people who care about science and human health, and I hope my audience will do the same.  That said, let's get to it.
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