Researchers have known for some time that the food and drink we all consume contains arsenic.
Should we be concerned? Aren’t we protected by federal regulations? Actually, no – we are not. In the US, as in many countries, the government regulates the concentration of arsenic in drinking water, but does not regulate the concentration of arsenic in any other drink or food. We have a mercury-in-food regulation; why don’t we have an arsenic-in-food regulation?
One important difference is that all of the compounds of mercury we find in food are equally toxic. This is not the case for arsenic. Although we normally think of arsenic compounds as potentially harmful, most of the arsenic we eat is harmless. Seafood, which contains by far the highest concentrations of arsenic, delivers it as arsenobetaine, an organic chemical containing arsenic that is innocuous to us humans.
How then should arsenic in food be regulated? To do that well, we need to develop better ways to determine the amounts of arsenic and other chemicals in our foods.
This article was originally published on The Conversation.
Food labels seem to provide all the information a thoughtful consumer needs, so counting calories should be simple. But things get tricky because food labels tell only half the story.
A calorie is a measure of usable energy. Food labels say how many calories a food contains. But what they don’t say is that how many calories you actually get out of your food depends on how highly processed it is.
Food-processing includes cooking, blending and mashing, or using refined instead of unrefined flour. It can be done by the food industry before you buy, or in your home when you prepare a meal. Its effects can be big. If you eat your food raw, you will tend to lose weight. If you eat the same food cooked, you will tend to gain weight. Same calories, different outcome.
For our ancestors, it could have meant the difference between life and death. Hundreds of thousands of years ago, when early humans learned to cook they were able to access more energy in whatever they ate. The extra energy allowed them to develop big brains, have babies faster and travel more efficiently. Without cooking, we would not be human.
Iodized salt is so commonplace in the U.S. today that you may never have given the additive a second thought. But new research finds that humble iodine has played a substantial role in cognitive improvements seen across the American population in the 20th century.
Iodine is a critical micronutrient in the human diet—that is, something our bodies can’t synthesize that we have to rely on food to obtain
—and it’s been added to salt (in the form of potassium iodide) since 1924. Originally, iodization was adopted to reduce the incidence of goiter, an enlargement of the thyroid gland. But research since then has found that iodine also plays a crucial role in brain development, especially during gestation.
today is the leading cause of preventable mental retardation in the world. It’s estimated that nearly one-third of the world’s population has a diet with too little iodine in it, and the problem isn’t limited to developing countries—perhaps one-fifth of those cases are in Europe (pdf), where iodized salt is still not the norm.
By Gary Taubes, author of Nobel Dreams (1987), Bad Science (1993), Good Calories, Bad Calories (2007), and Why We Get Fat (2011). Taubes is a former staff member at DISCOVER. He has won the Science in Society Award of the National Association of Science Writers three times and was awarded an MIT Knight Science Journalism Fellowship for 1996-97. A modified version of this post appeared on Taubes’ blog.
The last couple of weeks have witnessed a slightly-greater-than-usual outbreak of extremely newsworthy nutrition stories that could be described as bad journalism feasting on bad science. The first was a report out of the Harvard School of Public Health that meat-eating apparently causes premature death and disease (here’s how the New York Times covered it), and the second out of UC San Diego suggesting that chocolate is a food we should all be eating to lose weight (the Times again).
Both of these studies were classic examples of what is known technically as observational epidemiology, a field of research I discussed at great length back in 2007 in a cover article for in the New York Times Magazine. The article was called “Do We Really Know What Makes Us Healthy?” and I made the argument that this particular pursuit is closer to a pseudoscience than a real science.
As a case study, I used a collaboration of researchers from the Harvard School of Public Health, led by Walter Willett, who runs the Nurses’ Health Study. And I pointed out that every time that these Harvard researchers had claimed that an association observed in their observational trials was a causal relationship—that food or drug X caused disease or health benefit Y—and that this supposed causal relationship had then been tested in experiment, the experiment had failed to confirm the causal interpretation—i.e., the folks from Harvard got it wrong. Not most times, but every time.
Now it’s these very same Harvard researchers—Walter Willett and his colleagues—who have authored the article from two weeks ago claiming that red meat and processed meat consumption is deadly; that eating it regularly raises our risk of dying prematurely and contracting a host of chronic diseases. Zoe Harcombe has done a wonderful job dissecting the paper at her site. I want to talk about the bigger picture (in a less concise way).
This is an issue about science itself and the quality of research done in nutrition. Science is ultimately about establishing cause and effect. It’s not about guessing. You come up with a hypothesis—force x causes observation y—and then you do your best to prove that it’s wrong. If you can’t, you tentatively accept the possibility that your hypothesis might be right. In the words of Karl Popper, a leading philosopher of science, “The method of science is the method of bold conjectures and ingenious and severe attempts to refute them.” The bold conjectures, the hypotheses, making the observations that lead to your conjectures… that’s the easy part. The ingenious and severe attempts to refute your conjectures is the hard part. Anyone can make a bold conjecture. (Here’s one: space aliens cause heart disease.) Testing hypotheses ingeniously and severely is the single most important part of doing science.
The problem with observational studies like the ones from Harvard and UCSD that gave us the bad news about meat and the good news about chocolate, is that the researchers do little of this. The hard part of science is left out, and they skip straight to the endpoint, insisting that their causal interpretation of the association is the correct one and we should probably all change our diets accordingly.
Earlier this week, food columnist Ari LeVaux set off a storm of media reaction with a piece with this premise: tiny plant RNAs, recently discovered to survive digestion and alter host gene expression, are a major reason why genetically modified foods should be considered dangerous. For anyone familiar with the paper he referred to, or with molecular biology in general, the article was full of conflation and sloppy logic, and even as it became the most-emailed story on TheAtlantic.com, where it was published, biology bloggers and science writers were pointing out its significant flaws. To his credit, LeVaux revised the article to fix many (though not all) of the errors concerning genetics; the new version appeared yesterday at AlterNet and today replaced his original piece at The Atlantic.
So what did LeVaux get so wrong, and, once all of the wheat was sorted from the chaff, was there anything to what he was trying to say?
At the heart of the fracas is LeVaux’s claim that a class of molecules called miRNA is a reason to fear GMOs specifically, more than any other food plant or animal. miRNA, which is short for microRNA, is a class of molecules that perform various tasks in plants and animals. They were first discovered about twenty years ago, in nematode worms, and they regulate gene expression by binding the messenger RNA involved in translating a gene into a protein. The messenger RNA carries the “message” of the DNA’s sequence to a group of enzymes that translate it into the amino acid sequence of a protein. But if a miRNA binds to a messenger RNA, the message is destroyed, and the protein is never made. Thus, miRNA can be a powerful tool for preventing the expression of genes. In fact, that is what’s made it such an important lab tool in recent years: it allows researchers to knock down the expression of genes without physically removing them from an organism’s genome.
In the paper that LeVaux pegged his article on, Nanjing University researchers found that miRNAs usually seen in rice were circulating in the blood of humans, and that mice fed rice had the miRNA in their blood as well. That particular miRNA, in its native context, regulates plant development. When the researchers added it to human cells, it appeared to bind to the messenger RNA of a gene involved in removing cholesterol from the blood. Previous papers had found that plants have plenty of miRNA floating around in them [pdf] (as does just about everything we eat, since plants and animals make them by the thousands), but having them show up whole and unmolested in blood, apparently after digestion, was a new and very intriguing discovery.
by Richard Wrangham, as told to Discover’s Veronique Greenwood. Wrangham is the chair of biological anthropology at Harvard University, where he studies the cultural similarities between humans and chimpanzees—including our unique tendencies to form murderous alliances and engage in recreational sexual activity. He is the author of Catching Fire: How Cooking Made Us Human.
When I was studying the feeding behavior of wild chimpanzees in the early 1970s, I tried surviving on chimpanzee foods for a day at a time. I learned that nothing that chimpanzees ate (at Gombe, in Tanzania, at least) was so poisonous that it would make you ill, but nothing was so palatable that one could easily fill one’s stomach. Having eaten nothing but chimpanzee foods all day, I fell upon regular cooked food in the evenings with relief and delight.
About 25 years later, it occurred to me that my experience in Gombe of being unable to thrive on wild foods likely reflected a general problem for humans that was somehow overcome at some point, possibly through the development of cooking. (Various of our ancestors would have eaten more roots and meat than chimpanzees do, but I had plenty of experience of seeing chimpanzees working very hard to chew their way through tough raw meat—and had even myself tried chewing monkeys killed and discarded by chimpanzees.) In 1999, I published a paper [pdf] with colleagues that argued that the advent of cooking would have marked a turning point in how much energy our ancestors were able to reap from food.
To my surprise, some of the peer commentaries were dismissive of the idea that cooked food provides more energy than raw. The amazing fact is that no experiments had been published directly testing the effects of cooking on net energy gained. It was remarkable, given the abiding interest in calories, that there was a pronounced lack of studies of the effects of cooking on energy gain, even though there were thousands of studies on the effects of cooking on vitamin concentration, and a fair number on its effects on the physical properties of food such as tenderness. But more than a decade later, thanks particularly to the work of Rachel Carmody, a grad student in my lab, we now have a series of experiments that provide a solid base of evidence showing that the skeptics were wrong.
Whether we are talking about plants or meat, eating cooked food provides more calories than eating the same food raw. And that means that the calorie counts we’ve grown so used to consulting are routinely wrong. Read More