Why Was Chicken the Primary Source of Arsenic Exposure in Children?

What was the National Chicken Council’s response to public health authorities calling for the industry to stop feeding arsenic-based drugs to poultry?

“Dietary practices influence our exposure to pesticides, toxic heavy metals, persistent organic pollutants, and industrial pollutants….A diet high in fish and other animal products, for example, results in greater exposure to persistent organic compounds and metals than does a plant-based diet because these compounds bioaccumulate up the food chain.” Researchers at UC Davis analyzed the diets of children and adults in California to see just how bad things have gotten.

Cancer benchmark levels were exceeded by all children—100 percent of children—for arsenic, the banned pesticides dieldrin and DDT, metabolite DDE, as well as dioxins, and not just by a little. As you can see at 0:51 in my video Where Does the Arsenic in Chicken Come From?, researchers found more than a hundred times the acceptable daily exposure for arsenic in preschoolers, school-aged children, parents, and older adults, about ten times the acceptable levels for various pesticides, and up to a thousand times the daily dose for dioxins. Where are all these toxins coming from?

The number-one source of dioxins in the diets of Californian preschoolers, kids, parents, and grandparents appears to be dairy for all age groups, followed by meat, and then white potatoes, refined grains, mushrooms, poultry, and fish.

These days, our DDT legacy is also mostly from dairy. Dieldrin was created as a safer alternative to DDT, but it was banned just two years later, in 1974, though it’s still found in our bodies, mostly thanks to dairy, meat, and, evidently, cucumbers.

Chlordane made it into the 1980s before being banned, though we’re still exposed through dairy (and cukes). Lead is — foodwise — also mostly from dairy, and mercury is not surprisingly mostly from tuna and other seafood. But the primary source of arsenic in children? Surprisingly, mostly from chicken. Why?

Let me tell you a tale of arsenic in chicken. Arsenic is “well known as a poison by anyone who reads mysteries or the history of the Borgias, and with its long and colourful history, arsenic is not something that people want in their food.” So, when a biostatistics student went to the USDA in 2000 in search of a project for his master’s degree, he decided to look into it. He found a startling difference: Arsenic levels in chicken were three times higher than in other meats. His veterinary colleagues weren’t at all surprised and explained that four different types of arsenic-containing antibiotic drugs are fed to poultry—and have been fed to them since 1944.

“While arsenic-based drugs had been fed to poultry since the 1940s, recognition of this source of exposure [for humans] only occurred after appropriate statistical analysis of the data”—that is, after this student churned through the data. It was published in 2004 and expanded upon in 2006. The National Chicken Council (NCC) was none too pleased, saying lots of foods are contaminated with arsenic. “By focusing specifically on chicken, IATP [the Institute for Agriculture and Trade Policy] makes it clear that it is producing a publicity-oriented document focused on the objective of forcing [chicken] producers to stop using these safe and effective products”—by which the NCC means these arsenic-containing drugs. In fact, the NCC admits to using them but says we don’t need to worry because chicken producers use organic arsenic, “not the inorganic form made infamous in ‘Arsenic and Old Lace.’” Okay, so we don’t need to worry—until, apparently, we cook it. When chicken is cooked, it appears that some of the arsenic drug in the meat turns into the ”Arsenic and Old Lace” variety. So, the Poison-Free Poultry Act of 2009 was introduced into Congress, flopped, and was followed by the subsequent introduction of the Poison-Free Poultry Act of 2011. Did the second attempt fare any better? No, legislators once again said pish posh to poison-poor poultry. So, in 2013, a coalition of nine organizations got together and sued the FDA, and by December 31, 2015, all arsenic-containing poultry drugs were withdrawn. As of 2016, arsenic is no longer to be fed to chickens. The bad news is that without giving birds the arsenic-containing drug roxarsone, chicken may lose some of its “appealing pink color.”

In the end, the poultry industry got away with exposing the American public to arsenic for 72 years. “It should be noted that the European Union has never approved drugs containing arsenic for animal consumption” in the first place, saying, Hmm, feed our animals arsenic? No thanks, nein danke, no grazie, non, merci.

Europe has also long since banned the “urgent threat to human health” posed by feeding farm animals millions of pounds of human antibiotics. As you can see at 5:30 in my video, feeding chickens en masse literally tons of drugs like tetracyclines and penicillins to fatten them faster is a problem that gets worse every year instead of better and dates back to 1951 when drug companies whipped out the ALL CAPS in advertisements,  promising “PROFITS…several times higher!”, a dangerous practice the poultry industry has gotten away with for 68 years…and counting.


If you don’t eat poultry and are feeling a little cocky, you may want to check out my 12-video series on arsenic in rice before you gloat too much:

Think feeding arsenic to chickens is weird? Check out Illegal Drugs in Chicken Feathers.

And for more on the critical public health threat posed by antibiotic overuse in animal agriculture, see:

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

Açaí vs. Wild Blueberries for Artery Function

“Plant-based diets…have been found to reduce the risk of cardiovascular disease” and some of our other leading causes of death and disability. “Studies have shown that the longest living and least dementia-prone populations subsist on plant-based diets.” So why focus on açaí berries, just one plant, for brain health and performance?

Well, “foods rich in polyphenols…improve brain health,” and açaí berries contain lots of polyphenols and antioxidants, so perhaps that’s why they could be beneficial. If you’re only looking at polyphenols, though, there are more than a dozen foods that contain more per serving, like black elderberry, regular fruits like plums, flaxseeds, dark chocolate, and even just a cup of coffee.

As you can see at 1:02 in my video The Benefits of Açaí vs. Blueberries for Artery Function, in terms of antioxidants, açaí berries may have ten times more antioxidant content than more typical fruits, like peaches and papayas, and five times more antioxidants than strawberries. But blackberries, for instance, appear to have even more antioxidants than açaí berries and are cheaper and more widely available.

Açaí berries don’t just have potential brain benefits, however. Might they also protect the lungs against harm induced by cigarette smoke? You may remember the study where the addition of açaí berries to cigarettes protected against emphysema—in smoking mice, that is. That’s not very helpful. There is a long list of impressive-looking benefits until you dig a little deeper. For example, I was excited to see a “[r]eduction of coronary disease risk due to the vasodilation effect” of açaí berries, but then I pulled the study and found they were talking about a vasodilator effect…in the mesenteric vascular bed of rats. There hadn’t been any studies on açaí berries and artery function in humans until a study published in 2016.

Researchers gave overweight men either a smoothie containing about two-thirds of a cup of frozen açaí pulp and half a banana or an artificially colored placebo smoothie containing the banana but no açaí. As you can see at 2:26 in my video, within two hours of consumption of their smoothie, the açaí group had a significant improvement in artery function that lasted for at least six hours, a one or two point bump that is clinically significant. In fact, those walking around with just one point higher tend to go on to suffer 13 percent fewer cardiovascular events like fatal heart attacks.

As I show at 2:52 in my video, you can get the same effect from wild blueberries, though: about a one-and-a-half-point bump in artery function two hours after blueberry consumption. This effect peaks then plateaus at about one and a half cups of blueberries, with two and a half cups and three and a half cups showing no further benefits.

What about cooked blueberries? As you can see at 3:12 in my video, if you baked the blueberries into a bun, like a blueberry muffin, you get the same dramatic improvement in artery function.

Cocoa can do it, too. As shown at 3:30 in my video, after having one tablespoon of cocoa, you gain about one point, and two tablespoons gives you a whopping four points or so, which is double what you get with açaí berries.

One and a quarter cups’ worth of multicolored grapes also give a nice boost in artery function, but enough to counter an “acute endothelial insult,” a sudden attack on the vulnerable inner layer of our arteries? Researchers gave participants a “McDonald’s sausage egg breakfast sandwich and two hash browns.” They weren’t messing around! As you can see at 3:56 in my video, without the grapes, artery function was cut nearly in half within an hour, and the arteries stayed stiffened and crippled three hours later. But when they ate that McMuffin with all those grapes, the harmful effect was blunted.

Eat a meal with hamburger meat, and artery function drops. But if you eat that same meal with some spices, including a teaspoon and a half of turmeric, artery function actually improves.

What about orange juice? Four cups a day of commercial orange juice from concentrate for four weeks showed no change in artery function. What about freshly squeezed orange juice? Still nothing. That’s one of the reasons berries, not citrus, are the healthiest fruits.

For a beverage that can improve your artery function, try green tea. Two cups of green tea gives you that same effect we saw with cocoa, gaining nearly four points within just 30 minutes. And, as you can see at 5:05 in my video, that same crazy effect is also seen with black tea, with twice as powerful an effect as the açaí berries.

So, why all the focus on just that one plant? Why açaí berries? Well, the real reason may be because the author owns a patent on an açaí-based dietary supplement.


How do the antioxidant effects of açaí berries compare to applesauce? See The Antioxidant Effects of Açaí vs. Apples.

What about the effects of other foods on artery function? Coronary artery disease is, after all, our leading cause of death for men and women. See:

What else can blueberries do? Check out:

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

Kidney Toxins Created by Meat Consumption

As I discuss in my video How to Treat Heart Failure and Kidney Failure with Diet, one way a diet rich in animal-sourced foods like meat, eggs, and cheese may contribute to heart disease, stroke, and death is through the production of an atherosclerosis-inducing substance called TMAO. With the help of certain gut bacteria, the choline and carnitine found concentrated in animal products can get converted into TMAO. But, wait a second. I thought atherosclerosis, or hardening of the arteries, was about the buildup of cholesterol. Is that not the case?

“Cholesterol is still king,” but TMAO appears to accelerate the process. It seems that TMAO appears to increase the ability of inflammatory cells within the atherosclerotic plaque in the artery walls to bind to bad LDL cholesterol, “which makes the cells more prone to gobble up cholesterol.” So TMAO is just “another piece to the puzzle of how cholesterol causes heart disease.”

What’s more, TMAO doesn’t just appear to worsen atherosclerosis, contributing to strokes and heart attacks. It also contributes to heart and kidney failure. If you look at diabetics after a heart attack, a really high-risk group, nearly all who started out with the most TMAO in their bloodstream went on to develop heart failure within 2,000 days, or about five years. In comparison, only about 20 percent of those starting out with medium TMAO levels in the blood went into heart failure and none at all in the low TMAO group, as you can see at 1:21 in my video.

So, those with heart failure have higher levels of TMAO than controls, and those with worse heart failure have higher levels than those with lesser stage heart disease. If you follow people with heart failure over time, within six years, half of those who started out with the highest TMAO levels were dead. This finding has since been replicated in two other independent populations of heart failure patients.

The question is, why? It’s probably unlikely to just be additional atherosclerosis, since that takes years. For most who die of heart failure, their heart muscle just conks out or there’s a fatal heart rhythm. Maybe TMAO has toxic effects beyond just the accelerated buildup of cholesterol.

What about kidney failure? People with chronic kidney disease are at a particularly “increased risk for the development of cardiovascular disease,” thought to be because of a diverse array of uremic toxins. These are toxins that would normally be filtered out by the kidneys into the urine but may build up in the bloodstream as kidney function declines. When we think of uremic toxins, we usually think of the toxic byproducts of protein putrefying in our gut, which is why specially formulated plant-based diets have been used for decades to treat chronic kidney failure. Indeed, those who eat vegetarian diets form less than half of these uremic toxins.

Those aren’t the only uremic toxins, though. TMAO, which, as we’ve discussed, comes from the breakdown of choline and carnitine found mostly in meat and eggs, may be increasing heart disease risk in kidney patients as well. How? “The cardiovascular implication of TMAO seems to be due to the downregulation of reverse cholesterol transport,” meaning it subverts our own body’s attempts at pulling cholesterol out of our arteries.

And, indeed, the worse our kidney function gets, the higher our TMAO levels rise, and those elevated levels correlate with the amount of plaque clogging up their arteries in their heart. But once the kidney is working again with a transplant, your TMAO levels can drop right back down. So, TMAO was thought to be a kind of biomarker for declining kidney function—until a paper was published from the Framingham Heart Study, which found that “elevated choline and TMAO levels among individuals with normal renal [kidney] function predicted increased risk for incident development of CKD,” chronic kidney disease. This suggests that TMAO is both a biomarker and itself a kidney toxin.

Indeed, when you follow kidney patients over time and assess their freedom from death, those with higher TMAO, even controlling for kidney function, lived significantly shorter lives, as you can see at 4:44 in my video. This indicates this is a diet-induced mechanism for progressive kidney scarring and dysfunction, “strongly implying the need to focus preventive efforts on dietary modulation,” but what might that look like? Well, maybe we should reduce “dietary sources of TMAO generation, such as some species of deep-sea fish, eggs, and meat.”

It also depends on what kind of gut bacteria you have. You can feed a vegan a steak, and they still don’t really make any TMAO because they haven’t been fostering the carnitine-eating bacteria. Researchers are hoping, though, that one day, they’ll find a way to replicate “the effects of the vegetarian diet…by selective prebiotic, probiotic, or pharmacologic therapies.”


For more on this revolutionary TMAO story, see:

For more on kidney failure, see Preventing Kidney Failure Through Diet and Treating Kidney Failure Through Diet.

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations: