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:

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:

Can Soy Prevent and Treat Prostate Cancer?

As I discuss in my video The Role of Soy Foods in Prostate Cancer Prevention and Treatment, a compilation of 13 observational studies on soy food consumption and the risk of prostate cancer found that soy foods appear to be “protective.” What are observational studies? As opposed to interventional studies, in observational studies, researchers observe what people are eating but don’t intervene and try to change their diets. In these studies, they observed that men who ate more soy foods had lower rates of prostate cancer, but the problem with observational studies is that there could be confounding factors. For example, “people who choose to eat soy also make other lifestyle decisions that lower the risk of cancer (e.g., lower fat intake, higher vegetable and fruit intake, more frequent exercise),” maybe that is why they have less cancer. Most of the studies tried to control for these other lifestyle factors, but you can’t control for everything. What’s more, most of the studies were done in Asia, so maybe tofu consumption is just a sign of eating a more traditional diet. Is it possible that the reason non-tofu consumers got more cancer is that they had abandoned their traditional diet? If only we could look at a Western population that ate a lot of soy. We can: the Seventh-Day Adventists.

In the 1970s, more than 12,000 Adventist men were asked about their use of soy milk and then were followed for up to 16 years to see who got cancer and who did not. So, what did they find? Frequent consumption of soy milk was associated with a whopping 70 percent reduction of the risk of prostate cancer, as you can see at 1:33 in my video. Similarly, in a multiethnic study that involved a number of groups, soy intake appeared protective in Latinos, too.

Prostate cells carry beta type estrogen receptors, which appear to act as a tumor suppressor, a kind of “gatekeeper…inhibiting invasion, proliferation and…preventing” the prostate cells from turning cancerous. And, those are the receptors targeted by the phytoestrogens in soy, like genistein, which inhibits prostate cancer cell invasion and spread in a petri dish at the kind of levels one might get consuming soy foods. The prevention of metastases is critical, as death from prostate cancer isn’t caused by the original tumor, but its spread throughout the body, which explains why it “is recommended that men with prostate cancer consume soy foods, such as soybeans, tofu, miso and tempeh.”

Wait a moment. Dean Ornish and his colleagues got amazing results, apparently reversing the progression of prostate cancer with a plant-based diet and lifestyle program. Was it because of the soy? Their study didn’t just include a vegan diet, but a vegan diet supplemented with a daily serving of tofu and a soy protein isolate powder. There have been studies showing that men given soy protein powders develop less prostate cancer than the control group, but what was the control group getting? Milk protein powder. Those randomized to the milk group got six times more prostate cancer than the soy group, but was that due to the beneficial effects of soy or the deleterious effects of the dairy? Dairy products are not just associated with getting prostate cancer, but also with dying from prostate cancer. Men diagnosed with prostate cancer who then ate more dairy tended to die sooner, and “both low-fat and high-fat dairy consumption were positively associated with an increased risk of fatal outcome.”

The best study we have on soy protein powder supplementation for prostate cancer patients found no significant benefit, and neither did a series of soy phytoestrogen dietary supplements. But, perhaps that’s because they used isolated soy components rather than a whole soy food. “Taking the whole-food approach may be more efficacious,” but it can be hard to do controlled studies with whole foods: You can make fake pills, but how do you give people placebo tofu?

A group of Australian researchers creatively came up with a specially manufactured bread containing soy grits to compare to a placebo regular bread and gave slices to men diagnosed with prostate cancer awaiting surgery. As you can see at 4:31 in my video, they saw a remarkable difference in just about three weeks time. It was the first study to show that a diet incorporating a whole soy food could favorably affect prostate cancer markers, but you can’t just go out and buy soy grit bread. Another study was a little more practical. Twenty men with prostate cancer who had been treated with radiation or surgery but seemed to be relapsing were asked to drink three cups of regular soy milk a day. The PSA levels in each of the 20 patients were all rising before they started the soy milk, suggesting they had relapsing or metastatic cancer growing inside of them. However, during a year drinking soy milk, 6 out of the 20 subjects got better, 2 got worse, and the remaining 12 remained unchanged, as you can see from 5:02 in my video. So, they concluded that soy food may help in a subset of patients.

Based on all these studies, the results Ornish and his colleagues got were probably due to more than just the soy. Similarly, the low prostate cancer rates in Asia are probably because of more than just the soy, since the lowest rates are also found in parts of Africa, where I don’t think they’re eating a lot of tofu. Indeed, in the multiethnic study, other types of beans besides soy also appeared protective for Latinos and all the groups put together, when looking at the most aggressive forms of prostate cancer. So, the protection associated with plant-based diets may be due to eating a variety of healthy foods. 

That soy milk stat from the Adventist study is astounding. What about fermented soy foods, though? That was the subject of Fermented or Unfermented Soy Foods for Prostate Cancer Prevention?.

Reversing the progression of cancer? See How Not to Die from Cancer.

Given the power of diet, it’s amazing to me how difficult Changing a Man’s Diet After a Prostate Cancer Diagnosis can be. It’s not all or nothing, though. Check out Prostate Cancer Survival: The A/V Ratio.

For soy and breast cancer survival, see Is Soy Healthy for Breast Cancer Survivors?.

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: