Cancer Risk from Arsenic in Rice and Seaweed

A daily half-cup of cooked rice may carry a hundred times the acceptable cancer risk of arsenic. What about seaweed from the coast of Maine?

“At one point during the reign of King Cotton, farmers in the south central United States controlled boll weevils with arsenic-based pesticides, and residual arsenic still contaminates the soil.” Different plants have different reactions to arsenic exposure. Tomatoes, for example, don’t seem to accumulate much arsenic, but rice plants are really good at sucking it out of the ground—so much so that rice can be used for “arsenic phytoremediation,” meaning you can plant rice on contaminated land as a way to clear arsenic from the soil. Of course, you’re then supposed to throw the rice—and the arsenic—away. But in the South, where 80 percent of U.S. rice is grown, we instead feed it to people.

As you can see at 0:52 in my video Cancer Risk from Arsenic in Rice and Seaweed, national surveys have shown that most arsenic exposure has been measured coming from the meat in our diet, rather than from grains, with most from fish and other seafood. Well, given that seafood is contributing 90 percent of our arsenic exposure from food, why are we even talking about the 4 percent from rice?

The arsenic compounds in seafood are mainly organic—used here as a chemistry term having nothing to do with pesticides. Because of the way our body can deal with organic arsenic compounds, “they have historically been viewed as harmless.” Recently, there have been some questions about that assumption, but there’s no question about the toxicity of inorganic arsenic, which you get more of from rice.

As you can see at 1:43 in my video, rice contains more of the toxic inorganic arsenic than does seafood, with one exception: Hijiki, an edible seaweed, is a hundred times more contaminated than rice, leading some researchers to refer to it as the “so-called edible hijiki seaweed.” Governments have started to agree. In 2001, the Canadian government advised the public not to eat hijiki, followed by the United Kingdom, the European Commission, Australia, and New Zealand. The Hong Kong Centre for Food Safety advised the public not to eat hijiki and banned imports and sales of it. Japan, where there is actually a hijiki industry, just advised moderation.

What about seaweed from the coast of Maine—domestic, commercially harvested seaweed from New England? Thankfully, only one type, a type of kelp, had significant levels of arsenic. But, it would take more than a teaspoon to exceed the provisional daily limit for arsenic, and, at that point, you’d be exceeding the upper daily limit for iodine by about 3,000 percent, which is ten times more than reported in a life-threatening case report attributed to a kelp supplement.

I recommend avoiding hijiki due to its excess arsenic content and avoiding kelp due to its excess iodine content, but all other seaweeds should be fine, as long as you don’t eat them with too much rice.

In the report mentioned earlier where we learned that rice has more of the toxic inorganic arsenic than fish, we can see that there are 88.7 micrograms of inorganic arsenic per kilogram of raw white rice. What does that mean? That’s only 88.7 parts per billion, which is like 88.7 drops of arsenic in an Olympic-size swimming pool of rice. How much cancer risk are we talking about? To put it into context, the “usual level of acceptable risk for carcinogens” is one extra cancer case per million. That’s how we typically regulate cancer-causing substances. If a chemical company wants to release a new chemical, we want them to show that it doesn’t cause more than one in a million excess cancer cases.

The problem with arsenic in rice is that the excess cancer risk associated with eating just about a half cup of cooked rice a day could be closer to one in ten thousand, not one in a million, as you can see at 4:07 in my video. That’s a hundred times the acceptable cancer risk. The FDA has calculated that one serving a day of the most common rice, long grain white, would cause not 1 in a million extra cancer cases, but 136 in a million.

And that’s just the cancer effects of arsenic. What about all the non-cancer effects? The FDA acknowledges that, in addition to cancer, the toxic arsenic found in rice “has been associated with many non-cancer effects, including ischemic heart disease, diabetes, skin lesions, renal [kidney] disease, hypertension, and stroke.” Why, then, did the FDA only calculate the cancer risks of arsenic? “Assessing all the risks associated with inorganic arsenic would take considerable time and resources and would delay taking any needed action to protect public health” from the risks of rice.

“Although physicians can help patients reduce their dietary arsenic exposure, regulatory agencies, food producers, and legislative bodies have the most important roles” in terms of public health-scale changes. “Arsenic content in U.S.-grown rice has been relatively constant throughout the last 30 years,” which is a bad thing.

“Where grain arsenic concentration is elevated due to ongoing contamination, the ideal scenario is to stop the contamination at the source.” Some toxic arsenic in foods is from natural contamination of the land, but soil contamination has also come from the dumping of arsenic-containing pesticides, as well as the use of arsenic-based drugs in poultry production and then the spreading of arsenic-laced chicken manure on the land. Regardless of why south central U.S. rice paddies are so contaminated, we shouldn’t be growing rice in arsenic-contaminated soil.

What does the rice industry have to say for itself? Well, it started a website called ArsenicFacts. Its main argument appears to be that arsenic is everywhere, we’re all exposed to it every day, and it’s in most foods. But shouldn’t we try to cut down on the most concentrated sources? Isn’t that like saying look, diesel exhaust is everywhere, so why not suck on a tailpipe? The industry website quotes a nutrition professor saying, “All foods contain arsenic. So, if you eliminate arsenic from your diet, you will decrease your risk…and you’ll die of starvation.” That’s like Philip Morris saying that the only way to completely avoid secondhand smoke is to never breathe—but then you’ll asphyxiate, so you might as well just start smoking yourself. If you can’t avoid it, you might as well consume the most toxic source you can find?!

That’s the same tack the poultry industry took. Arsenic and chicken? “No need to worry” because there’s a little arsenic everywhere. That’s why it’s okay the industry fed chickens arsenic-based drugs for 70 years. If you can’t beat ’em, join ’em.

How can the rice industry get away with selling a product containing a hundred times the acceptable cancer risk? I cover that and so much more in my other videos on arsenic and rice, which also include concrete recommendations on how to mediate your risk.


Check out:

Pesticides were not the only source of arsenic. Poultry poop, too, if you can believe it! I cover that story in Where Does the Arsenic in Chicken Come From? and Where Does the Arsenic in Rice, Mushrooms, and Wine Come From?.

Chronic low-dose arsenic exposure is associated with more than just cancer. See The Effects of Too Much Arsenic in the 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:

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:

Balancing the Risks and Benefits of Vitamin C Supplements

Mainstream medicine has long had a healthy skepticism of dietary supplements, extending to the present day with commentaries like “Enough is enough.” In an essay entitled “Battling quackery,” however, published in the Archives of Internal Medicine, it’s argued that we may have gone too far in our supplement bashing, as evidenced by our “uncritical acceptance” of supposed toxicities; the surprisingly “angry, scornful tone” found in medical texts using words like “careless,” “useless,” “indefensible,” “wasteful,” and “insidious”; and ignoring evidence of possible benefit.

“To illustrate the uncritical acceptance of bad news” about supplements, the authors discussed the “well-known” concept that high-dose vitamin C can cause kidney stones, as I highlight in my video Do Vitamin C Supplements Prevent Colds but Cause Kidney Stones? Just because something is well-known in medicine, however, doesn’t mean it’s necessarily true. In fact, the authors couldn’t find a single, reported case.

We’ve known that vitamin C is turned into oxalates in the body, and, if the level of oxalates in the urine gets too high, stones can form, but, even at 4,000 mg of vitamin C a day, which is like a couple gallons’ worth of orange juice, urinary oxalates may not get very high, as you can see at 1:10 in my video. Of course, there may be the rare individuals who have an increased capacity for this conversion into oxalates, so a theoretical risk of kidney stones with high-dose vitamin C supplements was raised in a letter printed in a medical journal back in 1973.

When the theoretical risk was discussed in the medical literature, however, the researchers made it sound as if it were an established phenomenon: “Excessive intake of vitamin C may also be associated with the formation of oxalate stones.” Sounds less like a theoretical risk and more like an established phenomenon, right? That statement had seven citations supposedly suggesting an association between excessive vitamin-C intake and the formation of oxalate kidney stones. Let’s look at the cited sources, which you can see from 1:47 in my video. One reference is the letter about the theoretical risk, which is legitimate, but another listed citation, titled “Jaundice following the administration of niacin,” has nothing to do with either vitamin C or kidney stones. What’s more, the other five citations are just references to books. That may be acceptable if the books cited primary research themselves, but, instead, there was a kind of circular logic, where the books just cite other books citing that theoretical risk letter again. So, while it looks as if there’s a lot of evidence, they’re all just expressing this opinion with no new data.

By that time, there actually were studies that followed populations of people taking vitamin C supplements and found no increased kidney stone risk among men, then later, the same was shown in women. So, you can understand the frustration of the authors of “Battling quackery” commentary that vitamin-C supplements appeared to be unfairly villainized.

The irony is that we now know that vitamin-C supplements do indeed appear to increase kidney stone risk. The same population of men referenced above was followed further out, and men taking vitamin-C supplements did in fact end up with higher risk. This has since been confirmed in a second study, though also of men. We don’t yet know if women are similarly at risk, though there has now also been a case reported of a child running into problems.

What does doubling of risk mean exactly in this context? Those taking a thousand milligrams or so of vitamin C a day may have a 1-in-300 chance of getting a kidney stone every year, instead of a 1-in-600 chance. One in 300 “is not an insignificant risk,” as kidney stones can be really painful, so researchers concluded that since there are no benefits and some risk, it’s better to stay away.

But there are benefits. Taking vitamin C just when you get a cold doesn’t seem to help, and although regular supplement users don’t seem to get fewer colds, when they do get sick, they don’t get as sick and get better about 10 percent faster. And, those under extreme physical stress may cut their cold risk in half. So, it’s really up to each individual to balance the potential common cold benefit with the potential kidney stone risk.


What about intravenous vitamin C? I’ve got a whole video series on that, including:

If you’re not taking vitamin C supplements for pharmacological effects and just want to know how many vitamin C-rich fruits and vegetables to eat every day, check out my video What Is the Optimal Vitamin C Intake?.

Is there anything we can put into our mouth that really might help prevent colds? These videos will point you in the right direction:

And, if you’re interested in learning about the most important steps you can take to prevent and treat kidney stones, look no further than my videos How to Prevent Kidney Stones with Diet and How to Treat Kidney Stones with Diet.

What about high-oxalate vegetables such as rhubarb, spinach, beet greens and swiss chard? I’d encourage a moderation in intake. If you’re going to take my advice to ideally eat cups of dark green leafy vegetables a day I’d recommend sticking with other greens such as kale or collards.

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: