Treating Advanced Prostate Cancer with Diet

Dr. Dean Ornish showed that a plant-based diet and lifestyle program could apparently reverse the progression of prostate cancer for early stage, localized, watch-and-wait cancer. What about for more advanced stage life-threatening disease?

Dr. Dean Ornish showed that a plant-based diet and lifestyle program could apparently reverse the progression of prostate cancer by making men’s bloodstreams nearly eight times better at suppressing cancer cell growth. But this was for early-stage, localized, watch-and-wait prostate cancer.

What about for more advanced-stage, life-threatening disease? There have been sporadic case reports in the literature suggesting benefit. For example, a man with extensive metastatic disease who had been given about three years to live went on a strict plant-based diet. Four years later, it appeared the cancer had disappeared. After six years, he got a little too comfortable, backslid a bit on the diet and began eating “turkey, tuna fish, and chicken,” then the cancer came raging back and he died. But that could have been a total coincidence. That’s the problem with case reports, which are kind of glorified anecdotes. You have no idea how representative the outcome is unless it’s studied formally. But, throughout the 20th century, all we had were these kinds of case reports for more advanced prostate cancer until 2001.

We had “preliminary evidence” based on all the case reports that “prostate cancer may be sensitive to diet even after metastasis develops. Plant-based diets may be associated with prolonged survival and instances of remission of bone metastasis in men with advanced disease.” So, researchers decided to put it to the test in a four-month intervention. They thought that too much saturated fat, too little fiber, and too much meat may be the biggest players in tumor promotion and progression, so they put people on a whole food plant-based diet of whole grains, beans, seeds, and fruits. Figuring this would be quite the departure from their regular diet, the researchers included a stress reduction component in hopes of improving dietary compliance.

Who were the subjects? The ten men in the study didn’t just have prostate cancer—they had all undergone a radical prostatectomy to remove their primary tumor and then subsequently had increasing PSA levels, indicative of probable metastatic disease. PSA stands for prostate-specific antigen. It’s only made by prostate cells, but the ten men had just had their entire prostates removed so their levels should have been zero. The fact that they not only still had some PSA, but that it was rising suggests that the surgery had failed, and the cancer had spread and was making a comeback.

At 2:43 in my video Treating Advanced Prostate Cancer with Diet: Part 1, you can view a graph showing the PSA levels for each of the men before the study began and see the speed at which their PSAs went up. If their PSA trajectories had stayed the same after four months of eating healthfully, it would mean the diet had had no effect. In that case, presumably, the cancer would have still been powering away and spreading just as fast as before. Instead, in two of the men, it looked as if the cancer had accelerated and grew even faster, but in the other eight men, the intervention appeared to work, apparently slowing down cancer growth. And, in three of the ten men, it didn’t just slow or stop, but appeared to reverse and shrink.

Why the different responses? Well, in the Ornish study, the more people complied with the diet and lifestyle recommendations, the better they did, as you can see at 3:31 in my video. Dietary changes only work if you actually do them. Just because you tell people to start eating a whole food plant-based diet, doesn’t mean patients actually do it. One can use fiber intake as a proxy for dietary compliance because all whole plant foods have fiber, and Ornish’s patients about doubled their fiber intake from 31 grams to 59 grams.

How did the ten men in the 2001 study do? They started out even worse, averaging 14 grams of fiber a day, and only made it up to 19 grams a day. That’s not a whole food plant-based diet—that doesn’t even meet the recommended minimum daily intake. As you can see at 4:18 in my video, only four of the ten men even increased their fiber intake at all, so that may explain the different responses. In fact, the man whose fiber improved the most had the best PSA result, and the man whose fiber intake dropped the most had the worst PSA result. Indeed, it appears the more changes they made to their diet, the better their results.

The researchers concluded that “a plant-based diet delivered in the context of MBSR [Mindfulness-Based Stress Reduction]…may slow the rate of tumor progression,” and, unlike other treatments, may give patients some control over their disease. And, as Ornish pointed out, “the only side effects are beneficial ones.”

Dr. Ornish and colleagues were able to show an apparent reversal in the progression of early-stage, localized prostate cancer with a plant-based diet and lifestyle program, and researchers at the University of Massachusetts and elsewhere showed a similar diet may help slow the progression of even advanced prostate cancer over a period of four months.

How about over six months? As I discuss in my video Treating Advanced Prostate Cancer with Diet: Part 2, researchers at University of California, San Diego put cancer patients through the same protocol as the four-month study. Once again, these were patients who had already been treated for invasive prostate cancer by either radical prostatectomy or radiation therapy, yet still had rising PSA levels, suggesting the treatment didn’t work and the cancer was on the move. “In those who have undergone a [cancer] recurrence, PSA typically tends to rise exponentially after prostatectomy or radiation therapy, reflecting the gradual, inexorable growth of the cancer in the body. After local treatment, the rate of PSA rise is the single best predictor of…development of overt metastatic disease, as well as of overall survival.” The next step would be hormonal therapy, which is chemical or surgical castration, but that has a list of side effects, including loss of libido, sexual function, strength, and vitality. “Therefore, many physicians employ a strategy of active surveillance” and try to hold off for as long as possible. If we’re just waiting, why not give diet a try?

Patients were “taught to increase intake of whole grains, vegetables, fruit, and legumes and to decrease meat, dairy, and refined carbohydrates.” Of all possible lifestyle interventions, why a whole food plant-based diet? If you look around the world, there are huge differences in prostate cancer rates, as you can see at 1:42 in my video, and our We’re #1! USA! USA! rates are up to a hundred times higher than some places in Asia, for example—and it’s not just genetic. Within one generation of migrating to the United States, cancer rates shoot up, and the grandkids of the immigrants end up with the same top-of-the-pile “approximate US rates.” A whole range of lifestyle factors have been looked at, but diet appears to have the greatest influence.

Specifically, “consumption of meat and dairy appears to increase risk, and consumption of plant-based foods appears to decrease risk.” Hence, the plant-based diet. A possible mechanism found in both meat and dairy products is arachidonic acid, an inflammatory compound that we make from omega-6-rich oils, like corn, sunflower, safflower, and cottonseed oils. It also comes “preformed” in animal-based foods and, in the American diet, is found particularly in chicken and eggs. In a petri dish, arachidonic acid appears to stimulate prostate cancer cell growth as much 200 percent, as you can see at 2:43 in my video.

So what happened when those researchers at University of California, San Diego asked men to remove processed and animal foods from their diet for six months? At 2:57 in my video, you can see a graph showing how fast the cancer patients’ PSA levels had been rising before starting the study. “In the absence of treatment, absolute levels of PSA tend to increase exponentially,” but upon eating more healthfully, nine of the ten study subjects showed an apparent slowing of cancer growth and four of the nine showed an apparent reversal in cancer growth. The average doubling time, an estimate of how long it would take for their cancer to double in size, slowed from doubling every year to closer to every ten years.

Other studies have used various diets and nutritional interventions, like vitamin supplements, but none has worked as well as this one—and the subjects’ compliance wasn’t even all that great. As you can see at 3:41 in my video, they did well in boosting their whole grain consumption in the first three months, but then backslid a bit, and they ate more vegetables, including a serving of greens, and an extra serving of fruit, at least early on. And, in the beginning, they at least ate one whole serving of legumes a day. So the researchers “did observe some [dietary] recidivism by 6 months,” with subjects sliding back into old habits. Given that, they checked to see if the study participants were better able to beat off the disease during that earlier period. And, indeed, at the end of the first three months, on average, there was PSA reversal. “Changes in the rate of rise in PSA, an indicator of disease progression, were in the opposite direction as changes in the intake of plant-based food groups, raising the provocative possibility that PSA may have inversely tracked intake of these foods and suggesting that adoption of a plant-based diet may have therapeutic potential in the management of this condition.”

Their findings suggest that, without further surgery, radiation, or chemotherapy, disease progression can be slowed or even reversed, despite “the prevailing scientific consensus…that cancer progression is largely irreversible.” The researchers state their “findings do not refute the benefits of standard therapies or guarantee that a plant-based diet and stress reduction will always induce remission,” but their results “do contribute to a growing [medical] literature that suggests that in at least some circumstances, cancer may be partly reversible and that modification of dietary and lifestyle factors may be able to help prevent disease spread”—all without getting their testicles cut off.

Hold on. We can make men’s bloodstreams nearly eight times better at suppressing cancer cell growth? See How Not to Die from Cancer.

It’s not all or nothing, though. Any movement we make towards healthy eating may help. See Prostate Cancer Survival: The A/V Ratio .


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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:

Coconut Oil and the Boost in HDL “Good” Cholesterol

The effects of coconut oil were compared to butter and tallow. Even if virgin coconut oil and other saturated fats raise LDL “bad” cholesterol, isn’t that countered by the increase in HDL “good” cholesterol?

According to “the experience and wisdom of 200 of the country’s leading experts in cardiovascular diseases,” in a report representing 29 national medical organizations, including the American Heart Association and the American College of Cardiology, we’ve known for nearly half a century that “coconut oil is one of the most potent agents for elevating [blood] serum cholesterol level.” As I discuss in my video Coconut Oil and the Boost in HDL “Good” Cholesterol, studies showing coconut oil elevates cholesterol date back to 1955, when it was first shown experimentally that switching someone from coconut oil to soybean oil could drop cholesterol from around 200 down to 150, as you can see at 0:39 in my video.

Coconut oil can significantly raise cholesterol levels within hours of consumption. In fact, a significant increase in blood cholesterol was found within hours of eating a slice of cake made from either coconut oil (or cod liver oil for that matter), but not from the same cake made from flaxseed oil.

As you can see at 1:10 in my video, coconut oil may even be worse than tallow, or beef fat, but it is not as bad as butter. An interventional trial was published in March 2017: a month-long randomized, controlled, crossover study looking at the impact of two tablespoons per day of virgin coconut oil. The result? Coconut oil elevated cholesterol about 14 percent over the control, which was consistent with seven other interventional trials published to date in a 2016 review.

Hold on. Saturated fats can make HDL, the so-called good cholesterol, go up, so what’s the problem? The problem is that it doesn’t seem to help. Having a high blood HDL level is “no longer regarded as protective.” What? Wait a second. Higher HDL levels are clearly associated with lower risk of heart disease, as you can see at 2:01 in my video. In fact, HDL levels “are among the most consistent and robust predictors of CVD [cardiovascular disease] risk.” Ah, but there are two types of risk factors: causal and non-causal. Association does not mean causation—that is, just because two things are tightly linked, it doesn’t mean one causes the other.

Let me give you an example, which you can see at 2:30 in my video. I bet that the number of ashtrays someone owns is an excellent predictor of lung cancer risk and that study after study would show that link. But, that does not mean that if you intervene and lower the number of ashtrays someone has, their lung cancer risk will drop, because it’s not the ashtrays that are causing the cancer, but the smoking. The ashtrays are just a marker of smoking, an indicator of smoking, as opposed to playing a causal role in the disease. So, just like having a high number of running shoes and gym shorts might predict a lower risk of heart attack, having a high HDL also predicts a lower risk of heart attack. But, raising HDL, just like raising the number of gym shorts, wouldn’t necessarily affect disease risk. How do you differentiate between causal and non-causal risk factors? You put them to the test. The reason we know LDL cholesterol truly is bad is because people who were just born with genetically low LDL cholesterol end up having a low risk of heart disease. And, if you intervene and actively lower people’s LDL through diet or drugs, their heart disease risk drops—but not so with HDL.

People who live their whole lives with high HDL levels don’t appear to have a lower risk of heart attack, and if you give people a drug that increases their HDL, it doesn’t help. That’s why we used to give people high-dose niacin—to raise their HDL. But, it’s “time to face facts.” The “lack of benefit of raising the HDL cholesterol level with the use of niacin…seriously undermine[s] the hypothesis that HDL cholesterol is a causal risk factor.” In simple terms: “High HDL may not protect the heart.” We should concentrate on lowering LDL. So, specifically, as this relates to coconut oil, the increase in HDL “is of uncertain clinical relevance,” but the increase in LDL you get from eating coconut oil “would be expected to have an adverse effect” on atherosclerotic cardiovascular disease risk.

But, what about the MCTs, the medium-chain triglycerides? Proponents of coconut oil, who lament “that ‘coconut oil causes heart disease’ has created this bad image of [their] national exports,” assert that the medium-chain triglycerides, the shorter saturated fats found in coconut oil, aren’t as bad as the longer-chain saturated fats in meat and dairy. And, what about that study that purported to show low rates of heart disease among Pacific Islanders who ate large amounts of coconuts? I cover both of those topics in my video What About Coconuts, Coconut Milk, and Coconut Oil MCTs?.


I love topics that give me an excuse to talk about scientific concepts more generally, like various study designs in my video Prostate Cancer and Organic Milk vs. Almond Milk or my discussion of direct versus indirect risk factors in this one.

How do we know LDL is bad? Check out How Do We Know That Cholesterol Causes Heart Disease?.

But, wait. Isn’t the whole saturated fat thing bunk? No. 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:

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: