 It's crazy when you think about all the different kinds of foods we eat. We just swallow and hope it all works out for the best. Well, it turns out there are better ways to think about keeping our bodies humming healthfully along. Welcome to Nutrition Facts, I'm your host, Dr. Michael Greger. Today we try to help our bodies fight cancer that's metastasized, and we start with research about the perils of palmitic acid. This formation is the leading cause of death in cancer patients. That's how most people die of cancer. It's not the primary tumor, but the cancer spreading through the body. It's estimated that metastasis is responsible for 90% of cancer deaths, with little progress made in stopping the spread, despite our modern medical armamentarium. In fact, we can sometimes make it worse. Chemotherapy-induced metastasis. All the typical cancer treatments, radiation, chemotherapy, surgery, even just poking the tumors with fine needle biopsies, have the potential to contribute to the problem. I mean, you can imagine how cutting around a tumor, severing the blood vessels, might lead to the migration of residual tumor cells. But why chemotherapy? How might chemo exacerbate metastases? Despite reducing the size of primary tumors, chemotherapy can change the surrounding tissues, resulting in an increased escape of cancer cells into the bloodstream. Sometimes chemo-surgery radiation are entirely justified, but sometimes these treatments can make things worse, if only we had a way to treat the cause of the cancer spreading. The development of anti-metastatic therapies has been hampered by the fact that we haven't been able to identify the cells that initiate metastasis, but then this landmark study was published. Researchers found a subpopulation of human cancer cells unique in their ability to initiate metastasis, all expressing high levels of a fat receptor known as CD36, dubbed the fat controller. It turns out, palmitic acid or high-fat diet specifically boosts the metastatic potential of these cancer cells—mortified palmitic acid. Although originally discovered in palm oil, it's most concentrated in meat and dairy. Emerging evidence shows that palmitic acid serves as a signaling molecule regulating the progression and development of many diseases at the molecular level, and that's the saturated fat that is recognized by the CD36 receptor on the cancer cells. And we know that's to blame, because if you block the CD36 receptor, you block the metastasis. Now this was for human cancer, however it was a human cancer implanted into mice. But clinically, meaning in cancer patients, the presence of these CD36-studded metastasis initiating cells does indeed correlate with the poor prognosis. For example, CD36 appears to drive the progression of brain tumors. If you look the survival curves, those with tumors with less CD36 expression lived significantly longer—the same with breast cancer mortality. No surprise, since CD36 appears to play a critical role in the proliferation, migration, and growth of breast cancer cells. Inhibit CD36, and you can inhibit the migration and invasion of breast cancer cells. Cancer cell migration and invasion before and after CD36 inhibition. And not just in human melanoma and breast cancer-derived tumors, now we suspect that CD36 drives ovarian cancer progression and metastasis too, since we can inhibit ovarian cancer cell invasion and migration and block both lymph node and blood-borne metastases by blocking CD36. We see the same kind of effect with prostate cancer. Suppress the uptake of fat by prostate cancer cells, and you can suppress the tumor. This was all studied with like receptor-blocking drugs and antibodies in a laboratory setting, though. If these metastasis initiating cancer cells particularly rely on dietary fat to promote the spread of cancer, why not just block the dietary fat in the first place? Cancer cells love fat and cholesterol. The reason why fat metabolism may fuel cancer spread is because there's so much energy stored in fat. Hence, metastatic cells might take advantage of this feature to obtain the high amount of energy that is likely to be required for them to anchor and set up shop throughout the body. The time when sugar was considered as a major, if not only fuel, to support cancer cell proliferation is over. There appears to be a fatter way to metastasize. No wonder high-fat diets may play a crucial role in increasing the risk of different cancer types, including several advanced cancers. Okay, if dietary fat may be greasing the wheels of the cancer machine, might there be specific dietary regimens we could use to starve cancers of dietary fat? In our next story, we look at how randomized controlled trials show lowering saturated fat intake can lead to improved breast cancer survival. This is the leading cause of cancer-related death. Cancer kills because cancer spreads. For example, the five-year survival rate for women with localized breast cancer is nearly 99%, but that drops to just 27% in those with metastasized cancer. Yet our ability to effectively treat metastatic disease has not changed significantly in the past few decades. You know things are getting desperate when there are papers like this, targeting metastasis with snake toxins. Now we do have built-in defenses, natural killer cells that roam the body, killing off budding tumors, and I have videos on boosting natural killer cell activity. But as I explained in the last video, there's a fat receptor called CD36 that appears to be essential for cancer cells to spread, and these cancer cells respond to dietary fat intake, but not all fat. CD36 is upregulated by palmitic acid, as much as a 50-fold increase within 12 hours. Palmitic acid is a saturated fat found in junk food made from palm oil, but it's most concentrated in meat and dairy. This may explain why if you look at dietary fat and breast cancer mortality, there was no difference in risk of breast cancer-specific death for women in the highest versus lowest category of total fat intake, but you're about 50% more likely to die of breast cancer if you eat a lot of saturated fat. The systematic review and meta-analysis concluded that saturated fat intake negatively impacts upon breast cancer survival. This may explain why intake of high fat dairy, but not low fat dairy, was related to a high risk of mortality after a breast cancer diagnosis. If it was the dairy protein like casein, that was a problem. The skim milk might be even worse, but no, it was the saturated butter fat. Maybe because it triggered the CD36-induced cancer-spreading mechanism? Women who consumed one or more servings per day of high fat dairy had about a 50% higher risk of dying from breast cancer. We see the same thing with dairy intake in relation to prostate cancer survival. Drinking high fat milk appeared to increase the risk of dying from prostate cancer by as much as 600% in patients with localized prostate cancer. But low fat milk was not associated with such an increase in risk, so it seems to be the animal fat rather than the animal protein. And this is consistent with what Harvard researchers found in the United States. More evidence to the fat receptor CD36 is involved is that the risk of colorectal cancer from meat consumption increased from just doubling risk to octupling risk, multiplying the odds of getting cancer eightfold for those who carry a specific type of CD36 gene. So, is it time to give breast cancer patients, for example, a prescription for a low-fat diet? A cancer diagnosis is a teachable moment if there ever was one to motivate people to make changes to their lifestyle. But provision of evidence-based guidelines is essential. And you don't know until you put it to the test. A randomized prospective multicenter clinical trial to test the effect of a dietary intervention designed to reduce fat intake in women with resected early-stage breast cancer, meaning the women had their breast cancer surgically removed and were praying it doesn't come back. The dietary intervention group dropped their fat intake from about 30% of calories down to 20% of calories, dropped saturated fat intake about 40% and maintained that 40% lower intake after one year, three years, five years, and after approximately five years of fall-up, the women in the dietary intervention group had a 24% lower risk of relapse, a 24% lower risk of the cancer coming back. That was the women's intervention nutrition study. Then there was the women's health initiative study, where again women were randomized to drop their fat intake down to about 20% of calories. And again, those in the dietary intervention group experienced increased breast cancer survival, meaning a dietary change may be able to influence breast cancer outcomes. And not only was breast cancer survival significantly greater, the women also experienced a reduction in heart disease and a reduction in diabetes as a little side bonus. Finally today, the mighty power of cruciferous vegetables in fighting cancer. Both the women's intervention nutrition study and the women's health initiative study showed that women randomized to a lower fat diet enjoyed improved breast cancer-free survival. But wait a second. What about the women's health eating and living study, where women with breast cancer were also randomized to drop their fat intake down to 15 to 20% of calories? Yet after seven years, there was no difference in breast cancer relapse or death. Anytime you get an unexpected result, you always have to question whether people actually follow through with the instructions. Like if you randomized people to a stop smoking group and they ended up with the same lung cancer rates as the group not instructed to stop smoking, one likely explanation is that the group told to stop smoking didn't actually stop. In the women's healthy eating and living study, both the dietary intervention group and the control group started out at about 30% of calories from fat. Then the diet group was told to drop down to 15 to 20%. And by the end of the study, they dropped from 28.5% fat all the way down to 28.9% fat? They didn't change at all. No wonder they didn't experience any breast cancer benefit. But even if you include that flawed study and put all the trials together on the effect of lower fat diets and breast cancer survival, you see a reduced risk of breast cancer relapse and a reduced risk of death. Conclusion. Going on a low fat diet after a breast cancer diagnosis can improve breast cancer survival by reducing risk of cancer recurrence. And now perhaps we know why, by targeting metastasis initiating cancer cells through the fat receptor CD36, which I covered in my last two videos. We know that the cancer spreading receptor is up-regulated by saturated fat. Is there anything in our diet that can down-regulate it? Broccoli. Broccoli appeared to decrease CD36 expression by as much as 35%, but that was in mice. But of all fruits and vegetables, cruciferous vegetables like broccoli were the only ones associated with significantly less total cancer risk, and not just getting cancer in the first place. Those with bladder cancer who eat broccoli appear to live longer than those who don't. Those with lung cancer who eat more cruciferous veggies appear to survive longer as well. For example, one year out, about 75% of lung cancer patients eating more than one serving of cruciferous vegetables a day were still alive, whereas by then most who had been getting less than a half serving a day were already dead, killed off by their cancer. Ovarian cancer. Cruciferous vegetable intake significantly favored survival, whereas a survival disadvantage was shown for meats. Milk also appeared to double the risk of dying. Here are the survival graphs. Eight years out, for example. About 40% of ovarian cancer patients who averaged meat or milk every day were dead, compared to only about 20% who just had meat or milk a few times a week at most. Now it could just be that the fat and cholesterol on the meat increased circulating, estrogen levels, or because of meat's growth hormones or all the carcinogens, and galactose, the sugar naturally found in milk may also be directly toxic to the ovary, and dairy's got all the hormones too. However, the lowering of risk with broccoli and the increasing of risk with meat and dairy are also consistent with the CD36 mechanism cancer spread we've been talking about. So how about putting it to the test? Patients with advanced pancreatic cancer given pulverized broccoli sprouts or placebo. Compared to those in the placebo group, the average death rate was lower in the broccoli group. After a month, 18% of the placebo group was dead, but none in the broccoli group. By three months, another quarter of the placebo group had died, but still not a single death in the broccoli group. And by six months, 43% of the remaining patients in the placebo group were dead, along with the first 25% of the broccoli group. Unfortunately, the patients knew which group they were in because they were evidently getting broccoli burps, which gave it away, so you can't discount the placebo effect, and they weren't even properly randomized, since many of the patients refused to participate unless they were placed in the active treatment group, which is understandable, but it makes for a less rigorous result. But hey, a little broccoli can't hurt, and it's the no downside that leads to advising women undergoing treatment for breast cancer, for example, to include the liberal culinary use of cruciferous vegetables, and the same for reducing saturated fat. Is it time to give breast cancer patients a prescription for a low-fat diet? Although counseling women to consume a healthy diet after breast cancer diagnosis is certainly warranted for general health, read an editorial in the Journal of the National Cancer Institute, the existing data still fall a bit short of proving this will help reduce the risk of breast cancer recurrence and mortality. But what do you have to lose? After all, it's still certainly warranted for general health. To see any graphs, charts, graphics, images, or studies mentioned here, please go to the Nutrition Facts Podcast landing page. There you'll find all the detailed information you need, plus links to all the sources we cite for each of these topics. For our timely text on the pathogens that cause pandemics, you can order the e-book out of your book or hard copy of my latest book, How to Survive a Pandemic. For recipes, check out my new How Not to Diet Cookbook. It's beautifully designed with more than 100 recipes for delicious and nutritious meals. 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