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Tag: cancer survival

  • Eating to Downregulate a Gene for Metastatic Cancer  | NutritionFacts.org

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    Women with breast cancer should include the “liberal culinary use of cruciferous vegetables.”

    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 survival. However, in the Women’s Healthy Eating and Living Study, women with breast cancer were also randomized to drop their fat intake down to 15 to 20 percent of calories, yet there was no difference in breast cancer relapse or death after seven years.

    Any time there’s an unexpected result, you must question whether the participants actually followed through with study instructions. For instance, if you randomized people to stop smoking and they ended up with the same lung cancer rates as those in the group who weren’t instructed to quit, 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 percent of calories from fat. Then, the diet group was told to lower their fat intake to 15 to 20 percent of calories. By the end of the study, they had in fact gone from 28.5 percent fat to 28.9 percent fat, as you can see below and at 1:16 in my video The Food That Can Downregulate a Metastatic Cancer Gene. They didn’t even reduce their fat intake. No wonder they didn’t experience any breast cancer benefit. 

    When you put together all the trials on the effect of lower-fat diets on breast cancer survival, even including that flawed study, you see a reduced risk of breast cancer relapse and a reduced risk of death. In conclusion, going on a low-fat diet after a breast cancer diagnosis “can improve breast cancer survival by reducing the risk of recurrence.” We may now know why: by targeting metastasis-initiating cancer cells through the fat receptor CD36.

    We know that the cancer-spreading receptor is upregulated by saturated fat. Is there anything in our diet that can downregulate it? Broccoli.

    Broccoli appears to decrease CD36 expression by as much as 35 percent (in mice). Of all fruits and vegetables, cruciferous vegetables like broccoli were the only ones associated with significantly less total risk of cancer and not just getting cancer in the first place, as you can see here and at 2:19 in my video.

    Those with bladder cancer who eat broccoli also appear to live longer than those who don’t, and those with lung cancer who eat more cruciferous veggies appear to survive longer, too.

    For example, as you can see below and at 2:45 in my video, one year out, about 75 percent of lung cancer patients eating more than one serving of cruciferous vegetables a day were still alive (the top line in red), whereas, by then, most who had been getting less than half a serving a day had already died from their cancer (the bottom line in green).

    Ovarian cancer, too. Intake of cruciferous vegetables “significantly favored survival,” whereas “a survival disadvantage was shown for meats.” Milk also appeared to double the risk of dying. Below and at 3:21 in my video are the survival graphs. Eight years out, about 40 percent of ovarian cancer patients who averaged meat or milk every day were deceased (the boldest line, on the bottom), compared to only about 20 percent who had meat or milk only a few times a week at most (the faintest line, on the top). 

    Now, it could be that the fat and cholesterol in meat increased circulating estrogen levels, or it could be because of meat’s growth hormones or all its carcinogens. And galactose, the sugar naturally found in milk, may be directly toxic to the ovary. Dairy has all its 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 of cancer spread.

    Researchers put it to the test in patients with advanced pancreatic cancer who were given pulverized broccoli sprouts or a placebo. The average death rate was lower in the broccoli sprout group compared to the placebo group. After a month, 18 percent of the placebo group had died, but none in the broccoli group. By three months, another 25 percent of the placebo group had died, but still not a single death in the broccoli group. And by six months, 43 percent of the remaining patients in the placebo group were deceased, along with the first 25 percent of the broccoli group. Unfortunately, even though the capsules for both groups looked the same, “true blinding was not possible,” and the patients knew which group they were in “because the pulverized broccoli sprouts could be easily distinguished from the methylcellulose [placebo] through their characteristic smell and taste.” So, we can’t discount the placebo effect. What’s more, the study participants weren’t properly randomized “because many of the patients refused to participate unless they were placed into the [active] treatment group.” That’s understandable, but it makes for a less rigorous result. A little broccoli can’t hurt, though, and it may help. It’s the lack of downsides of broccoli consumption that leads to “Advising Women Undergoing Treatment for Breast Cancer” to include the “liberal culinary use of cruciferous vegetables,” for example.

    It’s the same for reducing saturated fat. The title of an editorial in a journal of the National Cancer Institute asked: “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, 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 we have to lose? After all, it’s still certainly warranted for general health.

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    Michael Greger M.D. FACLM

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  • Eating to Help Control Cancer Metastasis  | NutritionFacts.org

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    Randomized controlled trials show that lowering saturated fat intake can lead to improved breast cancer survival.

    The leading cause of cancer-related death is metastasis. Cancer kills because cancer spreads. The five-year survival rate for women with localized breast cancer is nearly 99 percent, for example, but that falls to only 27 percent in women with metastasized cancer. Yet, “our ability to effectively treat metastatic disease has not changed significantly in the past few decades…” The desperation is evident when there are such papers as “Targeting Metastasis with Snake Toxins: Molecular Mechanisms.”

    We have built-in defenses, natural killer cells that roam the body, killing off budding tumors. But, as I’ve discussed, 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 of consumption, as shown below and at 1:13 in my video How to Help Control Cancer Metastasis with Diet.

    Palmitic acid is a saturated fat made from palm oil that can be found in junk food, but it is most concentrated in meat and dairy. This may explain why, when looking at breast cancer mortality and dietary fat, “there was no difference in risk of breast-cancer-specific death…for women in the highest versus the lowest category of total fat intake,” but there’s about a 50 percent greater likelihood of dying of breast cancer with higher intake of saturated fat. Researchers conclude: “These meta-analyses have shown that saturated fat intake negatively impacts breast cancer survival.”

    This may also explain why “intake of high-fat dairy, but not low-fat dairy, was related to a higher risk of mortality after breast cancer diagnosis.” If a protein in dairy, like casein, was the problem, skim milk might be even worse, but that wasn’t the case. It’s the saturated butterfat, perhaps because it triggered that cancer-spreading mechanism induced by CD36. Women who consumed one or more daily servings of high-fat dairy had about a 50 percent higher risk of dying from breast cancer.

    We see the same with dairy and its relationship to prostate cancer survival. Researchers found that “drinking high-fat milk increased the risk of dying from prostate cancer by as much as 600% in patients with localized prostate cancer. 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 these findings are consistent with analyses from the Health Professionals Follow-up Study (HPFS) and the Physicians’ Health Study (PHS), conducted by Harvard researchers.

    There is even more evidence that the fat receptor CD36 is involved. The “risk of colorectal cancer for meat consumption” increased from a doubling to an octupling—that is, the odds of getting cancer multiplied eightfold for those who carry a specific type of CD36 gene. So, “Is It Time to Give Breast Cancer Patients a Prescription for a Low-Fat Diet?” A cancer diagnosis is often referred to as a ‘teachable moment’ when patients are motivated to make changes to their lifestyle, and so provision of evidence-based guidelines is essential.”

    In a randomized, prospective, multicenter clinical trial, researchers set out “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 had their breast cancer surgically removed. As shown below and at 4:02 in my video, the study participants in the dietary intervention group dropped their fat intake from about 30 percent of calories down to 20 percent, reduced their saturated fat intake by about 40 percent, and maintained it for five years. “After approximately 5 years of follow-up, women in the dietary intervention group had a 24% lower risk of relapse”—a 24-percent lower risk of the cancer coming back—“than those in the control group.” 

    That was the WINS study, the Women’s Intervention Nutrition Study. Then there was the Women’s Health Initiative study, where, again, women were randomized to lower their fat intake down to 20 percent of calories, and, again, “those randomized to a low-fat dietary pattern had increased breast cancer overall survival. Meaning: A dietary change may be able to influence breast cancer outcome.” What’s more, not only was their breast cancer survival significantly greater, but the women also experienced a reduction in heart disease and a reduction in diabetes.

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    Michael Greger M.D. FACLM

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  • Dietary Components That May Cause Cancer to Metastasize  | NutritionFacts.org

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    Palmitic acid, a saturated fat concentrated in meat and dairy, can boost the metastatic potential of cancer cells through the fat receptor CD36.

    The leading cause of death in cancer patients is metastasis formation. That’s how most people die of cancer—not from the primary tumor, but the cancer spreading through the body. “It is estimated that metastasis is responsible for ~90% of cancer deaths,” and little progress has been made in stopping the spread, despite our modern medical armamentarium. In fact, we can sometimes make matters worse. In an editorial entitled “Therapy-Induced Metastasis,” its authors “provide evidence that all the common therapies, including radiotherapy, chemotherapy, fine needle biopsies, surgical procedures and anaesthesia, have the potential to contribute to tumour progression.” You can imagine how cutting around a tumor and severing blood vessels might lead to the “migration of residual tumour cells,” but why chemotherapy? How might chemo exacerbate metastases? “Despite reducing the size of primary tumors, chemotherapy changes the tumor microenvironment”—its surrounding tissues—“resulting in an increased escape of cancer cells into the blood stream.” Sometimes, chemo, surgery, and radiation are entirely justified, but, again, other times, these treatments can make matters worse. If only we had a way to treat the cause of the cancer’s spreading.

    The development of antimetastatic therapies has been hampered by the fact that the cells that initiate metastasis remain unidentified. Then, a landmark study was published: “Targeting Metastasis-Initiating Cells Through the Fatty Acid Receptor CD36.” Researchers found a subpopulation of human cancer cells “unique in their ability to initiate metastasis”; they all express high levels of a fat receptor known as CD36, dubbed “the fat controller.” It turns out that palmitic acid or a high-fat diet specifically boosts the metastatic potential of these cancer cells. Where is palmitic acid found? Although it was originally discovered in palm oil, palmitic acid is most concentrated in meat and dairy. “Emerging evidence shows that palmitic acid (PA), a common fatty acid in the human diet, serves as a signaling molecule regulating the progression and development of many diseases at the molecular level.” It is the saturated fat that is recognized by CD36 receptors on cancer cells, and we know it is to blame, because if the CD36 receptor is blocked, so are metastases.

    The study was of a human cancer, but it was a human cancer implanted into mice. However, clinically (meaning in cancer patients themselves), the presence of these CD36-studded metastasis-initiating cells does indeed correlate with a poor prognosis. CD36 appears to drive the progression of brain tumors, for example. As seen in the survival curves shown below and at 3:21 in my video What Causes Cancer to Metastasize?, those with tumors with less CD36 expression lived significantly longer. It is the same with breast cancer mortality: “In this study, we correlated the mortality of breast cancer patients to tumor CD36 expression levels.” That isn’t a surprise, since “CD36 plays a critical role in proliferation, migration and…growth of…breast cancer cells.” If we inhibit CD36, we can inhibit “the migration and invasion of the breast cancer cells.” 

    Below and at 3:46 in my video, you can see breast cancer cell migration and invasion, before and after CD36 inhibition. (The top lines with circles are before CD36 inhibition, and the bottom lines with squares are after.)

    This isn’t only in “human melanoma- and breast cancer–derived tumours” either. Now we suspect that “CD36 expression drives ovarian cancer progression and metastasis,” too, since we can inhibit ovarian cancer cell invasion and migration, as well as block both lymph node and blood-borne metastasis, by blocking CD36. We also see the same kind of effect with prostate cancer; suppress the uptake of fat by prostate cancer cells and suppress the tumor. This was all studied with receptor-blocking drugs and antibodies in a laboratory setting, though. If these “metastasis-initiating cancer cells particularly rely on dietary lipids [fat] to promote metastasis,” the spread of cancer, why not just block the dietary fat in the first place?

    “Lipid metabolism fuels cancer’s spread.” Cancer cells love fat and cholesterol. The reason is that so much energy is stored in fat. “Hence, CD36+ 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 survive at sites distant from the primary tumour”—to set up shop throughout the body.

    “The time when glucose [sugar] was considered as the 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 (HFD) may “play a crucial role in increasing the risk of different cancer types, and a number of clinical studies have linked HFD with several advanced cancers.”

    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? You don’t know until you put it to the test, which we’ll look at next.

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    Michael Greger M.D. FACLM

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