New Studies on Breast Cancer

Hello and welcome to the Nutrition Facts podcast, I’m your host Dr. Michael Greger. 

Now, I know I’ve made a name for myself in explaining how not to do certain things – just look at my books – How NOT to Die – and my upcoming book, How NOT to Diet.  But what I want to share with you is actually quite positive: what’s the best way to live a healthy life? Here are some answers.

After skin cancer breast cancer is the most common cancer diagnosed in women in the U.S.  Fortunately there is more and more research coming out on what we can do to help prevent it in the first place.  Today we’re going to hear about a few of those studies.  Beginning with egg consumption and the question, how few eggs should we eat to reduce the risk of prostate, ovarian, colon, and breast cancer?

This nationwide study of dietary cholesterol intake and cancer concluded that not only may cutting down on cholesterol help “prevent cardiovascular diseases but also may reduce the risk of…cancer…” Therefore: “Limitation of…animal fat and cholesterol is…a favorable public health measure.” But the study didn’t find high cholesterol consumption correlated with all cancers. Yes, a significant association between high cholesterol intake was found for stomach cancer, colon cancer, rectal cancer, pancreatic cancer, lung cancer, breast cancer, kidney cancer, bladder cancer, and a type of bone marrow cancer called non-Hodgkin’s lymphoma, but the association was negative for prostate cancer.

If you look at studies on prostate cancer and eggs, though, which are one of the primary sources of cholesterol in the diet, a pooled analysis of 15 prospective cohort studies found that those who ate 25 grams a day or more of eggs, which is like a half an egg a day, versus like less than an egg a week, those averaging that half-egg had a significant 14 percent increased risk of advanced and fatal prostate cancer. They weren’t exactly sure how to explain it, “but eggs contain considerable amounts of choline,” which certain bad bacteria in the gut can turn into toxic TMAO, which I’ve described before.

There also appears to be a dose-response, meaning the more eggs, the more cancer risk. Increasing consumption by five eggs a week may increase the risk of fatal prostate cancer 47 percent, though that’s just for fatal prostate cancer. No relationship was found between eggs and prostate cancer in general; just eggs and the deadly forms. It’s not necessarily the cholesterol, though. Yes, “a large amount of cholesterol may support the rapid growth and proliferation” of cancer cells. But there’s also the choline, and the animal protein—all of which may link egg consumption to the risk of breast, ovarian, and prostate cancers.

And then, if you look at prostate cancer progression, meaning men who’ve already been treated for prostate cancer, had a radical prostatectomy to have their whole prostate removed, and are trying to keep the cancer from coming back. If you see what they were eating, a very high intake of eggs—by which they mean nearly an entire egg a day—was associated with the likelihood of recurrence of high-grade disease, meaning an aggressive form of cancer coming back.

Egg consumption is also associated with increased risk of ovarian cancer, where women make their own eggs, something we’ve known for over 15 years now. “Eggs can also be a source of heterocyclic amines, carcinogenic chemicals that are formed during high temperature frying.” That would be consistent with the bladder cancer data, suggesting fried egg consumption may double cancer risk, but not boiled eggs. The researchers considered the high cholesterol content of eggs, though, to be most plausible explanation for the ovarian cancer link. Eating lots of cholesterol-rich foods may increase the formation of toxic bile acids, which may at least affect colorectal cancer and lung cancer.

There does seem to be a dose-response relationship for egg consumption and cancers of the gut. Even just a few eggs a week may be associated with a 19 percent greater risk of colorectal cancer, but hit three or more eggs a week, and the increased risk may be as high as 71 percent.

And finally, breast cancer: a significant increase in breast cancer risk once women get up to around five eggs a week. Now this was putting together just all the forward-looking cohort studies. Adding together all the studies doesn’t change the conclusion: “egg consumption is associated with increased breast cancer risk.” A single serving of eggs may exceed the old 300 mg daily limit by like 40 percent. The latest dietary guidelines actually strengthened their limits on dietary cholesterol, saying forget 300, as recommended by the National Academy of Sciences Institute of Medicine; we “should eat as little dietary cholesterol as possible.”

In our next story we hear about how oxidized cholesterol (concentrated in products containing eggs, processed meat, and parmesan cheese) has cancer-fueling estrogenic effects on human breast cancer.

In 1908, the presence of cholesterol crystals was noted “in the proliferating areas of cancers,” suggesting that perhaps cholesterol, in some way, was “associated with the regulation of cancer proliferation.” A century later, we now recognize “the accumulation of cholesterol as a general feature of cancer tissue, and recent evidence suggests that cholesterol may indeed play critical roles in the progression of cancers, including breast, prostate, and colorectal cancers.”

Perhaps that could explain why “egg consumption was associated with increased breast cancer risk.” And, indeed, a systematic review of the evidence suggests that “dietary cholesterol intake increases risk of breast cancer,” and the more cholesterol you eat, the higher the risk appears to go. But, why?

One thought is that the “prolonged ingestion of a cholesterol-enriched diet induces a chronic, auto-inflammatory response,” and we know that “chronic inflammation can lead to the initiation, promotion, and progression of tumor development.” It’s true that sprinkling some cholesterol on white blood cells in a test tube can trigger the release of inflammatory compounds, and LDL cholesterol can induce breast cancer proliferation and invasion. But again, that’s in vitro, where you can show that like breast cancer cells can migrate nearly twice as far within a day in a petri dish in the presence of LDL cholesterol. But what about in people?

Well, the level of LDL cholesterol in the blood of women diagnosed with breast cancer does appear to be “a predictive factor of tumor progression.” About two years after surgery/chemo/radiation, not one of the women in the lowest third of LDL cholesterol levels had a cancer recurrence. The same could not be said for women with higher cholesterol. We know cholesterol can cause inflammation in our artery walls; maybe it’s also playing an effect on breast cancer initiation and progression? They speculate that the high cholesterol levels may have a “cancer-fueling effect.” And indeed, women with breast cancer who happen to be taking cholesterol-lowering statin drugs appear to live about 40 percent longer before the cancer comes back. But the data isn’t good enough to ensure the drug benefits outweigh the risks, though lowering cholesterol with diet, one may be able to get the best of both worlds. But what does this have to do with dietary cholesterol?

Sure, animal studies show that if you feed mice cholesterol, you can accelerate their cancers, “but extrapolation to humans is difficult as dietary cholesterol has limited effects on blood cholesterol levels in humans.” Thus, “dietary cholesterol might just be indicative of a lifestyle prone to health-related problems, including cancer.” Maybe people are just more likely to chase bacon and eggs down with a cigarette, compared to oatmeal? It’s hard to imagine how dietary cholesterol alone could promote cancer development. But that all changed recently, with the discovery that 27-Hydroxycholesterol, a metabolite of cholesterol, “can function as an estrogen and increase the proliferation” of most breast cancer cells.

Ah, so it’s not the cholesterol itself, but what it turns into in the body. “Scientists have long struggled to understand why women with heart disease risk factors are more likely to develop breast cancer.” Now, perhaps we know. “The discovery that the most abundant oxidized cholesterol metabolite” in our bloodstream can have estrogenic effects may explain the link between high cholesterol and the development and progression of breast cancer and prostate cancer. Yes, 27-Hydroxycholesterol also stimulates the proliferation of prostate cancer cells, boosting growth by about 50 percent.

I’ve explored before the role oxy-cholesterols may play in mediating pro-oxidative and pro-inflammatory processes in degenerative diseases, such as Alzheimer’s and heart disease, but now it looks like oxidized cholesterol can play a role in all three stages of tumor development as well: initiation, promotion, and then the progression of cancer. Not just promoting the growth of breast cancer cells, but also inducing their invasion and migration—potentially facilitating breast cancer metastasis through suppressing anti-cancer immunity, and then inducing angiogenesis, helping breast tumors hook up their blood supply.

This is all supported by “several lines of evidence[that point to a pathologic role” for this cholesterol metabolite. Yeah, you can feed mice cholesterol; their oxysterol levels go up and their tumors accelerate. It “also appears to dramatically hasten the spread, or metastasis, of breast tumors to other organs.” But turning to human breast tissue samples, they found that more aggressive tumors have higher levels of the enzyme that converts cholesterol into 27-HC. In breast cancer patients with estrogen receptor-positive tumors, the 27 Hydroxycholesterol content in their breast tissue is increased overall, and especially within the tumor itself—so much so that circulating oxysterol levels in the blood may one day be used as a prognostic factor. And “breast cancer patients with low tumor levels of the enzyme that breaks down 27-HC did not live as long” as women who can detoxify it better. “The bottom line is that some estrogen-driven breast tumors may rely on 27-HC to grow when estrogen isn’t available.” And that may explain a second breast cancer mystery.

Over 80 percent of breast cancers start out responding to estrogen, and so what we do is use hormone blockers—either aromatase inhibitors to stop the formation of estrogen in the first place, or tamoxifen to block its action. Despite the efficacy of these drugs, many patients relapse with resistant tumors. And that’s where oxidized cholesterol can come in. 27-HC can fuel breast cancer growth without estrogen, which could explain why sometimes these estrogen blockers don’t work.

And finally, 27-HC may explain why breast cancer patients with higher vitamin D levels appear to live longer. Vitamin D supplementation decreases 27-HC levels in the blood. The best way, though, may be to just lower overall cholesterol. Lower cholesterol, and you lower oxidized cholesterol. So, discovering this role of cholesterol is actually really good news, since “cholesterol is a highly amenable risk factor, either by lifestyle, dietary, or pharmacologic interventions.” The implications of these findings, according to the principal investigator, is that “lowering cholesterol with dietary changes or drugs could reduce a women’s breast cancer risk or slow tumor growth.”

In our last story today, we look at the potential link between antiperspirants and breast cancer.

A famous case report, called “The Mortician’s Mystery,” in the New England Journal of Medicine back in the 80s, described a man whose testicles started shrinking and breasts started growing. Turns out, he failed to wear gloves as he massaged embalming cream onto his corpse. They conclude there must have been some estrogenic compound in the cream that got absorbed through his skin into his body—one of the first such cases described.

This case was cited as inspiration by a group of researchers that came up with a new theory to explain a breast cancer mystery. Why do most breast cancers occur in the upper outer corner of the breast? The standard explanation was simply because that’s where most of the breast tissue is located, as the so-called tail of the breast extends up into the armpit.

But, that doesn’t explain this. It didn’t always used to be this way; there’s been a shift towards that upper corner. And, it doesn’t explain “greater genomic instability”—chromosome abnormalities that may signal precancerous changes. There definitely seems to be something happening to that side of the breast, and something relatively new—just in the last 50 years or so.

“Is it possible that the increasing use of underarm antiperspirant which parallels increasing breast cancer incidence could be an explanation for the greater number of tumours and the disproportionate incidence of breast cancer in the upper outer quadrant” of the breast near where the stick, spray, or roll-on is applied?

There’s a free flow of lymph fluid back and forth between the breast and the armpit. And, if you measure aluminum levels in breasts removed after mastectomies, “the aluminum content of breast tissue in the outer regions near the armpits was significantly higher”—presumably due to “closer proximity” to the underarm region.

This is a concern, because, in a petri dish at least, “it has been demonstrated that aluminum is a so-called metalloestrogen,” having pro-estrogenic effects on breast cancer cells. “Long-term exposure” of normal breast tissue cells in a test tube to aluminum concentrations “in the range of those” found in the breast results in precancerous-type changes. And then, once the cells have turned, those same concentrations can “increase the migratory and invasive activity” of human breast cancer cells in a petri dish. 

This is important, because women don’t die from the tumor in the breast itself, “but from the ability of the cancer cells to spread and grow at distant sites,” like the bones, lungs, liver, or brain. But, we don’t care about petri dishes; we care about people.

In 2002, a paper was published in the Journal of the National Cancer Institute, in which the underarm antiperspirant habits of 800 breast cancer survivors were compared to those of women who never got breast cancer. The first study of its kind, and they found “no indication” of a link between the two.

Based on this study, Harvard Women’s Health Watch assured women that antiperspirants do not cause breast cancer. “Women who are worried that antiperspirants might cause breast cancer can finally rest easy.”

But, two months later, “Frequency and early onset of antiperspirant/deodorant usage with underarm shaving was  associated with an earlier age of breast cancer diagnosis”—as much as 20 years earlier—in women using antiperspirant, and shaving their armpits more than three times a week. And, the earlier they started, before vs. after their sweet 16, appeared to move up their breast cancer 10 or 20 years. They conclude that “underarm shaving with antiperspirant use, may play a role in breast cancer” after all.

But what does shaving have to do with it? Shaving removes more than just armpit hair; it removes armpit skin. You end up shaving off the top skin layer. And, while there’s very little aluminum absorption through intact skin, when you strip off that outer layer with a razor, and then rub on some antiperspirant, you get a six-fold increase in aluminum absorption through the skin. So, good news for women who don’t shave, but “on the other hand, the high through-the-skin aluminum uptake on shaved skin should compel antiperspirant manufacturers to proceed with the utmost caution.”

European safety authorities and the FDA specifically advise against using aluminum antiperspirants on damaged or “broken skin.” Yet, shaving before antiperspirant application “can create abrasions in the skin.” I’m sure everyone knows about the FDA warning, having read title 21 part 350 subpart C50-5c1 of the Code of Federal Regulations.

But, we get so much aluminum in our diet from processed foods—”anti-caking agents in like pancake mix, melting agents in American cheese, meat binders, gravy thickeners, baking powder,” candy—that the contribution from underarm antiperspirants would presumably be minimal in comparison.

“But everything was turned topsy-turvy in 2004,” when a case was reported of “a woman with bone pain and fatigue” suffering from aluminum toxicity. But, within months of stopping the antiperspirant, which she was applying daily to her regularly-shaved pits, her aluminum levels came down, and “her symptoms” resolved. Although not everyone sucks up that much aluminum, the case “suggests that caution should be exercised when using aluminum-containing antiperspirants frequently.”

Recently, it was shown that women with breast cancer have twice the level of aluminum in their breasts, compared to women without breast cancer—though this doesn’t prove cause and effect. Maybe the aluminum contributed to the cancer, or maybe the cancer contributed to the aluminum. Maybe tumors just suck up more aluminum? Subsequent research suggests this alternative explanation is unlikely. So, where do we stand now?

The latest review on the subject concluded that as a consequence of the new data, given that aluminum can be toxic, and we have no need for the stuff, “reducing the concentration of this metal in antiperspirants is a matter of urgency.” Or, at the very least, it should say on the label: Do not use after shaving. Or, we could cease usage of aluminum-containing antiperspirants altogether.

But then, won’t we stink? Ironically, antiperspirants can make us stink worse. They increase the types of bacteria that cause body odor. It’s like the story with antidepressant drugs—how they can actually make you more depressed in the long run. The more we use antiperspirants, the more we may need them. Awfully convenient for a billion-dollar industry.

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