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 The findings of a large study from Denmark were a disappointment for those hoping that women taking or using low dose hormonal birth control (pills, IUD) would not show an increase in breast cancer (like the old higher dose birth control pills). This study found a small increase in the risk of breast cancer with the use of modern birth control pills and with a progestin-only intrauterine device. They pointed out that the biggest risk was in those using hormonal methods for over 10 years and in their 40s (most of the breast cancer cases occurred in this group of women). The risk goes up the longer one uses hormonal contraception.

Due to smaller numbers of women using a birth control patch, vaginal ring, and implants - they were unable to say one way or another if these also are linked to a higher incidence of breast cancer. But the sense from the researchers is that all hormonal contraception has a slight increase in risk of breast cancer. How big an increase in risk? There is a 20% increased risk overall, but the actual numbers are fairly small - 13 per 100,000 women or approximately 1 extra breast cancer for every 7690 women using hormonal contraception for 1 year. From Medical Xpress:

Small risk of breast cancer seen with hormone contraceptives

Modern birth control pills that are lower in estrogen have fewer side effects than past oral contraceptives. But a large Danish study suggests that, like older pills, they still modestly raise the risk of breast cancer, especially with long-term use. Researchers found a similar breast cancer risk with the progestin-only intrauterine device, and they couldn't rule out a risk for other hormonal contraceptives like the patch and the implant.

But the overall increased risk was small, amounting to one extra case of breast cancer among 7,700 women using such contraceptives per year. Experts who reviewed the research say women should balance the news against known benefits of the pill - including lowering the risk of other cancers.

Researchers analyzed health records of 1.8 million women, ages 15 to 49, in Denmark where a national health care system allows linking up large databases of prescription histories, cancer diagnoses and other information. Results were published Wednesday in the New England Journal of Medicine. Novo Nordisk Foundation funded the research, but played no role in designing the study.

Current and recent use of hormonal contraceptives was associated with a 20 percent increased risk of breast cancer. Risk increased with longer use, from a 9 percent increase in risk with less than a year of contraceptive use to a 38 percent increase after more than 10 years of use. Digging further, the researchers found no differences among types of birth control pills. Because of fewer users, the results for the patch, vaginal ring, implant and progestin shot were less clear, but the analysis didn't rule out an increased breast cancer risk for those methods. [Original study.]

A large study by researchers at the State University of NY, of 65,869 postmenopausal women found that those who have a history  of gum or periodontal disease also have an overall higher risk of cancer. The women with a history of periodontal disease also had an increased risk for several specific cancers: breast, esophageal, gallbladder, lung and melanoma cancers. This cancer and gum disease association occurred in both nonsmokers and smokers.

How is periodontal disease "promoting" cancer? How it occurs is still unclear, but one theory suggests the gum disease bacteria are in the saliva, which is swallowed, and so the bacteria get into the gut, esophagus, or lungs. Or bacteria from diseased gum tissues get into "systemic circulation" and so get to distant sites in the body.  One of the researchers pointed out that "Certain periodontal bacteria have been shown to promote inflammation even in tiny amounts, and these bacteria have been isolated from many organ systems and some cancers including esophageal cancers."

From Medscape: Gum Disease and Increased Link to Many Cancers

Brushing, flossing, and regular dental checkups appear to do much more than maintain a healthy smile. Now, a large prospective cohort study shows that postmenopausal women with a history of periodontal disease, including those who have never smoked, are at significantly increased overall risk for cancer as well as site-specific cancers, including lung, breast, esophageal, gallbladder, and melanoma skin cancers.

The study authors note that these results add to the growing body of evidence from smaller studies and studies in men that link periodontal disease to total cancer risk. The Centers for Disease Control and Prevention (CDC) estimate that 47% of adults 30 years of age and older in the United States have some form of periodontal disease, ranging from mild to severe. At age 65 years and older, however, 70% of adults have moderate to severe periodontal disease, according to the CDC.

The study involved almost 66,000 postmenopausal women in the United States, who were enrolled in the ongoing Women's Health Initiative Observational Study (WHI-OS). During a mean follow-up of 8.32 years, the team identified 7149 cancers and found that periodontal disease history was associated with a 14% increased total cancer risk. When analyses were limited to 34,097 never-smokers, there was also an increased risk for overall cancer.

An association between periodontal disease and site-specific cancers was observed in breast, lung, esophageal, gallbladder, and melanoma skin cancers. There was a borderline association with stomach cancer, the study authors report, and periodontal disease was not associated with cancers of the pancreas; liver; lower digestive tract organs; or lip, oral cavity, and pharynx combined. Similarly, there was no association with genitourinary and lymphoid and hematopoietic malignancies.

For the study, the investigators looked at periodontal disease information in 65,869 women aged 54 to 86 years at 40 US centers. Mean age was 68 years. Most women were non-Hispanic whites with some college education. All participants answered the question "Has a dentist or dental hygienist ever told you that you had periodontal or gum disease? (No/Yes)" between 1999 and 2003 on the annual Year-5 WHI-OS follow-up questionnaire. Cancer outcomes were documented through September 2013 with a maximum 15-year follow-up period.

 Women who reported a history of periodontal disease were also more likely to report a history of smoking, secondhand smoke exposure, alcohol use, hormone therapy (estrogen plus progestin), and a cancer diagnosis, the study authors report. At the same time, no significant differences were observed in body mass index, physical activity levels, or history of diabetes between women with periodontal disease and those without. [Original study.]

A recent study found that significantly increasing  dietary fiber intake after a diagnosis of colorectal cancer was associated with a lower death rate - from both colorectal cancer and overall mortality (from any cause). The 1575 men and women (all healthcare professionals) in the study had received a nonmetastatic colorectal cancer diagnosis (it had not spread beyond the colon), and the follow-up was about 8 years. These results were from food, not supplements.

How much did extra dietary fiber lower the death rate? For each additional 5  grams of fiber added to their daily diet (after diagnosis) was associated with a 18% lower colorectal cancer death rate, and a 14% lower death rate from any cause. In this study, whole grains, especially in cereals, were found to be the most beneficial. Current dietary guidelines recommend a fiber intake of 25 to 38 grams per day, but most Americans eat far lessDietary fiber is found in plant foods, such as beans, whole grains, nuts, seeds,  vegetables, and fruits. Plant fiber feeds the millions of gut microbes, especially beneficial microbes (here, here, and here) - something that was not really discussed in the study.

The researchers pointed out that a high fiber diet (especially from whole grains and cereals) is linked to a lower risk of getting colorectal (colon) cancer in the first place.  Also, that "higher intake of fiber, especially cereal fiber", has been linked to improved insulin sensitivity, reduced inflammation, type 2 diabetes, cardiovascular disease, and total mortality. Other studies have found that  vitamin D supplementation, exercise, and eating fish all increase survival from colorectal cancer. From From Medical Xpress:

Fiber-rich diet boosts survival from colon cancer

A diet rich in fiber may lessen the chances of dying from colon cancer, a new study suggests. Among people treated for non-metastatic colon cancer, every 5 grams of fiber added to their diet reduced their odds of dying by nearly 25 percent, said lead researcher Dr. Andrew Chan. He is an associate professor in the department of medicine at Harvard Medical School.

"What you eat after you've been diagnosed may make a difference," Chan said. "There is a possibility that increasing your intake of fiber may actually lower the rate of dying from colon cancer and maybe even other causes." Chan cautioned, however, that the study does not prove that the additional fiber caused people to live longer, only that the two were associated.

Fiber has been linked to better insulin control and less inflammation, which may account for better survival, he suggested. In addition, a high-fiber diet may protect people from developing colon cancer in the first place. The greatest benefit was attributed to fiber from cereals and whole grains, according to the report. Vegetable fiber was linked to an overall reduction in death, but not specifically in death from colon cancer, and fiber from fruit was not linked to a reduction in death from any cause. 

For the study, Chan and his colleagues collected data on 1,575 men and women who took part in the Nurses' Health Study and Health Professionals Follow-up Study, and who had been treated for colon or rectal cancer that had not spread beyond the colon. Specifically, the study looked at total fiber consumption in the six months to four years after the participants' cancer diagnosis. The researchers also looked at deaths from colon cancer and any other cause. In an eight-year period, 773 participants died, including 174 from colorectal cancer. [Original study.]

Once again the controversial herbicide (weed killer) glyphosate is in the news. Glyphosate is the active ingredient in Roundup (manufactured by Monsanto), and is the most commonly used pesticide in the world. Its use is increasing annually since the introduction of genetically modified crops that are tolerant of glyphosate being sprayed on them (Roundup Ready crops), and since the use of "preharvest" applications of Roundup. Over the years the US government has generally NOT been tracking how much glyphosate residues are in the foods we eat, but whenever a food is studied for glyphosate residues - they are found. (see all posts) Which means people are constantly ingesting low levels of glyphosate residues.

But what does that mean for humans? A  recently published study of 100 adults over the age of 50, residing in Southern California, and followed from 1993 to 2016, looked at detectable glyphosate and its metabolite aminomethylphosphonic acid (AMPA) residues in urine. They found that the number of people with detectable residues in urine, and also the actual levels found in the urine, really, really increased in the 23 years. The percentage of people who tested positive for glyphosate shot up by 500% in that time period - from 12 percent of the samples to 70 percent. WOW!

Are there health effects from constant ingestion in food from low levels of glyphosate? We don't know, because the studies on humans have not been done. There are a number of health concerns, including that it is a carcinogen (it has been classified as a "probable carcinogen" by some agencies), liver and kidney damage, that it acts as an antibiotic and disrupts the gut microbiome, and endocrine disruption. The researchers of this study are especially concerned about possible glyphosate health effects on the liver (liver disease), based on animal studies (animals exposed chronically to very low levels), and want to research this further.

However, the EPA keeps insisting it's safe (and to please ignore the conflicts and deals done with Monsanto in recent years), and actually raised the levels allowed in 2013 (due to corporate lobbying). Also, glyphosate is still not monitored by the Department of Agriculture's pesticide data program or the CDC's (Centers for Disease Control and Prevention) monitoring program of human exposure to environmental chemicals.

What can you do? Try to eat as many organic foods as possible because glyphosate (and Roundup) are not allowed to be used in organic farming. And don't use Roundup on your own property - because you can be exposed to it numerous ways (drinking and eating it in food, inhalation, through the skin).

From Medical Xpress: US study finds rise in human glyphosate levels

Levels of glyphosate, a controversial chemical found in herbicides, markedly increased in the bodies of a sample population over two decades, a study published Tuesday in a US medical journal said. The increase dated from the introduction of genetically-modified glyphosate-tolerant crops in the United States in 1994.

Researchers compared the levels of glyphosate in the urine of 100 people living in California. It covered a 23-year period starting from 1993, the year before the introduction of genetically-modified crops tolerant to Roundup. Glyphosate-containing Roundup, produced by US agro giant Monsanto, is one of the world's most widely-used weedkillers.

"Prior to the introduction of genetically modified foods, very few people had detectable levels of glyphosate," said Paul Mills, of the University of California at San Diego School of Medicine, the study's principal author. Among the study group, detectable amounts increased from an average of 0.20 micrograms per liter in 1993-1996 to an average of 0.45 micrograms in 2014-2016.

In July, California listed glyphosate as carcinogenic, and the World Health Organization International Agency for Research on Cancer called it "probably carcinogenic" in 2015. There are few human studies on the effects of glyphosate, but research on animals demonstrated that chronic exposure can have adverse effects, said Mills. Along with the European Commission's proposal on Tuesday, the European Parliament approved a non-binding resolution calling for the chemical to be banned by 2022.

Excerpts from Consumer Reports: We May Be Consuming More Glyphosate Than Ever Before

A 2016 report in the journal Environmental Health that looked at human and animal studies found a link between glyphosate exposure and a number of health problems, including liver and kidney damage, endocrine disruption, and an elevated risk of non-Hodgkin’s lymphoma. But a vast majority of those studies were done with animals.

In fact, very few human studies have been done on the health effects of glyphosate, and no federal agency monitors how much of the chemical makes it from the environment into our bodies. That lack of information makes it difficult to even begin to assess how much glyphosate is potentially harmful to humans and whether current exposure levels are above or below that mark.

Once again a study finds that pesticide exposure is linked to an adverse health effect - that pesticide exposure in the home during pregnancy and early childhood is linked to an elevated risk of brain tumor in the child. Other studies have also found that pesticides used in the home are associated with a higher risk of childhood cancers.

This is because pesticides do cross the placental barrier, as the study researchers point out: "There is evidence that pesticides cross the fetal-placental barrier since residues of some insecticides have been found in umbilical cord blood, neonatal hair, and meconium following maternal exposure during pregnancy." Also, the International Agency for Research on Cancer (IARC) has classified "more than twenty pesticide chemical compounds as potential human carcinogens".

The following are examples (but there are more) of other studies finding pesticide and childhood cancer links: A meta-analysis published in 2015 in Pediatrics by researchers at Harvard University found that children exposed to indoor insecticides (also herbicides) have a higher risk of certain childhood cancers, specifically leukemia, lymphomas, and brain tumors. A 2013 study published in Cancer Causes and Control found that professional pest control applications in the home within a year of conception and during pregnancy was associated with a higher risk of childhood brain tumors. A review of studies published in 2010 found that pesticide exposure during pregnancy and childhood increased the risk of childhood leukemia.

The good news is that there are alternatives to exposing fetuses and children to toxic pesticides at home - by using alternative ways of dealing with pests, such as least toxic Integrated Pest Management (IPM) or organic methods. That means doing other things (such as sealing or caulking holes, putting out traps and baits, vacuuming), a focus on least toxic methods and on prevention (here and here), rather than routinely applying toxic pesticides. If needed, least toxic pesticides include boric acid and vinegar. Other sources of pesticide exposure for pregnant women and children are foods and exposure in settings outside the home - perhaps even a friend's yard. By the way, pesticide exposure for everyone is linked to a higher risk of health problems, not just pregnant women and children.

From Science Daily: Pesticide use during pregnancy linked to increased risk of childhood brain tumors

Previous epidemiological studies have suggested that exposure to pesticides during pregnancy may have a possible role in the development of childhood brain tumors. In a new International Journal of Cancer analysis, researchers found a link between maternal residential pesticide use -- particularly insecticides -- and the risk of childhood brain tumorsThe analysis included 437 malignant childhood brain tumor cases and 3102 controls from two French studies. Pesticide use was associated with a 1.4-times increased risk of childhood brain tumors.

The investigators noted that many pesticide compounds are classified as probable carcinogens, and there is evidence that some insecticides can pass through the feto-placental barrier. "Although such retrospective studies cannot identify specific chemicals used or quantify the exposure, our findings add another reason to advise mothers to limit their exposure to pesticides around the time of pregnancy," said Nicolas Vidart d'Egurbide Bagazgoïtia, lead author of the study. [Original study.]

A major new report about colorectal cancer found that a number of lifestyle factors (diet, physical activity) increase or lower the risk of colorectal cancer. The report was an analysis of global research studies and was published by the American Institute for Cancer Research and World Cancer Research Fund.

They found that there is strong evidence that: being physically active, consuming whole grains, consuming foods containing dietary fiber, consuming dairy products, and taking calcium supplements all decrease the risk of colorectal cancer. On the other hand, there is strong evidence that: consuming red meat, consuming processed meat, consuming 2 or more alcoholic drinks per day, being overweight or obese, and being tall all increase the risk of colorectal cancer.

Also, that there is some evidence that: consuming foods containing vitamin C, consuming fish, vitamin D, consuming multivitamin supplements lower the risk of colorectal cancer. And there is some evidence that: low consumption on non-starch vegetables, low consumption of fruit, and consumption of foods containing haem iron might increase the risk of colorectal cancer. [NOTE: There are 2 types of iron in food: haem and non-haem iron. Haem iron is only found in meat, chicken, and fish, and is easily absorbed. Non-haem iron is found in plant foods, such as vegetables, cereals, beans, and lentils, but is not absorbed as well by the body.]

Finally, their cancer prevention recommendations for preventing cancer in general include: maintaining a healthy weight, being physically active and eating a healthy diet. (other posts on this - here, here, here). They also advise eating a healthy diet (think Mediterranean style diet) rather than relying on supplements to protect against cancer. The report also noted that inflammatory bowel disease and smoking increase the risk of colorectal cancer. From Science Daily:

Whole grains decrease colorectal cancer risk, processed meats increase the risk

Eating whole grains daily, such as brown rice or whole-wheat bread, reduces colorectal cancer risk, with the more you eat the lower the risk, finds a new report by the American Institute for Cancer Research (AICR) and the World Cancer Research Fund (WCRF). This is the first time AICR/WCRF research links whole grains independently to lower cancer riskDiet, Nutrition, Physical Activity and Colorectal Cancer also found that hot dogs, bacon and other processed meats consumed regularly increase the risk of this cancer. There was strong evidence that physical activity protects against colon cancer.

The new report evaluated the scientific research worldwide on how diet, weight and physical activity affect colorectal cancer risk. The report analyzed 99 studies, including data on 29 million people, of whom over a quarter of a million were diagnosed with colorectal cancer.

Other factors found to increase colorectal cancer include:  - Eating high amounts of red meat (above 500 grams cooked weight a week), such as beef or pork, - Being overweight or obese, - Consuming two or more daily alcoholic drinks (30 grams of alcohol), such as wine or beer. The report concluded that eating approximately three servings (90 grams) of whole grains daily reduces the risk of colorectal cancer by 17 percent. It adds to previous evidence showing that foods containing fiber decreases the risk of this cancer.

In the US, colorectal cancer is the third most common cancer among both men and women, with an estimated 371 cases diagnosed each day. AICR estimates that 47 percent of US colorectal cancer cases could be prevented each year through healthy lifestyle changes[The report.]

For years medicine has viewed cancer as a "malignant seed" and looked for ways to kill these seeds before they spread throughout the body (metastasis). This past week two provocative articles stresses that we should also look at the "environments" that the cancer cells grow in - that some environments in the person nourish and encourage the growth of cancer, while other environments suppress the growth of cancer and don't allow its spread.

This is a very different approach to cancer, but it also makes sense. Studies find that small cancers can just sit there harmlessly or regress on their own - even breast and prostate cancers, but it raises the questions: Why? Why do they regress or are suppressed in some people, but grow malignantly in others? What is different about those people and their bodies?

Researchers are starting to do research along these lines - that is, looking at the environment that cancer may or may not grow in. Yesterday's post discussed amazing research showing that cancer tumors are continuously shedding cancer cells in a person's body, but only in some people do they actually take root and grow. It's as if some people have environments that encourage growth of cancer, while other people have environments that do not.

Today's article, besides discussing the micro-environment in which cancer grows, also discusses the role of inflammation in cancer and how things causing inflammation (e.g., smoking, inactivity, poor diet) are also associated with cancer. So some micro-environments are good for cancer, and some are not. Some of the research I've posted in the past has tried to see if influencing the person's environment with "lots of exercise and activity"(here and here), or vitamin D levels in the body, or a person's diet somehow prevents or keeps cancer in check. From Nautilus:

The Problem with the Mutation-Centric View of Cancer

To better understand and treat cancer, physicians need to stop oversimplifying its causes. Cancer results not solely from genetic mutations but by adapting to and thriving in micro-environments in the body. That’s the point of view of James DeGregori, a professor in the Department of Biochemistry and Molecular Genetics at the University of Colorado School of Medicine.... In our conversation, DeGregori expanded on how a renewed focus on micro-environments and Darwinian evolutionary pressures can benefit cancer research.

How should we study the origins of cancer? My lab has been researching the origins of cancers for the last 15 to 17 years. We’re trying to understand cancer from an evolutionary viewpoint, understanding how it evolves. A lot of people think about cancer from an evolutionary viewpoint. But what sets us apart is that we’ve really come to understand cancer by the context these cells find themselves in.

What’s an example of such a context? While other people will think about aging as the time for mutations to cause advantageous events [for cancer] in cells, we see aging as a very different process. It’s not about the time you get mutations—you get many mutations when you’re young. It’s the tissue environment for the cells that changes dramatically as we age. Those new tissue environments basically stimulate the evolution. So the evolution isn’t a process that’s limited by the mutation so much as a process that is limited by micro-environment changes.

Instead of just attacking the cancer, we should be altering the micro-environment to disfavor the cancer. What we’ve shown is that you could take the same oncogenic mutation and put it into young cells in a young environment and it’s not advantageous [for cancer]. It doesn’t cause expansions and it doesn’t cause the cancer. You make that same mutation in old tissue and it can be adaptive for cancer.

When we’re young, our tissues are relatively constant and well maintained. If you look at the tissues of a 20-year-old and a 35-year-old, or maybe even a 40-year-old, you wouldn’t notice much of a difference. It’s not like we age linearly. It’s only after 45 or 50 that we start to really go downhill. Then that downhill accelerates. As those changes happen, our tissues are no longer presenting that same environment to our cells. What I argue is that we evolve stem cells, or the cells that are continuously making our tissues, to be well adapted to the youthful environment and not to be well adapted to an aged environment.

I’ve been criticized as putting forward a straw man because, essentially, they don’t really talk about micro-environment. But to me that’s the whole point—there’s a major factor that should be considered, and I would say not just “should.” You can’t really model cancer without it and yet they’re not taking it into account. In other words, the difference between a smoker and a nonsmoker isn’t just that the smoker has more mutations. The difference is the smoker’s lung—and I’m sure you’ve seen pictures of the charred blackened lungs of a smoker—and that presents a completely different environment for cells with mutations.

How can your ideas change the way doctors treat cancer? Mostly we now target the cancer cells. That’s changing somewhat. Immune therapies are in some ways targeting the environment. It’s almost like a predator strategy. Instead of just attacking the cancer, we should be altering the micro-environment to disfavor the cancer. If you just attack the cancer, you immediately select for resistance, which is what they see in the clinic so often. You can get a person into remission, but it’s keeping them in remission that’s the hard part. Cancer that comes back is inevitably worse than the cancer you started with.

.... If we can understand what factor about a smoker’s lung, or an old person’s lung, leads to more cancer, then we could modulate that factor to basically prevent the cancers from occurring in the first place. If it’s inflammation, for all we know maybe there are even dietary interventions that will reduce inflammation in the lungs. All the things we know that are associated with cancer are also associated with increased inflammation. Everything we know that basically leads to longer, healthier lives, is known to modulate inflammation. Exercise reduces it. Good diet reduces it. Not smoking, not exposing yourself to too much sun.

 Cancer cells. Credit:Wikipedia, National Cancer Institute

Image result for cancer cells wikipedia For years medicine has viewed cancer as a "malignant seed" and looked for ways to kill these seeds before they spread throughout the body (metastasis). This past week two provocative articles about new research stresses that we should also look at the "soil" that the cancer "seeds" grow in - that some "soils" or environments in the person nourish and encourage the growth of cancer, while other environments suppress the growth of cancer and don't allow its spread.

This is a very different approach to cancer, but it also makes sense. Studies find that small cancers can regress on their own - even breast and prostate cancers, but it raises the questions: Why? Why do they regress or are suppressed in some people, but grow malignantly in others? What is different about those people and their bodies?

Researchers are starting to do research along these lines - that is, looking at the environment or "soil" that cancer may or may not grow in. Amazing research shows that cancer tumors are continuously shedding cancer cells in a person's body, but only in some people do they actually take root and grow. It's as if some people have ecosystems that encourage growth of cancer, while other people have ecosystems that do not.

Of course Gilbert Welch's research is discussed - that many people have tiny cancers that are just sitting there without growing (here, here, here). And how early diagnosis of cancer is not really changing the percentage of deaths from many cancers (overdiagnosis). Some of the research I've posted in the past has tried to see if influencing the person's environment with "lots of exercise and activity" somehow keeps cancer in check (here and here), or vitamin D levels in the body, or a person's diet. Do go read the whole fascinating article. Excerpts from New Yorker:

Cancer’s Invasion Equation

We aren’t particularly adept at predicting whether a specific patient’s cancer will become metastatic or not. Metastasis can seem “like a random act of violence,” Daniel Hayes, a breast oncologist at the University of Michigan, told me when we spoke at the asco meeting in Chicago. “Because we’re not very good at telling whether breast-cancer patients will have metastasis, we tend to treat them with chemotherapy as if they all have potential metastasis.” Only some fraction of patients who receive toxic chemotherapy will really benefit from it, but we don’t know which fraction. And so, unable to say whether any particular patient will benefit, we have no choice but to overtreat.

There are deep roots to the idea that a cancer’s metastases depend on local habitats. In 1889, an English doctor named Stephen Paget set out to understand cancer’s “primary growth and the situation of the secondary growths derived from it.” .... But when Paget collected the case files of seven hundred and thirty-five women who had died of breast cancer, he found a bizarre pattern of metastatic spread. The metastases didn’t appear to spread centrifugally; they appeared in discrete, anatomically distant sites. And the pattern of spread was far from random: cancers had a strange and strong preference for particular organs. Of the three hundred-odd metastases, Paget found two hundred and forty-one in the liver, seventeen in the spleen, and seventy in the lungs. Enormous, empty, uncolonized steppes—anatomical landmasses untouched by metastasis—stretched out in between.

Why was the liver so hospitable to metastasis, while the spleen, which had similarities in blood supply, size, and proximity, seemed relatively resistant? As Paget probed deeper, he found that cancerous growth even favored particular sites within organ systems. Bones were a frequent site of metastasis in breast cancer—but not every bone was equally susceptible. “Who has ever seen the bones of the hands or the feet attacked by secondary cancer?” he asked. Paget coined the phrase “seed and soil” to describe the phenomenon. The seed was the cancer cell; the soil was the local ecosystem where it flourished, or failed to. Paget’s study concentrated on patterns of metastasis within a person’s body. The propensity of one organ to become colonized while another was spared seemed to depend on the nature or the location of the organ—on local ecologies. Yet the logic of the seed-and-soil model ultimately raises the question of global ecologies: why does one person’s body have susceptible niches and not another’s? .... Paget’s way of framing the issue—metastasis as the result of a pathological relationship between a cancer cell and its environment—lay dormant for more than a century.

In 2001, Joan Massagué, a cancer biologist at New York’s Memorial Sloan Kettering Cancer Center, came upon a scientific paper that radically changed his thinking about metastasis..... He had spent years studying cell biology, elucidating mechanisms of gene regulation that might prime breast cells to travel to the bone instead of to the brain. Then came a crucial piece of evidence, buried in an obscure journal and published nearly three decades earlier. Researchers at the National Institutes of Health had implanted a sac of breast-cancer cells into the ovarian pedicle of a female rat. The cells grew to form a bean-size tumor. The researchers then cannulated a large vein that was draining the tumor and siphoned blood from the vein every few hours in order to count the number of cancer cells that the tumor was shedding.

The results baffled the investigators. On average, they found, the tumor was sloughing off twenty thousand cancer cells into every millilitre of blood—roughly three million cells per gram of tumor every twenty-four hours. In the course of a day, the tumor molted nearly a tenth of its weight. Later studies, performed with more sophisticated methods and with animal tumors that had arisen more “naturally,” confirmed that tumors continually shed cells into circulation. (The rate of shedding from localized human tumors is harder to study; but available research tends to confirm the general phenomenon.)

But if primary human tumors shed cells continually, and if every cell is capable of forming visible metastasis, then every patient should have countless visible metastatic deposits all over his or her body.” Anna Guzello’s breast tumor should have stippled her brain, bones, and liver with mets. Why, then, did she have no visible evidence of disease anywhere else in her body? The real conundrum wasn’t why metastases occur in some cancer patients but why metastases don’t occur in all of them.

“The only way I could explain the scarcity of metastasis,” Massagué said, “was to imagine that an enormous wave of cellular death or cellular dormancy must restrict metastasis. Either the cells shed by the tumor are killed, or they stop dividing, becoming dormant. When tumor cells enter the circulation, they must perish almost immediately, and in vast numbers. Only a few reach their destination organ, such as the brain or the bone.” Once they do, they face the additional problem of surviving in unfamiliar and possibly hostile terrain. Massagué inferred that those few survivors must lie in a state of dormancy. “A visible, clinical metastasis—the kind that we can detect with cat scans or MRIs—must only occur once a dormant cell has been reactivated and begins to divide,” he said. Malignancy wasn’t simply about cells spreading; it was also about staying—and flourishing—once they had done so.

.... Rather than viewing invasiveness as a quality intrinsic to a cancer, researchers needed to consider invasiveness as a pathological relationship between an organism and an environment. “Together, cancer cells and host cells form an ecosystem,” Pienta reminded the audience. “Initially, the cancer cells are an invasive species to a new niche or environment. Eventually, the cancer-cell-host-cell interactions create a new environment.” Ask not just what the cancer is doing to you, Pienta was saying. Ask what you are doing to the cancer.

Evidence suggested, for example, that most men with prostate cancer would never experience metastasis. What made others susceptible? The usual approach, Welch knew, would be to look for markers in their cancer cells—to find patterns of gene activation, say, that made some of them dangerous. And the characteristics of those cells were plainly crucial. Pienta was arguing, though, that this approach was far too narrow. At least part of the answer might lie in the ecological relationship between a cancer and its host—between seed and soil. .....Once we think of diseases in terms of ecosystems, then, we’re obliged to ask why someone didn’t get sick

Image result for cancer cells wikipedia Cancer cells. Credit: Wikipedia, National Cancer Institute

Image result for calcium rich foods, wikipediaAgain, another study finds that taking supplements is not always best for health. Many studies find that eating foods with vitamin "X" is beneficial, but taking high dose supplements may be linked to health problems (here, here, and here). Now a new study finds that long-term high dose supplementation with vitamins B6 and B12 is associated with a 30 to 40% higher lung cancer risk in men (compared to men who didn't take these supplements). Smokers had the greatest increase in risk. But interestingly, long-term use use of  vitamins B6, folate, and B12 was not associated with lung cancer risk among women.

Good food sources of vitamin B6 are: poultry, fish, organ meats, potatoes and other starchy vegetables, chickpeas, and fruit (but not citrus). Good food sources of B12 are:  Beef liver, clams, fish, meat, poultry, eggs, milk, and other dairy products.  Bottom line: if you take vitamin supplements (such as daily multi-vitamin supplements), take a "low-dose" one - one that aims for 100% of minimum daily requirements, but not mega-doses of vitamins.  From Medical Xpress:

Clear link between heavy vitamin B intake and lung cancer

New research suggests long-term, high-dose supplementation with vitamins B6 and B12—long touted by the vitamin industry for increasing energy and improving metabolism—is associated with a two- to four-fold increased lung cancer risk in men relative to non-users.

Risk was further elevated in male smokers taking more than 20 mg of B6 or 55 micrograms of B12 a day for 10 years. Male smokers taking B6 at this dose were three times more likely to develop lung cancer. Male smokers taking B12 at such doses were approximately four times more likely to develop the disease compared to non-users..... This is the first prospective, observational study to look at the effects of long-term high-dose B6/B12 supplement use and lung cancer risk. These supplements have been broadly thought to reduce cancer risk.

For this study, Theodore Brasky, PhD, of the OSUCCC - James, and colleagues analyzed data from more than 77,000 patients participants in the VITamins And Lifestyle (VITAL) cohort study, a long-term prospective observational study designed to evaluate vitamin and other mineral supplements in relation to cancer risk. All participants were aged between 50 and 76 were recruited in the state of Washington between the years 2000 and 2002. Upon enrolling in the study, participants reported information to researchers about B-vitamin usage over the past 10 years. This included dosage information.

Brasky notes these findings relate to doses that are well above those from taking a multivitamin every day for 10 years. "These are doses that can only be obtained from taking high-dose B vitamin supplements, and these supplements are many times the U.S. Recommended Dietary Allowance," he said. Two additional studies are underway at The OSUCCC - James to further evaluate high dose, long-term B6 and B12 supplementation and lung cancer risk. [Original study.]

Image result for back of hair, wikipedia There has long been concern over the chemicals in hair dyes and chemical hair straighteners or relaxers, and whether they are linked to various cancers. Studies have had mixed findings with regard to breast cancer, but a review paper concluded that there is evidence to support a role of hair product use in the risk of early onset breast cancer, especially in African-American women. Other studies found that long term users of dark hair dyes have a significantly increased risk of non-Hodgkin's lymphoma, multiple myeloma, and bladder cancer. 

A recent study done in the New York City and New Jersey area looked at both African-American women and white women and their use of various hair chemical products. They found that regularly chemically relaxing hair or dying hair dark brown or black is associated with an elevated risk of breast cancer in both African-American and white women. And women using both types of products had an even higher risk of breast cancer.From Medscape:

Dark Hair Dye and Chemical Relaxers Linked to Breast Cancer

African-American and white women who regularly chemically straighten their hair or dye it dark brown or black have an elevated risk of breast cancer, new research suggests. The study of 4,285 African-American and white women was the first to find a significant increase in breast cancer risk among black women who used dark shades of hair dye and white women who used chemical relaxers.

Black women who reported using dark hair dye had a 51 percent increased risk of breast cancer compared to black women who did not, while white women who reported using chemical relaxers had a 74 percent increased risk of breast cancer, the study found. The risk of breast cancer was even higher for white women who regularly dyed their hair dark shades and also used chemical relaxers, and it more than doubled for white dual users compared to white women who used neither dark dye nor chemical straighteners.

The study included adult women from New York and New Jersey, surveyed from 2002 through 2008, who had been diagnosed with breast cancer, plus women of similar age and race but without a history of cancer.....While the vast majority - 88 percent - of blacks had used chemicals to relax their hair, only 5 percent of whites reported using relaxers. For dark hair dye, the numbers flipped, though the differences were not as dramatic. While 58 percent of whites said they regularly dyed their hair dark shades, only 30 percent of blacks did.

The most striking results showed increased risk in the minority of black women who used dark hair dye and white women who used chemical relaxers. Black women who used chemical straighteners and white women who used dark hair dyes were also at higher risk for breast cancer, but that might have been due to chance. James-Todd said that because so many of the black women used chemical relaxers and so many of the white women used dark hair dye, links would have been hard to detect. There’s no reason to believe that chemical relaxers and hair dyes would increase the risk for women of one race and not of another, she said. 

Previous studies have shown that long-term users of dark dyes have a four-fold increased risk of fatal non-Hodgkin’s lymphoma and fatal multiple myeloma, the authors write. Prior research also has associated dark hair dye use with an increased risk of bladder cancer. A 2016 report from the U.S. Centers for Disease Control and Prevention found that breast cancer rates are generally similar for black and white women, at around 122 new cases for every 100,000 women per year, although black women with the disease are more likely to die from it.  [Original study.]