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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.]

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Image result for lobster meal wikipedia A recent study provided evidence that higher levels of cadmium in women may increase the risk of endometrial cancer. Endometrial cancer is the fourth most common cancer in women, and it occurs primarily in postmenopausal women. Endometrial cancer is associated with estrogen exposure (for example, being obese, and also from external or environmental sources of estrogen).

Cadmium is a metal commonly found in foods such as kidneys, liver, and shellfish, but also tobacco (cigarette smoking). Cadmium is toxic, it accumulates in the body, it is an estrogen-mimicking chemical, and it is associated with several hormone-dependent cancers. The researchers found that a doubling of cadmium exposure (as compared to those with low levels) was associated with a 22% increased risk of endometrial cancer.  Bottom line: Go ahead and enjoy these foods, but try to eat foods with naturally high levels of cadmium in moderation - such as shellfish, kidneys, and liver. From Science Daily:

Increased endometrial cancer rates found in women with high levels of cadmium

More than 31,000 new cases of endometrial cancer are expected to be diagnosed in 2017. Through a five-year observational study recently published in PLOS One, researchers at the University of Missouri found that women with increased levels of cadmium -- a metal commonly found in foods such as kidneys, liver and shellfish as well as tobacco -- also had an increased risk of endometrial cancer. It's an observation the researchers hope could lead to new treatments or interventions to prevent the fourth most common cancer in women.

"Cadmium is an estrogen-mimicking chemical, meaning it imitates estrogen and its effects on the body," said lead author Jane McElroy, Ph.D., associate professor in the Department of Family and Community Medicine at the MU School of Medicine. "Endometrial cancer has been associated with estrogen exposure. Because cadmium mimics estrogen, it may lead to an increased growth of the endometrium, contributing to an increased risk of endometrial cancer."

The research team partnered with cancer registries in Missouri, Arkansas and Iowa to identify cases of endometrial cancer. The team enrolled 631 women with a history of endometrial cancer in the study and 879 women without a history of the cancer to serve as a control group. The participants were asked to complete a survey of more than 200 questions about risk factors potentially associated with endometrial cancer. Once they completed the questionnaire, participants were sent a kit to collect urine and saliva samples. Through tests conducted at the MU Research Reactor, the samples were analyzed for cadmium levels.

While more research is needed to better understand the risks associated with cadmium, researchers say there are steps individuals can take to limit their cadmium-associated cancer risks. "We all have cadmium present in our kidneys and livers, but smoking has been shown to more than double a person's cadmium exposure," McElroy said. "Also, we recommend being attentive to your diet, as certain foods such as shellfish, kidney and liver can contain high levels of cadmium. You don't necessarily need to cut these from your diet, but eat them in moderation. This is especially true if women have a predisposition to endometrial cancer, such as a family history, diabetes or obesity." [Original study.]

 Another reason exercise is good for you: A large study found that men who exercise after a diagnosis of prostate cancer (but which is not metastatic) had a lower risk of dying from prostate cancer - as compared to those men who don't exercise.

So get out there and do something that gets you moving - and yes, walking is an exercise (Note: 1 mile = 20 minutes of walking, thus 3 miles = 1 hour). In this study the average age at diagnosis was 71, but studies find that exercise has numerous benefits at all ages. Some doctors even think of exercise as "anticancer therapy" (here, here). Also, exercise has anti-inflammatory benefits, and current thinking is that chronic inflammation is linked to cancer.

The American Cancer Society in its cancer prevention guidelines recommends that adults should be physically active, and get at least 150 minutes of moderate physical activity or 75 minutes of vigorous intensity activity each week (or a combination of these), preferably spread throughout the week.

From Medscape: Exercise Linked to Lower Mortality With Early Prostate Cancer

Men with nonmetastatic prostate cancer may have longer survival the more they exercise, a recent study suggests. For these men, regular moderate or vigorous physical activity was associated with 31 percent to 37 percent lower likelihood of death during the study, compared to more modest amounts of exercise. “This confirms and expands on previous work that shows an inverse association between recreational physical activity after diagnosis and risk of prostate cancer-specific mortality,” said lead study author Ying Wang of the American Cancer Society in Atlanta, Georgia, in email to Reuters Health.

Wang and colleagues pulled data from a large, long-term study group established by the American Cancer Society in 1992, focusing on 7,000 men who were diagnosed with prostate cancer between 1992 and 2011. The average age at cancer diagnosis was 71, and there were 2,700 deaths through 2012, including 450 due to prostate cancer and 750 due to heart disease. The average time from diagnosis to death was about eight years for those who died from cancer and 10 years for those who died from other causes.

Men who were more active before diagnosis were more likely to have lower-risk cancer tumors and a history of prostate screenings. They were also leaner, more likely to be nonsmokers and vitamin users and they ate more fish. Both before and after diagnosis, walking accounted for 73 percent of the physical activity that men did, followed by 10 percent for cycling and 5 percent for aerobic exercise, according to the report online now in European Urology.

Based on exercise levels before diagnosis, moderate to vigorous exercise, including walking, was linked to lower risk of death from prostate cancer, but only for men with lower-risk tumors. But after the diagnosis, the same levels of exercise were linked to lower risk of death from prostate cancer for all men, although the apparent benefit of walking was no longer statistically meaningful. [Original study.]

  Two more studies found that higher levels of vitamin D in the blood are associated with better health outcomes - one study found a lower risk of breast cancer, especially among postmenopausal women, and in the other - better outcomes after a metastatic melanoma diagnosis.

The breast cancer study suggested that a fairly high blood level of vitamin D (25(OH)D serum level>38.0 ng/mL) was associated with a lower risk of breast cancer. But overall they found that women supplementing with vitamin D (more than 4 times a week) at any dose had a lower risk of breast cancer over a 5 year period than those not supplementing with vitamin D. From Environmental Health Perspectives:

Serum Vitamin D and Risk of Breast Cancer within Five Years

Vitamin D is an environmental and dietary agent with known anticarcinogenic effects, but protection against breast cancer has not been established. We evaluated the association between baseline serum 25-hydroxyvitamin D [25(OH)D] levels, supplemental vitamin D use, and breast cancer incidence over the subsequent 5 y of follow-up. From 2003-2009, the Sister Study enrolled 50,884 U.S. women 35-74 y old who had a sister with breast cancer but had never had breast cancer themselves. Using liquid chromatography-mass spectrometry, we measured 25(OH)D in serum samples from 1,611 women who later developed breast cancer and from 1,843 randomly selected cohort participants.

We found that 25(OH)D levels were associated with a 21% lower breast cancer hazard (highest versus lowest quartile). Analysis of the first 5 y of follow-up for all 50,884 Sister Study participants showed that self-reported vitamin D supplementation was associated with an 11% lower hazard. These associations were particularly strong among postmenopausal women.

In this cohort of women with elevated risk, high serum 25(OH)D levels and regular vitamin D supplement use were associated with lower rates of incident, postmenopausal breast cancer over 5 y of follow-up. These results may help to establish clinical benchmarks for 25(OH)D levels; in addition, they support the hypothesis that vitamin D supplementation is useful in breast cancer prevention.

The first sentence in the melanoma study lays out what is widely known: "Vitamin D deficiency (≤20 ng/mL) is associated with an increased incidence and worse prognosis of various types of cancer including melanoma." Studies show that the relationship between vitamin D, sunlight exposure, and melanoma is complicated in a number of ways, including: sun exposure may be associated with increased survival in patients with melanoma. which may mean that vitamin D has a protective role in patients with melanoma. Several studies suggest that vitamin D may delay melanoma recurrence and improve overall prognosis. The study also found that metastatic melanoma patients with vitamin D deficiency who are unable to or don't raise their vitamin D blood levels (25(OH)D3) have a worse outcome compared to those who are are able to markedly increase (by greater than >20 ng/mL) their 25(OH)D3 levels. From Oncotarget:

Vitamin D deficiency is associated with a worse prognosis in metastatic melanoma

Vitamin D deficiency (≤20 ng/mL) is associated with an increased incidence and worse prognosis of various types of cancer including melanoma. A retrospective, single-center study of individuals diagnosed with melanoma from January 2007 through June 2013 who had a vitamin D (25(OH)D3) level measured within one year of diagnosis was performed to determine whether vitamin D deficiency and repletion are associated with melanoma outcome.

A total of 409 individuals diagnosed with histopathology-confirmed melanoma who had an ever measured serum 25(OH)D3 level were identified. 252 individuals with a 25(OH)D3 level recorded within one year after diagnosis were included in the study .... A worse melanoma prognosis was associated with vitamin D deficiency, higher stage, ulceration, and higher mitotic rate. In patients with stage IV metastatic melanoma, vitamin D deficiency was associated with significantly worse melanoma-specific mortality. Patients with metastatic melanoma who were initially vitamin D deficient and subsequently had a decrease or ≤20 ng/mL increase in their 25(OH)D3 concentration had significantly worse outcomes compared to non-deficient patients who had a >20 ng/mL increase. Our results suggest that initial vitamin D deficiency and insufficient repletion is associated with a worse prognosis in patients with metastatic melanoma.

 Once again several studies found health benefits associated with drinking coffee daily - this time "reduced risk of death" in 2 studies, and in one study a reduced risk of gallbladder cancer.

Just keep in mind that the studies found associations, but did not establish that drinking coffee caused X (reduced risk of death) - so perhaps coffee drinkers differ in some still unknown way from non-coffee drinkers. But...so many studies are piling up showing an association with health benefits that it looks likely that it is actually the coffee causing the benefits. Both decaffeinated and regular coffee seem beneficial, and it doesn't matter how it is prepared (e.g., espresso, drip, cappuccino). (Earlier posts about coffee - here, here, here)

In the one study higher consumption of coffee was associated with a lower risk of death from heart disease, cancer, stroke, diabetes, and kidney disease in African Americans, Japanese Americans, Latinos, and whites. People who consumed a cup of coffee a day (decaffeinated or regular) were 12 percent less likely to die compared to those who didn't drink coffee, and those who drank two to three cups a day had an 18 percent reduced chance of death.

The conclusion of the other study of over half million adults in 10 European countries was similar: coffee drinking was associated with lower risk for death from "all causes", especially from circulatory diseases and diseases related to the digestive tract. This association held up among all the countries. The highest levels of consumption  group (3 cups or more of coffee per day)  had the lowest risk of death - as compared to those drinking none or less than 1 cup of coffee per day. However, the one negative result from drinking more than 3 cups of coffee daily was an increase in risk for ovarian cancer mortality in women (but only when compared to coffee non-drinkers).

From STAT News: Drink coffee? It won’t hurt you, and may reduce your risk of an early death

Good news, coffee drinkers: A couple of massive new studies that looked at hundreds of thousands of people for about 16 years finds that a few cups of coffee a day won’t hurt you and could lower your risk of dying prematurely. The studies reinforce previous findings that drinking an 8-ounce cup of joe (or three) won’t hurt you, but the authors of the new works and other experts say caveats abound.

Murphy told STAT his is the largest study on coffee and mortality to date. In the study, researchers with the WHO’s International Agency for Research on Cancer and Imperial College London tracked 521,000 adults from 10 European countries who self-reported their coffee consumption over an average of 16 years.... In investigating more than 40,000 deaths from this group, the team found that participants who fell into the highest 25 percent of coffee consumers had a lower risk of death due to any cause compared to non-coffee drinkers. They saw a reduced risk of early death by diseases related to the digestive and circulatory systems. The researchers also discovered a link between higher coffee consumption and lower risk of early death by lung cancer in men. And they also looked at suicide — completed suicides were lower for coffee drinkers, but only in men. [Original study.]

In a second study of 180,000 people tracked for an average of 16 years, University of Southern California investigators found drinking one to six cups of coffee per week led to a decreased risk of early death. The study was focused on non-white populations, andtheir findings proved consistent for coffee drinkers across racial and ethnic groups. One of the USC study’s senior authors, V. Wendy Setiawan... said coffee consumption may be linked a lower risk of early death for people with heart disease, cancer, chronic lower respiratory disease, stroke, and kidney disease.Drink one cup per day, and the risk of dying early from those diseases decreases by 12 percent, she said. [Original study.]

This 2016 study is from Medscape: Coffee Consumption and Risk of Gallbladder Cancer in a Prospective Study

Evidence indicates that coffee consumption may reduce the risk of gallstone diseasewhich is strongly associated with increased risk of gallbladder cancer. The association between coffee consumption and gallbladder cancer incidence was examined in a prospective cohort study of 72,680 Swedish adults (aged 45 − 83 years) who were free of cancer and reported their coffee consumption at baseline.....  In conclusion, coffee consumption was observed to be associated with a reduced risk of gallbladder cancer. A potential protective association between coffee consumption and risk of gallbladder cancer may be mediated via reduced gallstone formation or through other mechanisms such as reduction of oxidative damage and inflammation and regulation of DNA repair, phase II enzymatic activity, apoptosis, angiogenesis, and metastasis.

 Should the results of this study determine what kind of coffee one drinks? Does it really make a difference? Eh...Not for me (because all coffee seems to be beneficial), but it might for you.

Studies show that daily drinking of coffee appears to have health benefits. Studies have linked coffee consumption with lower rates of cancer (here and here), cardiovascular disease, and diabetes. Coffee contains beneficial chemicals (such as caffeine and chlorogenic acid) that are antioxidant and anti-inflammatory, and could help fight chronic inflammatory diseases. It turns out that how much coffee beans are roasted changes how much chlorogenic acid they contain, but the amount of caffeine basically stays the same among the different roasting levels.

Researchers in Korea compared the caffeine and chlorogenic acid components of Arabica coffee beans at different roasting levels: Light, Medium, City, and French roast. They then tested various protective antioxidant and anti-inflammatory properties of the different coffee extracts in various "cell models" (meaning in the lab, not on real people). They found that chlorogenic acid levels were higher in light roasted coffee extract than the other roasted groups, and also light roasted coffee extract had the highest antioxidant activity. The results found that increasing degrees of roasting reduced antioxidant and anti-inflammatory activities.

From the Journal of Medicinal Food: Cellular Antioxidant and Anti-Inflammatory Effects of Coffee Extracts with Different Roasting Levels

During roasting, major changes occur in the composition and physiological effects of coffee beans. In this study, in vitro antioxidant effects and anti-inflammatory effects of Coffea arabica green coffee extracts were investigated at different roasting levels corresponding to Light, Medium, City, and French roast. Total caffeine did not show huge difference according to roasting level, but total chlorogenic acid contents were higher in light roasted coffee extract than other roasted groups. In addition, light roasted coffee extract had the highest antioxidant activity.... The expression of mRNA for tumor necrosis factor-alpha and interleukin-6 was decreased in cells treated with the coffee extracts and the expression decreased with increasing roasting levels. These data suggest that coffee has physiological antioxidant and anti-inflammatory activities and these effects are negatively correlated with roasting levels in the cell models.

Coffee is one of the most popular beverages worldwide. Increasing consumption of coffee is related to the pleasing taste and aroma, as well as its physiological effects. Coffee is proposed to exert beneficial effects against cancer, cardiovascular disease, obesity, and diabetes. Coffee contains phenolic compounds such as caffeic acid, chlorogenic acid, ferulic acid, vanillic acid, and other phytochemicals. The quality of coffee is significantly related to the roasting process.... During roasting, there are numerous changes in coffee bean compound profiles and the aroma is increased. Major changes in coffee bean composition occur during roasting as a result of the Maillard reaction..... Roasting markedly affects chlorogenic acid, leading to hydrolysis of chlorogenic acid. New compounds are formed during the roasting process; one of these is melanoidin. Its formation might alter the overall antioxidant capacity of coffee beans after roasting.

Coffee is a rich source of antioxidants that may contribute to prevention of oxidative stress-related diseases. The antioxidant properties of coffee may reflect the presence of both phenolic and nonphenolic bioactive compounds, such as caffeine and chlorogenic acids. Previous studies have shown that coffee has protective effects against oxidation and DNA damage in human cell models and has been shown to possess an in vitro antioxidant activity that lessens lipid peroxidation and neoplastic activity. 

Caffeine is the major component in coffee extract and has antioxidant property. Chlorogenic acid is another well-known efficient antioxidant in coffee extract; it was highest in Light roast coffee extract and highest with low roasting temperature and lowest in Dark roasted extract. Carbohydrates, protein, and chlorogenic acid are all decreased in coffee during the roasting process.... Caffeine contents showed no differences among roasting levels, but chlorogenic acid content decreased as roasting degree increased..... The effect of coffee roasting on the antioxidant properties of coffee extracts was investigated in several earlier studies; antioxidant capacity decreased in Dark roast coffee. The antioxidant property of coffee extracts prepared with different roasting levels was also determined in this study. The best antioxidant activity was evident in Light roast coffee extract and the lowest in French roast coffee.