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Category: cancer

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Much discussion about the link between gut bacteria and liver cancer, as well as the link between inflammation and cancer. Gut microbiome imbalances can cause health harms.

Bottom line: Try to improve your gut microbiome by eating a diet rich in fruits, vegetables, seeds, nuts, legumes, and whole grains.

From the Dec.4, 2014 issue of Nature: Microbiome: The bacterial tightrope

Imbalances in gut bacteria have been implicated in the progression from liver disease to cancer. The team's research, published last year, suggests that gut bacteria — which are part of the microbiome of bacteria and other microorganisms that live in and on the body — can play a crucial part in liver-cancer progression.

There are trillions of microorganisms in the human microbiome — they outnumber their host's cells by around ten to one — and their exact role in health and disease is only now starting to be explored. Studies have found that people with non-alcoholic fatty liver disease have a different composition of bacteria in their gut from healthy individuals2, 3

 Instead, she sees an emerging picture of liver disease and cancer as a process in which various factors — including a high-fat diet, alcoholism, genetic susceptibility and the microbiome — can each contribute to the progression from minor to severe liver damage, and from severe liver damage to cancer.

Flavell's research suggests that the liver has an important role in immune surveillance and helps to maintain bacterial balance in the gut. Specialized cells in the liver and intestines monitor the microbiome by keeping tabs on bacterial by-products as they pass through. These cells can detect infections and help to fight them.

But they can also pick up on subtler changes in the bacterial populations in the gut. When certain types of bacteria become too numerous — a state called dysbiosis — the immune system becomes activated and triggers inflammation, although at a lower level than it would for an infection... Now, research is emerging that suggests that dysbiosis and the immune reaction it provokes can even contribute to cancer.

He thinks that at least part of this mechanism involves disruption in the balance of the various species of bacteria in the gut. An out-of-balance microbiome promotes a constant state of inflammation, which can contribute to cancer progression, Schwabe says. This aligns with the picture that is emerging of cancer, in general, as an inflammatory process: the same immune reactions that help the body to fight infection and disease can also promote unchecked cell growth.

Some of the earliest research on the human microbiome, published in 2006, demonstrated that the balance of gut bacteria in obese people is different from that in people of healthy weight. In particular, obese people tend to have greater numbers of the bacteria that produce DCA (deoxycholic acid) and other secondary bile acids.

This line of research points to the microbiome as one potential link between obesity and liver-cancer risk . And, much like Schwabe's work, Hara's results indicate that several factors converge to promote cancer: in this case, bacteria, diet and carcinogen exposure. Here, too, the ability to stave off the disease seems to depend on maintaining the appropriate microbial balance. Overweight mice and people have a different composition of gut microbiota from their lighter counterparts, and they have higher levels of DCA, too.

However, not everyone is convinced that individual bacterial species are to blame. Some researchers point out that dysbiosis, and therefore cancer risk, involves multiple strains of bacteria. And the bacterial mix can vary from person to person, meaning it is unlikely that scientists can pin all responsibility on a single species.

Others are looking for ways to promote the growth of healthy bacterial strains rather than target the bad ones....There is also some early clinical evidence that specially formulated probiotics — cocktails of good bacteria — can bump the microbiome back into balance. Hylemon and his colleagues gave people with cirrhosis a probiotic containing Lactobacillus bacteria and found that their blood markers of inflammation decreased along with their cognitive dysfunction (a common symptom of cirrhosis)6. Although the study was not designed to evaluate cancer risk, it does show that delivering bacteria to the gut can have positive therapeutic effects on the liver.

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Great reasons to eat walnuts. Yes, this study was done in mice, but it (as supported by other research) should also apply to humans.From Medical Xpress:

'Tis the season to indulge in walnuts

Researchers at UC Davis and other institutions have found that diets rich in whole walnuts or walnut oil slowed prostate cancer growth in mice. In addition, both walnuts and walnut oil reduced cholesterol and increased insulin sensitivity. The walnut diet also reduced levels of the hormone IGF-1, which had been previously implicated in both prostate and breast cancer. The study was published online in the Journal of Medicinal Food. 

Davis and colleagues have been investigating the impact of walnuts on health for some time. A previous study found that walnuts reduced prostate tumor size in mice; however, there were questions about which parts of the nuts generated these benefits. 

In the current study, researchers used a mixture of fats with virtually the same fatty acid content as walnuts as their control diet. The mice were fed whole walnuts, walnut oil or the walnut-like fat for 18 weeks. The results replicated those from the previous study. While the walnuts and walnut oil reduced cholesterol and slowed prostate cancer growth, in contrast, the walnut-like fat did not have these effects, confirming that other nut components caused the improvements - not the omega-3s.

While the study does not pinpoint which combination of compounds in walnuts slows cancer growth, it did rule out fiber, zinc, magnesium and selenium. In addition, the research demonstrated that walnuts modulate several mechanisms associated with cancer growth.

"The energy effects from decreasing IGF-1 seem to muck up the works so the cancer can't grow as fast as it normally would," Davis said. "Also, reducing cholesterol means cancer cells may not get enough of it to allow these cells to grow quickly." In addition, the research showed increases in both adiponectin and the tumor suppressor PSP94, as well as reduced levels of COX-2, all markers for reduced prostate cancer risk.

Although results in mice don't always translate to humans, Davis said his results suggest the benefits of incorporating walnuts into a healthy diet. Other research, such as the PREDIMED human study, which assessed the Mediterranean diet, also found that eating walnuts reduced cancer mortality.

Still, Davis recommends caution in diet modification. "In our study the mice were eating the equivalent of 2.6 ounces of walnuts," he said. "You need to realize that 2.6 ounces of walnuts is about 482 calories. That's not insignificant, but it's better than eating a serving of supersized fries, which has 610 calories. In addition to the cancer benefit, we think you also get cardiovascular benefits that other walnut research has demonstrated.

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Read the labels on personal care products, and do NOT buy those with triclosan! (See earlier posts for other reasons to avoid triclosan.) From Science Daily:

The 'dirty' side of soap: Triclosan, a common antimicrobial in personal hygiene products, causes liver fibrosis and cancer in mice

Triclosan is an antimicrobial commonly found in soaps, shampoos, toothpastes and many other household items. Despite its widespread use, researchers report potentially serious consequences of long-term exposure to the chemical.The study, published Nov. 17 by Proceedings of the National Academy of Sciences, shows that triclosan causes liver fibrosis and cancer in laboratory mice through molecular mechanisms that are also relevant in humans.

"Triclosan's increasing detection in environmental samples and its increasingly broad use in consumer products may overcome its moderate benefit and present a very real risk of liver toxicity for people, as it does in mice, particularly when combined with other compounds with similar action," said Robert H. Tukey, PhD, professor in the departments of Chemistry and Biochemistry and Pharmacology. 

Tukey, Hammock and their teams, including Mei-Fei Yueh, PhD, found that triclosan disrupted liver integrity and compromised liver function in mouse models. Mice exposed to triclosan for six months (roughly equivalent to 18 human years) were more susceptible to chemical-induced liver tumors. Their tumors were also larger and more frequent than in mice not exposed to triclosan.

The study suggests triclosan may do its damage by interfering with the constitutive androstane receptor, a protein responsible for detoxifying (clearing away) foreign chemicals in the body. To compensate for this stress, liver cells proliferate and turn fibrotic over time. Repeated triclosan exposure and continued liver fibrosis eventually promote tumor formation.

Triclosan is perhaps the most ubiquitous consumer antibacterial. Studies have found traces in 97 percent of breast milk samples from lactating women and in the urine of nearly 75 percent of people tested. Triclosan is also common in the environment: It is one of the seven most frequently detected compounds in streams across the United States.

More about this study plus a discussion about the FDA's lack of action. From The Atlantic:

The Ingredient to Avoid in Soap

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This article describes results of a research review showing cancer prevention benefits from eating fatty fish and fish oil. From Science News:

Marked benefits found for cancer prevention with a higher intake of fatty fish

A new research review will once again have people asking for a second helping of wild Alaskan salmon at the dinner table. While several other studies have recently challenged the long-held belief of the benefits of a diet high in omega-3 fatty acids, this new study cites compelling evidence that eating the right kinds of fatty fish, in the right quantity, and prepared the right way, can in fact help prevent the body’s development of adenocarcinomas, a common type of cancerous tumor. A high proportion of the cancers arising in the breast, prostate, pancreas, colon, and the rest of the gastrointestinal tracts are adenocarcinomas.

The authors first cite evidence that the recently-demonstrated ability of daily low-dose aspirin to decrease risk for adenocarcinomas is attributable to its ability to modestly decrease the activity of cyclooxygenase-2 (cox-2), an enzyme which contributes importantly to the genesis and progression of adenocarcinomas. They then propose that an ample dietary intake of omega-3 fats -- the type prominent in fatty fish -- could also be expected to oppose cox-2 activity, and thereby reduce risk for adenocarcinomas.

The authors emphasize that it is not only the amount of fish consumed daily, but also the nature of this fish, and how it is preserved or cooked, that can have a major impact on the potential of dietary fish to lower cancer risk. "An easy way to see the benefit of omega-3 is to look at Italy," Dr. DiNicolantonio said. "The staple oil used in cooking and as a salad dressing in Italy is olive oil, which is quite low in omega-6. Meanwhile, fish -- high in omega-3 -- is a staple food in the Italian diet, and this fish is rarely salt-preserved or fried. In Italians studies, subjects who consumed fish at least twice weekly as compared to those who ate fish less than once a week, were found to be at a significantly lower risk for a number of cancers, including ovarian, endometrial, pharyngeal, esophageal, gastric, colonic, rectal, and pancreatic."

The authors also focus on several recent studies in which regular consumption of fish oil is correlated with lower subsequent cancer risk. These studies have reported lower risks for colorectal, breast, and advanced prostate cancer in those taking such supplements. And a recent study from the University of Washington, which estimated total omega-3 intakes of its subjects from both fish and from supplements, found that a high omega-3 intake was associated with a 23 percent reduction in total cancer mortality. Indeed, mortality from all causes was significantly lower in those with higher omega-3 intakes. The authors also noted that cox-2 is significantly expressed in pre-malignant and early stage adenocarcinomas, but expression is sometimes lost as cancers mature. This may be why cox-2 inhibition (via increased omega-3 intake) seems to have greater potential for cancer prevention, than for cancer therapy.

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The latest results on this hotly debated subject. The researchers suggest that people instead use "hands free phones with the loud speaker feature". From Medscape:

Long-Term Cell Phone Use Linked to Brain Tumor Risk

Long-term use of both mobile and cordless phones is associated with an increased risk for glioma, the most common type of brain tumor, the latest research on the subject concludes.

The new study shows that the risk for glioma was tripled among those using a wireless phone for more than 25 years and that the risk was also greater for those who had started using mobile or cordless phones before age 20 years.

The recent worldwide increase in use of wireless communications has resulted in greater exposure to radio frequency electromagnetic fields (RF-EMF). The brain is the main target of RF-EMF when these phones are used, with the highest exposure being on the same side of the brain where the phone is placed.

The analysis included 1498 cases of malignant brain tumors; the mean age was 52 years. Most patients (92%) had a diagnosis of glioma, and just over half of the gliomas (50.3%) were the most malignant variety — astrocytoma  grade IV (glioblastoma multiforme). Also included were 3530 controls, with a mean age of 54 years.

The analysis showed an increased risk for glioma associated with use for more than 1 year of both mobile and cordless phones after adjustment for age at diagnosis, sex, socioeconomic index, and year of diagnosis. The highest risk was for those with the longest latency for mobile phone use over 25 years.

The risk was increased the more that wireless phones were used. The odds ratios steadily rose with increasing hours of use...Further, the risk was highest among participants who first used a mobile phone (odds ratio, 1.8) or cordless phone (odds ratio, 2.3) before age 20 years, although the number of cases and controls was relatively small.

As Dr Hardell explained, children and adolescents are more exposed to RF-EMF than adults because of their thinner skull bone and smaller head and the higher conductivity in their brain tissue. The brain is still developing up to about the age of 20 and until that time it is relatively vulnerable, he said.

There was a higher risk for third-generation (3G) mobile phone use compared with other types, but this was based on short latency and rather low numbers of exposed participants, said the authors. 3G universal global telecommunications system mobile phones emit wide band microwave signals, which "hypothetically" may result in higher biological effects compared to other signals, they write. 

Numerous studies have looked at the link between use of wireless phones and brain tumors. Studies by Dr Hardell and his colleagues dating back to the late 1990s have found a connection with mobile and cordless phones. But the INTERPHONE study (Int J Epidemiol 2011;39:675-694; Cancer Epidemiol 2011;32:453-464) failed to find strong evidence that mobile phones increase the risk for brain tumors.

In addition, a large prospective study (Int J Epidemiol 2013;42:792-802) found that mobile phone use was not associated with increased incidence of glioma or of meningioma or non–central nervous system cancers in middle-aged British women.

Pathophysiology. Published online October 28, 2014. Abstract

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This recent scientific (and yes, technical) article discusses the tantalizing promise of treating cancer, especially melanoma, with infections and certain vaccines. Much discussion of how two vaccines that are already out there may prevent some cancers such as melanoma and leukemia (vaccination with Bacille Calmette-Guerin (BCG) of newborns and vaccination with the yellow fever 17D vaccine of adults).This recent article is a further development on what was discussed in the last post (Injecting a person with a bacterial extract - called Coley's toxins or Coley toxins - to cause an infection, and so treat cancer). From BioMed Central:

The biography of the immune system and the control of cancer: from St Peregrine to contemporary vaccination strategies

In 1875 Campbell de Morgan, a surgeon at the Middlesex Hospital in London, reported that regressions and remissions of cancers sometimes occurred after post-operative infections, particularly the streptococcal infection erysipelas...

Campbell de Morgan’s observation that remissions sometimes occurred after post-operative streptococcal infections inspired some workers to undertake the risky procedure of deliberately inducing erysipelas in cancer patients. Subsequently, an American surgeon, William Coley, developed bacteria-free extracts of streptococci and other bacteria (“Coley toxins”) and reported their successful use in the therapy of cancers, especially sarcomas, between 1881 and 1936 . Unfortunately Coley, a mild mannered and unassuming gentleman, did not adhere to rigorous scientific protocols in his studies and he was marginalized by forceful personalities advocating radiotherapy. Notwithstanding, an analysis of his results with cancer deemed inoperable undertaken in 1994 revealed a remission rate of 64% and a five-year survival rate of 44%, results equal to or better than those with modern therapies [14]. 

It is also now appreciated that chronic inflammation is an essential element of cancers and it has indeed been termed ‘the other half of the tumour’ [37]. The normal healing process relies on inflammation, collagen production, angiogenesis and cell proliferation and, in a description of the similarities between tumour stroma formation and wound healing, tumours have been referred to as “wounds that do not heal” [38], 

The relationship between infection, and associated inflammation, and cancer is a complex and paradoxical one and there are several well described examples of cancer being the direct consequence of infection [41]. Around 2 million of the 12.7 million new cancer cases worldwide in 2008 (16.1%) were assumed to be related to infection, principally Helicobacter pylori, hepatitis viruses, and the human papilloma virus, with a higher proportion in developing countries (22.9%) than in developed ones (7.4%) [42]. The large majority of cases of cancer, especially those in the developed nations, are therefore not caused by infection – on the contrary, there is growing evidence that a history of certain infections and environmental exposure to certain populations of micro-organisms, as well as some types of vaccination, may induce patterns of immune reactivity that reduce the risk of at least some cancers. 

A study of an adult population in Italy demonstrated an association between a history of common childhood infectious diseases (measles, chickenpox, rubella, mumps and pertussis) and the risk of developing chronic lymphatic leukaemia (CLL), with a strong inverse relationship between the risk of CLL and the number of infections (p = 0.002) [47]. 

In the 1990s Kölmel and colleagues established a working group – Febrile Infections and Melanoma (FEBIM) – within the European Organization for Research and Treatment of Cancer (EORTC). Based on a pilot study [79] this group undertook a series of studies to establish the relationship between the risk for developing melanoma and a history of, initially, infectious diseases [80], and, subsequently, also of vaccinations [81,82].

In the first report of the FEBIM group a significant level of protection against melanoma in those with a history of certain severe infections (sepsis, Staph. aureus infection, pneumonia, pulmonary tuberculosis) with fever of over 38.5°C was demonstrated [80]. It should, however, be noted that these apparently melanoma-protective infectious diseases have become rare in the industrialized nations. 

It is claimed that, as a result of recent observational studies, measures for prevention of some malignancies such as melanoma and certain forms of leukaemia are already at hand: vaccination with Bacille Calmette-Guérin (BCG) of new-borns and vaccination with the yellow fever 17D (YFV) vaccine of adults. While the evidence of their benefit for prevention of malignancies requires substantiation, the observations that vaccinations with BCG and/or vaccinia early in life improved the outcome of patients after surgical therapy of melanoma are of practical relevance as the survival advantage conferred by prior vaccination is greater than any contemporary adjuvant therapy.

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This was written in 2009, but it discusses the amazing possibility of infections with high fever treating and curing cancer. This method, originally discovered by William Coley in the 1890s, used a bacterial extract (named Coley's toxins or Coley toxins) to cause an infection in the person with cancer. Try to read the whole fascinating article.From American Scientist:

Healing Heat: Harnessing Infection to Fight Cancer

Conventional wisdom long held that the human immune system was no match for cancer. Born of native cells, the logic went, cancer fooled the immune system into concluding it was harmless. Thus protected from attack, cancer easily thrived until its host died.

A deeper understanding of our biological defenses has changed that. The human immune system does battle cancer. But we could better optimize our defenses to fend off malignant disease. That’s clear from cancer treatments attempted in New York City and Germany as early as the 19th century. Those experiments and other undervalued evidence from the medical literature suggest that acute infection—in contrast to chronic infection, which sometimes causes cancer—can help a body fight tumors.

It’s not the pathogens that do the good work. But the way our bodies respond to the pathogens is key. Infection events, especially those that produce fever, appear to shift the innate human immune system into higher gear. That ultimately improves the performance of crucial biological machinery in the adaptive immune system. This lesson comes, partly, from doctors who risked making patients sicker to try to make them better.

Medicine back then offered little more than amputation and morphine to cancer patients... Shocked by his ineffectiveness, Coley dove into hospital records and the medical literature for clues to how to help more. He found about 90 sarcoma case reports. About half contained follow-up histories....In his literature search,William Coley found more than 40 cases of disappearance of malignancies during an erysipelas attack. 

In April 1891 an Italian immigrant, Mr. Zola, presented at New York Hospital with a large sarcoma tumor in his neck and an egg-sized metastasis in his right tonsil. He had been operated on twice before but was in hopeless condition. He could hardly speak or swallow and was unable to eat solid food. His life expectancy was, at the very most, a few months. He had nothing to lose by undergoing an experimental treatment.

Mr. Zola with large sarcoma in the neck. Credit: Discover magazine.

Since erysipelas was so hazardous, the hospital was reluctant to host Coley’s experiment, so it was performed in a private apartment. Colleagues at the College of Physicians and Surgeons, now part of Columbia University, prepared the bacteria. Three applications were delivered over three weeks, with minor success...Via a friend, Coley obtained fresh and potent bacteria culture from the leading German bacteriologist, Robert Koch. That fall, he again treated Zola, whose temperature that time rose above 104 degrees, with nausea, vomiting and severe pain. The infection almost killed him, but within two weeks, the neck tumor was not observable. The tonsil tumor stopped growing. Zola was in excellent health when Coley saw him four years later.

During the following two years Coley attempted to infect 12 patients who had inoperable cancer. He failed to induce a full-blown infection in four and succeeded in eight. All eight responded. Six had partial tumor remissions. Two showed full remission. But two patients died from infection. So Coley abandoned living cultures and turned toward what today we would call a bacterial extract.

In January 1893 Coley administered for the first time one variant of what today are still called “Coley’s toxins.” It was a heat-sterilized, combined culture of S. pyogenes and S. marcescens bacteria administered by injection. The patient was a 16-year-old boy with a large inoperable abdominal tumor, a malignant sarcoma. After receiving increasing doses over 10 weeks, the boy developed symptoms mimicking those of a heavy erysipelas infection: chills, headache, fever, local redness and swelling at injection sites. The tumor shrank by 80 percent. Coley kept in touch with his patient, who remained cancer-free for more than 20 years.

At the beginning of the 20th century radiation treatment came on the cancer therapy scene. This new procedure captured nearly the full attention of the oncology community due to its immediately visible effects. One could now, it seemed, x ray away tumors. Within the medical mainstream, interest in Coley’s methods faded. Still, some physicians did try to test Coley’s treatment.

Coley, throughout his 40-plus-year career, treated hundreds with multiple versions of his toxin. He never achieved a clear-cut, uniform result. Some patients responded...A five-year survival rate of zero after radiation and 38 percent after Coley’s treatments merited deeper scrutiny.

Helen Coley Nauts, Coley’s daughter, meticulously reexamined her father’s clinical cases after his death. This was not easy. Undoubtedly a man of determination, Coley was not a methodical scientist. His patient records were a mess, he treated different patients for different time periods and his bacterial extracts, over time, were inconsistently made. Coley Nauts counted 15 different preparations. Eleven of them, she concluded, were not potent enough to have a strong effect.

Coley Nauts determined that her father had treated several hundred patients by the time he died in 1936, many of whom had received radiation and sometimes surgery as well. To estimate the overall success of extracts, the analysis should be restricted to patients with inoperable cancer and treated by toxin alone. In another review from 1994, immunologist and oncology researcher Charles Starnes identified 170 such patients with adequate medical records (121 with some form of sarcoma, 43 with carcinoma and myeloma, and 6 with melanoma). The remission rate among them was 64 percent; the five-year survival rate was more than 44 percent.

According to the analyses of Coley Nauts and Starnes, treatment success correlated with length of therapy and the fevers induced by the toxins. Higher was better. This correlation was reported among several other observations but without emphasis or any explanation by the authors.

Only a few uncoordinated attempts to apply Coley’s ideas were pursued from mid-century on....Well-controlled studies of bacterial-extract cancer treatment that incorporate all the lessons from the retrospective analysis of Coley’s and other treatments have not been pursued since. But medical case studies, cancer epidemiology and our more precise understanding of immunology make a strong case that they should.

Spontaneous regression or remission is the partial or complete disappearance of an untreated malignant tumor or a tumor treated with a therapy considered inadequate to exert significant influence. It sounds like fantasy, but about 1,000 case studies in the medical literature during the past century detail spontaneous regression from cancer. Surely more have occurred. And there’s a pattern to some of the cases. A prior fever was recorded in 25 to 80 percent of documented cases of spontaneous regression of cancer.

It is not true, as Coley believed of S. pyogenes, that all these pathogens produce some cagey anti-cancerous substance...Much more likely is that the sequence of immune reactions triggered by the infections was the same...Cancer cells can carry hundreds of mutations that distinguish them from healthy cells. But the immune system often remains in an “observer” state in their presence rather than engaging in battle as it does against bacterial or viral infections. The reason for this incomplete immune response is a long-standing puzzle in cancer immunology. William Coley’s experiments may help today’s scientists solve it.

There may be prophylactic potential here as well. Epidemiological studies suggest that a personal history that includes several infections with fever sometimes significantly reduces the likelihood a person will develop cancer later (see What the Literature Says). One potential explanation is that feverish infections reduce would-be malignant cells. If that’s true, the implications are profound.

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The following medical article (actually an interview with Prof. Cedric F Garland, Department of Family & Preventive Medicine, University of California San Diego School of Medicine) is strongly in favor of Americans getting their Vitamin D levels tested, and taking vitamin D3 (if needed) to raise serum levels of vitamin D's metabolite 25(OH)D to at least 30 ng/mL and preferably more.

It is suggested that taking 1000 IU of vitamin D3 daily would achieve these levels in most people. From Medscape:

Vitamin D and Mortality Risk: Should Clinical Practice Change?

Traditionally associated with skeletal disease including osteoporosis and fractures, low levels of serum 25-hydroxyvitamin D (25[OH]D), the metabolite usually measured as a mark of vitamin D status, more recently have been linked to a wide range of nonskeletal diseases, including some cancers and autoimmune, cardiometabolic, and neurologic diseases. A number of studies also have reported an inverse association between 25(OH)D concentration and all-cause mortality.

To explore this association more, Medscape reached out to Dr. Cedric Garland, a well-known expert on vitamin D. Dr. Garland is a professor in the Division of Epidemiology, Department of Family and Preventive Medicine, and a Fellow of the American College of Epidemiology. He has a Doctor of Public Health degree from University of California San Diego and studied epidemiology at Johns Hopkins. His research has focused on vitamin D status in health and the association between vitamin D deficiency and increased risk for disease, including some common cancers (breast cancer, colon cancer, leukemia, and melanoma) and diabetes. He is active in seeking to reduce the risk for cancer and diabetes by improving vitamin D status among the US population.

To examine the relation between serum 25(OH)D and mortality, Dr. Garland and colleagues at the University of California San Diego and others in the United States pooled data from 32 studies published between 1966 and 2013.[6] They found an overall relative risk of 1.8 (95% confidence interval [CI]: 1.7-1.8; P <.001) comparing the lowest (0-9 ng/mL) with the highest (>30 ng/mL) category of 25(OH)D for all-cause mortality. Serum 25(OH)D concentrations ≤30 ng/mL were associated with higher all-cause mortality than concentrations >30 ng/mL (P <.01).

The investigators noted that these findings confirmed observations from the Institute of Medicine (IOM) that 25(OH)D levels of <20 ng/mL are too low for safety,[8] but they suggested a cut-off point of >30 ng/mL rather than >20 ng/mL for all-cause mortality reduction. This level "could be achieved in most individuals by intake of 1000 IU per day of vitamin D3," the investigators said, noting that this is described as a safe dose in almost all adults by both the IOM[8] and Endocrine Society[9] clinical guidelines on dietary intake of vitamin D.

In particular, a randomized clinical trial by Lappe et al[12] had demonstrated a reduced risk for all cancers with vitamin D supplementation in postmenopausal women.... Only one third of the US population is below 20 ng/mL,[15] but two thirds of the population is below 30 ng/mL.[16]

We decided to look at what would happen if we put together all the existing studies that have looked at the survival of "ordinary" people; that is, mostly people in general practices who did not, for the most part, have illnesses. Studies that only included people who were already ill were not eligible for inclusion in our analysis. We found 88 relevant studies, of which 32 presented their data by quartiles of intake, allowing us to see a dose response

The incidence of colon cancer is very high in countries like Iceland and Sweden, and other countries nearer the North Pole, and in countries like New Zealand, which is closer to the South Pole, and intermediate in countries at intermediate latitudes such as the United States, which is, on average, 38º north of the Equator. By the time you get down within the tropics, which is 23º from the Equator, it begins to decrease, and within 5º of the Equator there are vanishingly low incidence rates of colon cancer. In the past, some scientists theorized that the low incidence rates near the equator were due to intake of a high-fiber diet, but now my group believes -- and many others are leaning more in this direction -- that it is the high UVB irradiance and high circulating 25(OH)D year-around nearer the equator rather than a high-fiber diet that best explains the inverse association with solar UVB irradiance

Raising the serum 25(OH)D from 30 to 40 ng/mL reduces the incidence of breast, bowel, and lung cancer by 80%, as reported by Lappe and colleagues in their clinical trial.[12]On the other hand, if you lump all cancers together, in both sexes, and include countries where there is a whole lot of cigarette smoking, then you may obscure the effect of the vitamin D. Vitamin D is not able to overcome the effect of heavy smoking, and the CHANCES analysis[7] included data from people in countries like the Czech Republic, Poland, and Lithuania, where there is a huge amount of smoking. Although the effects are still there, they are weakened.

Studies such as our meta-analysis have provided us an opportunity to not just be locked into the present but to predict mortality on the basis of vitamin D levels in the present. I had expected our results to be convincing, but we were shocked at the persistence of the belief that very low levels of vitamin D, such as approximately 20 ng/mL, are safe. They are not safe with regard to breast and colon cancer, several other cancers, diabetes in youth and adulthood, fractures, and other complications of 25(OH)D <30 ng/mL. Even higher levels, such as 40-60 ng/mL, would be even safer, according to a letter of consensus of expert vitamin D scientists and physicians.

In addition, 2 ongoing trials, the CAPS study[23] (aiming to replicate the findings of Lappe et al[12]) and the VITAL study,[22] are both using a vitamin D3 dose of 2000 international units (IU)/day. I think that if I were to design a trial, knowing what we know today, I would use 4000-5000 IU/day. It seems as though each time we do a clinical trial, by the time the trial is completed, we know that the doses were too small to elicit an effect.

I am also concerned that there may be not enough calcium to see an effect. In CAPS, the women are being given 1500 mg of calcium, which was done in the original randomized controlled trial in which 80% of the cancers in postmenopausal women were prevented. I would have stayed with this design and dose for the VITAL trial. We know that it helps because in their original trial, Lappe and colleagues[12]examined the effects of vitamin D alone vs vitamin D plus calcium, and the effects were stronger when the calcium was included.

Testing should be universal. And ideally it should be done in March when the vitamin D is at its lowest levels. This will prevent hundreds of thousands of cases of serious diseases worldwide annually, beginning with postmenopausal breast cancer and including colon cancer and types 1 and 2 diabetes. Skipping this test would be equivalent to not measuring blood pressure, serum lipids, or weight at an annual exam.

No one should run a serum 25(OH)D less than 30 ng/mL. This means that two thirds of the US population needs supplementation. You may have noticed that President Obama was recently tested for his vitamin D, and it was 22.9 ng/mL.[35] His physicians wisely decided to treat him, and he is now taking vitamin D.

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Another study finding health benefits from eating dairy foods (vs not eating any dairy foods).

From Science Daily: A heart-felt need for dairy food: Small serving beneficial, large not necessary

A daily small serve of dairy food may reduce the risk of heart disease or stroke, even in communities where such foods have not traditionally formed part of the diet according to new research.

A study of nearly 4000 Taiwanese, led by Emeritus Professor Mark Wahlqvist from Monash University's Department of Epidemiology and Preventive Medicine and the Monash Asia Institute, considered the role increased consumption of dairy foods had played in the country's gains in health and longevity.

"We observed that increased dairy consumption meant lower risks of mortality from cardiovascular disease, especially stroke, but found no significant association with the risk of cancer," Professor Wahlqvist said.

Milk and other dairy foods are recognised as providing a broad spectrum of nutrients essential for human health. According to the study findings, people only need to eat small amounts to gain the benefits.

"Those who ate no dairy had higher blood pressure, higher body mass index and greater body fatness generally than other groups. But Taiwanese who included dairy food in their diet only three to seven times a week were more likely to survive than those who ate none."

For optimal results, the key is daily consumption of dairy foods -- but at the rate of about five servings over a week. One serving is the equivalent to eight grams of protein: a cup of milk, or 45 grams of cheese. Such quantities rarely cause trouble even for people considered to be lactose intolerant, Professor Wahlqvist said.

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Eating more tomatoes is doable, tastes delicious, and reduces prostate cancer risk! From Science Daily:

Fighting prostate cancer with tomato-rich diet

Men who eat over 10 portions a week of tomatoes have an 18 percent lower risk of developing prostate cancer, new research suggests. With 35,000 new cases every year in the UK, and around 10,000 deaths, prostate cancer is the second most common cancer in men worldwide. Rates are higher in developed countries, which some experts believe is linked to a Westernised diet and lifestyle.

To assess if following dietary and lifestyle recommendations reduces risk of prostate cancer, researchers at the Universities of Bristol, Cambridge and Oxford looked at the diets and lifestyle of 1,806 men aged between 50 and 69 with prostate cancer and compared with 12,005 cancer-free men.

The NIHR-funded study, published in the medical journal Cancer Epidemiology, Biomarkers and Prevention, is the first study of its kind to develop a prostate cancer 'dietary index' which consists of dietary components -- selenium, calcium and foods rich in lycopene -- that have been linked to prostate cancer. Men who had optimal intake of these three dietary components had a lower risk of prostate cancer.

Tomatoes and its products -- such as tomato juice and baked beans -- were shown to be most beneficial, with an 18 per cent reduction in risk found in men eating over 10 portions a week. This is thought to be due to lycopene, an antioxidant which fights off toxins that can cause DNA and cell damage. 

The researchers also looked at the recommendations on physical activity, diet and body weight for cancer prevention published by the World Cancer Research Fund (WCRF) and the American Institute for Cancer Research (AICR). Only the recommendation on plant foods -- high intake of fruits, vegetables and dietary fibre -- was found to be associated with a reduced risk of prostate cancer.