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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

 A study was just published by researchers at the University of California that reviewed the role of Lactobacillus bacteria in a variety of diseases and conditions. What was surprising was that while we generally think of Lactobacillus bacteria as beneficial, some studies suggest that in certain diseases or conditions they may not be. But it is unknown if in those cases whether they're causing harm or why they are there in increased amounts.

Studies have found that Lactobacillus numbers are decreased ("depleted") in: some infectious diseases such as human immunodeficiency virus (HIV), in diarrhea-dominant irritable bowel syndrome (IBS) patients, type 1 diabetes, multiple sclerosis, colorectal cancer, and maternal prenatal stress (resulted in the infant having decreased levels of Lactobacillus bacteria). Lactobacillus levels were found to be either increased or decreased (depending on the study) in: cancer [but breast cancer, head and neck squamous cell cancer had increases in Lactobacillus levels], type 2 diabetes, and obesity. Increased amounts (intestinal "abundance") of Lactobacillus species has been found in: Crohn’s disease (CD) patients and rheumatoid arthritis (RA) patients. Studies also found benefits for consuming probiotics (with varying strains of Lactobacillus) for treating most of these diseases and conditions.

It used to be thought that Lactobacillus species were main species of the gut, but as genetic sequencing tests were developed, it became clear that Lactobacillus species are less than 1% of the bacterial species of the gut - thus a "minor member" of the gut microbiome. But as can be seen in the review study - much is still unknown about Lactobacillus species. What is true for one Lactobacillus species may not apply to another one. Studies find that feeding or nourishing beneficial microbes in the gut is good (e.g., eat foods with lots of fiber), as well as eating foods with lots of naturally occurring microbes (e.g., raw fruits and vegetables, cheeses, and fermented foods).

NOTE: In the following excerpts autochthonous = native (to the gut), and allochthonous - not native (originates elsewhere - such as from ingested probiotics). Excerpts from Current Opinion in Biotechnology:

Intestinal Lactobacillus in health and disease, a driver or just along for the ride?

Similarly, a number of recent publications in which culture independent methods were employed (e.g. 16S rRNA gene amplicon sequencing) identified Lactobacillus as being significantly enriched in the distal gut during either health or disease.....Lactobacillus species have been isolated from the entirety of the human GI tract (oral cavity to feces) as well as the skin and vagina. This genus is estimated to constitute 6% of the total bacterial cell numbers in the human duodenum and approximately 0.3% of all bacteria in the colon..... Lactobacillus can also dominate the human vaginal microbiota (90 to 100% of total bacteria present) and is found on the skin, but in much lower relative abundance.

Only a few out of the >200 known Lactobacillus species  have been consistently and repeatedly associated with the human GI tract. Recently, this number was increased to over 50 Lactobacillus species that were repeatedly detected in the stools of healthy volunteers. The most abundant Lactobacilli included L. casei, L. delbruckeii, L.murinus, L. plantarum, L.rhamnosus, and L. ruminus. Some of these species (e.g. L. rhamnosus and L. murinus) are rarely isolated from environments outside the intestine and are considered gut-autochthonous microorganisms. Other mucosal sites are colonized by distinct species (e.g. L. crispatus in the vagina). 

Both human immunodeficiency virus (HIV)-infected humans and simian immunodeficiency virus (SIV)- infected rhesus macaques harbor reduced numbers of intestinal Lactobacillus..... Several recent animal studies have indicated a broader role for Lactobacillus in prevention and resolution of infectious disease. Tryptophan metabolites (indole aldehydes) produced by indigenous L. reuteri strains activate host aryl hydrocarbon receptors (AHR) to promote gut and vaginal epithelial barrier and antimicrobial responses required for limiting the expansion of Candida albicans, an opportunistic pathogen. Autochthonous Lactobacillus might also have a role in the resolution of infectious disease and recovery of immune homeostasis.

A meta-analysis of reports investigating the fecal microbiomes from IBS patients and healthy subjects concluded Lactobacillus was depleted in diarrhea-dominant, IBS patients..... Consistent with these results, meta-analysis of probiotic intervention studies randomized controlled trials (RCTs)) for treatment of IBS concluded that multi-species probiotics diminish symptoms (abdominal pain, bloating, and flatulence scores). Conversely, intestinal abundance of Lactobacillus and other genera including Bifidobacterium were recently positively correlated with Crohn’s disease (CD)patients .... These findings contrast with ulcerative colitis (UC) in which probiotic Lactobacillus consumption has been with improved clinical symptoms.

The intestinal microbiota of patients with severe and early onset rheumatoid arthritis (RA) were shown to have increased proportions of L. salivarius, L. ruminus, and L. iners when compared to healthy, age-matched individuals..... These results are in opposition to recent RCTs of probiotics in RA patients.... Such findings might indicate species or strain-specific differences between autochthonous and allochthonous Lactobacillus on RA disease activity.

There are conflicting reports on the association of intestinal Lactobacillus with obesity in humans..... Moreover, metaanalysis of RCT studies found that probiotic Lactobacillus improved weight management outcomes in obese adults. Consumption of yogurt and other dairy products fermented by Lactobacillus is also correlated with protection from T2D and obesity. Because Lactobacillus species appear to be either associated with weight gain or weight loss, the disparate findings among obese individuals might be due to genetic differences among the lactobacilli. Strain and species distinctions could result in variations in carbohydrate metabolism and production of fermentation end-products, such as lactate.

In a systematic review of thirty-one studies, Lactobacillus along with a limited number of butyrogenic genera were consistently diminished in colorectal cancer patients. Preventative and therapeutic roles of Lactobacillus in cancer are supported in studies with preclinical, rodent models, including a recently study in which a multi-strain probiotic altered Th-cell polarization away from Th17 cells in a mouse model of hepatocellular carcinoma. However, Lactobacillus might not always be beneficial in certain extra-intestinal sites as shown by the higher levels of Lactobacillus in malignant breast cancer compared to benign-disease tissues. There was also a positive association between the levels of this genus in the oral microbiome and head and neck squamous cell carcinoma.

Image result for thunderstorm wikipediaThunderstorm asthma? This is an asthma attack triggered by a thunderstorm - it is still relatively rare, but predicted to increase with the coming climate changes. During thunderstorms there are downdrafts of cold air which sweep up particles of pollens and mold spores into the clouds. There they absorb moisture and rupture into small, fragments (into a size easily inhaled into the lungs), which then are dispersed by rain and wind. When inhaled they  can enter the lungs and trigger an asthma attack - thunderstorm asthma. [Note that normally larger pollen grains are usually filtered by hairs in the nose - so they don't make it to the lungs.] It seems that people with "hayfever" and allergies to grass pollen are at highest risk - at least in Australia. From Medscape:

Thunderstorm Asthma on the Rise

For seasonal allergy sufferers, rain is usually thought of as a friend—it washes the pollen out of the air. However, there are circumstances in which a particular type of wet weather event can make things much worse: thunderstorms. Asthma epidemics have occurred under such circumstances and have affected patients who have never exhibited asthmatic symptoms before. The most recent severe episode occurred in Melbourne, Australia, in 2016, with 8500 emergency asthma visits and nine deaths.[1]

Recently in the Journal of Allergy and Clinical Immunology, Dr Gennaro D'Amato and colleagues[1] explored the nature of this phenomenon and implications for the future. The authors point out that although rare, these events are expected to occur more often with anticipated climate change. According to the authors, the evidence for this so far is limited to pollen and outdoor mold seasons—but even in the northeastern United States, that is about three quarters of the year.

Pollen grains are large (up to 35 µm in diameter)[2] and usually do not make their way down to the bronchial tree. During a thunderstorm, however, these grains are swept up by a dry updraft, ruptured by high humidity at the cloud base, then forced down by cold air. These smaller grains contains allergens of the just the right size (< 3 µm) to reach the bronchial tree, resulting in asthma symptoms in patients with allergic rhinitis who perhaps have never exhibited asthma before.

The first reported case of thunderstorm asthma was in the United Kingdom in 1983. Since then it has happened in Australia, Canada, the United Kingdom (Alternaria species), the United States, and Italy (olive and Parietaria pollens). Evidence for the role of the Parietaria pollen in the outbreak in Naples, Italy, was supported by high levels of the pollen grains as opposed to low levels of measured particulates and pollutants, including ozone and nitric oxide.

Certainly, people who are sensitized to the relevant allergens are at risk. Beyond that, we can presume that patients who already have poorly controlled asthma or more bronchial hyperresponsiveness would be at risk, as would patients who have other concurrent risk factors for allergic asthma (such as rhinovirus infection).

It seems like I can't stop writing about coffee (here and here). Coffee drinkers rejoice: another study (presented at the European Society of Cardiology) finds health benefits from drinking several cups of coffee daily. This study, like other previous studies, found an inverse relationship between drinking coffee and early death ("all-cause mortality") - meaning the more one drinks coffee, the less likely one is to have a premature death. The biggest effect was in drinking 4 cups daily in people aged 45 and older! It was an observational study, so can't prove it definitely - can only say there's an association. But still... it's looking good. From Medical Xpress:

Higher coffee consumption associated with lower risk of death

Higher coffee consumption is associated with a lower risk of death, according to research presented today at ESC Congress. The observational study in nearly 20,000 participants suggests that coffee can be part of a healthy diet in healthy people. 

The purpose of this study was to examine the association between coffee consumption and the risk of mortality in a middle-aged Mediterranean cohort. The study was conducted within the framework of the Seguimiento Universidad de Navarra (SUN) Project, a long-term prospective cohort study in more than 22,500 Spanish university graduates which started in 1999. This analysis included 19,896 participants of the SUN Project, whose average age at enrollment was 37.7 years old. .... Patients were followed-up for an average of ten years. 

During the ten year period, 337 participants died. The researchers found that participants who consumed at least four cups of coffee per day had a 64% lower risk of all-cause mortality than those who never or almost never consumed coffee. There was a 22% lower risk of all-cause mortality for each two additional cups of coffee per day.

The researchers examined whether sex, age or adherence to the Mediterranean diet had any influence on the association between baseline coffee consumption and mortality. They observed a significant interaction between coffee consumption and age. In those who were at least 45 years old, drinking two additional cups of coffee per day was associated with a 30% lower risk of mortality during follow-up. The association was not significant among younger participants.

Two recent studies, both done in California, looked at different aspects of pesticide exposure. They highlight how people can be exposed to pesticides in the air they breathe, especially if they live in areas where pesticides are heavily applied (such as farms). But keep in mind that even in suburbia, every time a neighbor applies pesticides on the lawn or trees - there is drift, and so you are also exposed (e.g., breathing it, droplets on the skin).

The first study found that pregnant women with high pesticide exposure (living in areas near farms using pesticides) had increases in adverse birth outcomes (low birth weight, shorter pregnancy length, preterm birth, birth defects or abnormalities). No effects were seen with low pesticide exposure. But note that these results are what could be seen at birth - they do not include effects that can only be seen later, such as delayed development, learning disabilities, lower intelligence, asthma, autism - all effects found in some studies.

The other was a California Department of Pesticide Regulation (CDPR) 2016 report on air monitoring results (from 6 sites) of 32 chemicals (pesticides and breakdown products) in California. Some pesticides were not detected, some were only at trace amounts, and some were detected at higher amounts  - and the amounts fluctuated over the year and from site to site. [NOTE: They did not monitor for 2 widely used pesticides: glyphosate, which is in Roundup, and 2,4-D. Hmm...]. A Kern County high school monitoring site showed levels of the pesticide chlorpyrifos more than 18 times higher than EPA's "level of concern for pregnant women" - but yet these levels are considered OK for the general public.

Chlorpyrifos is "controversial" in that scientists (including EPA scientists), medical professionals, and farmworker organiztions asked that its use be banned due to its serious health effects on humans, but this year EPA chief Scott Pruitt refused to do so (he gave in to pesticide industry lobbying). The bottom lineWhat effect do the mixtures of pesticides (at chronic low levels) that we're exposed to have on us? Unknown. 

From Medical Xpress: Researchers unravel the negative effects of pesticide exposure on birth outcomes

Although common opinion holds that exposure to pesticides increases adverse birth outcomes, the existing body of scientific evidence is ambiguous..... A new study by researchers at UC Santa Barbara addresses the issue in a novel way—by analyzing birth outcomes in California's San Joaquin Valley. With more than one-third of the country's vegetables and two-thirds of its fruits and nuts produced there, the San Joaquin Valley, not surprisingly, is a heavy pesticide-use region. The UCSB team investigated the effect of exposure during pregnancy in this agriculturally dominated area and observed an increase in adverse outcomes accompanying very high levels of pesticide exposure

"For the majority of births, there is no statistically identifiable impact of pesticide exposure on birth outcome," said lead author Ashley Larsen, an assistant professor in UCSB's Bren School of Environmental Science & Management. "Yet mothers exposed to extreme levels of pesticides, defined here as the top 5 percent of the pesticide exposure distribution, experienced between 5 and 9 percent increases in the probability of adverse outcomes with an approximately 13-gram decrease in birth weight."

Using individual birth certificate records for more than 500,000 single births between 1997 and 2011, coupled with pesticide use data at a fine spatial and temporal scale, the scientists were able to determine if residential agricultural pesticide exposure during gestation—by trimester and by toxicity—influenced birth weight, gestational length or birth abnormalities.

They found negative effects of pesticide exposure for all birth outcomes—birth weight, low birth weight, gestational length, preterm birth, birth abnormalities—but only for mothers exposed to very high levels of pesticides—the top 5 percent of the exposure distribution in this sample.... Numerous chemicals are used daily in close proximity to residential areas, making it difficult to ascertain a specific responsible agent. As a result, in this study, the researchers looked at the combined results from all pesticides used in the region[Original study.]

Excerpts from Beyond Pesticides: Neurotoxic Pesticide Detected in Air at High Levels in California County

The California Department of Pesticide Regulation (CDPR) released its 2016 air monitoring data where it was revealed that chlorpyrifos air concentrations for a one-month period at the air monitoring site on the campus of Shafter High School in Kern County was 39.4 nanograms per cubic meter (ng/m3) – more than 18 times higher than EPA’s level of concern for pregnant women (2.1 ng/m3).  Shafter High School is some distance from fields in an area where chlorpyrifos use is not as high as in other parts of Kern County or elsewhere in California. 

High chlorpyrifos levels at a school means that children and unsuspecting teachers and parents, especially those that may be pregnant, are breathing in unusually high levels of chlorpyrifos. Children exposed to high levels of chlorpyrifos have developmental delays, attention problems, attention-deficit/hyperactivity disorder problems, and pervasive developmental disorders.

Image result for psoriasis wikipediaCould probiotics have a role to play in the treatment of psoriasis? A recent analysis and review of studies suggests that they might. Psoriasis is a non-contagious, chronic disease affecting about 2 to 4% of the population, and which is characterized by patches of abnormal skin. These skin patches are typically red, itchy, and scaly, and can cover small areas to covering the entire body. There is no cure for psoriasis, but various treatments can help control the symptoms, such as steroid creams, vitamin D3 cream, ultraviolet light, and immune system suppressing medications. 

What did the researchers find? They said that "new evidence suggests that the microbiome may play a pathogenic role in psoriatic disease" - meaning the community of microbes (microbiome) may be involved in this disease. There is dysbiosis of the skin microbiome (microbial community is out of whack) in areas of skin lesions or patches. Areas of skin lesions had a different microbiome ("lesional psoriatic microbiome") compared to healthy skin - and in these skin lesions or patches some microbial species increase which leads to a decrease or elimination of others. Not just differences in bacteria, but also in fungi and viruses.

in psoriasis the microbial community of the gut is also out of whack (dysbiosis of the gut microbiome). And the gut microbiome is different in those with psoriasis limited to just skin patches, and those with complications of psoriasis (e.g., psoriatic arthritis) - and several studies found that these shifts in the gut microbiome occurred before the psoriatic complications became evident. That suggests that probiotics might help. But which ones?

The researchers state: "Other changes observed in gut microbiome studies include a decrease in Actinobacteria. This may suggest a protective role of Actinobacteria, a phylum which includes Bifidobacterium species that have been shown to reduce intestinal inflammation, suppress autoimmunity, and induce Tregs." They go on to state that one 2013 study by Groeger et al demonstrated that eating Bifidobacteria infantis 35,624 for 6–8 weeks in a randomized, double-blind, placebo-controlled clinical trial reduced inflammatory markers (plasma CRP and TNF-a) in psoriasis patients. Bifidobacterium species, including B. infantis, are commonly found in many multi-strain supplements. So I wonder, what happens if people with psoriasis take them over an extended period? Will the skin psoriasis skin patches improve? This is currently unknown. But...If you've had success with probiotics as a  psoriasis treatment - please let me know. What microbes? And for what symptoms of psoriasis?

From Current Dermatology Reports : The Role of the Skin and Gut Microbiome in Psoriatic Disease

Our review of studies pertaining to the cutaneous microbiome showed a trend towards an increased relative abundance of Streptococcus and a decreased level of Propionibacterium in psoriasis patients compared to controls. In the gut microbiome, the ratio of Firmicutes and Bacteroidetes was perturbed in psoriatic individuals compared to healthy controls. Actinobacteria was also relatively underrepresented in psoriasis patients relative to healthy individuals.

Summary: Although the field of the psoriatic microbiome is relatively new, these first studies reveal interesting differences in microbiome composition that may be associated with the development of psoriatic comorbidities and serve as novel therapeutic targets.

Image result for psoriasis medscape  Psoriasis.  Credit: Medscape

Surprised...is how I felt after reading this study. According to the study, activity levels and exercise in mid-life are not linked to cognitive fitness and dementia later on in life. Instead, higher levels of physical activity and exercise has a beneficial effect on the brain in the short term (e.g., within 2 years or so). This finding of no long-term benefits, but only short-term benefits to the brain from exercise, is contrary to some other (cross-sectional) studies, but is supported by another recent study ("no evidence of a neuroprotective effect of physical activity").

The beauty of this study is that it followed 646 people for 30 years (from a median age of 46 years in 1978 and 77 years in 2008). The negative is that according to this study, physical exercise in mid-life does not seem to delay or prevent the onset of dementia and Alzheimer's later on in life. Eh... From Medical Xpress:

Physical activity in midlife not linked to cognitive fitness in later years, long-term study shows

A study led by Johns Hopkins Bloomberg School of Public Health researchers that tracked activity levels of 646 adults over 30 years found that, contrary to previous research, exercise in mid-life was not linked to cognitive fitness in later yearsThe finding suggests that physical activity may not help maintain cognitive function, or help avoid or delay the onset of the debilitating conditions like dementia and Alzheimer's

The study, which appears online in the Journal of Alzheimer's Disease, did find that activity levels among study participants in the later years were associated with high cognitive function two years later. This supports earlier research findings that exercise may help to maintain cognitive fitness in the short term.

There is no known treatment or cure for Alzheimer's or dementia, syndromes that involves declining memory, confusion and eventually limited ability to perform daily tasks. To date, there are no preventive measures, such as physical exercise, brain games or a diet regimen, that have been proven to help delay or altogether prevent its onset. The researchers undertook the study because of a growing consensus that physical activity levels helps prevent Alzheimer's, however much of the evidence for this thinking is based on cross-sectional studies that compare responses from one group of participants with another at a given point in time or within a very short duration, typically several years..... That's where longitudinal studies, which look at the same group of participants over a long time, are more helpful.

The researchers used data from the Johns Hopkins Precursors study.... The researchers used responses from 1978 through 2008 from 646 participants (598 men, 48 women) to calculate so-called metabolic equivalents, which quantify physical activity levels. Participants were also asked whether they regularly exercise to a sweat. The team administered cognitive tests in 2008, and, using participants' medical records, scored for dementia through 2011. The researchers identified 28, or 4.5 percent of the cohort, to have Alzheimer's.

No physical activity measure in mid-life was associated with late-life cognitive fitness or onset of dementia. The study confirmed findings of other cross-sectional studies, that higher levels of physical activity and exercise measured close in time to the cognitive testing were associated with better cognitive functioning. The authors also looked at whether patterns of change in physical activity levels over the life span were associated with cognitive health and found no relationships.

The idea that exercise might play a role in preventing or limiting Alzheimer's makes sense, the researchers say, because physical activity, at least in mouse models, has shown less accumulation of B-amyloid plaques, which are thought to play a role in dementia, including Alzheimer's. In addition, physical activity improves blood flow to the brain, which is linked to better cognitive performance. This may explain why studies find that exercise may contribute to cognitive fitness in the short term.

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.]

 Could something as simple as giving a probiotic and a sugar for 7 days prevent sepsis in babies? Sepsis is a life-threatening infection that is a HUGE problem in developing countries such as India. It is a major cause of death in babies throughout the world, even with antibiotic treatment. So this new research (done in India) finding that giving newborn babies a probiotic plus the sugar fructooligosaccharide (FOS) for only one week had the result of lowering the incidence of sepsis and death by 40%, and also infections is huge news. A game changer.

The researchers found that the strain given to the babies was very important. They first tried Lactobacillus GG and Lactobacillus sporogenes, but didn't have success. But a strain of Lactobacillus plantarum was amazingly effective. They gave it together with a sugar - fructooligosaccharide (FOS) - which together worked as a synbiotic. Synbiotics are combinations of probiotics with an FOS supplement that promotes growth and colonization of the beneficial bacteria. FOS (which is naturally found in breast milk and such plants as onion, chicory, garlic, asparagus, banana, artichoke, agave, leeks, wheat, barley), is food for the probiotic bacteria.

It must be pointed out that other studies have tried other probiotics in the prevention of sepsis, but have not been successful. Probiotics that did not work work in other studies were Streptococcus thermophilus, Bifidobacterium infantis, Bifidobacterium lactis, and Bifidobacterium breve. However, they did not also use prebiotic supplements (the FOS) - just the probiotic alone - and studied premature or low birth weight babies (while this study focused on healthy babies of approximately normal weight.) This is why research now needs to be done looking at other groups of babies. From Medical Xpress:

Study shows probiotics can prevent sepsis in infants

A research team at the University of Nebraska Medical Center College of Public Health has determined that a special mixture of good bacteria in the body reduced the incidence of sepsis in infants in India by 40 percent at a cost of only $1 per infant...... The special mixture included a probiotic called Lactobacillus plantarum ATCC-202195 combined with fructo-oligosaccharide (FOS), an oral synbiotic preparation developed by Dr. Panigrahi.

Probiotics are live bacteria and yeasts that are good for your health, especially your digestive system. Synbiotics are combinations of probiotics with an FOS supplement that promotes growth and sustains colonization of the probiotic strain. FOS, naturally found in breast milk and such plants as onion, chicory, garlic, asparagus, banana, artichoke and others, is food for the probiotic bacteria.

Sepsis is a severe complication of bacterial infection that results in around one million infant deaths worldwide each year, mostly in developing countries. It occurs when the immune system stops fighting germs and begins to turn on itself and can lead to tissue damage, organ failure and death. It is estimated that 40 percent of patients with severe sepsis in developing countries do not survive.

The team enrolled more than 4,500 newborns from 149 villages in the Indian province of Odisha and followed them for their first 60 days, the most critical period when they get sick and die. During their first days of life, the newborns were administered the oral preparation for seven days. Results of the randomized, double-blind, placebo-controlled study showed that sepsis and deaths in the first two months of infancy were reduced by 40 percent, more than twice the anticipated reduction of 20 percent. The synbiotic treatment also lowered respiratory tract infections. The effectiveness demonstrated in Dr. Panigrahi's study was so successful the study was halted early. 

An interesting article about this research from The Atlantic: At Last, a Big, Successful Trial of Probiotics

  Amazing if this holds up in larger studies - a treatment for peanut allergy! As the researchers said -  the treatment (2 grams of peanut protein plus a specific strain of the probiotic Lactobacillus rhamnosus daily for 18 months) provided "persistent suppression of the allergic immune response to peanuts 4 years" after the treatment had ended This was a nicely done multi-year study in children - a randomised, double-blind, placebo-controlled trial (to eliminate biases).

The researchers also wrote in the Discussion section of the study: "PPOIT [combined probiotic and peanut oral immunotherapy] was associated with long-lasting peanut tolerance 4 years after stopping treatment. Two-thirds of PPOIT treated participants were able to continue regular peanut ingestion, and more than half were ingesting moderate to-large amounts of peanut on a regular basis, compared with only one (4%) of 24 placebo-treated participants. Allergic reactions from intentional peanut ingestion were uncommon and all reactions were mild, suggesting that those who achieved PPOIT-induced sustained unresponsiveness can safely continue peanut ingestion." In other words - WOW! (Other posts on peanut allergies - here and here, and earlier progress report of this study.) From Medical Xpress:

Australian researchers in peanut allergy breakthrough

Australian researchers have reported a major breakthrough in the relief of deadly peanut allergy with the discovery of a long-lasting treatment they say offers hope that a cure will soon be possible. In clinical trials conducted by scientists at Melbourne's Murdoch Childrens Research Institute, children with peanut allergies were given a probiotic along with small doses of a peanut protein over an 18-month period. When the experiment ended in 2013 some 80 percent of the kids were able to tolerate peanutsThe research, published Wednesday in medical journal The Lancet, found that four years on, about 70 percent could still eat peanuts without an adverse reaction.

"The importance of this finding is that these children were able to eat peanuts like children who don't have peanut allergy and still maintain their tolerant state, protected against reactions to peanut," lead researcher Mimi Tang said. "These findings suggest our treatment is effective at inducing long-term tolerance, up to four years after completing treatment, and is safe. Food allergy affects one in 20 children and about two in 100 adults, with seafood, cow's milk, eggs and peanuts among the most typical triggers. Peanuts are one of the most common foods to cause anaphylaxis, a potentially fatal allergic reaction.

The researchers said the Murdoch study provides the "strongest evidence yet that a cure may be possible for peanut allergy"..... Ten-year-old Olivia May suffered a reaction when she tried to eat a peanut butter sandwich seven years ago. "We visited the allergist the first time [and] he said 'sorry, you're going to have to go home and empty your pantry out, clear it of all nuts, anything with nuts in it'," Oliver's mother Tanya told the Australian Broadcasting Corporation. But after taking part in the trial, Oliva no longer suffers from her allergy.

Fifty-six children completed the study, with half receiving a placebo and half receiving the treatment, which encourages the immune system to develop a tolerance to the allergy. Researchers are now aiming to confirm the results with a larger study of the treatment they say "holds important implications for attacking the modern food allergy epidemic". [Original study.]