Gut Infections May Be Linked to Inflammatory Bowel Disease

Came across a really interesting article about some new research that suggests that gut infections could be a trigger sending the immune system into a downward spiral where it can't distinguish between good and bad bacteria in the gut.

The hypothesis (that still needs to be confirmed) is that a gut infection potentially causes good bacteria to act strangely (e.g. overgrowing), your gut to be leaky (i.e. let bacteria invade other parts of your body like your bloodstream), and then your immune system is forced to respond to these bacteria and start treating them as bad.  At that point, your body has trained itself to treat these good bacteria as bad bacteria, and then your immune system is just totally thrown off.

I blogged about this before, but I had several serious bouts of food poisoning when I was younger and I've often wondered if those events threw my system off.  Interesting research though.

Here's an excerpt:

Most likely, Hand said, the immune system is indirectly responsible for spreading the good gut bacteria around. A strong immune response can damage body cells, including the gut cells that usually keep beneficial bacteria on the inside of the intestines. 

Once the parasite infection is over, the researchers found, the immune system locks in a memory of the invaders it fought in memory T cells. These cells are able to mount a fast immune response if they encounter the same pathogens for a second or third time. 

Unfortunately, the T cells remember the beneficial gut bacteria as well as the parasite, the researchers report online today (Aug. 23) in the journal Science. This memory seems to last as long as the mouse lives, Hand said.

Caltech Researchers Discover that Gut Bacteria Affect Multiple Sclerosis

I've had a couple blog posts about multiple sclerosis (MS), including links to both viral and bacterial infections. I just came across another study, this one from Caltech, that found that gut bacteria can affect the onset of MS. The researchers found that gut bacteria could influence the creation of Th17 cells (certain kinds of immune helper cells).

The bacteria aren't necessarily the entire cause of the disease, but they may represent the "environmental" component that when combined with genetic susceptibility causes the disease to kick into gear. Here's an excerpt:

Mazmanian and his colleagues don't, however, suggest that gut bacteria are the direct cause of multiple sclerosis, which is known to be genetically linked. Rather, the bacteria may be helping to shape the immune system's inflammatory response, thus creating conditions that could allow the disease to develop. Indeed, multiple sclerosis also has a strong environmental component; identical twins, who possess the same genome and share all of their genes, only have a 25 percent chance of sharing the disease. "We would like to suggest that gut bacteria may be the missing environmental component," he says.

It's amazing that inflammation of something as sterile as the central nervous system and brain could be impacted by what's going on in your gut. But there does indeed seem to be a connection. Hopefully they can find the bacteria (or type of bacteria) that triggers Crohn's Disease as well.

When Good Germs Go Bad - Friendly Bacteria Triggers Arthritis in Mice

Saw a really interesting article in Scientific American about a study regarding a link between a specific strain of bacteria and rheumatoid arthritis (RA) in mice. The study found that the introduction of a single type of bacteria could increase the amount of IL-17 (interleukin 17), a protein that signals the immune system to cause inflammation, in the mouse. The "friendly" bacteria that causes this accelerated the onset of arthritis in the mice. The mice were selected to already be genetically predisposed to having arthritis, so all mice in the study developed arthritis. But the mice that were given the bacteria developed RA much more quickly.

Why is this important? This could mean that exposure to even a single bacteria or virus could trigger an autoimmune reaction in genetically susceptible individuals. Here's an excerpt:

Mathis emphasized that one should not take away from these mouse studies "that mice or humans can 'catch' an autoimmune disease or arthritis," she says. She added that the better way to think about it is that individuals have varying degrees of genetic susceptibility, and when exposed to certain environmental factors may then go on to develop disease. "It's really an interaction between genetics and environment," Mathis says.

Crohn's Disease or Inflammatory Bowel Disease (IBD) may have a similar pattern to RA. It could also mean that there is a single bacteria or virus responsible for the disease. Or ... it could also mean that there are any number of bacteria or viruses that trigger the disease. Either way, it's a very study and reinforces previous theories and studies I've seen.

Virus infection may trigger unusual immune cells to attack the brain and spinal cord in multiple sclerosis

I came across a really interesting article regarding a possible causative mechanism for multiple sclerosis (MS). As you most likely know, MS is an autoimmune disease (similar to IBD and Crohn's) where immune cells misguidedly attack the body's own cells. In the case of MS, the body is attacking the protective sheath around major nerves. In the case of IBD, the body is attacking your intestinal tissue.

The above mentioned article found that a viral infection could incite certain rare immune cells to be released in the body that attack both the virus and (in the case of MS) nerve cells. The rare immune cells do this because they have receptors for both the virus' proteins and proteins present in nerve tissue (myelin). I found this research interesting given the recent talk from Amy Proal that I blogged about regarding the viral and bacterial metagenome and the recent study (similar to the MS one) that found a possible link between errant T-cells and diabetes.

The study about MS suggests that there's not necessarily a single virus that causes the disease, but instead a combination of factors that generate the errant T-cells:

The authors explained that it's possible that multiple viruses could influence susceptibility to multiple sclerosis. The ability of any particular virus to contribute to the disease could depend on an individual's own repertoire of other predisposing genes, exposure to other predisposing environmental factors, and the random chance that T cells had been generated that recognize a myelin protein and a pathogen.

Receptors on T cells are randomly generated during their development. This observation helps explain why multiple sclerosis is partly a matter of chance. Some people with a genetic predisposition and environmental exposure develop the disease, while others with similar genetic predisposition and environmental exposure do not.

This suggests some really interesting (and challenging) directions for future research. Many current studies are focusing on finding a single bacteria or virus (e.g. MAP) that someone is infected with or a single genetic mutation (e.g. NOD2) that cause IBD. This is a potentially flawed approach, though. This study suggests that even after the infection is cleared, the errant T-cells that cause the autoimmune reaction may persist (i.e. there's no smoking gun). It certainly makes finding the root-cause difficult! But it suggests a different direction to take research.

Meat Proteins Linked to Bowel Disease in Women

A new study from France revealed that eating lots of animal protein appears to increase the risk of inflammatory bowel disease (IBD) in women. The study was conducted on 67,000 women in France over a long time period to find risk factors for different diseases, including cancer and other common illnesses. There are no conclusions that are being drawn from the study, but it does suggest that diet does potentially play a role in the disease.

An excerpt:

Women who consumed the most protein were at more than triple the risk of being diagnosed with IBD, the researchers found; animal protein accounted for most of the risk. Risk was specifically associated with high intake of meat and fish, but not with dairy products or eggs.

While experts have long suspected that diet might play a role in inflammatory bowel disease, Carbonnel and his colleagues note, the only links identified previously were with eating a lot of fats and certain kinds of sugars. Those studies were more prone to error than forward-looking or prospective studies like the current investigation. There have also been several studies linking vitamin D deficiency to IBD.

Another excerpt regarding the potential link to IBD:

Meat could contribute to inflammatory bowel disease risk because digestion of animal protein produces many potentially toxic "end products," such as hydrogen sulfide and ammonia, the researchers note. Also, Carbonnel pointed out, a high-protein diet could alter the mix of bacteria that live in the colon.

The article doesn't comment on it, but I would argue that there is potentially another possible causation here. The reasons suggested are that the high intake of proteins is either generating toxic end-products or causing dysbiosis of the bacterial mix. If that were the case, though, this type of correlation would be present with other types of animal protein sources, including dairy and eggs. But there was not. (As an aside, I would also expect that other food types - e.g. starches, sugars, etc. - also produce these types of toxic end-products as well). I think another alternative cause could be the bacteria present in meat and fish stocks. Contamination from these food sources (e.g. MAP), could also be an explanation. Hopefully that's a third alternative they'll do additional research on. Either way, interesting study.

Amy Proal on Viral and Bacterial Metagenome

Just watched a really interesting talk by Amy Proal about how the interaction and symbiosis (i.e. reinforcing relationship) between bacteria and viruses could lead to autoimmune disorders by interfering with Vitamin-D receptors (VDR's). I've embedded the video below, but here's a link to the post. It looks like she's working on some really interesting research.

The idea is that autoimmune disorders are caused by multiple bacteria and viruses working together to suppress the immune response. This causes a vicious cycle as it supports additional bacterial and viral infection. She suggests that traditional therapies like immunosuppression (which I have mentioned repeatedly seems counterintuitive) may actually prolong and worsen diseases in the long run. They have been working on alternative therapies that are meant to boost the innate immune response. Her blog seems pretty interesting as well, so worth a look as well: http://bacteriality.com/.

Antibiotics in Infancy Potentially Linked to IBD Risk

A small study showed that there might be an increased risk of IBD for infants that are given antibiotics in their 1st year of life. The study compared 36 children with IBD with 360 children that did not have IBD. 60% of the group with IBD had been given antibiotics compared to only 40% for the non-IBD group. The difference was even more pronounced for boys than girls. The study suggests a possible root cause or causative agent in the development of the disease. But again, this was a very small study, so this just suggests areas for additional research.

Pathobionts, Dysbiosis, and IBD

Saw an article about some research at Caltech. Biologists have identified bacteria that lie between the traditional categories of "symbionts" and "pathogens". An example is the Helicobacter hepaticus bacterium. An excerpt:

"The bacteria appear to have struck a deal with their host," Mazmanian says. They keep their own numbers low so they don't overwhelm the immune system, and in return, the immune system leaves them alone. "The bacteria need the secretion system to put the host in 'don't attack' mode." In return, the presence of the bacteria does not induce inflammation, as would be the case with a pathogen that has not evolved a similar "agreement."

"There has to be communication. It could be peaceful—as is the case for symbionts—or it could be an argument—as is the case for pathogens. But when this molecular dialogue breaks down, it's probably harmful to both microbe and man," Mazmanian says.

Disrupt that communication, and the balance gets thrown out of whack. "Inflammation leads to cancer, and this bacterium has been associated with inflammation and colon cancer in animals," he says. Understanding if dysbiosis causes disease in humans could lead to therapies based on restoring the healthy microbial balance in the gut.

Gene Sequencing Yields Picture of Human Gut

Read this article in Business Week about how researchers have identified 160 different species of bacteria in the gut. One interesting finding - people with inflammatory bowel disease (IBD) have 25% fewer bacterial genes than healthy people, indicating that those with IBD have less diversity in their gut.

An excerpt:

"This is so rich. It could help in so many different ways. It could help us understand diseases like inflammatory bowel disease [IBD], Crohn's and ulcerative colitis. It could help us with problems like malnutrition and obesity. It could help us understand many different metabolic problems from liver disease to kidney to heart disease," said Dr. Martin Blaser, chairman of the department of medicine at New York University Langone Medical Center and a professor of microbiology at New York University School of Medicine in New York City. "This is really a landmark study."

Italian researchers discover a possible onset mechanism for Multiple Sclerosis

I just read an interesting article on how bacterium might be a trigger for the onset of Multiple Sclerosis. One theory regarding the cause of MS is that it is an autoimmune triggered. A recent study in mice found that a harmless bacterium made to look like a nerve cell allows T-cells to modify to the point where they can repeatedly break into the central nervous system. Normally, T-cells can not do this. However, in mice where this modified bacterium has been introduced, the T-cells modify in the inflammatory response. These modified T-cells persist well after the bacterium has been killed and continue to cause inflammation in the central nervous system.

I think it's interesting to see how other immune disorders operate as there may be analogs in Crohn's.

Here's an excerpt:

This is the hypothesis that the researchers coming from the Institutes of General Pathology, Microbiology and Anatomy of the Catholic University of Rome have been testing with their two-year long work. To demonstrate the viability of this idea, scientists have fooled the mouse immune system, modifying subtly a bacterium of the common family of mycobacteria (the same family to which also the bacterium causing tuberculosis belongs) to make it look like to myelin, the protein coating nerve cells. This modified mycobacterium is completely innocuous. As all external agents, though, it is capable to trigger the reaction of the T-cells of the immune systems. They intervene to destroy it. Since they are innocuous bacteria, although very common in the environment, and since they induce an immune reaction, they are the ideal bacteria scientists can use to study the environmental factor contributing, together with the genetic factor, to cause multiple sclerosis.

"Normally, T-cells cannot penetrate into the Central Nervous System", adds Rea, "because the hematoencephalic barrier prevents them from doing so. But the bacterium modifies the characteristics of the T-cells and allows them to overcome the barrier. In 15 days the bacterium disappears completely from the body".

Yet these T-cells can now enter into the brain. This way, they begin to attack the myelin of the nerve cells, and here is how the immune disease breaks out.

"We basically demonstrate – explains Rea – that in an animal model it is possible to be infected with something not carrying any disease, and later on develop a purely autoimmune disease".

Pretty interesting.

MAP and its Relationship to Crohn's Disease

I just read a really great paper ("Mycobacterium avium subspecies paratuberculosis and its relationship with Crohn’s disease") that summarized recent literature on the role of Mycobacterium avium paratuberculosis (MAP) in Crohn's Disease. I've had several previous posts regarding MAP's potential role in Crohn's and IBD, but this paper was much more comprehensive and cited studies I had not heard of.

It's really worth reading the whole thing if you're looking for background on this topic. Here were the topics covered:

• Introduction
• MAP - description and background on the MAP bacterium
• Detection of Map in Crohn's Disease - intro of detection techniques
• MAP Culture - different methods of culturing MAP and results of studies related to Crohn's
• Detection of Insertion Sequence IS900 - methods of detecting the IS900 gene sequence (which is unique to MAP)
• Serologic Studies of MAP - looking for antibodies in the blood of Crohn's patients
• MAP and Genetic Susceptibility to Crohn's Disease - interaction between genetic susceptibility (via the NOD2/CARD15 Crohn's gene mutations) and MAP (e.g. overgrowth, etc.)
• Anti-Mycobacterial Antibiotics for Crohn's Disease - review of studies that tried (unsuccessfully) to cause long-term remission of Crohn's through use of antibiotics. MAP is very resilient and the interaction between antibiotics and immunosuppressive agents (which may also impact MAP function) leave room for doubt in the studies.
• Epidemiologic Evidence for MAP as a Cause of CD - lots of epidemiologic evidence for why MAP is likely not the cause of Crohn's, but some support of it being a cause.
• Conclusion (full excerpt below)

For reference, I'm including an excerpt of the conclusion of the paper:

MAP is the causative agent of Johne’s disease. It seems likely that chronic infection with MAP does occasionally occur in humans. MAP is widely present in our food chain and the DNA of this organism can be recovered from the intestine of CD patients. Studies have shown that a high percentage of subjects with CD are infected with MAP, though whether the association of this bacterium and CD is causal or coincidental is not known. Epidemiologists have gathered enough information to indicate an association between MAP and CD. Nonetheless, the role of MAP in CD etiology is not known, and may be determined from consistent results of studies using improved methods of isolation and detection of MAP bacilli and/or MAP-elicited immune responses in the host.

Probiotics May Help Prevent Crohn's Disease

Saw an interesting mention of a research report in a Wall Street Journal article. Here's the excerpt:

Crohn's Disease: Probiotics—live microorganisms that appear to improve gastrointestinal health—may prevent the onset of Crohn's disease, according to a study in the Proceedings of the National Academy of Sciences. The researchers fed young mice, who had been bred to develop a Crohn's-like inflammatory bowel disease, diets that included a high dose of eight probiotic bacteria strains. The disease, ileitis, was entirely prevented in five of those 11 mice, and markedly less severe in five of the remaining six. A lower dose of the bacteria, given to another set of mice, provided little beneficial effect. The researchers suggested, based on necropsies of the mice, that the probiotics guarded against ileitis by stimulating the immune system of the gut lining.

Caveat: It's not known whether probiotics would prevent actual Crohn's disease in humans, or what dose would be required. (Read the Report)

This kind of raises an interesting question around the Specific Carbohyrdrate Diet (which I'm using). How do you train or sensitize your immune system to handle different types of gut bacteria if you're on a diet that is targeted at eliminating many strains of bacteria in the gut? Perhaps you slowly introduce new bacteria (or foods that allow those other bacteria to develop). That way your body can slowly develop (or re-develop) it's sensitivity to these.

Crohn's blamed on lazy immune cells

Saw this article. Not necessarily anything new here.

It still wasn't clear, however, what caused the weakened immunity in the first place. So Segal's team focused on cells called macrophages, the immune system's whistle-blowers. In people with Crohn's disease, they found that macrophages secrete lower levels of cytokines, the chemicals that rally other immune cells to infection sites (Journal of Experimental Medicine, DOI: 10.1084/jem.20091683).

The team concluded that ineffectual rallying of immune cells in people with defective macrophages is what allows intestinal bacteria to run amok in the early stages of an infection, setting in motion the series of events that leads to Crohn's disease.

Johne's Disease (and MAP) in as Many as 70% of U.S. Herds

I saw an article today that shared some startling news about the spread of Johne's Disease. In the last 15 years (from 1996 to 2009), the prevalence of Johne's has increased from only 22% to as much as 70% of U.S. dairy herds. Johne's Disease is caused by the MAP bacteria (see previous blog posts), which many people have found links with to Crohn's Disease.

Here's an excerpt:

"Studies showed that in 1996, Johne's disease was in about 22 percent of the U.S. herds, but because of rapid expansion of herds across the country, producers unknowingly purchased young heifers and older cows which were infected with the disease and thus has raised the prevalence of Johne's to be present in nearly 70 percent of the herds," she said.

Could the recent rise in Crohn's Disease be linked to this rise in the spread of MAP?

Gut Bacteria Linked to Immune Response

Just read this article about a new finding of a bacteria linked to a specific immune response in mice. The bacteria induced higher Th17 response. The finding suggests additional bacteria to look at in the formation of autoimmune disease. Here's an excerpt:

If the effect is present in humans, it suggests a clinical use for the findings, Littman said. "So you can immediately see some practical application of this, if one can mimic the presence of these commensal bacteria to strengthen resistance to pathogenic microbes," he said.

On the other hand, the level of the microbes could also play a role in the development of autoimmune disease, he said. "You have to have the right balance," Littman said.

With hundreds of strains of bacteria, the "right balance" seems very difficult to find.

Wildlife May Cause Livestock Infections of MAP

A study by Scottish researchers found a possible source of Mycobacterium avium paratuberculosis (MAP) infections in livestock -- wild animals. The transmission of infection may be from wild animals to livestock to humans.

Just Say No To Antibacterial Burgers

Read a good Washington Post article about the extreme use of antibiotics in our livestock and food supply. An astonishing 70% of antibiotics used in the US are used for the raising of livestock (primarily in disease prevention rather than treatment). That means were are steadily getting small doses of antibiotics through our food supply our entire lives. But those antibiotics lets us keep our food cheap and accessible for the masses, right? How could we eliminate it? I thought this excerpt was good:

There's also the argument that the pennies we're saving on each burger are being spent in our hospitals. A 2005 study out of Tufts University estimated that antibiotic-resistant infections add $50 billion to the annual cost of American health care. On the other side of the coin, a National Academy of Sciences study found that eliminating non-therapeutic antibiotics from animals would cost only about $5 to $10 per person per year. I'd pay that for a lower risk of super-staphylococcus.

That's very reasonable.

Contamination of food products with Mycobacterium avium paratuberculosis: a systematic review

A study published back in March 2009 conducted a systematic review of previous studies of the potential threats to exposure to the MAP bacteria. Here's the abstract from the research:

Although a causal link between Mycobacterium avium subspecies paratuberculosis (MAP) and Crohn's disease has not been proved, previous studies suggest that the potential routes of human exposure to MAP should be investigated. We conducted a systematic review of literature concerning the likelihood of contamination of food products with MAP and the likely changes in the quantity of MAP in dairy and meat products along their respective production chains. Relevant data were extracted from 65 research papers and synthesized qualitatively. Although estimates of the prevalence of Johne's disease are scarce, particularly for non-dairy herds, the available data suggest that the likelihood of contamination of raw milk with MAP in most studied regions is substantial. The presence of MAP in raw and pasteurized milk has been the subject of several studies which show that pasteurized milk is not always MAP-free and that the effectiveness of pasteurization in inactivating MAP depends on the initial concentration of the agent in raw milk. The most recent studies indicated that beef can be contaminated with MAP via dissemination of the pathogen in the tissues of infected animals. Currently available data suggests that the likelihood of dairy and meat products being contaminated with MAP on retail sale should not be ignored.

One of the tables that summarizes the rates of infection of MAP in livestock was pretty telling. In the US, rates of infection in herds ranged from 2% to 74%. Main take-away is that there is substantial risk to exposure to MAP in the US (and in most other countries - regardless of how developed they are).

Urban Cluster of Crohn's Potentially Explained by MAP

I just came across a new research report published Sept 23, 2009 (Possible Transmission of Mycobacterium avium subspecies paratuberculosis through Potable Water: Lessons from an Urban Cluster of Crohn's Disease) that found a geographical cluster of people that developed Crohn's Disease.

Here's an excerpt that describes the clustering they found (only three people, but still warrants further research):

Despite the documented presence of MAP in tap water and its probable growth on tap water pipes, clusters of Crohn's disease have not previously been described in relationship to tap water pipes supplying patients' homes. This report describes three unrelated individuals who lived on the same block along a street in a midwestern American city and developed Crohn's disease within four years of each other in the 1960's. A common tap water pipe supplied their homes. This is the first reported cluster of Crohn's disease possibly linked to fully treated drinking water, and is consistent with previously reported clusters of Crohn's disease linked to an infectious microorganism in water.

The full article can be found here.

Vitamin D and Why Immunosuppressants May Be Counterproductive

I just saw a post from the Napa County Science News Examiner (thank Google Alerts for that) commenting on an upcoming research paper that will be published in the September issue of "Annals of the New York Academy of Sciences" regarding Vitamin D's role in auto-immune diseases. The post talks about a recent research paper that discusses why Vitamin D may be even more important for women than in men (and could also explain higher rates of auto-immune diseases in women). The paper found that women have a higher number of Vitamin D receptors in their body, in particular in the endometrial cells (lining of the uterus). When Vitamin D binds with these receptors, many genes are expressed that help kick-up the immune system.

Here's an excerpt:

The key to how vitamin D plays its part is to understand what the VDR does. When the correct form of vitamin D (a form known as 1,25-D or calcitriol) binds to VDR, VDR then directly causes the expression of over 900 genes to occur. Two of the genes that are turned on produce proteins that are directly responsible for kicking the immune response into active mode. The reason for VDR in the endometrium is that it provides protection against infection for the developing fetus.

Another key to the puzzle has been the growing evidence that bacteria may play a role in the development of autoimmune disease. If so, why wouldn’t women, who have more VDRs, be better off than men? The problem is that bacteria of various kinds can interfere with VDRs and prevent vitamin D from binding. If vitamin is unable to bind, then the immune response is disrupted. Not only is the immune system affected, but thyroid hormone problems can result too.

There are many clear links that have been established between Crohn's and bacteria. However, this finding could point to why immunosuppressants could be hurting rather than helping the problem. Here's another excerpt:

Although these results do not provide a clear path to treatment, “the potential role of persistent pathogens in autoimmune disease mandates reconsideration of the use of corticosteroids as a first-line treatment for many autoimmune diseases. Corticosteroids effectively reduce the ability of the immune system to respond to pathogens, including persistent microbiota, which is counterproductive to recovery.”

This would suggest that Vitamin D supplementation, particularly in women, is important in recovery. Plus, it really calls into question usage of corticosteroids as a treatment for Crohn's.

With all that said, though, you don't want too much Vitamin D apparently. Another study (from 2004) conducted at UCLA found that people with Crohn's had very high levels of Vitamin D in their blood. The high Vitamin D level (contrary to what you would think) actually causes loss of bone density, which could lead to osteoperosis. Here's the excerpt:

ISLAMABAD: Contrary to expectations, people with the inflammatory bowel condition Crohn’s disease are likely to have excessive levels of the active form of vitamin D in their blood, researchers have found. This is associated with low bone mineral density, they report.

Dr. Maria T. Abreu from the Inflammatory Bowel Disease Center at Cedars-Sinai Medical Center in Los Angeles led the study. She told Reuters Health, "Most doctors think that Crohn’s patients automatically have decreased vitamin D levels and encourage supplementation with vitamin D. We would like to urge doctors to check vitamin D levels before making that recommendation."

As Abreu’s team explains in the medical journal Gut, under certain circumstances too much active vitamin D can actually contribute to the breakdown of bone, leading to osteoporosis. The researchers found "inappropriately high" blood levels of the active form of vitamin D in 42 percent of the 138 people they studied with Crohn’s disease. This was true of only 7 percent of 29 patients with ulcerative colitis, another type of inflammatory bowel disease.

Also, the higher the blood levels of active vitamin D in Crohn’s patients, the lower was their bone density -- regardless of whether they were treated with steroids -- the investigators found. "We believe that high vitamin D levels are most likely a manifestation of the underlying gut inflammation," Abreu said. A high vitamin D level is "an additional risk factor predisposing to development of osteoporosis" for some Crohn’s disease patients, the team concludes. Treatment of the underlying inflammation, "may improve metabolic bone disease."

I suppose it's a mixed verdict then. But at the very least it's worth getting your Vitamin D level checked to see where you are and then only supplement if necessary.