Guest guest Posted February 12, 2007 Report Share Posted February 12, 2007 Hi , Thanks a bunch for sending this article. I found it very interesting. I haven't checked the links that it references yet but I was wondering if you wouldn't mind telling us how much Vit D you take daily? The article didn't seem to mention a specific amount that is recommended? Tracey > > Hi Folks - a while back I mentioned this article, about Vitamin D possibly > protecting against the common cold (and being generally good at helping us > ward off infection). Someone wrote back that I posted the wrong URL for the > article, so I'm attaching the whole thing here. Hope you find it > interesting, as I did. > > Best, > > R > > ========== > > The Antibiotic Vitamin > > Deficiency in vitamin D may predispose people to infection > Janet Raloff > > In April 2005, a virulent strain of influenza hit a maximum-security > forensic psychiatric hospital for men that's midway between San Francisco > and Los Angeles. J. Cannell, a psychiatrist there, observed with > increasing curiosity as one infected ward after another was quarantined to > limit the outbreak. Although 10 percent of the facility's 1,200 patients > ultimately developed the flu's fever and debilitating muscle aches, none did > in the ward that he supervised. > > > WINTER WOES. Cold-weather wear and the sun's angle in the winter sky limit > how much ultraviolet light reaches the skin. This can add up to a deficiency > in production of vitamin D, which might explain why respiratory infections > are common and severe in winter. > " First, the ward below mine was quarantined, then the wards on my right, > left, and across the hall, " Cannell recalls. However, although the 32 men on > his ward at Atascadero (Calif.) State Hospital had mingled with patients > from infected wards before their quarantine, none developed the illness. > Cannell's ward was the only heavily exposed ward left unaffected. Was it by > mere chance, Cannell wondered, that his patients dodged the sickness? > A few months later, Cannell ran across a possible answer in the scientific > literature. In the July 2005 FASEB Journal, F. Gombart of the > University of California, Los Angeles (UCLA) and his colleagues reported > that vitamin D boosts production in white blood cells of one of the > antimicrobial compounds that defends the body against germs. > Immediately, Cannell says, the proverbial lightbulb went on in his head: > Maybe the high doses of vitamin D that he had been prescribing to virtually > all the men on his ward had boosted their natural arsenal of the > antimicrobial, called cathelicidin, and protected them from flu. Cannell had > been administering the vitamin D because his patients, like many other > people in the industrial world, had shown a deficiency. > The FASEB Journal article also triggered Cannell's recollection that > children with rickets, a hallmark of vitamin D deficiency, tend to > experience more infections than do kids without the bone disease. He shared > his flu data with some well-known vitamin D researchers, and they urged him > to investigate further. > On the basis of more than 100 articles that he collected, Cannell and seven > other researchers now propose that vitamin D deficiency may underlie a > vulnerability to infections by the microbes that cathelicidin targets. These > include bacteria, viruses, and fungi, the group notes in a report available > online <http://dx.doi.org/10.1017/S0950268806007175> for the December > Epidemiology and Infection. > This is only a hypothesis, " but a very credible one " that deserves testing, > says immunologist Zasloff of town University in Washington, > D.C. > Behind the hypothesis are recent studies that link vitamin D intake to > revved-up cathelicidin production. These investigations point to an > infection-fighting role for vitamin D, which is produced in skin exposed to > sunlight but is present in few foods. > A study published earlier this year that investigated the relationship > between vitamin D and susceptibility to tuberculosis also bolsters the idea > proposed by Cannell's team. Scientists have already planned a handful of > clinical trials to evaluate the antimicrobial benefits of vitamin D > supplementation. > Zasloff argues that if studies support the hypothesis, " we can imagine one > day treating infections not by giving somebody a drug, but by giving them > safe and simple substances‹like a vitamin. " > Innate protection > Legions of germs come into contact with our bodies every day. Each microbe > seeks a host in which it can multiply. Most would-be invaders, however, > don't succeed; if not barred entry outright, they're destroyed by cellular > recruits called up to participate in local immune militias. > Scientists hadn't been sure what serves as the call to arms for these immune > cells and what triggers the production of their antibiotic arsenal, which > includes several chemical weapons. > Over the past 5 years, a spate of studies began to shed light on the rollout > of one of those munitions‹cathelicidin. Dermatologist and immunologist > L. Gallo of the University of California, San Diego, a coauthor of > many of these studies, explains that cathelicidin " targets the bad guys. " It > kills invaders by punching holes in the external membrane of a microbe, > permitting its innards to leak out. > Molecular geneticist H. White of McGill University in Montreal and his > colleagues were the first to observe that cathelicidin production is ramped > up by vitamin D‹or, more specifically, by the hormone 1,25-D, the vitamin's > active form (SN: 10/9/04, p. 232: > http://www.sciencenews.org/articles/20041009/bob8.asp > <http://www.sciencenews.org/articles/20041009/bob8.asp> ). Through a cascade > of events, vitamin D transforms into a compound, called a prehormone, that > circulates in blood and then is converted locally, as needed, into 1,25-D. > In the nucleus of cells, 1,25-D binds to short sequences of DNA. Known as > response elements, these sequences switch on the activity of adjacent genes. > " We wanted to find out what genes were next to the vitamin D response > elements, " White recalls. > Two of these response elements proved to be neighbors of genes that make > antimicrobial peptides, cathelicidin and beta-defensin 2, the researchers > reported in 2004. When the researchers administered 1,25-D to a variety of > cells, production of beta-defensin 2 increased " modestly, " White told > Science News. In contrast, he says, the gene for making cathelicidin " went > boom! Its induction was very, very strong. " > Almost a year later, while hunting for triggers for cathelicidin production, > Gombart confirmed the McGill finding. His group had been administering > various natural signaling agents to white blood cells, which the immune > system sends out to vanquish germs. > In these cells, " nothing turned on the cathelicidin gene to any degree > except vitamin D. And it really turned that gene on‹just cranked it up, " > Gombart says. " I was completely surprised. " > Independently, dermatologist Mona Ståhle of the Karolinska Institute in > Stockholm reached a similar conclusion when she realized that both vitamin D > and several antimicrobials, including cathelicidin, are produced in the > skin. She says, " It just came to me‹an intuitive thought‹that maybe the sun, > through vitamin D production, might help regulate the skin's antimicrobial > response. " > So, her team administered an ointment containing a drug mimic of 1,25-D to > the skin of four healthy people. The salve hit " the jackpot, right away, " > Ståhle says. In the May 2005 Journal of Investigative Dermatology, her team > reported that where the ointment had been applied, cathelicidin-gene > activity skyrocketed as much as 100-fold. The team also found evidence of a > localized increase in the concentration of cathelicidin. > Tackling TB and more > Those studies, though suggestive, didn't reveal whether vitamin D directly > reduced infection risk in people. Together with Gallo, microbial > immunologist Modlin of UCLA and his colleagues moved closer to that > goal: They evaluated the vitamin's role in fending off the tuberculosis (TB) > germ Mycobacterium tuberculosis. > This group, working independently of Gombart's team, had been focusing on > macrophages, a type of white blood cell deployed by the immune system to > gobble up and destroy germs. These defense cells have features, called > toll-like receptors, that identify biochemical patterns characteristic of > invading microbes. If the receptors sense an invader, they can trigger > cathelicidin production. > Modlin's team showed that before making that antibiotic, those cells briefly > boosted their production of vitamin D receptors and of an enzyme that > converts the vitamin D prehormone into 1,25-D. However, the data suggested > that significant concentrations of 1,25-D would develop only in the presence > of the TB bacteria. This indicated that the microbe, and perhaps other > germs, must be present for the enzyme to maximize its production of 1,25-D, > Modlin says. > His group then tested whether people's blood concentrations of the > prehormone are high enough to drive the production of germ-killing > concentrations of cathelicidin. Black people, because of the sun- filtering > effect of dark pigments in their skin, are far more likely than whites to be > vitamin D deficient (SN: 10/16/04, p. 248: > http://www.sciencenews.org/articles/20041016/bob9.asp > <http://www.sciencenews.org/articles/20041016/bob9.asp> ). Furthermore, > blacks tend to be more susceptible to TB than whites and to develop a more > severe illness when infected. > The team collected blood serum from white people and from blacks. When the > researchers added TB bacteria, macrophages in the serum from black > participants produced 63 percent less cathelicidin‹and were less likely to > kill the germs‹than were macrophages incubated in serum from whites. > The scientists then added vitamin D to the serum from blacks until > concentrations of the prehormone matched those in the serum from whites. > This boosted the macrophages' cathelicidin production and rates of > TB-microbe killing to those seen when such cells were incubated in serum > from whites. Modlin's group reported its findings in the March 24 Science. > The new data may explain the difference between blacks and whites in TB > susceptibility. Modlin says, " We showed that serum from African American > individuals did not support the production of the antibiotic by immune > cells, until the serum received supplemental vitamin D. " > " We're now planning to do a clinical trial and treat African Americans who > are deficient with vitamin D to correct their serum levels [of the > prehormone] and see if this will change their antimicrobial response, " > Modlin says. > Gallo is also planning a new trial. His group will compare the effectiveness > of supplemental vitamin D in elevating cathelicidin concentrations when > administered as oral supplements or as a skin treatment. > The team expects to see the biggest benefit in skin wounds. However, Gallo > predicts that even healthy skin will exhibit somewhat elevated antimicrobial > concentrations, signaling an improved resistance to infection. > Sun exposure‹in moderation‹might also prove therapeutic, Ståhle's team > suggested in the November 2005 Journal of Investigative Dermatology. The > scientists showed that in eight fair-skinned people, a single dose of > ultraviolet-B radiation‹just enough to evoke some skin reddening the next > day‹activated the vitamin D receptor and the cathelicidin gene in the > exposed skin. > Ståhle is now beginning a trial of people with skin infections. A drug > analog of 1,25-D will be applied to see whether it speeds wound healing. > > Flu too? > Many other findings also suggested to Cannell's team that flu vulnerability > might be tempered by adequate vitamin D intake. The researchers have > marshaled data, gleaned from 120 or so reports over the past 70 years, > suggesting a link between vitamin D and resistance to infections. > For instance, the researchers point to studies showing that in winter, > colds, flu, and other respiratory diseases are more common and more likely > to be deadly than they are in summer. During winter, ultraviolet- light > exposure tends to be low because people spend more time indoors and the > atmosphere filters out more of the sun's rays, especially at mid and high > latitudes. > Cannell's group cites a 1997 study showing that the rate of pneumonia in > Ethiopian children with rickets, and therefore a likely vitamin D > deficiency, was 13 times as high as in children without that disease. The > researchers also point to five studies since the 1930s that have linked > reduced risks of infectious disease to dietary supplementation with cod > liver oil, a rich source of vitamin D. > Although the arguments in the paper by Cannell's group " are provocative, " > White says, " I find them believable. " > So does Gallo. " There are many microbes out there that rarely-to- never cause > disease in immunocompetent individuals. It's not because the microbes don't > choose to infect us, " he notes. " It's because the body's immune defense > against the microbes is sufficient to control their proliferation. " > It's possible, he says, that a shortfall in vitamin D might seriously > compromise that defense. > Gombart's group is developing rodents in which vitamin D modulates > cathelicidin. > Until such lab animals are available, vitamin D's impact‹even on flu > risk‹ " should be explored in clinical trials, " Zasloff says, because the > treatment poses little risk to people. > Moreover, he argues, the payoff from any positive finding " would be amazing. > Imagine being able to block the spread of epidemic flu with appropriate > doses of this vitamin. " > Quote Link to comment Share on other sites More sharing options...
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