Re: Vitamin D and Common Cold

[Guest guest]

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. "

>