Sunday, November 09, 2008

CELLPHONE ALLERGY- OCT 2008

Do you have a child/ grandchild with facial rash ?
Does she use a cell phone ?


Did you ever think why the hell she gets a rash after using cellphone ?

Did you change her telephone two, three times ? But she gets the rash no matter what telephone she uses.

Did you send her to a dermatologist ?
Did you have her use a lot of steroid creams ?

Until it happens to some one close to you, you will not realize how important this is.

I am sure I am not the only MD with some one in the family with cell phone allergy.

I thought I will share my experience with you.

See attached : this was published this year. Almost none of us know about it.



Take one look at the picture and make the diagnosis, please.

So what do you do ?


After investigations we found Nokia phones do not have any nickel in it as it says in table 1. After spending some money on other phones once we found the answer and switched to Nokia phone the facial skin got back to normal.

Thought this will help some one in my 100 MD net work study group. I hope most people in my group benefit from these educational pieces and each of you is better off after reading these, than before reading these.

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CMAJ • January 1, 2008; 178 (1). doi:10.1503/cmaj.071233.
© 2008 Canadian Medical Association or its licensors
All editorial matter in CMAJ represents the opinions of the authors and not necessarily those of the Canadian Medical Association.
This Article
from JOURNAL OF CANADIAN MEDICAL ASSOCIATION- CMAJ JAN 1, 2008

Teaching Case Report

Cellphone contact dermatitis with nickel allergy

Lionel Bercovitch, MD* and John Luo
*Department of Dermatology, Warren Alpert Medical School of Brown University; Liberal Medical Education, Brown University, Providence, Rhode Island

The case: An 18-year-old male presented with pruritic lichenified dermatitis on his lower abdomen and eczematous dermatitis on his extremities, flanks and face that had lasted several weeks. We suspected his belt buckle had led to allergic contact dermatitis with subsequent autoeczematization. Patch testing using the expanded North American Contact Dermatitis Group allergen battery of 65 allergens1 disclosed an edematous and papulovesicular reaction to nickel at 72 hours. The patient had no other positive reactions, nor did he react to other metals tested, including gold, cobalt, chromium, copper and palladium.

The patient suspected that his recurrent facial dermatitis was related to contact with the headset of his cellphone. We spot tested both the antenna and the headset for free nickel. The test of the antenna, which was plastic coated with metallic paint, was negative. The test of the headset was strongly positive for free nickel. The patient began using a cellphone that contained no nickel, and his facial dermatitis cleared. He decided to resume using his old cellphone to confirm that it had caused his dermatitis and the eruption recurred (Figure 1).

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Figure 1: Patches of eczematous dermatitis on patient's face (left) in areas that came into contact with the headset of his cellphone (right).

We performed spot tests for free nickel on 22 different popular models of cellphones from 8 manufacturers and a Bluetooth headset. We used a commercially available kit (Allertest Ni, Allerderm Laboratories, Phoenix, Arizona), in which we applied a drop of dimethylglyoxime and a drop of ammonium hydroxide solution to a cotton-tipped applicator and rubbed it on the part of the equipment being tested (Figure 2, left). A pink colour on the applicator indicates the presence of free nickel. We performed spot tests on the menu button, the headset, the area bordering the screen and any other metallic areas that could come into contact with the skin (Figure 2, right). The results of the nickel spot testing are summarized in Table 1.


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Figure 2: Spot tests for free nickel were performed by adding a dimethylglyoxime and ammonium hydroxide solution to a cotton-tipped applicator and then rubbing the applicator on areas of cellphones likely to have skin contact. A pink colour on the applicator tip indicates the presence of free nickel (left). In some models, the area around the screen and the menu button tested positive for free nickel (right).

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Table 1.


In the last few years, use of wireless devices for basic communication has risen significantly around the world. In December 2006 the Canadian Residential Telephone Service Survey reported that two-thirds of Canadian households had at least 1 cellphone and that 80% of Alberta households had cellphone service.2 In the same year, a news report in the United States indicated that 53% of American adolescents aged 12–17 owned cellphones, up from 39% in 2005 and 33% in 2002.3 Given the widespread use of cellphones, the presence of metal in the exterior casing of these phones and the high prevalence of nickel sensitization in the population, it is not surprising that cellphones can cause allergic contact dermatitis. Recently, facial contact dermatitis from exposure to hexavalent chromium plating4,5 and to nickel6 in cellphones has been reported.

Although cellphone batteries containing nickel have received much attention as an environmental concern, little has been written about the presence of nickel in cellphone cases. Nearly half of the phones we spot tested contained some free nickel. The menu buttons, decorative logos on the headsets and the metallic frames around the liquid crystal display (LCD) screens were the most common sites.

There appears to be a relation between cellphone models and nickel content. Cellphones intended for rugged use, such as the Motorola i series (i580 and i870), often have rubber coating and no surface nickel. Those with more fashionable designs often have metallic accents and are more likely to contain free nickel in their casings.

Cellphone use should be considered in the differential diagnosis of facial and ear contact dermatitis in individuals who are sensitive to nickel. Manufacturers and industrial designers should be aware of the potential for cellphones to cause allergic reactions related to nickel. Before purchasing cellphones, individuals sensitive to nickel should consider spot testing phones for free nickel. Nickel spot-test kits such as the one we used are readily available for consumer use. These tests are sensitive enough to detect the presence of free nickel at a level as low as 10 ppm — a threshold below which only individuals with the most pronounced sensitivity to nickel would experience a reaction. In addition, we recommend that cellphone retailers allow users with a medically documented allergy to metallic parts of their phones to exchange the equipment without penalty.




Footnotes

This article has been peer reviewed.
Competing interests: None declared.




REFERENCES
Top
REFERENCES

Pratt MD, Belsito DV, DeLeo VA, et al. North American Contact Dermatitis Group patch-test results, 2001–2002 study period. Dermatitis 2004;15:176-83.[Medline]
Residential Telephone Service Survey. Ottawa: Statistics Canada. Available: www.statcan.ca/Daily/English/070504/d070504a.htm. (accessed 2007 Oct 31).
Meyerson B. Schools crack down on cellphones. MSNBC; 2006 Available: www.msnbc.msn.com/id/14912068 (accessed 2007 Oct 31).
Seishima M, Oyama Z, Yamanura M. Cellular phone dermatitis. Arch Dermatol 2002;136:272-3.
Seishima M, Oyama Z, Oda M Cellular phone dermatitis with chromate allergy. Dermatology 2003;207:48-50.[CrossRef][Medline]
Wohrl S, Jandl T, Stingl G, et al. Mobile telephone as new source for nickel dermatitis. Contact Dermatitis 2007;56:113.[Medline]

LIST OF POSTINGS

NEW MEDICINE FOR LIVING LONGER HEALTHIER- 5 oz WINE-HEARD OF RESVERATROL?- NOV 2008

ALLERGY TO CELLPHONE- OCT/NOV 2008

SUNSHINE VITAMIN- JULY 2008

CAN YOU POSTPONE YOUR DATE WITH CANCER AND MI- SEPT 2007

ARE YOU TREATING UNCOMPLICATED UTIS CORRECTLY- FEB 2007

ARE YOU STILL USING ATENOLOL FOR HTN? - OCT 2006

VITAMIN D AND YOU- AUG. 2006

LOVENOX AND BLEEDING- JULY 2006

TREATMENT OF HYPOCALCEMIA- JUNE 2006

TRAZODONE AND SLEEP- MAY 2006

Sunday, July 06, 2008

QUESTIONS AND ANSWERS ON SUNSHINE VITAMIN

In answer to many of the questions you ask let me bring you
uptodate in the form of questions and answers on sunshine vitamin - Vitamin D

1) Q : How much vitamin D you should I recommend to my patients
?

A: vitamin D ( CVS/ Walgreens /store brand/ ) 1000 units
capsules at least 1000 is needed. This is in addition to the vitamin D you make from sun exposure and vitmain D you may consume and vitamin D in multivitamin pills
you may be taking. ( the other day my wife got me a multivitamin bottle which
says that contains 1000 units vitamin D per capsule, that is an exception,
usually it contains - 200 units plus ./ minus. In older people, nursing home
residents you may need to give 2000 units howeve. So the dose is 1000 units or higher dailyin any case

2) Q: Do I need to do vitamin D level before starting vitamin
D suppliment. ?

A: No, vitamin D level test is $ 100 per test in 2008 -
Not necessary. vitamin D capsule costs 2 cents

3) Q: What if my blood level is OK and if I take extra vitamin
D is there any harm ?

A: No harm at all, vitamin D 3- cholecalciferol, even 10,000 units daily for three months has been studied - no harm at all. Hypervitaminosis D without extra calcium can do no harm as far as we know.

4) Q: If I order vitamin D 1000 units for hospital patients is
that enough ?

A : Commonest mistake : If you order like that they get
the wrong vitamin D, in my opinion. When MDs order vitamin D in hospitals (
at least the ones I know of ) they get vitamin D2- Ergocalciferol, which is not
the vitamin D we are talking about. I see a lot of patients with that order,
every time I see that order I change it to vitamin D3 - cholecalciferol-
"Ergo" in much less potent than "chole" unit for unit 1 to 3 . ie Chole is three times stronger than Ergo.
Vitamin D without further qualification means vitamin
D2 in NSMC. So if you really want to give "vitamin D 1000 units"- you need to
write vitamin D3 or cholecalciferol which is a mouthful and you may forget it,
remember # 3, if you can

5) Q: When patients go to pharmacy OTC and get vitamin D what
do they get ?

A : vitamin D3- cholecalciferol-
vitaminD2 - Ergocalciferol- is prescription and not OTC in USA . I do
not know why. In USA Ergo- vitamin D is prescription only.
6) Q: How much vitamin D2 should patients get on
prescription-

A: 10,000 units a day or 50,000 units a week . If patients does not want to pay for vitamin D and wants to get it on prescription you
should order vitamin D2- Ergocalciferol- 50,000 units weekly or q 2 weeks or at least q monthly for maintenance

7) Q : My patient takes calcium with vitamin D- 200 units BID
May be I should double the dose.?

A : May be but giving extra calcium with vitamin D
increases risk of hyperclacemia and kidney stones. All the new data is on
vitamin D alone. No calcium with it, just vitamin D

8) Q: Patients already has cancer is it any good to give
vitamin D now ?

A : Yes it is , if you take vitamin D even after the
diagnosis of cancer you live longer.

In fact in my opinion all cancer patients of course with a
small number of exceptions should be on extra vitamin D. All oncologists on
board please. Exceptions may be patients with hypercalcemia to begin with, or perhaps calcium oxalate kidney stones, may be some other exceptions too

9) Q: Is it true Vitamin D prevents diabetes and improves
cardiac problems ?

A: Yes. Your cadiac muscle as well as pancreatic cells need
vitamin D . You have a better chance of postponing the DX of MI or diabetes
if you take extra vitamin D (see the last reference -for all the
cardiologists, second reference: for diabetes prevention) All
cardiologists on board please.

10) Q: How much vitamin D is in there in cow's milk ?
A: Close to zero, my take on that is: even well fed,
well grazing cows, non vitaminD deficient cows will have only as much vitmain D
in mild as it is in cow's blood/ serum may be say 30/ liter. Vitamin D is not
secreted into the milk.
However all milk in cartons have extra vitamin D added
into it, so if you drink extra milk or dairy products you are probably OK but
even there you should not get into problem if you take 1000 units vitamin D3 in addition.

11) Q :Africans , Indians and others who live in the tropics do they need vitamin D, they get plenty of sun. ?
A : They do , melanin pigment works like a sunscreen and
protect the skin but it unfortunatley also block vitmain D production in the
skin from UV-B rays . So even pigmented people need synthetic vitamin D.
Sunscreen used when you go to the beach also shuts off vitamin D production by
the skin.


Did any of your patients tell you 50,000 units is too much ,
give them less ?. One of the medical students said so last year to me. In fact
now it is in milligrams. 1 mg is 40,000 units. So 50,000 units is 1.25 mgs .
thought you should know









Vitamin D helps colorectal cancer patients: studyThu Jun 19 05:28:41 UTC 2008


By Will Dunham
WASHINGTON (Reuters) - Vitamin D may extend the lives of people with colon and
rectal cancer, according to a study published on Wednesday suggesting another
health benefit from the so-called sunshine vitamin.
Previous research has indicated that people with higher levels of vitamin D may
be less likely to develop colon and rectal cancer, also called colorectal
cancer.
The new study led by Dr. Kimmie Ng of Dana-Farber Cancer Institute in Boston
involved 304 men and women diagnosed with colorectal cancer from 1991 to 2002,
to see if higher levels of vitamin D in the patients affected their survival
chances.
In fact, that turned out to be the case.
The researchers in the study, published in the Journal of Clinical Oncology,
used blood samples to determine vitamin D levels of the patients, and they were
tracked for an average of about 6-1/2 years.
Those in the highest 25 percent of vitamin D levels were about 50 percent less
likely to die during the study from their cancer or any other cause compared to
the patients in the lowest 25 percent of vitamin D levels.
During the study, 123 of the patients died, 96 of them from colorectal cancer.
"It's probably premature to say that we should be recommending this as treatment
for colon cancer, but vitamin D should definitely be studied in the setting of a
clinical trial to see if it has any benefit to treating colorectal cancer," Ng
said in a telephone interview.
Ng said a clinical study is being planned to test vitamin D as part of
colorectal cancer treatment. It would involve patients who already have gotten
their cancer surgically removed, with some getting chemotherapy with vitamin D
after surgery and the others getting just the standard chemotherapy.
"Definitive evidence of a benefit of vitamin D in treating colon cancer would
have to come from a clinical trial," Ng said.
The body makes vitamin D when the skin is exposed to sunlight, thus earning its
nickname the "sunshine vitamin." Milk commonly is fortified with it, and it is
found in fatty fish like salmon. But many people do not get enough of it.
Vitamin D helps the body absorb calcium and is considered important for bone
health. In adults, vitamin D deficiency can lead to osteoporosis, and it can
lead to rickets in children.
A number of recent studies have indicated vitamin D also may offer a variety of
other health benefits, including protecting against types of cancer such as
breast cancer, peripheral artery disease and tuberculosis.
According to the American Cancer Society, about 1.2 million new cases of
colorectal cancer are diagnosed a year, and the disease kills about 630,000
people a year, accounting for 8 percent of all cancer deaths.
In addition, a study published on June 9 in the journal Archives of Internal
Medicine found that men with low levels of vitamin D had an elevated risk for a
heart attack.
The American Medical Association, the largest U.S. doctors group, voted this
week to urge the Food and Drug Administration to re-examine recommendations for
vitamin D intake in light of new scientific findings showing its benefits.

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Chronic Kidney Disease Expert Column



Vitamin D and the Diabetic Patient



Posted 04/28/2008

Daniel W. Coyne, MD
Author Information


Vitamin D


Vitamin D and its active metabolite, 1,25-di(OH)-vitamin D or calcitriol, have
long been recognized as important regulators of serum calcium and bone health.
Production of calcitriol is dependent on adequate vitamin D. Following
constitutive conversion of vitamin D to 25(OH)-vitamin D by the liver, most
circulating calcitriol (hormonal calcitriol) is made by the highly regulated
1alpha-hydroxylase (CYP27B1) present in the kidneys. Numerous other tissues also
possess 1alpha-hydroxylase and appear to produce calcitriol locally at high
concentrations. The receptor for calcitriol, the vitamin D receptor (VDR), is
expressed in virtually all tissues. Thus, this latter form of calcitriol
production constitutes a classic paracrine-autocrine system. Local production of
calcitriol may even be important in the classic calcitriol target tissues of
bone and the parathyroid gland because investigators have demonstrated the
presence of 1alpha-hydroxylase in bone and parathyroid
cells.[1,2]

Activation of the VDR by hormonal or locally produced calcitriol generally
promotes differentiation of tissues and inhibits proliferation. Some regulatory
actions of VDR are even independent of calcitriol. Scientists have investigated
the relationship of vitamin D deficiency to cancer, cardiovascular disease,
neuromuscular function, and autoimmune diseases.

A large proportion of the population has low vitamin D levels, which are
generally defined as a serum level of 25(OH)-vitamin D less than 20 or 30 ng/mL.
Although sunlight stimulates skin production of vitamin D, many in modern
society are dependent on ingestion of vitamin D in milk or supplements to
maintain normal vitamin D levels, especially during the winter months. Vitamin D
deficiency is particularly common in hospitalized individuals, those with
chronic diseases, and African Americans. Over the past decade, the relationship
of vitamin D deficiency to the risk of developing diabetes mellitus (DM) and the
risk for diabetic complications has been of great interest to scientists.

Dialysis patients have an enormous burden of vitamin D abnormalities, and this
burden also falls on diabetics, who constitute almost 50% of new dialysis
patients. Due to the loss of renal function, dialysis patients are unable to
produce adequate calcitriol. Consequently, these patients have very low hormonal
calcitriol levels. Without supplementation with calcitriol or a calcitriol
analog, they have profoundly diminished activation of the VDR in tissues
throughout the body. Wolf and colleagues examined incident hemodialysis
patients, and found that diabetics were more likely to be severely
25(OH)-vitamin D-deficient (< 10 ng/mL) than nondiabetics (22% vs 17%).[3] Lower
25(OH)-vitamin D levels and lower calcitriol levels strongly correlated with an
increased risk for death during the first 90 days in patients not given
injectable calcitriol or an analog.[3]


Vitamin D and the Risk of Developing DM



Several observational studies have suggested that either low vitamin D levels or
low vitamin D intake may predispose to the development of both type 1 and type 2
DM. The Nurses' Health Study found that vitamin D intake above 800 IU/day and
more than 1200 mg of calcium per day were associated with a 33% reduction in the
risk of developing type 2 DM compared with an intake of < 600 mg of calcium and
< 400 IU of vitamin D.[4] A meta-analysis of largely observational studies
concluded that there was "a relatively consistent association between low
vitamin D status, calcium or dairy intake, and prevalent type 2 DM or metabolic
syndrome.[5]" Evidence from interventional trials suggests that combined vitamin
D and calcium supplementation may help prevent type 2 DM in only some
populations at high risk for diabetes.[5]

Low vitamin D levels, low sun exposure, and low intake of vitamin D have each
been associated with an increased risk for the development of type 1 DM. In
animal models, induction of type 1 DM by streptozocin induces a marked fall in
calcitriol levels, whereas 25(OH)-vitamin D levels remain normal. Treatment with
insulin restores calcitriol levels to normal. Calcitriol has an immunomodulatory
effect. In a nonobese diabetic mouse model, administration of calcitriol or
1alpha-(OH)-vitamin D (a precursor of calcitriol) has been shown to
significantly reduce the likelihood of development of type 1 DM.[6]


Low Vitamin D levels and the Presence of DM or Glucose Intolerance


A report from Martins and colleagues on data from over 15,000 adults in the
Third National Health and Nutrition Examination Survey is perhaps the best
recent evidence on vitamin D and the general population.[7] The 25(OH)-vitamin D
levels were lower in diabetics, women, the elderly, and racial minorities,
groups that are at increased risk of having chronic kidney disease (CKD).[7]
Scragg and colleagues reported in 1995 the association of low 25(OH)-vitamin D
levels with the presence of DM or glucose intolerance.[8] Consistent with these
findings, low vitamin D levels are associated with obesity, as assessed by body
mass index or waist circumference, and weakly with elevated glycated hemoglobin
(A1C) levels.[9]


Vitamin D and Diabetic Complications


Wang and colleagues studied 1739 Framingham offspring participants without prior
cardiovascular disease, and found that low 25(OH)-vitamin D levels (< 15 ng/mL)
were significantly associated with an increased incidence of a first
cardiovascular event during the mean 5.4 years of follow-up.[10] Among diabetics
in this cohort, low 25(OH)-vitamin D levels were significantly more common than
nondiabetics (11% vs 7%), but the association of low vitamin D levels to first
cardiovascular event remained after adjustment for diabetics and other known
risk factors.

Low 25(OH)-vitamin D levels have been shown to correlate with the presence of
cardiovascular disease in diabetics.[11] Similarly, hypovitaminosis D has been
independently associated with carotid artery intimal-medial thickening, a
harbinger of cerebrovascular and cardiovascular events.[12] Suzuki and
colleagues found that microvascular complications were more frequent when
vitamin D levels were low, despite similar duration of disease and other
clinical characteristics compared with control patients without
complications.[13]

These data suggest that diabetic patients are at greater risk of being vitamin
D-deficient and harmed by this deficiency. The presence of CKD will compromise
the production of calcitriol, and potentially further contribute to inadequate
vitamin D signaling. Consistent with this, among 463 diabetics with CKD, low
vitamin D levels were independently associated with the presence of
cardiovascular disease.[14]


VDR Activators and Improved Outcomes in Patients on Dialysis and CKD



Vitamin D receptor activators (VDRAs) are calcitriol or related analogs capable
of binding to the VDR and activating it. Use of a VDRA is common in patients
with CKD and dialysis for the treatment of secondary hyperparathyroidism. In
nephrology, the first suggestion that use of a VDRA may be related to survival
was the sentinel study in 2003 by Teng and colleagues reporting an association
of improved survival in hemodialysis patients given paricalcitol, a VDRA and
analog of calcitriol, compared with native calcitriol.[15] Critics of that study
suggested that either agent may be worse than no VDRA therapy. These critics
noted that both paricalcitol and calcitriol increase serum calcium and
phosphorus, which are associated with lower survival in some observational
studies of the dialysis population.

A subsequent observational study by Teng and colleagues found that use of either
paricalcitol or calcitriol in dialysis patients was associated with improved
survival compared with no VDRA therapy.[16] The strength and consistency of the
association of VDRA use with improved survival has increased over the succeeding
years, with diverse studies of CKD and dialysis populations confirming the
associations.[17-19]


Diabetes, Vitamin D, and Future Research

Most of the data outlined above show associations of vitamin D, calcitriol, or
calcitriol analogs with cardiovascular burden and survival in diabetic patients.
The potential mechanisms by which treatment of vitamin D and calcitriol
deficiency can lead to improved survival and lower cardiovascular events reflect
the diverse actions of vitamin D in the body. Studies are ongoing to determine
through randomized trials whether use of vitamin D can lower inflammation,
moderate cardiac and vascular disease, and lower proteinuria. Significant work
is still required to determine whether this decade of associating vitamin D
deficiency with diabetics and their complications will be followed by results
showing that treatment can mitigate those complications, and even lower the
prevalence of diabetes.

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Lack Of Vitamin D May Increase Heart Disease Risk



ScienceDaily (Jan. 8, 2008) - The same vitamin D deficiency that can result in
weak bones now has been associated with an increased risk of cardiovascular
disease, Framingham Heart Study researchers report in Circulation: Journal of
the American Heart Association.

*
*

"Vitamin D deficiency is associated with increased cardiovascular risk, above
and beyond established cardiovascular risk factors," said Thomas J. Wang, M.D.,
assistant professor of medicine at Harvard Medical School in Boston, Mass. "The
higher risk associated with vitamin D deficiency was particularly evident among
individuals with high blood pressure."

In a study of 1,739 offspring from Framingham Heart Study participants (average
age 59, all Caucasian), researchers found that those with blood levels of
vitamin D below15 nanograms per milliliter (ng/mL) had twice the risk of a
cardiovascular event such as a heart attack, heart failure or stroke in the next
five years compared to those with higher levels of vitamin D.


When researchers adjusted for traditional cardiovascular risk factors such as
high cholesterol, diabetes and high blood pressure, the risk remained
significant with a 62 percent higher risk of a cardiovascular event in
participants with low levels of vitamin D compared to those with higher levels.

Researchers observed the highest rate of cardiovascular disease events in subset
analyses dividing 688 participants according to high blood pressure status.
After researchers adjusted for conventional cardiovascular risk factors,
participants with hypertension and a vitamin D deficiency had about 2 times the
risk of having a cardiovascular disease event in five years.

Researchers also found an increase in cardiovascular risk with each level of
vitamin D deficiency.

"We found that people with low vitamin D levels had a higher rate of
cardiovascular events over the five-year follow-up period," Wang said. "These
results are intriguing and suggestive but need to be followed up with further
study."

Study participants had no prior cardiovascular disease and were tested for
vitamin D status and then followed for an average of 5.4 years.

The participants attended the offspring examinations between 1996 and 2001.
Researchers obtained medical history, physical examinations and laboratory
assessments of vascular risk factors. They also obtained medical records related
to cardiovascular disease.

Overall, 28 percent of individuals had levels of vitamin D below15 ng/mL and 9
percent had levels below10 ng/mL. Although levels above 30 ng/mL are considered
optimal for bone metabolism, only 10 percent of the study sample had levels in
this range, researchers said.

During follow-up:

* 120 participants developed a first cardiovascular event including fatal
and nonfatal coronary heart disease;
* 28 participants had fatal or nonfatal cerebrovascular events such as
nonhemorrhagic stroke;
* 19 participants were diagnosed with heart failure; and
* 8 had occurrences of claudication, fatigue in the legs during activity.

"Low levels of vitamin D are highly prevalent in the United States, especially
in areas without much sunshine," Wang said. "Twenty to 30 percent of the
population in many areas has moderate to severe vitamin D deficiency."

Most of this is attributed to lack of sun exposure, pigmented skin that prevents
penetration of the sun's rays and inadequate dietary intake of vitamin D
enriched foods, researchers said.

"A growing body of evidence suggests that low levels of vitamin D may adversely
affect the cardiovascular system," Wang said. "Vitamin D receptors have a broad
tissue distribution that includes vascular smooth muscle and endothelium, the
inner lining of the body's vessels. Our data raise the possibility that treating
vitamin D deficiency, via supplementation or lifestyle measures, could reduce
cardiovascular risk.

"What hasn't been proven yet is that vitamin D deficiency actually causes
increased risk of cardiovascular disease. This would require a large randomized
trial to show whether correcting the vitamin D deficiency would result in a
reduction in cardiovascular risk."

Therfore, Wang doesn't recommend physicians check for vitamin D deficiency or
that those with a known vitamin D deficiency be treated to prevent heart disease
at this time.

During the past decade, researchers have studied several other vitamins that
initially showed promise in reducing heart disease. But the vitamins didn't
reduce heart disease in subsequent large randomized trials.

"On the flip side, just because other vitamins haven't succeeded doesn't
preclude the possibility of finding vitamins that might prevent cardiovascular
disease," Wang said. "This is always an area of great interest. Vitamins are
easy to administer and in general have few toxic effects."

The American Heart Association recommends that healthy people get adequate
nutrients by eating a variety of foods in moderation, rather than by taking
supplements. Food sources of vitamin D include milk, salmon, mackerel, sardines,
cod liver oil and some fortified cereals. Vitamin or mineral supplements aren't
a substitute for a balanced, nutritious diet that limits excess calories,
saturated fat, trans fat, sodium and dietary cholesterol. This dietary approach
has been shown to reduce coronary heart disease risk in healthy people and those
with coronary disease.

Co-authors are: Michael J. Pencina, Ph.D.; Sarah L. Booth, Ph.D.; Paul F.
Jacques, D.Sc.; Erik Ingelsson, M.D., Ph.D.; Katherine Lanier, B.S.; Emelia J.
Benjamin, M.D.; Ralph B. D'Agostino, Ph.D.; Myles Wolf, M.D.; and Ramachandran
S. Vasan, M.D. The National Institute of Health, U.S. Department of Agriculture
and American Heart Association funded the study.