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Post by Yvonne » Mon 11 Feb 2008 20:09

Ugeskr Laeger. 2007 Oct 22;169(43):3655-60. Links
Comment in:
Ugeskr Laeger. 2007 Dec 10;169(50):4374; author reply 4374.

Vitamin D insufficiency--possible etiologic factor of autoimmune diseases
[Article in Danish]

Jørgensen SP, Bartels LE, Agnholt J, Glerup H, Nielsen SL, Hvas CL, Dahlerup JF.
Arhus Universitetshospital, Arhus Sygehus, Medicinsk Hepato-gastroenterologisk Afdeling V.

The primary source of vitamin D in humans is sun exposure to the skin. The incidence of certain autoimmune diseases correlates positively with latitude. As vitamin D production increases with sun exposure, vitamin D insufficiency is hypothesised to influence the development of autoimmune diseases. In experimental animal and cellular studies in vitro 1.25-(OH)2-vitamin D reduces inflammation. This article discusses the role of vitamin D in inflammatory bowel disease, type 1 diabetes mellitus, multiple sclerosis, and rheumatoid arthritis.

PMID: 17967265

Arq Bras Endocrinol Metabol. 2006 Feb;50(1):25-37. Epub 2006 Apr 17. Links

Vitamin D deficiency in adults: to better understand a new presentation of an old disease
[Article in Portuguese]

Premaor MO, Furlanetto TW.
Departamento de Medicina Interna, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS.

Vitamin D is synthesized in skin through a reaction mediated by sunlight, and it is metabolized to 25-hydroxyvitamin D, in liver, and in 1,25-dihydroxyvitamin D, in kidney. This last reaction has a tight feedback mechanism. 1,25-dihydroxyvitamin D is the active hormone, and its actions are mediated mainly by nuclear receptors. Its major functions are in calcium metabolism and bone mass maintenance. Hypovitaminosis D, as a disease in adult people, manifests itself with hypocalcemia and secondary hyperparathyroidism with subsequent loss of trabecular bone, thinning of cortical bone, and, eventually, a higher risk of fractures. Hypovitaminosis D is a very common condition in Europe, Africa, North America and some South American countries, such as Chile and Argentina. Measurement of serum total 25-hydroxyvitamin D concentration is the gold standard to diagnose vitamin D deficiency. Serum concentrations below 50 nmol/L are associated with an increase in parathyroid hormone concentration, and bone loss. Risk factors for vitamin D deficiency, like poor sunlight exposition, aging skin and factors that interfere with normal vitamin D metabolism, are well established. Oral vitamin D supplementation, an easy and inexpensive treatment, is needed to treat this illness.

PMID: 16628272

Arch Intern Med. 2007 Sep 10;167(16):1730-7. Links
Comment in:
Arch Intern Med. 2007 Sep 10;167(16):1709-10.

Vitamin D supplementation and total mortality: a meta-analysis of randomized controlled trials.
Autier P, Gandini S.
International Agency for Research on Cancer, 150 cours Albert Thomas, F-69372 Lyon, France.

BACKGROUND: Ecological and observational studies suggest that low vitamin D status could be associated with higher mortality from life-threatening conditions including cancer, cardiovascular disease, and diabetes mellitus that account for 60% to 70% of total mortality in high-income countries. We examined the risk of dying from any cause in subjects who participated in randomized trials testing the impact of vitamin D supplementation (ergocalciferol [vitamin D(2)] or cholecalciferol [vitamin D(3)]) on any health condition. METHODS: The literature up to November 2006 was searched without language restriction using the following databases: PubMed, ISI Web of Science (Science Citation Index Expanded), EMBASE, and the Cochrane Library. RESULTS: We identified 18 independent randomized controlled trials, including 57 311 participants. A total of 4777 deaths from any cause occurred during a trial size-adjusted mean of 5.7 years. Daily doses of vitamin D supplements varied from 300 to 2000 IU. The trial size-adjusted mean daily vitamin D dose was 528 IU. In 9 trials, there was a 1.4- to 5.2-fold difference in serum 25-hydroxyvitamin D between the intervention and control groups. The summary relative risk for mortality from any cause was 0.93 (95% confidence interval, 0.87-0.99). There was neither indication for heterogeneity nor indication for publication biases. The summary relative risk did not change according to the addition of calcium supplements in the intervention. CONCLUSIONS: Intake of ordinary doses of vitamin D supplements seems to be associated with decreases in total mortality rates. The relationship between baseline vitamin D status, dose of vitamin D supplements, and total mortality rates remains to be investigated. Population-based, placebo-controlled randomized trials with total mortality as the main end point should be organized for confirming these findings.

PMID: 17846391

Current Understanding of the Molecular Actions of Vitamin D : ... =relevance
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Re: Vitamins

Post by Yvonne » Mon 11 Feb 2008 20:13

Multivitamin/Mineral Supplements and Prevention of Chronic Disease

Structured Abstract
Objective. To review and synthesize published literature on the efficacy of multivitamin/mineral
supplements and certain single nutrient supplements in the primary prevention of chronic disease
in the general adult population, and on the safety of multivitamin/mineral supplements and
certain single nutrient supplements, likely to be included in multivitamin/mineral supplements, in
the general population of adults and children.
Data Sources. All articles published through February 28, 2006, on MEDLINE,® EMBASE,®
and the Cochrane databases.
Review Methods. Each article underwent double reviews on title, abstract, and inclusion
eligibility. Two reviewers performed data abstraction and quality assessment. Differences in
opinion were resolved through consensus adjudication.
Results. Few trials have addressed the efficacy of multivitamin/mineral supplement use in
chronic disease prevention in the general population of the United States. One trial on poorly
nourished Chinese showed supplementation with combined β-carotene, vitamin E and selenium
reduced gastric cancer incidence and mortality, and overall cancer mortality. In a French trial,
combined vitamin C, vitamin E, β-carotene, selenium, and zinc reduced cancer risk in men but
not in women. No cardiovascular benefit was evident in both trials. Multivitamin/mineral
supplement use had no benefit for preventing cataract. Zinc/antioxidants had benefits for
preventing advanced age-related macular degeneration in persons at high risk for the disease.
With few exceptions, neither β-carotene nor vitamin E had benefits for preventing cancer,
cardiovascular disease, cataract, and age-related macular degeneration. β-carotene
supplementation increased lung cancer risk in smokers and persons exposed to asbestos. Folic
acid alone or combined with vitamin B12 and/or vitamin B6 had no significant effects on
cognitive function. Selenium may confer benefit for cancer prevention but not cardiovascular
disease prevention. Calcium may prevent bone mineral density loss in postmenopausal women,
and may reduce vertebral fractures, but not non-vertebral fractures. The evidence suggests dosedependent
benefits of vitamin D with/without calcium for retaining bone mineral density and
preventing hip fracture, non-vertebral fracture and falls.
We found no consistent pattern of increased adverse effects of multivitamin/mineral
supplements except for skin yellowing by β-carotene.


Multivitamin/mineral supplement use may prevent cancer in individuals with poor
or suboptimal nutritional status. The heterogeneity in the study populations limits generalization
to United States population. Multivitamin/mineral supplements conferred no benefit in
preventing cardiovascular disease or cataract, and may prevent advanced age-related macular
degeneration only in high-risk individuals. The overall quality and quantity of the literature on
the safety of multivitamin/mineral supplements is limited. ... ltivit.pdf
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Re: Vitamins

Post by Yvonne » Mon 11 Feb 2008 20:16

Meta-Analysis: High-Dosage Vitamin E Supplementation May IncreaseAll-Cause Mortality

Edgar R. Miller III, MD, PhD; Roberto Pastor-

Background: Experimental models and observational studies
suggest that vitamin E supplementation may prevent cardiovascular
disease and cancer. However, several trials of high-dosage
vitamin E supplementation showed non–statistically significant increases
in total mortality.
Purpose: To perform a meta-analysis of the dose–response relationship
between vitamin E supplementation and total mortality
by using data from randomized, controlled trials.
Patients: 135 967 participants in 19 clinical trials. Of these trials,
9 tested vitamin E alone and 10 tested vitamin E combined with
other vitamins or minerals. The dosages of vitamin E ranged from
16.5 to 2000 IU/d (median, 400 IU/d).
Data Sources: PubMed search from 1966 through August 2004,
complemented by a search of the Cochrane Clinical Trials Database
and review of citations of published reviews and metaanalyses.
No language restrictions were applied.
Data Extraction: 3 investigators independently abstracted
study reports. The investigators of the original publications were
contacted if required information was not available.

Data Synthesis: 9 of 11 trials testing high-dosage vitamin E
(>400 IU/d) showed increased risk (risk difference > 0) for allcause
mortality in comparisons of vitamin E versus control. The
pooled all-cause mortality risk difference in high-dosage vitamin E
trials was 39 per 10 000 persons (95% CI, 3 to 74 per 10 000
persons; P 0.035). For low-dosage vitamin E trials, the risk
difference was 16 per 10 000 persons (CI, 41 to 10 per 10 000
persons; P > 0.2). A dose–response analysis showed a statistically
significant relationship between vitamin E dosage and all-cause
mortality, with increased risk of dosages greater than 150 IU/d.
Limitations: High-dosage (>400 IU/d) trials were often small
and were performed in patients with chronic diseases. The generalizability
of the findings to healthy adults is uncertain. Precise
estimation of the threshold at which risk increases is difficult.

High-dosage (>400 IU/d) vitamin E supplements
may increase all-cause mortality and should be avoided.
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Re: Vitamins

Post by Yvonne » Fri 22 Feb 2008 19:39

1: Photodermatol Photoimmunol Photomed. 2007 Oct;23(5):179-85. Links

Treatment of vitamin D deficiency with UV light in patients with malabsorption syndromes: a case series.

Chandra P, Wolfenden LL, Ziegler TR, Tian J, Luo M, Stecenko AA, Chen TC, Holick MF, Tangpricha V.
Graduate Program in Nutrition and Health Sciences and Department of Medicine, Emory University School of Medicine, Atlanta, GA 30307, USA.

BACKGROUND: Cystic fibrosis (CF) and short bowel syndrome (SBS) patients are unable to absorb vitamin D from the diet and thus are frequently found to be severely vitamin D deficient. We evaluated whether a commercial portable ultraviolet (UV) indoor tanning lamp that has a spectral output that mimics natural sunlight could raise circulating 25-hydroxyvitamin D [25(OH)D] levels in subjects with CF and SBS. METHODS: In initial pilot studies, two SBS subjects came to the outpatient clinic twice weekly for 8 weeks for UV light sessions of 6 min each. In a follow-up study, five CF subjects exposed their lower backs in a seated position to the sunlamp at a distance of 14 cm for 5-10 min depending on the skin type five times a week for 8 weeks. Blood samples for 25(OH)D and parathyroid hormone (PTH) measurements were performed at baseline and at the end of the study. RESULTS: In our study, with two SBS subjects, the indoor lamp increased or maintained circulating 25(OH)D levels during the winter months. We increased the UV lamp frequency and found an improved response in the CF patients. Serum 25(OH)D levels in CF subjects at baseline were 21 +/- 3 ng/ml, which increased to 27 +/- 4 ng/ml at the end of 8 weeks (P=0.05). PTH concentration remained largely unchanged in both population groups. CONCLUSION: A UV lamp that emits ultraviolet radiation similar to sunlight and thus produces vitamin D(3) in the skin is an excellent alternative for CF, and SBS patients who suffer from vitamin D deficiency due to fat malabsorption, especially during the winter months when natural sunlight is unable to produce vitamin D3 in the skin. This UV lamp is widely available for commercial home use and could potentially be prescribed to patients with CF or SBS.

PMID: 17803596
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Re: Vitamins

Post by Nick » Sat 23 Feb 2008 17:28

Yvonne wrote: BACKGROUND: Cystic fibrosis (CF) and short bowel syndrome (SBS) patients are unable to absorb vitamin D from the diet and thus are frequently found to be severely vitamin D deficient. We evaluated whether a commercial portable ultraviolet (UV) indoor tanning lamp that has a spectral output that mimics natural sunlight could raise circulating 25-hydroxyvitamin D [25(OH)D] levels in subjects with CF and SBS.
interesting, because many Lymies seem to have gut problems (either from Lyme itself, or from the antibiotics) which might be the cause for the frequently found vitamin D deficits. Because of that the usual recommendations regarding vitamin D intake (difficult to develop a shortage with normal diet) might not apply for them. Maybe Lymies need to go outside more than average, or purchase such an UV lamp.

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Re: Vitamins

Post by Yvonne » Tue 11 Mar 2008 20:11

Eur J Immunol. 2007 Feb;37(2):395-405. Links

The vitamin D receptor gene FokI polymorphism: functional impact on the immune system.

van Etten E, Verlinden L, Giulietti A, Ramos-Lopez E, Branisteanu DD, Ferreira GB, Overbergh L, Verstuyf A, Bouillon R, Roep BO, Badenhoop K, Mathieu C

Laboratory for Experimental Medicine and Endocrinology (LEGENDO), Katholieke Universiteit Leuven, Leuven, Belgium.

1Alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3) has important effects on the growth and function of multiple cell types. These pleiotropic effects of 1,25(OH)2D3 are mediated through binding to the vitamin D receptor (VDR). Several polymorphisms of the human VDR gene have been identified, with the FokI polymorphism resulting in VDR proteins with different structures, a long f-VDR or a shorter F-VDR. The aim of this study was to investigate the functional consequences of the FokI polymorphism in immune cells. In transfection experiments, the presence of the shorter F-VDR resulted in higher NF-kappaB- and NFAT-driven transcription as well as higher IL-12p40 promoter-driven transcription. Marginal differences were observed for AP-1-driven transcription, and no differential effects were observed for transactivation of a classical vitamin D-responsive element. Concordantly, in human monocytes and dendritic cells with a homozygous short FF VDR genotype, expression of IL-12 (mRNA and protein) was higher than in cells with a long ff VDR genotype. Additionally, lymphocytes with a short FF VDR genotype proliferated more strongly in response to phytohemagglutinin. Together, these data provide the first evidence that the VDR FokI polymorphism affects immune cell behavior, with a more active immune system for the short F-VDR, thus possibly playing a role in immune-mediated diseases.

PMID: 17274004
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Re: Vitamins

Post by Yvonne » Tue 11 Mar 2008 20:14

Vitamin D: its role and uses in immunology


In recent years there has been an effort to understand possible noncalcemic roles of vitamin D, including its role in the immune system and, in particular, on T cell-medicated immunity. Vitamin D receptor is found in significant concentrations in the T lymphocyte and macrophage populations. However, its highest concentration is in the immature immune cells of the thymus and the mature CD-8 T lymphocytes. The significant role of vitamin D compounds as selective immunosuppressants is illustrated by their ability to either prevent or markedly suppress animal models of autoimmune disease. Results show that 1,25-dihydroxyvitamin D3 can either prevent or markedly suppress experimental autoimmune encephalomyelitis, rheumatoid arthritis, systemic lupus erythematosus, type I diabetes, and inflammatory bowel disease. In almost every case, the action of the vitamin D hormone requires that the animals be maintained on a normal or high calcium diet. Possible mechanisms of suppression of these autoimmune disorders by the vitamin D hormone have been presented. The vitamin D hormone stimulates transforming growth factor TGFß-1 and interleukin 4 (IL-4) production, which in turn may suppress inflammatory T cell activity. In support of this, the vitamin D hormone is unable to suppress a murine model of the human disease multiple sclerosis in IL-4-deficient mice. The results suggest an important role for vitamin D in autoimmune disorders and provide a fertile and interesting area of research that may yield important new therapies.—DeLuca, H. F., Cantorna, M. T. Vitamin D: its role and uses in immunology.
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Re: Vitamins

Post by Yvonne » Tue 11 Mar 2008 20:27

Vitamin D3: Higher Doses Reduce Risk of Common Health Concerns

Vitamin D3 is one of the most useful nutritional tools we have at our
disposal for improving overall health. This nutrient is unique in that even
though it is a vitamin it has hormone-like actions and controls phosphorus, calcium,
and bone metabolism and neuromuscular function. Vitamin D3 is the only vitamin
the body can manufacture from sunlight.
Yet, with today’s indoor living and the use of sunscreens due to concern about skin
cancer, we are now a society with millions of individuals deficient in life-sustaining vitamin D3.
For more than a century, scientists have recognized that vitamin D3 is involved in
bone health. Research has continued to accumulate that it can reduce the risk of
fractures to a signifi cant degree. The latest research, however, shows that Vitamin D3
defi ciency is linked to a surprising number of other health conditions such as depression,
back pain, cancer, insulin resistance and pre-eclampsia in pregnancy, impaired
immunity and macular degeneration.
At the same time it’s becoming clear that vitamin D3 may play a wide role in overall
health, it’s becoming equally clear that a large percentage of individuals are defi cient
in this important nutrient. The fear of skin cancer has stopped many individuals from
obtaining benefi cial amounts of sunlight,which the skin converts into vitamin D3.
Even individuals who venture out into the sun often use suntan lotion and may be defi -
cient in vitamin D3. Furthermore, as we age, we are less equipped to produce suf-
fi cient quantities of this vital nutrient. One study found that age-related declines in
kidney function may require older people to ingest more vitamin D to maintain the
same blood levels as younger people.1
The Recommended Daily Intake (RDI) is set so low that individuals who consume
this small amount are still likely to be defi -cient. In fact, researchers have discovered
that the RDI, which was considered adequate to prevent osteomalacia (a painful
bone disease) or rickets, is nowhere near high enough to protect against the majority
of diseases linked to vitamin D3 deficiency.
For example, an analysis of the medical literature found that at least 1,000
to 2,000 IU of vitamin D3 per day is necessary to reduce the risk of colorectal cancer
and that a low dose of vitamin D3 did not have the same protective effect.2
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Re: Vitamins

Post by Yvonne » Sat 22 Mar 2008 16:42

Making Up For An 'Inborn' Vitamin C Deficiency

A new study appears to explain how humans, along with other higher primates, guinea pigs and fruit bats, get by with what some have called an "inborn metabolic error": an inability to produce vitamin C from glucose.

Unlike the more than 4,000 other species of mammals who manufacture vitamin C, and lots of it, the red blood cells of the handful of vitamin C-defective species are specially equipped to suck up the vitamin's oxidized form, so-called L-dehydroascorbic acid (DHA), the researchers report in the March 21st issue of Cell, a publication of Cell Press. Once inside the blood cells, that DHA--which is immediately transformed back into ascorbic acid (a.k.a. vitamin C)--can be efficiently carried through the bloodstream to the rest of the body, the researchers suggest.

"Evolution is amazing. Even though people talk about this as an 'inborn error'- a metabolic defect that all humans have - there is also this incredible manner in which we've responded to the defect, using some of the body's most plentiful cells," said Naomi Taylor of Université Montpellier I and II in France, noting that the body harbors billions of red blood cells. "[Through evolution], we've created this system that takes out the oxidized form of vitamin C and transports the essential, antioxidant form."

Meanwhile, the red cells of other mammals apparently take up very little, if any, DHA, which might explain why they need to produce so much more vitamin C than we need to get from our diets, Taylor said. The recommended daily dose of vitamin C for humans is just one mg/kg, while goats, for example, produce the vitamin at a striking rate of 200 mg/kg each day.

In essence, the red cells of animals that can't make vitamin C recycle what little they've got. Earlier studies had described the recycling process, Taylor said. "Our contribution to the whole story is to show that this process of recycling exists specifically in mammals that don't make vitamin C."

Scientists knew that the protein called Glut1, found in the membranes of cells throughout the body, is the primary transporter of glucose. They also knew that Glut1 can transport DHA too, thanks to the structural similarities between the two molecules. In biochemical assays, it appeared that the glucose transporter would move glucose and DHA interchangeably.

But, in the new study, Taylor's group made a surprising discovery: The Glut1 on human red blood cells strongly favors DHA over glucose. In fact, the human blood cells are known to carry more Glut1 than any other cell type, harboring more than 200,000 molecules on the surface of every cell. Nevertheless, the researchers found, as red blood cells develop in the bone marrow, their transport of glucose declines even as Glut1 numbers skyrocket.

The key to the glucose transporters switch to DHA, they show, is the presence of another membrane protein called stomatin. (Accordingly, in patients with a rare genetic disorder of red cell membrane permeability wherein stomatin is only present at low levels, DHA transport is decreased by 50% while glucose uptake is significantly increased, they report.)

Then, another surprise: The researchers found that the red cells of mice, a species that can produce vitamin C, don't carry Glut1 on their red blood cells at all. They carry Glut4 instead. They suspected that the differences in human red blood cells might be linked to our inability to synthesize the reduced form of DHA, vitamin C, from glucose. In fact, they confirmed Glut1 expression on human, guinea pig and fruit bat red blood cells, but not on any other mammalian red cells tested, including rabbit, rat, cat, dog and chinchilla. Next, they took a closer look at primates. Primates belonging to the Haplorrhini suborder (including prosimian tarsiers, new world monkeys, old world monkeys, humans and apes) have lost the ability to synthesize vitamin C, whereas primates in the Strepsirrhini suborder (including lemurs) are reportedly able to produce this vitamin, Taylor explained.

Notably, they detected Glut1 on all tested red blood cells of primates within the higher primate group, including long-tailed macaques, rhesus monkeys, baboons and magot monkeys. In marked contrast, Glut1 was not detected on lemur red blood cells. Moreover, they report, although DHA uptake in human and magot red cells was similar, the level of transport in cells from three different lemur species was less than 10% of that detected in higher primates.

"Red blood cell-specific Glut1 expression and DHA transport are specific traits of the few vitamin C-deficient mammalian species, encompassing only higher primates, guinea pigs and fruit bats," the researchers concluded. "Indeed, the red cells of adult mice do not harbor Glut1 and do not transport DHA. Rather, Glut4 is expressed on their cells. Thus, the concomitant induction of Glut1 and stomatin during red blood cell differentiation constitutes a compensatory mechanism in mammals that are unable to synthesize the essential ascorbic acid metabolite," otherwise known as vitamin C.
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Re: Vitamins

Post by Cobwebby » Mon 24 Mar 2008 1:16

Well I sort of read these articles-as in skimmed them.

My personal experience is that I went to an endocrinologist for hypothyroidism(is that a word?), and routine blood work showed my vitamin D was exceedingly low. I was given a booster dose of 40,000 mg 3x week for 8 weeks.

Now I just take 400iu a day to maintain.

Dr. said it was malabsorption syndrome-and I should be tested for Celiac Disease. I just changed my diet to gluten free.

Now my level is normal-but I still plan to sun myself on the deck this summer-wonder what percentage of exposed skin I should have for maximum benefit? :)
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