UV-B therapy

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UV-B therapy

Postby trisca » Mon Dec 10, 2012 10:22 am

Has anyone tried it? Did it make a difference to your symptoms?
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Re: UV-B therapy

Postby jimmylegs » Mon Dec 10, 2012 2:03 pm

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Re: UV-B therapy

Postby trisca » Mon Dec 10, 2012 3:11 pm

I'm thinking of buying a narrow band uv b lamp (full length medical grade) and wondered if anyone else has any personal experience in using one.

I did the link in one of your links above on calculating how much time in the sun is necessary. I used today's conditions (in London, UK) and it answered 12:00 to 12:00, which I take it means it's just not possible.

I'm not so convinced by the supplements alone.
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Re: UV-B therapy

Postby trisca » Mon Dec 10, 2012 3:17 pm

Here is one of the studies I'm thinking of:

http://www.abdn.ac.uk/news/details-13016.php
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Re: UV-B therapy

Postby jimmylegs » Mon Dec 10, 2012 6:03 pm

i have personally found the efficacy of d3 supplements to be heavily zinc dependent. and zinc status is not great in your typical ms patient. i will check out that study.
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Re: UV-B therapy

Postby jimmylegs » Mon Dec 10, 2012 7:13 pm

i think the linked article above is just about trying to help people value sunlight rather than hide from it for fear of cancer.

here's an unexpected find:

Treatment and Prevention of Vitamin D Insufficiency in Cystic Fibrosis Patients: Comparative Efficacy of Ergocalciferol, Cholecalciferol, and UV Light
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2690417/
Abstract
Background: The optimal treatment for correcting or preventing vitamin D insufficiency in cystic fibrosis (CF) patients has not been established.
Objective: The aim of the study was to assess the relative efficacy of three modes of vitamin D therapy: cholecalciferol (D3), ergocalciferol (D2), and UV light in raising or maintaining 25(OH)D levels above 30 ng/ml.
Design: Thirty adult CF subjects with vitamin D insufficiency were randomized into one of three treatment arms: D3, D2, or UV light. Subjects randomized to D3 or D2 ingested 50,000 IU of vitamin D weekly, and those randomized to UV exposed their skin to UV light from a lamp five times a week. Serum was collected for 25(OH)D and PTH at baseline and at 12 wk.
Results: Treatment with D3 and D2 raised 25(OH)D levels significantly, from a mean of 21.2 ± 10.18 to 47.1 ± 20.5 ng/ml (P < 0.001) and 24.4 ± 10.3 to 32.7± 9.7 ng/ml (P = 0.01), with 100% and 60% reaching 25(OH)D levels above 30 ng/ml, respectively. Treatment with UV did not raise 25(OH)D levels significantly; however, only 55% of subjects were adherent with UV therapy.
Conclusion: This study demonstrates that CF subjects are able to achieve or maintain optimal vitamin D status (>30 ng/ml) with two oral regimens of either D3 or D2 treatment, the former being more efficacious. A confounding variable for this observation is the fact that the D3 and D2 capsules contained different carriers, powder-based vs. oil-based, respectively. UV therapy did not alter vitamin D status, possibly due to poor adherence to UV therapy.

also possibly that they had insufficient nutrient status to manufacture the enzymes required to synthesize d3 from 7-dehydrocholesterol in the skin??? - i'm investigating that but it's challenging.

in the meantime, is it possible that CF subjects are zinc deficient, and could that be playing a role? yes to the first part, and i think the answer to the second part may be yes also:

PLASMA-ZINC IN HEALTH AND DISEASE (1970!!)
http://www.sciencedirect.com/science/ar ... 3670907014
"Plasma-zinc levels were measured by atomic-absorption spectrophotometry in healthy adults and children, in patients with a variety of diseases, in pregnancy, and in women taking oral contraceptives. ... Abnormally low values were obtained in alcoholic cirrhosis, other types of liver disease, active tuberculosis, indolent ulcers, uræmia, before and after a single hæmodialysis, myocardial infarct, non-tuberculous pulmonary infection, Down's syndrome, cystic fibrosis with growth retardation, growth-retarded Iranian villagers, pregnancy, and in women taking oral contraceptives. In cystic fibrosis without growth retardation and in inactive tuberculosis, there was no significant decrease. No conditions have been observed with a higher-than-normal plasma-zinc concentration."
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Re: UV-B therapy

Postby lyndacarol » Mon Dec 10, 2012 8:50 pm

Strong New Evidence That MS Risk Affected by Birth Month, Mom's Vitamin D Status:

http://articles.mercola.com/sites/artic ... _DNL_art_2


In this article on vitamin D by Dr. Joseph Mercola, he writes (about two thirds of the way down the page), "If you cannot get your vitamin D requirements from Sun exposure, I recommend using a safe tanning bed… Safe tanning beds also have less dangerous UVA than sunlight, while unsafe ones have more UVA than sunlight."

http://articles.mercola.com/sites/artic ... stake.aspx


In Mercola's opinion, if sunshine is not a possible source of vitamin D, a safe tanning bed is the next best option:

http://articles.mercola.com/sites/artic ... cause.aspx
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Re: UV-B therapy

Postby jimmylegs » Mon Dec 10, 2012 9:16 pm

i wish i had full text access to this one. a less than ideally informative abstract.

Ultraviolet-B radiation increases serum 25-hydroxyvitamin D levels: The effect of UVB dose and skin color
http://www.sciencedirect.com/science/ar ... 2207005002
Background
Ultraviolet (UV)-B light increases vitamin D levels, but the dose response and the effect of skin pigmentation have not been well characterized.
Objective
We sought to define the relationship between UVB exposure and 25-hydroxyvitamin D (25-OH-D) concentrations as a function of skin pigmentation.
Methods
Seventy two participants with various skin tones had 90% of their skin exposed to UVB light (20-80 mJ/cm2) 3 times a week for 4 weeks. Serum 25-OH-D was measured weekly.
Results
Eighty percent of the variation in treatment response was explained by UVB dose and skin tone. Therapeutically important changes in 25-OH-D were achieved with minimal tanning.
Limitations
Four weeks was not long enough to reach a steady state at the higher dose rates.
Conclusions
The response of 25-OH-D levels to UVB light is dependent on skin pigmentation and the amount of UVB given, and useful increases in vitamin D status can be achieved by defined UVB doses small enough to produce only minimal tanning.

omg this is practically brand new

Changes in serum 25-hydroxyvitamin D and cholecalciferol after one whole-body exposure in a commercial tanning bed: a randomized study
http://link.springer.com/article/10.100 ... z?LI=true#
We wanted to evaluate the cutaneous synthesis of 25OHD and cholecalciferol after one whole-body exposure to ultraviolet radiation type B (UVB) in a randomized setup. Healthy volunteers were randomized to one whole-body exposure in a commercial tanning bed with UVB emission (UVB/UVA ratio 1.8–2.0%) or an identical placebo tanning bed without UVB. The output in the 280–320 nm range was 450 µW/cm2. Blood samples were analyzed for 25OHD and cholecalciferol at baseline and during 7 days after treatment. We included 20 volunteers, 11 to UVB and 9 to placebo treatment. During the first 6 h, no significant differences in 25OHD between the groups were found. At the end of the study, we found a mean increase of 25OHD in the UVB group of 4.5 nmol/l (SD 7 nmol/l) compared to a decline of −1.2 nmol/l (SD 7 nmol/l) in the placebo group (p = 0.1). A linear mixed model yielded an increase of 25OHD in the UVB group of 1.0 nmol/l per 24 h (p < 0.01). For cholecalciferol, we found a near significant increase of 1 pmol/l per hour in the UVB group compared to the placebo group during the first 6 h (p = 0.052). One tanning bed session had significant, but modest impact on the level of 25OHD during 7 days after exposure to UVB.

oral dose response study
Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol
http://ajcn.nutrition.org/content/77/1/204.short
From a mean baseline value of 70.3 nmol/L, equilibrium concentrations of serum 25-hydroxycholecalciferol changed during the winter months in direct proportion to the dose, with a slope of ≈0.70 nmol/L for each additional 1 μg cholecalciferol input. The calculated oral input required to sustain the serum 25-hydroxycholecalciferol concentration present before the study (ie, in the autumn) was 12.5 μg (500 IU)/d, whereas the total amount from all sources (supplement, food, tissue stores) needed to sustain the starting 25-hydroxycholecalciferol concentration was estimated at ≈96 μg (≈3800 IU)/d. By difference, the tissue stores provided ≈78–82 μg/d.
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: UV-B therapy

Postby trisca » Tue Dec 11, 2012 1:45 am

This is the other bit of research I'm thinking of that I didn't have time to find last night:

The mice exposed to UV rays suppressed the effects of MS-like disease better than the control mice, the researchers found, even though the amount of radiation wasn’t enough to greatly increase the animals’ blood concentrations of vitamin D.

In another test, the researchers gave injected mice varying doses of vitamin D supplements, but no UV radiation. The supplements failed to control the disease onset, severity or progression.

“We concluded that UV light is doing something beyond [making] vitamin D,” DeLuca says.

http://www.sciencenews.org/view/generic ... s_symptoms

The type of uvb therapy I'm talking about is the same type that is used for psoriasis (yet another autoimmune disease with a vitamin d link.) Like in this article:

"For those who have access to UVB treatment at their local dermatology unit, a course usually entails three visits each week for between eight to 10 weeks.
It works by dampening down the immune overreaction in the skin." http://news.bbc.co.uk/1/hi/health/8038206.stm

lyndacarol, have you tried any light therapy?

BTW, I was born in November.
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Re: UV-B therapy

Postby trisca » Tue Dec 11, 2012 4:14 am

Here's the actual article in the mouse link above.

http://www.pnas.org/content/107/14/6418.short
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Re: UV-B therapy

Postby trisca » Tue Dec 11, 2012 4:19 am

Here is another study I was thinking of,

Conclusions: Sun exposure and vitamin D status may have independent roles in the risk of CNS demyelination.

http://www.pnas.org/content/107/14/6418.short
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Re: UV-B therapy

Postby trisca » Tue Dec 11, 2012 4:28 am

Here is a study with vitamin d supplements and ms symptoms.

"Supplementation with 20,000 IU vitamin D3 weekly did not result in beneficial effects on the measured multiple sclerosis-related outcomes. This study was not powered to address clinical outcomes, but none of the results were suggestive of an effect in this unselected population of fully ambulatory persons with multiple sclerosis."

http://msj.sagepub.com/content/18/8/1144.abstract

I would like to see that study done using light therapy (instead of supplements), does such a study exist?
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Re: UV-B therapy

Postby jimmylegs » Tue Dec 11, 2012 6:27 am

i wonder what the mice in the above study had for dietary calcium

Dietary Calcium Is a Major Factor in 1,25-Dihydroxycholecalciferol Suppression of Experimental Autoimmune Encephalomyelitis in Mice1
http://jn.nutrition.org/content/129/11/1966.full
The active form of vitamin D (1,25-dihydroxycholecalciferol) is a potent immune system regulator. Treating mice with 1,25-dihydroxycholecalciferol and feeding them diets high in calcium can completely suppress the induction of experimental autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE). Experiments described here were carried out on mice in which development of EAE was induced. Mice were fed diets containing various amounts of calcium and 1,25-dihydroxychole-calciferol. Variables measured were as follows: 1) incidence and severity of EAE; 2) serum calcium concentrations; 3) body weight; 4) total number of cells in the lymph nodes; and 5) interleukin-4 (IL-4) and transforming growth factor-ß1 (TGF-ß1) mRNA levels. When calcium was removed from the diet, the incidence of EAE was reduced 20% in both males and females. Further, the lower the dietary level of calcium, the higher was the dose of 1,25-dihydroxycholecalciferol required to prevent the symptoms. Thus, 1,25-dihydroxycholecalciferol was found most effective in mice fed a diet adequate or high in calcium. 1,25-Dihydroxycholecalciferol treatment of mice fed high dietary calcium resulted in a decreased number of lymphocytes in the lymph nodes and increased IL-4 and TGF-ß1 mRNA levels. When calcium was omitted from the diet, 1,25-dihydroxycholecalciferol supplementation increased TGF-ß1 mRNA. Increased IL-4 mRNA and decreased lymphocytes in the lymph nodes in response to 1,25-dihydroxycholecalciferol occurred only when dietary calcium was adequate or high. Our results suggest that dietary calcium and 1,25-dihydroxycholecalciferol are both involved in the prevention of symptomatic EAE.

in humans, we know about the calcium magnesium and zinc requirements but as a fat soluble vitamin, absorption is also fat-dependent. last night i ran across the relevant study but i'm not using the right search terms to find it again. for the nonce, a study on another fat soluble vit:

The absorption of vitamin E is influenced by the amount of fat in a meal and the food matrix.
http://www.ncbi.nlm.nih.gov/pubmed/15522126
Abstract
Vitamin E absorption requires the presence of fat; however, limited information exists on the influence of fat quantity on optimal absorption. In the present study we compared the absorption of stable-isotope-labelled vitamin E following meals of varying fat content and source. In a randomised four-way cross-over study, eight healthy individuals consumed a capsule containing 150 mg (2)H-labelled RRR-alpha-tocopheryl acetate with a test meal of toast with butter (17.5 g fat), cereal with full-fat milk (17.5 g fat), cereal with semi-skimmed milk (2.7 g fat) and water (0 g fat). Blood was taken at 0, 0.5, 1, 1.5, 2, 3, 6 and 9 h following ingestion, chylomicrons were isolated, and (2)H-labelled alpha-tocopherol was analysed in the chylomicron and plasma samples. There was a significant time (P<0.001) and treatment effect (P<0.001) in (2)H-labelled alpha-tocopherol concentration in both chylomicrons and plasma between the test meals. (2)H-labelled alpha-tocopherol concentration was significantly greater with the higher-fat toast and butter meal compared with the low-fat cereal meal or water (P<0.001), and a trend towards greater concentration compared with the high-fat cereal meal (P=0.065). There was significantly greater (2)H-labelled alpha-tocopherol concentration with the high-fat cereal meal compared with the low-fat cereal meal (P<0.05). The (2)H-labelled alpha-tocopherol concentration following either the low-fat cereal meal or water was low. These results demonstrate that both the amount of fat and the food matrix influence vitamin E absorption. These factors should be considered by consumers and for future vitamin E intervention studies.

it's key to separate the influence of light period, from the influence of vitamin d3. what the uv light is doing for symptoms is possibly related moreso to melatonin and hippocampal neurogenesis than straight vit d3.
http://wolfweb.unr.edu/homepage/vpravos ... memory.htm
ms patients have characteristic hippocampal atrophy, and the eae virus attacks and kills murine hippocampal pyramidal neurons.

dietary tryptophan is a key ingredient for melatonin production.

Biological Synthesis and Metabolism of Melatonin
http://www.ch.ic.ac.uk/local/projects/s ... synth.html

so now the question is, does the wavelength matter. thought back to some chats we had about 5 yrs ago, found this tidbit:
post15775.html?hilit=murine d3#p15775

kasuku, i just ran across something related to zinc and thought of your comment some time back:
also would like to attract your attention to the paper on vit. D in the latest posts. The paper described that people with depression did better if they were located in the side of the hospital with sun exposure as well as people recovering from surgery. I assume that the exposure is mostly sunlight filtered by windows so in theory no UVB exposure. Light itself stimulates the pituitary gland resulting in hormone secretions and that could explain quicker recovery from depression as opposed to people kept in darker rooms. Perhaps light itself plays a role in addition to vit D. from UVB exposure. I guess my understanding is that UVB are filtered by glass. Am I right on this? What do you think Jimmylegs?
K

(i didn't answer that question about filtering originally, but the answer is yes..)
i have the feeling i have made this connection before but in case i didn't post it:
i was just reading these bits and pieces which reminded me of the light exposure sans D3 production element:
Quote:
Med Hypotheses. 2000 Sep;55(3):239-41.
The possible role of gradual accumulation of copper, cadmium, lead and iron and gradual depletion of zinc, magnesium, selenium, vitamins B2, B6, D, and E and essential fatty acids in multiple sclerosis.
Johnson S.
Multiple sclerosis (MS) has a much higher incidence among caucasians that in any other race. Furthermore: females are much more susceptible than males and white females living in colder, wetter areas are much more susceptible than those living in warmer areas. On the other hand, menstruating women have increased copper (Cu) absorption and half-life, so they tend to accumulate more Cu than males. Moreover, rapidly growing girls have an increased demand for zinc (Zn), but their rapidly decreasing production of melatonin results in impaired Zn absorption, which is exacerbated by the high Cu levels. The low Zn levels result in deficient CuZnSuperoxide dismutase (CuZnSOD), which in turn leads to increased levels of superoxide. Menstruating females also often present with low magnesium (Mg) and vitamin B6 levels. Vitamin B6 moderates intracellular nitric oxide (NO) production and extracellular Mg is required for NO release from the cell, so that a deficiency of these nutrients results in increased NO production in the cell and reduced release from the cell. The trapped NO combines with superoxide to form peroxinitrite, an extremely powerful free radical that leads to the myelin damage of MS. Iron (Fe), molybdenum (Mo) and cadmium (Cd) accumulation also increase superoxide production. Which explains MS in males, who tend to accumulate Fe much faster and Cu much less rapidly than females. Since vitamin D is paramount for Mg absorption, the much reduced exposure to sunlight in the higher latitudes may account for the higher incidence in these areas. Moreover, vitamin B2 is a cofactor for xanthine oxidase, and its deficiency exacerbates the low levels of uric acid caused by high Cu levels, resulting in myelin degeneration. Finally Selenium (Se) and vitamin E prevent lipid peroxidation and EPA and DHA upregulate CuZnSOD. Therefore, supplementation with 100 mg MG, 25 mg vit B6, 10 mg vit B2, 15 mg Zn and 400 IU vit D and E, 100 microg Se, 180 mg EPA and 120 mg DHA per day between 14 and 16 years of age may prevent MS.
also found this...
Quote:
Melatonin: Where It Comes From
Melatonin is a naturally occuring hormone that is synthesized from the neurotransmitter serotonin which in turn is synthesized from the amino acid tryptophan. This synthesis or production occurs primarily in a gland located at the center of the brain called the pineal gland. The pineal gland is light-activated, i.e., it is controlled by the amount of light seen by the eyes each day. This light activation gives rise to the belief that the pineal gland functions as the body's internal clock, regulating functions that are time-related such as sleep and the ageing process. Melatonin production via serotonin synthesis occurs at its peak during the dark hours around 2:00 a.m. Inversely, during daylight hours, melatonin production is low. It is for this reason that melatonin is believed to aid in regulating our sleep cycle and help stimulate sleep. Also, evidence exists that the pineal gland not only controls our 24 hour clock but our "life clock", meaning that it appears to be a major controller regarding our ageig process. As we age, several things happen to our pineal gland that result in it producing less melatonin. Since the pineal gland is derived from nerve tissue, the gland's cells do not replicate when damaged or lost. This loss of pineal gland cells may result from chemical or biological injury to the gland, or for a myriad of other reasons. Therefore, as we age, the pineal gland literally decreases in size or atrophies which has a direct effect on the amount of melatonin it is capable of synthesizing. Additionally, the gland itself is susceptible to the ageing processes that occur, such as calcium deposits and a decreased blood supply due to atherosclerosis. These in conjunction with other ageing processes interfere with the pineal gland’s melatonin-producing activities.
i am working on finding some info on pineal gland nutrition and support, i found one 2001 rat study but will keep looking

Hi Jimmylegs,
Very interesting! Do you recall the work coming out of Stanford where they found that tryptophan giving to mice in the EAE model not only stopped the progression of the disease, but also improved the clinical signs. The connection between tryptophan, melatonin and light is definitely interesting. I wonder if there are ways to stimulate the pineal gland other than with light. Taking melatonin may have the opposite effect due to biofeedback. What do you think?
K
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Re: UV-B therapy

Postby trisca » Tue Dec 11, 2012 6:53 am

Maybe a SAD light is the way to go.

Have there really been no studies on this? Or no anecdotal information?
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Re: UV-B therapy

Postby trisca » Tue Dec 11, 2012 8:47 am

I just saw someone I vaguely know that I know has psoriasis and asked her if she's done the uv b therapy. She said yes and it works but them you get 'immune' to it and they have to keep raising the dose and now she's at the point where she has to soak in some sort of chemical bath first. Thought that might be interesting.
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