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xo++
03-07-2009, 11:56 AM
A few interesting Vitamin D studies in this year's batch of abstracts.

First, women with MS appear to benefit more from Vitamin D than men.

Secondly a small trial of Vitamin D3 found high-doses of D3 to be safe and to alter the immunological profile of patients in a manner thought to be beneficial in MS.

Third, a study found that the lower levels of Vitamin D are associated with disease severity in MS.

Finally, an Australian study found relapses higher in the northern hemisphere in spring and southern hemisphere in autumn (which could be explained by lower levels of Vitamin D in these seasons).


[S39.004] Gender Differences in Immunomodulatory Effects of 1,25 Dihydroxyvitamin D3 in Multiple Sclerosis

Jorge Correale, María C. Ysrraelit, María I. Gaitán, Buenos Aires, Argentina

OBJECTIVE: To study gender differences in the immunomodulatory effects of Vitamin D in MS.

BACKGROUND: Vitamin D has a protective effect against MS development, supported by reduced disease risk associated with sun exposure and Vitamin D supplement use. Elevated Vitamin D blood levels have also been associated with lower risk of MS. However, Vitamin D inhibits EAE in female but not in male mice. DESIGN/

METHODS: Serum 25(OH)D3 and 1,25(OH)2D3 levels were measured using ELISA in 58 relapsing remitting MS (RRMS) patients during remission, 34 RRMS patients during relapse, 40 primary progressive MS (PPMS) subjects and 60 healthy controls. Cell proliferation was measured using [3H]-thymidine incorporation assays. Vitamin D receptor, CYP27B1, CYP24A1, and Vitamin-D binding protein (DBP) expression was measured by RT-PCR, while cytokine production was evaluated using ELISA. CD4+CD25+ regulatory T cells were studied using flow cytometry.

RESULTS: Female and male patients showed similar levels of 25(OH)D3 and 1,25(OH)2D3 in all groups studied. However, inhibition of proliferation of MBP-specific T cells, as well as secretion of Interferon- and IL-17 by 1,25(OH)2D3 were significantly stronger in females compared to males (p< 0.01). Likewise, enhancement of IL-10 secretion, and increased number of CD4+CD25+ regulatory T cells induced by Vitamin D was higher in female MS patients compared to males (p < 0.001). Female MS patients had significantly lower levels of CYP24A1 mRNA, encoding the inactivating 24-OHase enzyme, and increased amounts of DBP compared to males, indicating gender differences in Vitamin D metabolism. Finally, treatment of MBP-specific T cells with 17beta-estradiol significantly reduced CYP24A1 mRNA expression and increased DBP expression favoring Vitamin D uptake.

CONCLUSIONS/RELEVANCE: Gender differences in the metabolism of Vitamin D suggest a higher protective effect of Vitamin D-based therapeutic strategies in women. Supported by: Institute for Neurological Research Dr. Raul Carrea, FLENI

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[P01.110] Immunological Analysis of a Phase I/II Dose-Escalation Trial of Oral Vitamin D3 with Calcium Supplementation in Patients with Multiple Sclerosis

Jodie M. Burton, Samantha Kimball, Amit Bar-Or, Hans-Michael Dosch, Donald Gagne, Roy Cheung, Cheryl D'Souza, Melanie Ursell, Reinhold Vieth, Paul O'Connor, Montreal, QC, Canada, Etobicoke, ON, Canada, Toronto, ON, Canada

OBJECTIVE: To characterize the safety and immunological profile of high-dose oral vitamin D3 (VD3) in multiple sclerosis (MS).

BACKGROUND: Low UV radiation and 25-hydroxyvitamin D (25(OH)D) are associated with increasing risk and prevalence of MS. We have recently established that high-dose oral VD3 is safe in MS with apparent clinical benefit. This is presumably mediated through immune-regulation and a hypothesized shift away from the pro-inflammatory state believed to be key in MS.

DESIGN/METHODS: A prospective controlled 52-week trial matched MS patients for demographic and disease characteristics, with randomization to treatment and control groups. Treatment patients started VD3 at 4,000 IU/d and escalated over 28 weeks to 40,000 IU/d, at which they spent 6 weeks. This was followed by maintenance with 10,000 IU/d for 12 weeks, 4,000 IU/d for 8 weeks and a 4-week wash-out (roughly 14,000 IU/d over 52 weeks). Calcium (1,200 mg/d) was given throughout the trial. T-scores (a measure of T-cell reactivity to test antigens) were measured at the first and last visit. MMP-9/TIMP-1 values and cytokines profiles were measured at visits 1 (0 IU/d), 4 (10,000 IU/d), 7 (40,000 IU/d) and 11 (0 IU/d). Statistical methods included sign rank, Mann-Whitney U, McNemar, Chi-square and repeated measures modeling.

RESULTS: Forty-nine patients were enrolled (25 treatment, 24 control). Despite a maximum mean 25(OH)D of 413nmol/L (66-729), no adverse events, including calcium abnormalities, occurred. T-scores (TCS) dropped significantly over 52 weeks in treatment patients (p=0.002), but not in controls. The proportion of patients with a TCS below the pre-determined threshold was also greater in treatment patients (p=0.032). Reduction in TCS was significantly greater in patients with an end of trial 25(OH)D => 100nmol/L (p=0.032). MMP-9/TIMP-1 and cytokine analyses will be presented.

CONCLUSIONS/RELEVANCE: High-dose VD3 (10,000 IU/d, possibly higher) in MS is safe and tolerable with immunodulatory effects. Such effects may explain clinical improvement in treated patients. Supported by: Direct-MS and the Multiple Sclerosis Society of Canada.

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[P04.142] Serum Vitamin D Levels Are Associated with Multiple Sclerosis Disease Severity

Bijal K. Mehta, Allison S. Drake, Barbara E. Teter, Murali Ramanathan, Nupur Batra, Nitin Agarwal, Robert Zivadinov, Bianca Weinstock-Guttman, Buffalo, NY

OBJECTIVE: To evaluate whether 25-hydroxyvitamin D (25(OH)D) levels are associated with disease severity in patients with multiple sclerosis (MS).

BACKGROUND: Vitamin D deficiency has been implicated as a risk factor for MS. Higher circulating levels of 25(OH)D are associated with a decreased risk of developing MS. In vivo studies have demonstrated that 25(OH)D inhibits EAE induction in mice and also prevents disease progression. However, the association between 25(OH)D and MS disease severity in humans has yet to be elucidated.

DESIGN/METHODS: Clinical, demographic and 25(OH)D data from 228 MS patients enrolled in the New York State Multiple Sclerosis Consortium (NYSMSC) were analyzed (mean age 50.59.5yrs). The Expanded Disability Status Scale (EDSS) was used to measure MS disease severity (median 3.0); serum 25(OH)D level results were obtained from the same commercial laboratory. Serum 25(OH)D levels <32ng/mL were considered less than sufficient. Ordinal regression was performed to assess the impact of several factors on EDSS score.

RESULTS: Mean serum 25(OH)D level was 29.8ng/mL, with 63.4% of patients considered 25(OH)D deficient/insufficient. The ordinal regression model contained the following variables: sex, age, age at symptom onset, season and 25(OH)D level (Chi-square = 49.9, p < 0.001). Correcting for sex, season, age and age of onset, 25(OH)D levels were found to be significantly predictive of EDSS scores (Wald parameter = 4.9, p<0.05).

CONCLUSIONS/RELEVANCE: The results of this study indicate that 25(OH)D levels are significantly associated with MS disease severity. While further studies regarding the role of 25(OH)D in MS are warranted, these results support a potential disease modifying effect of high levels of 25(OH)D.

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[P08.027] Temporal Variation of Onset of Relapses in Multiple Sclerosis: Results from the Northern and Southern Hemispheres in the MSBase Registry

Orla Mary Gray, Damien Jolley, et. al.

OBJECTIVE: To determine if there is a temporal variation in onset of relapses using the MSBase registry, a large, multi-centre cohort study of MS outcomes. To compare the time of onset of relapses in the northern and southern hemispheres.

BACKGROUND: Previous studies into time of onset of relapses have suggested that relapses are seasonal, with more relapses in spring and fewest in winter. The proposed mechanism is that reduced vitamin D levels at spring onset precipitate relapses. However small numbers, differing diagnostic criteria and the involvement of single regions limited these studies.

DESIGN/METHODS: Data was extracted on 16th July 2008. The dataset comprised 7,860 cases with all forms of MS from 33 centres in 16 countries, including 25,784 documented relapses. Relapses with 1st January recorded as day of onset were excluded, leaving 22,684 in total including 5,542 first demyelinating events. Relapses were stratified by hemisphere of residence and compared by season, quartile and month of onset. Statistical analysis was performed using chi-squared test.

RESULTS: 22,684 relapses (19,775 northern, 2,909 southern) were included. Relapses were significantly more common in spring in the northern hemisphere (P<0.0001) and autumn in the southern hemisphere (P<0.0001). June had the highest number of relapses than any other month in either hemisphere (P<0.0001). These results were replicated with analysis of the 5,542 first demyelinating event in MS cases (4,801 northern, 741 southern).

CONCLUSIONS/RELEVANCE: A highly significant temporal variation in onset of relapses is present in both northern and southern hemispheres. However, peak relapse incidence does not occur in the same season in the northern and southern hemispheres.

lady_express_44
03-07-2009, 12:28 PM
RESULTS: 22,684 relapses (19,775 northern, 2,909 southern) were included. Relapses were significantly more common in spring in the northern hemisphere (P<0.0001) and autumn in the southern hemisphere (P<0.0001). June had the highest number of relapses than any other month in either hemisphere (P<0.0001). These results were replicated with analysis of the 5,542 first demyelinating event in MS cases (4,801 northern, 741 southern).

CONCLUSIONS/RELEVANCE: A highly significant temporal variation in onset of relapses is present in both northern and southern hemispheres. However, peak relapse incidence does not occur in the same season in the northern and southern hemispheres.

WTHeck?

Unfortunately we can't see if there was a variance depending on "where" people reside within the northern vs. southern hemisphere's, i.e. "above 35th parellel might be different then below . . . but given the purpose of the study, you'd think if they observed a pattern if there was one.

So, in the northern hemisphere we relapse mostly in the spring, and in the southern they relapse more in the fall. The fall doesn't follow a lack of sunshine/vitamin D, so that wouldn't seem to be the environmental difference.

I wonder if it might have more to do with viruses that occur in those months, depending on the hemisphere? For instance, in Canada viruses can lag the US because of the colder weather (hitting us in Spring), but in the southern hemisphere they might travel faster due to warmer weather (hitting them in Fall). :confused:

Are you coming to Vancouver, Mark?

Cherie

xo++
03-07-2009, 12:36 PM
Hi Cherie,

But in the southern hemisphere, winter occurs in June, July, August ...

No I'm sad but while I'm going to be in Seattle for a few days at a conference and wanted to go to Vancouver, my brother and sister-in-law put a lot of pressure on me to drop down to California and visit after the conference, and I didn't feel I had time to go both to Vancouver and California.

Mark

lady_express_44
03-07-2009, 01:48 PM
Hi Cherie,

No I'm sad but while I'm going to be in Seattle for a few days at a conference and wanted to go to Vancouver, my brother and sister-in-law put a lot of pressure on me to drop down to California and visit after the conference, and I didn't feel I had time to go both to Vancouver and California.

Mark

Well, the weather is probably nicer in CA right now anyway. :) Maybe next time.

But in the southern hemisphere, winter occurs in June, July, August ...

Maybe I am confused . . . :confused:

If the majority of relapses happen in June, all over the world ...

. . . then in the Northern hemisphere that would be OUR Spring/Pre-summer months (after months without "sufficient" vitamin D)

. . . and in the Southern hemisphere, that would be THEIR late Fall months (after many months with "ample" vitamin D from summer).

If it was theroetically due to lack of sunshine/vitamin D, why would they experience most of their relapses in Dec, at the end of the season where they haven't had much exposure ~ like we do? Why not the same season no matter which hemisphere?

Cherie

xo++
03-07-2009, 02:04 PM
Oh ok. :) I was just referring to this result:

"Relapses were significantly more common in spring in the northern hemisphere (P<0.0001) and autumn in the southern hemisphere (P<0.0001)."

But yes you're right the June result doesn't fit the hypothesis (I assume they're advancing) even though the seasonal result does.

Ikoiko
03-07-2009, 03:00 PM
Thanks, Mark!

Ted Hutchinson
03-07-2009, 05:24 PM
This is a bit more detailed (http://www.neurology-asia.org/articles/20082_199.pdf)
Conclusions: A temporal variation in onset of relapses is present in both northern and southern hemispheres. However, peak relapse incidence does not occur in the same season - relapses are more common in spring in the northern hemisphere and autumn in the southern hemisphere. The highest incidence of relapses in the northern hemisphere is at the end of spring in the month of June, not spring onset in this large cohort.

I don't understand why the removed relapses occurring on Ist January. Any ideas.

Association of vitamin D metabolite levels with relapse rate and disability in multiple sclerosis (http://msj.sagepub.com/cgi/content/abstract/14/9/1220) shows relapse rate is vitamin d status related.

It's possible that as vitamin d levels have declined year on year for the last 15 yrs that we have go to the point that latitude is not making much difference to UVB exposure. Certainly in Australia/NZ it's not a good idea to sunbathe any month of the year because the ozone prevents UVB getting down to ground level so unless folks are taking effective amounts of D3 they will be vit d deplete every month of the year. There are other factors that drag 25(OH)D down Wheat/high fibre diets can halve Vitamin d half life.
HFCS by raising leptin levels can antagonise D3 metabolism.

More details here about why Australians don't get UVB and why sunscreens cause more cancer than they prevent.
http://i2.ytimg.com/vi/eeXtGHSt-5o/default.jpgSkin Cancer/Sunscreen - the Dilemma (http://www.youtube.com/watch?v=eeXtGHSt-5o)

lady_express_44
03-07-2009, 07:47 PM
There were 16 countries involved in the study, so Canada, the USA, Australia and NZ would only represent 4.

Either way, it doesn't make sense that Vitamin D deficiency is the culprit, if the wave of relapses came at the end of June in both hemispheres.

The very best time to be outdoors in the Northern hemisphere is Spring, and chances are that is when people get the very most exposure to sunshine; Mar, April, May, June. This is when it is not yet too hot, the days are longer, etc.

Probably the very best time to be outdoors in the Southern hemisphere is throughout Fall to Winter. Chances are that this is when they have the least worry of all about ultraviolet rays, and probably the most exposure to direct sunshine; Mar, April, May, June.

Of ALL the months that people would be having relapses, and IF it is due to reduced Vitamin D levels, June makes the least sense of all for all of us.

Cherie

BBS1951
03-07-2009, 10:33 PM
Ah, but that is assuming that the relapse occurs as the level of D drops. It could be something more complex than that.

mmcc53
03-07-2009, 11:50 PM
I don't understand why the removed relapses occurring on Ist January. Any ideas.
Probably because people putting down January 1st are more likely to not have put in an accurate date, and just put down Jan. 1st to avoid leaving the form blank.

I know people do this because I have done it myself when an answer is a "required field" but I don't know.

lady_express_44
03-08-2009, 01:55 AM
Ah, but that is assuming that the relapse occurs as the level of D drops. It could be something more complex than that.

What, we are to surmise that relapses are most likely to occur 4.5 months after a substantial drop in vitamin D levels, but once vitamin D levels are back in check to their optimum ability . . . ?

Yep, I agree that the disease probably has a much more complex solution than simply trying to fit a round peg in a square hole.

Cherie

notasperfectasyou
03-08-2009, 03:07 AM
Hi Mark,
I haven't seen you here in a long time. Great to see your post. Kim's ABX Neurologist recently wrote her a script for 50k iu/w but we found out it was d2 and he said it was ok to use d3, so Kim is now on 8k/d. I will hope to read your post and the articles more thoroughly next week.
Ken

Ted Hutchinson
03-09-2009, 03:05 PM
Dr. Cannell: I have been a subscriber since the early days, six years ago, and have been following your work with great admiration. I am a medical malpractice attorney in Seattle, Washington diagnosed with multiple sclerosis three years ago. I was told there was no effective treatment. I read hundreds of articles and studies. I read last week where an MS gene has been isolated that is regulated by vitamin D.

I have stopped the progression of my MS by getting my 25(OH)D level to approximately 80 ng/mL (200 nmol/L) and keeping it there for a little over 2 years now. I just had another gadolinium MRI (18 months after the fist "clean" MRI) and I still have no active MS lesions. I have maintained my 25(OH)D level >80 ng/mL throughout, and have obtained serial 25(OH)D levels and blood calcium testing, and have had no increase in blood calcium or other side effects.

The research I have attached strongly suggests that vitamin D may stop the progression of MS, and I have 3 gadolinium MRIs that show that it does work. There are hundreds of thousands of individuals in just the U.S. that will benefit from this therapy, and research shows that there are no side effects to this therapy. There is good science behind this—can you help me get the word out? Kate, Seattle

Yes a number of epidemiological studies suggest vitamin D has a treatment effect in MS, such as fewer exacerbations in the summer, not just a preventative effect. However, we now have more direct evidence that vitamin D helps treat MS. In an open study of 12 patients by Kimball, et al, the number of lesions per patient (assessed with a nuclear magnetic brain scan) decreased in the treatment group from the initial mean of 1.75 to the end-of-study mean of 0.83. Kimball SM, Ursell MR, O'Connor P, Vieth R. Safety of vitamin D3 in adults with multiple sclerosis. Am J Clin Nutr. 2007 Sep;86(3):645–51.

The question is what do you do if you have MS, while we are waiting for more studies? If you have MS, do you wait and see if your MS is going to progress? Does your doctor? In my opinion, it is unethical for doctors to ignore vitamin D deficiency in serious diseases, such as MS, and most doctors do. MS patients should take the initiative themselves, getting their 25(OH)D into the high range of normal (70–90 ng/mL) while we are waiting for more science. This may require up to 10,000 IU/day in some people, an indoor UV light, or a sun tan parlor.

Full text of whole letter (http://www.vitamindcouncil.org/newsletter/2009-march.shtml) With active links.

BBS1951
03-09-2009, 08:37 PM
Hi Ted, FYI I emailed one of the prominent researchers of Vitamin D and asked about whether I can manufacture Vitamin D while swimming. Perhaps you recall that I wondered whether being bathed in the cool pool waters would make it hard to manufacture Vitamin D due to (1) the cooling of the water, and (2) whether it washed away something important on skin surface.

The researcher informed me that there is no problem of the skin making Vitamin D while swimming in the sunshine. This was very good news to me since I swim every day in the sunshine of Florida.

Ted Hutchinson
03-10-2009, 05:32 AM
Hi Ted, FYI I emailed one of the prominent researchers of Vitamin D and asked about whether I can manufacture Vitamin D while swimming. Perhaps you recall that I wondered whether being bathed in the cool pool waters would make it hard to manufacture Vitamin D due to (1) the cooling of the water, and (2) whether it washed away something important on skin surface.

The researcher informed me that there is no problem of the skin making Vitamin D while swimming in the sunshine. This was very good news to me since I swim every day in the sunshine of Florida.But take into account what Dr Cannell has to say here. (http://www.vitamindcouncil.org/newsletter/2009-march.shtml)
These last two studies raise the possibility that sunbathing or using UV lights may not produce much vitamin D if you shower with soap after exposure. Water cleans the body but does not destroy as much sebum, human body oil. When you think about it, God made the perfect body oil for humans—sebum—but humans wash off her body oil and then apply body oils made by the cosmetic industry. I doubt she likes that.

I'd also like to make it clear that water will reduce the penetration of UVB. So the deeper you go the less UVB.

In one relatively clear lake in Ontario, Canada, with a low DOC level of 0.5 milligram (mg) per liter, only about 34% of surface UVB radiation reached a depth of 20 centimeters (cm) (http://goliath.ecnext.com/coms2/gi_0199-2885045/Shedding-light-on-ultraviolet-radiation.html)( 8inches)

So don't think you will make as much D3 as quickly and don't towel or wash it off as soon as you emerge and don't forget also it is a self regulating process and if you stay under UVB longer than is necessary for D3 production that is counterproductive as any/all D3 remaining near the skin surface gets processed on into supra sterols that are not used by the body at all. So It's important, even for people who think they MUST be getting sufficient sunlight exposure to have levels above 60~70ng/mL to get tested regularly to be certain that what you are doing is actually working out and is effective, in practice.

BBS1951
03-10-2009, 07:53 PM
Ok. I will next time I have my check up.

SInce D3 is manufactured inside the skin cells, I do not see how water can "wash" it off.

'Lissa
03-10-2009, 08:53 PM
Here's my theory of why more flare ups occur in the Spring. Our immune cells take a while for the body to manufacture and for them to mature. The cells that are being developed during the winter, when Vit. D is probably at its lowest, are the ones that get unleashed on the body come Spring. Vitamin D is supposed to act as a regulator of properly developed immune cells. If there isn't enough Vit. D while the cells are being "hatched', they don't mature properly and run amok.

I don't claim that this is a scientifically supported theory. It is just my mad ponderings. What do you all think, am I on to something?

BBS1951
03-10-2009, 09:03 PM
Maybe on to marijuana--LOL--Just kidding. Your theory is interesting, but I do not know enough to know if its accurate!