[Natalie8]

This was just published a few days ago. Preliminary suggestions only but still very interesting.

http://www.ctv.ca/servlet/ArticleNew...90524/20090525

[AfterMyNap]

Interesting article, it would be cool if they did a study with a larger sample, 25 is such a small population.


This one paragraph caught my attention:

Recent research has found that proteins activated by vitamin D attach to a certain type of DNA, called DRB1-1501, which is believed to cause the disease.

I've never heard this claim, has anyone else?

[SandyC]

I haven't heard that either Cin. I heard some time ago there was a defective gene they were looking at that is sometimes passed through families. I wonder if that is the one?

Jim's was put on D3 for low VitD just recently. I was pushing for it since I also heard low VitD is related to more pain in spinal cord patients. Interesting.

[mrsD]

I put up a comment about this here.

http://neurotalk.psychcentral.com/thread88283.html

The information continues to come in about Vit D and its potential for improving health.

I find it interesting that very little negative information is coming forth as well.

So we can only read the studies, and be monitored by a doctor,
while trying high Vit D treatments.

There has just been a Vit D3 topical ointment approved in US for psoriasis. (in the previous years, only one patient developed hypercalcemia with topical D that I read about.)
http://www.vectical.com/?gclid=CLi8s...FSQeDQodMRZoCQ
The risk of hypercalcemia accompanies this new ointment.
Previously, Vit D ointments were not considered safe. But newer studies are showing different results.
It might be that eventually, all of us may be using this rather than oral capsules. I see this coming in 5 or more years, based on if there is a lack of toxicity with this new product.

[Dejibo]

wouldnt you have to worry about kidney stones?

[mrsD]

Not everyone gets hypercalcemia from Vit D ointments/supplements. It is a potential, but not that common.

Kidney stones (most of them anyway) are formed from high oxalate in the diet. --this is for calcium oxalate stones.

There are also uric acid stones.

pH of the urine may cause them -- citrate supplements are used
sometimes for calcium oxalate stones.

For the calcium oxalate ones, giving calcium citrate may prevent them. Eating a low oxalate diet too. It is believed that the excess oxalate may come from foods eaten, when the beneficial organism Oxalobacter formigenes dies from antibiotic use. Also vitamin B6 for some reason helps kidney stone prone patients prevent them. (for some odd reason).

There are some kidney stones that have bacteria as centers, and it is thought that they begin the process for some people.

The old belief that high calcium causes stones, is just not the total reasons for them. Calcium can be lost thru the urine commonly. The common diuretic furosemide (Lasix) causes a loss of calcium thru the urine.

[lady_express_44]

Then you run into studies like this:

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.

That doesn't make sense . . . since June is "fall" in the southern hemisphere (following a ton of sun), and is after a few months of tolerable sunshine that we would most be exposed to in the northern hemisphere. Many of us might stay indoors in July/Aug, cause it's too hot, but June is a great month for having seen enough sun ....

You'd think it would be late fall or winter that we would have the most relapses, if it was due to lack of vitamin D.

Cherie

[mrsD]

That is interesting.

There is a circadian trigger for cluster headache. Spring and fall.
The specialty headache clinics are using melatonin for it, as one treatment.

Also I attended a pain conference (including the cluster headache info last Friday) and they had information about central pain states and receptors.

1) The changing estrogen levels (drops) in female brains can be correlated to triggering migraines (in genetically prone women, not all women) and also may be a factor in fibromyalgia.

2) using opiates for head pain, stimulate glial cells which actually release inflammatory trigger molecules which create MORE pain.

It is possible that Vit D is acting as a hormone in the brain and that day length, light stimulation of the retina where melatonin receptors are, may be involved. Recently studies have found melatonin receptors in the pancreas, and so this circadian action may involve glucose levels as well.

The melatonin information is very interesting of late. It appears that melatonin does much more than facilitate sleep.

Here is a link to the estrogen connection/pain:
http://www.med.umich.edu/opm/newspag.../painbrain.htm

BTW melatonin is synthesized from serotonin, using MethylB12 as a cofactor. So people who do not have adequate B12 will have poor or little melatonin to work with.

[Kitty]

I found this article......it's got some interesting info:

http://www.nutritionalwellness.com/a...06_vasquez.php

What are the consequences of long-term vitamin D deficiency? The answer to this question has become increasingly clear in the past few years. Actually, the first evidence in support of sun exposure as a source of vitamin D was published in 1941 by Apperly, who showed in the journal Cancer Research that cancers of various types were much less frequent in populations that lived closer to the equator. Since then, additional research has shown that vitamin D deficiency is a risk factor for breast cancer, prostate cancer, and numerous autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, and type-1 diabetes. The most convincing study ever published on this topic was authored by Hypponen and colleagues in the November 2001 issue of The Lancet. In this remarkable study, the investigators administered 2,000 IU of vitamin D per day to more than 10,000 infants, who were supposed to receive the vitamin D supplement every day for the first entire year of life. Thereafter, the risk of developing type-1 diabetes was calculated and a dose-response relationship was established. The results showed a positive dose-response relationship: the more regularly vitamin D was consumed, the greater the protection afforded against the development of type-1 diabetes. Children who were given vitamin D supplements on a regular basis had their risk of type-1 diabetes reduced by an amazing 88 percent! No adverse effects were noted.

[Bearygood]

Well, definitely interesting to me since I'm holding the radiologist's report from my newest MRI in my hand. As some of you know, I found out I was vitamin D deficient last month after being normal the month before. Yup, you guessed it -- at least according to the radiologist's report I have a new lesion, actually, a non-enhancing black hole. I've felt okay in the 15 months in-between MRIs and I'm not going to worrry about this, at least until I see my neuro-ophthalmologist tomorrow. Even my lower eyelid twitching has subsided. BUT -- of course I wonder if there could be a relationship to this new lesion and the deficiency. And even in regard to the eyelid thing and some of the intermittent fasciculations, the new lesion (or black hole) is in the right posterior frontal lobe which I believe affects pre-motor and motor functions. Almost makes too much sense, doesn't it? Anyway, I'll find out more tomorrow and as for my deficiency, my new blood test will be this month.

Thanks for continuing to post vitamin D (D3) info. as it comes in. I know I was definitely deficient before I was diagnosed but have no idea for how long. I had many lesions, none enhancing, and other than my Optic Neuritis, I've never had a clear relapse. (And my MS specialist still says that was NOT a relapse. ).