This Is MS Multiple Sclerosis Knowledge & Support Community

Marcia
Do you feel better when you are in Florida? I definitely do, which is why we moved from Ohio. Get your husband to move! You will be glad you did!
Lori

The little bit of what we consider cold weather here in Texas hurts me so bad. I don't know how people in the northern areas do it? If the temp get below 60 degs I am looking fo a coat. I go fishing just about every weekend and I feel so much better after a good afternoon in my boat in the sun. It is normally 95 degs here with 100% humidity. The wonderful Gulf breeze! Gotta love it.[/b]

so being from 'the north' as it were, i am still wondering why i can get such a fierce sunburn on my face in winter, working outdoors as i do, and still not be making vitamin D. i mean, i could look it up i'm sure it's just x and y amounts of energy input needed for pigmentation vs d3 production, but i guess i'm just lazy

Do you feel better when you are in Florida?

Yes I do! I can get out of the house and breathe fresh air. I'm from Kentucky and the bone chilling cold winters which spill into April and begin in September make me stiff and uncomfortable. I feel that for 6 or so months out of the year I'm a hermit cooped up in my house. It's not the way I want to live. Any ammunition you can give me to support my position on moving I'll gladly use.

Thanks!
Marcia

Talking about skin pigmentation. Strange, but I have slightly redish/blonde hair. Normally people with my hair color you would associate with having light colored skin, but in my case I have a dark tan. My neuro is always saying how dark I am for someone with my hair color. For what it worth. arti

This is fascinating. I take 4000IU per day while my wife and daughter each take 2000 per day. I hope that's enough to shield my little girl from possible MS. I about cried when I read that if it's the father that has it, the offspring are more likely than if it is the mother. I quit putting sunscreen on her years ago. When I was growing up, we would burn the first day, and then we would just be dark brown all summer. Every time I see parents just hammering their kids with 50 SPF every half hour I always want to tell them to back off a bit. Now I think I'll just give them this article!

I worry about my five year old son. he is sandy blonde with extremely dark skin. his mother is french/coonass. i hope you all know what a coonass is!!!LMAO....arti

OK....I live in southern California, and the weather is really beautiful here all year round (Please don't hate me!) I was just in West Palm last week too, visiting my Dad. We played tennis, and I got quite a burn!

My Californian husband has had three basal cell sites cut off his face and torso. He's been outside in the sun his whole life, and he got MS. I KNOW his MS isn't from lack of vitamin D thru his skin, but maybe through his digestive system. I think leaky gut and malabsorption were the culprits in his vitamin imbalances.

Lew, PLEASE put sunscreen on your precious daughter...fifteen minutes w/out suncreen a day is all she needs. You can also give her more vitamin D fortified food and milk. Melanoma isn't any better than MS. My socal son is at the beach all summer, and he wears a rash guard shirt and sunscreen...and I'm not worried about his vit. D levels, because he's outside everyday. No need to burn, folks!

-the very fortunate Calfornian cheerleader

I do wear sunscreen especially on my face at SPF 30. I put SPF 50 on my kids when they go outside especially when swimming and they still come home with a beautiful tan. Of course I do not. I am as fair skinned as they come. My freckles get darker but that's all. I'm of germanic descent with brown hair, blue eyes, and fair skin. Do you think my skin might just have problems accepting vitamin D?

Marcia

nope i don't think so... light young skin makes vit d the best. the older you get, the less you make. the darker you are, the more clothing you wear (duh), the more you are inside, the worse your vitamin d status.
of course vitamin d is not the single determining factor in whether someone gets cancer (or other inflammatory condition) but it's looking like it's a big chunk.
if your levels are low after being out in the sun with pale skin, then i'd have to hypothesize some kind of failure in the hydroxylation processes in the liver and kidney?

hmm let me see if i can find that reference... it's about clothing and skin colour and d... ah ha, grover and morley... WOW awesome i can link you right to a table (box 2) i used in an essay in '06!
http://www.mja.com.au/public/issues/175 ... .html#box2

G'day people. The results are in from Direct-MS'ssponsored trial outlined here.

A Phase I/II Dose Escalation Trial of Oral Vitamin D3 with Calcium Supplementation in Patients with Multiple Sclerosis

Jodie M. Burton, Samantha Kimball, Reinhold Vieth, Amit Bar-Or, Montreal, QC, Canada, Hans-Michael Dosch, Louise Thibault, Sally Kilborn, Ste. Anne de Bellevue, QC, Canada, Cheryl D'Souza, Melanie Ursell, Paul O'Connor, Toronto, ON, Canada

OBJECTIVE: The main objective of the trial was to determine the safety of high-dose vitamin D3 (VD3) in Multiple Sclerosis (MS).

BACKGROUND: A clear inverse relationship exists between VD3 status and the probability of developing MS, likely through VD3 s immunoregulatory effects. If VD3 plays a role in MS development, it may also play a beneficial role after MS has developed, but a safe, effective dose must be established.

DESIGN/METHODS: This prospective controlled phase I/II 52-week trial matched clinically definite MS patients for age, gender, MS duration, EDSS, disease modifying drugs, and MS subtype. Patients were randomized to treatment or control groups. Treatment patients started at VD3 doses of 4,000 IU/d and escalated over 28 weeks to 40,000 IU/d. They were then maintained on 10,000 IU/d for 12 weeks, 4,000 IU/d for 8 weeks and a 4-week wash out. Calcium was given throughout the trial. The primary endpoint was mean change in serum calcium concentration in treatment patients over the year. Secondary endpoints included change in 25(OH)D, parathyroid hormone and urinary calcium/creatinine. EDSS and relapse rate were also evaluated, as were cytokine profiles, lymphocyte assays and matrix metalloproteinases across VD3 doses and between treatment and control groups.

RESULTS: Fifty patients were enrolled, with mean age 40.5y (21-54), EDSS 1.25 (0-6.5), and baseline 25(OH)D of 78nmol/L ( 27). Groups were balanced at baseline on all relevant parameters. Two patients dropped out, one before screening and one (treatment) at visit 3 for reasons unknown. With a mean serum 25(OH)D of 409nmol/L ( 152) at 40,000 IU/d, no hypercalcemia occurred nor did persistent hypercalciuria, with no significant differences in serum calcium values between the two groups. A trend of greater reduction in annualized relapse rate favoured treatment patients. Immunological results will be presented.

CONCLUSIONS/RELEVANCE: High-dose VD3 appears to be safe and tolerable in MS patients. Supported by: Direct-MS.

Category - MS and Related Diseases

SubCategory - Clinical Science

This following is another study conducted by some of the same researchers as the above trial. It was NOT funded by Direct-MS. Sorry for the confusion.

1: Am J Clin Nutr. 2007 Sep;86(3):645-51.

Safety of vitamin D3 in adults with multiple sclerosis.

Kimball SM, Ursell MR, O'Connor P, Vieth R.

Department of Nutritional Sciences, University of Toronto, Toronto, Canada. samantha.kimball@utoronto.ca

BACKGROUND: Vitamin D3 may have therapeutic potential in several diseases, including multiple sclerosis. High doses of vitamin D(3) may be required for therapeutic efficacy, and yet tolerability--in the present context, defined as the serum concentration of 25-hydroxyvitamin D [25(OH)D] that does not cause hypercalcemia--remains poorly characterized. OBJECTIVE: The objective of the study was to characterize the calcemic response to specific serum 25(OH)D concentrations.

DESIGN: In a 28-wk protocol, 12 patients in an active phase of multiple sclerosis were given 1200 mg elemental Ca/d along with progressively increasing doses of vitamin D3: from 700 to 7000 microg/wk (from 28,000 to 280,000 IU/wk). RESULTS: Mean (+/- SD) serum concentrations of 25(OH)D initially were 78 +/- 35 nmol/L and rose to 386 +/- 157 nmol/L (P < 0.001). Serum calcium concentrations and the urinary ratio of calcium to creatinine neither increased in mean values nor exceeded reference values for any participant (2.1-2.6 mmol/L and <1.0, respectively). Liver enzymes, serum creatinine, electrolytes, serum protein, and parathyroid hormone did not change according to Bonferroni repeated-measures statistics, although parathyroid hormone did decline significantly according to the paired t test. Disease progression and activity were not affected, but the number of gadolinium-enhancing lesions per patient (assessed with a nuclear magnetic brain scan) decreased from the initial mean of 1.75 to the end-of-study mean of 0.83 (P = 0.03).

CONCLUSIONS: Patients' serum 25(OH)D concentrations reached twice the top of the physiologic range without eliciting hypercalcemia or hypercalciuria. The data support the feasibility of pharmacologic doses of vitamin D3 for clinical research, and they provide objective evidence that vitamin D intake beyond the current upper limit is safe by a large margin.
PMID: 17823429 [PubMed - indexed for MEDLINE]


As the abstact states, the subjects were initally given 4,000 IU/d and at trial end, 40,000 IU/d. For optimal immunoregulation as suggested here and here, Direct-MS advocates taking 4,000 IU/d.

Cheers
Nick

G'day people. The results are in from Direct-MS'ssponsored trial outlined here.

A Phase I/II Dose Escalation Trial of Oral Vitamin D3 with Calcium Supplementation in Patients with Multiple Sclerosis

Jodie M. Burton, Samantha Kimball, Reinhold Vieth, Amit Bar-Or, Montreal, QC, Canada, Hans-Michael Dosch, Louise Thibault, Sally Kilborn, Ste. Anne de Bellevue, QC, Canada, Cheryl D'Souza, Melanie Ursell, Paul O'Connor, Toronto, ON, Canada

OBJECTIVE: The main objective of the trial was to determine the safety of high-dose vitamin D3 (VD3) in Multiple Sclerosis (MS).

BACKGROUND: A clear inverse relationship exists between VD3 status and the probability of developing MS, likely through VD3 s immunoregulatory effects. If VD3 plays a role in MS development, it may also play a beneficial role after MS has developed, but a safe, effective dose must be established.

DESIGN/METHODS: This prospective controlled phase I/II 52-week trial matched clinically definite MS patients for age, gender, MS duration, EDSS, disease modifying drugs, and MS subtype. Patients were randomized to treatment or control groups. Treatment patients started at VD3 doses of 4,000 IU/d and escalated over 28 weeks to 40,000 IU/d. They were then maintained on 10,000 IU/d for 12 weeks, 4,000 IU/d for 8 weeks and a 4-week wash out. Calcium was given throughout the trial. The primary endpoint was mean change in serum calcium concentration in treatment patients over the year. Secondary endpoints included change in 25(OH)D, parathyroid hormone and urinary calcium/creatinine. EDSS and relapse rate were also evaluated, as were cytokine profiles, lymphocyte assays and matrix metalloproteinases across VD3 doses and between treatment and control groups.

RESULTS: Fifty patients were enrolled, with mean age 40.5y (21-54), EDSS 1.25 (0-6.5), and baseline 25(OH)D of 78nmol/L ( 27). Groups were balanced at baseline on all relevant parameters. Two patients dropped out, one before screening and one (treatment) at visit 3 for reasons unknown. With a mean serum 25(OH)D of 409nmol/L ( 152) at 40,000 IU/d, no hypercalcemia occurred nor did persistent hypercalciuria, with no significant differences in serum calcium values between the two groups. A trend of greater reduction in annualized relapse rate favoured treatment patients. Immunological results will be presented.

CONCLUSIONS/RELEVANCE: High-dose VD3 appears to be safe and tolerable in MS patients. Supported by: Direct-MS.

Category - MS and Related Diseases

SubCategory - Clinical Science

This is another study conducted by some of the same researchers as the above trial. It was NOT funded by Direct-MS. Sorry for the confusion.

1: Am J Clin Nutr. 2007 Sep;86(3):645-51.

Safety of vitamin D3 in adults with multiple sclerosis.

Kimball SM, Ursell MR, O'Connor P, Vieth R.

Department of Nutritional Sciences, University of Toronto, Toronto, Canada. samantha.kimball@utoronto.ca

BACKGROUND: Vitamin D3 may have therapeutic potential in several diseases, including multiple sclerosis. High doses of vitamin D(3) may be required for therapeutic efficacy, and yet tolerability--in the present context, defined as the serum concentration of 25-hydroxyvitamin D [25(OH)D] that does not cause hypercalcemia--remains poorly characterized. OBJECTIVE: The objective of the study was to characterize the calcemic response to specific serum 25(OH)D concentrations.

DESIGN: In a 28-wk protocol, 12 patients in an active phase of multiple sclerosis were given 1200 mg elemental Ca/d along with progressively increasing doses of vitamin D3: from 700 to 7000 microg/wk (from 28,000 to 280,000 IU/wk). RESULTS: Mean (+/- SD) serum concentrations of 25(OH)D initially were 78 +/- 35 nmol/L and rose to 386 +/- 157 nmol/L (P < 0.001). Serum calcium concentrations and the urinary ratio of calcium to creatinine neither increased in mean values nor exceeded reference values for any participant (2.1-2.6 mmol/L and <1.0, respectively). Liver enzymes, serum creatinine, electrolytes, serum protein, and parathyroid hormone did not change according to Bonferroni repeated-measures statistics, although parathyroid hormone did decline significantly according to the paired t test. Disease progression and activity were not affected, but the number of gadolinium-enhancing lesions per patient (assessed with a nuclear magnetic brain scan) decreased from the initial mean of 1.75 to the end-of-study mean of 0.83 (P = 0.03).

CONCLUSIONS: Patients' serum 25(OH)D concentrations reached twice the top of the physiologic range without eliciting hypercalcemia or hypercalciuria. The data support the feasibility of pharmacologic doses of vitamin D3 for clinical research, and they provide objective evidence that vitamin D intake beyond the current upper limit is safe by a large margin.
PMID: 17823429 [PubMed - indexed for MEDLINE]


As the abstact states, the subjects were initally given 4,000 IU/d and at trial end, 40,000 IU/d. For optimal immunoregulation as suggested here and here, Direct-MS advocates taking 4,000 IU/d.

Cheers
Nick

good stuff nick. is there anything in the works for the magnesium connection to d3 and calcium?

Not that I am aware of.

Nick wrote: Liver enzymes, serum creatinine, electrolytes, serum protein, and parathyroid hormone did not change according to Bonferroni repeated-measures statistics, although parathyroid hormone did decline significantly according to the paired t test.

Thanks for the info, Nick.

Good catch, JL....they need to add magnesium to the mix in order to avoid hypoparathyroidism.

Low levels of parathyroid can be caused by too little magnesium-

The element magnesium is closely related to the action of calcium in the body. When magnesium levels are too low, calcium levels may also fall. It appears that magnesium is important for parathyroid cells to make PTH normally.
http://parathyroid.com/hypoparathyroidism.htm

mg!
AC