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Kristi 06-18-2008 09:50 PM

Vitamin D and MS ?
 
Earlier, today I got a call from my neuro about a blood test I had last week when I went for my 6 month check-up she wanted to check my Vitamin D level. And she said my level was very low so she prescribed Vit D2 50,000 units,I take one softgel once a week for 6 weeks and then one pill once a month until finished,and then in 8 weeks she do another blood test to check the levels. She's also has me taking calcium pills one pill twice a day. It's kinda scary I've been doing research on this and low levels of vit D and the higher risk of breast cancer and now I really don't want to make a appointment for my first mammagram I've been putting it off for a year now. MS is scary enough for me thank you. I'm just wondering if maybe this is partly why I got MS I know there is a connection with low levels of Vit D and MS.See when I was a little kid I was always out in the sun we had a pool and I was as brown as a bear in the summertime but when I got older I just didn't go out in the sun that much because I burn very easy. I would really like to have your guys opinion on the subject. Thanks Kristi.

lady_express_44 06-18-2008 10:18 PM

Vitamin D deficiencies are the latest "trend" in MS. :cool:

In testing for vitamin D deficiencies, there are two methods that labs use for reporting Vitamin D levels:

1. nanograms per milliliter (ng/mL)
(To convert ng/mL to nmol/l: multiply by 2.5, eg. 40 ng/mL *2.5 = 100 nmol/L)
2. nanomoles per liter [nmol/L]
(To convert nmol/l to ng/mL: divide by 2.5, eg. 100 nmol/L /2.5 = 40 ng/mL)

The optimum levels of vitamin D are defined as:

1. LESS THEN 20 ng/mL (50 nmol/L) is generally considered inadequate.

2. Between 20 (ng/mL) – 100 (ng/mL) is “normal”, by most accounts.

Where someone is deemed deficient (< 2o ng/mL), which can occur because of:

- dietary inadequacy, i.e. exposure to sunlight is limited or diet restrictions (milk allergies/lactose intolerance, vegetarianism, etc.)
- impaired absorption, i.e kidneys cannot convert vitamin D to its active form, or absorption of vitamin D from the digestive tract is inadequate

. . . The "normal" recommended FNB daily intake of vitamin D range is from 200 IU (5 mcg) to 600 IU (15 mcg) . . . dependant on age (as provided by the NIH & Food and Nutrition Board).

The best way to source Vitamin D naturally is by getting 5-30 minutes of DIRECT sun exposure between 10 AM and 3 PM, at least twice a week. This exposure can be to (NOTE: EITHER) the face, arms, legs, or back. However, one must realize that:

- complete cloud cover can reduce UV energy by 50%
- shade (including that which is produced by severe pollution) reduces UV energy by 60%
- Sunscreens with a sun protection factor of 8+ may block vitamin D-producing UV rays (but people generally do not apply sufficient amounts, or reapply their sunscreen frequently enough to cover all sun-exposed skin anyway)

People can also source sufficient vitamin D from their diet:

- fortified foods will provide most of the vitamin D people need, ie. U.S. milk is fortified with 100 IU/cup of vitamin D (which is already 25% - 50% of the daily recommended value, depending on age).
- 1 tbsp of cod liver oil = 1360 IU’s per serving (almost 3 X the average daily recommended requirment)
- The flesh of fish (such as salmon, tuna, and mackerel) = 200 – 350 IU’s per serving
- fish liver oils
- beef liver, cheese, and egg yolks (15 – 60 UI).
- some ready-to-eat breakfast contain added vitamin D, as do some brands of orange juice, yogurt, and margarine, ie. cereal flours and related products, milk and products made from milk, and calcium-fortified fruit juices and drinks.
- moderate use of commercial tanning beds (that emit 2-6% UVB radiation)

There have been some “theories” about lack of vitamin D being contributory to the initial development of MS, based on the “gradient latitude” hypothesis, . . . but the prevalence and distribution of MS has changed so significantly over recent years, that theory is becoming more and more obsolete. There is also no proof what-so-ever that increased vitamin D will affect the disease process in any way.

Can you find out what your vitamin D levels are right now?

Cherie

Kristi 06-18-2008 10:27 PM

Quote:

Originally Posted by lady_express_44 (Post 304471)
Vitamin D deficiencies are the latest "trend" in MS. :cool:

In testing for vitamin D deficiencies, there are two methods that labs use for reporting Vitamin D levels:

1. nanograms per milliliter (ng/mL)
(To convert ng/mL to nmol/l: multiply by 2.5, eg. 40 ng/mL *2.5 = 100 nmol/L)
2. nanomoles per liter [nmol/L]
(To convert nmol/l to ng/mL: divide by 2.5, eg. 100 nmol/L /2.5 = 40 ng/mL)

The optimum levels of vitamin D are defined as:

1. LESS THEN 20 ng/mL (50 nmol/L) is generally considered inadequate.

2. Between 20 (ng/mL) – 100 (ng/mL) is “normal”, by most accounts.

Where someone is deemed deficient (< 2o ng/mL), which can occur because of:

- dietary inadequacy, i.e. exposure to sunlight is limited or diet restrictions (milk allergies/lactose intolerance, vegetarianism, etc.)
- impaired absorption, i.e kidneys cannot convert vitamin D to its active form, or absorption of vitamin D from the digestive tract is inadequate

. . . The "normal" recommended FNB daily intake of vitamin D range is from 200 IU (5 mcg) to 600 IU (15 mcg) . . . dependant on age (as provided by the NIH & Food and Nutrition Board).

The best way to source Vitamin D naturally is by getting 5-30 minutes of DIRECT sun exposure between 10 AM and 3 PM, at least twice a week. This exposure can be to (NOTE: EITHER) the face, arms, legs, or back. However, one must realize that:

- complete cloud cover can reduce UV energy by 50%
- shade (including that which is produced by severe pollution) reduces UV energy by 60%
- Sunscreens with a sun protection factor of 8+ may block vitamin D-producing UV rays (but people generally do not apply sufficient amounts, or reapply their sunscreen frequently enough to cover all sun-exposed skin anyway)

People can also source sufficient vitamin D from their diet:

- fortified foods will provide most of the vitamin D people need, ie. U.S. milk is fortified with 100 IU/cup of vitamin D (which is already 25% - 50% of the daily recommended value, depending on age).
- 1 tbsp of cod liver oil = 1360 IU’s per serving (almost 3 X the average daily recommended requirment)
- The flesh of fish (such as salmon, tuna, and mackerel) = 200 – 350 IU’s per serving
- fish liver oils
- beef liver, cheese, and egg yolks (15 – 60 UI).
- some ready-to-eat breakfast contain added vitamin D, as do some brands of orange juice, yogurt, and margarine, ie. cereal flours and related products, milk and products made from milk, and calcium-fortified fruit juices and drinks.
- moderate use of commercial tanning beds (that emit 2-6% UVB radiation)

There have been some “theories” about lack of vitamin D being contributory to the initial development of MS, based on the “gradient latitude” hypothesis, . . . but the prevalence and distribution of MS has changed so significantly over recent years, that theory is becoming more and more obsolete. There is also no proof what-so-ever that increased vitamin D will affect the disease process in any way.

Can you find out what your vitamin D levels are right now?

Cherie


Thanks Cherie for replying to me good information. I will find out soon what my Vitamin D levels are my neuro also sends my test results in the mail so probably this week or next week I should know.

mom23angels 06-19-2008 06:32 AM

When I went to the MS Expo, the doctor speaking talked about Vitamin D and it's effects on MS. I was born in Mass, so I definitely was in cold weather for most of my life. The theory this man explained was to have your residence closer to the equator BEFORE you're 13. Such as: if you lived in GA for 12 years of your life and then moved to the cold.. you would have the immunity of someone that's "protected" *lol* Unfortunately for me I had 27 yrs of cold Mass. weather and yes it has to do with being in the sun.

There are of course exceptions to this rule.. there was a woman there that moved to a warmer climate before she was 13, but of course she still got MS.

I was getting sick and tired of waiting for dr's to treat my lack of minerals/electrolytes so I started to take Vit. C& E, Magnesium/Zinc/Calcium, B12, Fish Oil, Potassium, etc. to bring all my levels up to normal levels.. I do feel better but taking all these pills - YUCK!

Girlie Girl 06-19-2008 11:42 AM

Kristi, I take vitamin D and Calcium daily because of MS. I don't know if it is helping. Make your appointment for your mammo! It is very important!

jackD 06-19-2008 11:43 AM

Special MS Vit D3 needs
 
For almost ALL MS folks getting MORE than a sufficient amount of Vit D is a VERY VERY good idea.

Taking between 2,000 and 4,000 IUs of Vitamin D3 (Cholecalciferol) will result in VERY favorable changes in blood chemistry. Actual good changes start at 1,000 IUs.

MS folks are "ABNORMAL" i.e. SICK and EXCESS Vit D3 is for them GOOD.

Think "outside normal" when it comes to MS needs. Vit D3 is the best non-Rx version to take. Getting some blood testing done before and after starting a Vit D3 supplementing program is a good idea but not really an absolute necessity. The upper limit for Vit D3 supplementing is 10,000 IUs.

The calcium issue is more complex and varies by gender, age and many other complex things. In my situation I am concerned about excess calcification in soft tissues.

I will post some abstracts/articles to explain some of my comments.

jackD

jackD 06-19-2008 12:51 PM

The benefit in reducing MMP-9s is enormous. They make the hole in the BBB Blood Brain Barrier and cut up myelin. I discussed this in my recent Avonex posting.

They do not mentuion MS in this abstract probably because it was done in 2002 and the MS MMP-9 connection was not published in detail until 2001.

jackD

Quote:

1: QJM 2002 Dec;95(12):787-796

Circulating MMP9, vitamin D and variation in the TIMP-1 response with VDR
genotype: mechanisms for inflammatory damage in chronic disorders?

Timms PM, Mannan N, Hitman GA, Noonan K, Mills PG, Syndercombe-Court D, Aganna
E, Price CP, Boucher(2) BJ.

Departments of. Clinical Biochemistry, Diabetes and Metabolic Medicine and.
Haematology, Barts and The London, Queen Mary's School of Medicine and
Dentistry, University of London and. Department of Cardiology, 'Barts and The
London' NHS Trust, London, UK.

BACKGROUND:Vitamin-D deficiency and vitamin-D receptor genotype (VDR) are risk
factors for several disorders with inflammatory components, including coronary
heart disease (CHD) and diabetes, though the mechanisms involved are unclear.
Aim: To examine the hypothesis that vitamin D status modulates the matrix
metalloproteinase (MMP) system in a population with a high prevalence of vitamin
D deficiency, a situation affecting susceptibility to CHD and diabetes.

DESIGN:
Prospective cross-sectional, interventional and embedded studies.

METHODS:
Circulating MMP2,9, the inhibitor TIMP-1 and C-reactive protein (CRP) were
measured during studies of vitamin-D deficiency as a risk factor for type 2
diabetes and CHD in 171 healthy British Bangladeshi adults, free of known
diabetes or major illness. Vitamin D status, VDR genotype, body-build, blood
pressure, lipid and insulin profiles, glucose tolerance, fibrinogen, PAI-1,
folate and homocysteine were measured. Vitamin-D-deficient subjects were
re-assessed after 1 years' supplementation. MMP, TIMP-1 and CRP levels were
measured in 41 subjects halfway through 5-year follow-up. Independent
determinants of circulating concentrations of MMP9, TIMP-1 and CRP were assessed
by multiple regression analysis.

:wink:RESULTS: Vitamin D status was the sole
determinant of circulating MMP9 (inversely) and an independent determinant of
CRP (inversely). Determinants of TIMP-1 were MMP9, systolic blood-pressure
(directly) and VDR genotype (TaqI). :)Significant reductions in MMP9 (-68%),
TIMP-1 (-38%) and CRP (-23%) concentrations followed vitamin-D supplementation.

DISCUSSION: Vitamin-D insufficiency is associated with increased circulating
MMP2,9 and CRP, correctable by supplementation. This finding provides a possible
mechanism for tissue damage in chronic inflammatory conditions, including and diabetes.

PMID: 12454321 [PubMed - as supplied by publisher]

jackD 06-19-2008 01:04 PM

1000 IU Vit D3 positive effects for MSers
 
Here is one study done at Penn Stata Univ funded by the National Multiple Sclerosis Foundation which back in 2001 showed how Vit D3 supplements can help blood chemistry. This is from their public press release at that time.

jackD



Quote:

Study points to positive results from vitamin D supplements for MS sufferers
University Park, Pa. --- A small study conducted by researchers at Penn State
and Helen Hayes Hospital in New York has shown that:) a daily dose of vitamin D –
1000 IU or two and a half times the recommended dose for adults -- causes
changes in blood chemistry that indicate positive effects for multiple sclerosis
patients
.:)

Dr. Margherita Cantorna, assistant professor of nutrition, says the study has
not been in progress long enough to observe changes in the clinical symptoms of
the disease in the patients who participated. However, blood samples drawn after
just 6 months of Vitamin D supplementation, show an increase in transforming
growth factor beta-1 (TGF-Beta) which is associated with the remission and
suppression of the immune response which produces symptoms in MS patients. In
addition, the researchers found a decrease in interleuken-2 which is associated
with the cells that induce MS.

Cantorna's student, Brett Mahon, a doctoral candidate in nutrition, detailed the
study results today (April 3) at the Experimental Biology 2001 conference in
Orlando, Fla. The paper, "Altered Cytokine Profile in Patients with Multiple
Sclerosis Following Vitamin D Supplementation," is co-authored by Dr. Felicia
Cosman, medical director, Clinical Research Center, S. A. Gordon and J. Cruz,
all of Helen Hayes Hospital, and Cantorna. Mahon is first author.

As a postdoctoral fellow at the University of Wisconsin, Madison, Cantorna and
others had shown, in experiments with mice, that vitamin D supplementation could
completely prevent the development of MS in susceptible animals. After Cantorna
joined the faculty at Penn State, she learned of Dr. Cosman's research program
which centers on investigating whether a low level vitamin D deficiency in MS
patients might account for the incidence of brittle bones.

Cantorna asked Cosman for blood samples from the participating patients to see
if the same changes she had observed in mice also occur in humans who receive
vitamin D supplementation. She found that the results were, in fact, similar at
the blood chemistry level. Multiple sclerosis is an autoimmune disease in which
the victim's own immune system attacks the spinal cord and brain. The disease
afflicts about 350,000 people in the United States alone and its cause is
thought to be a complex interaction of genetics and environmental forces that
are not completely understood.

Cantorna and others hypothesize that one crucial environmental factor involved
in the development of the disease is the amount of sunlight a person receives.
Exposure to sunlight catalyzes the production of vitamin D in the skin. In low
sunlight, the skin produces significantly less vitamin D.

In support of a connection among sunlight, vitamin D and multiple sclerosis,
Cantorna points out that the incidence of the disease is nearly zero near the
equator and increases with latitude in both hemispheres. In addition,
Switzerland has high MS rates at low altitudes and low MS rates at high
altitudes. Ultraviolet light is more intense at higher altitudes, resulting in
the skin manufacturing more vitamin D.

Other evidence of an MS/vitamin D link comes from Norway where MS rates are
higher inland than on the coast where larger quantities of fish are consumed
which are rich in vitamin D.

While Cantorna's research and MS's geographical distribution suggest a
connection between vitamin D and MS, she cautions that the vitamin's exact role
is still unclear.

"I think that if you are an MS patient, it would be best to continue to follow
your personal physician's advice," says the College of Health and Human
Development faculty member. Since vitamin D can be toxic in high doses, it would
not be a good idea to begin taking vitamin D pills available over-the-counter in
large amounts.

"On the other hand, since adequate amounts of vitamin D are difficult to get
from diet and because MS patients often have to stay out of the sun, you might
want to consider taking a vitamin D supplement at the current recommended daily
requirement level. There are potential benefits for bone health and for the
immune system as well."

The project was supported by two grants from the National Multiple Sclerosis
Foundation -- one to Cantorna and the other to Cosman.

starfish 06-19-2008 03:43 PM

Thank you for these studies. It is not easy to find nutrition research that relates to MS.

It is predicted that the minimum requirement for Vitamin D will be increased in 2010, when the decade cycle on nutrition updates is scheduled.

Anytime a nutritional requirement is changed it affects food programs, such as food stamps, WIC, and school lunches to name a few. They try not to change them too frequently.

barb02 06-19-2008 06:25 PM

There was a news story on vitamin D and MS on the news tonight. It dealt with a study that examined twins and preventing MS. You can read it on their web site. Just click on the health search engine.

tkrik 06-19-2008 09:44 PM

Being cognitively challenged at times, that was quite a bit of information to absorb so bear with me if this was in Jack's post. In order to get an adequate amount of D3 one must get an adequate amount of sunlight with ultraviolet B. This is challenging for some in many parts of the country. Not so for the southwestern states. When the weather is cooler, I sit out in the sun for 15 minutes a day give or take. When it is hot, as in now, I will sit by a window. Would sitting by the window be enough?

BTW - I lived most my life on Long Island and CT. Additionally, I know of 4 people that were born and raised in AZ that have MS. So I am not 100% convinced on the vitamin D theory.

watsonsh 06-19-2008 09:52 PM

There is also a good thread on Vitamin D in the vitamin forum.

also I remember an article where they did a test on people in Hawaii (sunny all the time right) and there was a good proportion that had low vitamin D.

So there are people that either do not absorbe well through the sun or dont convert well was what I think it said.

My Vit D was low and I have been supplementing with 1000 iu a day and it has definitely helped with muscle pain and fatigue.

Kristi 06-19-2008 10:25 PM

In Rod we trust Go Blue !!! love it Shelley.Well, I sure hope my Vit D levels will be normal in 8 weeks when my neuro will do another blood test to check my levels again,I wonder if she'll want me to stay on Vit D I don't know because I want to stay on it as it sounds like it really can help me.

Go Blue !!!!!

starfish 06-20-2008 03:34 PM

vit D
 
FYi: I had posted this on another forum in May.

There is a great article on Vitamin D starting on page 44 of May 2008 Cooking Light magazine. It predicts that when the new levels get reset in 2010, they will be increased. ( They don't reset nutrition levels but every 10 years.)

"In the absence of it, you're asking the body to defend itself with one hand tied behind its back."

I was surprised b/c it said that a fair skinned person manufactures as much as 15,000 IU in 30 minutes with optimal sunlight conditions, so that is why they think giving people 10,000 IU as a supplement is okay!

The normal values for daily intake are 200 to 400 IU according to your age, but this information is a decade old.

It gives guidelines on the time of day for the sun to be at a 45 degree angle above the horizon and speaks about those of us who live above the 35 degree of latittude ( North Carolina to Southern California).

An spf of just 8 will block 98 percent of your skin's vitamin D production. So we should not have it on all the time.

They suggest having Vitamin D levels checked with bloodwork for something that insurance usually covers like a cholesterol panel or any other annual test. However they think you should always check with your insurance company first.

Most public libraries have Cooking Light magazine in the periodical area.

starfish 06-20-2008 03:37 PM

FYI: I had posted this in another forum last month.

There is a great article on Vitamin D starting on page 44 of this month's Cooking Light magazine. It predicts that when the new levels get reset in 2010, they will be increased. ( They only reset nutrition level every 10 years.)

"In the absence of it,"... (vitamin D) ..." you're asking the body to defend itself with one hand tied behind its back."

I was surprised b/c it said that a fair skinned person manufactures as much as 15,000 IU in 30 minutes with optimal sunlight conditions, so that is why they think giving people 10,000 IU as a supplement is okay!

The normal values for daily intake are 200 to 400 IU according to your age, but this information is a decade old.

It gives guidelines on the time of day for the sun to be at a 45 degree angle above the horizon and speaks about those of us who live above the 35 degree of latittude ( North Carolina to Southern California).

An spf of just 8 will block 98 percent of your skin's vitamin D production. So we should not have it on all the time.

They suggest having Vitamin D levels checked with bloodwork for something that insurance usually covers like a cholesterol panel or any other annual test. However they think you should always check with your insurance company first.

Most public libraries have Cooking Light magazine in the periodical area.

starfish 06-20-2008 03:42 PM

Tkrik, you would be surprised how people modifiy life in Arizona and Texas.

I have lived in both places. By May it is 105 in Az. You go out very early in the am or late evening, when less direct sun to do anything outside. Cars have tint so the temperature does not get so hot your windows blow out.

I'll never forget TX. I remember sticking my head out the door and it felt like I was putting it in an oven. Only when we could go to the pool club did we go out during the day.

watsonsh 06-20-2008 03:43 PM

Quote:

Originally Posted by Kristi (Post 305281)
In Rod we trust Go Blue !!! love it Shelley.Well, I sure hope my Vit D levels will be normal in 8 weeks when my neuro will do another blood test to check my levels again,I wonder if she'll want me to stay on Vit D I don't know because I want to stay on it as it sounds like it really can help me.

Go Blue !!!!!

Yep Kristi,

Counting down to the start of the season.

If I were you after the 8 weeks I would go on a maintainence dose of like 1000iu a day of D3. Otherwise over time it will just deplete again.

tkrik 06-20-2008 04:13 PM

Starfish - Thank you so much. That is the information I was kind of looking for.

jackD 06-20-2008 06:43 PM

Risk assessment for vitamin D
 
I think it is very unwise for amost anyone to exceed 10,000 IU of Vitamin d3.

I take a total of 4,200 IUs of Vit D3 in supplement form daily.

jackD

p.s UL = Upper Level intake safe amount


Quote:

1: Am J Clin Nutr. 2007 Jan;85(1):6-18.

Risk assessment for vitamin D.

Hathcock JN, Shao A, Vieth R, Heaney R.

Council for Responsible Nutrition, Washington, DC 20036-5114, USA.

The objective of this review was to apply the risk assessment methodology used by the Food and Nutrition Board (FNB) to derive a revised safe Tolerable Upper Intake Level (UL) for vitamin D. New data continue to emerge regarding the health benefits of vitamin D beyond its role in bone.

The intakes associated with those benefits suggest a need for levels of supplementation, food fortification, or both that are higher than current levels. A prevailing concern exists, however, regarding the potential for toxicity related to excessive vitamin D intakes.

The UL established by the FNB for vitamin D (50 microg, or 2000 IU) is not based on current evidence and is viewed by many as being too restrictive, thus curtailing research, commercial development, and optimization of nutritional policy.

Human clinical trial data published subsequent to the establishment of the FNB vitamin D UL published in 1997 support a significantly higher UL.

We present a risk assessment based on relevant, well-designed human clinical trials of vitamin D.

Collectively, the absence of toxicity in trials conducted in healthy adults that used vitamin D dose > or = 250 microg/d (10,000 IU vitamin D3) supports the confident selection of this value as the UL.

PMID: 17209171 [PubMed - indexed for MEDLINE]

tkrik 06-20-2008 07:00 PM

Quote:

Originally Posted by jackD (Post 305922)
I think it is very unwise for amost anyone to exceed 10,000 IU of Vitamin d3.

I take a total of 4,200 IUs of Vit D3 in supplement form daily.

jackD

p.s UL = Upper Level intake safe amount

Too much of a "good" thing can actually be really bad if not toxic. I have seen it over and over. Very sad.

watsonsh 06-20-2008 07:18 PM

Yeah not sure I would exceed 1000 iu a day. Slow and steady is the way I am building mine back up.

starfish 06-20-2008 09:05 PM

This is the most comprehensive information about Vitamin D I have yet to find. As you get towards the bottom ( long) it explains why doses are being given above 2000 IU a day.

It is very interesting because it cites how steroids affect calcium and Vitamin D, and how other medications alter absorption.

http://ods.od.nih.gov/factsheets/vitamind.asp

For more info google: vitamin + D + absorption

Thanks for the article from the Journal of Clinical Nutrition!

Dejibo 06-21-2008 07:22 AM

I cant keep my Vit D level up. I have taken lots of different over the counter stuff too. I was recently placed on Rx stuff. I hope that helps. I already feel better after just a couple of weeks on it.

Bearygood 06-21-2008 12:22 PM

D2 vs. D3
 
Kristi, I'm quite surprised you were prescribed D2 as opposed to D3 (aka Cholecalciferol). D3 is the equivalent to the "sunshine" factor and is processed in the body as a hormone -- it's specifically that form that's been the hot topic.

I started reading a lot about D3 after I was dxed and have been taking a little over 3,000 IUs daily for at least 9 months. (I ADD UP the D in my calcium and mult-vitamin and then supplement with two 1,000 capsules made by Jarrow.) Vitamin D can build up in the body and can be toxic so your levels should be monitored, as well as your liver function. I don't know if my levels were low before I started supplementing but my endocrinologist tested me a few months ago and even with the amount I'm taking, I was still within normal range (and my liver function was fine). However, I will continue to be monitored, having these tests repeated in future blood work. My endo explained to me that for some reason, they're finding that those high 50,000 IU doses weekly do not seem to present the same problems as high doses building up over time.

The RDA UL for "healthy" people has been raised to 600 IUs. There have been several studies about vitamin D (D3 specifically) possibly being helpful with various neurological disorders, not only MS (and not only in terms of prevention). I know many people with MS in the U.S. whose doctors have been recommending (if not prescribing) vitamin D3 to their patients even if their levels are not low. Most of the things I've read about using this supplement like a "drug" recommend up to 4,000 IUs daily but to reduce intake in the summer or if you live in a sunny climate year round. Again, do be careful though -- do your own research, speak to your doctors and if you DO take it, have your D levels and liver function tested periodically.

jackD 06-21-2008 12:41 PM

The dark side & Vit K1 &K2
 
I have recently added Vit K to my supplement list because I found in the
MPEG of my body CT Scan noticeable Calcium deposits around my heart aorta
and some considerable Calcification in my right Femoral Artery.

One of the causes of this is Vitamin D supplementation!!!

Note --- there are different kinds of vit K

K1 (phylloquinone) is present naturally in plants.
K2 (menaquinone) is made by bacteria in the intestinal tract of humans and
animals
K3 (menadione) is man made.
K4 (menadiol) is man made. It can be used by intestinal bacteria to make K2.
Unlike the fat-soluble compounds K1, K2 and K3, K4 is water-soluble

I have discovered that Vit K supplements will stop and help remove this
excess calcium. I also believe that Vinpocetine may have a similar action(at
least in rabbit tests). I am taking the LEF(life Extension Foundation)
"SUPER K with K2" supplement which has 9 mg of Vit K1 and 1 mg of Vit K2

http://www.lef.org/newshop/items/ite...ced-K2-Complex

jackD

Quote:

1: Z Kardiol. 2001;90 Suppl 3:57-63.Links
Role of vitamin K and vitamin K-dependent proteins in vascular calcification.Schurgers LJ, Dissel PE, Spronk HM, Soute BA, Dhore CR, Cleutjens JP, Vermeer C.
Department of Biochemistry, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands.

OBJECTIVES: To provide a rational basis for recommended daily allowances (RDA) of dietary phylloquinone (vitamin K1) and menaquinone (vitamin K2) intake that adequately supply extrahepatic (notably vascular) tissue requirements.

BACKGROUND: Vitamin K has a key function in the synthesis of at least two proteins involved in calcium and bone metabolism, namely osteocalcin and matrix Gla-protein (MGP). MGP was shown to be a strong inhibitor of vascular calcification. Present RDA values for vitamin K are based on the hepatic phylloquinone requirement for coagulation factor synthesis. Accumulating data suggest that extrahepatic tissues such as bone and vessel wall require higher dietary intakes and have a preference for menaquinone rather than for phylloquinone.

METHODS: Tissue-specific vitamin K consumption under controlled intake was determined in warfarin-treated rats using the vitamin K-quinone/epoxide ratio as a measure for vitamin K consumption. Immunohistochemical analysis of human vascular material was performed using a monoclonal antibody against MGP. The same antibody was used for quantification of MGP levels in serum.

RESULTS: At least some extrahepatic tissues including the arterial vessel wall have a high preference for accumulating and using menaquinone rather than phylloquinone. Both intima and media sclerosis are associated with high tissue concentrations of MGP, with the most prominent accumulation at the interface between vascular tissue and calcified material. This was consistent with increased concentrations of circulating MGP in subjects with atherosclerosis and diabetes mellitus.

CONCLUSIONS: This is the first report demonstrating the association between MGP and vascular calcification. The hypothesis is put forward that undercarboxylation of MGP is a risk factor for vascular calcification and that the present RDA values are too low to ensure full carboxylation of MGP.

PMID: 11374034 [PubMed - indexed for MEDLINE]

Quote:

1: J Neurosci. 2003 Jul 2;23(13):5816-26. Links
Novel role of vitamin k in preventing oxidative injury to developing oligodendrocytes and neurons.Li J, Lin JC, Wang H, Peterson JW, Furie BC, Furie B, Booth SL, Volpe JJ, Rosenberg PA.
Department of Neurology, Division of Neuroscience, Children's Hospital, Boston, MA 02115, USA.

Oxidative stress is believed to be the cause of cell death in multiple disorders of the brain, including perinatal hypoxia/ischemia. Glutamate, cystine deprivation, homocysteic acid, and the glutathione synthesis inhibitor buthionine sulfoximine all cause oxidative injury to immature neurons and oligodendrocytes by depleting intracellular glutathione.

Although vitamin K is not a classical antioxidant, we report here the novel finding that vitamin K1 and K2 (menaquinone-4) potently inhibit glutathione depletion-mediated oxidative cell death in primary cultures of oligodendrocyte precursors and immature fetal cortical neurons with EC50 values of 30 nm and 2 nm, respectively. The mechanism by which vitamin K blocks oxidative injury is independent of its only known biological function as a cofactor for gamma-glutamylcarboxylase, an enzyme responsible for posttranslational modification of specific proteins. Neither oligodendrocytes nor neurons possess significant vitamin K-dependent carboxylase or epoxidase activity. Furthermore, the vitamin K antagonists warfarin and dicoumarol and the direct carboxylase inhibitor 2-chloro-vitamin K1 have no effect on the protective function of vitamin K against oxidative injury.

Vitamin K does not prevent the depletion of intracellular glutathione caused by cystine deprivation but completely blocks free radical accumulation and cell death. The protective and potent efficacy of this naturally occurring vitamin, with no established clinical side effects, suggests a potential therapeutic application in preventing oxidative damage to undifferentiated oligodendrocytes in perinatal hypoxic/ischemic brain injury.

PMID: 12843286 [PubMed - indexed for MEDLINE]


Arterial calcification is characterized as a buildup of calcium in the
arterial walls. It is a process that can begin as early as the second decade
of life and continue throughout adulthood. Although calcium is an essential
nutrient in maintaining human bone integrity, the trick is to keep it out of
the arteries. Studies have revealed that adequate levels of vitamin K may
help in keeping calcium in bones and out of arterial walls.



Caution
Those taking anticoagulant drugs such as Coumadin or heparin should avoid
vitamin K supplements.

Bearygood 06-21-2008 12:47 PM

Thanks, Jack. I'd heard about this in regard to calcium supplementation and have been meaning to look to research it more thoroughly. I'm definitely going to mention it to my endocrinologist when I see him in September.

jackD 06-21-2008 01:12 PM

Vinpocetine & MS
 
Here is the rabbit thing plus the Bladder thingie. I take 10mg of Vinpocetine twice a day.

jackD

p.s. It is also the BEST cure for MS(58% reduction in lesion activity) and fixes my bladder problems. There is some considerable hyperboyle in the preceding statement but that is what the study showed.


Quote:

1: J Int Med Res. 1990 Mar-Apr;18(2):142-52.

Calcium, phosphorus and aluminium concentrations in the central nervous system, liver and kidney of rabbits with experimental atherosclerosis: preventive effects of vinpocetine on the deposition of these elements.

Yasui M, Yano I, Ota K, Oshima A.

Division of Neurological Diseases, Wakayama Medical College, Japan.

Calcium, phosphorus and aluminium concentrations in the central nervous system, liver and kidneys were determined in 16 rabbits with atherosclerosis experimentally induced by a cholesterol-rich diet and the protective effect of 3 or 10 mg/kg.day vinpocetine (14-ethoxycarbonyl-(3 alpha,16 alpha-ethyl)-14,15-eburnamenine) given orally on the deposition of these elements was assessed.

Rabbits fed a cholesterol-rich diet developed atherosclerosis after 3 months and these rabbits possessed high concentrations of calcium, phosphorus and aluminium in the central nervous system, determined by neutron activation analysis.

In atherosclerotic rabbits fed a vinpocetine supplement, there was a decrease in concentrations of these elements in tissues.

It is suggested that calcium, phosphorus and aluminium may be implicated in the aetiology of atherosclerosis and that vinpocetine may have a preventive action on the deposition of these elements in central nervous tissue, liver and kidney.

PMID: 2340946 [PubMed - indexed for MEDLINE]

Quote:

1: Mult Scler. 2000 Feb;6(1):56-8.

Drop in relapse rate of MS by combination therapy of three different phosphodiesterase inhibitors.

Suzumura A, Nakamuro T, Tamaru T, Takayanagi T.
Department of Neurology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-0813, Japan.

Phosphodiesterase inhibitors (PDEIs), when used in combination, synergistically suppress TNFalpha production by various cells and also suppress experimental demyelination at very low concentrations.

We conducted a pilot study to determine whether the combination of three PDEIs suppresses the relapse of MS at the usual therapeutic doses. Of the 12 relapsing remitting MS, the mean relapse rate/year dropped remarkably (from 3.08+/-3.32 to 0.92+/-1.86) after PDEI treatment. Seven out of 12 (58.3%) were relapse-free in the follow up period (499+/-142 days).

The combination of three PDEIs can be safe and useful strategy for the future treatment of MS. - 58

PMID: 10694847 [PubMed - indexed for MEDLINE]

Bladder - thingie


Quote:

1: World J Urol. 2000 Dec;18(6):439-43.

Initial clinical experience with the selective phosphodiesterase-I isoenzyme inhibitor vinpocetine in the treatment of urge incontinence and low compliance bladder.

Truss MC, Stief CG, Uckert S, Becker AJ, Schultheiss D, Machtens S, Jonas U.
Department of Urology, Medizinische Hochschule Hannover, Germany. truss.michael@mh-hannover.de

Current pharmacological treatment modalities for urge incontinence and low compliance bladder are limited by a low clinical efficacy and the significant side effects of the standard drugs available. Previous in vitro studies indicated a possible functional relevance of the intracellular phosphodiesterase (PDE)-1 isoenzyme in the regulation of human detrusor smooth muscle contractility.

We therefore investigated the effect of the PDE-1 inhibitor vinpocetine in nonresponders to standard pharmacological therapy. In 11/19 patients (57.9%) clinical symptoms and/or urodynamic parameters were improved. Although these initial data are preliminary, they represent the first evidence that isoenzyme-selective PDE inhibition may be a novel approach to the treatment of lower urinary tract disorders.

PMID: 11204266 [PubMed - indexed for MEDLINE]

Natalie8 06-21-2008 04:15 PM

Quote:

Originally Posted by lady_express_44 (Post 304471)
The best way to source Vitamin D naturally is by getting 5-30 minutes of DIRECT sun exposure between 10 AM and 3 PM, at least twice a week. This exposure can be to (NOTE: EITHER) the face, arms, legs, or back.
Cherie

When I got diagnosed 10 months ago I was told I had an extremely low Vitamin D level. To be perfectly honest I was shocked since I had lived in San Diego for 10 years (sun all the time) and moved to sunny/hot Texas and have been here the past 4 years. Thus, I'm not sure everyone's bodies can get the Vitamin D they need from the sun -- clearly that wasn't the case for me over the past 14 years and I spend a lot of time outdoors.

I took the 50,000 IU pills once a week for 9 weeks. It bumped my level up into low normal range. I am now taking 1,000 IU a day.

The MS specialist I saw at the Mayo Clinic in MN. said that I should be taking Vitamin D supplements every day. The MS specialist I saw in my own city 2 weeks ago said that Vitamin D deficiency is a risk factor for MS (apparently I hit the MS jackpot and as she put it "the stars lined up" because I had 4 risk factors: 1) Vitamin D deficiency 2) grew up in Mass. until age 22 3) mother just diagnosed with MS last year right before me 4) wicked mono/epstein barr infection the year before my diagnosis).
Lucky me! <heavy sarcasm> :rolleyes:

Anyhow, nothing proves that taking Vitamin D after the fact will slow the disease down but why not take the supplement? There does appear to be a correlation of some sort.

Kristi 06-21-2008 08:05 PM

Quote:

Originally Posted by Bearygood (Post 306407)
Kristi, I'm quite surprised you were prescribed D2 as opposed to D3 (aka Cholecalciferol). D3 is the equivalent to the "sunshine" factor and is processed in the body as a hormone -- it's specifically that form that's been the hot topic.

I started reading a lot about D3 after I was dxed and have been taking a little over 3,000 IUs daily for at least 9 months. (I ADD UP the D in my calcium and mult-vitamin and then supplement with two 1,000 capsules made by Jarrow.) Vitamin D can build up in the body and can be toxic so your levels should be monitored, as well as your liver function. I don't know if my levels were low before I started supplementing but my endocrinologist tested me a few months ago and even with the amount I'm taking, I was still within normal range (and my liver function was fine). However, I will continue to be monitored, having these tests repeated in future blood work. My endo explained to me that for some reason, they're finding that those high 50,000 IU doses weekly do not seem to present the same problems as high doses building up over time.

The RDA UL for "healthy" people has been raised to 600 IUs. There have been several studies about vitamin D (D3 specifically) possibly being helpful with various neurological disorders, not only MS (and not only in terms of prevention). I know many people with MS in the U.S. whose doctors have been recommending (if not prescribing) vitamin D3 to their patients even if their levels are not low. Most of the things I've read about using this supplement like a "drug" recommend up to 4,000 IUs daily but to reduce intake in the summer or if you live in a sunny climate year round. Again, do be careful though -- do your own research, speak to your doctors and if you DO take it, have your D levels and liver function tested periodically.

Hi,Bearygood

I don't know why my neuro prescribed vit D2,heck I didn't know there was a
D2 and D3, I just thought there was just Vit D period. I'm glad I started this thread,I've found out alot of good information from alot people here.

jackD 06-23-2008 08:45 PM

Nerve Growth Factor -good Stuff
 
Most folks do not know much about this but NGF Nerve Growth Factor is great stuff to have in sufficient quantity to take care of those small? brain repair jobs common to MS folks.

If you are LOW in Vitamin D then you are probably LOW in NGF Nerve Growth Factor also.

I probably should start a new thread to elaborate on this topic.(Nerve Growth/Repair)

Suffice it to say that Vitamin D makes the body make NGF as stated in the below abstract.

http://www.copewithcytokines.de/cope.cgi?key=NGF (a GREAT sources of my info)

This is why I take 4000 IUs of Vit D3 supplement each day. The excess is GOOD for MS folks because our NEED is greater.

jackD

http://www.ncbi.nlm.nih.gov/pubmed/9...ubmed_RVDocSum

Quote:

1: Nippon Yakurigaku Zasshi. 1997 Oct;110 Suppl 1:39P-43P.

[Novel pharmacological activity of a vitamin (novel pharmacological action of vitamin D)][Article in Japanese]


Fukuoka M, Ohta T, Kiyoki M.
Teijin Institute for Bio-Medical Research, Tokyo, Japan.

The endocrine system to maintain calcium homeostasis involves the active vitamin D, as well as parathyloid hormone (PTH). Based on this 'classical' calcium-regulatory function, 1,25-(OH)2D3 and 1 alpha OHD3 was developed as the drug for vitamin D resistant rickets, renal dystrophy, and osteoporosis. Psoriasis is a chronic skin disease which is characterized by hyperproliferation and abnormal differentiation of epidermis. As an anti-psoriatic drug, 1,24R-(OH)2D3 has been on clinical use. The efficacy for psoriasis is explainable by the differentiation-inducing activity of this compound. 1,25-(OH)2D3 was also reported to suppress proliferation and induce differentiation of tumor cells including breast cancer, colon cancer and so forth, suggesting the possible therapy of malignant tumors.

:)In immune system, active vitamin D3 exerts various effects; 1,25-(OH)2D3 suppresses proliferation and cytokine production in T cells and antibody production in B cells. Animal models of autoimmune diseases and skin-graft suggest active vitamin D becomes a novel immuno suppressant.

:eek: Since 1,25-(OH)2D3 induces the synthesis of nerve growth factor (NGF), it will be a new therapy for the treatment of neuronal degenerative diseases.

PMID: 9503403 [PubMed - indexed for MEDLINE]

jackD 06-24-2008 05:38 PM

NGF - Calcium - The Degenerative Stage of MS
 
Numerous neurotrophic growth factors help determine which neurons develop in the immature brain and which are retained in the adult brain.

Neurotrophic factors can also induce neurons to sprout axons capable of growing into new locations and forming new synaptic connections, a process that continues in the mature brain.

NGF (Nerve Growth Factor) is one essential neurotrophic growth factor. The below links describe how calcium is used in this process and how Glutamate toxicity kills neurons using Calcium in the Second stage of MS.


http://www.psychiatrist.com/pcc/brainstorm/br5904.htm (main article)

http://www.psychiatrist.com/pcc/brainstorm/br5906.htm (therapeutic potential)

http://www.psychiatrist.com/pcc/brainstorm/br5806.htm (Glutamate assassin/excitotoxic neuron murder)

The Second Stage of MS is "The Degenerative Stage" in which "excess Glutamate" runs wild on a killing spree. First phase, of course, is the "Inflammatory Stage" of MS.

http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf

jackD

Kristi 06-24-2008 07:10 PM

Quote:

Originally Posted by jackD (Post 308753)
Numerous neurotrophic growth factors help determine which neurons develop in the immature brain and which are retained in the adult brain.

Neurotrophic factors can also induce neurons to sprout axons capable of growing into new locations and forming new synaptic connections, a process that continues in the mature brain.

NGF (Nerve Growth Facto)r is one essential neurotrophic growth factor. The below links describe how calcium is used in this process and how Glutamate toxicity kills neurons using Calcium in the Second stage of MS.


http://www.psychiatrist.com/pcc/brainstorm/br5904.htm (main article)

http://www.psychiatrist.com/pcc/brainstorm/br5906.htm (therapeutic potential)

http://www.psychiatrist.com/pcc/brainstorm/br5806.htm (Glutamate assassin/excitotoxic neuron murder)

The Second Stage of MS is "The Degererative Stage" in which "excess Glutamate" runs wild on a killing spree. First phase, of course, is the "Inflammatory Stage" of MS.

http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf

jackD


Thanks, Jack for all your good information on the subject.

starfish 06-24-2008 08:21 PM

Hi jackD! You are making want to go to the library and get a biochem book!! I am sure I got rid of my college book when it was 25 years old.

I am concerned that NGF also influences the activity of B and T cells. I would have to understand how a little better.

I did find vitamin D3 at BJs Wholesale Club in 1000 IU capsules. I understand why we may need more.

I very much liked your last link because it had the best graphic explaining the nerve issues with the chemicals and how Copaxone works in certain situations.If anyone has a little knowledge about biochem you really should take a peek.

I don't know how you are finding this material, in its complete form, but I am glad you are sharing it. Its not easy to find more than just an abstract.

I know that our dendrites can grow and elongate,

http://www-als.lbl.gov/als/science/s...9receptor.html

and that is why my neuro told me about Wii actually helping to grow these for folks who can't get enough activity outside of the home.

So to keep this back to Vitamin D, it supports the NGF, if I am interpretting this properly.

jackD 06-24-2008 08:31 PM

Quote:

Originally Posted by starfish (Post 308895)
Hi jackD! You are making want to go to the library and get a biochem book!! I am sure I got rid of my college book when it was 25 years old.

I am concerned that NGF also influences the activity of B and T cells. I would have to understand how a little better.

I did find vitamin D3 at BJs Wholesale Club in 1000 IU capsules. I understand why we may need more.

I very much liked your last link because it had the best graphic explaining the nerve issues with the chemicals and how Copaxone works in certain situations.If anyone has a little knowledge about biochem you really should take a peek.

I don't know how you are finding this material, in its complete form, but I am glad you are sharing it. Its not easy to find more than just an abstract.

I know that our dendrites can grow and elongate,

http://www-als.lbl.gov/als/science/s...9receptor.html

and that is why my neuro told me about Wii actually helping to grow these for folks who can't get enough activity outside of the home.

So to keep this back to Vitamin D, it supports the NGF, if I am interpretting this properly.

THANKS!!

You are right about the Vit D and NGF connection.

That techie site...

http://www.copewithcytokines.de/cope.cgi?key=NGF

says that ...
Quote:

Serum, phorbol 12-myristate 13-acetate (see also: Phorbol esters), and :)vitamin D3 are potent inducers of NGF synthesis. Glucocorticoids inhibit the synthesis of NGF.
.

That comment about Glucocorticoids (STEROIDS) blocking NGF production is a real bummer.

jackD

jackD 06-24-2008 08:54 PM

idebenone - NGF
 
I also take some IDEBENONE to get some extra NGF production in my brain. It is a bit expensive and you need to take 2 caps daily.

jackD

p.s. It a modified form of CQ-10 and is somewhat difficult to find in stores. I hear the rats love the stuff. I can now make it thru the water maze in a flash.

Quote:

1: Naunyn Schmiedebergs Arch Pharmacol. 1994 Apr;349(4):401-7.

Oral administration of idebenone induces nerve growth factor in the brain and improves learning and memory in basal forebrain-lesioned rats.

Nitta A, Murakami Y, Furukawa Y, Kawatsura W, Hayashi K, Yamada K, Hasegawa T, Nabeshima T.

Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine, Japan.

Nerve growth factor plays an important role in the survival and maintenance of cholinergic neurons in the central neuronal system. In senile dementia of the Alzheimer type, learning and memory are impaired by the loss of neurons in the magnocellular cholinergic neuronal system.

It is therefore, of interest to investigate the role of nerve growth factor in this degenerative disorder.

:mad:Since nerve growth factor does not cross the blood-brain barrier and is easily metabolized by peptidases when administered peripherally, it can be used for medical treatment only when directly injected into the brain.

:)We demonstrate here that the oral administration of idebenone, a potent in vitro nerve growth factors synthesis stimulator, induced an increase in nerve growth factor protein and mRNA, and in choline acetyltransferase activity, in basal forebrain lesioned rats, but not in intact rats.

Idebenone also ameliorated the behavioral deficits in habituation, water maze, and passive avoidance tasks in these animals.

:)These results suggest that idebenone stimulated nerve growth factor synthesis in vivo and ameliorates the behavioral deficits which were accompanied with the recovery of the reduced choline acetyltransferase activity in the basal forebrain-lesioned rats.

PMID: 8058112 [PubMed - indexed for MEDLINE]
Quote:

1: Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(4):27-32.Links
[Noben (idebenone) in the treatment of dementia and memory impairment without dementia][Article in Russian]


[No authors listed]
Noben (idebenone) was administered in dosage 120 mg during 6 months to 35 patients, aged from 60 to 86 years, with dementia, Alzheimer's type and mixed type, and with memory disturbances which did not reach the level of dementia. The assessment of patient's state before and after treatment was based on the results of somatic, neurological and psychiatric examination as well as neuropsychological testing and using of psychometrical and other scales. The significant improvement on the MMSE scale was found in patients with mild and moderate dementia.

:)The improvement of daily activity was observed in 27% of patients. The neuropsychological study revealed the improvement of short-term and delayed memory and attention, speech functions, the performance on kinesthetic, spatial and dynamic praxis tests, visual-spatial gnosis, reasoning and writing.

:)The positive therapeutic effect assessed by the CGI scale was observed in 37% of patients, the stable state--in 48%.

PMID: 18454094 [PubMed - in process]

jackD 06-25-2008 10:53 AM

Other reason for taking Vit (K1 & K2) combo
 
Not a bad side effect for something that stops/removes excess calcium deposits from Vit D/calcium supplementing.

jackD


Quote:

1: J Neurosci. 2003 Jul 2;23(13):5816-26.

Novel role of vitamin k in preventing oxidative injury to developing oligodendrocytes and neurons.

Li J, Lin JC, Wang H, Peterson JW, Furie BC, Furie B, Booth SL, Volpe JJ, Rosenberg PA.
Department of Neurology, Division of Neuroscience, Children's Hospital, Boston, MA 02115, USA.

Oxidative stress is believed to be the cause of cell death in multiple disorders of the brain, including perinatal hypoxia/ischemia.

:mad:Glutamate, cystine deprivation, homocysteic acid, and the glutathione synthesis inhibitor buthionine sulfoximine all cause oxidative injury to immature neurons and oligodendrocytes by depleting intracellular glutathione.

:) Although vitamin K is not a classical antioxidant, we report here the novel finding that vitamin K1 and K2 (menaquinone-4) potently inhibit glutathione depletion-mediated oxidative cell death in primary cultures of oligodendrocyte precursors and immature fetal cortical neurons with EC50 values of 30 nm and 2 nm, respectively. The mechanism by which vitamin K blocks oxidative injury is independent of its only known biological function as a cofactor for gamma-glutamylcarboxylase, an enzyme responsible for posttranslational modification of specific proteins. Neither oligodendrocytes nor neurons possess significant vitamin K-dependent carboxylase or epoxidase activity. Furthermore, the vitamin K antagonists warfarin and dicoumarol and the direct carboxylase inhibitor 2-chloro-vitamin K1 have no effect on the protective function of vitamin K against oxidative injury.

:)Vitamin K does not prevent the depletion of intracellular glutathione caused by cystine deprivation but completely blocks free radical accumulation and cell death.

The protective and potent efficacy of this naturally occurring vitamin, with no established clinical side effects, suggests a potential therapeutic application in preventing oxidative damage to undifferentiated oligodendrocytes in perinatal hypoxic/ischemic brain injury.

PMID: 12843286 [PubMed - indexed for MEDLINE

jackD 06-25-2008 01:59 PM

NGF & Vit K1 K2 & neurons
 
Interesting to see how NGF and the Vit Ks work together to protect and enhance neuron outgrowth.

jackD


Quote:

Neurosci Lett. 2002 Apr 19;323(1):9-12.

Novel effect of vitamin K(1) (phylloquinone) and vitamin K(2) (menaquinone) on promoting nerve growth factor-mediated neurite outgrowth from PC12D cells.

Tsang CK, Kamei Y.
Marine and Highland Bioscience Center, Saga University, 152-1 Shonan-cho, Karatsu, 847-0021, Saga, Japan.


The nerve growth factor (NGF)-potentiating effect of K vitamins on PC12D cells was investigated.

Treatment of PC12D cells with vitamin K(1) or K(2) in the presence of NGF significantly enhanced the proportion of neurite-bearing cells and acetylcholinesterase activity compared with NGF treatment alone.

The K vitamins-enhanced neurite outgrowth on PC12D cells was completely blocked by a protein kinase A (PKA) inhibitor or mitogen-activated protein kinase (MAPK) kinase inhibitor PD98059, whereas a protein kinase C inhibitor chelerythrine chloride did not significantly inhibit the enhancing effect of the K vitamins.

These results suggest that the K vitamins enhance neurite outgrowth via the activation of PKA and MAPK-mediated signaling pathways in PC12D cells.

PMID: 11911978 [PubMed - indexed for MEDLINE]

Bentnub 06-25-2008 03:15 PM

glutamate excitotoxicity
 
Neurologische Universitätsklinik, Robert-Koch-Strasse 40, D-37075 Göttingen, Germany.

Axonal destruction and neuronal loss occur early during multiple sclerosis, an autoimmune inflammatory CNS disease that frequently manifests with acute optic neuritis. Available therapies mainly target the inflammatory component of the disease but fail to prevent neurodegeneration. To investigate the effect of minocycline on the survival of retinal ganglion cells (RGCs), the neurons that form the axons of the optic nerve, we used a rat model of myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis. Optic neuritis in this model was diagnosed by recording visual evoked potentials and RGC function was monitored by measuring electroretinograms. Functional and histopathological data of RGCs and optic nerves revealed neuronal and axonal protection when minocycline treatment was started on the day of immunization. Furthermore, we demonstrate that minocycline-induced neuroprotection is related to a direct antagonism of multiple mechanisms leading to neuronal cell death such as the induction of anti-apoptotic intracellular signalling pathways and a decrease in glutamate excitotoxicity. From these observations, we conclude that minocycline exerts neuroprotective effects independent of its anti-inflammatory properties. This hypothesis was confirmed in a non-inflammatory disease model leading to degeneration of RGCs, the surgical transection of the optic nerve.

PMID: 17239606 [PubMed - indexed for MEDLINE]

jackD 06-25-2008 04:36 PM

Quote:

Originally Posted by Bentnub (Post 309456)
Neurologische Universitätsklinik, Robert-Koch-Strasse 40, D-37075 Göttingen, Germany.

Axonal destruction and neuronal loss occur early during multiple sclerosis, an autoimmune inflammatory CNS disease that frequently manifests with acute optic neuritis. Available therapies mainly target the inflammatory component of the disease but fail to prevent neurodegeneration. To investigate the effect of minocycline on the survival of retinal ganglion cells (RGCs), the neurons that form the axons of the optic nerve, we used a rat model of myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis. Optic neuritis in this model was diagnosed by recording visual evoked potentials and RGC function was monitored by measuring electroretinograms. Functional and histopathological data of RGCs and optic nerves revealed neuronal and axonal protection when minocycline treatment was started on the day of immunization. Furthermore, we demonstrate that minocycline-induced neuroprotection is related to a direct antagonism of multiple mechanisms leading to neuronal cell death such as the induction of anti-apoptotic intracellular signalling pathways and a decrease in glutamate excitotoxicity. From these observations, we conclude that minocycline exerts neuroprotective effects independent of its anti-inflammatory properties. This hypothesis was confirmed in a non-inflammatory disease model leading to degeneration of RGCs, the surgical transection of the optic nerve.

PMID: 17239606 [PubMed - indexed for MEDLINE]


THANKS!

Targeting "things" to reduce BOTH Inflammation and glutamate excitotoxicity makes a lot of sense.

I am not a fan of minocycline treatment because I feel that it's main benefit comes from reducing MMP-9s and the damage the MMP-9s do in the MS's destructive processes. I have been researching safe ways to reduce glutamate excitotoxicity via a number of common supplements.

I hope you realize that it is NOT the antibiotic nature of minocycline that provides its MS benefit. I would not take it or recommend taking it for a long period of time. There are better & safer alternatives.

jackD

Quote:

Breakthrough in research for multiple sclerosis (MS)
28 Oct 2004

Paratek Pharmaceuticals, Inc announced results of preclinical studies demonstrating that a new class of compounds, orally available non-antibacterial tetracyclines, has shown promising activity in a preclinical animal model of multiple sclerosis (MS). Affecting approximately two million people worldwide, MS is a chronic, inflammatory condition of the nervous system and the most common, non-traumatic, neurological disease in young adults. Dr. David McKenney, a Paratek scientist, will present the findings during an oral presentation at 2:30 p.m. PST (5:30 p.m. EST) today at Neuroscience 2004, the Society for Neuroscience's 34th Annual Meeting in San Diego.
For the first time, Paratek is presenting data showing that its non-antibacterial tetracycline compounds in a preclinical model of MS have efficacy comparable to minocycline, an antibiotic also in the tetracycline family. A previous clinical study directed by Dr. Luanne Metz at the University of Calgary has demonstrated disease protection in MS patients treated with minocycline. Unfortunately, long-term treatment with minocycline or any other broad-spectrum antibiotics causes many patients to experience intolerability related to antibiotic side effects. In today's presentation, Paratek will report that three non-antibacterial tetracycline compounds, with different structures, demonstrated activity in reducing limb paralysis in the preclinical EAE (Experimental Autoimmune Encephalomyelitis) model of MS. These compounds have no detectable antibacterial activity.

Paratek Pharmaceuticals, Inc. and Serono (virt-x: SEO and NYSE: SRA) announced today that they have entered into an agreement to discover, develop and commercialize an orally-available disease modifying treatment for multiple sclerosis (MS). The agreement covers the compounds for which Dr. McKenney presents data today.

Stuart Levy, Paratek's Vice Chairman, Chief Scientific Officer and Co-Founder, commented, "The clinical research community has long regarded a pill for MS as an ultimate goal, but so far attempts to develop a safe, feasible, orally available drug candidate have failed. Our team has successfully modified the tetracycline molecule, keeping the core structure that confers anti-MS activity while removing portions of the molecule with antibacterial effects. This represents an exciting advance not only for MS, but potentially for many other inflammation-related disease areas. "

Dr. Michael Draper, Associate Director at Paratek, stated, "Paratek has developed world-class expertise in modifying the tetracycline class, which has a 30-year track record in the marketplace and a favorable, well-documented safety profile. This new, proprietary class of non-antibacterial tetracycline compounds will avoid the negative consequences associated with long-term antibiotic use and will not further contribute to the development of antibiotic resistance. We believe that these highly active, orally available compounds will also prove to be well-tolerated for MS, and we are very proud of this accomplishment."

About Multiple Sclerosis

Multiple sclerosis is a chronic, inflammatory condition of the nervous system and is the most common non-traumatic neurological disease in young adults. Multiple sclerosis may affect approximately two million people worldwide. While symptoms can vary, the most common symptoms of multiple sclerosis include blurred vision, numbness or tingling in the limbs and problems with strength and coordination. The relapsing forms of multiple sclerosis are the most common.

About Paratek Pharmaceuticals
Paratek Pharmaceuticals, Inc. is engaged in the discovery and commercialization of new therapeutics that treat serious and life-threatening diseases, with a particular focus on the growing worldwide problem of antibiotic resistance. Paratek's lead programs are advancing novel compounds that can circumvent or block bacterial resistance, as well as drugs that can prevent infection by interfering with Multiple Adaptational Response (MAR) mechanisms in bacteria. Out of these efforts, Paratek has discovered a new class of antibiotics, the aminomethylcyclines that target the need for new and potent antibacterials to overcome the problem of rapidly growing bacterial resistance. The Company's lead antibiotic clinical candidate, BAY 73-7388, the first product from this class, is being developed in a collaborative partnership with Bayer HealthCare AG for the treatment of serious infections.

Outside the antibacterial therapeutic area, Paratek has also established an internal effort to exploit its novel families of compounds and their unique mechanism of action in selected anti-inflammatory and neurodegenerative conditions. Paratek has an active chemical synthesis effort to produce novel and diverse small molecules, with the goal of developing non-antibacterial products with improved activity in serious diseases based upon a growing body of clinical and basic research supporting this approach.

Paratek is privately held and headquartered in Boston, Massachusetts, USA. For more information, visit Paratek's website at http://www.paratekpharm.com

Multiple Sclerosis - Paratek is developing orally available non-antibacterial tetracyclines for the treatment of multiple sclerosis (MS). These compounds are disease modifying agents to reduce demyelination, relapses and progression in patients suffering from various forms of MS, including relapsing and remitting MS. This effort follows the recent publication of very favorable clinical data with minocycline (reference 26). Paratek’s novel compounds offer the potential to show improved activity but without the side effects associated with broad spectrum antibiotics, which can be a problem with long-term use of minocycline. Paratek established a Collaborative Research and License Agreement with Serono SA in October 2004 to develop novel and improved tetracycline derived compounds for MS. Paratek presented data on its novel non-antibacterial tetracycline derivatives in the EAE model in October 2004 Lead candidate compounds for preclinical development are expected to be designated by mid 2006.
The second stage of MS -THE NEURODEGENERATIVE STAGE - where the excess glutamate kills neurons.

http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf

Below pic/chart is from this report. NOTE EXCESS GLUTAMATE

http://home.ix.netcom.com/~jdalton/two%20stage%20MS.jpg

karilann 06-26-2008 05:51 PM

vitamin D3
 
I asked my doc to check my levels and they were excessively low. She put me on the mega dose for awhile and now I take 1000IU a day to maintain. I don't feel any different, but I do believe no one should have low levels of anything without paying consequences later on.
I grew up in Michigan so enough said.
Perhaps people with low vit D levels get sick....or maybe sick people develope low levels of vit D.....I'm not sure...but getting your levels up is optimal.


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