A half-dozen papers on this back to 1991. Yet we never heard of it?


1: Brain Res Mol Brain Res. 2002 Dec;108(1-2):143-6.

1,25-Dihydroxyvitamin D(3) increases striatal GDNF mRNA and protein expression
in adult rats.

Sanchez B, Lopez-Martin E, Segura C, Labandeira-Garcia JL, Perez-Fernandez R.

Department of Physiology, School of Medicine, University of Santiago de
Compostela, Spain.

Glial cell line-derived neurotrophic factor (GDNF) has been postulated as a
possible candidate for therapeutic treatment in Parkinson's disease (PD). Recent
in vitro data suggest that 1,25-dihydroxyvitamin D3 [1,25(OH)(2)D(3)] treatment
may enhance GDNF mRNA expression. In the present study, using semiquantitative
RT-PCR and Western blot, we have shown that 1,25(OH)(2)D(3) administration
intraperitoneally, significantly increases GDNF mRNA and protein levels in the
striatum of adult rats.

PMID: 12480187 [PubMed - indexed for MEDLINE]

Not being too familiar with the scientific lingo, I looked up intraperitoneally, and it means injected into a body cavity as opposed to a blood vessel...where did they inject it in the rats, if you know, and where would one ask a doc to inject it, assuming you could find one willing to do so?

Also, is the D3 they used the same D3 we can get? Be interesting to see what this might lead to...we already know PWP are low in D from the sunlight (hey, I think it's D3 that our body makes from sunlight, using cholesterol from our bodies (another thing PWP are typically low in, cholesterol), hmmmmm no this is getting interesting....need to give this some more thought...

Purely anecdotal information based upon a subject number of 1: husband's serum vitamin D levels were low. his doc ordered Vit D 3 @ 50,000IU to be taken every 4 weeks X 4 doses. Husband's symptoms increased after 1st dose, though both of us attributed that to the incredible variability of his symptoms day to day. This happened again after the 2nd dose 4 weeks later (version of a rechallenge dose of the drug) --he will not take a third dose. This could be an idiosyncratic response and not universal for patients with PD. Husband has taken 2,000 IUs of Vit D3 daily for the past 2 yrs without adverse effects we could discern (and his serum levels were still low). perhaps it was the massive dosage of D3 that upset some equilibrium--or another reason?
Just FYI--should one take this dosage, be vigilant to changes in symptoms/intensity of symptoms and act accordingly. madelyn

From http://www.life-enhancement.com/arti...te.asp?id=1707

A paper we recently obtained reports that vitamin D3 attenuates damage induced by 6-hydroxydopamine, a powerful free radical-generating oxidant, both in cell culture of rat midbrain neurons and in rats whose brains were lesioned with 6-hydroxydopamine.1

The paper reports that vitamin D3 has been shown to be a �potent inducer� of endogenous GDNF (glial-derived neurotrophic factor), which is neuroprotective against the toxicity of 6-hydroxydopamine and MPTP in animal models of Parkinson�s disease. GDNF is upregulated in response to neuronal injury and in cortex after ischemia, as well as in response to the cytotoxic effects of kainate in rats and has also been found to reduce the extent of infarction in cerebral cortex of rats. The authors note that, in addition to inducing GDNF, vitamin D3 also increases nerve growth factor and transforming growth factor beta2 expression in neuroblastoma cells and neurotrophin3/neurotrophin4 mRNA levels in astrocytes. Moreover, the authors note, vitamin D3 (in contrast to GDNF) can pass through the blood-brain barrier, making it possible to take vitamin D3 orally to reach brain tissues.

The researchers found that vitamin D3-pretreated 6-hydroxydopamine-lesioned rats had significantly higher peak locomotor activity as compared to lesioned animals that had received saline pretreatment. Peak mean rest time was significantly lower in D3-pretreated animals. �These results suggest that D3 treatment attenuates the hypokinesia produced by 6-hydroxydopamine lesions.� Vitamin D3 pretreatment also normalized nigral dopamine and dopamine metabolites in the lesioned animals in vivo. The authors conclude, �� since D3 can pass through the blood-brain barrier and elevate GDNF levels, this vitamin may be potentially useful in treatment of Parkinson�s disease and other neurodegenerative disorders.� As dopaminergic neurons are damaged and destroyed in the process of ordinary aging, even in the absence of overt Parkinson�s disease, this paper supports the use of vitamin D3 as a possible antiaging treatment for the brain.

Reference

1. Wang et al. Vitamin D3 attenuates 6-hydroxydopamine-induced neurotoxicity in rats. Brain Res 904:67-75 (2001).

Madelyn-
That's quite a dose! This is from a proposed clinical trial last year:
This trial examines the safety of high dose oral Vitamin D3 titrated up to a maximum of 40,000 IU per day over a 12 month period. Fifty patients matched for MS and non-MS characteristics will be divided into two groups: one group receiving the high dose Vitamin D regimen, and the other restricted to a maximum of 4000 IU per day. The hypothesis is that patients with MS can tolerate seemingly high doses of Vitamin D3 without adverse events and/or calcium-related abnormalities. It is also hypothesized that those receiving the higher doses will demonstrate improved relapse and disability status compared to controls, and that the treatment group will show improved markers of bone health and immune indicators of reduced inflammation.
http://clinicaltrials.gov/ct2/show/NCT00644904

Note that if you access this abstract through Medline that while it does not say so, you can access the full text PDF by clicking on the AMR logo. The Alternative Medicine Review publishes some of the best work around.


1: Altern Med Rev. 2008 Mar;13(1):6-20.

Use of vitamin D in clinical practice.

Cannell JJ, Hollis BW.

The recent discovery--from a meta-analysis of 18 randomized controlled
trials--that supplemental cholecalciferol (vitamin D) significantly reduces
all-cause mortality emphasizes the medical, ethical, and legal implications of
promptly diagnosing and adequately treating vitamin D deficiency. Not only are
such deficiencies common, and probably the rule, vitamin D deficiency is
implicated in most of the diseases of civilization. Vitamin D's final metabolic
product is a potent, pleiotropic, repair and maintenance, seco-steroid hormone
that targets more than 200 human genes in a wide variety of tissues, meaning it
has as many mechanisms of action as genes it targets. One of the most important
genes vitamin D up-regulates is for cathelicidin, a naturally occurring
broad-spectrum antibiotic. Natural vitamin D levels, those found in humans living
in a sun-rich environment, are between 40-70 ng per ml, levels obtained by few
modern humans. Assessing serum 25-hydroxy-vitamin D (25(OH)D) is the only way to
make the diagnosis and to assure treatment is adequate and safe. Three treatment
modalities exist for vitamin D deficiency: sunlight, artificial ultraviolet B
(UVB) radiation, and vitamin D3 supplementation. Treatment of vitamin D
deficiency in otherwise healthy patients with 2,000-7,000 IU vitamin D per day
should be sufficient to maintain year-round 25(OH)D levels between 40-70 ng per
mL. In those with serious illnesses associated with vitamin D deficiency, such as
cancer, heart disease, multiple sclerosis, diabetes, autism, and a host of other
illnesses, doses should be sufficient to maintain year-round 25(OH)D levels
between 55 -70 ng per mL. Vitamin D-deficient patients with serious illness
should not only be supplemented more aggressively than the well, they should have
more frequent monitoring of serum 25(OH)D and serum calcium. Vitamin D should
always be adjuvant treatment in patients with serious illnesses and never replace
standard treatment. Theoretically, pharmacological doses of vitamin D (2,000 IU
per kg per day for three days) may produce enough of the naturally occurring
antibiotic cathelicidin to cure common viral respiratory infections, such as
influenza and the common cold, but such a theory awaits further science.


PMID: 18377099 [PubMed - indexed for MEDLINE]

It might be better to do it daily with lower doses...say 4000IU. D3 is short lived in the body. I am not comfortable with those 50,000 IU doses. Also you want to get liquigel types of D3. I think they are absorbed better.

Hi all.
Got this info out of NIH clinical studies website which was updated a few days ago. It looks like they are recruiting PWPs for Vit D and PD study/ But look at the dates!!! Start date was supposed to be June 07!
Study design is what you were all talking about.

http://clinicaltrials.gov/ct2/show/r...ease%22&rank=2

Clinical Effects of Vitamin D Repletion in Patients With Parkinson's Disease
Brief Summary

1. A statement of the problem of interest Retrospective review of records in the Emory Movement Disorders clinic suggests vitamin D deficiency occurs in over 80% of patients with Parkinson's Disease (PD), much more frequently than in internal medicine clinics. Laboratory studies have suggested vitamin D could play a role in the development of PD. In addition, low vitamin D levels have been associated with slower walking speeds, worse memory and thinking, and depression.
2.

General statement of how the problem will be studied About 150 persons who have PD and low vitamin D levels will participate in this study. Subjects will be randomly (like flipping a coin) assigned to either high dose vitamin D supplement (54,200 IU weekly) or the Recommended Daily Allowance (RDA) for older persons (4200 IU weekly of vitamin D).

Subjects will be examined in the clinic before, then 3- and 6- months after taking vitamin D supplement. Tests of walking speed, Parkinson's rating scales, memory tests and questionnaires of mood, anxiety and fatigue will be administered.
3. How the research will advance scientific knowledge and/or human health If this study confirms that vitamin D deficiency is occurs in 80% of patients, other patients may benefit because awareness of the problem will be increased. Also, this study will help determine whether vitamin D improves patients' functioning.
4. What the standard of care, if any, is Currently, there is no "standard of care" for persons with low vitamin D. At the VA Medical center providers use a variety of supplement regimens. The Institute of Medicine (IOM) has published 600 IU per day (4200 IU per week) as the Recommended Daily Allowance (RDA). By definition, the RDA is the amount of a vitamin or supplement that will prevent 97-98% of the population from becoming deficient.

I think there's a lot to this Vitamin D thing. Here's a link a to a page of Vitamin D resource links. Dr. Mercola says it's really important what lab does your Vitamin D testing. Will find out more.
Fiona

That clinical trial, which should have been as straight-forward as it gets, was to be completed this past December. But I have searched pretty thoroughly and it seems to have vanished down the memory hole. A lot of hits in 2007 when it was announced but nothing since. I have emailed the contact asking about it and will let you know what I hear back.

The doc in charge was one Marian L. Evatt, MD, Assistant Professor of Neurology, Emory University, School of Medicine, and Assistant Chief of Neurology, Movement Disorders Program, Wesley Woods Geriatric Hospital, Inc, Atlanta .

Searching for her turned up a CE leture she gave less than three months ago titled: " Vitamin D and Neurologic Disorders". The lecture abstract is at http://www.cme-ce-summaries.com/fami...ce/fp5712.html

The section about PD says nothing at all about a major trial that should have been complete just 90 days earlier. That seems kind of odd. Hmmmm...