I didn't want to answer mrs. D 's question because i thought it was so low that I might have heard my doctor wrong. Mine was a whopping 7.

Well,the low readings here are not unusual to NeuroTalk. In fact the websites (both grassrootshealth and Vitamin D council) both have statistics to show many people in US and elsewhere are very low.

One thing to consider if you decide to do high dose Vit D3 (more than 2000IU daily) is not to take alot of calcium. One cardiologist has a blog, and he is recommending not to go over 600mg a day of calcium in supplement form. In fact I don't take any!
Vit D increases calcium absorption from food, and it is possible with a good diet to no longer need high dose calcium in supplement form while on high dose Vit D 3 supplementation.

Both my husband and I take 5000IU daily from Sept, to July. Once we are outside in the sun more, I stop ours. It has made a huge difference for both of us as far as mental and physical stamina, and neither of us gets colds or sick anymore too.

It is recommended for patients with sarcoidosis to not take supplements of D without a doctor's supervision. This is because the research into this uncommon condition of inflammation is not well founded with Vit D issues. The Marshall Protocol and all that. (you can Google it if you haven't heard of it but I bet most of you have!

Upped my dosage to 5000 IU yesterday and took part of it at the same time as meds. Seemed like they worked much better. Did it a little more deliberately today and it was not my imagination. Has anyone else noticed a similar effect?

Rick,

Now that you mention it, I have had an incredibly smooth day with meds. They nearly always work but today I didn't have much of a wearing off sensation. I am at 4000 IU and my Vita D is at 13.

-Laura

I havent noticed a bit of difference

Vitamin D Levels Associated with Parkinson's Disease Risk
http://www.sciencedaily.com/releases...0712162624.htm

Over 65s Should Take High Dose Vitamin D to Prevent Falls, Say Researchers
http://www.sciencedaily.com/releases...1001191659.htm

Rick, I find that when I get one of those shaky "spells" such as you and Laura describe, it's because I haven't been taking my D3. When I'm in that zombie state, the D3 helps within a couple of hours.

Jaye

Hmmm?? do you know if UTI's and some urology problems are connected to Vit. D deficiency?

Hey, Jaye - I hope you are feeling better after that hospital stay.
Peg

Much better, thanks, Peg. Wish I'd been more faithful to the D3. Kidney infections, though not terribly painful when caught early, are no fun. The hospital was totally cool about my PD meds, btw.

And a Happy Birthday to you, my dear.

Jaye

1. Brain Res Mol Brain Res. 1994 Jul;24(1-4):70-6.

1,25-dihydroxyvitamin D3 regulates the synthesis of nerve growth factor in
primary cultures of glial cells.

Neveu I, Naveilhan P, Jehan F, Baudet C, Wion D, De Luca HF, Brachet P.

Institut National de la Santé et de la Recherche Médicale, Unité U.298, Centre
Hospitalier Régional et Universitaire, Angers, France.

The effect of 1,25-dihydroxyvitamin D3 (1,25-(OH)2 D3) on nerve growth factor
(NGF) synthesis was investigated in primary cultures of astrocytes prepared from
brain of neonatal rats. 1,25-(OH)2 D3 elicited a dose-dependent increase of NGF
mRNA with a maximal effect at 10(-7) M, which persisted for at least 48 h.
Northern blot analysis revealed an expression of the vitamin D3 receptor (VDR)
gene in primary glial cells. Treatment of cells with 1,25-(OH)2 D3 led to an
increase in the VDR mRNA levels. Similar results were obtained in C6 glioma
cells. Exposure of primary glial cells to 10(-8) M 1,25-(OH)2 D3 caused only a
2-fold increase of the levels of cell-secreted NGF after 3 days of treatment.
However, a 5-fold increase was observed three days after a second addition of
vitamin D3. Likewise, a pretreatment with lower doses of hormone such as 10(-10)
M or 10(-9) M enhanced the responsiveness of the cells to a 24 h treatment with
10(-8) M hormone. It appears, therefore, that the duration of the treatment
influences the level of synthesis of NGF, possibly as a consequence of the
increase of the VDR gene expression. The specificity of 1,25-(OH)2 D3 is
supported by the fact that a concentration of 10(-7) M of an another vitamin D3
metabolite, 24,25-(OH)2 D3, had no effect on NGF synthesis. Several lines of
evidence indicate that astrocytes constitute the major cell type responsive to
1,25-(OH)2 D3 in primary cultures of glial cells.(ABSTRACT TRUNCATED AT 250
WORDS)


PMID: 7968379 [PubMed - indexed for MEDLINE]

------
1. Neuroreport. 1996 Sep 2;7(13):2171-5.

1,25-Dihydroxyvitamin D3, an inducer of glial cell line-derived neurotrophic
factor.

Naveilhan P, Neveu I, Wion D, Brachet P.

Institut National de la Santé et la Recherche Médicale, Centre Hospitalier
Universitaire, Angers, France.

Glial cell line-derived neurotrophic factor (GDNF) has significant therapeutic
potentials, in particular for neurodegenerative disorders. To determine factors
that would enhance GDNF expression, we analysed the effect of 1,25-(OH)2 D3 in C6
glioma cells. Treatment of C6 cells with 10(-7) M, 1,25-(OH)2 D3 for 48 h
elicited an 18.5-fold increase in the level of GDNF mRNA. In addition, our
results indicate that 1,25-(OH)2 D3 is effective at concentrations as low as
10(-10) M and that retinoic acid has additive effects. These data indicate that
1,25-(OH)2 D3 is a potent inducer of GDNF expression and suggest that 1,25-(OH)2
D3 may contribute to the regulation of GDNF in vivo.


PMID: 8930983 [PubMed - indexed for MEDLINE]

----


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]

-----


1. J Neurosci Res. 2009 Feb 15;87(3):723-32.

1,25-Dihydroxyvitamin D3 administration to 6-hydroxydopamine-lesioned rats
increases glial cell line-derived neurotrophic factor and partially restores
tyrosine hydroxylase expression in substantia nigra and striatum.

Sanchez B, Relova JL, Gallego R, Ben-Batalla I, Perez-Fernandez R.

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

It has previously been demonstrated that 1,25-dihydroxyvitamin D(3)
[1,25(OH)(2)D(3)] administration, whether in cell cultures or in vivo to rats,
increases glial cell line-derived neurotrophic factor (GDNF) expression levels,
suggesting that this hormone may have beneficial effects in neurodegenerative
disorders. This study was carried out to explore the effects of 1,25(OH)(2)D(3)
administration in a 6-OHDA-lesioned rat model of Parkinson's disease on GDNF and
tyrosine hydroxylase (TH) expression in substantia nigra (SN) and striatum. Two
groups of animals received 1,25(OH)(2)D(3) intraperitoneally, the first group 7
days before the unilateral injection of 6-OHDA into the medial forebrain bundle
(MFB) and the second group 21 days (days 21-28) after the unilateral injection of
6-OHDA. Animals of both groups were sacrificed on day 28. In addition, two other
groups received a unilateral injection of either saline or 6-OHDA into the MFB.
Rats were killed, and the SN and striatum were then removed for GDNF and TH
determination. Striatal GDNF protein expression was increased on the ipsilateral
with respect to the contralateral side after 6-OHDA injection alone as well as in
1,25(OH)(2)D(3)-treated rats before or after 6-OHDA administration. As expected,
6-OHDA injection induced an ipsilateral decrease in TH-immunopositive neuronal
cell bodies and axonal terminals in the SN and striatum. However, treatment with
1,25(OH)(2)D(3) before and after 6-OHDA injection partially restored TH
expression in SN. These data suggest that 1,25(OH)(2)D(3) may help to prevent
dopaminergic neuron damage.


PMID: 18816795 [PubMed - indexed for MEDLINE]

...but whatcha' gonna' do?

I think there is something big here and it is staring us in the face. The studies that I just posted are about all there are relating to the relationship between Vit D and GDNF. They all point to a major role. Other studies, including Amgen's notorius work, have made it clear that GDNF is capable of magic if it is in the right place. The studies above indicate a role for Vit D in getting it to that place.

Almost overnight the medical community has gone from saying that 400 IU of Vit D is all we need to saying that some of us may need 1000x that. This tells me that everything needs to be re-examined. The potential here is huge. If a chronic deficiency of Vit D is blocking the natural production of GDNF and the ability to heal ourselves, I want to know.

A lot of PWP have found that they have low Vit D. Have you heard of any of us who reported high levels? Me neither. As Paula mentioned, the general result of GDNF studies has been mixed. But Vit D levels were not considered.

I am going to post an assortment of files for consideration.

In order to keep this readable I am going to use the PubMed ID for citation purposes:

18852350: " RESULTS: Significantly more patients with PD (55%) had insufficient vitamin D than did controls (36%) or patients with AD
(41%"

20625085 : "CONCLUSIONS: The
results are consistent with the suggestion that high vitamin D status provides protection against Parkinson disease."

9371907 : "High prevalence of vitamin D deficiency and reduced bone mass in Parkinson's disease."

20586743 : "Hypovitaminosis D is also associated with several other neurological diseases
that is less likely mediated by dysregulated immune responses, including
Parkinson's disease and Alzheimer's disease, schizophrenia and affective
disorders, suggesting a more diverse role for vitamin D in the maintenance of
brain health. Accordingly, both the vitamin D receptor and the enzymes necessary
to synthesize bioactive 1,25-dihydroxyvitamin D are expressed in the brain, and
hypovitaminosis D is associated with abnormal development and function of the
brain."

17935548 : "CONCLUSION: Vitamin D therapy with conventional treatment improves serum levels
of 25 hydroxy vitamin D but still leaves some patients with significant insufficiency and therefore the same dose of vitamin D is not appropriate for all."

3838342 : "The present studies measure the transport of retinol, retinoic acid,
1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], and 25-hydroxyvitamin D3 [25-(OH)D3]
through the rat brain capillary endothelial wall, i.e., the blood-brain barrier
(BBB). The vitamin A and D derivatives bind both to albumin and to specific
high-affinity binding proteins in plasma. In the presence of physiologic
concentrations of plasma proteins, the extraction by brain of all four compounds
was 5% or less."

------

The last indicates that although the quantities are small, oral vitamin D can make its way to the brain. That is not likely to be an accident. If not, then what is being "starved" by these low levels?