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Mind and Muscle Forums > Chemically Correct > Advanced Hypothesis, Theory & Discussion
Benson
I caught a little of this debate on NPR this morning. The growing body of evidence is that we are not getting nearly enough vitamin D, depsite its inclusion in milk and other "fortified" foods and that hypovitamin D may be a contributing factor in the pathology of a whole host of human diseases. The general advice: get out in the sun more without sunscreen...

Eur J Clin Invest. 2005 May;35(5):290-304.
Vitamin D and calcium deficits predispose for multiple chronic diseases.

Peterlik M, Cross HS.

Department of Pathophysiology, Center for Physiology and Pathophysiology, University of Medicine Vienna, Vienna, Austria. meinrad.peterlik@meduniwien.ac.at

There is evidence from both observational studies and clinical trials that calcium malnutrition and hypovitaminosis D are predisposing conditions for various common chronic diseases. In addition to skeletal disorders, calcium and vitamin D deficits increase the risk of malignancies, particularly of colon, breast and prostate gland, of chronic inflammatory and autoimmune diseases (e.g. insulin-dependent diabetes mellitus, inflammatory bowel disease, multiple sclerosis), as well as of metabolic disorders (metabolic syndrome, hypertension). The aim of the present review was to provide improved understanding of the molecular and cellular processes by which deficits in calcium and vitamin D cause specific changes in cell and organ functions and thereby increase the risk for chronic diseases of different aetiology. 1,25-Dihydroxyvitamin D(3) and extracellular Ca(++) are both key regulators of proliferation, differentiation and function at the cellular level. However, the efficiency of vitamin D receptor-mediated intracellular signalling is limited by the negative effects of hypovitaminosis D on extrarenal 25-hydroxyvitamin D-1alpha-hydroxylase activity and thus on the production of 1,25-dihydroxyvitamin D(3). Calcium malnutrition eventually causes a decrease in calcium concentration in extracellular fluid compartments, resulting in organ-specific modulation of calcium-sensing receptor activity. Hence, attenuation of signal transduction from the ligand-activated vitamin D receptor and calcium-sensing receptor seems to be the prime mechanism by which calcium and vitamin D insufficiencies cause perturbation of cellular functions in bone, kidney, intestine, mammary and prostate glands, endocrine pancreas, vascular endothelium, and, importantly, in the immune system. The wide range of diseases associated with deficits in calcium and vitamin D in combination with the high prevalence of these conditions represents a special challenge for preventive medicine.

Br J Nutr. 2003 May;89(5):552-72.
Vitamin D in preventive medicine: are we ignoring the evidence?

Zittermann A.

Department of Nutrition Science, University of Bonn, Endenicher Allee 11-13, 53115 Bonn, Germany. a.zittermann@uni-bonn.de

Vitamin D is metabolised by a hepatic 25-hydroxylase into 25-hydroxyvitamin D (25(OH)D) and by a renal 1alpha-hydroxylase into the vitamin D hormone calcitriol. Calcitriol receptors are present in more than thirty different tissues. Apart from the kidney, several tissues also possess the enzyme 1alpha-hydroxylase, which is able to use circulating 25(OH)D as a substrate. Serum levels of 25(OH)D are the best indicator to assess vitamin D deficiency, insufficiency, hypovitaminosis, adequacy, and toxicity. European children and young adults often have circulating 25(OH)D levels in the insufficiency range during wintertime. Elderly subjects have mean 25(OH)D levels in the insufficiency range throughout the year. In institutionalized subjects 25(OH)D levels are often in the deficiency range. There is now general agreement that a low vitamin D status is involved in the pathogenesis of osteoporosis. Moreover, vitamin D insufficiency can lead to a disturbed muscle function. Epidemiological data also indicate a low vitamin D status in tuberculosis, rheumatoid arthritis, multiple sclerosis, inflammatory bowel diseases, hypertension, and specific types of cancer. Some intervention trials have demonstrated that supplementation with vitamin D or its metabolites is able: (i) to reduce blood pressure in hypertensive patients; (ii) to improve blood glucose levels in diabetics; (iii) to improve symptoms of rheumatoid arthritis and multiple sclerosis. The oral dose necessary to achieve adequate serum 25(OH)D levels is probably much higher than the current recommendations of 5-15 microg/d.

Benson

See how far out in front we were with this one, gents?
nightop
I thought this was well known for years.
Benson
QUOTE(nightop @ Feb 17 2008, 12:16 PM) [snapback]458780[/snapback]
I thought this was well known for years.


At least 2.5 years anyway wink.gif
Proton Soup
i think i first started reading about it at LEF
ATB
Yes, first popularised argument I am aware of goes back to an article in Nexus magazine that was to be echoed in its conclusions by a subsequent, more recent one in New Scientist, and then by the popular press. ANd somewhere in between we've been championing it too. The work on associating D3 and behavior and brain dissorders is where we might be found really original, although scientists had made similar propositions, I think we have expanded it, popularised it and put some very relevant fuindings together to conclude probable contribution of D3 variations in racial patterns of mental illness, particularly being able to explain the vast disparity in schizophrenia, type 1 diabeties between white and immigrant asian and african populations, and some of the mechanisms as to why.

It could even explain psychotic behavior and paranoia in fundamentalists who probably have the lowest whole-life D3 levels in the population (mothers cover up, stay indoors in inner city environments and have usually darker skin).

We've also pushed its potential role as an antidepressant through various roles, including an assumed anti-inflammatory effect and stimulation of certain brain receptors. It turns out that more recently, scientists have been surprised to discover a strong anti-depressant effect of Vitamin D3, which gave test volunteers an 'inner glow'.
lynx
QUOTE(Proton Soup @ Feb 17 2008, 03:21 PM) [snapback]458852[/snapback]
i think i first started reading about it at LEF

First I recall was Dr. David Perlmutters Book, BrainRecovery.com published May, 2000. In one place he cites a Japanese study in which Parkinson's sufferers were found to have really low Vit D and the authors therefore concluded that the patients should be careful of falling. That was the state of Vit D awareness at the time.
Proton Soup
QUOTE(lynx @ Feb 17 2008, 04:08 PM) [snapback]458867[/snapback]
First I recall was Dr. David Perlmutters Book, BrainRecovery.com published May, 2000. In one place he cites a Japanese study in which Parkinson's sufferers were found to have really low Vit D and the authors therefore concluded that the patients should be careful of falling. That was the state of Vit D awareness at the time.


yeah, we've certainly known about vit D and bone health for a long time, but (and someone correct me if i'm wrong here) i think what has been learned recently is just how common vitamin D receptors are throughout the body. so just within the past few years, the effects of D on other tissues has become an interest. things like muscle function in the elderly, etc.
FunkMasterFlex
Carlson ( the company) had it in its newsletter atleast 6 years ago. Talking about 1000 to 2000iu's a day. I personally have been buying theirs for the last 5 years now. Respect to them. Especially since their cod liver oil actually tastes like lemon. lol
lynx
QUOTE(Proton Soup @ Feb 17 2008, 05:33 PM) [snapback]458882[/snapback]
yeah, we've certainly known about vit D and bone health for a long time, but (and someone correct me if i'm wrong here) i think what has been learned recently is just how common vitamin D receptors are throughout the body. so just within the past few years, the effects of D on other tissues has become an interest. things like muscle function in the elderly, etc.

I was pointing out the effect of Vit D on Neurodegenerative diseases, ie Parkinson's and demonstrating that the Drs in the study couldn't see the forest for the trees.
maxhealth
I take a 1000iu tab every day along with some extra in my ortho core. That plus a moderate amount of unavoidable sun should be enough.
ShuffleUp
QUOTE(maxhealth @ Feb 18 2008, 03:21 PM) [snapback]459119[/snapback]
I take a 1000iu tab every day along with some extra in my ortho core. That plus a moderate amount of unavoidable sun should be enough.


Depends on how moderate is moderate. I think you can definately get there but I get very little sun and it's taking quite a bit more D3 to get adequate levels:

(My post from another thread):

I've been using NOW brand's D3 which are 1000IU gelcaps, the d3 suspended in Olive Oil. I started taking this 3 months ago at between 4 or 5 per day, just depending on how many came out of the bottle when I poured it. I would say consistently I was between these units the entire time, with little to no sun exposure. The last meaningful sun exposure I had was in June in Mexico for a week.

I just bought a Vit D3 blood test through LEF and had it done a week ago. Results came in the envelope today and I was at 45.2 ng/mL which I asume is pretty decent. The ref range was 32.0 - 100. Below the test they write, "Recent studies consider the lower limit of 32.0 ng/mL to be a threshold for optimal health. Hollis BW. J Nutr. 2005 Feb; 135(2):317-22.

Davis recommends to get between 50 and 60. I'm unsure what to add to my doseage to get there, but I'm thinking a consistent 5000IU - 6000IU should do the trick for me. Maybe back to 4000IU in the summer.

I didn't have a previous test before supplementation so no clue where I was before, but quite possible I was under 32 if it took ~4500IU's to get me to 45.

I also take 100 micrograms of K2 daily from Source Naturals brand. This is the MK-7 form. Studies showed reduced cardiovasular problems at somewhere over 30-some micrograms / day levels.

ScottL - if you read this, you mentioned you were getting your levels checked - how did that come out for you & at what d3 dose?
D Sade
I've been doing anywhere between 3000 and 5000 i.u around 11am (to mimic when natural sunlight would be the strongest, and theoretically when the body would be producing the MOST...I have been doing this in conjunction with a Havoc cycle.

Too early to quantify, but subjectively what I notice the most of an enhanced mind/muscle connection.
avantgarde
Any side effects from taking D3 supps ?

oswaldosalcedo
.


Int Urol Nephrol. 2008 Jan 10.

Vitamin D, the renin-angiotensin system, and insulin resistance.


Rammos G, Tseke P, Ziakka S.

Department of Clinical Therapeutics, General Hospital of Athens, “Alexandra”, Athens, Greece.

Insulin resistance is characterized by the systemic impairment of insulin action and is usually the result of aging, obesity, chronic inflammation, or another factor that may contribute to the inhibition of the insulin signaling pathway. Insulin resistance is accompanied by defects in lipid metabolism and blood coagulation, hypertension, obesity, and vascular inflammation in a syndrome called syndrome X or metabolic syndrome. Metabolic syndrome is involved in the development of atherosclerosis with consequent cardiovascular complications including acute myocardial infarction, stroke, and vascular disease. Recent data have shown that vitamin D acts as a negative regulator of the renin gene and that vitamin D deficiency is followed by increased renin-angiotensin II expression. The link between the insulin signaling pathway/insulin resistance and the renin-angiotensin system has been well documented in previous studies. The present review focuses on disorders characterized by a reduction in vitamin D concentration or its receptor function and the development of insulin resistance or metabolic syndrome, and discusses also possible therapeutic interventions.









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Proton Soup
QUOTE(lynx @ Feb 17 2008, 09:53 PM) [snapback]458936[/snapback]
I was pointing out the effect of Vit D on Neurodegenerative diseases, ie Parkinson's and demonstrating that the Drs in the study couldn't see the forest for the trees.


yeah, but i'm not sure that low vitamin D status is peculiar to that segment of the elderly population.
liorrh
raising your calcitriol and killing your PTH levels with a(oh)d3.

I got 1ug softgels of this baby sitting around. now, this study talks about taking more than 2 mug a day, I assume its mili-ug?

I barely get sun lately so yeah, this should be good for fatloss/strength/immune/mood

anyone else take alpha(oh)d3? (aka alfacalcidol, alpha-hydroxyvitamin d3)


QUOTE
Comparison of effects of 1 alpha-hydroxy-vitamin D3 and 1,25-dihydroxy-vitamin D3 in man.
A S Brickman, J W Coburn, G R Friedman, W H Okamura, S G Massry, and A W Norman
Small right arrow pointing to: This article has been cited by other articles in PMC.
Abstract
The effects of short-term treatment with 1,25-dihydroxy-vitamin D3 [1,25(0H)2D3] or 1 alpha-hydroxy-vitamin D3 [1 alpha(OH)D3] on intestinal absorption of 47Ca were compared in 41 experiments in normals and 72 experiments in patients with chronic renal failure. 11 patients were studied a second time after treatment for 2-5 mo. Doses varied from 0.14 to 5.4 mug/day to establish dose-response relationships. Urinary calcium was monitored in normal subjects, nine of whom received a constant calcium intake on a metabolic unit. There was an increase in intestinal absorption of 47Ca and urinary calcium in normals receiving 1,25 (OH)2D3, 0.14 mug/day or greater, and 0.28 mug/day or greater augmented intestinal absorption of 47Ca in chronic renal failure. In contrast, 2.6 mug/day of 1 alpha (OH) D3 was required to increase intestinal absorption of 47Ca in both groups. The increase in urinary calcium to maximal levels was delayed during treatment with 1 alpha (OH) D3, 5-10 days vs. 2-5 days with 1,25 (OH)2D3. Moreover, half times for urinary calcium to decrease to pretreatment levels after stopping treatment were greater after 1 alpha-(OH) D3 (1.5-2.7 days) than 1,25(OH)2D3 (1.1-2.0 days). With long-term administration there was a progressive increase in intestinal absorption of 47Ca in the patients receiving 1 alpha (OH)D3; this was not observed with 1,25(OH)2D3. The pharmacologic differences between 1 alpha(OH) D3 and 1,25(OH)2D3 may be explained by the requirement for 25-hydroxylation of 1alpha(OH) D3 before biologic effects occur; at low doses (less than 1 mug/day), 1 alpha(OH) D3 competes with vitamin D3 for 25-hydroxylation. With prolonged treatment or larger doses (greater than 2 mug/day),, 1alpha(OH) D3 could accumulate and then be hydroxylated resulting in production of higher levels of 1,25(OH)2D3.
ShuffleUp
QUOTE(avantgarde @ Feb 26 2008, 01:28 PM) [snapback]461306[/snapback]
Any side effects from taking D3 supps ?


No sides that I have seen but you do want to take some K2 with it to help prevent soft tissue calcification.

liorrh
QUOTE(ShuffleUp @ Feb 29 2008, 06:42 PM) [snapback]462451[/snapback]
No sides that I have seen but you do want to take some K2 with it to help prevent soft tissue calcification.

how important is that? soft tissue calcification.. WTF
ScottL
QUOTE(liorrh @ Mar 1 2008, 08:12 AM) [snapback]462490[/snapback]
soft tissue calcification.. WTF


not a good thing.
liorrh
QUOTE(ScottL @ Mar 1 2008, 08:00 AM) [snapback]462503[/snapback]
not a good thing.

so staying in the sun will calcify my soft tissue? please expand.
Benson
QUOTE(liorrh @ Mar 1 2008, 05:08 PM) [snapback]462585[/snapback]
so staying in the sun will calcify my soft tissue? please expand.


Here is the interesting thing...your skin produces tens of thousands of IU of vitamin D every hour of solar exposure and yet, nobody ever overdosed on vitamin D from sunbathing...
liorrh
QUOTE(Benson @ Mar 1 2008, 05:09 PM) [snapback]462598[/snapback]
Here is the interesting thing...your skin produces tens of thousands of IU of vitamin D every hour of solar exposure and yet, nobody ever overdosed on vitamin D from sunbathing...


bump! please reference that soft tissue calcification thingy.
Benson
QUOTE(liorrh @ Mar 2 2008, 04:14 AM) [snapback]462661[/snapback]
bump! please reference that soft tissue calcification thingy.


Don't worry about it. It would take a daily dose of 100,000 IU for several months to create hypercalcimia that you would need to be concerned about.
ShuffleUp
QUOTE(liorrh @ Mar 2 2008, 03:14 AM) [snapback]462661[/snapback]
bump! please reference that soft tissue calcification thingy.


Here's a mention of it. I really don't know if there is legitimate cause for concern but Vit K2 is good for you anyway so what they hey.


http://www.westonaprice.org/basicnutrition...indmiracle.html

VITAMIN D UPDATE-A WARNING, Fall 2002
By Krispin Sullivan, CN

I have reported in this magazine on the substantial benefits that can be gained from vitamin D therapy (Wise Traditions, Fall 2000). However, my own clinical experience and the research of others is clearly showing chronic subclinical vitamin D toxicity is possible, from both supplements or tropical sunlight. Elevated levels of serum vitamin D can cause significant bone loss and calcification of soft tissues.

If you are using supplements of vitamin D (natural or synthetic) or are light skinned and have had significant sun exposure in tropical or subtropical areas and haven't done so before, it is very important to test your blood levels of D.

Optimal values of 25(OH)D are 40-50 ng/ml
Acceptable values of 25(OH)D are 35-55 ng/ml
Levels above 55 ng/ml will be toxic for some individuals.

There is no good reason to maintain levels of D in this higher range and strong evidence showing potential harm.

You need to TEST. The correct test to order is 25(OH)D, also called 25-hydroxyvitamin D. Make sure this is the test you get. Labs often give the test for 1,25-dihydroxyvitamin D, the active hormone. This test is the wrong test as it offers no meaningful data regarding D status.

Lab One offers the least expensive testing I have found nationwide and is available in most states. Your physician can reach them at 1-800-646-7788. The test is 25-hydroxyvitamin D. The Lab One test number, just to be sure you get the right test, is #3247. Rarely does insurance cover the cost for this test, which is about $60 including lab fees. Other labs I have queried charge $100-180 for the same test.

The important thing to remember if you are doing vitamin D therapy, or spending lots of time in the sun, is to TEST!
lynx
QUOTE
Dietary supplementation exerts neuroprotective effects in ischemic stroke model.Yasuhara T, Hara K, Maki M, Masuda T, Sanberg CD, Sanberg PR, Bickford PC, Borlongan CV.
Department of Neurology, Medical College of Georgia, Augusta, Georgia.

ABSTRACT This study examined whether dietary supplementation can be used to protect against ischemic stroke. Two groups of adult male Sprague-Dawley rats initially received NT-020, a proprietary formulation of blueberry, green tea, Vitamin D3, and carnosine (n = 8), or vehicle (n = 7). Dosing for NT-020 and vehicle consisted of daily oral administration (using a gavage) over a 2-week period. On day 14 following the last drug treatment, all animals underwent the stroke surgery using the transient 1-hour suture occlusion of middle cerebral artery (MCAo). To reveal the functional effects of NT-020, animals were subjected to established behavioral tests just prior to stroke surgery and again on day 14 post-stroke. ANOVA revealed significant treatment effects (p < 0.05), characterized by reductions of 11.8% and 24.4% in motor asymmetry and neurologic dysfunction, respectively, in NT-020-treated stroke animals compared to vehicle-treated stroke animals. Evaluation of cerebral infarction revealed a significant 75% decrement in mean glial scar area in the ischemic striatum of NT-020-treated stroke animals compared to that of vehicle-treated stroke animals (p < 0.0005). Quantitative analysis of subventricular zone's cell proliferative activity revealed at least a one-fold increment in the number of BrdU-positive cells in the NT-020-treated stroke brains compared to vehicle-treated stroke brains (p < 0.0005). Similarly, quantitative analysis of BrdU labeling in the ischemic striatal penumbra revealed at least a three-fold increase in the number of BrdU-positive cells in the NT-020-treated stroke brains compared to vehicle-treated stroke brains (p < 0.0001). In addition, widespread double labeling of cells with BrdU and doublecortin was detected in NT-020-treated stroke brains (intact side 17% and ischemic side 75%), which was significantly higher than those seen in vehicle-treated stroke brains (intact side 5% and ischemic side 13%) (p < 0.05). In contrast, only a small number of cells in NT-020-treated stroke brains double labeled with BrdU and GFAP (intact side 1% and ischemic side 2%), which was significantly lower than those vehicle-treated stroke brains (intact side 18% and ischemic side 35%) (p < 0.0001). Endogenous neurogenic factors were also significantly upregulated in the ischemic brains of NT-020-treated stroke animals. These data demonstrate the remarkable neuroprotective effects of NT-020 when given prior to stroke, possibly acting via its neurogenic potential.

PMID: 18260778 [PubMed - in process
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