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if a patient tests the zinc and magnesium levels while supplementing and testing d3, he or she can see the interrelationships and ensure optimal levels of all three. it's an interesting project that allows a patient to see how their personal situation line up (or don't) with available research.

A quick point to consider with this discussion is the interplay that Porphyria and Secondary Porphyria have in the MS causation and especially the symptom picture.
Sugars whether Natural, modified or Artificial are very common and problematic in Western Diets and growing more problematic in the last 100 years yet are not suspected because they sell Products!
I know this is taken from a different angle and different reason I will link more why, check the Glucose involvement in symptoms please,
CPn Help/secondary_porphyria_in_cp

Somewhere in this connection is the glucose, fructose, sucrose and the symptom expressions in MS.

Chronic infection with CPn causes acquired porphyria (which is known to mimic MS). Was browsing porphyria help sites, I saw that the Australian organisation which helps people with Porphyria actually operates from the same premises as Multiple Sclerosis Limited! They also seem to share some human resources (Andrew Long in Secretary of Porphyria Association Inc and Multiple Sclerosis Limited). http://www.porphyria-australia.org/who.htm

I don't how this all links but the diet and the increase in Asia, for one example of MS, presumably from diet changes to Western and hi sugar use is interlinked and I think also in the mix is Sun exposure, the trend to avoid Sun is very high in Asian folks.

So some how there is synergy with Vit D, Glucose and Diet in general and MS type symptoms.

A third factor that is being spoken of more and more (thanks Joan B for still pushing this along) is the general health of our veins and arteries for instance,


Food for thought?
Nigel

answering in part, re the asian/western angle, i think the transition from rice (gluten free) to wheat and associated impacts on zinc levels could be a factor. gluten with its impacts on zinc status also has the potential to impair dietary d3 absorption, exacerbating poor environmental exposure.

as for porphyria, here's the list of deficient enzymes depending what p subtype
http://en.wikipedia.org/wiki/Porphyria

might be useful to find out what these various enzymes are dependent upon, why said enzymes might be deficient, if there's anything to be done on the genetic expression front etc

I guess most have seen this, I hadn't!

From
RJ Lewis

Research has confirmed that "catching" colds and flu may actually be a symptom of an underlying vitamin D deficiency. The research is quite clear: less than optimal vitamin D levels will significantly impair your immune response and make you far more susceptible to contracting colds, influenza, and other respiratory infections.Vitamin D is an amazingly effective antimicrobial agent, producing 200 to 300 different antimicrobial peptides in your body that kill bacteria, viruses and fungi. http://articles.mercola.com/sites/artic ... t-one.aspx

Another article with some Conclusions? I think the conclusions are based on limited knowledge and available variables.

http://www.neurology.org/content/76/5/425.short

Background: French farmers and their families constitute an informative population to study multiple sclerosis (MS) prevalence and related epidemiology. We carried out an ecological study to evaluate the association of MS prevalence and ultraviolet (UV) radiation, a candidate climatologic risk factor.

Methods: Mean annual and winter (December–March) UVB irradiation values were systematically compared to MS prevalence rates in corresponding regions of France. UVB data were obtained from the solar radiation database (SoDa) service and prevalence rates from previously published data on 2,667 MS cases registered with the national farmer health insurance system, Mutualité Sociale Agricole (MSA). Pearson correlation was used to examine the relationship of annual and winter UVB values with MS prevalence. Male and female prevalence were also analyzed separately. Linear regression was used to test for interaction of annual and winter UVB with sex in predicting MS prevalence.

Results: There was a strong association between MS prevalence and annual mean UVB irradiation (r = −0.80, p < 0.001) and average winter UVB (r = −0.87, p < 0.001). Both female (r = −0.76, p < 0.001) and male (r = −0.46, p = 0.032) prevalence rates were correlated with annual UVB. Regression modeling showed that the effect of UVB on prevalence rates differed by sex; the interaction effect was significant for both annual UVB (p = 0.003) and winter UVB (p = 0.002).

Conclusions: The findings suggest that regional UVB radiation is predictive of corresponding MS prevalence rates and supports the hypothesis that sunlight exposure influences MS risk. The evidence also supports a potential role for gender-specific effects of UVB exposure.

Another article on Vit D dosages and MS

http://blog.lef.org/2013/01/vitamin-d-r ... rosis.html

Experiencing Fewer MS Symptoms with Vitamin D

Researchers from the University of California, San Francisco reported a reduction in brain lesions and disease activity in multiple sclerosis patients who had higher levels of vitamin D.2

This conclusion came after a 5-year study, involving 469 men and women with MS. All participants underwent yearly blood testing for vitamin D and brain magnetic resonance imaging (MRI) to evaluate disease progression.

The researchers determined that with each 10 ng/ml increase in serum 25-hydroxyvitamin D, there was a corresponding 15% reduction in the risk of new brain lesions characteristic of MS.

They also noted a 32% lower risk of areas of active disease as indicated by “white spots” or areas of inflammation visible on MRI images.

To put this into perspective, a 10-point increase in your vitamin D level can often be achieved by adding only 1 gram of it to your diet.3

Considering that the average cost-per-pill is around 8 cents, for a mere fraction of the cost of current treatments, people with MS could experience significant improvements in their quality of life.

Optimal Vitamin D Dosing & Blood Levels for Fighting MS

So what is the optimal vitamin D dose? Well, that depends on your blood level — and how much is in your blood is really the question we should be asking.

According to the Office of Dietary Supplements, a department of the National Institutes of Health, the optimal vitamin D blood level is between 20 and 50 ng/ml.4

This is optimal, by the way, if preventing bone disease is your only goal. But to reap the full benefits of vitamin D, including helping with MS symptoms and preventing new brain lesions, you’ll probably need to fall between 50 and 70 ng/ml, considerably higher than the NIH recommendations.

So we suggest obtaining a vitamin D blood level first and then taking a dose that will help you optimize your blood level, 10 points at a time.

Sun exposure helps to optimize blood levels as well. However, our ability to convert precursors into vitamin D under the influence of UVB light from the sun becomes less efficient with age5.

In addition, this process is influenced by multiple other factors, including season, latitude, time of the day, and sunscreen use5.

For these reasons, and given the many benefits attributed to vitamin D, it’s probably best to supplement with it daily. Are you?

Interesting insights to Wavelengths and Vit D interactions!

http://news.softpedia.com/news/UV-Radia ... 8211.shtml

According to University of the Wisconsin-Madison (UWM) Steenbock Research Professor of Biochemistry Hector DeLuca, vitamin D may indeed play some part in stopping MS from grabbing a hold on people. However, he proposes that UV wavelengths in the sunlight exert a more important influence on the disease. Details of his investigations, which were conducted with first author Bryan Becklund, were published in the latest online issue of the esteemed publication Proceedings of the National Academy of Sciences (PNAS).

“Since the 1970s, a lot of people have believed that sunlight worked through vitamin D to reduce MS. It's true that large doses of the active form of vitamin D can block the disease in the animal model. That causes an unacceptably high level of calcium in the blood, but we know that people at the equator don't have this high blood calcium, even though they have a low incidence of MS. So it seems that something other than vitamin D could explain this geographic relationship,” DeLuca says. He adds, however, that the new finding may not be helpful in any way. It is still too early to say whether the results will have any applications in humans or not.

“There are several ways this could go. If we can find out what the UV is producing, maybe we could give that as a medicine. In the short term, if we can define a specific wavelength of light that is active, and it does not overlap with the wavelengths that cause cancer, we could expose patients who have been diagnosed with MS to that wavelength,” he concludes.

Possibly relevant...for the first time in more than 25 years I laid out in the sun (no tan line style) with no sunscreen for 1-3 hours weekly (and swam wo sunscreen for hours every week) from May 2012 thru August 2012 at relatively high elevation. I had vitamin d tested in August and it was only 30.

This makes me believe that something is interfering with our vitamin d synthesis. Some Internet sources say its cortisol.

the common denominator there would be, as you can no doubt imagine, zinc. low zinc, poor d3 absorption. low zinc, high cortisol. optimize zinc levels, cortisol drops.

http://link.springer.com/content/pdf/10 ... 9254424394
Twenty-five mg of ZnCC were administered intravenously during 1 min, ... The Plasma cortisol levels decreased significantly, which is consistent with our previous findings.

since zinc is known to be lower in ms patients, it's reasonable to expect it to help.

my own lab tests support the idea of zinc supplementation helping to alter processes in ms patients, read more here http://www.thisisms.com/forum/general-d ... ml#p202977

Jimmy, you know I love my zinc but I might love my hpa axis dysreg obsession more. lol

What do you think about this?

http://www.pnas.org/content/107/7/2818.full

Adrenal insufficiency increases serum zinc concentrations whereas administration of glucocorticoids, corticotropin, and the excess cortisol production in Cushing’s Syndrome decrease these concentrations [reviewed in (38)]. Hypercortisolemia and hypozincemia are associated with chronic alcoholism (39). Excess cortisol could accelerate pancreatic zinc release and produce a systemic zinc deficiency as observed in alcoholism. Radiotracer kinetic studies with humans reveal that carbohydrate-active steroids (glucocorticoids) may alter rate constants of the fecal excretion of zinc (38). Hypozincemia associated with glucocorticoid action has been related to induced synthesis of MT in rodents (40). GR involvement in pancreatic tissue organization and the differentiation of acinar cells, as well as enzyme and zymogen granule production is compatible with a role in ZnT2 regulation. Furthermore, the control zinc provides via MTF-1 responsive ZnT2 expression is consistent with a homeostatic role in endogenous zinc secretion. However, how the correlation of serum zinc and cortisol levels influences pancreatic ZnT2 expression requires further studies. To our knowledge ZnT2 may represent the first member of either the ZnT or Zip families to be glucocorticoid regulated.

clearly strong interconnections. found an amazing article that breaks it all down in super detail
http://dc.library.okstate.edu/cdm/singl ... _container

"In general, cortisol is seen together with pro-inflammatory factors due to the fact that high blood cortisol levels are triggered by inflammatory cytokines. As well, immunological constraints like protein energy malnutriton or zinc deficiency are known to cause high serum cortisol (32, 202). ... low dietary zinc is associated with oxidative damage of DNA ... Zinc status is also associated with cortisol (24). Cortisol is a glucocorticoid hormone from the hypothalamic-pituary-adrenal (HPA) axis that acts as an important stress marker. Stress of any kind, such as anxiety, strenuous exercise, inflammation or malnutrition triggers the excretion of cortisol from the adrenal glands (25, 26). For instance, protein energy malnutriton is often seen in conjunction with low zinc intake and increased serum cortisol concentrations. Elevated cortisol in turn suppresses inflammatory cytokines and prevents an overwhelming inflammatory reaction (27-29) by downregulating the expression of inflammatory cytokines (30, 31)."

so given these causes for elevated cortisol: anxiety and exercise both cause nutritional depletion, obviously so does mal- or mis- nutrition, and the inflammation deal is a catch 22 of sorts given that inflammation would increase cortisol resulting in inflammation etc etc etc.

"... Zinc deficiency is widespread in developing countries and can still be found in developed countries. The main reason for zinc deficiency is poor dietary intakes (86). ... In developing countries where women and children are especially likely to have low meat intake, diets are also typically high in fiber and phytate. This may also be true for certain diets found in developed countries (e.g., the vegan diet). Low meat consumption and high intake of minimally processed grains are suspected to be the root cause of impaired zinc status. In plant-based diets with small amounts of animal-source foods, multiple nutrient deficiencies are likely to develop (64, 90)."

and that would be me...

refer also to figure 6 in the pdf doc. note that all causes of stress heading for the HPA axis are either caused by or can cause nutrient deficits:
Figure 6: Effect of stress from different sources, such as malnutrition, exercise, trauma, inflammation, on the cortisol pathway via the HPA axis, adapted from Bowen, 2006 (200).

"Vitamin D research is discussed in light of the hypothesis that the lower average levels of vitamin D frequently observed in autoimmune disease are not a sign of deficiency.
Instead, it is proposed that the lower levels result from chronic infection with intracellular bacteria that dysregulate vitamin D metabolism by causing vitamin D receptor (VDR) dysfunction within phagocytes."
http://autoimmunityresearch.org/transcr ... eprint.pdf


Very very interesting article, I personally like the Atheist Advocate angle of looking at things and this appears to have merit.
"Marshall reviewed recent large meta-analyses
looking at vitamin D and autoimmune disease,
overall mortality, cancer mortality and bone
density and found that in general, they did not
show a clear benefit for vitamin D supplementation. Problems with many studies on vitamin D
include failure to adequately consider confounding
factors, failure to measure the active metabolite
(1,25-D), inadequate study lengths, overreliance
on in vitro and animal studies, lack of
randomization and a failure to consider the
alternative hypothesis for low vitamin D levels."
and
"The choice of a VDR agonist is very important
so as to achieve the right level of VDR activation
without negatively impacting the activity of other
nuclear receptors also involved in the immune
response.
2
So far, olmesartan is the only agent that
seems to satisfy these requirements. In addition, a
careful control of antibiotic timing and dosage by
a schedule determined by experience and modified
according to individual reactions,* is required in
order to reduce immunosuppressive effects of the
antibiotics and maximize their ability to target
these treatment-resistant bacteria.
"

NZer1 wrote:"Vitamin D research is discussed in light of the hypothesis that the lower average levels of vitamin D frequently observed in autoimmune disease are not a sign of deficiency.
Instead, it is proposed that the lower levels result from chronic infection with intracellular bacteria that dysregulate vitamin D metabolism by causing vitamin D receptor (VDR) dysfunction within phagocytes."
http://autoimmunityresearch.org/transcr ... eprint.pdf

Vitamin D will be consumed at high rates whenever there is injury to the cell.

It doesn't have to be a bacteria. Could be a virus. Could be injury from turbulent blood flow.

If there is injury, whatever the cause, vitamin D will set off an immune cascade and each part of that cascade needs its own vitamin D.

So,
I take from that Ed that testing for Vit D is much more complex in the reading of results and there often needs to be further tests to decide if it is high use or VDR dysregulation by Bacteria or viruses?

Plus the calcium balance in this equation as well!

Just when I thought I was beginning to understand I am sat on my arse once again with lack of knowledge at a new level, and that's life all over ;)

? I wonder what this will mean?
So far, olmesartan is the only agent that
seems to satisfy these requirements.

Nigel

NZer1 wrote:So,
I take from that Ed that testing for Vit D is much more complex in the reading of results and there often needs to be further tests to decide if it is high use or VDR dysregulation by Bacteria or viruses?

Plus the calcium balance in this equation as well!

Just when I thought I was beginning to understand I am sat on my arse once again with lack of knowledge at a new level, and that's life all over

The goal is not just to take a certain amount of vitamin D, but to attain a level of 25(OH)D.

That means at least two tests. The first to see what your current level is and the second to see if you have reached your target level. There is a standard formula for estimating the loading dose needed to reach a target level.

[cen]Loading dose = 40 * (Target nmol/L - Serum nmol/L) * BodyWeight Kg [/cen]

Using this formula, you can also tell whether you may have vitamin D gene processing deficiencies. If you don't reach the target after taking the loading dose, then you may not be processing vitamin D properly and will need to take more just to reach and maintain a target level.

Finally, you need a third test to see if your maintenance dose is maintaining the target 25(OH)D level. If you are using up vitamin D at a faster rate than normal, then you may have to take more and if it is pushing you over the target level, then you would need less.

I don't know about complex, but you would need these three tests to know whether you are getting too much or too little vitamin D.