Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Re: Vit D3 Supply from iHerb in California

Postby MarkW » Fri Jan 04, 2013 3:35 am

Squeakycat wrote:Standing naked at noon with full UV-B exposure as you would have in East Africa year around, your body would make 1,000 IU a minute, but only up to a limit of 20,000 IU for the day unless you have greater need, the most studied being pregnancy and bone growth where the body allows you to make more. So wouldn't natural or evolutionary history suggest that 5,000 IU is on the low end while the "natural" number is closer to 20,000 or even half that.
Ed


Hello Ed,
You are absolutely correct that our body's exposure to UVB will produce excess D3 above human needs. Diet (oily fish) also makes a big differece.
There is very little data on what D3 levels a healthy outside dwelling human would maintain. I recall that Lifeguards in St Louis, USA had a natual level D3 of 150 mmol/L. (Hopefully I referenced the paper in this thread, otherwise it needs a PubMed search). The other data is that pwMS with higher D3 levels have fewer relapses (try page 12 of thread). This effect reaches a plateau around around 110 mmol/L.
My recommendation on D3 blood level in pwMS is 125mmol/L or 50ng/ml (now as a minimum target).
Just my educated guess.

Different people could acheive this level in different ways:
Sunbathing; Oily Fish; D3 supplements
D3 levels make the news in Scotland - http://www.bbc.co.uk/news/uk-scotland-16255962.
As the Scottish Government will not act on Prof Ebers advice, I am just giving my advice on ThisIsMS/CCSVI and not wasting effort on MS Experts/politicians who are deaf.
MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Re: FIRST STEP-Take Vitamin D3 Before & After De-Stenosis.

Postby Squeakycat » Fri Jan 04, 2013 4:50 am

NZer1 wrote:MS Australia is running the world first randomised controlled trial to see if Vitamin D can actually prevent MS after an initial incident, there are different dose levels being trialled so some clarity might come from that :

http://www.msra.org.au/australia-rolls- ... tion-trial

ARGH(*%^%^(&*^)*&^()

1. There appears to be no plan to:
    1. Raise the 25(OH)D level of participants to a high level to start! The selected doses will mean that during most of the trial, people will just be getting up to a high enough level to have any effect and perhaps even more critically
    2. Without calcium of at least 1,200 mg/day, the study will fail. This was identified as the critical dimension in the pivotal EAE trial of vitamin D. It had no effect without calcium. This has also been shown to be true in human trials.

These are show stoppers!

There is simply no rational for the two lower doses in the trial. NONE. And Bruce Taylor who heads the trial should know this well. All he has to do is look at the results of other trials. Why repeat their errors? It is a waste of time and resources.

Rather than testing doses of 1,000 IU and 2,000 IU, the trial should probably test doses starting at the current high level of 10,000 IU. Levels of up 40,000 IU have been shown to have effect and be safe.

There is already ample evidence in the context of MS that these higher levels, PULSED, not taken daily, are safe.

It would appear that the primary goal of this trial is to prove that Vitamin D is useless. If it goes forward as planned, bet my last penny that it will FAIL.

What a waste.
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Re: Vit D3 Supply from iHerb in California

Postby Squeakycat » Fri Jan 04, 2013 5:26 am

MarkW wrote:There is very little data on what D3 levels a healthy outside dwelling human would maintain. I recall that Lifeguards in St Louis, USA had a natual level D3 of 150 mmol/L. (Hopefully I referenced the paper in this thread, otherwise it needs a PubMed search).

Here's the paper in case you didn't list it.

© 1999 American Society for Clinical Nutrition
Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety
Reinhold Vieth
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Re: FIRST STEP-Take Vitamin D3 Before & After De-Stenosis.

Postby NHE » Fri Jan 04, 2013 5:46 am

Squeakycat wrote:Thanks. I've read the Vieth pieces. In 2006 he said toss D2, there was no role for it. Now he is saying we need more studies to find out how they differ in terms of how they are metabolized and whether there are health differences as a result of these metabolic differences.

That sounds to me as though the jury is still somewhat undecided. They know the D3 raises 25(OH)D levels more effectively than D2, but they don't know if that is a health benefit since there may be some reasons for the difference that do have a direct health effects.


What I found interesting was the Medscape article which mentioned that vitamin D2 binds to the vitamin D receptor with lower affinity than vitamin D3. This could easily explain the lower efficacy of D2.

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Re: Vit D3 Supply from iHerb in California

Postby Squeakycat » Fri Jan 04, 2013 9:39 am

EJC wrote:I found a firm on eBay UK selling the brand you mentioned earlier in this thread.

I ordered a 360 day supply of the Healthy Origins Product in 10,000 iu liquicaps for £31 incl delivery.

http://stores.ebay.co.uk/SupplementsThatWork

The 5000iu caps are £14.96 + P&P

I do need to know what multivitamins/minerals Emma should be balancing this with though.

EJC,

What all the studies are showing is that you need to take calcium for vitamin D supplementation to be effective. Calcium requires adequate levels of magnesium and zinc to be fully absorbed. Several trials have been done with a level of 1,200 mg/day calcium. I found one product online, Nature's Life Calcium with Magnesium that also has zinc and 1000 mg of calcium.

High dosed vitamin D really should not be undertaken without first assessing kidney and liver function and being sure that calcium, phosphorus and parathyroid hormone (PTH) are all within normal limits or low. The danger is that high levels of vitamin D will induce hypercalcemia which can be extremely dangerous since it can cause the kidneys, heart and other organs to calcify while robbing bones of calcium and releasing toxic levels of phosphorus.

You minimize the risk of hypercalcemia at least at doses up to 20,000 IU a day by pulse dosing, taking a week's worth all at once. Since high levels of vitamin D can cause nausea, you can also divide the week's worth into two smaller batches taken 3.5 days apart.

So, to summarize: Emma will need to take a daily dose of calcium. It is highly advisable that you do blood work to check current 25(OH)D levels and kidney and liver function as well as levels of calcium, phosphorus and PTH to be sure they are within or below normal limits. The daily dose of vitamin D should be pulsed weekly or in two doses 3.5 days apart.
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Re: FIRST STEP-Take Vitamin D3 Before & After De-Stenosis.

Postby NZer1 » Fri Jan 04, 2013 1:51 pm

Ed, Australians have approached this like they have their CCSVI trials at the Alfred Hospital. It appears at times that there is a time warp where they don't notice what else happens around the World in Research and they follow the old model of thinking anyway, it's either that or it takes a decade or so to get Studies through red tape and funding.

Anyway, I read this earlier and I believe if you look at the article and merge Vit D knowledge of the influences it has in multiple body functions, I believe that the picture for MS and most diseases takes on a more progressive approach to returning Health.

"From; CCSVI in New Zealand (Me)
The hypothalamic-pituitary-adrenal axis and the sympathetic nervous system
http://www.envita.com/lyme-disease/fina ... e-disease/
Idiopathic disease is defined as one that develops without any apparent or known causes. That is the term used for fibromyalgia, autoimmune diseases, including Lupus and Chronic Fatigue Syndrome. While many of these diseases have recognizable signs and symptoms, the lack of causality haunts medical schools, doctors, practices, and hospitals. The only one benefitting from the lifelong symptom treating associated with Chronic Fatigue Syndrome, Lupus, Autoimmune disease, or Fibromyalgia are the pharmaceutical companies who sell billions in medication to treat them. A long list of pain medications, sleep-aids, anti-depressants, and anti-inflammatories is not sufficient because the diagnosis is incorrect. So let’s look at what the possible causes are to these diseases.
Below, is a quick list of causes and we will give a clinical review and explanation as to what takes place.
Chronic Fatigue Syndrome and Fibromyalgia have been linked with genes involved in the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. These genes regulate response to trauma, injury, and other stressful events. Our ten years of clinical experience shows that while such traumas could play a role in the etiology (the trigger to exhibiting symptoms) of the disease, they are unlikely the conditions’ causes.
HPA makes up a multi-set of direct influences and feedback interactions among the hypothalamus, the pituitary gland (a pea-shaped structure located below the hypothalamus), and the adrenal, also called “suprarenal,” glands which are small, conical organs on top of the kidneys.
The interactions among these organs constitute the HPA axis, a major part of the neuroendocrine system. From here the body regulates reactions to stress as well as processes such as digestion, the immune system, mood, emotions, sexuality, as well as energy. Infectious disease, such as chronic Lyme Disease Complex, impacts the HPA-axis via neurotoxins that compete for the same receptor sites used by the HPA-axis. In fact, such infections can bring about identical symptoms of some idiopathic diseases listed above and many of the symptoms associated therewith. This should bring our attention to the Lyme Disease Complex, which is composed of a number of infections and neurotoxins that bring about even more symptoms than those listed earlier in this article.
Abnormal levels of certain chemicals regulated in the HPA axis area of the brain system, have been proposed as a cause of Chronic Fatigue Syndrome and also have some influence in Fibromyalgia. This system controls important functions, including sleep, stress response, and depression. Of particular interest to researchers, are the chemicals and other factors listed below that are controlled by the HPA axis.
The HPA axis is involved in the neurobiology of mood disorders and functional illnesses, including anxiety disorder, bipolar disorder, insomnia, post-traumatic stress disorder, borderline personality disorder, ADHD, major depressive disorder, burnout, chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome, and alcoholism. Antidepressants, which are routinely prescribed for many of these illnesses, serve to regulate HPA axis function. All of these conditions and their symptoms are commonly seen in Chronic Lyme disease patients that contain a host of infections and neurotoxins that block serotonin receptors in the brain.
Patients may have contracted an infection at any point in their life-time; however, the symptoms of Chronic Lyme disease Complex or its co-infections may remain unseen or dormant until the individual is weakened by a trauma or trigger. This could be anything from child birth or a car accident to the death of a loved one, a divorce, or even a vaccine as seen among children with weakened immune systems.
In the etiology of chronic infectious disease, the traumatic event is a trigger but not the cause of autoimmune disease, Chronic Fatigue Syndrome, or Fibromyalgia. Nevertheless, treating these triggers is critically important to the new patient’s care. What we find is that infection and not genetic defects are at the root of HPA axis disruption in the brain itself.
A number of studies have found that alterations in genes are caused by infections involving immune function, intercellular communication and energy transfer.
Researchers have identified many different genes in patients with Chronic Fatigue Syndrome that relate to blood disease, immune system function, and infection. However, despite these identifications, there is no clear pattern to them and it is quite possible that it is the infections alone that are altering these genes and are responsible for impacting mental and emotional health as well. It is very possible that the infections can alter these genes that impact mental and emotional health as well.
Some patients with Chronic Fatigue Syndrome have abnormally high levels of serotonin – a neurotransmitter (chemical messenger in the brain), and also show deficiencies in dopamine – an important neurotransmitter associated with feelings of reward. In some cases there is also a demonstrable imbalance between norepinephrine and dopamine.
A number of studies on Chronic Fatigue Syndrome have shown patients with lower cortisol levels, a stress hormone produced by the adrenal glands. It has been suggested that such cortisol deficiencies are responsible for Chronic Fatigue Syndrome patients having impaired or weakened responses to psychological or physical stresses like worry, infection, or exercise. However, administering replacement cortisol improves symptoms only in some patients. Why? Infection and their toxins (neurotoxins) must be cleared before hormone replacement can begin to be effective in these patients. It is also common for these patients to have thyroid, testosterone and cortisol issues.
Evidence suggests that certain CFS, Fibromyalgia, and Autoimmune patients have disturbed circadian rhythms (disorder of the sleep-wake cycle), which is regulated by the so-called circadian clock, a nerve cluster in the HPA axis. These are commonly seen in Lyme Disease Complex along with a number of other neurological symptoms.
A mentally or physically stressful event, such as a viral infection, may disrupt natural circadian rhythms. An inability to reset these rhythms results in a perpetual cycle of sleep disturbances. Medications that improve sleep can be very helpful for certain patients with Chronic Fatigue Syndrome, Fibromyalgia, and Autoimmune diseases. But, until the infections are cleared and hormones are rebalanced, long-term improvement is unlikely.
Psychological, personality, and social factors are strongly associated with Chronic Fatigue Syndrome, Fibromyalgia, and Autoimmune disease like Lupus. There is a distinct complex relationship between physical and emotional factors.
Because most of the features of Chronic Fatigue Syndrome resemble those of a lingering viral illness, many researchers have focused on the possibility that a virus or some other infectious agent, in some cases, causes the syndrome.
We have clinically determined that these patients usually have a group of viral, bacterial, parasitic, and fungal infections that make up what we call Lyme Disease Complex. Some patients may or may not have actual Lyme disease but may have another type of tick-borne illness along with a host of co-infections that have brought about immunological, hormonal, and neuroendocrine changes.
Still, not all Chronic Fatigue Syndrome patients show signs of infection. And although experts have long been divided on whether infections play any role in this disorder at all, it does seem clear that subtypes of both viral and non-viral Chronic Fatigue Syndrome exist. That being said, researchers have seemingly overlooked the complexity of mute-infections, multi-toxins, and heavy metal components that complicate these conditions making them extremely difficult to diagnose on a case to case basis. When a complex of infections exists, they can affect the activation and replication of each other via biofilm communities. To be certain, most patients are never tested thoroughly and correctly for all the infections that make up, chronic Lyme Disease Complex.
The theory for Chronic Fatigue Syndrome having a viral cause is not based on hard evidence, rather, on an ever-growing series of observations that suggest this association:
Chronic Fatigue Syndrome as well as Fibromyalgia and Autoimmune disease patients are often found with elevated levels of antibodies to many organisms that cause fatigue and other Chronic Fatigue Syndrome symptoms. Such organisms include those that cause Lyme disease, Candida (“yeast infection”), herpes virus type 6 (HHV-6), human T cell lymph tropic virus (HTLV), Epstein-Barr, measles, coxsackie B, cytomegalovirus, or parvovirus.
Many of these infectious agents are very common; however, none have emerged as a definitive cause of CFS. Well-designed studies of patients who met strict criteria for CFS without any known cause have not found an increased incidence of any specific infection(s).
In up to 80% of cases, CFS starts suddenly with a flu-like condition. In the U.S., there have been reports of cluster outbreaks of CFS occurring within the same household, workplace, and community (but most have not been confirmed by the Centers for Disease Control and Prevention). However, most cases of CFS occur sporadically in individuals, and do not appear to be contagious. These all have the pattern of infections and more importantly, complexes of infections taking over the patient’s immune system, which is clearly seen in the depressed CD57 markers found in almost all of this population.
CFS is sometimes referred to as “Chronic Fatigue Immune Dysfunction Syndrome.” In many cases, studies have detected many immune system irregularities. Some components appear to be over-reactive, while others appear to be under-reactive, but no consistent picture has emerged to explain CFS as a disease of the immune system in conventional medical practices. Chronic Lyme Disease patients almost always have depressed CD57 marker called the striker panel and this is almost never run on chronic fatigue patients when they go to their doctor. Almost 100% of the time we find decreased key immune function in all CFS patients because we are running the correct diagnostics.
Some studies have reported that a majority of CFS patients have allergies to foods, pollen, metals (such as nickel or mercury), or other substances. One theory is that allergens, like viral infections, may trigger a cascade of immune abnormalities leading to CFS. However, most allergic people do not have CFS. In our clinical setting, patients often have pesticide, heavy metal and chemical toxicity along with chronic infections which explains the abnormal and inconstant responses to allergies. Environmental toxins complicate these conditions and require targeted treatments to overcome them.
The risk profile for CFS is similar to the risk profiles for a number of autoimmune diseases. Studies are inconsistent with regards to the presence of auto-antibodies (antibodies that attack the body’s own tissues) in CFS, so the disease is unlikely to be due to auto-immunity – making it more likely connected to infectious disease. In Lyme disease patients, we typically see that the patient was diagnosed at one time or another with several autoimmune diseases but almost certainly the previous physicians were confused."

Another angle that comes into focus in the interlinking is the Dyautonomia link that Mike Arata is pushing. Linking the Vascular changes to the Autonomic System creates a continuum of thinking from the above article.
The other insight that shows a Protein in the BBB that is missing in MS has some more Jigsaw pieces to ponder, yet it also fits in the context of combinations to achieve a dx of MS.

From; CCSVI in New Zealand (Me again!)
"Sounds promising!

(Medical Xpress)—Research led by Queen Mary, University of London, has opened up the possibility that drug therapies may one day be able to restore the integrity of the blood-brain barrier, potentially slowing or even reversing the progression of diseases like multiple sclerosis (MS). The study, funded by the Wellcome Trust, is published in Proceedings of the National Academy of Sciences.
The blood-brain barrier (BBB) is a layer of cells, including endothelial cells, which line the blood vessels in the brain and spinal cord. These cells act as a barrier, stopping certain molecules, including immune cells and viruses, passing from the blood stream into the central nervous system (brain and spinal cord).

In a number of neurodegenerative brain diseases, including MS, the BBB is compromised, allowing inappropriate cells to pass into the brain with devastating consequences.

In this study the researchers identified a specific protein – known as Annexin A1 (ANXA1) – as being integral in maintaining the BBB in the brain. The authors initially found that mice bred to lack this protein showed a decrease in integrity of the BBB compared to controls.

Taking this finding, they then investigated the potential role of ANXA1 in conditions which involve progressive breakdown of the BBB, including MS and Parkinson's disease, by examining post-mortem human brain tissue samples. ANXA1 was present in the cells of samples from individuals who did not have a neurological disease and also in samples from patients who had died with Parkinson's disease. However, it was not detectable in the endothelial cells in samples from patients who had died with MS.

Crucially, the researchers found that treating in vitro brain endothelial cells with human recombinant ANXA1 restored the key cellular features needed to reinstate the integrity of the BBB. The same was seen with the ANXA1 knockout mice, where administering the protein reversed the permeability of the BBB within 24 hours.

Dr Egle Solito, from Barts and The London School of Medicine and Dentistry, part of Queen Mary, who co-ordinated the study said: "Our findings suggest this protein plays a key role in maintaining a functioning BBB and, more importantly, has the potential to rescue defects in the BBB. We now need to carry on our research to see how much this molecule may be exploited for therapeutic uses in conditions such as MS, or as a biomarker to help in early diagnosis."
Provided by Queen Mary, University of London
http://m.medicalxpress.com/news/2013-01 ... rrier.html"

Mixing Bowl stuff, which is the most important ingredient? All I guess!
Nigel
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Re: Vit D3 Supply from eBay in UK

Postby EJC » Fri Jan 04, 2013 2:13 pm

MarkW wrote:
EJC wrote:I found a firm on eBay UK selling the brand you mentioned earlier in this thread.
I ordered a 360 day supply of the Healthy Origins Product in 10,000 iu liquicaps for £31 incl delivery.
http://stores.ebay.co.uk/SupplementsThatWork
The 5000iu caps are £14.96 + P&P

I do need to know what multivitamins/minerals Emma should be balancing this with though.


Thanks for the info EJC. I would check that the eBay importer know how to store the D3 as the price is close to what I would pay direct from iHerb.

I would not add any extra vit/min at this stage, as it complicates assessing changes. If Emma's D3 level is not over 125mmol/L with 10k iu/day then consider the points that Jimmylegs made on minerals. Your GP is able to conduct a test for D3 in blood on the NHS (mine does). I suggest 2 months of D3 then a test, maybe Feb/Mar, as we are unlikely to get any sun before then in southern England.
MarkW


Thanks Mark (and all who have replied).

I'll ply Emma with these D3 tabs for 8 weeks then get some bloods done and will post on here what they are.

She does get B12 shots every 6 weeks - which I hope have no conflict with these?
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Re: FIRST STEP-Take Vitamin D3 Before & After De-Stenosis.

Postby jimmylegs » Fri Jan 04, 2013 3:30 pm

hi nigel sorry i missed your question the other day, patchy access.

yes ensure optimal zinc and magnesium status, not just calcium, to ensure optimal d3 status.

i find i can't even take calcium, i absorb it too well b/c of all my dark leafy greens etc. if i take calcium i feel my muscles heading for spasticity.

serum magnesium is one useful test, ensure serum levels are at LEAST 0.90 mmol/L. that's the middle of the 'normal' range.

serum zinc is another important one. levels should be upper teens. based on lots of studies looking at zinc levels in healthy controls, i aim for 18-19 umol/L. that is the top end of the 'normal' range. my d3 absorption more than tripled when i got my zinc level optimized. i had been deficient previously. you still absorb the d3, but you do it way better with optimal zinc status. i can only imagine all the other things that are also working better with optimal zinc in the picture.

yes selenium is important too. brazil nuts are supposed to be an excellent source (2-3 a day) ugh :S i mainly get my dietary selenium from good old egg yolks! selenomethionine is supposed to be a good supplemental form. generally, i take 200mcg supplemental selenomethionine daily.
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: Vit D3 Supply from eBay in UK

Postby Squeakycat » Fri Jan 04, 2013 5:33 pm

EJC wrote:I would not add any extra vit/min at this stage, as it complicates assessing changes.
Thanks Mark (and all who have replied).

I'll ply Emma with these D3 tabs for 8 weeks then get some bloods done and will post on here what they are.

She does get B12 shots every 6 weeks - which I hope have no conflict with these?


EJC, calcium is not an "add on" it is a "co-factor" of vitamin D. Vitamin D manages calcium in the body and is prompted to do much of what it does by calcium. They are a team.

If Emma, like Jimmylegs, is eating 1,000 mg worth of dietary calcium a day, then she wouldn't need a calcium supplement, but otherwise, you might as well just put the vitamin D capsules at the foot of your Buddha and hope that works. :>)

This is going to sound a little contradictory, but it isn't. High doses of vitamin D, if it is pulsed as it needs to be to avoid hypercalcemia, will lower PTH which will lower calcium absorption. This is the goal when you use high dose vitamin D for people (and my cats) with renal failure.

So as soon as you start taking vitamin D in high doses, you have a calcium deficit and if not addressed, will cause vitamin D to be unable to do what it is supposed to be doing just as surely as low vitamin D levels have this effect.

So you need the higher levels of calcium to offset the action vitamin D has on PTH which then lowers calcium absorption. Isn't the body wonderfully complicated.

Without adequate supplies of calcium, vitamin D will not be able to do what it is supposed to do, in this case, repair damage to the blood brain barrier and dampen the immune response somewhat.

The thing that got all this rolling in MS was the study of vitamin D supplementation in EAE mice. The effect was so dramatic and the fear of losing the market for worthless pharamaceuticals so great, that everyone decided to run trials, I think to put it to bed as they've been doing with CCSVI.

In the EAE study, the authors note that the mice were fed a high calcium diet and this was why they got such dramatically different results than two earlier studies: "It is important to note that in these experiments, unlike previous experiments (13, 14), the animals were fed a high calcium diet with the only variable being the administration of 1,25-(OH)2D3."

In all the Kimball/Veith human trials of vitamin D and MS, they use calcium, in sharp contrast to almost all other trials. I haven't yet found their explanation for this. It seems that they are saying, "Of course we are using calcium. How else would vitamin D work?" This may be explained in some of their other papers before these trials. They do explain the dose which is the recommended daily allowance by noting that most people do eat things which have calcium in them which they say probably, on average, adds up to around 800 mg. That makes the total for the day 2,000 which is the standard upper limit for calcium above which you set off a hypercalcemia cascade.

It is all a delicate balance which is why it really should be under the supervision of a medical professional.

Scream if any of this is unclear or you disagree. I'll marshal up a crowd of authorities. :>) Meanwhile, I'm going to follow Jimmylegs' lead and go see how vital zinc is to all of this. I know that magnesium is and I know that the same receptors vitamin D has various genes create to move calcium around in the cell, also will allow manganese to pass. There has to be a reason for this too, though so far, no one has actually looked at that question as far as I can tell.
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Re: Vit D3 Supply from eBay in UK

Postby MarkW » Sat Jan 05, 2013 4:44 am

EJC wrote:
MarkW wrote:
EJC wrote:I found a firm on eBay UK selling the brand you mentioned earlier in this thread.
I ordered a 360 day supply of the Healthy Origins Product in 10,000 iu liquicaps for £31 incl delivery.
http://stores.ebay.co.uk/SupplementsThatWork
The 5000iu caps are £14.96 + P&P
I do need to know what multivitamins/minerals Emma should be balancing this with though.

I would not add any extra vit/min at this stage, as it complicates assessing changes. If Emma's D3 level is not over 125mmol/L with 10k iu/day then consider the points that Jimmylegs made on minerals. Your GP is able to conduct a test for D3 in blood on the NHS (mine does). I suggest 2 months of D3 then a test, maybe Feb/Mar, as we are unlikely to get any sun before then in southern England.
MarkW

Thanks Mark (and all who have replied).
I'll ply Emma with these D3 tabs for 8 weeks then get some bloods done and will post on here what they are.
She does get B12 shots every 6 weeks - which I hope have no conflict with these?


Hello EJC,
My approach differs for Emma from the info from population studies. I suggest changing one vit/min at a time then test D3 levels after each change. My logic stems from the differences in diet and uptake of vits/mins by humans - there is a lot of variabilty. If one needed to raise D3 blood levels in a group of people and did not wish to test after each change then one would give D3 plus calcium plus zinc plus magnesium plus selenium. However, you have a population of one (Emma), who I guess prefers to take the minimum number of pills/capsules every day. The objective is the same - a minimun blood D3 level of 125mmol/L, how you get there depends on your approach and how co-operative Emma's GP is on conducting tests.
Looking forward to reading the results in a couple of months.
Best wishes,
MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Aus Study on Vitamin D3

Postby MarkW » Sat Jan 05, 2013 4:55 am

Hello NZer1,
Should you inform the researchers and sponsors of the Aus trial that they are wasting their time and money???
Wear a bullet proof jacket if you do, as you could be the messenger who gets shot.
MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Re: FIRST STEP-Take Vitamin D3 Before & After De-Stenosis.

Postby EJC » Sat Jan 05, 2013 5:03 am

OK I seem to be getting different advice here.

Should Emma be taking anything with the 10,000iu D3 supplements?
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Re: FIRST STEP-Take Vitamin D3 Before & After De-Stenosis.

Postby Squeakycat » Sat Jan 05, 2013 7:02 am

EJC wrote:OK I seem to be getting different advice here.

Should Emma be taking anything with the 10,000iu D3 supplements?

I think she has to have calcium for the reasons I explained.

Vitamin D will suppress calcium absorption by depressing PTH. If you don't add calcium, then the vitamin D will have little effect, even though you will be able to raise her 25(OH)D level. Most of what vitamin D does involves calcium. Calcium acts on vitamin D and is acted upon by vitamin D.

As far as the other minerals, the Nature's Life brand of calcium citrate maleate also has magnesium and zinc so is an easy way to take the necessary calcium and at the same, cover some of the magnesium and zinc that may play a role in vitamin D metabolism.

The calcium comes as a 1,000 mg tablet which is the recommended daily allowance. It leaves enough margin so that her normal intake of calcium which likely fluctuates on a day to day basis, plus the supplement, will still be under the daily upper limit of 2,000 mg of calcium.

Again, the reason for taking calcium is because it's absorption will be suppressed by vitamin D and it is a co-factor of vitamin D. Vitamin D alone will have little effect without adequate supplies of calcium.
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Re: Aus Study on Vitamin D3

Postby Squeakycat » Sat Jan 05, 2013 7:37 am

MarkW wrote:Hello NZer1,
Should you inform the researchers and sponsors of the Aus trial that they are wasting their time and money???
Wear a bullet proof jacket if you do, as you could be the messenger who gets shot.
MarkW

It appears that this trial got started months ago so there is probably no way to change the design at this stage.

We need to lay out the sine qua non of these trials and hope that the people conducting them will look at this and design trials to answer the real questions.

We have no idea how much vitamin D is needed by someone with MS or how that varies with the course of the disease. It could turn out to be very little, or it could turn out to be a lot. It would be nice if the different trials tested this. It seems rather easy to test.

Logic and a few studies tell us that if you suppress calcium absorption you need to add calcium for vitamin D to have effect in MS. While we have a few studies that suggest that this is the case, it hasn't been examined in a double blind, placebo controlled fashion just testing this.

I feel comfortable saying that if there was no breakdown in the blood brain barrier, there would be no MS. We need to know if the principle effect of vitamin D is in maintaining the blood brain barrier and as a result, dampening the immune response.

As such, it may be addressing the root cause of demyelination, but we don't know if it has a role in remyelination.

As such, I would not expect it to have much impact on EDSS, but it should cause gadolinium enhanced lesions to go away. That should lessen the number of relapses.

It won't fix malformed veins. It probably isn't enough to stop damage caused by smoking, alcohol, poor dietary habits.

At the same time, it could have a direct effect on any viral, bacterial or I suppose, even a protozoan infectious agent.

Basically, we need to tease out how it is working, but with the initially focus on whether it is working and at what levels of 25(OH)D, what co-factors are necessary.
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Squeakycat
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Re: FIRST STEP-Take Vitamin D3 Before & After De-Stenosis.

Postby EJC » Sat Jan 05, 2013 8:03 am

calcium it is then.

Anything else?
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