Todd,

Sorry you're having such a rough time... The trip to the ER proves you need an Rx for home oxygen therapy...  That... or take up welding...

V/R, Batch

3-Foot,

No question about it... you were clearly vitamin D3 deficient at the time of that lab test.  If you haven't taken any supplemental vitamin D3 or spent any time in the mid day sun clad in a bathing suit without sun block... your 25(OH)D serum concentration will not have changed.

The following table lists the supplements and doses needed in the anti-inflammatory regimen.

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The following photo illustrates the supplements I take that meet the requirements in the table above.  I buy most of them at Costco...  I buy the super K and vitamin B 50 over the Internet from Amazon.

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The vitamin B 50 is not shown in the photo above.

You're a good candidate for the accelerated vitamin D3 loading schedule.  This will build your 25(OH)D serum concentration rapidly but at a measured pace.

Start the anti-inflammatory regimen at 10,000 IU/day vitamin D3 for a couple days just to make sure there's no reaction to any of the supplement then proceed with the loading schedule below.

The following loading schedule totals 700,000 IU of vitamin D3 over a 4-week period.  That should result in a 25(OH)D serum concentration response of 70 ng/mL on top of your starting serum concentration of 25(OH)D at 10 ng/mL. 

At the end of the 4-week loading schedule, try to get another lab test for 25(OH)D.  You should be up around 80 ng/mL at that point which will make 10,000 IU/day vitamin D3 a good maintenance dose.

Week 1 - 50,000 IU/day vitamin D3
Week 2 - 25,000 IU/day vitamin D3
Week 3 - 15,000 IU/day vitamin D3
Week 4 - 10,000 IU/day vitamin D3

Be sure to take all the other supplements daily.  Magnesium is the most important cofactor. 

Regarding the verapamil...  The only possible interaction comes from the calcium which can lower verapamil's effectiveness.  The Mature Multi is formulated with 220 mg of calcium so that shouldn't impact verapamil as long as you separate the dosing time for verapamil and Mature Multi by 10 to 12 hours.

I'd take the verapamil in the morning and the entire anti-inflammatory regimen with the evening meal.  This will also improve vitamin D3 absorption.

Please feel free to ask questions...

Take care and please keep us posted.

V/R, Batch

Hey Sue,

Great news, great lab results and a great question.  In order to better understand the relationship between vitamin D3 metabolism and PTH you also need lab tests for serum calcium as you'll see below.

The pharmacokinetics of vitmamin D3 (what the body does to vitamin D3) is fascinating.  Once vitamin D3 is metabolized to 25(OH)D in the liver, the 25(OH)D travels along two separate paths of metabolism.

In the first path, called the endocrine path, 25(OH)D is further metabolized to 1,25(OH)3D3 by the kidneys.  This path is tightly controlled by calcium homeostasis, the mechanism that controls serum calcium concentrations to maintain it in a very narrow range.

This is also where the parathyroids and their hormone, PTH, come into play.  If the serum calcium concentration is near the low end of the normal reference range or below, the parathyroids sense this condition and increase production of PTH. 

The increased serum concentration of PTH signals the kidneys to increase the rate of metabolism of 25(OH)D to 1,25(OH)2D3, the active hormonal form of vitamin D3. The increased serum concentration of 1,25(OH)2D3 pulls more calcium from the gut and transports it into blood serum to increase its serum concentration.

If the serum calcium concentration is near the upper end of its normal reference range, the parathyroids sense this condition and down-regulate or suppress production of PTH.  This slows metabolism of 25(OH)D to 1,25(OH)2D3 in the kidneys so less calcium is pulled from the gut.

Again, the above discussion covers the endocrine path of vitamin D3 metabolism and how it sustains calcium homeostasis  along with maintenance of bone mineral density.  From a life sustaining standpoint, this is the most important path... 

Not enough vitamin D3 means insufficient 25(OH)D and that results in serum calcium concentrations dropping below the normal reference range...  When that happens... bone mineral density suffers, nerve cells don't fire properly, calcium channels break down and the wheels come off... In other words, health declines rapidly...

The second path of vitamin D3 metabolism gets really exciting.  This is called the autocrine or autocrine/exocrine path that results in genetic expression...

In the autocrine path of vitamin D3 metabolism, the 25(OH)D produced by the liver is metabolized extrarenal (outside the kidneys) at the cellular, nuclear and genetic level throughout the body. 

For CH'ers, when 25(OH)D is metabolized in nerve cells within the trigeminal ganglion, this is where the magic occurs resulting in a cessation or reduction of CH symptoms.

The following graphic illustrates the two paths of vitamin D3 metabolism.  As you can see roughly 20% of the 25(OH)D produced in the liver travels along the endocrine path and 80% along the autocrine path.

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In the autocrine path of vitamin D3 metabolism, 25(OH)D enters the cell wall where the the same enzyme, 1-α hydroxylase, that adds another hydroxyl ion [OH]^- at the 1st position on the vitamin D3 molecule in the kidneys, does the same thing within the cell. 

As a side note, the 1-α hydroxylase enzyme requires magnesium and some of the other vitamin D3 cofactors to function properly.

Within the cell nucleus at the genetic level, 1,25(OH)2D3 combines with retinol (vitamin A) to form a 2-molecule chain polymer, (dimer), that attaches to a vitamin D receptor (VDR) at one end on one part of the gene and a retinoid X receptor (RXR) at the other end on another part of that gene.  When this happens, the cell's genetic library of instructions are opened and the cell begins to follow these instructions...

The following graphic illustrates bonding of the vitamin D3-vitamin A dimer to a gene at a vitamin D response element (VDRE).  This is a DNA sequence that is found in the promoter region of vitamin D regulated genes...

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The leading theory on the role of vitamin D3 in preventing cluster and migraine headaches deals with the autocrine path of vitamin D3 metabolism.  This is where 1,25(OH)2D3 and vitamin A (retinol) signal the nerve cell to down-regulate calcitonin gene-regulated peptide (CGRP).   CGRP has been found elevated during the pain phase of CH and migraines.

Molecular biologists and geneticists are just starting to peal back the onion skin layers when it comes to the role of vitamin D regulated genes... and the extent vitamin D3 plays in our overall health.

A 2010 study identified 2776 genomic positions occupied by the VDR and 229 genes with significant changes in expression in response to vitamin D...  Cluster headache is only one of these...

Hope this helps answer the mail...

Take care,

V/R, Batch