Visperas,

Great questions...  Let's start with your 25(OH)D serum concentration...  Yours is between 95 and 98 ng/mL and you're staying mostly CH pain free so this appears to be a good therapeutic range to maintain...

The serum concentration of 25(OH)D is essentially a biological marker of vitamin D3 status... 

The higher the 25(OH)D serum concentration the better and 80 ng/mL is a good target...  Above that, there's really no problem until you start approaching 200 ng/mL...  Routine serum 25(OH)D, calcium and PTH lab tests are prudent if you need to maintain a 25(OH)D serum concentration above 100 ng/mL

The 25(OH)D serum concentration also represent an indication of vitamin D3 reserves once you've reached a reasonably stable serum concentration... and your 25(OH)D serum concentration is relatively stable... 

Higher 25(OH)D reserves near the target serum concentration mean the incidence of a CH relapse is much lower in the event of a viral or bacterial infection or an allergic reaction... These conditions trigger an immune response that will consume 25(OH)D rapidly as do injury or surgery.

1,25(OH)2D3 serum concentrations are generally a 1000 times less than 25(OH)D and they fluctuate rapidly from day to day as a function of calcium homeostasis.

It all depends on the serum calcium concentration and the serum concentration of the parathyroid hormone PTH.  When the serum calcium concentration starts to drop, the parathyroids sense this condition and start pumping out PTH. 

PTH signals the kidneys to metabolize more 25(OH)D into 1,25(OH)2D3 which in turn pulls more calcium from the gut and pushes it into the blood stream.  As the serum concentration of calcium rises, PTH drops so less 1,25(OH)2D3 is produced...   It's all a very tightly controlled balancing act to maintain serum calcium concentration in a very narrow range.

Vitamin D3 intoxication occurs under a couple situations...  A hyperactive parathyroid produces too much PTH and this triggers the kidneys to produce too much 1,25(OH)2D3 and this pulls too much calcium from the gut resulting in calcium serum concentrations above its normal reference range...  (vitamin D3 intoxication).

If we take too much vitamin D3, (a lot more than called for in the anti-inflammatory regimen) our liver will produce too much 25(OH)D.  This overloads the body's mechanisms for controlling 25(OH)D metabolism and this can also result in a calcium serum concentration above its normal reference range...   (vitamin D3 intoxication).

Magnesium plays an essential roll in the enzymatic processes involved in metabolizing vitamin D3 into 25(OH)D and then on to 1,25(OH)2D3, (Calcitriol), the active hormonal metabolite of vitamin D3.  Magnesium levels can also be affected by other blood electrolytes...

Most of the above discussion deals with the endocrine mode of vitamin D3 metabolism and calcium homeostasis...  Roughly 20% of the 25(OH)D metabolized from vitamin D3 in the liver is further metabolized by the kidneys into 1,25(OH)2D3 to maintain calcium homeostasis... 

The other 80% of the 25(OH)D produced by the liver is metabolized and consumed at the cellular and nuclear level throughout the body in what is called the autocrine path of vitamin D3 metabolism...

It's this path of vitamin D3 metabolism we think is responsible for preventing CH and migraines.  The leading theory is the genetic expression made possible by vitamin D3, [1,25(OH)2D3] and retinol (vitamin A) trigger the nerve cells to stop producing calcitonin gene-related peptide, (CGRP).

CGRP is a vasodilator and responsible for not only pain transmission but also neurogenic inflammation...  both are part of the pathophysiology of cluster headache.

In this path of vitamin D3 metabolism, 25(OH)D and vitamin A (retinol) are absorbed in the cell wall and metabolized to 1,25(OH)2D3 and a family of retinoids within the cell.  The 1,25(OH)2D3 then combines with retinoids to form a bridge attaching to specific genes at a vitamin D3 receptor (VDR) and Retinoid-X receptor (RXR).

This process unlocks the cell's genetic library and triggers the cell to perform any one of a number of functions...  In our case as CH'ers, the cell slows or stops producing CGRP.  It's also important to note that 1,25(OH)2D3 and retinol are consumed in this process so more will be needed to maintain this cell function.

So there you have it... How to build a Swiss watch when you only wanted the time...

The takeaway is simple, we need all the vitamin D3 cofactors...

Hope this helps...

Take care,

V/R, Batch

Hey Gracie,

Good question...  The biggest difference between vitamin D3 and vitamin D2 is the human body produces it's own vitamin D3 and there are hundreds of biological processes that depend on vitamin D3 in ample quantities...

Supplemental vitamin D3 is available over the counter without prescription.  It's also distilled from animal fatty acids.

Vitamin D2 is primarily synthesized in a lab...  Here in the US it's only available by prescription...

There are several studies that show vitamin D3 is 30% to 60% more effective than vitamin D2 in treating medical conditions due to a vitamin D deficiency.  You can read more about why you should be taking vitamin D3 and not D2 at the following VitaminDwiki link:

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Here's the latest list of supplements and doses used in the anti-inflammatory regimen along with a photo of the supplements I take:

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The Mature Multi contains the rest of the vitamin D3 cofactors shown in the table above.  Not shown in this photo is the vitamin B 50 recommended by Dr. Stasha Gominak, MD.  She's a neurologist in Tyler, TX who suggests a 3-month course of vitamin B 50 to take care of any possible B vitamin deficiencies... 

Dr. Gominak has been treating her patients with sleep, chronic pain and headache disorders for over 6 years with a regimen very similar to the anti-inflammatory regimen.  The only real difference is she adds the 3-month course of vitamin B 50.

Vitamin B 50 is a formulation of all seven B vitamins at 50 mg each plus 400 mg of Folic acid.

Many CH'ers have found the following vitamin D3 loading schedule elevates their 25(OH)D serum concentration and achieves a pain free response a lot faster than taking 10,000 IU/day vitamin D3... 

Take the complete anti-inflammatory regime with 10,000 IU/day vitamin d3 on the first day.  As long as you don't experience an allergic reaction (very rare) to the vitamin D3, proceed with the loading schedule.

The vitamin D3 loading schedule calls for 20,000 IU/day vitamin D3 for two weeks plus a 50,000 IU loading dose once a week during the first two weeks.

Take 15,000 IU/day vitamin D3 for the next two weeks then drop the vitamin D3 intake to a maintenance dose of 10,000 IU/day. 

This loading schedule totals 600,000 IU of vitamin D3 over the 4-week schedule.  I know that sounds like a lot of vitamin D3, but it averages out to a little over 20,000 IU/day vitamin D3... 

Our skin can make that much vitamin D3 with a 30 minute exposure to the UVB in direct sunlight at mid day if clad in a bathing suit without any sun block.

This vitamin D3 loading schedule should result in a 25(OH)D response of 60 ng/mL above the starting serum concentration by the end of the 4th week. 

Be sure to see your PCP for the 25(OH)D lab test at that point.

Take care and please keep us posted.

V/R, Batch

Visperas,

Glad to hear the anti-inflammatory regimen is preventing your CH... and sorry my last explanation wasn't clear.

Regarding your questions... Under normal conditions, in the endocrine mode of vitamin D3 metabolism where calcidiol, [25(OH)D] is metabolized in the kidneys calcitriol, [1,25(OH)2D3] is controlled by a complex set of biological mechanisms involving the parathyroid hormone (PTH) to ensure an optimum level of serum calcium.

A slight dip in serum calcium (within the normal calcium reference range) is all it takes to stimulate calcitriol production in the kidneys.  Accordingly, you'll need to track total calcium serum concentration and serum PTH with lab tests to see their relationship with serum calcitriol.

Serum levels of calcitriol produced along the endocrine path of vitamin D3 metabolism can clearly help prevent the incidence of CH. 

That said, the autocrine path of vitamin D3 metabolism where calcidiol is metabolized within the nerve and other types of cells throughout the body at the nuclear and genetic level to calcitriol.  This process triggers genetic expression and consumes the calcitriol so it never reenters the blood stream.  Calcidiol, vitamin A (retinol) and magnesium are the primary reagents in the process we think down-regulates CGRP and in the process, prevents CH.

Vitamin D3 intoxication is very rare at the doses we take to control CH.  It would take 50,000 IU or more for several months to overload the 1,25(OH)2D3 control mechanisms and this would likely take 25(OH)D serum concentrations well above 200 ng/mL (closer to 300 ng/mL 25(OH)D).

There are exceptions... If the parathyroids are hyperactive (hyperparathyroidism) where too much PTH is produced, this can trigger an uncontrolled metabolism of 25(OH)D, (calcidiol) to 1,25(OH)2D3, (calcitriol). 

This excess calcitriol would then pull too much calcium from the gut and bones causing serum calcium concentrations to exceed the normal reference range. This is how a vitamin D3 intoxication is determined...

A vitamin D3 dose of 10,000 IU/day is very safe...  Your skin can make that much in as little as 10 minutes exposure to mid day sun clad in a bathing suit without sun block.

The average normal 25(OH)D response to a 5000 IU dose of vitamin D3 is a serum concentration of 60 ng/mL.  While this may prevent some CH, a serum concentration this low leaves no reserves for other consumers of 25(OH)D like your immune system...  See the following chart:

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Exposure to virus, bacteria or even allergens (this happens all the time) can trigger an immune response that will suck up available 25(OH)D leaving not enough to prevent CH... 

Accordingly, CH'ers are better off taking 10,000 IU/day vitamin D3 to maintain an average 25(OH)D serum concentration at 80 ng/mL...

I hope this answers the mail...

Take care,

V/R, Batch

Hey Gracie,

Watch Dr. Stasha Gominak's videos at the following link...  She explains sleep, why quality sleep is very important and why we need vitamin D3, the cofactors and a 3-month course of vitamin B 50.

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Take care

V/R Batch

Gracie,

Thanks for the update...  I understand the frustration that you're not completely pain free.  It's only been a week since you started the anti-inflammatory regimen and you've already experienced a favorable response with a reduction in the frequency and severity of your CH...

I'm confident, with a little more time, your CH symptoms will continue to decrease until you're pain free.  Once you've been taking this regimen for a month, try to see your PCP for another lab test for 25(OH)D. After that, the best course of action is to continue taking this regimen year-round at a vitamin D3 maintenance dose of 10,000 IU/day.

Take care and please keep us posted.

V/R, Batch