Hey Joseph,
Thanks for the update... Off hand, I'd say you're starting to respond to this regimen...
Good questions too... but my question for you is how much vitamin D3 are you taking daily?
With a starting 25(OH)D serum concentration of 10 ng/mL, it could take as long as two months at an intake of 10,000 IU/day vitamin D3 to get your concentration of this vitamin D3 metabolite up to 60 ng/mL. That's the lower threshold of the green zone (60-110 ng/mL) where CH'ers who respond to this regimen have a favorable response.
If you've been on the basic anti-inflammatory regimen at 10,000 IU/day vitamin D3 along with the 2000 mg/day Omega 3 Fish Oil, 500 mg/day calcium (the calcium citrate tablets formulated with the other basic cofactors: 80 mg/day magnesium, 10 mg/day zinc and boron) for 12 days, and you've had no problems, you may want to try like several other CH'ers have... an increased dose of 20,000 IU/day vitamin D3 with a 50,000 IU loading dose once a week.
As high a weekly dosing schedule as this sounds... 190,000 IU/week vitamin D3 is safe... It's also well below the 350,000 IU/week (average of 50,000 IU/day) vitamin D3 you would need to take for at least 12 weeks to reach the lower threshold of vitamin D3 intoxication at 200 ng/mL 25(OH)D... This condition would be clinically indicated by serum and urine calcium concentrations above normal.
This increased dosing strategy will build 25(OH)D levels much faster and hopefully get you into the green zone with a more favorable response at a serum concentration of 60 to 110 ng/mL in less time.
When you've experienced a cessation of CH attacks or a significantly reduced frequency and severity of attacks for at least a week, you can throttle back to 10,000 IU/day vitamin D3 as a maintenance dose.
Keep the cofactors at the original dose.
As to your questions...
1. The reason for the higher oxygen flow rates that support hyperventilation (25 to 45 liters/minute) is simple but likely not obvious unless you're a student of respiratory physiology.
Most neurologists and CH'ers assume it's the 100% oxygen inhaled resulting in an increased arterial partial pressure of oxygen above normal that aborts the cluster headache.
In fact, it's the increased arterial partial pressure of oxygen above normal
AND a decrease in the arterial partial pressure of CO2 below normal that aborts CH faster and more reliably than the lower oxygen flow rates.
Flow rates that support hyperventilation are also very safe... There are a lot of old wives tales about people passing out at high oxygen flow rates... For otherwise healthy people with CH, they're not true.
I've prayed to pass out during this method of oxygen therapy when I got to the oxygen late and the beast had a head start... it never happened...
In five years using this method of oxygen therapy at an average of 3 times a day... I've never passed out... nor have I seen reports of any other CH'ers having problems with higher flow rates... I'm also 68 and still here...
Why is a lower partial pressure of CO2 important during oxygen therapy?
You lower the arterial partial pressure of CO2 by hyperventilating... breathing faster and deeper than needed. In doing this, you're essentially blowing off CO2 faster than your body generates it through normal metabolism...
This pushes your system into voluntary respiratory alkalosis... In other words you've intentionally hyperventilated long enough to raise the alkalinity of arterial blood.
This accomplishes two other important physiological conditions. Blowing off more CO2 than normal lowers the acid content of the blood making it more alkaline (a higher pH). This stimulates the vasoconstriction needed to abort the CH.
A higher pH also increases blood hemoglobin's affinity for oxygen to the point where it carries up to 11% more oxygen. This results in a super-oxygenated flow of blood to the brain further increasing vasoconstriction...
The net effect is faster and more reliable aborts with oxygen therapy.
A couple things happen when you reach respiratory alkalosis... Most of us will experience the symptoms of paresthesia... a very slight tingling or prickling of the fingertips, lips or back of the neck. Some of us also experience a slight dizziness... I lean against a wall if I get dizzy.
Both of these symptoms of respiratory alkalosis are very normal and strange as it may sound, they are your friend. They tell you you're getting the fastest abort possible with oxygen therapy...
Why too much CO2 (an elevated arterial partial pressure of CO2) makes oxygen therapy ineffective...
If you're like most of us, when the CH pain reaches 6 to 8 on the 10 point headache pain scale, you're unable to stand still. Most of us do the CH 2-step or dance. Some of us pace in circles or rock back and forth.
This physical activity generates more CO2 and the body's response is to the elevated CO2 is to breath faster to keep CO2 levels in the normal range. Too much CO2 also triggers vasodilation throughout the body to increase blood flow to the lungs.
Here's the kicker... If your level of physical activity is greater than sitting motionless and you're doing the CH 2-step, pacing or just rocking back and forth... You'll need a volume of lung ventilation equal to 25 liters/minute or higher (a minute volume of 25 liters or greater) just to maintain normal CO2 levels...
However, if you constrain your lung ventilation to a minute volume of 15 liters (a flow rate of 15 liters/minute) with a non-rebreathing oxygen mask... and you have any physical activity above being completely at rest, you'll be unable to cast off sufficient CO2 to maintain normal levels... As a result, your arterial partial pressure of CO2 rises above normal and vasodilation increases. That's the exact opposite of what you want to happen with oxygen therapy...
This triggers an uncontrollable urge to breath faster but as your respiration is now limited or constrained to 15 liters/minute flow rate by the regulator, you'll start feeling increased anxiety and possibly panic attacks... even though you're still breathing 100% oxygen...
Under these conditions, an abort with oxygen therapy may not be bpossible or the time to abort will be greater than 20 minutes...
I know that was a long-winded answer. However, I've found that once CH'ers understand why oxygen flow rates that support hyperventilation are safe and far more effective with faster abort times than 15 liters/minute, they tend to have a much greater success rate aborting their CH with oxygen therapy.
2. Why take Omega 3 Fish Oil, Calcium and the other cofactors: magnesium, zinc, vitamin K2, vitamin A and boron.
The simple answer is they're all needed to make vitamin D3 therapy more effective.
Aside from the well published cardiovascular benefits of Omega 3 Fish Oil and it's anti-inflammatory properties, recent studies have linked the intake of Omega 3 Fish Oil to increased production of 1,25(OH)2D3, the active vitamin D3 metabolite and hormone that appears to be effective as a CH preventative.
Calcium is essential any time we take vitamin D3. The main reason is vitamin D3 pulls calcium from the gut and pushes it into the blood stream. Under normal conditions, this excess calcium in the blood is passed into the bones to maintain and increase bone mineral density (BMD). This process is tightly controlled by the parathyroid hormone to maintain serum calcium levels in a very narrow range.
If there is insufficient dietary calcium in the gut, vitamin D3 will take calcium from the bones... Hence, a minimum intake of 500 mg/day calcium will ensure sufficient calcium for better BMD and good bone health.
Magnesium, zinc and boron aid in vitamin D3 metabolism in the liver and kidneys.
Vitamin K2 helps direct serum calcium to the bones. It also helps prevent calcium plaque buildup in the arteries...
Vitamin A is the sleeper... and likely a key enabler in the CH preventative role of vitamin D3...
The normal path of vitamin D3 metabolism that maintains calcium homeostasis starts in the liver where vitamin D3 (cholecalciferol) is metabolized into 25(OH)D (calcidiol), and from there to the kidneys where 25(OH)D is further metabolized to 1,25(OH)2D3, (calcitriol).
A number of studies indicate vitamin A (retinol) is essential for an alternate pathway for peripheral metabolism of 25(OH)D into the active metabolite 1,25(OH)2D3. This takes place as needed when needed by affected cells throughout the body.
In this mode of metabolism, vitamin D3 acts as an autocrine signalling hormone unlocking genentic code within the cells DNA to produce whatever the cell needs to heal or reproduce itself. This peripheral mode of vitamin D3 metabolism can only take place when 25(OH)D reaches affected cells in the presence of vitamin A.
Dr. Robert Heaney, M.D. uses the following example of peripheral vitamin D3 metabolism and genetic expression:
A tuberculin bacillus lands on a cell within the lung's alveole and starts to infect it. The cell says "I don't have the material to fight this bacillus... but if I had some 25(OH)D and some vitamin A, I could use these two ingredients to make 1,25(OH)2D3 to unlock my genetic library for the recipe to make the appropriate tuberculosis anti-bodies..."
You can watch Dr. Heaney's presentation of
Vitamin D: Nutrient, Not A Drug at the following link for a better explanation of this peripheral mode of vitamin D3 metabolism:
Multimedia File Viewing and Clickable Links are available for Registered Members only!! You need to
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Although we don't have the exact mechanism by which vitamin D3 acts as a CH preventative, it's looking more and more like this peripheral mode of vitamin D3 metabolism and genetic expression is responsible.
I hope this answers your questions without creating too much confusion...
Take care and please keep us posted.
V/R, Batch
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123 Days PF And I Think I know Why (Read 534520 times)
