Vitamin D and Autoimmune Disease - Tex's Book

[aquilegia]

Tex,
I just finished reading your book and I thought it was excellent. I am going to read it again as more than one reading is necessary.
I have a couple of questions having to do with steroids and Vitamin D. I think you said that steroids increase the number of VDRs. Given that, how does discontinuing the steroid before complete healing has occurred affect the amount of Vit D one should take? Should it be increased?
I think that you also said that Vit D increases the number of VDRs so I am inferring that increasing the Vit D after discontinuing budesonide would make up for the loss of the steroid.
I realized that after I increased my Vit D from 4000 units daily to 6000 units daily was when my symptoms started to improve and I was able to stop taking the budesonide - two weeks now. I am thinking that I should increase the Vit D to 8000 units daily to make up for the loss of the budesonide. What do you think?
You also say in the book that steroids deplete the reserves of Vit D. Is that because they increase the number of VDRs so the circulating Vit D is taken up?

[tex]

You also say in the book that steroids deplete the reserves of Vit D. Is that because they increase the number of VDRs so the circulating Vit D is taken up?

Yes, that is exactly what happens. Steroids promote the conversion of the inactive form of vitamin D to the active form (to bind to the VDRs, to suppress inflammation) and this of course depletes the supply of 25(OH)D3 circulating in the blood.

Given that relationship (with corticosteroid use), I'm not sure that the dosage would need to be increased when the use of a corticosteroid is discontinued (because the demand for D3 should go down). This is assuming that a adequate amount of vitamin D3 was being taken while the corticosteroid was being used. Of course, if not enough vitamin D3 was available while a corticosteroid was in use, then a deficit would be created, which would need to be filled. IOW, this will depend on our own personal situation.

I'm not aware of any research data that provides a way to accurately assess the increased demand on vitamin D3 supplies due to the use of a corticosteroid, so this is all pretty much a fly-by-the-seat-of-our-pants procedure. Probably the best way to deal with it would be to test our vitamin D level (the 25[OH]D3 level) as we reach the final stages of the corticosteroid withdrawal taper, or soon after we have stopped taking it. That way we wouldn't have to guess at whether we might need to increase our vitamin D intake.

I would love to see some research data that shows quantitatively how steroid use affects vitamin D utilization, but I would be surprised if anyone ever pursues that research (because the drug companies are not going to fund it).

Tex

[aquilegia]

I read the book a second time. I highly recommend it. There is a lot of compelling evidence in this book that Vitamin D deficiency is implicated in many medical conditions. I have always been a great believer in taking Vitamin D in higher doses than doctors recommend. My Vitamin D level has been tested once in 2010 and it was low even though I was taking 1000 units daily which was considered to be a high dose in those days. I doubled it after that.

Now I am going to increase it to 8000 units daily. I was taking 6000.

One has to pay now to get the vitamin D level tested in Ontario, but it seems like it is well worth it.

[Zizzle]

I take 5,000 IU every other day, and I've been on prednisone for 2 years. Even on Pred, my blood levels of D have been in the 40s. My doc said today she wants me above 50, so I must take 5,000 IU daily. Now that I'm down to 2 mgs pred, does that mean I should expect my blood levels of D to rise?

[tex]

Now that I'm down to 2 mgs pred, does that mean I should expect my blood levels of D to rise?

Stopping prednisone completely should cause an increase in serum vitamin D level, but I'm not sure that reducing the dose of prednisone will always cause a significant increase, because whether or not the VDR response significantly changes with corticosteroid dose changes may depend on circumstances (IOW, the VDR population may or may not be saturated/maxed out). But if you double your vitamin D daily dose, then it should certainly increase for that reason, whether the prednisone dosage is decreased or not.

Tex

[Lilja]

Hi Tex,

In my country the pharmaceutical industry insists on using grams instead of international units.

So, I buy vitamin D3, (colecalsiferol) and each tablet contains 20 micrograms. No other D3 product contains more than this per tablet.

How many tablets would I have to take, in order to match 7.000 i.u.?

There is a special conversion table on the internet as to D-vitamins, because you cannot convert from grams to i.u. automatically, you have to know which vitamin you want to convert.

Even with the table in front of me, I have trouble in understanding how to calculate ...

http://www.thecalculatorsite.com/articl ... to-mcg.php

I would appreciate your help in doing the math



Lilja

[BearcatRx]

I would recommend against taking an enormous about of Vitamin D on a daily basis. Vitamin D is a fat soluble vitamin and CAN become toxic if taken at high levels. 10,000 IU is the most I've seen over the counter and that should only be taken once weekly. I had my D levels checked at was below 13. My doctor put me on 50,000 IU once weekly for 12 weeks and 2,000 IU daily.

[tex]

Lilja,

With vitamin D, 1 IU is equal to 0.025 mcg. Therefore, 20 mcg is equal to 20/0.025 = 800 IU. Apparently whoever is in charge of deciding on the potency of vitamin D supplements for sale in Norway is extremely conservative. They probably assume that everyone in Norway should get most of their vitamin D from their diet (which isn't very practical these days).

If you are sure that you need to take 7,000 IU daily, that would require 8 or 9 of those tablets (the math comes out at 8.75 tablets).

Tex

[Lilja]

Lilja,

With vitamin D, 1 IU is equal to 0.025 mcg. Therefore, 20 mcg is equal to 20/0.025 = 800 IU. Apparently whoever is in charge of deciding on the potency of vitamin D supplements for sale in Norway is extremely conservative. They probably assume that everyone in Norway should get most of their vitamin D from their diet (which isn't very practical these days).

If you are sure that you need to take 7,000 IU daily, that would require 8 or 9 of those tablets (the math comes out at 8.75 tablets).

Tex

Thank you, Tex.

Yes, they are extremely conservative, and that is in a country that has so little sunshine.

I'm not sure that I need to take 7.000 i.u. daily, but as long as I'm on Entocort I thought that I would take this much, and lower it substantially when I'm off Entocort and the inflammation has cooled down.

Is this a bad idea?

Lilja

[tex]

Bearcat,

Your point is well taken, and I certainly agree with you that one should not take "an enormous about of Vitamin D on a daily basis". However, IMO your cautionary statement about not taking more than 10,000 IU per week is not only way too conservative, but potentially counterproductive for treating MC.

MC typically causes the malabsorption of fat. Therefore most fat soluble vitamins tend to have rather low absorption rates (whether in food or supplements), whenever MC is active. It is well known that not only does a vitamin D deficiency increase the risk of developing an IBD (as you have experienced), but all IBDs (including MC) deplete serum vitamin D levels. Not only that, but corticosteroids deplete serum vitamin D levels, so anyone following the standard medical protocol (using Entocort or Uceris) to treat MC is virtually guaranteed to eventually have a vitamin D deficiency (if they didn't already have a deficiency before they started taking the medication), unless they take a supplement sufficient to overcome the depletion rate.

In addition, my own research suggests that the primary reason why corticosteroids stop working for many MC patients is because their serum vitamin D level has become depleted (and this has been verified by the experience of members here, who have increased their vitamin D supplementation and thereby enabled their Entocort to begin working again (after it had "mysteriously" stopped working).

Vitamin D supplements offering 50,000 IU are readily available from several sources, and these are based on D3, not the poorly-utilized D2 provided by all subscription-based vitamin D. Here is my opinion of the vitamin D2 that's found in all vitamin D prescriptions, from page 46 of my book about vitamin D and AI diseases:

Many decades ago, vitamin D2 was thought to be the equivalent of vitamin D3, but that assumption can no longer be justified. Why physicians continue to prescribe vitamin D2 is somewhat of a mystery, since research shows that vitamin D3 supplements are consistently more effective than vitamin D2 supplements. Houghton and Vieth, (2006), summed up the case against vitamin D2 supplements with this statement:7

The case that vitamin D2 should no longer be considered equivalent to vitamin D3 is based on differences in their efficacy at raising serum 25-hydroxyvitamin D, diminished binding of vitamin D2 metabolites to vitamin D binding protein in plasma, and a nonphysiologic metabolism and shorter shelf life of vitamin D2. Vitamin D2, or ergocalciferol, should not be regarded as a nutrient suitable for supplementation or fortification. (p. 696)

Here is reference 7 from that quote:

7. Houghton, L. A., & Vieth, R. (2006). The case against ergocalciferol (vitamin D2) as a vitamin supplement. American Journal of Clinical Nutrition, 84(4), 694–697. Retrieved from http://ajcn.nutrition.org/content/84/4/694.full

Vitamin D toxicity (due to overdose) is certainly a potential risk, but the facts suggest that the risk appears to be very overblown by many in the medical community, and they tend to err on the low side (often the very low side). IMO, the main problem here is that most doctors fail to recognize that AI issues (especially IBDs) place huge demands on our serum vitamin D supplies, and that demand is further compounded if a corticosteroid is prescribed for treatment.

Of course all of the confusion and many of the problems can be minimized by regular vitamin D tests. But unfortunately that's a valuable tool that few doctors use often enough.

They could prevent the development of many AI diseases if they only had more respect for the value of that simple test. But of course, they're not in the business of preventing disease — they're trained to treat disease after it develops.

Tex

[tex]

I'm not sure that I need to take 7.000 i.u. daily, but as long as I'm on Entocort I thought that I would take this much, and lower it substantially when I'm off Entocort and the inflammation has cooled down.

Is this a bad idea?

No, that sounds very practical, especially during the season when there is so little sunlight available.

Tex

[BearcatRx]

Tex,

True. 10,000 IU once weekly I'd say is a fair dosage for a person who is simply trying to supplement D without having MC. I just try to urge caution in patients who seem to be arbitrarily increasing their daily intake of D supplement without proper knowledge. If it were a water soluble vitamin I wouldn't care because they'd literally be pissing it away. I am curious as to what you've found as far as clinical improvement of symptoms, if any, by getting our D level back to "normal." As I said I'm taking 50,000 IU once weekly and 2,000 daily and honestly don't see any clinical response or improvement in symptoms. If it is not going to improve symptoms I'd rather not take the additional pill per day. I've always been taught to treat the patient and not simply chase numbers, in this case my vitamin D level.

[tex]

I am curious as to what you've found as far as clinical improvement of symptoms, if any, by getting our D level back to "normal."

That's certainly a fair question. We have several members who have posted that they were sure (as sure as anyone can be, short of rigidly-controlled random, double-blind testing), that increasing their vitamin D supplementation was responsible for resolving their acid reflux/GERD problems, for example. I have a hunch that this is associated with the fact that calcium is involved in the regulation of the lower esophageal sphincter and vitamin D is critical in the regulation of calcium utilization.

At least one member (who was posting for her mother), was able to regain efficacy from Entocort, after the corticosteroid had stopped working for her mother (who is reluctant to carefully follow diet restrictions), simply by restarting/increasing her vitamin D supplementation. As she posted:

Just wanted to report back to let you know the stopping Vit D was the problem - a week or so after restarting (this time on 2000 IU instead of 1000) all is back to how it has been for the past couple of years (not 100% well, but D mostly under control)

You can read the entire thread here. Of course, this is not likely to be much help unless one's vitamin D level is insufficient, but it appears that virtually every disease has a different insufficiency level, and that level is almost always above the minimum levels recommended by most authorities (except for rickets — minimal vitamin D will treat/prevent rickets). You might find the chart from GrassrootsHealth at the following link to be helpful:

Disease Incidence Prevention by Serum 25(OH)D Level

As I said I'm taking 50,000 IU once weekly and 2,000 daily and honestly don't see any clinical response or improvement in symptoms. If it is not going to improve symptoms I'd rather not take the additional pill per day. I've always been taught to treat the patient and not simply chase numbers, in this case my vitamin D level.

I hear you. I agree that it's never a good idea to ingest medications, supplements, (or higher doses of medications or supplements), food, water, or anything else, in excess amounts (my definition of excess being more than we actually need). Have you tracked down and eliminated from your diet all traces of food sensitivities that are causing your immune system to produce antibodies? For most of us, certain food sensitivities are not only the reason for the self-perpetuating inflammation that causes MC, but those food sensitivities will even trump treatment by corticosteroids or any other anti-inflammatory meds. My tag line is not a joke — it's the difference between remission and being dependent on drugs for the rest of one's life with MC.

When the genes that predispose to MC are triggered, the genes that predispose to gluten sensitivity and other food (and drug) sensitivities are also triggered at the same time. Any gastroenterologist who argues otherwise doesn't have the foggiest idea how to successfully treat MC, and the persistence of that gap in medical knowledge is the primary reason for the existence of this discussion and support board. Many of us here have been in remission for over 10 years, by diet changes alone. Most members stop posting of course, after they are able to get their life back, but fortunately, some stick around to help new members.

If you are relying on negative results on the celiac blood tests as the basis of your assumption that you have no food sensitivities, then you are relying on a test that is virtually useless for anything less than fully-developed celiac disease. Those tests will not detect any stage of intestinal damage below a Marsh 3 level (which typically takes at least several years to develop after the onset of symptoms). That makes those tests worthless for our purposes as MC patients. We have to utilize IgA-based stool tests to detect the antibodies in the intestines (where they are produced). By the time those antibody levels rise to detectable levels in serum, years of damage have accrued. That's why the average length of time from first onset of symptoms to an official celiac diagnosis is still 9.6 years in this country (according to the most recently-published data). From page 108 of the book Microscopic Colitis:

The blood tests used to screen for celiac disease appear to be the primary problem. Research shows that for all practical purposes, they are capable of detecting only fully-developed cases of celiac sprue, and they even miss a large percentage of those. One such study looked at 115 subjects with biopsy-proven celiac disease and found that only 77 % of those who had total villus atrophy showed a positive serum anti-endomysial antibody test result.6 Furthermore, in this particular study, only 71 % of the total number of subjects had total villus atrophy, and for those who had partial villus atrophy, only 33 % showed a positive anti-endomysial antibody test result. As the research report so eloquently pointed out, “Serologic tests, in clinical practice, lack the sensitivity reported in the literature” (Abrams, et al., 2004, p. 547).

The red emphasis was added for this post. Here is reference 6 from that quote:

6. Abrams, J. A., Diamond, B., Rotterdam, H., & Green, P. H. (2004). Seronegative celiac disease: increased prevalence with lesser degrees of villous atrophy. Digestive Diseases and Sciences, 49(4):546–550. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/15185855

The goal of the medical community is to treat the symptoms of MC, by the use of expensive medications. Our goal on this board is to treat MC by eliminating the root causes. We're not above using medications if they will make life easier while the diet changes are healing our gut, but in the long run, we prefer to control the disease by diet changes, (since that carries the least amount of risk to our long-term health and well-being).

Tex

[BearcatRx]

Tex,

I've been reading up on a few elimination diets and am trying to find a solid one that I'm able to work with. My symptoms have mostly been controlled with Lialda alone but as I've stated before, I'd rather keep hold of my money in my HSA for something more important. I've kept basically the same diet that I've always had. When the symptoms overpower the medication and I experience loose stool (not necessarily full on D), I try to go back over my food consumption over the last 24-48 hours to try to determine anything that may be the cause. Thusfar I have not been able to pinpoint anything in particular. At least, none of the common allergens seem to be the culprit. I've been able to consume dairy, gluten and even hot wings with no problems.

[Gabes-Apg]

BearcatRX
keep in mind that triggers are not always just food ingredient related...

it can be stress (emotional, and/or mental, and/or physical)
it can be environmental, mould, air conditioning, pollutants, chemicals,
change in eating routine
not enough sleep or rest
immune system fighting germs (cold, virus etc)

a combo of any or all of the above....

It may be helpful to include activities, locations as part of the food journal.

some examples:
one member here used to react to the heating system in her daughter's house (it had mould)
another member in remission, had major flare due to death in family
a combo of a bad nights sleep and exposure to chemicals was enough to cause me to react - or a really stressful day at work.

Elimination diet wise - I eliminated all the common triggers that affected the people here and then when stable, tested them.
are you following a low fibre, low inflammation eating plan??
common irritants: Soy, Eggs, beans/green veges (just at first), any meal or food item that has lots of ingredients, ie more than 7 different ingredients.

you may do ok with gluten and dairy, but if you consume too much of both in the one day maybe that is triggering issues..