Stopping inflammation while raising vitamin D levels

Many discussions of late have talked about vitamin D as well as increasing vitamin D levels.  In addition, many discussions lately also have talked about inflammation and how to reduce it.  The problem is that those two objectives may have obstacles that counter the other.  My question and the discussion I want to have is how can we do that?

I have previously thought that I could take NSAIDs to circumvent the problem but now read that the  NSAID that I've been using, Naproxen Sodium, is in fact both a COX-1 and COX-2 inhibitor.  Not good.  That impairs my bodie's ability to absorb vitamin D and covert it to the active hormone form.  I want to avoid that.  But again, I also want to reduce inflammation at the same time.  How can this be done?  Ideas?  My thoughts about an approach to it are sadly lacking.

John,

There is nothing I can contribute to this discussion, since I have taken only two Aleve pills (Naprosyn, I believe) in the last 10 years. 

My contribution which may be useful is that three months ago my Vit D level was 49.6 and yesterday was 70, by the same doctor and same lab.  I have been taking about 4000 iu until three months ago, when I learned the results of 49.6, and increased my intake to 8000, aiming for +/- 75. I am close to my target, so will cut back to a daily 4000.   Somewhere I picked up a "comfort zone" of 75-100.  My doctor has been testin many of his patients of late (!), finding levels of 4, 5, 10 ...These are in "women on calcium with D ", people in the Carolinas, and people who are "out in the sun a lot".

3/9 Symptoms returning. Began 5 abx protocol 5/9 Rifampin 600, Amox 1000, Doxy 200, MWF Azith 250, flagyl 1000 daily. Began Sept 04 PPMS EDSS 6.7 Now good days EDSS 1 Mind, like parachute, work only when open. Charlie Chan  In for the duration.&am

Ken

I would love it if it were that simple; however, I don't believe it is.  Once you have COX and/or 5-LOX inhibitors in the bloodstream, they're in the bloodstream for a while.  I don 't know the half lives of the various herbs or drugs but I really doubt they would be removed from the bloodstream quickly enough.  Plus, if they weren't in the bloodstream, inflammation would reign, or so I believe.

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

Rica            

It's a contribution to say that you haven't really used NSAIDs much.  I was on curcumin and stopped it thinking I could replace it with an NSAID but that appears to be  counter to the idea of raising vitamin D levels at the same time.  There is ample documentation of how NSAIDs interfere with vitamin D due to their status as COX inhibitors.

The only thing I've come across that _might_ work without being a COX inhibitor are Omega 3 acids or Fish Oil.  It's hard to say why they might work though.  I'm not well versed in the science about it only that it has been mentioned in the past in documents I've read on the subject.

Needless to say, I have to stop the NSAID (naproxen sodium) and now have nothing to reduce inflammation.  Not good.  There has to be something that we can use or some strategy for taking inflammation reducing agents while permitting vitamin D levels to go up and stay in the healthy range.  Finding out what those are is why I started this thread.

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

Anti-Inflammatory Curcumin Benefits  

 

So does Curcumin need to be take apart from D3 too?

 

I'm going back through this thread and I picked up on the curcumin comment.  Kim takes curcumin and I thought I'd add some info about it.

Curcumin is a COX-2 inhibitor
Plummer et al. 1999 Inhibition of cyclo-oxygenase 2 expression in colon cells by the chemopreventive agent curcumin involves inhibition of NF-B activation via the NIK/IKK signalling complex

Curcumin induces apoptosis
Cipriani et al. 2001 Curcumin Inhibits Activation of V{gamma}9V{delta}2 T Cells by Phosphoantigens and Induces Apoptosis Involving Apoptosis-Inducing Factor and Large Scale DNA Fragmentation

Curcumin is anti-inflammatory
Lim et al. 2001 The Curry Spice Curcumin Reduces Oxidative Damage and Amyloid Pathology in an Alzheimer Transgenic Mouse

 

 

In pursuit of ABX

Don't Allow What You Know To Get In The Way Of What Might Be

notasperfectasyou        

You do not need to worry about Cox2 inhibitors interfering with vitamin D.  My interpretation of how it worked was confused with 5-Lox inhibitors, which do interfere with the underlying process that you go through to produce and absorb vitamin D.  So by all means, go ahead with the Curcumin!

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

Red

Hi Rica,

This is great news!  Glad to hear your Vit D levels are getting up there.   Also very interesting (and scary) about your doc's other patients...

 

 

Hi John,

I've read and posted a lot on Vit D3 and 5-LOX inhibitors, but I haven't read anything on interactions between COX inhibitors and Vitamin D.   Can you post a link to a study on this?  Thanks...

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Maybe I'm asking the wrong question.  Maybe the question should be should we be concerned about vitamin D levels while trying to fight inflammation.  Or the reverse of the - should we be worried about inflammation while trying to raise vitamin D levels?  Sounds ridiculous to me but then again, wouldn't be the first time I was mistaken.

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

Red

Hi John,

While I'm certainly no expert, I'd personally stay away from the 5-LOX inhibitors given what I've managed to dig up on their potential to increase pathogen burdens, but I'd say if you need to use an NSAID like Naproxen or Ibuprofen (COX-1 and COX-2 inhibitors) to counter the inflammation right now in order to function, do it.  Once you are better, you can always stop the NSAIDs...

Hang in there...

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Hi Red         

Thanks for the comment but it leaves the question out there of increasing vitamin D levels at the same time?  If we're wanting to lower pathogen burdens, should we not be doing that also?  And if we do that, doesn't using an NSAID or an herbal COX\5-LOX inhibitor counter that effort?  My limited knowledge indicates that it does.

So, where are we left?  What is the best course of action?  Are we pissing into the wind either way we go?

A couple of things that I think might give us a way to formulate a plan of action.  First, knowing the half lives of either the anti-inflammatory herbs or the NSAIDS.  That's key to me and I haven't been able to come up with anything on it thus far.  Second, the inpact on vitamin D absorbtion that various COX-1, COX-2, and 5-LOX inhibitors have.  Maybe simply increasing intake of vitamin D  offsets the reduced absorbtion??

So two possible strategies that have come to mind, neither of which I have any idea of the value of trying.

  1. Take the inhibitor that has the shortest half life at a time where it is less likely to impact vitamin D...or alternate days on vitamin D intake so that one day you take it, the next day you take the inflammation inhibitor
  2. Take an increased amount of vitamin D to offset the impact of the inflammation  inhibitor and take vitamin D every day.

I have no idea if either of those strategies work but those are the two which come to mind.  I'm sure there are more but those are all I can think of at the moment.  Any help anyone can give in determining which way to go is the better way or what the better way is, is greatly appreciated.

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

Information on NSAID half lives...

The information I have found is sketchy in my opinion, not as reliable as more scientific information.  But still, it's information to start from.

My understanding of the half lives of NSAIDS is that they remain in blood plasma a shorter time then in humna tissues.  To me this poses a problem with vitamin D.  Here is some information I've found and where I got it from.

From http://arthritis.about.com/cs/nsaids/a/factsofnsaids.htm I found...

  • Pain and inflammation sometimes occur in a circadian rhythm (daily rhythmic cycle based on a 24 hour interval). Therefore NSAIDs may be more effective at certain times.
  • NSAIDs can be divided into two groups: those with plasma (blood) half-lives less than 6 hours (i.e. aspirin, diclofenac, ibuprofen) and those with half-lives greater than 10 hours (i.e. diflunisal, piroxicam, and sulindac). Since it takes three to five half-lives to stabilize blood levels, NSAIDs with longer half-lives require a loading dose to be given (large dose given initially). The "half-life" is the time it takes a drug to go down to half of its initial level.
  • Prostaglandins, which are inhibited by NSAIDs, function in the body to protect the stomach lining, promote clotting of the blood, regulate salt and fluid balance, and maintain blood flow to the kidneys when kidney function is reduced. By decreasing prostaglandins, NSAIDs can cause stomach irritation, bleeding, fluid retention, and decreased kidney function.
  • Synovial fluid (joint fluid) concentrations are 60% of plasma concentrations regardless of type of NSAID or its half-life. Synovial fluid is mostly the site of action of NSAIDs.
  • NSAIDs are 95% albumin (protein) bound. The unbound fraction of the NSAID is increased in patients with low albumin concentrations such as in active rheumatoid arthritis and the elderly.

From http://www.medicineau.net.au/clinical/palliative/NSAIDS.html I found...

Drug Half-life (hr)

Short half-life

  • Aspirin 0.25 0.03
  • Diclofenac 1.1 0.2
  • Flufenamic acid 1.4;9.0
  • Ibuprofen 2.1 0.3
  • Indomethacin 4.6 0.7
  • Ketoprofen 1.8 0.4
  • Tiaprofenic acid 3.0 0.2

Long half-life

  • Diflunisal 13 2
  • Naproxen 14 2
  • Phenylbutazone 68 25
  • Piroxicam 57 22
  • Salicylate 2 - 15
  • Suldinac (sulfide) 14 8
  • Tenoxicam 60 11

This information is good but only addresses blood plasma half life and not tissue half life.  So, it's only partially there.  I've been trying to find the tissue half life but my guess is that it isn't out there.  How does a researcher known how long a drug remains in the brain/spine or heart/lungs?  I haven't a clue how that works.

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

The search continues and I found another site with more information about NSAIDS...

http://rheumatology.oxfordjournals.org/cgi/content/full/kem070v1#F1

Here is an interesting diagram from one of their figures

Image removed.

I can't claim to completely understand what the diagram or arcticle is talking about but it does seem relevant, so I included it here.  From the review of the information above, it would seem that the half life of most of the NSAIDS is less then 10 hours.  If that is correct, how does that impact the tissue concentration?

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

Just a footnote about the diagram above.  The column Tmax is the time to maximum plasma levels and T1/2 is the half life time.

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

I found a good paper that describes some of the more common herbal COX inhibitors and the difference between COX-1, COX-2, AND 5-LOX.  According to what the author writes, two things stand out to me from the paper.

The first is that inflammation is a function of the COX-2 enzyme, not COX-1.  The second thing is that BROMELAIN apparently isn't a COX inhibitor as I thought I read else where.  I'll be looking for a counter statement elsewhere after I post this.  Either way, this is an interesting paper:

http://www.hchs.edu/files/HerbalCox_2_HSR.pdf

 

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

I did find several counter statements so I have no idea what's true...

http://pubs.acs.org/doi/abs/10.1021/jf052390k

http://www.abouthormones.org/bromelain

...for example.  There are plenty of others but these are two.

 

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

I came across this study that seems to indicate that a specific COX-2 inhibitor works in conjunction with vitamin D rather then prevent absorbtion.  All very confusing and I have been having difficulty getting the issue clarified in a concise way.

The study was in reference to a prostate cancer treatment...

http://oai.dtic.mil/oai/oai?&verb=getRecord&metadataPrefix=html&identifier=ADA472121

 

The incidence of prostate cancer has increased and effort is needed towards understanding mechanisms involved in development/progression of prostate cancer and developing new strategies for prevention/treatment. Studies suggested nonsteroidal anti-inflammatory drugs, such as COX-2 inhibitor, act as chemopreventative agents and found COX-2 expression in prostate cancer correlated with cancer progression. Treatment of prostate cancer cells with COX-2 inhibitor, NS-398, induces VDR expression, and might increase vitamin D sensitivity. Treatment of prostate cancer cells with 1,25-VD results in reduced COX- 2 expression. Based on the bi-directional regulation of vitamin D and COX-2 inhibitor, we hypothesize that combining vitamin D and COX-2 inhibitor in treatment of prostate cancer will be beneficial. Over the past year, we identified the molecular mechanism by which vitamin D inhibits prostate cancer angiogenesis through IL-8, finding a strong correlation of IL-8 expression with prostate cancer disease progression, therefore, inhibition of IL-8 by vitamin D supports the chemotherapeutic effects of vitamin D in preventing prostate cancer progression.....

 

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

This study has found that a form of vitamin D3 acts as a potent anti-inflammatory agent

Résumé / Abstract

Inducible cyclooxygenase-2 (COX-2) has been implicated to play a role in inflammation and carcinogenesis and selective COX-2 inhibitors have been considered as anti-inflammatory and cancer chemopreventive agents. 1α,25-dihydroxyvitamin D3 (1α,25(OH)2D3), the active hormonal form of vitamin D3 also has been considered to be a cancer chemopreventive agent in addition to its important role in maintaining calcium homeostasis. Based on these observations, we studied the direct effect of 1α,25(OH)2D3 and one of its less calcemic synthetic analogs, 1 α,25(OH)2-1 6-ene-23-yne-D3 on the activity of both COX-1 and COX-2 in an in vitro enzyme assay. Preliminary data indicated that both 1α,25(OH)2D3 and 1α,25(OH)2-16-ene-23-yne-D3 inhibited selectively the activity of COX-2 with no effect on the activity of COX-1. Out of the two compounds, 1α,25(OH)2-16-ene-23-yne-D3 was found to be more effective with an IC50 of 5.8 nM. Therefore, the rest of the experiments were performed using 1α,25(OH)2-16-ene-23-yne-D3 only. 1α,25(OH)2-16-ene-23-yne-D3 inhibited the proliferation of lipopolysaccharide (LPS) stimulated mouse macrophage cells (RAW 264.7) with a reduction in the expression of COX-2 along with other inflammatory mediators like inducible nitric oxide synthase (iNOS) and interleukin-2 (IL-2). Furthermore, 1α,25(OH)2-16-ene-23-yne-D3 also inhibited carrageenan induced inflammation in an air pouch of a rat and effectively reduced the expression of COX-2, iNOS, and IL-2 in the tissues of the same air pouch. In both cases, 1α,25(OH)2-16-ene-23-yne-D3 did not show any effect on the expression of COX-1. In summary, our results indicate that 1 α,25(OH)2-16-ene-23-yne-D3, a less calcemic vitamin D analog, exhibits potent anti-inflammatory effects and is a selective COX-2 inhibitor.

http://cat.inist.fr/?aModele=afficheN&cpsidt=20518002

 

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

Wow, John great detective work. The last one seems to indicate that vitamin d is pretty effective as a cox 2 and the authors are not really saying as they often do that more studies are needed. They seem pretty sure of themselves! Vitamin d has been known for a long time to be antiinflammatory; Interesting that the mechanism is the cox 2 pathway. I take both an nsaid and vitamin d personally. Thanks for this good work marie

On CAP since Sept '05 for MS, RA, Asthma, sciatica. EDSS at start 5.5.(early cane) Now 6 (cane full time) Originally on: Doxy 200, Azith 3x week, Tini cont. over summer '07, Revamp of protocol in Summer '08 by Stratton due to functional loss; clarithro

Thanks Marie.  I'm not sure I deserve the praise as it's not very definitive information in my opinion, but it's the best I could find so far. 

I still have a couple of loose ends I haven't tracked down yet.  The first is determining if and how much vitamin D absorbtion is affected by any NSAID or 5-LOX inhibitor.  The second is to settle on a strategy based on information that is trustworthy and complete.  There may be more but those two are what readily comes to mind.  So, the search continues.

Actually, there is a third thing and that is to enumerate the various herbs that fit into the aforementioned categories, and show what their half life is, and how much they impact vitamin D.

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

John,

Wow!  I had no idea this was such a key issue, but I agree that it's important.  I'm not clear as to whether there is a recommendation that's come out of this.  How much vitamin D have you been taking?  Kim's taking 6000 D3 daily.  I get the impression that Ibuprophen has a shorter half life, would this be preferable to use?

Ken

In pursuit of ABX

Don't Allow What You Know To Get In The Way Of What Might Be

Ken           

No, there's no clear-cut recommendation about taking herbal COX or 5-LOX inhibitors at the same time as taking vitamin D.  However, a few things we've figured out.

First, there are two or three COX inhibitor pathways.  COX-1, COX-2, and recently COX-3 was discovered.  From what I've read, my understanding is that it is the COX-2 pathway that is chiefly responsible for inflammatory responses/inflammation.  I suspect 5-LOX as well but know less about that and have only a little bit to go on with it, as well as research that Red has done and reported on this site about how one's immune system is impaired by 5-LOX.   I may not be quoting him correctly so maybe you can look for some of his threads and/or he'll chime in here to correct me.

I have been taking 4000 IU of vitamin D continuously for about 3 years, and before that about 3000 IU for 5 years.  I just recently started taking 6000 IU and am at that level now.

Ibuprofen does have a shorter half life; however, I would not necessarily make a recommendation cart blanche about taking one NSAID versus the next.  The half life is just one thing to consider.  What COX pathways that inhibit is the other.  Finally, knowing how much they inhibit/impair vitamin D absorbtion is the last thing I would consider.  I don't have an answer for the last question and haven't been able to find anything on it.  I'm still looking but it may be that the information is not available where I will find it.

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

Okay, I'm posting this to bump this topic up since it's relevant to the vitamin D discussion we have been having here for some time. Given that inflammation is part of the CPn story, as are low vitamin D levels, I think talking about this and putting together some ideas about an approach or strategy is needed.

In the intervening 2 months since I was a frequent poster here, I have made no progress on this front with respect to coming up with a strategy.  My only choice has been to put vitamin D at the highest priority and deal with the inflammation by just accepting it.  Not an ideal approach, but without some real strategy, I have no other options that come to mind but one is definitely needed.

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

John, how much VitD3 have your worked your dosage up to at this point?  When did you start increasing?  How long were you on it prior to that attempt to increase it and for how long at that dosage?  I ask to get a picture of what you have done.  You may have said it all before but if you want to start the discussion again I would find a recap helpful.

I have been taking vitamins for the better part of 35 years, and intermittent multivits prior to that time.  During my first pregnancy I had foot  cramps, my OBdoctor told me to chew some Maalox tablets when I complained.   I asked myself what is in that OTC antacid that would be helpful.  Magnesium.  I began to read the work of Adele Davis way back then in the 70's and I was hooked on nutrition to support my state of being.  The magnesium has always been my mainstay if I went longer than 3 weeks almost to the day without it I would be back there again with middle of the night foot cramps.  I have been taking handfuls of supplements for the better part of 30+ years.  I still got infected, was likely so for many, many years.  VitD was stressed by good old Adele so I have always supplemented in the 400 - 800 IU level.  Never was tested until May 07 and although my reading was just above the low normal line, it was a Quest lab test which has since been implicated in false readings, so I was likely below range even on the multi that I was taking.

I start to take a bone health combination supplement which had 3000IU and calcium and more.  I took it intermittently during the first 6 months of CAP due to massive nausea secondary to doxy.  At 6 mos I was insufficient still and advised to take 6000IU which I did for 4 months and still I was insufficient on testing.  In the fall retested once again insufficient level.  This is when I went up to 10,000, I was just tested early January and the results now a level of 68 more acceptable range but my MD wants me to get my test up to 100.  I will likely continue on 10,000 and retest again in April or May and see what the level is once again.   I think that frequent testing, at least quarterly until you find your optimal dosage is a good idea.  You can self test.   I may go that way eventually as I will want to follow myself over time as I want to keep within the upper limits of the current acceptable levels.   You need to titrate your dosage to your particular situation.  Some get lots of sun and make their own Vit D3 even then you need to shower less I understand so it actually stays on your skin and is absorbed.    I live in a locality where lots of skin exposure year round is quite limited.  And with cousins with hx of MS and Lupus I have stayed out of the sun for extended period for years.  Then there were all those years that I worked indoors and once again had limited time in the sun.  Getting D from sun exposure is just not practical as a way to sustain VitD for myself. 

I hope there are a few more posts for you with suggestions.  I am not fighting spasticity and I did not really have an idea for any untoward die off effect when I initially ramped up so if it caused me any troubles I did not know enough to atribute them to VitD3!

Louise

  • CAP(TiniOnly): 06/07-02/09 for CFS
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDN 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support

Hi Louise      

I was at 4000 IU for something like 6 or 7 years and just recently increased to 6000 IU since November.  I got on the D3 bandwagon quite a while ago though my levels could be higher and I'm working on that.  I was on most of the supplements that a recommended adjuncts to the CAP since 2001.  When I was diagnosed with MS, my first step was to ignore my neurologist because I was seeing a reaction from the food I was eating (porphyria).  That lead me to the MS Direct group and the BBD, along with their recommended supplements at the time.  It did significantly improve my symptoms but I never got back to where it all started, but it did stabilize to where it was up until I started the CAP some almost 3 years ago now.  It stay stabilized but there have been super subtle improvements.  Tiny little things that cumalitively are bigger but still not big.  Like I said in another post...nibble nibble nibble.

I do believe that the increase in my D intake recently had somewhat worsened my condition; however, I believe that's just a temporary situation, likely to remit over time as I aclimate to higher D levels.

I had my D levels checked in August or September.  They were in the high 40s, which was lower then I expected.  So, I'm working on increasing the levels and will be tested again in March.  I wanted to get tested sooner but my doctor wanted to give the higher level intake time to increase the levels before testing.

In any case, none of that has any bearing on the topic of this thread directly.  The topic of this thread is how to plan the intake of inflammation reducing agents such as NSAIDs which also negatively impact vitamin D while simultaneously increasing vitamin D levels.  Not an easy task to work out.  The only idea that I or someone else here came up with was Ibuprofen because of it's shorter half life.  I don't know if a shorter half life is going to be enough and this may just be a case where the science isn't there to work out this problem.

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

My question about your Vit D was because I did not know if you were just now increasing with this new wave of VitD info.  Sound like you have taken a substantial amount over a good long period of time.  For me finally stepping up to 10,000 is what was needed to bring me to the mid range, below the target level of my provider.    Guess you will find out in March what you have from the dose that you have been taking these past months.   Then your dose can be adjusted again if needed.  Guess I don't have any other suggestions for inflamation to share.  Louise 

  • CAP(TiniOnly): 06/07-02/09 for CFS
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDN 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support

Hi John,

In addition to the supplements of CAP for inflammation, I use ibuprofen and Traumeel drops.  I've also taken another Heel remedy called Lymphomyosot for symptoms of that flu like feeling which were both recommended to me by a naturopath physician as well as an MD that uses it for his patients for die off symptom relief during antibiotic treatment.  

Thanks for reminding me of these!  I just began using Traumeel again lately which may be why I'm feeling better.  Image removed.

NAC 2.4g, Zith 250mg/MWF, mino 200mg, Tini 5day/1g/5 pulses, Valcyte
Supplements, CFIDS/FMS, Hashimoto's, Psoriasis, PA, IBS, Sec Addisons

Don't believe everything you think!  

Hi Reenie

It's good to hear that those are working for you.  I followed the links you provided and also went out to Wikipedia.  I didn't find much about their exact mechanism of action although I may have missed it.  It does appear from one of the diagrams I saw that it's not a COX inhibitor.  That may or may not be right, it may in fact be one, either Traumeel or Lymphomyosot.  Or they may be taking a different approach.  The question I have about it is what do they do and how might they impact vitamin D asorbtion, if at all?

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

Traumeel is a homeopathic combination remedy.
  • CAP(TiniOnly): 06/07-02/09 for CFS
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDN 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support

John,

Neither one of these remedies are supposed to affect Vit D.  In fact, the MD using them has many patients on the MP, although the MP suggests not to use much of anything that is alternative but this Dr does use them (with a few supplements as well) for his patients.  

Traumeel is one of the only homeopathic medications I'm aware of that has actually been studied like a drug with clinical trials.  I think you have to understand how homeopathy works to understand how or why it helps.  

HERE's some info on trials. 

And... you can read the rest of the statement from below, HERE

As with many pharmaceuticals including the conventional NSAIDs, the exact mechanism of action of TRAUMEEL® is not fully understood. However, it appears to be the result of modulation of the release of oxygen radicals from activated neutrophils, and inhibition of the release of inflammatory mediators (possibly interleukin 1 from activated macrophages) and neuropeptides.

And... be sure to click on the link for PDR reference in the above link too.  Image removed.

NAC 2.4g, Zith 250mg/MWF, mino 200mg, Tini 5day/1g/5 pulses, Valcyte
Supplements, CFIDS/FMS, Hashimoto's, Psoriasis, PA, IBS, Sec Addisons

Don't believe everything you think!  

Reenie and Louis     

I understand that Traumeel is a homeopathic remedy; however, the assertion that it's not supposed to affect vitamin D absorbtion gives me little confidence that it doesn't.  I can't read the PDR right now and will take a look this evening and see what it says.

The one thing that stands out is the comparison to NSAIDS.  It may be more effective but have a similar mode of action, although they do say another mode that may be unrelated to the COX2 pathway.

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day