oops! Lymetutu
I thought she was doing well.
Anyone know what went down?
Chris
As if that's not enough, the MP site has made changes and they've deleted 2 of their forums. "Off Topic" and "Skeptic's Corner" have both disappeared. I still don't understand those changes, because they deleted and censored anything they didn't want to discuss anyway. There were some excellent topics and information that was lost as a result of the decision to do away with those forums.
With Paula and TXLM gone, they have lost their CFS and Lyme experts. There is no one else on the MP board staff who is thoroughly familiar with these two diseases. It has become a second Sarcoidosis board, because all the key board staff members have Sarcoidosis diagnoses, and all of the answers being given pertain to Sarc. They are very dismissive of any of the special problems which pertain either to Lyme or to CFS.
Both Paula and TXLM have been to countless major medical conferences pertaining to both CFS and Lyme. I do understand that the new administrator at that site is a licensed massage therapist according the recent conference brochure (M.T.), so she does qualify as a medical professional of sorts.
It states that Paula resigned and that the topic is closed out of respect for her privacy. I saved this page to my hard drive, as well as the page that shows very clearly that she was "banned" and did NOT resign.
[This message has been edited by Lonestartick (edited 17 March 2005).]
So maybe TM didn't like the "negative" aspect of dealing with Lyme patients...???
------------------
oops!
Lymetutu
QUOTE:
I would like to state that I have been banned from the Marshall Protocol
website where I used to be a moderator. I have no further connection with
this website or with Dr. Trevor Marshall.
I was banned because I expressed concern for a patient who had been vomiting
three days, had elevated kidney tests, and needed IV fluids. This patient's
doctor had stated these things. When I encouraged this patient to follow the
doctor's directions, and that minocycline and Benicar both can affect kidney
function, my post was deleted.
When I protested the deletion of my cautionary message I was banned.
Dr. Marshall wrote me the following warning:
"There is no way that any of us should be talking in such a manner such as
might induce a mother to believe that IV fluids are either necessary or
desirable."
I replied on this:
"I did not suggest IV fluids. Her doctor called her and left a message on
her answering machine to BRING HIM IN FOR IV FLUIDS. I suggested she do that
NOW. This boy had extreme vomiting for three days, elevated markers for
kidney malfunction which had existed in the past, and needed electrolytes.
He remained so dizzy he could not stand. I gave this woman NO advice her
doctors had not already given her...Yet my post was the one deleted."
I am still on the Marshall Protocol and had encouraging conversations with
doctors at the Chicago conference. I will be writing an article on this for
the Wisconsin CFIDS organization.
I feel that in order to protect myself and other patients I must distance
myself from the MP website. I find that I frequently disagree with the
advice given there, and several of my posts have been deleted in the past
because of this.
I hear it has been posted at the MP website that they will not discuss why I
was banned to protect my privacy. The information I have stated above is the
reason I was banned. I am not trying to protect my privacy. They are trying
to hide the reason why I was banned.
Paula Carnes
END OF QUOTE
No wonder we have such problems with Lyme disease being diagnosed and treated when we have to deal with doctors like that....
Too many doctor's have God complex's.
I had promised to stay on as a Board Staff member until after the Chicago conference had ended because I had been instrumental in inviting one of the keynote speakers, Dr. Lida Mattman, to speak, as well as persuading several medical professionals from the RA community to attend the meeting as VIP guests.
My continuation on the MP Board Staff following the conference was contingent upon our ability to resolve several problems which have existed at the MP website to our mutual satisfaction. Unfortunately, however, there was no agreement that any of my concerns were considered to be significant or worthy of further discussion.
I find it unrealistic to try to contribute anything meaningful or useful in an atmosphere of such heavy censorship, where my messages were sometimes deleted or, even worse, where my messages were subject to being edited WITHOUT ANY NOTICE that such editorial changes had occurred.
Before I had a chance to compose my letter of resignation, however, I discovered much to my great relief that my status had already been changed for me, without the necessity of a formal request from me to initiate this change.
This change in my status at the MP website will allow me more spare time for participation in other groups where I can speak my own mind freely and without any inhibitions or sanctions.
I am still very genuinely optimistic that the MP program will prove to be both safe and cost-effective for treating chronic, late-stage Lyme disease. I am also realistic enough to recognize that it is much too early to make any premature claims that the MP is any kind of proven sure cure for chronic, late-stage Lyme disease.
I want to clear up a not uncommon misperception about Trevor Marshall's credentials.
He is not a medical doctor (MD) Dr. He is a PhD Dr.
I believe that this is clear in his publications but it is not prominently posted anywhere at mp.com and is a source of confusion for some people.
Ticked
<< The following message was deleted from marshallprotocol.com after about 30 minutes. Since I am still getting messages from people who don't know that I am no longer board admin there, I am posting messages at other message boards with hopes that word will spread. Thank you.
<< I hope that Board Staff will indulge me this one message:
Most of you do not know this, but I am "Suzanne", former "Admin" for this site. In some recent correspondence with board members, it has come to my attention that it is not generally known that I am no longer the admin for this board.
It is important to me that board members know that I resigned my position here on or about Feb. 1, 2005, and no longer am associated in any way with Board Staff [at marshallprotocol.com].
Anyone who needs help with board operations should correspond with the new admin who now controls the "Admin" account.
My email address is visible in my profile for anyone who would like to correspond with me privately about non-board related issues.
Thank you,
Suzanne/"pepper" >>
>>
Please note that, while we are very critical of the way mp.com is run, we still believe that the protocol has merit, even if it might not yet have totally evolved.
The jury is still out, but there are a number of open-minded, forward thinking doctors who are on board with this, along with the many who are not.
Sounds to me like it is no different than the situation with other current Lyme treatments?
As someone said, let's not throw the baby (science and protocol) out with the bath water (mp.com).
Ticked
I thought you were still the admin, because it's the same contact address you used, [email protected] . Did you turn that address over to someone else?
Who's "officially" administering the board now?
penny
quote:
Originally posted by tickedntx:
I posted this elsewhere earlier today but it seems appropriate to post it here, too:<< The following message was deleted from marshallprotocol.com after about 30 minutes. Since I am still getting messages from people who don't know that I am no longer board admin there, I am posting messages at other message boards with hopes that word will spread. Thank you.
<< I hope that Board Staff will indulge me this one message:
Most of you do not know this, but I am "Suzanne", former "Admin" for this site. In some recent correspondence with board members, it has come to my attention that it is not generally known that I am no longer the admin for this board.
It is important to me that board members know that I resigned my position here on or about Feb. 1, 2005, and no longer am associated in any way with Board Staff [at marshallprotocol.com].
Anyone who needs help with board operations should correspond with the new admin who now controls the "Admin" account.
My email address is visible in my profile for anyone who would like to correspond with me privately about non-board related issues.
Thank you,
Suzanne/"pepper" >>>>
I don't believe that's the case.
Protocols don't 'evolve' by themselves, but are adjusted as those responsible for their creation learn and grow from experience.
In this case, the protocol's creator not only refuses to learn himself but works overtime to 'protect' mp.com members from being contaminated by outside sources of information.
If the Protocol was 'evolving', the D-deprivation element would have been dispensed with for most patients, whose measured serum levels of vitamin D and its active metabolite have been normal or deficient, not toxic and dysregulated.
If the Protocol was 'evolving', instead of lashing out at those who report poor results and accusing them of non-compliance, the site staff would re-evaluate their starting assumptions in light of empirical results.
If the Protocol was 'evolving,' the last thirty years of research on 1,25-D as an immune modulator would not be excluded from discussion on the mp.com website. Most of that research concerns the ability of 1,25-D to both enhance immunity to cancer and bacteria and selectively suppress those immune responses implicated in auto-immune disease.
If the Protocol was 'evolving,' evidence that Benicar suppresses aldosterone, a hormone that is already suppressed in many chronically ill people, would be acknowledged, and appropriate warnings and workarounds added.
It was for the high crime of posting a Benicar study showing significant reduction in aldosterone after 6 months (at the standard hypertensive dose), that I was banned from the mp.com site.
If the protocol was evolving, a succession of recent studies showing the vitamin D deprived have significantly higher cancer rates, as well as rates of MS and other chronic inflammatory diseases, would have been accurately conveyed to members, many of whom are already at elevated risk for these conditions.
If the protocol was evolving, it would not continue to rely on an obsolete range for 'healthy, normal' 1,25-d in the Merck manual, ignoring the upward revision in both the level of that metabolite our bodies need and the level our bodies can safely tolerate.
If the protocol was evolving, the fact that out of 'over three hundred' Sarcoidosis patients who've begun the MP 'maybe 50, maybe 20' have stuck with it and are registering improvements would strike a note of caution.
Never, to my knowledge, has a protocol with such flimsy results against its original target disease been rewarded with broad application to a legion of other ills.
If the protocol was evolving, the response to questioning over time would have become more relaxed, confident, not more shrill and intolerant.
If the protocol was evolving, when researchers whose work Marshall has cited point out that he's misconstrued their findings, he might actually listen.
The protocol is not evolving, because it's assumptions are so rigidly maintained that anything which calls them into question is immediately rejected. Fiddling with antibiotic selections in the later stages of the protocol does not qualify as 'evolving.'
Indeed, these changes have been used to intensify the secrecy surrounding the MP and intimidate questioning members by threatening to withhold the latest secret formula from their doctors if they don't behave like good compliant little sheep.
Araneli recently suggested the protocol's rigidities may be necessary for an 'experiment' of this kind. Araneli is unaware, I think, that Marshall rages at any suggestion that he is involved in an 'experiment,' and explicitly rejects the notion that he is bound by the ethical and procedural norms which experimental treatments are properly subject to.
Several times during my stay on the board staff of mp.com, I suggested to Marshall that this was, after all, clearly experimental, and that publically acknowledging that was the most appropriate way to respond to skeptics. For my efforts, I was told to shut up.
The protocol is not evolving, most critically, because the careful selection and monitoring of participants that allow a trial to be meaningful have been rejected by Marshall from day one.
Instead of gathering information that would allow an ongoing assessment of the protocol's performance, Marshall used his support staff's time to issue uniform, generic responses to patient queries. The staff members who have stayed on embrace that role, and have by now posted the same, un-evolved Marshallisms on that site many hundreds or thousands of times. These are seldom actually responsive to patient questions.
When a very thoughtfully designed survey was introduced by a site member to collect that information, Marshall used harrassment and legal threats to shut it down. Not only is the information not collected and analyzed by the staff, but any attempt by members themselves to do so is verbotten.
You cannot adapt to information you go out of your way never to see.
The protocol is also not evolving because at the very point of entry, when 'candidates' submit their D-test results to Mangin for 'interpretation', the obvious fact that most do NOT have excessively high 1,25-D levels is cast aside as irrelevant.
Members will find that any subsequent developments that do not fit the MP orthodoxy will be just as blithely dismissed.
The MP is not evolving, but grows more narrow, inbred, and non-responsive with every passing day.
The only sense in which aspects of the MP are evolving is that some patients, who know pathological rigidity when they see it, have had the courage and wisdom to do what the protocol's creator will not, and adapt those elements which might be useful to their own needs and understanding of the relevant science.
Many of them posted on the old Infection and Inflammation site, declaring superior results with lower doses of Benicar, or higher doses of antibiotics, or both. For that reason alone, the I & I site could not be allowed to continue.
I am glad to see that others who have been involved at a staff level with mp.com are now speaking more candidly about problems in how the site is run. But the problems go a lot deeper than that. The site problems aren't just a product of one man's ego and bad temper.
The censorship, the blaming attitude expressed towards patients who report poor results, the need to shut down critical discussion not just within mp.com but in other public forums...these things arise naturally out of the original act of egoism that declared this weakly established remedy for Sarcoidosis a broad cure for every 'autoimmune' disease known to man.
Reality is intrinsically hostile to that claim, and those who advance that claim will inevitably become hostile to reality.
quote:
Originally posted by tickedntx:
I want to clear up a not uncommon misperception...He is not a medical doctor (MD) Dr. He is a PhD Dr.
Not only that, he has a degree in electrical engineering, and apparently has spent most of his time working with computers and trying to unsuccessfuly run a computer related business, Sarc Systems. It went bankrupt and was involved in a number of legal actions. See: http://tinyurl.com/3ksdr
or: http://www.sec.gov/Archives/edgar/data/843650/0000843650-00-000001.txt
Most people with this kind of PhD rarely refer to themselves as "doctor" but it's his perogative.
[This message has been edited by pennyhoule (edited 23 March 2005).]
I have my suspicions about who replaced me as Admin but do not know for certain so prefer not to speculate publicly.
Suzanne
[This message has been edited by tickedntx (edited 18 March 2005).]
I believe that other scientists/medical professionals will evolve the protocol if Marshall does not.
This may be wishful thinking, but based on attendance at his recent conference, I believe that there is growing (if currently limited) interest in his work in the medical community, and am hopeful that this will happen.
Only time will tell.
Suzanne
Thanks for posting Paula's comments with her permission! I hope you got a private email from me today with info.
I have asked for last 2 days specifically what the first name of the new admin is & twice; they would not address it, and deleted that out of my post to them.
Someone mentioned a physical therapist I believe above who WENT to the conference; is that Reenie? I believe she is the one who did that type of work prior to lyme.
I applaud you & Paula for going to the conference, but then Paula didn't know then she was banned, correct?
Suzanne, please answer this publicly on this board also.
Are the PRIVATE MESSAGE area on MP private between sender/receive OR do other board members & admin have acces to everything there? Thanks for explaining how that worked.
That was a wonderful feature I enjoyed daily. Thanks for answering my questions.
You were ONE IN A MILLION over there; your management skills & tact were the best I have ever encountered on a message board. Atta girl Suzanne/Pepper.
Bettyg, Iowa
[This message has been edited by bettyg (edited 20 March 2005).]
:-) I am most definitely not Tx Lyme Mom! I'm not even a mom! :-)
To the best of my knowledge, Reenie was a massage therapist. On the conference brochure/web site, it said "MT" after her name. I assume it means "massage therapist" but am not certain. Yes, she was at the conference. (I did not attend.)
Private messages at mp.com are accessible by administrators, but not Board Staff.
Suzanne
Some researchers and studies suggest that Lyme can evolve into MS, with that trademark type of auto-inflammation that attacks myelin and causes the death of axons, neurons and other central nervous system cells.
Low vitamin D is a known risk factor for MS.
For several months, after first becoming acquainted with the Marshall Protocol, I adhered to the ban on sun exposure, bright light in the eyes, and dietary vitamin D.
Then last December I had my 3rd brain MRI. For the first time, the report came back citing marked brain volume loss and atrophy.
My symptoms are more of a match symptomatically with MS than they were a year ago.
I also developed much more severe arthritic pain in my knees over the same period.
I should note that I did not take MP doses of Benicar (no physician I spoke with would even consider such doses), but did take a higher daily dose of Diovan for blood pressure than was used and found effective in the first version of the MP.
There were multiple posts by Marshall and other staff indicating that D-deprivation was therapeutic in itself for "Th1 diseases."
The point is that if I had known that there is a huge body of research implicating D deficiency in the onset and progression of our illnesses, I would never have risked Marshall's experiment.
I can't know that the months of D-deprivation are a culprit in my decline, but I also can't know that they weren't.
Others had adverse responses on the full protocol that were more acute and debilitating than mine. I've talked to several former MP patients who feel that they were set back, and have not yet recovered the degree of health and well-being they started out with.
The relationship between vitamin D and MS is widely known. The MS Map of the United States, if you haven't seen it, will absolutely put to rest any doubts you have about the case for this relationship - the vast majority of cases occur in areas with long "vitamin D winters" where UV exposure is too low for vitamin D synthesis to occur.
Indeed, Trevor Marshall's favored authors on the subject of vitamin D, Adams and Lemire, are well aware that low vitamin D is a risk factor for MS, and believe that vitamin D is protective against a number of other 'autoimmune' diseases, including Lyme arthritis.
Marshall does not disclose this information, nor does he allow it to be posted to the website.
One of the fundamental principles governing innovative medicine is informed consent. Patients should not be encouraged to embark on an experimental regimen without being aprised of all relevant risks.
It is my strong belief that if most patients with CFS, RA, Lyme, FM, etc, were apprised of what is now known about the immune-modulating role of vitamin D and its metabolites, they would not choose to embark on a sustained regimen of D-deprivation.
Not only does the active metabolite of vitamin D increase bacterocidal activity in infected macrophages (the very kernel of the 'Marshall Pathogenesis' is infected macrophages), it has been shown in vitro, in vivo, in animals, in humans to contain and limit auto-inflammation. This is the exact opposite of what patients on the mp.com website are told.
One could critique these findings about vitamin D, but they reflect the emerging medical consensus, and to pretend they do not exist is inexcusable.
(I am very well aware that there are patients, particularly those who have granuloma forming diseases, who do in fact need to limit vitamin D - it is not a one-size fits all proposition, and that is precisely my point).
Then there is the FDA data which according to Marshall certifies the safety of taking 3 to 4x the recommended maximum dose of Benicar. (Actually, the mp site's recommendations for Benicar use during 'intolerable herxes' gets you to 6x the maximum recommended dose).
In fact, no one was tested at anything like 160mg of Benicar daily OVER TIME; the study the mp.com site refers to was much shorter in duration than the 18 to 36 months specified by the protocol.
Studies like this have to balance the need to determine safety against the need not to subject human test subjects to unnecessary risks. So there were animal studies, notably a two year rat study that found 'dose-dependent' increases in kidney tumors and tubular cell hyperplasia.
The FDA formally found those results "relevant to man." The same report that discusses them concludes by advising that a starting dose lower than 20mg be established, and that this be the recommended starting dose for all patients.
Patients taking Benicar at the standard dose have had kidney problems. A very suggestive animal study indicates that ARBs generally may actually increase the risk of renal fibrosis. More than one MP patient has reported kidney pain, and some have had persistent lab abnormalities as well.
MP patients who don't experience any of these problems and perceive some benefit can be glad. That does not make the protocol any more 'safe and effective' for those who don't respond or respond negatively.
But the operators of the mp.com site are unusual in their insistence that problems NEVER arise from the protocol itself, only from patients who fail to adhere to it.
This dishonest and dangerous attitude is not excused by the evangelical fervor expressed by Marshall and some of his more ardent followers. Indeed, Messianic pretensions are always, for me at least, a warning sign of imminent danger.
I write about these things at some length here because it is not possible to do so on mp.com, and in my opinion it is indecent for patients not to know these things when they weigh their medical options.
quote:
Originally posted by TX Lyme Mom:This change in my status at the MP website will allow me more spare time for participation in other groups where I can speak my own mind freely and without any inhibitions or sanctions.
------------------
oops!
Lymetutu
I've learned quite a lot during my departure from LymeNet while I was spending almost all of my spare time learning about the MP program and helping to mentor patients at the MP website -- so it was not time wasted at all.
This is just a quick note to say that I never really intended to stay away from LymeNet for so long, but there just aren't enough hours in the day to keep up with everything that there is to learn out there on the big wide internet.
More later, when time permits.
Tickedntx aka Pepper, former MP admin is Suzanne... and not the same person as TX mom..
TexasLyme Mom, former MP board Staff is the real-life mom of Lonestartick (who is a Lymie & former MP patient).
Is that right?.. I guess not that it really matters, but since it's come up..
I know Texas is big, but do you'all live in the same town?;-)
Barb
You got it right. : ) Nope, none of us live in the same cities unfortunately.
Hi Betty,
I'm almost 90% certain that Reenie is not a Physical Therapist (P.T.). I believe she is a Massage therapist (M.T.? or L.M.T), but you might ask her.
I have a few close friends who are physical therapists - Note that this is different from Physical Therapy Aides. The programs my Physical Therapist friends completed were nearly as competitive as medical school. They each spent a year with a cadaver just like medical students do. One of my friends has a master's degree and another has a doctorate degree (D.P.T.) in Pysical Therapy. Their education is much different from the limited requirements for massage training.
One must take undergraduate courses in Biology, Anatomy & Physiology, Chemistry, and Physics prior to being admitted into a Physical Therapy program here in Texas. It is very competitive, a high GPA (grade point average) is required to be admitted into a P.T program.
Massage therapy, on the other hand, does not even require college course credits. The certification process usually requires about 6 months of training.
It takes years of at university in order to become a Physical Therapist, and only months at a massage school in order to become licensed. I hope this helps. http://stats.bls.gov/oco/ocos080.htm
-Lonestartick/Kris
[This message has been edited by Lonestartick (edited 20 March 2005).]
Do you have any thoughts on this? Also, I know Barb Peck may have some good ideas. Thanks for any input.
Paula Carnes
It is my strong belief that if most patients with CFS, RA, Lyme, FM, etc, were apprised of what is now known about the immune-modulating role of vitamin D and its metabolites, they would not choose to embark on a sustained regimen of D-deprivation.
Not only does the active metabolite of vitamin D increase bacterocidal activity in infected macrophages (the very kernel of the 'Marshall Pathogenesis' is infected macrophages), it has been shown in vitro, in vivo, in animals, in humans to contain and limit auto-inflammation. This is the exact opposite of what patients on the mp.com website are told.
One could critique these findings about vitamin D, but they reflect the emerging medical consensus, and to pretend they do not exist is inexcusable.
(I am very well aware that there are patients, particularly those who have granuloma forming diseases, who do in fact need to limit vitamin D - it is not a one-size fits all proposition, and that is precisely my point).
Firstly,
An assumtion is being made that the adverse reactions on the low dose abx therapy is a herxheimer.
I have repeatedly questioned whether these reactions are from bacteria die off (and the subsequent immune reaction.. i.e herx) or something else entirely. IMO this question hasn't been answered.
Secondly,
The literature supports that Benicar (and other ARBS,) , have immune modulating properties. It's ptetty well accepted, that for chronic inflammatory conditions, a modulator modulates to improves the condition by reducing the inflammation by various mechanisms.
But you're lumping Vit D restriction along with angiotensin II receptor blocking making certain assumptions and somehow tieing it in with herxheimer.
As far as low dose abx:
I have never under stood the theory put forth about very low dose Mino (between 25-100mg 3 times per week) and the statements about how "as it degrades from the tissues" it kills bacteria... and I beleive that statement underlies much of the assumptions made about low dose equalling herxheimer.
Maybe now that you and TxLyme mom are back here you can explain some of these assumptions.
And finally- the term immune modulating just means that the substance changes in some way the way the immune system is currently operating...good or bad..
And with the dual role alot of substances play in the body - one cannot assume that the immune modulating effects of D resitriction and off-label high dose ARBS are going to be good for everyone or in every disease or syndrome.
Barb
edited to correct spelling- gotta use spell check!
[This message has been edited by bpeck (edited 20 March 2005).]
Thanks for the clarification; I was quoting this from my bad "brain fog" memory.
Paula, WELCOME to the lymenet board! I'm very sorry about how you, TLM, and Suzanne were all treated by Trevor. He is rude enough to members, but to be that way with the VOLUNTEER board staff is unforgiveable.
Paula, you mentioned vit.D, etc. and I have this question for you/other former board moderators:
My last D tests were 20 on 25; 21 on H125.
Sorry, again I'm doing this from my poor memory & can't remember the proper names...uffda.
My LLMD recommended that I start taking a vit D supplement. I have NOT. Wearing the NOIR sunglasses really help my eyes which then has lowered the 125 D; right?
I know I have NEVER been on the MP treatment program. I'm on my LLMD & VET Dr. Scott Taylor's treatment plan. Scott has lyme & he is the reason why I tested for lyme last summer.
Would any of your moderators take the D or NOT as I have chosen to do at this point.
I am NOT getting any better on treatment plan I'm on. I wouldn't say I'm much worse, but the fatigue is awful. I even tend to fall asleep while on pc.
QUESTION: tomorrow I go see my LLMD. I feel I should be tested for co-infections since it was NOT done earlier.
Do I test for all? Would you recommend MDLabs which accepts most insurances?
=====================================
We've had countless expenses with my neuro psy testings last Dec. & my Jan. sleep apnea study plus buying the cpap machine which is NOT working! I got a humidifier based on folk's input from here.
I stated I wanted a HOT/WARM AIR one only; what I received blows COLD arctic air at me all night long. Cpap machine has a meter reader on it, and does NOT count at least 50% of time I sleep with it on.
I've complained for the entire last 3 weeks. Gotten the run around including to MICROWAVE the water first, which I did that lasted 11 minutes staying warm
Will talk to supervisor tomorrow.
I apologize Suzanne for HIJACKING your post, but know that Paula, TLM, Paul, and you will most likely read this post.
Betty G.
First of all, let me state that I'm not convinced that the excess light exposures trigger as many of the so-called "Herx" symptoms as it is being claimed that they trigger -- but I'm also not 100% sure that they don't. My vote is still out on that whole issue, based on my second-hand (but close-up) observations of what I've seen our daughter go through.
She and I usually agree on almost everything, but we are still trying to decide what to make of this paradox, and we have been batting it around and trying to sort it out, based on her various reactions during the last 7+ months on the MP program. I'm not sure if she and I are in total agreement yet on our interpretation of everything or not, so please take what I am saying here with a grain of salt.
We both reserve the right to change our minds about our interpretations of why excess light exposures seem to trigger so many unpleasant symptoms, as we continue to accumulate more and more experience with it. Maybe the dogmas being expounded at the MP website about this are right, but until we can verify this effect by means of our own experience, we are reserving judgement on its validity.
OK, now to the meat of the matter. Lowering the secosteroidal hormone 1,25-D by avoiding excess exposure to sun and bright lights and by means of dietary restrictions of vitamin D is effective because it lessens the ability of these occult intracellular bacteria to survive. The low-dose antibiotics weaken them even further so that the immune system can then do its job properly to kill them instead of protecting them in a safe niche where the antibiotics cannot penetrate in high enough concentrations to kill them.
Without the help of Benicar to block the angiotensin receptors on the host's macrophages, the bacteria which reside safely sequestered inside these phagocytic WBCs are able to convert the precursor vitamin 25-D into the active secosteroidal form, known as 1,25-D. Too much 1,25-D is toxic to the host.
This excess conversion of vit 25-D to 1,25-D does not occur in healthy, normal individuals who are not infected with these intracellular bacteria though because their kidneys manage to control the level of conversion of 25-D to 1,25-D so that it remains at a physiological, healthy level instead.
Toxic levels of 1,25-D suppress the host's immune system and also throw out of balance many other of the host's steroidal hormones. However, if the angiotensin receptor sites are blocked by the Benicar blockade, then the bacteria inside the host's macrophages cannot utilize 25-D to convert it to excess 1,25-D -- therefore, no immuno-suppression and no hormonal imbalances.
Here is the link to a Trevor's published scientific papers which explain all of this in great detail so that you can see for yourself if I've explained it right or not. I know my explanation is pretty close, but until I spend some more time reviewing it again, I'm hesitant to state for sure that I've got it down exactly right.
http://trevormarshall.com/papers.htm
What we have found, though, based on experience is that Benicar potentiates the effect of the antibiotics more than anyone could ever imagine who hasn't experienced it or witnessed it up close in a family member sho has gone through it. It's absolutely indescribable, amazing and unbelievable just how much difference Benicar can make when it is combined with the right antibiotics taken at the right dosage levels and also at the proper frequency of dosing.
quote:
Originally posted by TX Lyme Mom:
What we have found, though, based on experience is that Benicar potentiates the effect of the antibiotics more than anyone could ever imagine who hasn't experienced it or witnessed it up close in a family member sho has gone through it. It's absolutely indescribable, amazing and unbelievable just how much difference Benicar can make when it is combined with the right antibiotics taken at the right dosage levels and also at the proper frequency of dosing.
I'm sorry, but this just doesn't add up to what you're claiming it does. I know at least 5 people who have done full dose abx while on high dose Benicar with no adverse effects. No one ever addresses this. It was just stated at some point in time that Benicar potentiates abx, and miraculoulsy follows the bugs' life cycle exactly to kill bugs, and then it became part of an entire belief system package. Don't you think the Sankyo package insert would warn of combining Benicar with abx, if there were really such a huge risk?
You're completely ignoring the possibility that it may be the low dose abx that's causing the activation of the bug's defense mechanisms, and in turn its proliferation, which is causing these horrible so-called "herxes". Or perhaps there's something else altogether going on. Some people have no "herx" with mino and Benicar, other's have terrible herxes with a few milligrams. Maybe it's because people metabolize the drugs differently, or they're simply having negative reactions to mino, which is described abundantly throughout the medical literature?
This conjecture, which has become a kind of mythology, really needs to stop if we're ever going to know whether Benicar or other ARBS can truly help us or not.
penny
p.s. If this approach of low dose abx being potentiated by Benicar is so true, why have none of the original mper's announced that they've come off the abx or the benicar?
Anybody that trust the FDA in these matters and the drug industy should look at the example of the drugs cited above. I myself was on the Marshall Protocol and kept getting sicker and sicker. The more I followed it the worse it became until it was intolerable. The climax came when I had two episodes of gastrointestinal bleeding ten days apart. People have bled to death from using anti-inflmatory drugs.
So given the small number of people who have actually tried the MP I submit that the incident of mine may posess a significance I would really not care to think about. But it, among other things is something that needs to be addressed. My point being, that benicar, while potentially very attractive, has very real, if hidden risks. Cheers. Thomas Parkman
Not all antibiotics are going to have this same effect an an increased Herx effect when takent together with Benicar because some antibiotics work differently from the special antibiotics which are being used in the MP program.
For example, antibiotics which belong to the cell wall inhibiting (CWI) families of antibiotics, such as the penicillins and the cephalosporins, do not seem to work the same way as the protein synthesis inhibiting (PSI) antibiotics do.
Lyme patients are very familiar with how good they feel on CWI antibiotics because these antibiotics work by getting rid of the cell walls of the pathogens, where the antigens which cause so many of the symptoms are located. However, when one gets rid of the cell wall, what is left is a cell wall-less pathogen instead -- ie, a pathogen which is even more capable of penetrating host tissue cells and of hiding out intracellularly as a stealth pathogen in its CWD form. (CWD = cell wall deficient/divergent)
Therefore, it would depend in large part on several factors: 1.) what antibiotic is used in combination with the Benicar; 2.) the dosing schedule, since pulsed antibiotics of the PSI classes tend to cause more die-off effects.
The reason that the pulsing schedule of taking the antibiotics only every other day is so effective is that these PSI antibiotics inhibit protein synthesis in the host as well as in the pathogen. If you inhibit protein synthesis in the host on a continuous basis, then the host's immune system cannot manufacture enough WBCs with enough potency to be able to kill the intracellular pathogens at a very high rate. That's why one experiences a stronger Herxheimer reaction on the day OFF of the antibiotic than he does on the day ON the antibiotic.
Dr. Thomas McPherson Brown explained this concept about the importance of "pulsing" the antibiotics on an every other day dosing schedule in his classical laymen's text book on this subject published over 10 years ago.
One of the modifications to the MP program being suggested for patients who have an unusally heavy bacterial load, such that they cannot tolerate taking minocycline together with Benicar, is to cut the dosage of minocycline while increasing the frequency of the dosages. This alteration of the dosing schedule lessens the die-off by maintaining a steadier concentration level of the antibiotic in the host's blood stream, thereby not allowing his own immune system to be quite as effective. Then later on, when his pathogen load has been reduced enough that he can start to move towards the recommended pulsing schedule for taking the antibiotics, he can start to pulse his antibiotics by skipping a day between dosages.
Also, I suspect that some/many of the so-called adverse reactions and side-effects listed on the package insert and other drug warnings for Benicar have been noted because this drug has been tested on persons who are not in perfectly good health themselves and that the symptoms which result are a sign that the person might have a low-grade infection with one or several stealth pathogens.
This infection would not be a high enough of a pathogen load to cause acute symptoms and maybe not even very many chronic minor symptoms either. Nevertheless, these individuals may be in the early stages of some yet unidentified chronic infection which will later be diagnosed as some kind of chronic, degenerative (and maybe autoimmune) disease several years later on.
I don't know why, but it always cheers me to read you. (Apparently, even when you're writing warnings.) I love your humor and your eloquence. I find I smile every time I see your name by a post.
Your points are valid. In my case I reached the point where I began to feel that Lyme and co-infections would be the death of me if I didn't do anything. I have tried other things, but I always relapsed. I was miserable and desperate, so after weighing things very carefully, I was willing to accept risks - risks I was aware of as well as those I can only imagine. To be blunt, I would like to be comfortable and enjoy a few good years before I die.
This topic reminds me of the wonderful days at Lymenet when people could agree to discuss heated topics openly and,for the most part, politely. Oh, my have I ever missed open, uncensored communication. It's so nice to be able to agree to disagree.
[This message has been edited by Lonestartick (edited 20 March 2005).]
I haven't done high dose antibiotics while on Benicar. I do know that at least one patient at the MP forum experienced awful symptoms that I do NOT believe was Herxing while she was on just 3mgs of Minocin. Her experience did NOT seem to me to be Herxing. In fact, it made me wonder whether or not this dose was merely low enough to stimulate, and not actually inhibit the bacterial growth. (I have a hard time believing that Minocin and ABX kill the most bacteria when their levels are approaching zero.)
Maybe the super-low-dose of Minocin contributed to exacerbated symptoms by stimulating the bacterial growth, not by killing anything. I see by your response that I'm not the only one who has been thinking along these lines.
My lab work verifying high levels of 1,25 D causes me to believe that TM's model may apply to me. I also felt improvement in symptoms simply by avoiding D foods and sun & light exposures. When I first started taking Benicar, oh my, did it ever make me feel good! (Again, this is my experience.) I didn't start out at super low doses of Minocin when I was on the MP. I began at 25mgs and moved up to the full 100mgs qod as quickly as I could. This worked really well for me. (Again, my experiences only.
I have NOT used high dose antibiotics at all while I've been on Benicar because I was interested in seeing how this protocol built on the foundation that Dr. Thomas McPherson Brown. I do know people like you who have done so successfully, without any adverse effects.
I did experience symptoms that so closely mirrored my actual Herxing responses during times when I was taking high doses of multiple antibiotics for Lyme and co-infections. My experience causes me to believe that one can Herx on a lower dose of ABX when it is combined with Benicar. I've never felt as if I was staying anywhere close to the super-low-dose that might be encouraging bacterial growth. I do actually feel like I'm Herxing when I feel like I'm Herxing. (Yikes, I hope you figure out my meaning there.)
My perceived Herxes follow a very predictable pattern on my calendar. They are almost like clock work and that does tend to influence my belief in this aspect of the model. (I should admit that, for the most part, I believe much of the model, even if I can NO longer believe in the man. I hope that makes sense too.)
I understand that McPherson-Brown's protocol is a 2+ year process for curing autoimmune disease. Given that precedence, I will feel better about evaluating this protocol's success/failure at the 2-year mark. I'm still only 6+ months into this process, so it's too soon for me to know anything, let lone to claim a cure. It does seem to help symptom management though.
I agree with you that much of TM's speculations have become myth and that we need to be discussing these things openly without the cult like dogma. Please forgive me my tendency to focus entirely on my current improvements in light of his model. This is what makes sense for me right now from my own patient perspective and my own experiences with this protocol. That's really all I have to go on as I sort through things. I do know a Sarc patient who claims to be recovered. She reported that she has now gone off antibiotics and has not relapsed yet. We at this site seem to recognize that Sarc is different from CFS and Lyme
I must say, TM's behavior towards you saddened me. It was a real eye opener.
[This message has been edited by Lonestartick (edited 20 March 2005).]
Is there more bacterial die-off going on with the MP than there would be, with the same doses of antibiotics alone?
My answer is that I very much doubt it.
quote:
Originally posted by paulscha:
Paula, if I interpret your question narrowly, it reads like this:Is there more bacterial die-off going on with the MP than there would be, with the same doses of antibiotics alone?
My answer is that I very much doubt it.
I am suggesting that if we took the same doses of antibiotics WITHOUT Benicar and reduction of D we might get the same results. There may well be something going on with pulsed antibiotics (not just the low dose, but the timing) that kills borrelia.
I tried to simply explain the concept behind pulsed antibiotics. It is not that the antibiotic kills best at a low level. It is that the bacteria cannot mount the same defense over time when the antibiotic threat has been decreased and then increased in a cyclical fashion. I guess they think it is safe to come out and play, then they get whacked. It is like they run out of bullets.
Also, the triple combo Trevor is using may well be key. He has selected effective antibiotics which would require the bacteria to develop 3 mutations to survive. This is not likely to happen. Of course, this might lead one to ask why not start all three at once. Would that mean death by herx??? LOL
That wasn't really funny was it?
Then there is the aspect of reduced inflammation. We know that the SARS patients died from lung inflammation, not the virus. So is Benicar the key?
I don't know the answers. I think I know the questions. Meanwhile I feel like LoneStar, so far it is working for me.
Paula Carnes
Nice to hear a voice of reason.
I also think that elements of the protocol hold promise, but it's just way too early to know how or why, or for whom. And the information we've been fed so far (since so many reports are censored or edited or ignored) is just too biased to evaluate objectively, IMO.
I'm still responding really well to Benicar, but am definitely concerned about the possibility of long term side effects. I'm also the classic case of someone who can't take minocycline. There are SO many studies that show that minocycline can be really dangerous for certain people. So far, I'm doing fine with Zithromax.
I'm truly praying that Sankyo and the other ARB companies will do some serious research in this area. Gary Smith did a wonderful, highly acclaimed study on the benefits of ARBS as anti-inflammatories and their potential for curing cancer. He believes there are implications for all kinds of "autoimmune" disease. I sure hope we hear more from him. We used to have his research in the files at Infection and Inflammation, before we were suddenly and "mysteriously" shut down. You can read it at the Journal Of Inflammation:
http://www.journal-inflammation.com/content/1/1/3
We really need more good research in this area asap, as it holds such promise. But we can't allow ourselves to be brainwashed out of desperation.
penny
[This message has been edited by pennyhoule (edited 20 March 2005).]
Tetracyclines and Zitho are common antibiotics prescribed for many many things. If there was any potentation aspects then given the number of years that ARBs have been used and how heavily they are used with this high-blood pressure nation.... I would expect that to have been very well documented in the literature. It is not.
Some one has suggested that there are two things going on with this odd herx:
Hormone changes from both benicar and vitamin D deficiency
The reduction of vitamin D is actually turning off the immune system so all of the auto-immune responses are being turned off [no symptoms] and the infection is allowed to grow uninhibited. Remember, it is the body RESPONSES to the infection that causes the symptoms. Turn off the immune system by starving it of Vitamin D and the symptoms will disappear [and any existing infection will thrive -- so 1 mg of a tetracycline would cause a massive toxin dump because the body is full of infections!]
quote:
Originally posted by TX Lyme Mom:Not all antibiotics are going to have this same effect an an increased Herx effect when takent together with Benicar because some antibiotics work differently from the special antibiotics which are being used in the MP program.
[/B]
On low dose abx, the field of dentistry made some interesting paradoxical findings, back in, I think, the mid 1980s(?)
If I'm not mistaken one finding 'may'have had to do with somehow 'fooling' bacteria by giving a low dose instead of a high dose.
A line of investigation into this might provide some clues.
pq
Keen insight Wabbit! 
I'm very inclined to agree.
Been investigating this line of reasoning for some time.
Its 3am now, and I'm too comatose write anything longer than this.
To sleep I go with this to contemplate.
Back another day.
pq
You didn't mention which 3 abx you were talking about
Did you sign a confidentiality agreement not to reveal the 3 abx? If so, then it's going to be mighty hard to discuss anything with any substance.
Are you talking about Mino, bactrin and Zith?
I was involved in discussions about the efficacy of low dose abx with your group.
As a matter of fact, I supplied your group with abstracts showing that some pathogens's variants are susceptible to abx under the MIC while the classical or parent form was not susceptible to low doses at all. SO, while there is evidence that low dose can kill some variants (but it's not quite so simple as just taking a tiny amount).
There is alot of data out there about how low a dose you can go with certain abx and still either control or kill bacteria that has come out of the AIDS research, and I forwarded plenty of papers to your group about those abx classes and how AIDS patients need to ramp up Bactrim to avoid side-effects, how many times per week you need to take Bactrim to keep the populations of certain pathogend down. etc, etc...
The idea to use more than one abx at a time (one to get the classical form and the otehr to get it's variant) is not new- it's used in H. pylori and Lyme therapy.
For Lyme, I used Mino, Bactrim and Zith - all three together, not at low dose, but at therapeutic doses. (200mg Mino, 500mg Bactrim, 500mg zith perday).
This triple comb followed over a year of other abx for Lyme and I think it was excellent for the remaining neuro (eye) symptoms that remained.
I left these discussions NOT being convinced by your group that their suppositions about the benefits of LOW DOSE abx (even in combo) outweighed the risks. ... the risks being the development of mtuants of other pathogens you aren't even targeting.. or just keeping the bacteria colonized (not killing them), and building a dependance on low dose.
And this doesn't even get into the high dose ARB Benicar discussion - or the Herx VS adverse drug reaction discussions.
In any case- I still have exactly the same questions to you guys as I stated earlier in the thread. ESPECIALLY the statement coming out of your group about Minocycline
working the best (at killing) as it degrades out of the tissues.. I've been trying to get an answer to that one since I saw it in print.
Barb
Paula wrote:
Also, the triple combo Trevor is using may well be key. He has selected effective antibiotics which would require the bacteria to develop 3 mutations to survive. This is not likely to happen. Of course, this might lead one to ask why not start all three at once. Would that mean death by herx??? LOL
quote:
Originally posted by bettyg:
Someone mentioned a physical therapist I believe above who WENT to the conference; is that Reenie? I believe she is the one who did that type of work prior to lyme.....I applaud you & Paula for going to the conference, but then Paula didn't know then she was banned, correct?
Are the PRIVATE MESSAGE area on MP private between sender/receive OR do other board members & admin have acces to everything there? Thanks for explaining how that worked.
That was a wonderful feature I enjoyed daily. Thanks for answering my questions.
You were ONE IN A MILLION over there; your management skills & tact were the best I have ever encountered on a message board. Atta girl Suzanne/Pepper.
Bettyg, Iowa
[This message has been edited by bettyg (edited 20 March 2005).]
BettyG,
The best way to defeat the lack of capability for truly private messaging at the MP website would be for everyone to display his/her e-mail address in his/her "profile" so that other members could use private e-mails, which would indeed be private, rather than being forced to use only the website's PM function, which can easily be read by the two Administrators (Trevor and Reenie), although not by other Board Staff mentors.
Betty, if you will send me a private e-mail (since your own e-mail address isn't displayed), then there's more that I can tell you, but I dare not post it openly, even here in this forum.
To the best of my knowledge, Paula's and my status was not changed until after the Chicago conference ended.
Ditto for what you said about the former MP administrator, Suzanne. She's one in a million.
1) As Barb worries, and I do, low dose abx may create resistant organisms. It certainly does so in much simpler organisms, in our animals for instance. REsistant e-coli is now rampant. Same with resistant staph.
Why would abx resistance be such a huge deal, and people believe that low dose or pulsing works?
2) Please attend carefully to the fact that suppressing cox-2 pathway was seriously harmful--50,000 people died of related heart attacks etc.
Please consider the recent scandal with tysabri--2 people got PML a rare fatal brain virus, one died, the other didn't. Tysabri is an immune "modulator" ie suppressor
It is well known that other anti inflammatories INCREASE the risk of cancer, such as enbrel, remicade etc.
Why do you guys think this is any different?
quote:
Originally posted by Lonestartick:
Hi Penny,
I haven't done high dose antibiotics while on Benicar. I do know that at least one patient at the MP forum experienced awful symptoms that I do NOT believe was Herxing while she was on just 3mgs of Minocin. Her experience did NOT seem to me to be Herxing. In fact, it made me wonder whether or not this dose was merely low enough to stimulate, and not actually inhibit the bacterial growth. (I have a hard time believing that Minocin and ABX kill the most bacteria when their levels are approaching zero.)Maybe the super-low-dose of Minocin contributed to exacerbated symptoms by stimulating the bacterial growth, not by killing anything. I see by your response that I'm not the only one who has been thinking along these lines.
Yes, I have a couple of data points from authoritative sources that say that these ultra-low doses of minocycline (below 12.5 mg) might actually be stimulating the growth of some pleomorphic bacteria, rather than inhibiting them. One such reference is Lida Mattman's medical textbook, "Cell Wall Deficient Forms: Stealth Pathogens" (CRC Press). There are passages in her textbook which describe that same phenomenon.
Another authoritative source to reconfirm Mattman's observations of this phenomenon comes from Luther Lindner, MD, PhD, who teaches pathology in the College of Medicine at TAMU and who also runs a private research lab on the side which deals with culturing CWD pathogens from the blood of CFIDS and MS patients. He has made the exact same observation, that different dosages of the same antibiotic may either inhibit or stimulate the growth of certain organisms in vitro.
It is unfortunate the the Phase 1 Treatment Guidelines were so hastily revised in a one week period of time and without sufficient review by other experienced Board Staff members, just prior to the ILADS conference late last October. It took quite a long time and a good bit of behind-the-scenes effort (by Paula and myself) to point out that serious discrepancy before they finally realized that that unwise revision needed to be re-revised again. We realized right away that this was hurting patients, but it was difficult for us to get our points across until several patients had been hurt by this mistake.
Instances like that were what compelled the two of us to hang in as long as we did, thinking that we could have some kind of positive influence. I hate to think how many more people could have been hurt if we had not stood up for correcting that very obvious error.
We both still believe that the MP program deserves a fair trial, but we also believe that its further evolution needs to be in the hands of the doctors who are qualified to implement it and to make modifications to it to fit the special needs of the various cohorts of patients who might benefit from it.
QUOTE from above: (I have a hard time believing that Minocin and ABX kill the most bacteria when their levels are approaching zero.) UNQUOTE
My Comment: DITTO. That dogma was incorporated into a FAQ, which neither Paula nor I were permitted to have any in-put into writing, and which I never agreed with because I felt it was overly-simplistic and blatantly false. I tried to address this concept in subsequent messages myself, but those explanations got lost in the shuffle while this erroneous dogma remained, enshrined into an FAQ, as if it were unquestionably true.
There is neither space nor time right now for me to address all of the other worthy concerns which several other posters have already mentioned here. Busy day ahead for me today. Must stop. More later, when time permits.
Did you sign a confidentiality agreement
which prohibits discussion of some aspects of the protocol? Or are you worried about a Lawsuit?
Something's up - based on your reply to Betty (below.)
If you can't discuss certain technical aspects, then IMO it's a waste of time to skirt around the issues, or talk about what one either 'beleives' in or not..
If that's the case it's a big waste of my time.
Barb
TxLymeMom wrote:
Betty, if you will send me a private e-mail (since your own e-mail address isn't displayed), then there's more that I can tell you, but I dare not post it openly, even here in this forum.
quote:
Originally posted by oxygenbabe:
Important points to consider:1) As Barb worries, and I do, low dose abx may create resistant organisms. It certainly does so in much simpler organisms, in our animals for instance. REsistant e-coli is now rampant. Same with resistant staph.
Why would abx resistance be such a huge deal, and people believe that low dose or pulsing works?
Why do you guys think this is any different?
As I see it, CFIDS and chronic, late-stage Lyme patients are already infected with those "resistant" pathogens -- in the form of CWD organism which hide out intracellularly inside host tissue cells, including the very phagocytic WBCs of the immune system, which are supposed to be killing them, but which are parasitized and "paralyzed" by them instead.
This is what the MP program's approach is uniquely qualified to deal with -- namely, granuloma formations and also intracellular pathogens, which have paralyzed the host's immune system's ability to function properly.
If you want to understand this important basic concept better, please start reading Trevor's published scientific papers on this subject.
http://trevormarshall.com/papers.htm
quote:
Originally posted by bpeck:
TXLMom:
You've just replied without answering any of the questions I raised.. with the most impoertant being:Did you sign a confidentiality agreement
which prohibits discussion of some aspects of the protocol? Or are you worried about a Lawsuit?
Barb,
Nope, no confidentiality agreements. I do have other separate concerns though, and they aren't about any kind of lawsuit either.
It's just better not to spell everything out openly though, for reasons which should be obvious to anyone who is intimately acquainted with the way the MP website operates.
For that reason, I do not feel free to elaborate about these concerns to anyone new whom I do not recognize from earlier associations.
I'll try to address some of the other in-depth scientific concers to the best of my ability, as time permits. I have several other pressing matters to attend to today, so my time at the computer is still very limited right now.
Therefore those issues, which require a lot of time to compose complicated responses to, will simply have to wait for another more convenient time for me to address them, later.
For the third time in this thread you have not adressed my questions.
So I'm going to make some assumptions of my own, based on your avoidance of the direct questions, and your replies to others in this thread.
This thread to me is looking like an advertisment to try some Alt.Off-Label
therapy, based on subjective beliefs with no interest in discussing the drug mechanism, or lack of, for this protocol.
So..
Sorry - and don't take this personally, becuase that's not the way it's meant..
But this is a waste of my time.
Barb
[This message has been edited by bpeck (edited 21 March 2005).]
Yet none who claim to have achieved this 'cure' have stopped taking Benicar.
We know that many people have taken Benicar at MP doses combined with high doses of antibiotics. The 'potentiated' mega-herx that should have ensued did not.
The official explanation - that tiny, homeopathic doses of antibiotics devastate bacteria but inhibitory concentrations do not - is simply not credible. Elizabeth concedes this.
So why does she repeat the claim?
Not because of something she has read in Marshall's papers. I have read them, read each several times, read many of their referenced materials (which often contradict the claims they are invoked to support).
It was precisely by reading those papers closely that I discovered I had been sold a bill of goods.
So why? Why is the claim repeated?
When patients report an exacerbation of symptoms in response to a given behavior (it hurts when I do this) the common sense answer is 'don't do that'.
Elizabeth has said repeatedly now that this answer does not apply to symptom exacerbation experienced on the MP, because antibiotics are being potentiated and infection is being cleared.
Elizabeth, this is not an academic question. You propose to offer guidance to patients who either are, or are not, helping themselves by combining massive doses of Benicar, D-deprivation and sub-inhibitory doses of antibiotics.
You have participated in an enterprise that tirelessly assures patients who feel worse on this regimen, 'not to worry, you may feel worse but you are certainly GETTING better.'
Here, in this forum, where all anyone asks is that you be candid, you have been asked a straightforward question: on what BASIS do you say that these patients are getting better?
All that is asked, Elizabeth, is that you clearly indicate whether you have a rational basis for that claim, or are articulating a belief, grounded in faith, not fact.
Can't you just please answer that question?
quote:
Originally posted by TX Lyme Mom:
This is what the...approach is uniquely qualified to deal with -- namely, granuloma formations and also intracellular pathogens, which have paralyzed the host's immune system's ability to function properly.
Uniquely Qualified. Uniquely Qualified?
On what basis should an experimental treatment be considered "qualified" to deal with intracellular pathogens? I would think to "qualify" there would first have to be a diagnosis of identifiable pathogens and then undisputable evidence that the pathogens are eradicated with treatment, at least in a portion of the patients. Barring that, then some good hard statistics of full remission?
I don't mind people having their opinions, or their theories. I don't mind optimism, but if opinion is going to be shrouded in scientific sounding mumbo jumbo and unsubstantiated claims, then I'm going to demand some accuracy, because this kind of stuff is misleading and is exactly the reason so many people buy into something without understanding it.
This is like political double speak. If you really care about people as you claim, you'll stop it, you'll stop glossing over the evidence you have of people you say were "harmed" and start telling the truth. "Helping people" should be completely egoless, who cares what others think of you? Otherwise it's a corrupted activity. So far, I feel like I'm right back where we started months ago, where concern for struggling patients comes last, especially if they get in the way of our personal agendas. (Oh, except the language has been cleaned up, prettified for prime time viewing.)
penny
What's really sad, is that all the conjecture and hyperbole and spin is probably doing way more damage than good. It's completely clouding, and potentially damaging, the kind of work being done by great researchers like Gary Smith and colleagues.
I'm sure Sankyo and other ARB manufacturers are none too pleased by these whacko developments surrounding their drugs. It's totally impossible to determine what's true and what isn't based on this kind of dialogue.
We need to focus on science, on evidence, on the potential benefits and the potential harm, and stop getting side tracked by the particular biases of certain individuals. We are sorely in need of objectivity, and we need the support of companies like Sankyo. That means moving forward with objective investigation, not dogma and blind belief. The sooner we can discuss this objectively, the sooner progress will be made. Which of course is what we were trying to do at Infection and Inflammation, despite numerous claims that open discussion was "harming patients". Of course, that's before we got "mysteriously" shut down.
penny
I did read Marshall's work early on and I saw that he cited a paper where half the sarc patients improved on Vitamin D and half got worse. I asked him about this and I never got a good answer. I posted on his list a roundup showing the importance of Vitamin D.
I don't doubt some people have excess Vitamin D metabolites. But I don't think its the majority and I don't think staying out of the sun longterm is a good idea. Killing the infection is a better idea.
I never found this protocol very attractive, theoretically, and I don't see that too many people actually did well on it. Each to their own. I personally would not be suppressing an inflammatory pathway longterm. Too many other drugs that do so have been shown to be harmful.
I am disappointed that this topic has degenerated into a free for all. I do not feel comfortable participating in an atmosphere of such intense negativity. Those who have deemed this conversation to be ``a waste of time' have insured by their attitudes that it is, indeed, a waste of time for everyone involved.
quote:
Originally posted by TX Lyme Mom:
I'll try to address some of the other in-depth scientific concerns to the best of my ability, as time permits. I have several other pressing matters to attend to today, so my time at the computer is still very limited right now.Therefore those issues, which require a lot of time to compose complicated responses to, will simply have to wait for another more convenient time for me to address them, later.
I had every good intention of coming back to this topic later, when I would have adequate time to discuss these ideas in greater depth, but I have concluded that this is turning into an unnecessarily confrontational argument, frought with negativity.
Anything further which I might have intended trying to say here in this forum would only prove to be a complete waste of time for everyone.
Each person is free to draw whatever conclusions of his or her own about the potential value of the MP -- but NO one should claim to draw any conclusions whatsoever about what my own views might be on any of the unanswered questions which I did not have sufficient opportunity to address previously, because that would me a most unfair thing to try to do.
[This message has been edited by TX Lyme Mom (edited 21 March 2005).]
quote:
Originally posted by TX Lyme Mom:
[B] I had every good intention of coming back to this topic later, when I would have adequate time to discuss these ideas in greater depth, but I have concluded that this is turning into an unnecessarily confrontational argument, frought with negativity.Anything further which I might have intended trying to say here in this forum would only prove to be a complete waste of time for everyone.
Each person is free to draw whatever conclusions of his or her own about the potential value of the MP -- but NO one should claim to draw any conclusions whatsoever about what my own views might be on any of the unanswered questions which I did not have sufficient opportunity to address previously, because that would me a most unfair thing to try to do.[B]
Maybe you should have thought of that, back when we tried to follow the very same principles at I & I, but instead were continously vilified and attacked, and eventually shut down.
Forgive me if I don't feel like sitting here now and hearing how pretty everything is. If you really don't want to waste people's time, then try to get real.
penny
[This message has been edited by pennyhoule (edited 21 March 2005).]
penny
[This message has been edited by pennyhoule (edited 21 March 2005).]
This started out as a good thread. So much so that I almost got up the courage to share my experience with 10 months on the MP. Now I remember why I choose lurk mode on these lists.
Can't those of you who are so angry (rightfully so), see how in your passioned attempts to preserve our right of free speech and help/protect others you are creating the same negative atmosphere by a different route?
If you can't find your way to forgiveness, at least get out of the way and let people express their experiences and opinions. And I don't mean opinions about other people's intentions, motives or agendas, just opinions about the protocol, and the research.
"Know won nose" (if you don't read phonetically, say it aloud)
"you will understand that my peer-reviewed publications lend my opinion a certain credibility, and international reputation"
Attempt at humor
* So he has gotten a bunch of PhD's in Electrical Engineering to review his work?
* Or, did he post it on a board of people with the same illness (and thus obtained review from his peers)? Gee whiz, all of us have peer-reviewed literature now!
* I recall that someone pointed out that he owns the "journal" where his stuff is published. Any critical comment on it would not be published.
So my opinion about the research is that it is likely far less worth than reading CFS-L; and there is such an appearance of a lack of any intregity in Trevor Marshall that any research claim should be validated independently before being acted upon.
quote:
Originally posted by Digby:
just opinions about the protocol, and the research."Know won nose" (if you don't read phonetically, say it aloud)
Now, I will proceed to my main topic of the science of vitamin D, which is a complex and difficult one and was brought up at some length by Paul.
I know this post is somewhat long and technical and may be difficult for readers who are not very familiar with the subject. One might look at the vitamin D article I mention (where many of the references can be found) and also an overview article of the MP that I wrote for Issue 7 of CISRA's Synergy Health Newsletter at members.aol.com/SynergyHN. I tried to make the overview article somewhat simpler.
By the way, although I am doing well on the MP myself, I am still independent and write on a variety of subjects, and do my best to study the science, sort things out and write them up to the best of my ability.
Like Paul, I have been researching the topic and trying to learn to what extent Trevor Marshall's data and views can be reconciled with other studies supporting more widespread vitamin D supplementation.
First, I will address the issue of why some people at the MP sites with normal levels of 25 D and 1,25 D are being told the protocol is still appropriate for them. For one thing, as time has passed, they have found that in people with a clinical picture compatible with the MP and with these normal levels, they still tend to respond in the same way to the MP drugs. So now, they view the D tests as useful as indicating to a rough degree the degree of inflammation in areas of the body with plenty of blood flow (like heart and lungs), but perhaps more importantly, as a tool to rule out a TH2 viral process like AIDS or chronic hepatitis, where the 1,25 D was truly very low.
As Marshall explains, the paracrine or local levels of 1,25 D in areas with less blood flow, like joints, may be much higher. In addition, the body has a certain level of regulatory ability, particularly in the kidneys. If peripheral tissues are producing extra 1,25 D, most people's kidneys have the ability to slow production of 1,25 D in order to compensate and thus have the end result of a normal serum level. However, beyond a certain point and perhaps more so in different people (perhaps with more kidney inflammation?), this compensatory regulatory ability is exceeded by the unregulated production of 1,25 D in inflamed tissues.
My personal experience has been that I had been taking about 600-1000 IU vitamin D in supplements for most of my illness. Last August, when I had my D levels tested, my 25 D was fairly low at 11 ng/ml, but my 1,25 D was elevated at 65 pg/ml, well above the Merck maximum of 42, though near many lab's normal upper end. Thus, inflammation was causing a rapid conversion of 25 D to 1,25 D, just as in sarcoidosis.
My serum calcium levels were not the slightest bit elevated, so there appeared to me to be no reason to suspect that my 1,25 D was so high based on traditional criteria (this is usually the case with regard to serum calcium and 1,25 D values, according to Dr. Marshall's data). The calcium levels are of importance, since most of the reviews supporting higher vitamin D supplementation say that one can avoid excess 1,25 D levels by monitoring serum calcium, which they say will identify excess D levels. The new data being posted at the MP sites and published by Marshall show this is not an adequate way of monitoring for high 1,25 D.
I was surprised how much better I felt when I began avoiding D and sun and then began the Benicar. Of course, for some people, who's immune systems are in a different stage, they may feel worse on lower vitamin D. According to the MP theory, this is because the Herx symptoms may increase once the D is lower and the immune function begins killing the bacteria. Despite short term improvements, the potential for a later relapse may be there as the bacteria are able to continue to increase unhindered. And so it seems, if one is to evaluate whether the MP theory is correct, that short term improvements in a variety of studies may need to be reexamined, as the vitamin D may have been acting in a manner somewhat analogous to high doses of prednisone at least in certain illnesses (though it apparently differs from prednisone in that it mainly suppresses CWD bacterial killing, not all immune function).
According to Marshall, the above phenomenon of Herx suppressions can explain the improvement in many of the studies that claim vitamin D to be beneficial. In many cases, this seems to me to be feasible, though more data is needed. The studies are too short term to know if there is an ultimate benefit to this increased D level or if there would be an ultimate relapse. Even studies showing seasonal variation in MS lesions could be showing a process similar to what would happen if the patient was given immunosuppressive drugs only in the summer (instead of the greater sun exposure).
Regarding MS, I have several points to make (see article from Issue 7 at members.aol.com/SynergyHN for references). First, I think it may be true that very low levels of vitamin D that truly reflect a deficiency of active 1,25 D as well as the inactive precursor 25 D, might lead to a greater incidence of people getting MS to begin with. I see this as possibly being due to the fact that as with other hormones, we all need a level of 1,25 D in a certain range surrounding the mean for normal functioning. In far northern latitudes, where people, particularly older people are indoors or almost entirely covered up for a large part of the year, this may not happen, unless they consume enough vitamin D containing foods. But this doesn't necessarily mean that once one has MS, and the macrophages may be producing a lot of 1,25 D in response to CWD bacteria, that one would benefit by having so large an amount of vitamin D that it suppresses immune function.
Second, to my knowledge, only one epidemiological study seems to show that there is better survival for MS patients who have outdoor jobs and thus presumably more vitamin D. I will just say that these kind of epidemiological studies have a lot of potential for bias. For instance, people choose their jobs for all sorts of reasons that could correlate with characteristics of their disease and influence the results, and I think it unwise to base too much on this study alone.
However, even if it turned out that this study's conclusions were validated, it may just mean that immune suppression with high D limited inflammatory damage to some degree and extended their life a little longer (as opposed to sarcoidosis, where it would seem to be more likely to hasten their death). But that doesn't mean that low D plus the MP's treatment or perhaps other antibacterial treatment of a proposed bacterial cause wouldn't have far better results than giving just vitamin D. Perhaps the antibiotic based treatments might even cure the disease.
As for the animal studies showing a benefit of vitamin D in autoimmune illnesses, there are also many problems. The mouse model for the autoimmune diseases involves causing a condition that looks similar to MS or other AI diseases by injecting certain antigens into the animal. It may be that they are able suppress the immune reaction to the antigens with too much vitamin D, and if this is the case, it is not surprising that the disease would improve. But, if this is not a true model of the disease, but it is actually caused by bacteria that would eventually proliferate more with immune suppression, the mice experiments are probably of little value. There are other problems too, like the experiments are short and mice are adapted to much dirtier environments, but I personally find the first reason most convincing.
I have also begun looking at the data for cancer, especially looking at the work of William Grant, Ph.D., (www.sunarc.org) who does a lot of epidemiological cancer research. He sent me a very recent paper he wrote where he discusses data that shows that prostate cancer rates had a J shaped relationship with light intensity (Int. J. Cancer. 111:470-471, 2004). His brief article also cited a paper (Tuohiman et al., Int. J. Cancer 108:104-8, 2004) that showed the lowest prostate cancer rates were in the range of 40-60 nmol/l (about 16-24 ng/ml) and this was supported by the correlation being J shaped when looking at the relationship between living at various latitudes and prostate cancer.
This J shaped curve suggests that people with too high a level of vitamin D are more prone to get prostate cancer than those in the moderate range for D. For the study that actually measured 25 D, those with too low a level of 25 D (the inactive precursor) could reflect two different situations, and perhaps both may occur. The very low 25 D may be associated with a true deficiency and in that case the active hormone, 1,25 D would also be very low and supplementation might be appropriate. However, the 25 D could also be low due to a TH1 inflammatory process depleting the 25 D precursor through conversion by macrophages into 1,25 D. In that case, the 1,25 D would then be high and supplementation would be inappropriate. Clearly, these two different possibilities to explain low 25 D can not be distinguished until studies start also measuring 1,25 D.
I do think that the studies that showed evidence for higher colon cancer mortality rates in parts of the world with very low light levels might suggest that very low levels of sun exposure might increase the colon cancer mortality rate, especially since calcium deficiency has also been linked independently with colon cancer (Grant et al, Nutrition and Cancer 48(2): 115-123.) It may be, however, that if everyone got adequate calcium, that the D levels would no longer be a factor. It is also interesting that the above relationship for colon cancer did not hold up for women, when the data were analyzed separately in several studies. It seems to me that the higher rate of autoimmune and related diseases in women, (presumably the undiagnosed cases, as obvious cases would probably have been excluded from the study) might have caused the correlation to disappear. In women, the 1,25 D levels might be more frequently elevated due to TH1 disease, so even very low light exposure would not cause them to be deficient.
For breast cancer, the relationship with D was weaker, and other dietary factors seemed to be much more important (Grant, Cancer 94:272-81, 2002). I have yet to look further into this data, but I thought it interesting that I have seen maps of the U.S. showing breast cancer in the areas of highest industrial activity (CIIN conference, 2004, ciin.org). These areas were in the Northeast, especially. This relationship might confound the vitamin D effect for the U.S., as a large part of the breast cancer correlation was related to finding higher cancer rates in the Northeast, as compared to the Southwest. But I need to look into this more.
Another area I plan to look into is the relationship some have observed between sun exposure, vitamin D and depression. I know my own mood fluctuations have improved since I lowered D, while others have responded differently. The link between inflammation and depression and other mental disorders has received a lot of interest of late. Many of us experience this link when we undergo Herx reactions and feel rather depressed and/or anxious, even having bad dreams on the nights of our biggest Herxes due to the antibiotics. I intend to look further into this in future, but it seems possible that at least some cases of depression being helped by sun or vitamin D could be due to high levels of D suppressing the inflammation from Herxes (occurring when the immune system kills CWD bacteria).
I plan to write a more detailed article on these issues in the coming months, but I thought I'd share these preliminary observations. I hope they may be of some help in giving a different perspective on this complex subject.
Best Wishes to All,
Joyce Waterhouse, Ph.D.
(for those who are interested, information on my background can be found at members.aol.com/SynergyHN and members.aol.com/jcwat101, but I will say briefly that I have a bachelor's in Biology (much of it pre medical), a Ph.D. in Systems Ecology with a minor in Statistics from U.T. Knoxville, did research at Oak Ridge National Laboratory, and published several papers in scientific journals before becoming ill with chronic fatigue and immune dysregulation syndrome (CFIDS or CFS), fibromyalgia and Lyme Disease. Since then I have spent nearly 20 years studying these and other illnesses, including reading a number of medical textbooks)
FIRST: Would you please give some MEDLINE citations that validates this speculation that 1,25D is a valid indicator for TH1 / TH2 determination?
--------------------------
SECOND, I see from the literature that HIV patients will often have 1,25 levels of 45 pg/mL (actually 25% are still higher than THAT).
[U]Subnormal serum concentration of 1,25-vitamin D in human immunodeficiency virus infection: correlation with degree of immune deficiency and survival.[/U]Haug C, Muller F, Aukrust P, Froland SS. J Infect Dis. 1994 Apr;169(4):889-93.
What confuses the matter even more is that the lowest levels of 1,25D are seen with HIV patients that have a Mycobacterium infection (which ain't a viral infection).
[U]Disseminated Mycobacterium avium complex infection in AIDS: immunopathogenic significance of an activated tumor necrosis factor system and depressed serum levels of 1,25 dihydroxyvitamin D.[/U] Haug CJ, Aukrust P, Lien E, Muller F, Espevik T, Froland SS. J Infect Dis. 1996 Jan;173(1):259-62.
Looking at the posted numbers on Marshall Protocol.com for 1,25D, I see SIXTY FIVE people (of 125 checked) with lower levels than seen with HIV, yet Trevor Marshall deem them to be candidates!!! 1,25 D levels are a poor differiator -- since you have a stats background:
What value is the critical value?
What is the alpha error risk with this vlaue?
What is the beta error risk with this vlaue?
Inquiring (trained) minds want to know
Where is he and you getting your numbers and literature from?????? You wrote up a storm, Trevor talks up a strom -- but upon inspection there seems to be nothing but speculation.
---------------------
quote:
Originally posted by joycejcwat101:
but perhaps more importantly, as a tool to rule out a TH2 viral process like AIDS or chronic hepatitis, where the 1,25 D was truly very low.
I also agree that a study of the long-term response of MS to outdoor avocation does not really yield. You dont mention whether the authors tried to do a matched control group - but even if they did I dont see how it could ever have been "matched enough," given that many salient indices of mild MS are quite subjective [edit: and may be the very same indicies/phenomena that might affect a sickies decision on whether to take an outdoor job, since most of them are physical].
You dont mention whether you started D-avoidance and benicar simultaneously - if so one wonders if the effect on your symptoms might not have been solely from benicar.
In any case, it may be impossible to demonstrate that rapid effects of D-modulation on symptoms are not simply due to reversal of hypervitaminosis D. Hence I dont see any clear evidence that 1,25d can actually act as a pro-inflammatory (contrary to its usual effect) in our diseases of interest - ie human inflammatory diseases that are probably due more (as we all tend to believe) to alloimmunity than to autoimunity.
Regardless of by what mechanism D-avoidance may improve sx in the short run for *some* people (the contrary for others)... the question remains as to whether it is ultimately of larger benefit in vanquishing infections. I realize you havent addressed that yet here. But - regarding this question there are no nitty-gritty immunological-molecular proposals to explore; there is only what I would call hopeful speculation. Hence there are really only patient reports to go on.
Eric Hodologica, contemplator of bacteria
[This message has been edited by hodologica (edited 21 March 2005).]
Merck states:
". In healthy persons .. 20 to 45 pg/mL (48 to 108 pmol/L) for 1,25(OH)2D3." http://www.merck.com/mrkshared/mmanual/section1/chapter3/3d.jsp
Why the ALARMIST phrasing of Merck maximum of 42?
Vitamin D status: effects on parathyroid hormone and 1,25-dihydroxyvitamin D in postmenopausal women" Am J Clin Nutr 2000;71:1577-81. shows 135pmol/L (or 54pg/ml ) occuring in that population.
And I see many readings over 200 pmol/L (80pg/ml) in this newer article...
Age-Related Changes in the 25-Hydroxyvitamin D Versus Parathyroid Hormone Relationship Suggest a Different Reason Why Older Adults Require More Vitamin D J Clin Endocrinol Metab, January 2003, 88(1):185-191 REINHOLD VIETH, YASMIN LADAK, AND PAUL G. WALFISH
For example, deeming the normal level to START at 100 (which is above the Merck maximun)
Functional indices of vitamin D status and ramifications of vitamin D deficiency Am J Clin Nutr 2004;80(suppl):1706S-9S. Robert P Heaney,
Would it not be better to get the 25D up to to 100 before you do 1,25D testing?
quote:
Originally posted by joycejcwat101:
Last August, when I had my D levels tested, my 25 D was fairly low at 11 ng/ml, but my 1,25 D was elevated at 65 pg/ml, well above the Merck maximum of 42, though near many lab's normal upper end.[B]
Can't those of you who are so angry (rightfully so), see how in your passioned attempts to preserve our right of free speech and help/protect others you are creating the same negative atmosphere by a different route?
If you can't find your way to forgiveness, at least get out of the way and let people express their experiences and opinions. And I don't mean opinions about other people's intentions, motives or agendas, just opinions about the protocol, and the research.
"Know won nose" (if you don't read phonetically, say it aloud)
posted by digby
********************************************
There are so many valuable points for contemplation here, and of interest both extrapalated from various research points and patient experience.
I hope we can stick to focusing on those things, because surely there could be great value in open, respectful discussion.
Even in as much as understanding the bacteria/immune relationship..
as well as what to do about it.
Despite all the questions this approach has created, it is certainly a new and refreshing angle from which to learn from and perhaps apply.
That said..I have wondered whether there have been..or would be patients who could run basic CBC's, WBC with Dif.. and reactive Lymphocytes, immune complexes, C-reactive protein and SED rate, platelets (making new blood) as well as comprehensive metabolic panel (watch energy, liver, kidney health)..as a means of tracking what is going on.
If patients and Docs would be willing to run these orders...say...weekly...
perhaps some insight into whether herxing (in those cases/situations where there is uncertainty)...perhaps some insight into whether infection killing, die off, immune response is taking place in and around the time that herx reactions are experienced?
I wondered this some time ago when the discussions were new, and understood that..at the time..or for Sarc patients..
the bulk of testing was leaning upon the D tests..but really wonder if TBD's patients would have more to follow along these lines.
I have also branched off in some immunotherapy study for some time (where I landed after choosing/needing to pull myself out of Marshall discussions, actually)..
and this is what one might track in straight immunotherapy and infection.
This could apply to an immune-modulating therapy (where by the immune system is to be ultimately causing the herx activity)..in a much diferent way than if we follow these results in high dose abx therapy..
where the abx's do most of the work, and often times other immune system activity is dampened (ie: the immune system takes a break as the abx does the work)..
Just a random thought..
There could be reason's why this would not apply using the MP that I am not aware of.
Mo
[This message has been edited by Mo (edited 21 March 2005).]
Before you can use test result data, and draw conclusions from that data, the data has to be clean.
The literature shows that 1,25D3 fluctuates throughout the ovulation cycle of fertile women (Reference 1)
and testosterone (Reference 2).
Therefore, at the very least, before you can use the results from 1,25 D3 testing for any analysis from which conclusions are drawn, the tests have to be standardized for these hormonal differences.
The labs that do these tests do not standardize for hormonal fluctuations.
so
comaring these levels amongst women of different age and hormonal status groups and men is not comparing apples to apples...
REFERENCE (#1)
PMID: 6897337 [PubMed - indexed for MEDLINE]
Am J Obstet Gynecol. 1982 Dec 15;144(8):880-4.
Fluctuation of serum concentration of 1,25-dihydroxyvitamin D3 during
the menstrual cycle.
Gray TK, McAdoo T, Hatley L, Lester GE, Thierry M.
________________________________________
REFERENCE 2
PMID: 9115169 [PubMed - indexed for MEDLINE]
: Calcif Tissue Int. 1997 May;60(5):485-7.
The metabolism of vitamin D3 in response to testosterone.
Otremski I, Lev-Ran M, Salama R, Edelstein S.
Biochemistry Department, The Weizmann Institute of Science, Rehovot,
Israel.
I was talking about using basic methods to track immune system activity and infection.
..not specifically about the D testing, of which I admittedly know little about.
If I were to try the protocol, I'd want to follow these tests I listed just to see what I could see..
of course, not knowing till I saw it..or not.. 
Mo
There are people who have Ploymorphous Light Eruptions (PLE)...
Very Very common with Lupus - and Sarc.. and one of the
hypersensitivites from chronic inflammatory conditions. And I guess 20% of the healthy
population suffers from this condition at one time or another.
The Journal of Immunology, Vol 149, Issue 12 3865-3871, Copyright �
1992 by American Association of Immunologists
----------------------------------------------------------------------
----------
ARTICLES
Systemic suppression of delayed-type hypersensitivity by supernatants
from UV-irradiated keratinocytes. An essential role for keratinocyte-
derived IL-10
JM Rivas and SE Ullrich
Department of Immunology, University of Texas, M. D. Anderson Cancer
Center, Houston 77030.
Exposing murine keratinocyte cultures to UV radiation causes the
release of a suppressive cytokine that mimics the immunosuppressive
effects of total-body UV exposure.
Injecting supernatants from UV- irradiated keratinocyte cultures
into mice inhibits their ability to generate a delayed-type
hypersensitivity reaction against allogeneic histocompatibility Ag,
and spleen cells from mice injected with supernatant do not respond
to alloantigen in the in vitro MLR.
A unique feature of the immunosuppression induced by either total-
body UV- exposure or injecting the suppressive cytokine from UV-
irradiated keratinocytes is the selectivity of suppression.
Although cellular immune reactions such as delayed-type
hypersensitivity are suppressed antibody production is unaffected.
Because the selective nature to the UV-induced immunosuppression is
similar to the biologic activity of IL- 10, we examined the
hypothesis that UV exposure of keratinocytes causes the release of IL-
10.
Keratinocyte monolayers were exposed to UV radiation and at specific
times after exposure mRNA was isolated or the culture supernatant
from the cells was collected. IL-10 mRNA expression was enhanced in
UV-irradiated keratinocytes. The secretion of IL-10 by the irradiated
keratinocytes was determined by Western blot analysis. A band
reactive with anti-IL-10 mAb was found in supernatants from the UV-
irradiated but not the mock-irradiated cells. IL-10 biologic activity
was determined by the ability of the supernatants from the UV-
irradiated keratinocytes to suppress IFN-gamma production by Ag-
activated Th 1 cell clones. Anti-IL-10 mAb neutralized the ability of
supernatants from UV-irradiated keratinocytes to suppress the
induction of delayed-type hypersensitivity in vivo. Furthermore,
injecting UV- irradiated mice with antibodies against IL-10 partially
inhibited in vivo immunosuppression.
These data indicate that activated keratinocytes are capable of
secreting IL-10 and suggest that the release of IL-10 by UV-
irradiated keratinocytes plays an essential role in the induction of
systemic immunosuppression after total-body UV exposure.
___________________________________________________________________
Differential Expression of Cytokines in UV-B-Exposed Skin of Patients
With Polymorphous Light Eruption
Correlation With Langerhans Cell Migration and Immunosuppression
Wendy K�lgen, MSc; Marjan van Meurs, BSc; Marjan Jongsma, BSc; Huib
van Weelden, MSc; Carla A. F. M. Bruijnzeel-Koomen, MD; Edward F.
Knol, PhD; Willem A. van Vloten, MD; Jon Laman, PhD; Frank R. de
Gruijl, PhD
Arch Dermatol. 2004;140:295-302.
Background Disturbances in UV-induced Langerhans cell migration and
T helper (TH) 2 cell responses could be early steps in the
pathogenesis of PLE.
Objective To establish whether UV-B exposure induces aberrant
cytokine expression in the uninvolved skin of patients with
polymorphous light eruption (PLE).
Design Immunohistochemical staining and comparison of microscopic
sections of skin irradiated with 6 times the minimal dose of UV-B
causing erythema and the unirradiated skin of patients with PLE and
of healthy individuals.
Setting University Medical Center (Dutch National Center for
Photodermatoses).
Patients Patients with PLE (n = 6) with clinically proven
pathological responses to UV-B exposure and normal erythemal
sensitivity. Healthy volunteers (n = 5) were recruited among students
and hospital staff.
Main Outcome Measures Expression of cytokines related to Langerhans
cell migration (interleukin [IL] 1, IL-18,and tumor necrosis factor
[TNF] ); TH2 responses (IL-4 and IL-10); and TH1 responses (IL-6, IL-
12, and interferon ). Double staining was performed for elastase
(neutrophils), tryptase (mast cells), and CD36 (macrophages).
Results The number of cells expressing IL-1 and TNF- was reduced in
the UV-B-exposed skin of patients with PLE compared with the skin of
healthy individuals (P<.05 for TNF-). No differences were observed in
the expression of TH1-related cytokines but fewer cells expressing IL-
4 infiltrated the epidermis of patients with PLE 24 hours after
irradiation (P = .03). After UV exposure TNF-, IL-4, and, to a lesser
extent, IL-10 were predominantly expressed by neutrophils.
Conclusions The reduced expression of TNF-, IL-4, and IL-10 in the
UV-B-irradiated skin of patients with PLE appears largely
attributable to a lack of neutrophils, and is indicative of reduced
Langerhans cell migration and reduced TH2 skewing. An impairment of
these mechanisms underlying UV-B-induced immunosuppression may be
important in the pathogenesis of PLE.
From the Department of Dermatology, University Medical Center
Utrecht, Utrecht (Ms K�lgen, Mr van Weelden, and Drs Bruijnzeel-
Koomen, Knol, and van Vloten); Department of Immunology, Erasmus
Medical Center, Rotterdam (Ms van Meurs and Dr Laman); and Department
of Dermatology, Leiden University Medical Center, Leiden (Ms Jongsma
and Dr de Gruijl), the Netherlands. The authors have no relevant
financial interest in this article.
2000 IU/day have been give to 1 year old child (and kept up for 20 years) with only positive effects being recorded (i.e. 80% drop in diabetes rate).
Source: The Lancet, 2001 Nov 3;358(9292):1500-3.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11705562
This level (2000 IU/day) is being advocated by quite a wide range of sources.
quote:
Originally posted by bpeck:
I am posting the following papers in full, because, for people who feel better AVOIDING UV exposure -
it's a little more complicated than just the reduction in vit D formation.
[This message has been edited by joycejcwat101 (edited 24 March 2005).]
[This message has been edited by joycejcwat101 (edited 24 March 2005).]
[This message has been edited by joycejcwat101 (edited 24 March 2005).]
[This message has been edited by joycejcwat101 (edited 24 March 2005).]
[This message has been edited by joycejcwat101 (edited 24 March 2005).]
Thanks for your patience.
< It is true, as some have said, that a number of his initial research papers on sarcoidosis have been published in non peer reviewed journals such as clinmed and JOIMR, but his work has broken through that barrier in that he now has a PubMed listed article on the sarcoidosis research in Autoimmunity Reviews. Also, he was chosen to speak at an International Conference among recognized biomedical researchers, and was selected to participate in a collection of works on sarcoidosis by a Russian scientific publisher. Here is a link to the Autoimmunity Reviews journal, published by Elsevier, a well-known publisher of scientific work: http://authors.elsevier.com/JournalDetail.html?PubID=622356&Precis=DESC and ones to the International Conference he spoke at: http://www.kenes.com/autoim2004/ He touches on the points of his education and career most relevant to his current work at: http://www.immunesupport.com/library/showarticle.cfm/ID/5784/T/CFIDS_FM/searchtext/Trevor%20Marshall Joyce Waterhouse, Ph.D. [This message has been edited by joycejcwat101 (edited 24 March 2005).] [This message has been edited by joycejcwat101 (edited 24 March 2005).]
[This message has been edited by joycejcwat101 (edited 24 March 2005).]
You're missing the point - at least you're missing my point. You're Sooooooo missing my point. I'd like to discuss the posibile mechanisms at work (or not) with a novel theory. I think that's what most people on the list want... to learn something. Joyce: can you address the technical issues in the thread? If not, Barb You all bring up some good questions and comments on vitamin D and other issues related to the Marshall Protocol and I will do my best to try to address many of them. On the 1,25 D as an indicator of TH1 immunity, I think one has to look at the entire body of Marshall's recent writings and look at the references (like Mawer et al, Evidence for Nonrenal Synthesis of 1,25 -Dihydroxyvitamin D in patients with inflammatory arthritis, J. Bone and Mineral Res. 6(7): 1991) as well as Abreu et al, which I post the abstract for below. The basic fact that activated macrophages in sarcoidosis produce 1,25 D is well-known and can be found in any textbook (like Harrison's Principles of Internal Medicine). But the use of it more widely as an indicator is something fairly new, though supported to some degree by the Abreu et al and Mawer et al and other studies in molecular medicine. If it were something widely established, then Marshall's work wouldn't be considered so innovative. The references I've looked at cited by Marshall do suggest it to be a promising way of looking at things and there are a number of references that support the underlying processes (and I also cite and discuss some of them in my vitamin D article at http://members.aol.com/SynergyHN ). His work makes the leap of connecting all the basic research he cites with his newer observations. But I agree, there is still much more work to be done. On the AIDS study, I am going by the one cited in Marshall's Autoimmunity Review article (Haug et al 1998). See http://trevormarshall.com/papers.htm for links to all his papers and within those papers you will find many of those he cites, including this one. Haug finds an average for 1,25 D in HIV infected patients of 48 pmol/L. I think the misunderstanding has arisen because they are using different units. To convert to the units used usually in the U.S., you have to divide by about 2.5 to get 18.5 pg/ml (they also state that sometimes the 1,25 D is undetectable, which I suppose may be related to the severity of the infection). This 18.5 is a lower value than I recall seeing posted at the Marshall Protocol.com site. If any were near that, they would have suggested a retest if the sample may have not been frozen or consideration of another diagnosis. I think with regard to the Mycobacterium, the cause and effect may be reversed, since in HIV the the factor of the destruction of the TH1 immune system is there, which is not occurring in sarcoidosis. Perhaps they are having the Mycobacterium problems because their TH1 immune systems have declined to the point that they have virtually no TH1 cells to fight off the bacteria and thus also have little 1,25 D being produced by macrophages (part of the TH1 response). I can also say that Dr. Marshall has also analyzed some of the same data that Vieth uses and disagrees with many of his interpretations of it. He is not the only one that disagrees, since Vieth is pushing for higher requirements and a different way of looking at D than the established one. < I have still to look more deeply into Vieth's work myself, but another example that would seem to contradict Vieth's work is this study by Adams et al ( http://www.annals.org/cgi/content/full/127/3/203 ) involving generally healthy patients rather than ones with TH1 disease, who have had bone loss due to too much 25 D from supplements (much of it not even being on the label). Some of their data in Table 1 and the graphs, shows that they were losing bone at some of the levels of 25 D that Vieth seems to think to be O.K. or even recommended (remember to divide by 2.5 for 1,25 D and 2.6 for 25 D). Their bone mineral density improved by stopping D supplementation. The amount they took would have been a much greater problem if they had sarcoidosis or a related disease with D dyregulation. If one looks at the data in Table 1, their 1,25 D levels aren't nearly as high as they would be in a sarc. patient, given their very high 25 D levels. I don't mean to say that some of the studies showing that older people, especially who live in the North, like in Canda or Finland etc... may not need more vitamin D in their diet for osteoporosis prevention. But I think Vieth goes too far in the levels he recommends and he doesn't know about this new data that shows that the situation of sarcoidosis, of dysregulated vitamin D, is not just a tiny fraction of the public, but may occur in more like 5-10 %. I also don't think his view that a certain amount of increase of PTH is necessarily synonymous with bone loss, and I don't think it is accepted very widely yet by others either, but the PTH part is something I need to look into more. This paper by Abreu et al., on Crohns and Ulcerative Colitis (see abstract below), indicates that 60 pg/ml of D or greater would be detrimental and lead to bone loss. They use a somewhat higher cut off for the point at which bone loss occurs than the 45 pg/ml, but lower than my own 1,25 D value, I believe. I don't know the basis for Merck's value, but I believe there is one, and will have to get back to you on that. In any case, the issue of bone loss isn't what is most significant in Marshall's use of the 1,25 D test, which he is now using as an indicator, though not a perfect one, of the TH1 vs TH2 dominance. Title: Measurement of vitamin D levels in inflammatory bowel disease patients reveals a subset of Crohn's disease patients with elevated 1,25-dihydroxyvitamin D and low bone mineral density. In response to another question, I believe I did feel some improvement on lowered D before I started the Benicar, and others have reported this, also. On the subject of whether taking vitamin D might protect against diabetes, it is intriguing, and I plan to look into that research. But it may fall into the situation I suggested might be true of MS, that a deficient vitamin D state might allow the bacteria to become established, but it doesn't necessarily follow that too much D would be beneficial after it is established. Just like with other hormones, being hypo is as bad as being hyper. But more needs to be researched on this. But I should note that a very new study by a well-known researcher (see Marshall's discussion of this on the upcoming DVD from the conference from http://autoimmunityresearch.org for more on this) found that in mice that typically got diabetes, inoculation with bacterial antigens in their first 5 weeks caused a dramatic reduction in the rate at which they got diabetes. I also wanted to say on the subject of whether very low mino. levels might really promote bacterial growth, although it might occur in certain circumstances with certain bacteria, that did not at all fit with my experience. The first dose I used on the MP was 3 mg Mino (at a time before they changed the recommendation to begin at 25 mg) and I did get a big Herx. within the first 12 hours (bigger than with 100 mg Mino pre-MP). But over time, the Herxes at the 3 mg dose declined to hardly noticeable, indicating that my immune system, working with the antibiotic, had mostly killed off the bacteria that could be reached using that dose of that one drug. Each time the dose was raised, it seemed as though the Mino was penetrating a little deeper and reaching new bacteria, and then the Herx declined after a while at each dose. I can't think of any more plausible explanation of this pattern of response, since it has also been accompanied by improvements in my health. I think the pulsing and low doses of antibiotics may well be more effective than constant dosing, particularly if one thinks of it as being the immune system that is really doing the killing and it's not simply the antibiotic, which just weakens the bacteria. The way I view it at present, is that too big an initial die-off with too big a dose of antibiotics may raise the inflammation and 1,25 D levels, which then help suppress the immune killing of the bacteria. But it is probably a lot more complicated than that. However, my point on pulsing is that the bigger Herx at 3 mg on the MP than 100 mg pre-MP in the first 12 hours supports the view that its not only the pulsing that is the difference with the MP, because when comparing only the very first 12 hours of Herxing from the first dose, pulsing can not become an issue. I'm sure there are others on the MP who have done pulsing before they got on the protocol and probably could directly address the issue of whether the MP enhanced the effect independent of the pulsing. On the issue of fluctuations of 1,25 D with ovulation, I think they may have some relevance for women who are menstruating. But I noticed that paper was rather old and the technique they used was quite new at the time they published and they had only a small sample size, so I'm not sure how much it can be relied on by itself. I wish it were all more simple and I could do better at explaining it, but for now, this is the best I can do, since I have other demands on my time and am going out of town. As I said, I plan to write more in future and will let you know when I do. Also, I wanted to mention that I think I may be doing better than some on the MP because I had already minimized my hidden food and chemical allergies/sensitivities. And believe me, for most people, it takes a lot more than one or two allergy tests to accomplish this. I also think that many with CFS and Lyme who may not do as well on MP may have more severe problems with allergies/sensitivities worsening many symptoms and this may be due to a new parasitic roundworm, C. pulmoni (which I also have). You can read about some easy, at-home methods for reducing your sensitivities in articles I have written at the web site below (Issue 5 and 8 and other for food allergy and Issue 7 for the roundworm). Joyce Waterhouse, Ph.D. http://members.aol.com/SynergyHN [This message has been edited by joycejcwat101 (edited 23 March 2005).]
Just for the record and in the interests of accuracy... According to the Manager of Archives and Records at the University of Western Australia, "Dr Trevor Gordon Marshall was admitted to the degree of Doctor of Philosophy from the University of Western Australia on 23.4.1985. His thesis was entitled "Modelling and Simulation in Diabetes Care"." and "Dr Marshall's student file and academic record...both confirm that his PhD was obtained in the unit 064.920 ie Ph.D thesis Electric. There is no other information that refers to a particular discipline although he majored in Electronic Engineering." The thesis is on file at the library but not available for loan. http://tinyurl.com/6xv2x He has publicly stated (immunesupport.com) that he came to the U.S. in 1982. According to the University of Western Australia, his PhD was awarded in 1985. [This message has been edited by pennyhoule (edited 23 March 2005).]
penny
Joyce, Your statement infered that all PubMed citations represent articles that are peer-reviewed--that is absolutely incorrect. Not all publications that submit to PubMed are peer-review publications. Indeed, I looked at the Marshall citations you referenced, particularly #2 and #6 since they are related to his current endeavor. One of the references is in Autoimmunity Review which is NOT a peer-reviewed journal. Papers are generally requested by the editorial board and do not go through a blind peer-review process. Moreover, the papers in this publication represent overviews of existing literature, not original research. As for the other reference (regarding Vitamin D) you cite, that is a LETTER Marshall sent in. Again, not at all a peer-reviewed paper. I did not look at #7 & #8 as they are not related to the "protocol." In short, (a) he (yet) has no protocol-related original research that has withstood a rigorous academic review process, and (b) neither of the (non-original research) protocol-related citations were peer reviewed. While I do not necessarily think that all treatment suggestions (e.g., Abx combo's frequently used in Lyme) need to go through such a process (although that would be optimal), I am instead taking issue with the claim that you made regarding the peer-reviewed nature of these papers. Finally, one's abilities in one sub-discipline (e.g., engineering) has little relevence to one's abilities in another (e.g., medicine). I do not expect colleagues to read my old work in visual development and be able to make any inferences about my current work in human memory (even though perception and memory are more related than engineering and medicine). Another PhD researcher, [This message has been edited by Sue vG (edited 23 March 2005).]
Thank you for taking the time to detail Your post is very helpful in understanding these concepts. I attended Marshall's presentation at ILADS.. Any insight is always helpful. Mo It is not uncommon for people to complete their thesis or dissertation work in absentia. There can be a lengthy delay while the committee reviews the dissertation and revisions, and there's no need for the candidate to be present at the university during that time. They just have to return for the defense. So I don't see a problem there. [This message has been edited by Sue vG (edited 23 March 2005).]
It is not uncommon for people to complete their thesis or dissertation work in absentia. There can be a lengthy delay while the committee reviews the dissertation and revisions, and there's no need for the candidate to be present at the university during that time. They just have to return for the defense. So I don't see a problem there. Sue vG is absolutely correct about locations and the awarding of degrees. In fact, I earned my first master's degree from a university in Canada in 1989 but left Canada to come back to the states in 1988. I just made a few trips back and forth to meet with my committee and then present at my final oral defense. This is quite common in graduate work when the data have already been collected and analysis and write-up is all that is left. Nature of the graduate work beast. Nothing suspicious about it at all.
I am guily of asking 1 question early on here, and then it has gotten totally out of hand. Joyce Waterhouse, please copy/paste your comments to a NEW thread so that the replies go to you. Delete ALL the duplicate posts at that time. Show a very specific title of what the post is about please. Joyce, please start a NEW thread about Trevor Marshall's credentials so comments only on that will go there. FYI, I am NOT a moderator on this or any other board. I'm an active lymenet reader who is learning a lot from majority of you more experienced lyme folks. If we have a NEW topic, please start your OWN thread so the replies apply only to your subject area and not 2-6 other things. Thank you for your consideration. The moderators of this board are not actively involved, so that leaves it up to the members to get things straightened out again. Happy postings. Penny, I am very sorry for the terrible way you were treated by Trevor on MP. I did not know that yours & Dr. Scott Taylor's I&I board was stopped. I used to read & post a little there. Betty G., Iowa Edited to remove Penny's name from the Trevor comment, and showed Joyce's name who originated that part of the post. Sorry Penny for my mistake. BG [This message has been edited by bettyg (edited 24 March 2005).]
Joyce or: http://www.sec.gov/Archives/edgar/data/843650/0000843650-00-000001.txt Most people with this kind of PhD rarely refer to themselves as "doctor" but it's his perogative. [This message has been edited by pennyhoule (edited 23 March 2005).] [This message has been edited by joycejcwat101 (edited 23 March 2005).]
It is not uncommon for people to complete their thesis or dissertation work in absentia. There can be a lengthy delay while the committee reviews the dissertation and revisions, and there's no need for the candidate to be present at the university during that time. They just have to return for the defense. So I don't see a problem there. [This message has been edited by Sue vG (edited 23 March 2005).] I didn't imply there's anything suspcious about that. Just stating the facts. From then to now, the details of his public resume are somewhat sparse. If Joyce is trying to claim that he's been devoting himself to medical research most of that time, I don't see a lot of evidence to support that scenario. If he has been, then please correct me. I'd feel better if I knew this to be the case. penny [This message has been edited by pennyhoule (edited 23 March 2005).]
Betty G., Iowa Hi Betty, I did not raise the topic of TM's credentials. Most recently, Joyce responded with her version, "in the name of accuracy". So I corrected her statements "in the name of accuracy". My concern, considering everything that has happened, is that people get only the facts and the truth. And that anything that is not know for sure, be identified for what it is. Speculation. penny Bettyg
Joyce, Your statement infered that all PubMed citations represent articles that are peer-reviewed--that is absolutely incorrect. Not all publications that submit to PubMed are peer-review publications. Indeed, I looked at the Marshall citations you referenced, particularly #2 and #6 since they are related to his current endeavor. One of the references is in Autoimmunity Review which is NOT a peer-reviewed journal. Sorry my statements were not quite precise enough. I take your points. I did put in the link to Autoimmunity Reviews and the list of his published work because I thought people could judge for themselves the quality of the journals and could see what work he has been doing. Personally, I consider being chosen by Editors and Board members of the International journal, Autoimmunity Reviews to be a type of peer review that is as significant as the typical blinded peer review. For instance, one of the Editors, Schoenfeld, is an expert in autoimmunity and infection, so I think I would take his recommendation over the majority of academic researchers in autoimmunity. But in any case, I thought by putting in the links showing his publications and that he did have publications in PubMed where most of the best journals are indexed, might be of significance and of interest. Thanks for pointing out my errors-- I did not intend to mislead. I think people have enough links and viewpoints on his career and publications that they can judge for themselves regarding his credentials. Ultimately, the evidence and the science must be judges on its own merits by reading his work and seeing how it stands up over time. Joyce Joyce, please start a NEW thread about Trevor Marshall's credentials so comments only on that will go there. Betty G., Iowa [This message has been edited by bettyg (edited 24 March 2005).] Betty: I only brought up the credentials in response to several previous comments in this thread and perhaps we can leave it where it is now without a new thread. Thanks for pointing out all the duplicate posts and to Penny for letting me know how to effectively get rid of them. It is good to get to interact again with some of you who I knew from the MP sites previously. I hope to learn from you some of the ideas and experiences that you have been sharing on other non MP sites in this more free wheeling and wider ranging atmosphere. Joyce
[This message has been edited by Jellybelly (edited 07 April 2005).]
members.aol.com/SynergyHN
>>
Posted by joycejcwat101 (Member # 6848) on :
edit
Posted by bpeck (Member # 3235) on :
Joyce:
I'm not sure anyone's really interested in re-hashing someones credentials, or lack of..
That kind of discussion should really be in the "Off-Topic" section.
Posted by joycejcwat101 (Member # 6848) on :
Now, on to the technical issues, now that I have had time to prepare my response.
This is clear from his disagreement with the establishment that he expresses in the first 2 sentences of this abstract:
Source: J Steroid Biochem Mol Biol, 89-90(1-5): 571-3 2004
Abstract: Official nutrition committee reports in both North America and Europe now state that Vitamin D is more of a hormone than a nutrient. These statements are wrong, and do not reflect the definitions of either vitamin or hormone.>>
Author: Abreu MT , Kantorovich V , Vasiliauskas EA , Gruntmanis U , Matuk R , Daigle K , Chen S , Zehnder D , Lin YC , Yang H , Hewison M , Adams JS
Source: Gut, 53(8): 1129-36 2004
Abstract: OBJECTIVES: Many patients with Crohn's disease (CD) have low bone mineral density (BMD) that may not be solely attributable to glucocorticoid use. We hypothesised that low BMD in patients with CD is associated with elevated circulating levels of the active form of vitamin D, 1,25-dihydroxyvitamin D (1,25(OH)(2)D). We further hypothesised that this was secondary to increased synthesis of 1,25(OH)(2)D by inflammatory cells in the intestine. The aim of this study was to examine the relationship between 1,25(OH)(2)D levels and BMD in patients with CD. METHODS: An IRB approved retrospective review of medical records from patients with CD (n = 138) or ulcerative colitis (UC, n = 29). Measurements of vitamin D metabolites and immunoreactive parathyroid hormone (iPTH) were carried out. BMD results were available for 88 CD and 20 UC patients. Immunohistochemistry or real time reverse transcription-polymerase chain reaction (RT-PCR) for the enzyme 1alpha-hydroxylase was performed on colonic biopsies from patients with CD (14) or UC (12) and normal colons (4). RESULTS: Inappropriately high levels of serum 1,25(OH)(2)D (>60 pg/ml) were observed in 42% of patients with CD compared with only 7% in UC, despite no differences in mean iPTH. Serum 1,25(OH)(2)D levels were higher in CD (57 pg/ml) versus UC (41 pg/ml) (p = 0.0001). In patients with CD, there was a negative correlation between 1,25(OH)(2)D levels and lumbar BMD (r = -0.301, p = 0.005) independent of therapeutic glucocorticoid use. 1,25(OH)(2)D levels also correlated with CD activity. Lastly, immunohistochemistry and RT-PCR demonstrated increased expression of intestinal 1alpha-hydroxylase in patients with CD. CONCLUSIONS: These data demonstrate that elevated 1,25(OH)(2)D is more common in CD than previously appreciated and is independently associated with low bone mineral density. The source of the active vitamin D may be the inflamed intestine. Treatment of the underlying inflammation may improve metabolic bone disease in this subgroup of patients.
I don't argue that a truly deficient vitamin D level might not be harmful to immunity, in fact I think it is, but it may be that an even more effective prevention method might eventually turn out to be an immunization to certain bacteria. (Edit: I don't give a link to the study because I need to verify information on it when I able to hear the conference again. But I think the researchers name is Bach and that he had previously published in the NEJM and his current work is not yet published).
Posted by pennyhoule (Member # 5611) on :
quote:
Originally posted by joycejcwat101:
Just for the record and in the interests of accuracy, I wanted to clarify some things about the credentials of Trevor Marshall, Ph.D.,
Posted by pennyhoule (Member # 5611) on :
Joyce, you can delete the majority of those multiple posts yourself, by editing them down to just a few words. Be sure to check the previous page as well, as you've got about 6 duplicates of the same or similar posts on the previous page.
Posted by duramater (Member # 6480) on :
Joyce Waterhouse said:
"One can see that he has at least 4 articles in PubMed, where peer-reviewed biomedical research is indexed (for the PubMed ones, see the ones with a PMID number, references # 2, 6, 7 and 8, at http://trevormarshall.com/papers.htm )."
Dura Mater.
Posted by Sue vG (Member # 3143) on :
.
Posted by Mo (Member # 2863) on :
Hi Joyce..
specifics of the very 'meat' of the theories
surrounding this protocol.
there are just so many levles to try and understand and then apply to its use in multiple infections.
Posted by Sue vG (Member # 3143) on :
I have no opinion on Marshall, but just wanted to say that his coming to the US in '82 and getting his PhD in '85 from W. Aust. is not suspicious.
Posted by duramater (Member # 6480) on :
quote:
Originally posted by Sue vG:
I have no opinion on Marshall, but just wanted to say that his coming to the US in '82 and getting his PhD in '85 from W. Aust. is not suspicious.
[This message has been edited by Sue vG (edited 23 March 2005).]
Posted by bg (Member # 46416) on :
Everyone, this thread concerning Paula Carnes only got really hijacked over & over here.
Posted by joycejcwat101 (Member # 6848) on :
Barb,
It was this statement and another one about Trevor Marshall implying that he only publishing in non peer reviewed journals that caused me to post his credentials etc... Sorry, I didn't do the quotes to make that clearer the reason for my posting them. I think if one sort of statement is O.K., then mine is appropriate too.quote:
Originally posted by pennyhoule:
Not only that, he has a degree in electrical engineering, and apparently has spent most of his time working with computers and trying to unsuccessfuly run a computer related business, Sarc Systems. It went bankrupt and was involved in a number of legal actions. See: http://tinyurl.com/3ksdr
Posted by pennyhoule (Member # 5611) on :
quote:
Originally posted by Sue vG:
I have no opinion on Marshall, but just wanted to say that his coming to the US in '82 and getting his PhD in '85 from W. Aust. is not suspicious.
Posted by pennyhoule (Member # 5611) on :
quote:
Originally posted by bettyg:
Penny, please start a NEW thread about Trevor Marshall's credentials so comments only on that will go there.
Posted by bg (Member # 46416) on :
Penny, sorry about my mistake! I went back in and corrected my error to read Joyce's name....not yours. My apologies.
Posted by joycejcwat101 (Member # 6848) on :
quote:
Originally posted by duramater:
[b]Joyce Waterhouse said:
"One can see that he has at least 4 articles in PubMed, where peer-reviewed biomedical research is indexed (for the PubMed ones, see the ones with a PMID number, references # 2, 6, 7 and 8, at http://trevormarshall.com/papers.htm )."
Another PhD researcher,
Dura Mater.[/B]
Posted by joycejcwat101 (Member # 6848) on :
quote:
Originally posted by bettyg:
Joyce Waterhouse, please copy/paste your comments to a NEW thread so that the replies go to you. Delete ALL the duplicate posts at that time. Show a very specific title of what the post is about please.
I am rather new to posting here.
You are right, I will start another thread where we can discuss the science. I will copy my posts on the science and perhaps we can get some more discussion on that.
Posted by Jellybelly (Member # 7142) on :
Ooops, I shoulod have read the entire thread before I posted, never mind.
Posted by nomoremuscles (Member # 9560) on :
Since there's been much MP talk here lately, I thought it would be a good idea for newer members considering this therapy to read this thread.