22 Sep 2008
On Monday, I returned from the 6th International Congress on Autoimmunity held in Porto, Portugal. You can watch my presentation here.
The Congress on Autoimmunity is a biennial event. It features dozens of talks, 1,800 registered delegates, and takes place over the course of five days.
The meeting has a decidedly international flavor. Participants hail from Germany, Italy, Russia, Italy, South Africa, even Mongolia. For many researchers and scientists in the field of immunology, this is an ideal forum to learn about and discuss advances in their field.
Participants include researchers presenting their work, physicians gaining continuing medical education credits, and vendors hawking seemingly sophisticated technology. Who knows — maybe that five-foot chamber with the three LCD screens and dozens of buttons was no more than a glorified alarm clock. I probably should have gotten a brochure.
As host cities go, you can’t do much better than Portugal’s second largest city, Porto. The weather was cool and, except for the skater punks outside my hotel room, the locals were lacking artifice. (One grizzled fellow told me in broken English that Porto was so named, because once upon a time the city’s fathers said, “Let us call it Porto, because it is on a port.” Now there’s something you can’t get in a guidebook.) And what better place to have a conference on immunology than a city dominated by winding streets and dead ends? More than once, I completed a taxi ride thinking I couldn’t tell if I had been taken to my destination using the world’s most clever series of shortcuts or was simply being ripped off.
The meeting itself was held in a historic waterfront building with high pillars and a floor with curious metal tracks leading between one room and the next. Although as good scientists, we spent a lot of time hypothesizing about how the tracks might have been used in the past, no one we talked to could tell us why they were there.
In his speech during the opening ceremony, Dr. Yehuda Shoenfeld, the President of the Congress, proved himself to be something of a jokester. Shoenfeld said he had a particular fondness for Porto, no small part of it due to the fact that his wife had won a beauty contest held in Porto in 1975. When he wasn’t showing pictures of previous years’ attendees ogling belly dancers or introducing the night’s band - the Anti-Phospholipids - he was telling the audience that the three winners of lifetime service awards each would receive prizes of one million dollars (not true!).
One of the award winners was Dr. Eric Gershwin who, in addition to his studies in the field of autoimmune disease, maintains an informal medical clinic for handicapped animals including tortoises, horses, and skunks among others. Dr. Shoenfeld related that Gershwin is a direct descendant of the famous composer George Gershwin. We learned that Shoenfeld’s son, who incidentally turned out to be the keyboardist for the Anti-Phospholipids, received a gift from Dr. Gershwin: an original copy of “Rhapsody in Blue” signed by the composer himself.
Shoenfeld confessed it was the first time the son thought his father’s scientific connections were of actual value. Incidentally, the other half of the Anti-Phospholipids was a violinist who presented at the Congress.
On a more serious note, Dr. Shoenfeld also noted how more diseases - including, for example, depression - are now considered by some to be autoimmune in nature. Interestingly, the list of diseases thought to be autoimmune closely parallels those which the Marshall Protocol treats. Several talks even discussed cancer and autoimmune disease. I find it interesting that when it comes to the MP, some people have a hard time accepting the hypothesis that nearly every inflammatory condition can have the same basic pathogenesis. Yet as the “autoimmune community” continues to attribute more and more diseases to their same basic disease model few people raise an eyebrow.
I arrived with a contingent of others who work closely with Autoimmunity Research Foundation (ARF). ARF’s time in the limelight came early in the Conference, on Thursday afternoon. The session on vitamin D was two hours long and was chaired by Dr. Trevor Marshall. In addition to the four of us associated with ARF, we heard from four others including Dr. Howard Amital of Israel and Dr. Maurizio Cutolo of Italy, both prominent researchers in the field of vitamin D. The last speaker slated to speak, a researcher from Iran, actually failed to show, presumably because he didn’t want to share the stage with an Israeli researcher. This is not the first time this has happened, we were told.
As the chair, Dr. Marshall spoke first. Marshall’s talk had a decided focus on bacteria. He began by reminding the audience that bacterial cells outnumber human cells by a factor of 10 to 1. He went on to argue that the microbiota we harbor has evolved to decrease antimicrobial peptide expression by dysregulating the vitamin D receptor.
Dr. Greg Blaney is an MP physician. Dr. Blaney presented data, serum blood values mostly, from his own sizable cohort of MP patients. Using that data, he articulated a rationale for why 25-D is an inferior marker of inflammatory disease compared to 1,25-D. He showed how, among his cohort, measures of 25-D had a high level of variability and 1,25-D tended to be more consistent with disease status. One of his sickest patients, he reported, had a 1,25-D in excess of 100 pg/ml. Hopefully, his talk will challenge, in at least some small measure, doctors’ and researchers’ practice of testing only 25-D.
Later on, Captain Tom Perez, RPh, MPH spoke. He gave some details of the Marshall Protocol study including statistics on how many patients, by autoimmune diagnosis, experience improvement by time frame.
In my talk, I made a case for why autoimmune diseases such as Hashimoto’s Thyroiditis are much more likely to occur in women than in men, especially during the childbearing years. My contribution had value because I was able to show how one can use the alternate hypothesis for vitamin D to formulate viable hypotheses that logically explain other aspects of autoimmune disease. In the parlance of software engineers, the MP is extensible.
Some people are wary of public speaking. As you can surmise from the above video, I am not such a person. Also, I’ve been longing for the chance to connect with researchers and doctors in a larger forum. In any case, I could have spent much more time talking! I actually was so focused on covering all the main points in my talk that I didn’t even notice the Citizen Kane-like screen behind me.
This Congress marks an important, though certainly not the final, milestone in the increasing acceptance of the Marshall Protocol as a therapy for chronic disease. It was telling that speakers supporting the MP model ranged from a molecular biologist to physician to public health official.
As expected, the other speakers in the vitamin D session offered more traditional perspectives on vitamin D. Prior to my opportunity to speak, Dr. Amital showed data connecting a low level of 25-D to lupus severity. Dr. Cutolo offered a similar conclusion for rheumatoid arthritis.
I take issue with observers who conclude that a low level of 25-D is necessarily a cause of the disease process. They could have just as well identified the measure as a result of the disease state. As epidemiologists repeat ad nauseam, “Correlation does not equal causation.” (I’ve been told that it is a rare epidemiologist indeed who doesn’t have this phrase tattooed somewhere on his or her person.)
In listening to the speakers in the vitamin D session, I imagine that even the least attentive audience member must have felt a certain amount of dissonance, even whiplash. I was disappointed that the forum didn’t allow for a more spirited dialogue, one we desperately need to have.
Being the penultimate speaker allowed me to at least briefly address the disconnect. I concluded my speech with this impromptu observation: “When it comes to correlating disease incidence with low levels of vitamin D, it’s also incredibly important to consider the alternate hypothesis, which is that the low levels of vitamin D may not be causing the disease but may simply be a result of the disease process.”
After the session concluded, Dr. Cutolo introduced himself and we spoke for about 20 minutes. There’s a lot to like about Dr. Cutolo. He’s a jocular guy, but he’s also a serious scientist and was therefore willing to consider the alternate hypothesis. What seemed to intrigue him most was Dr. Blaney’s point that 1,25-D is a more reliable biomarker of autoimmune disease status than 25-D. Perhaps we can expect future studies of autoimmune disease from Dr. Cutolo to rely on this measure. We also talked about my hypothesis: how a muted immune response during pregnancy could lead women to feel greater well-being.
The Congress concluded with a final group dinner held in a winery overlooking the Douro River. Trevor outed himself as a port aficionado. During dinner, he turned down the waiter’s offers of wine and held up his port glass in order to signal how eager he was to drink the local beverage. Also, we finally got to hear genuine native Portuguese music. The band played a series of “old country” ballads including “Do the Hustle” and “I Will Survive.”
The truth is, I can’t say with certainty what effect our speeches and our side conversations had on our fellow attendees. I had the distinct impression that a substantial minority had come to the Conference to conclude business deals. The sparkling booths were evidence of that. Nevertheless, I think we did succeed in presenting the research and hypotheses that underlie the Marshall Protocol to many of the world’s leading researchers and physicians. Thanks to the Internet, the videos of our speeches have the potential to reach an even greater audience.
17 Responses for "Notes from the 2008 International Congress on Autoimmunity"
Amy,
As always, the latest breaking good news seems to be here on your site. I particularly enjoy your consistent attack on the problem while loving the people who are currently lost in the problem. I think I have “Correlation does not equal causation” tatooed already in my heart.
Thank you for that reminder, and thank you for making that important statement to help everyone understand better who came to the session: “When it comes to correlating disease incidence with low levels of vitamin D, it’s also incredibly important to consider the alternate hypothesis, which is that the low levels of vitamin D may not be causing the disease but may simply be a result of the disease process.”
I really enjoyed your presentation too. Very, very well done. I’m so glad you are here.
As usual great writing and ‘color’ on the conference. Particularly liked
“And what better place to have a conference on immunology than a city dominated by winding streets and dead ends?”
Studying Janeway’s Immunobiology has always left we with the firm conviction that, as presently conceived, immunology is a Ptolemaic system.
Janet,
I’m glad you enjoyed the piece. Thanks for reading.
Terry,
I’m glad you picked up on my innuendo. You know, it is such a rewarding experience to talk to researchers, because many of them are just as frustrated as we are. Like any good scientists, I’ve seen that they are open to alternative hypotheses.
The best way for anyone to understand the MP is in the context of conversation where one can address objections and pull the different parts of the model together. That’s why I feel conferences are so valuable in helping the MP gain acceptance in the mainstream research community.
Amy
Hi Amy.
Is your Georgetown thesis on CFS posted somewhere for us to read?
Any major surprises between your thoughts then and now?
Thanks for your wonderful presentation.
-Erik
Hi Erik,
My Georgetown thesis is bound somewhere in the science library. Unfortunately, there is no online version.
That’s no huge loss, because part of the thesis went through the “science” beyond several of the treatments for CFS and their flaws. Then I focused the rest on the MP, basically explaining the MP up to that point, citing Marshall’s work to date and other literature on bacteria. It’s nothing that isn’t on Bacteriality or that isn’t communicated on the MP site. There are no nuggets of wisdom!
My conclusion was that the MP seemed like the most logical treatment for CFS, and I think I was right.
I’m glad you enjoyed the presentation.
Best,
Amy
Amy, I guess nothing speaks louder than success.
But CFSers are necessarily suspicious, having been scammed by countless opportunists who have ALL developed compelling-sounding sales pitches.
Do you, Paul and the other recovered MP’s have some kind of demonstration of physical prowess planned that can set these doubts to rest, and clinch the deal?
-Erik
(Prof Marshall’s protocol clearly has an unfair marketing advantage with such an eye-catching spokesperson)
Interesting description of the effects of extra calcitriol on the expression of other AMPs, and on thyroid dysfunction. Thanks for that.
Hi Amy-
Brilliant presentation! I’m a Phase 3 MPer and your talk described me to a T. My big issues started during pregnancy and quickly deteriorated after my son was born. With T3, testosterone and progesterone being displaced, estrogen got to work on my soft tissue receptors with resulting severe joint hypermobility. Over the years, I’ve had to supplement with the aforementioned hormones. I never new why my endocrine system was off until I found the MP.
Now I take nothing but Benicar and abx…and my joint are largely back to normal.
Anyway, thanks again for showing me with science that I wasn’t crazy for the last 9 years.
This website is great too!
Eppie
Hi Eppie,
Thanks for sharing!
I’m glad to know that yet another woman’s experiences fits with the hypothesis I presented at the Conference.
No, you are definitely not crazy! My hormone levels plummeted as well when my CFS was at its worst. So many women suffering from inflammatory disease also display hormonal deficiencies.
I’m so glad that you joints are returning to normal thanks to Benicar and the MP abx. I hope you continue to make good progress!
Best,
Amy
Amy, are you familiar with the history of Chronic Fatigue Syndrome?
(Osler’s Web. Inside the Labyrinth of the Chronic Fatigue Syndrome Epidemic, by Hillary Johnson)
Dr Peterson called up the CDC because he had a cluster of a little more than two hundred people with some really bizarre and “unheard-of” complaints that had no explanation in the medical literature.
This phone call by Dr Peterson initiated the investigation which led to the creation of the “Holmes Committee” and the subsequent “Research tool” of “CFS” which was originally intended to investigate these anomalies.
One of these abnormalities was a “pathologically low Erythrocyte Sedimentation Rate” (SED rate).
Dr Peterson told me at the time, that “Doctors are taught ‘The lower, the better’ so they don’t perceive a low SED rate as an abnormality, but a ZERO SED rate is absolutely ridiculous”.
This was later confirmed by Dr Byron Hyde.
Are you seeing a 3-or-less SED rate in these TH shifted illnesses? And is it being corrected by the MP?
- Erik Johnson
1985 Incline Village CFS survivor
Osler’s Web
Antecedent Epidemics page 215:
*The following year, Anthony Komaroff and his associate Dedra Buchwald told an audience of doctors and researchers at the University of Washington in Seattle that approximately 40% of patienst with the disease had abnormally low sed rates. “With the exception of sickle-cell disease,” Buchwald said, “we’ve never seen sedimentation rates that are consistently zero, one, or two, with any other illnesses. We’ve speculated these patients may have difficulty forming red cell membranes, as is the case with sickle cell disease, because of a distorted red cell pathology.” Two years later, Canadian clinician Byron Hyde reported in the fall 1989 issue of his newsletter to sufferers, “To my knowledge, there are only five diseases that have a pathological low sedimentation level: myalgic encephalomyelitis (the British, Australian, and Canadian term for the chronic illness) sickle-cell anemia, hereditary sperocytosis, hyper-gammaglobulinemia, hyper-fibrogenemia.”
Amy,
In your talk you mention and show images of how 1,25 DiHydroxy interferes with Thyroid, adrenal and gonadal hormones. Do you have this information in a document/article available here. I just tested for low 25 Hydroxy and have had problems with all three hormonal systems for 5 years.
Do you think lyme, chlamydia pneumonia, etc. testing is necessary to detect the presence of TH1 bacteria or would the low 25 Hydroxy combined with the high 1,25 Dihydroxy be enough?
I’ve also been reading in popular magazines declaring an epidemic of low Vitamin D. Do you think this might be related to the increasing prevalence of TH1 infection?
Thanks,
Shawn
Hi Shawn,
A transcript of my speech is available here. I am also in the process of writing a paper for the Annals of the New York Academy of Science which will discuss 1,25-D’s ability to dysregulate the nuclear receptors in greater detail. The paper should be published in about 2 months.
In the meantime, I got the in silico data on 1,25-D’s affinity for the thyroid, adrenal, and glucocorticoid receptor from Dr. Marshall’s paper that was recently published in BioEassys. The info is near the end of the paper:
http://TrevorMarshall.com/BioEssays-Feb08-Marshall-Preprint.pdf
I don’t think chlamydia testing or testing for other co-infections will give you any indication of whether the MP will work for you. The D tests are a good indication of infection under some circumstances, but in my opinion, the best way to figure out whether or not you can benefit from the MP is to do a therapeutic probe. I discuss the D tests and a therapeutic probe in this article:
http://bacteriality.com/2008/02/23/misconceptions/#10
Yes, what mainstream medicine views as an “epidemic of vitamin D “deficiency” simply indicates to those of us familiar with the MP that an increasing number of people are suffering from infection with the Th1 pathogens, and at an earlier age. In light of the fact that rates of chronic disease are skyrocketing as vitamin D advocates continue to convince the public to take more of the secosteroid, our alternate hypothesis seems to hold more water.
Best,
Amy
Amy,
Thanks for those. I’m trying to convince my doc to try me on Cytomel (T3). Klinghart mentions that giving T3 and Forskolin help remove the lyme blocks of the receptors in the thyroid and adrenals respectively.
“The more difficult objective is to choose agents and
methods to trigger the release of neurotoxins from
their respective binding sites. Only then can they be
transported to the liver, processed and enter the small intestine from where they can be carried out by the binding agents. The toxins occupying the T3 receptor are competitively displaced by oral T3 - cycled with the Wilson protocol (available at most compounding pharmacies). The toxins blocking the cortisol receptor are mobilized with the herb forskolin.”
From:
http://www.samento.com.ec/sciencelib/4lyme/KlinghardtArticle.pdf
Amy,
On the subject of T3 if you’ve heard of Wilson’s Temperature syndrome (http://www.wilsonssyndrome.com/)
I suspect that many of not most of these Chronic Fatigue type illnesses are TH1 pathogen based. If so then the different types of cures/treatments for these may be effective at either destroying the TH1 Pathogen or effectively putting it in remission.
WTS treatment is basically to give the patient T3 for a month to “reset” the thyroid.
From:
http://www.knoxintegrativemed.com/wilson%27s%20syndrome.htm
“However, when a person experiences prolonged stress, the adrenal glands respond by manufacturing a large amount of cortisol. Cortisol inhibits the conversion of T4 to T3 and favors the conversion of T4 to RT3. If stress is prolonged, a condition called Reverse T3 Dominance occurs and persists even after the stress passes and cortisol levels fall. Apparently, RT3 itself acts like cortisol and blocks the conversion of T4 to T3.”
I know I’ve read the Lyme patients run cold. Possibly part of the pathology of the TH1 bacteria which might be the “stress trigger” that allows them to escape from dormancy.
It is interesting to think that giving T3 for a few weeks might right the balance. I know that typical chronic Lyme treatment involves a year or more of various antibiotic with strong herx. Once the temperature is back up the lyme goes dormant once again and waits for another stressful event to return it to the throne.
Hi Shawn,
Thanks for sharing, but the treatment you propose does not fit the MP model of chronic disease.
Well, it does in the sense that we both seem to agree that most inflammatory diseases are caused by the Th1 pathogens.
But the goal of every MP patient is to avoid any form of supplementation. Rather the MP aims to target the root cause of hormonal dysregulation and in the process allow the body to re-balance thyroid levels through it’s own natural homeostatic mechanisms.
In the case of many autoimmune diseases, T3 is low because of the flow on effects of Vitamin D Receptor blockage by bacteria that cause the diseases in the first place. So by killing these pathogens, MP patients allow their hormone levels to naturally return to a normal range. Indeed, many subjects in our trial have blood tests to prove that their hormones have re-stabilized.
I am writing a paper on the topic of thyroid hormone dysregulation and autoimmune disease for the Annals of the New York Academy of Sciences. It should be published in February when I will link to it on this site. I hope the paper will give you an even better idea of how T3 levels can be managed with the MP.
Best,
Amy
>Thanks for sharing, but the treatment you propose does not fit the MP model of chronic disease.
I know…. I’m not quite sold on the MP yet although I am deciding what to do next in the way of testing. If I can the doc to run a 1,25 DiHydroxy and if that turns out high I might consider trying to persue MP if I can find an open minded doc in Alabama.
I was just trying to decide if there was an easier path than taking antibiotics with all the herxing involved and such and save the patient even more suffering. The idea that you can ever completely erradicate lyme is something I question. Another tick or mosquito or biting Fly and it’s back. Wouldn’t it be better to figure out how to shut if off then go through a year of antibiotics each time?
This blog might interest you. This MD is a very intelligent Lyme Doc in Maryland. He discusses Vitamin D and Marshall in this postl:
http://lymemd.blogspot.com/2008/05/whats-deal-with-vitamin-d.html
> Rather the MP aims to target the root cause of hormonal dysregulation and in the process allow the body to re-balance thyroid levels through it’s own natural homeostatic mechanisms.
How long does this treatment usually take? How long did it take for you? (thanks for putting up will all my questions
Hi Shawn,
Most people on the MP are quite intelligent and have tried numerous therapies for their diseases before doing the MP. If there was an easier route to recovery than the MP then why would so many patients be sticking with the MP even when it is a difficult treatment?
The decision to do the MP begs this question - how badly do you want to get a completely normal life back? Not a life where you might have good days and bad days and still have to take supplements and drugs - but a totally healthy existence again.
Taking supplemental T3 may well palliate your disease symptoms and allow you to live a more active life. But without killing the bacteria causing your disease you will not actually be well. But perhaps you would rather take this route then have to deal with several years of difficult herxing on the MP? It’s your decision.
Once on the MP another tick or mosquito bite will not make you ill again because
a) the pathogens the insect harbors will be killed by the antibiotics
b) the MP strengthens the innate immune system so that even when the treatment is stopped it can still fend off the pathogens transmitted by insects.
While the Dr. your reference in Maryland seems open to looking at vitamin D through a new lens his interpretation of the MP is unfortunately very wrong. I would suggest he read Dr. Marshall’s published papers before writing blog posts.
Most MP patients who are seriously ill take 3-5 years to complete the treatment. They do get better as time wears on and herx reactions become easier and easier. But the MP is still tough and requires commitment.
I recommend that you continue reading about the MP, and try to speak to Lyme patients who are currently on the treatment to get a real perspective of what they are dealing with.
Best,
Amy
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