Monday, April 29, 2013

Fish or Cut Bait

Regarding the April 25-26th FDA meeting, this much can be said. There is the real world - and then there is the world of the government. These two worlds do not intersect at any point.

In the real world of ME/CFS, research and treatment are moving along, government or no government. There are hints and suggestions that a certain dynamism is occurring - perhaps for the first time ever.

One extremely bright spot is the upcoming InvestinME conference in London on May 31, 2013. I cannot say enough positive things about this conference, and the reader can access my previous posts about this conference. This is the sixth year I have attended this conference. Thanks (in abundance) goes to Pia and Richard Simpson (and their friends), the organizers of this 8th annual InvestinME conference. The title of this year's conference is: "Infection, Immunity and Myalgic Encephalomyelitis - Mainstreaming Research into ME". I cannot imagine a more apt title to describe where this conference is headed this year.

This conference is an intense, compact, knockout set of presentations, entirely directed towards biological research into ME/CFS. There is no bullshit here, no fluff, no pandering - and the day is long and difficult. But it is also enthralling. The organizers tailor the presentations to provide a strong research thread from the past, while, at the same time, offering new research avenues to a broadening understanding of this illness.

The conference Chair this year is Dr. Ian Gibson. In this tight-packed day, this job takes on a heightened importance, requiring the chair to forge links between research threads, and to guide speakers along in a commonly focussed direction - so that the entirety takes on some cohesion. I personally am a great admirer of the skills, nudging abilities and humor of Professor Malcolm Hooper, who has done this task at a number of these conferences.

Dr. Andy Kolgenik will return for the third year in a row. Dr. Kolgenik's research and treatment is ever expanding with more clinical data. Most likely Dr. Kogelnik will present updated ideas coming out of his Open Medicine Institute. (It is generally known that Dr. Kogelnik and Dr. Dan Peterson have a close and strong working relationship. Dr. Peterson is a regular attendee at this conference and has lectured here on a number of occasions. (Dr. Peterson will be attending this year's conference.) Dr. Peterson recently presented a retrospective study of infused Vistide in ME/CFS patients. The results, generated by his research institute, Simmaron, were impressive - and give further weight to the reality that here are existing treatments for this illness, a reality that the CDC has completely ignored. Cort Johnson reports on this study here. Not only does the study encourage broader use of Vistide but it also points with some optimism to the future use of an analogue of Vistide, CMX001, now in clinical trials.

Dr Sonya Marshall-Gradnisdik will return, presenting further her work on NK cells. This research is very promising for a marker or markers, and perhaps clinical tracking for this illness. (Incidentally Dr. Jose Montoya indicated to me at the FDA meeting that he was working hard on a cytokine signature for this illness and should have some results in the next six months or year. Dr. Montoya does not want to be rushed and wants to "get it right".)

Dr. Fluge and Dr. Mella will also be returning, perhaps with new information about their follow-up treatment on the original Rituximab patient cohort and perhaps on their trial of Enbrel. (Some might remember that Dr. Jonathan Kerr proposed a study on Enbrel in 2007, but he was turned down in his funding application.) Hopefully the momemtum on Rituximab treatment options in ME/CFS will gain some traction.

New researchers this year include Dr. Mady Hornig from Columbia. She promises to describe some results of the pathogens study under the aegis of the Chronic Fatigue Initiative, financed by the Hutchins Family Foundation and directed by Dr. Ian Lipkin.

Two new immunologists will speak - Dr. Carmen Shelbenbogen from the Berlin Charitie and Dr. Amolak Bansal from Epsom and St. Helena University Hospitals in Surrey. Professor Greg Towers, a virologist from the University College London will also speak.

This year's conference promises to yield more and deeper collaborative efforts between researchers and clinicians as bonds are formed among individuals who have a certain like-mindedness. More importantly, these individuals are not confused about whether this illness exists, nor are they disbelieving of the serious nature of this illness. None of these presenters have to be convinced that these patients are seriously ill and debilitated with measurable immunological abnormalities.

Dr. James Baraniuk will not be able to return this year - as he has a conflicting engagement. I was able to speak at some length with Dr. Baraniuk at the FDA. His brain research is terrifically exciting. In presentation, Dr Baraniuk generates a certain confidence and clarity. I have long felt that Dr. Baraniuk's research is going to have a profound impact in the field. His most recent study can be read here. I understand that other papers will be forthcoming. His NIH grants are continuing at a sufficient level where his research can be ongoing.

Fortunately Dr. Baraniuk's colleague Dr. Rakib Rayhan will be making a presentation at the InvestinME conference. From the InvestinME website: "Dr. Rayhan's desire is to identify potential biomarkers that provide objective support to disease criteria and that are translated into new and affordable therapies leading to a better quality of life for patients."

Last year InvestinME introduced a pre-conference, invitational roundtable (with the same subject as the conference). The roundtable took place on the day before the conference. Last year's subject was autoimmunity and featured a number of researchers from potentially allied autoimmune illnesses. The invited guests, including the conference speakers, spent a full day exchanging ideas. This exchange has proven to be very effective in forging new and sometimes unexpected alliances. What could be better? There are various ways in which to encourage exchanges between experts inside and outside the field and all conferences and university research facilities should be exploring ways to do this. The Ratna Ling model, ending in 2008, sets a nice example.

In the evening of this roundtable day, there is a dinner where further, important exchanges occur.

It is my hope that various clinicians, researchers, advocates (and perhaps a few semi-well or partially recovered or recovered patients) from the United States can go to this conference. This conference has always been woefully underattended by Americans (except for presenters). It is a black hole in the United States. This makes no sense. Shit happens at this conference, and more American "doers and thinkers" should just suck it up and go.

There should be two of these conferences per year - with the other one taking place in the United States. Someone in the US should "look and learn". The current US model for an ME/CFS  conference - a four-day biannual conference for "Professionals of all stripes" - really sucks.

By the way, the FDA should fish or cut bait. After this two-day FDA conference on April 25th and 26th, the FDA can no longer plead ignorance about the true nature of this illness. They have an opportunity now to "send a signal". They should start with a significant move to get Ampligen approved for this patient population. What has happened with Ampligen is a first-rate travesty.

Tuesday, April 23, 2013

Lisa Petrison's comments and notes on Dr. Paul Cheney's 2013 lecture

The following is reprinted from Facebook with permission of Lisa Petrison:

"Thanks much to patient advocate Chris Cairns for sharing Dr. Paul Cheney's new video series, which I just finished watching. Here is a brief summary.

Video #1:  This is a recap of material from Cheney's previous videos, including background info on CFS, descriptions of heart dysfunction and presentation of the concept of oxygen toxicity. This continues onto Video #2.

Video #2: At about 16:00, Cheney moves into some very interesting new material related to the idea that due to heart problems in the disease, CFS patients do not push enough oxygen/nutrients into their brains/livers and also do not remove toxins from the brains/livers.  He discusses VIP (subject of a new paper by Dr. Ritchie Shoemaker) as a possible way of addressing this problem, and as an aside mentions that Shoemaker's "CIRS-Water Damaged Building" patients are the same clinically as his own CFS patients. 

Video #2:  At the end of this video, he discusses MAF.  The treatment seems to work best when it brings nagalese to a moderate level, he says.  If nagalese is too high, the immune system is not working well enough, whereas if it is too low, the immune system is way too active, he says.  So he only seems willing to use it on certain patients, for certain lengths of time.  The yogurt/kefir version works better than the chemical version on his patients, he suggests.

Video #3:  These are some random Q&A's.  They include his explanation for why thyroid is not a good treatment for most CFS patients; his suggestions for patients who want to exercise (walking, pilates and light swimming/walking in water); and his justification of his fees. He also responds to a question about Chronic Lyme, pointing out that a leading NY Lyme doctor said that he had seen lots of patients with _acute_ Lyme disease between 1970 and 1980, but that he had never seen any of them go _chronic_ until after 1980.  Cheney says that because CFS appeared in NY and SF in 1980, and because the Chronic Lyme patients look exactly the same as the CFS patients, he thinks that something changed in 1980 and that chronic Lyme is an effect rather than a cause of whatever that is. 

I personally would likely agree with that, and would expand it to include chronic mold reactivity as well. I also agree that the CCSVI & CHVI findings have the potential to be really important, based on my own experiences of recovering from the disease.  It's interesting that VIP is related to them.


My Lecture Notes:

CCSVI (Chronic Cerebral Spinal Venous insufficiency) -- seen in 100% of Cheney’s CFS patients tested (n=20 to date). Back-and-forth flow reversal of the deep cerebral spinal veins. That’s going to destroy capillary function in the central nervous system.

CHVI (Chronic Hepatic Venous Insufficiency) -- seen in 100% of Cheney’s CFS patients tested (n=20 to date). Capillary flow reversal in the liver.

This is a complication of right ventricular squeeze compensation for diastolic dysfunction.  It is probably the most serious complication that I’ve ever found in CFS. It will destroy effective capillary function in the brain and in the liver.

Results are catastrophic, because if you don’t have proper capillary flow in the brain, you neither deliver sufficient oxygen and nutrients to the brain nor do you remove toxins from the brain.

Likewise in the liver, you just knock out important liver function, ranging from detoxification, which will put you at risk for food sensitivities and drug sensitivities. You will create xenobiotic toxicity of all kinds of things. Worst of all, it’s your center of gravity for redox control. The primary center of gravity for redox control, especially NADPH production, is in the liver, and that’s going to be impaired.

CCSVI: A doppler ultrasound technique used on cerebral venous outflow tracts in the neck and in deep cerebral vessels developed by Dr. Paola Zamboni in Italy in 2008. First characterized in MS patients by Dr. Zamboni; later discovered in autism and chronic Lyme disease; currently observed in 100% of CFS cases to date; somewhat controversial in respect to invasive vascular interventions even though such interventions have helped some but not all patients with CCSVI.

CHVI: A doppler ultrasound technique used on hepatic venous outflow tracts in the liver first described by Dr. Cheney (“I know no one else who has even looked for this”). First characterized in CFS patients by Dr. Cheney; also seen in what some have called chronic lyme; currently observed in 100% of CFS cases to date; associated with CCSVI in 100% of CFS cases to date; findings of CHVI confirmed by two ultrasound certified radiologists in California and Italy; linked to the physiology of pure diastolic dysfunction.

Because of the big artery squeeze, you get a very high tricuspid regurgitant flow that’s passing from the right ventricle through the tricuspid valve going in the opposite direction of venous return. This pressure pulse (which is almost 30 ml of mercury, which is pretty high) going in the opposite direction leads to a return blood flow that’s actually low, because there is a low (aortic?) output. Therefore with the low return pressures, meeting a high pressure pulse going in the opposite direction, you have the potential to reverse the flow of blood. That’s what you see in some of the pictures -- that red splash is a flow reversal in the hepatic vein.
It’s supposed to be blue, with blood moving toward the heart. When it’s red, the blood is moving from the heart up toward the liver. Reversal is never normal, and unbelievably that’s what I see in 100% of my patients.

The cause of it is that big RV cavitation to compensate for diastolic dysfunction. And enough that the venous return is actually low. 
With a low return coming back and a big powerful squeeze pushing blood the other way. That will knock out effective liver capillary function and a lot of problems will ensue.

This is our first attempt to treat this. We’re using Vasoactive Intestinal Peptide (VIP). This was developed by Dr. Ritchie Shoemaker who recently published a paper on the use of nasal VIP. This is the TRmaxPG  pre-VIP treatment and then 5 minutes post.  What we saw was a derogation of the TRmaxPG, which is the pressure pulse causing reversal flow. That dropped by 8, 22 and 38% respectively in three consecutive patients.

If you can drop out this pressure pulse, you can actually stop refluxing in the liver. Because what VIP does is it’s a potent nasal dilator. So a squirt up your nose will cause the cardiovasculator to dilate, which means that when the right ventricle squeezes, blood goes out the pulmonary artery rather than back through the tricuspid valve. You’re reducing the pressure so it moves in the right direction and much less of it goes in the wrong direction, causing these big drop-offs in the TRmaxPG.

See this big red blotch here?  That’s flow reversal. If you watched it in real time, it would be blue-red, blue-red, blue-red. Five minutes after nasal VIP treatment, we completely abolished it. No more blue-red, blue-red.  Just blue, blue, blue. Very odd, very impressive and very encouraging, because to date no one has had any idea how one might actually reverse CCSVI or CHVI. This could have tremendous clinical impacts on these patients.

* 28 Amino Acid Peptide
* Member of the Glucagon/Secretin Superfamily
* Similar to Growth Hormone Releasing Hormone
* Produced in the gut, pancreas and hypothalmus
* VIP receptors (GPCR) found in CNV, liver, lung, intestine, T-lymphocyte, heart, adipose tissue, kidney, skeletal muscle, testis, stomach
* Responsible for circadian rhythm
* Increases intestinal motility, pancreatic secretion, biliary secretion (this may be one of the reasons we see reduced biliary secretion ejection fractions in the gall bladder in almost every patient), stomach pepsin secretion, inhibits stomach Hcl, increases chronotropism and inotropism in the heart (Rx chronic heart failure?)
* Potent pulmonary vasodilator (Rx PAH - FDA approved for that)

If you dilate the pulmonovascular bed, you promote forward flow and stop flow reversal, which is what we think the primary mechanism is. Certainly that explains why it does it so quickly.

This is Dr. Shoemaker’s paper, which is going to be an important one. He just published it this week actually, using nasal VIP on 20 patients who had what he calls Chronic Inflammatory Response Syndrome related to Water Damaged Buildings, because he’s a mold expert.

By the way, there is no clinical difference between CIRS due to water damaged buildings and Chronic Fatigue Syndrome. We trade patients. I get his patients that he can’t seem to fix with mold, and he gets my patients that I can’t seem to fix because maybe they have mold. So we keep trading patients, and we can’t tell the difference between them.

This 18 month therapy with nasal VIP corrected numerous inflammatory biomarkers (C4a, TGF-beta 1, VEGF, MMP9); corrected numerous hormones (estrogen-M, testosterone-M, D3); reduced pulmonary artery systolic pressure; increased T-reg cell levels (CD4+ CD25+’s), which means it tends to reduce some of the pro-inflammatory effects of the disease; and enhanced quality of life in 100% of cases.

No doubt: if you can reverse flow reversal into the brain and the liver, you will get better.

This is what we think the mechanism is.  Due to the low cardiac output, we see a big right ventricular squeeze. If you squeeze really really hard, this little tricuspid valve held by very weak capillary muscles will give way. And when it gives way, a jet of blood from this squeezing right ventricle will shoot into the right atrium or shoot right up into the superior vena cava. And if the return is low, you will see flow reversal.

In the case of the inferior vena cava, you see blood moving down into the liver and cause flow reversal with every beat.

We have observed a respiratory component so that when they inhale, you get a greater return and you don’t see the flow reversal stop, because there’s not blood coming back in to be reversed. On the exhalation, there’s a much lower return, and that’s when you see the red flash.

Requirements for Reflux:
1.  Low cardiac output to produce low venous return.
2. Excess RV ejection fraction percentage to produce high TR
3. All caused by diastolic dysfunction.

All diastolic dysfunction is caused by energy impairment, caused by redox impairment. And we do not know what causes redox impairment."

Paul Cheney lecture - March 22, 2013

Here is the first part of a Paul Cheney lecture given in North Carolina on March 22, 2013. It is entitled "Compassionate Use Treatment of Chronic Fatigue Syndrome using both chemical and probiotic (MAF 314) forms of GcMAF".

The lecture was given at the Forsyth Center Maya Angelou Center for Women's Heatlth and Wellness in Winston Salem, NC. It was sponsored by the Winston Salem Chronic Fatigue Syndrome, Fibromyalgia and Lyme disease support group.

The lecture was free to the public.

Teresa Simmons provides this title of one of the lectures: "Chronic Fatigue Syndrome as a cellular energy disorder related to poor redox buffering followed by progressive complications arising from a low cardiac energy system related to energy-linked cardiac diastolic dysfunction". The title itself gives a clue of what the viewer will engage in these videos.

Dr. Cheney has evolving and innovative treatments and this lecture will present his latest ideas. Thanks to Teresa Simmons for this video presentation of this important lecture.

Dr. Cheney gives public presentations every few years, encapsulating his unique treatment ideas and protocols. His lectures are long, usually three hours, and complex. They invite repeated viewing as they encompass so much information and presented in his inimitable manner.

Great progress is being made in the availability of research and treatment ideas in these complicated illnesses. I saw the 2009 lecture of Dr. Cheney in VA, which was only available to the wider audience on a DVD at a significant cost. Times are changing and now others worldwide have access to Dr. Cheney's latest thinking. Maybe other clinicians will view this and connect the dots - adding in and  testing out some of Dr. Cheney's ideas. And maybe some ideas will flow the other way, from the outside into Dr. Cheney's brain, made possible by the information disseminated in this lecture video.

The second and third part are here.

Sunday, April 21, 2013

Mycotoxins and Mold

Mycotoxins and mold have been on my mind for a number of years now. They routinely fall into line with a host of variables: gut ecology, hormone regulation, diet, resting and pacing, viruses, bacteria, mycoplasma, Lyme disease, mitochondrial and methylation deficiencies, sleep abnormalities and mercury. It is a vast juggling act. I have written elsewhere about my experience trying to remediate the mold in my daughter's former apartment. I am interested in the idea of mycotoxins as a confounder to recovery in ME/CFS.

Yesterday I watched once again Dr. Ritchie Shoemaker's astonishing 15 minute lecture at the IAMECFS conference in 2009. I remember thinking how important this information was when he presented - but no one seemed to notice, and his profound insights were just buried under a pile of mediocre presentations. This lecture unfortunately is not online. Eric Johnson has the written lecture on his website.

Yesterday I also read a long review article on Water Damaged Buildings, Mold and Mycotoxins. It is by Janette Hope and can be read here. This article clarifies and consolidates known information on mold, mycotoxins, various bacteria and endotoxins, deals with the mechanism of illness, outlines symptoms, neurological and otherwise, and suggests treatments.

Among the treatments are FIR sauna and Cholestryramine. I was particularly interested to read about "Probiotics and Dietary Interventions" - "These treatments have the potential to have significant beneficial effects, as much of the metabolism of toxins occurs via intestinal biotransformation". So here we have a potential cross-over of gut ecology treatment and mycotoxin remediation. Maybe these same ME/CFS patients in Dr. Brewer's study have a functional imbalance in their gut biome. I think it would be worth finding out.

Lisa Petrison has written to Dr. Joseph Brewer regarding his experience with mycotoxins and mold. Dr. Brewer's answer follows:


Although I am an infectious disease specialist, I had no focus whatsoever on "mold issues". Prior to February 2012 (when I first heard about the urine mycotoxin assay at RealTime Laboratories) I didn't even have an interest in mycotoxins or environmental illness. These findings surprised me as much as anyone as the results began to unfold last year.

These patients were all randomly tested. These are long standing patients of mine that were previously diagnosed with CFS/ME (basically"average CFS patients"). We discussed the test and offered it to them at routine follow-up clinic visits. Very few suspected mold illness until I brought it up at their routine visits.

We only found that they "lived/worked in buildings with visible mold" after we asked. Some patients didn't even remember the exposure until we prodded a bit (mainly because the exposure had been so far in the past - such as an apartment they lived in college).

I now see patients every week that are shocked when I bring up mold. They have very impressive exposure histories but no one asked.

If these CFS patients who are on the blogs get tested, I suspect ~90% will be positive. A doctor from the East coast has found almost identical results to mine in their cases (90% positive). Same for a physician on the West coast.

Anyone who sends a specimen to RealTime Lab must pay for the test "up front" but many of the patients ended up getting reimbursed (at least for most of the testing cost) from the insurance. They were not biased since most were hoping to get reimbursed.

I think it is hard for people to get their "arms around this" and want to implicate selection bias but that simply was not the case.

I hope this helps.

Joe Brewer, MD

Thursday, April 11, 2013

Dr. Joseph Brewer and Mycotoxins

A study was released today entitled the "Detection of Mycotoxins in Patients with Chronic Fatigue Syndrome".

Abstract: Over the past 20 years, exposure to mycotoxin producing mold has been recognized as a significant health risk. Scientific literature has demonstrated mycotoxins as possible causes of human disease in water-damaged buildings (WDB). This study was conducted to determine if selected mycotoxins could be identified in human urine from patients suffering from chronic fatigue syndrome (CFS). Patients (n = 112) with a prior diagnosis of CFS were evaluated for mold exposure and the presence of mycotoxins in their urine. Urine was tested for aflatoxins (AT), ochratoxin A (OTA) and macrocyclic trichothecenes (MT) using Enzyme Linked Immunosorbent Assays (ELISA). Urine specimens from 104 of 112 patients (93%) were positive for at least one mycotoxin (one in the equivocal range). Almost 30% of the cases had more than one mycotoxin present. OTA was the most prevalent mycotoxin detected (83%) with MT as the next most common (44%). Exposure histories indicated current and/or past exposure to WDB in over 90% of cases. Environmental testing was performed in the WDB from a subset of these patients. This testing revealed the presence of potentially mycotoxin producing mold species and mycotoxins in the environment of the WDB. Prior testing in a healthy control population with no history of exposure to a WDB or moldy environment (n = 55) by the same laboratory, utilizing the same methods, revealed no positive cases at the limits of detection.
Keywords: mycotoxin; mold exposure; chronic fatigue syndrome; Stachybotrys

The full study can be found here. This is important work.

Mycotoxins are one of those unheralded co-factors in ME/CFS -along with mercury, mold, and other environmental factors. Mycotoxins can be added to the list of "the usual suspects" that need to be considered, and treated - gut ecology, mitochondrial defects, diet, hormonal irregularities, viral activations, bacterial complications, mycoplasmas and so forth. It is a long list. Mycotoxins might be an important confounding factor in this illness.

Dr. Joseph Brewer has worked on this study. Dr. Brewer is one of the foremost clinicians/researchers in ME/CFS and Lyme disease.  Dr. Brewer is an Infectious Disease doctor who practices in Kansas City, MO. Dr. Brewer has worked with both HIV and CFS patients for 25 years. He has also treated many Lyme patients. In my estimation Dr. Brewer is among the very best physicians dealing with this illness. Dr. Brewer has shown interest in identifying causes of or confounders associated with the immune dysfunction in ME/CFS. After his full day of treating patients, Dr. Brewer reads ME/CFS research late into the night.

In this study Dr. Brewer has teamed up with Dr. Dennis Hooper of Realtime labs. Dr. Hooper gave a talk at the recent Physicians Roundtable in Tampa, FL. Dr. Hooper has developed an important mycotoxin test that was used in this study. The test is a urine test and looks for three mycotoxins: aflatoxins, ochratoxin A, and macrocyclic trichothecenes. More about mycotoxins and Realtime labs mycotoxin testing can be found here.

My daughter has done this test twice. The first time she came back with elevated Ochratoxin A. As far as I can determine Ochratoxin A is associated with water damaged buildings. Several ERMI tests indicated mold associated with water. It appears that my daughter's apartment was in a building built on a stream bed. While there was no visible water damage or mold, I could never remediate the building and get a reasonable ERMI test result. I write about this experience here.

Eventually I helped my daughter move (for non-mold related reasons) to another apartment. I was expecting that a repeat Mycotoxin test would reveal that the Ochratoxin A had disappeared. This turned out not to be true as the Ochratoxin A was still elevated. (I have no idea about the relativity of this elevation). The suspicion has to be that she was moved into another water damaged building.

Treatment of mycotoxins is: Avoidance, FIR sauna, and cholestryamine. I would imagine that other detox regimes might be helpful.

This study highlights once again the complexity of ME/CFS and gives us a good chance to look in this direction to see if there are problems (confounders) that can be remedied.

Saturday, April 6, 2013

Dr. Derek Enlander, NYC

Dr. Derek Enlander has treated ME/CFS patients in New York City for many years. He is a terrific hands-on clinician, who is highly respected and beloved by many of his patients. Dr. Enlander is known for his empathy, and for a willingness to try different treatments on this illness.

Today we are fortunate to be able to read an interview with Dr. Enlander on Phoenix Rising, an interview which gives the reader a good look into Dr. Enlander's treatment and research concerns. The interview, conducted by an editor named Joel, does a thorough job of asking the right questions of this sympathetic and gifted physician. Phoenix Rising has profiled various clinicians or clinician/researchers in the past, but never, to my knowledge, have they interviewed or profiled Dr. Enlander. This interview is especially welcome and perhaps reflects a change in direction.

As a ME/CFS physician, Dr. Enlander is unique.  He is one of a few ME/CFS physicians in America, perhaps the only one, who is associated with a major medical school and hospital - Mt. Sinai in NYC. (The only other such case of which I am aware was Dr. Philip Peterson's clinical and research center at Hennepin County Hospital in Minneapolis years ago). About a year ago, Dr. Enlander formed the Mt. Sinai ME/CFS Center, which fuses the work of various researchers - Eric Schadt, Miriam Merad and Ila Singh. This Center was funded by a generous gift of a patient of Dr. Enlander's, a patient who, I believe, wants to remain anonymous. This generous gift could not have been better placed, and upcoming, tangible results will encourage further gifts, both from this donor and others. The ME/CFS Center at Mt. Sinai is currently conducting a Post Exertional Malaise trial, due to be completed this year. The ME/CFS Center at Mt. Sinai has made it clear that they are interested in collaborating with other institutions in the pursuit of concrete research into this illness.

Dr. Enlander's belief in the seriousness of this illness and its devastation on patients is grounded in an understanding of Dr. Melvyn Ramsey's definition of ME, formulated so many years ago. Being of Irish descent, Dr. Enlander has embraced patients and advocates in Ireland and the UK. He has worked with conferences and patients in Ireland and the UK, trying to extend his treatment and research ideas and to help a thoroughly abandoned patient population.

The Chronic Fatigue Initiative (CFI) is currently conducting important work into the role of pathogens in Neuroimmune illnesses. Five patient cohorts from selected physicians in America are supplying the samples. An article by Cort Johnson, highlighting the positive activity of one of the CFI collaborators, Simmaron Research, can be found here.

Interestingly enough, however,  Dr Enlander was not among those clinicians selected for the Lipkin CFI study. This seems "an unfortunate oversight" as Dr. Enlander has ME patients from all over the world - and his office is a few miles from Dr. Ian Lipkin's Columbia lab. Not utilizing Dr. Enlander's clinical experience and not using the assets that he has assembled at Mt. Sinai seems like "a bit of a mistake".

Meanwhile, we have this interview to consider, and we applaud the efforts of this fine physician.