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.

VIP:
* 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."

7 comments:

  1. When the syndrome of CFS was created in 1988, we did not think of our illness as being identical to the Gidget Faubion/chronic mono - Dubois- Straus- Jones "CEBV Syndrome" phenomenon that took place in the early 1980's.

    The CDC argued with Cheney and Petersons suspicions that the mystery illness might be a variant, because the Tahoe phenomenon was so obviously not CEBV Syndrome.

    The incubation period of EBV made it impossible to have a huge outbreak of illness.

    When Dr Komaroff came to Tahoe after seeing a similar sporadic illness in Boston, he thought there must be some difference because he wasn't seeing clusters.
    Stephen Straus, James Jones, Irena Brus all said the same thing. Epidemic style outbreaks were not associated with the CEBV Syndrome.

    The CDC said our outbreak was more like the Royal Free disease outbreak of 1955.

    By insisting that the Tahoe outbreak is the same as all the others, this obviates any reason to find out if there was anything that made this one different.

    If there had been no differences, we would be known as the 1985 Tahoe CEBV Syndrome outbreak.

    ReplyDelete
  2. Thank you for posting the Cheney videos and notes on them. I found them very, very helpful.

    I posted a summary of Cheney's thoughts on thyroid on my blog, with reference and link to your blog. I hope you don't mind.

    ReplyDelete
  3. http://www.scilogs.com/in_scientio_veritas/cfs-leptin/

    Glimpse of an elusive diagnostic biomarker for Chronic Fatigue Syndrome
    23 April 2013 by Kausik Datta, posted in Inflammation, Research Blogging, Science, Science Communication, Science Education, Scientific Research




    http://www.meactionuk.org.uk/Quotable_Quotes_Updated.pdf
    1989
    "The crucial differentiation between ME and other forms of postiviral fatigue syndrome lies in the striking variability of the symptoms not only in the couirse of a day but often within the hour. This variability of the intensity of the symptoms is not found in post viral fatigue states"
    (Dr Melvin Ramsay, President UK ME Association. ME Association Newsletter, Winter 1989 20-21)
    ---------------------------------------------


    Mold Warriors
    by Dr Ritchie Shoemaker


    Chapt. 10
    Saratoga Springs. NY, Birthplace of the American Mold Revolution
    page 201

    How quickly does leptin, MMP9 and VCS change with -re-exposure and re-aquisition of illness?
    It was one thing to be able to show what the mold illness had as markers, but truly understanding
    the physiology of the illness meant seeing changes in both hyperacute and chronic illness, as well
    as hyperacute changes with "new" illness. The changes from normal suggested by the Biotoxin
    pathway were present in spades in mold illness.



    During the Incline epidemic, I saw this same pattern of severity corresponding to certain months of the year, just as Acheson did.
    I also noted my own condition was seriously exacerbated by
    "cold and damp weather".

    I knew that neither cold or damp, per se had any effect on me,
    so I asked myself what was it that cold and damp might


    increase during those winter months?
    What would "release" when the weather changes?

    The answer seemed obvious. It could only be mould.

    I told Dr Cheney and Dr Peterson that until they find out what the "Weird flu" was, that I am just going to work
    on staying away from the mould. (although we spell it differently in the U.S of A.)

    http://www.meresearch.org.uk/information/keypubs/Acheson_AmJMed.pdf

    The Clinical Syndrome Variously Called Benign Myalgic Encephalomyelitis,
    Iceland Disease and Epidemic Neuromyasthenia
    E.D. Acheson, D.M., M.R.C.P.
    Department of Medicine, State University of New York, College of Medicine of New York, and
    Department of Medical Services, Maimonides Hospital, Brooklyn, New York

    >
    Cold damp weather
    frequently increased pain and a sense of
    illbeing in patients in whom a definite
    recrudescence was not precipitated.
    ------------------------------------------------

    “Disease is very old and nothing about it has changed. It is we who change as we learn to recognise what was formerly imperceptible.” J.M. Charcot

    ReplyDelete
  4. As to why Dr Cheney and all CFS researchers had no interest in the actual evidence that started the "Chronic Fatigue Syndrome"....
    I have no explanation.

    --------------------------------

    Dr Shoemaker is "The Last Semmelweis", the ONLY RESEARCHER in the entire world who responded to the evidence at Ground Zero for CFS as a Semmelweis would.
    There were no others.

    http://survivingmold.createsend1.com/t/ViewEmail/r/5E3AF582A3B80E4C/F2F08E63E1D25E36F99AA49ED5AF8B9E

    ReplyDelete
  5. Given the nearly universal desire of CFS researchers and CFS patients to suppress the evidence that started this syndrome, it seems reasonable that doctors and the CDC/NIH/FDA should ignore it, as well.

    I can't imagine why such a vast majority of patients think it is to their benefit to disregard the CFS history and demolish clues.

    I have never understood it.

    ReplyDelete
  6. I never cease to be stunned and amazed by the absolute refusal of the CFS community to take an interest in the phenomenon.

    We just handed you an incredible chunk of information, and receive total unresponsiveness in return. Apparently with the intent to see that it slips away into abysmal oblivion.


    The CFS community can never pretend to be searching for real answers, after proving beyond a shadow of doubt that all they really want...

    is to destroy them.

    ReplyDelete
  7. Of course, there is no such thing as a "CFS community"

    Just a rabble of people with a mob-mentality who have wildly diverse "opinions" upon something they call CFS, of which there is absolutely zero agreement.

    Zero collaboration.
    Zero cooperation.

    I can prove it.
    Ask a "CFS group", "Is CFS a syndrome that was coined in 1988?" and not a single "Yes" will result.

    Only protesations of "That doesn't matter"
    "CFS has moved on since then" "CFS was redefined in 1994" "CFS is just a label"

    "CFS is a psychological illness invented by psychiatrists" (and never mind the exclusion of "psychiatric disease" in the Holmes definition.)

    "CFS is different things to different people"

    "CFS IS JUST FATIGUE"

    The one and only thing they ALL agree on is that "CFS" has nothing to do with the original evidence or illness that brought the syndrome into existence.

    Don't bother to blame the CDC.
    They didn't demolish and trivialize the syndrome into total oblivion.

    The "CFS dis-unity" did.

    ReplyDelete