chronic illness/FMS

[Guest guest]

According to Medline research and Dr. Cheney, FM sufferers are not only low

on HGH but are also low on glutathione that is increased with the Immunocal.

Either of these therapies can work, but they work better together.

How it will benefit us is that this is a therapy we can do it AT HOME for

the most part, using an amino acid stack like SomaLife gHP, with only

occasional or rare trips to the doctor for monitoring purposes. This

benefits people who can afford about $100-$200 a month, while previously the

HGH therapy component alone cost upwards of $1200 a month, exclusive of the

doctor's lab work and appointments.

Both of these therapies can be had from one website for about $30 less than

the second lowest price on the web,

http://members.shaw.ca/widewest/HMS-90.html and I understand from postings

to the group oxyplus that US buyers of HMS-90 (Immunocal) who use the

" Canada " button to purchase get it for less than distributor cost in the

USA.

________________________________________________

Audio tape #2

Cheney, M.D.

Feb. 5-7, 1999. Afternoon workshop and case studies, with slides.

This session is on the clinical management of Chronic Fatigue Syndrome.

And I'll go through a series of slides that I think outline a number of

key issues and their management, and then go through a treatment paradigm

[pyramid actually, I think] that I developed over many years to treat

these patients. Then maybe we'll open up to questions.

One of the things that I think is important to know about these people is

that they're complicated in the beginning, but I think they become ever

more complicated at time goes on. I'm constantly amazed at how complicated

the disease is, especially as the years roll by. We'll discuss some of the

reasons why. I think they are, interestingly, most approachable from a

therapeutic standpoint in the early stages of the illness. But as things

go along, they can be more and more difficult. I think there's an end

stage to this disease that may not be well treated no matter what you do,

and we'll talk a little about what makes those people so treatment

resistant.

I'm going to begin by sort of coupling to the talk this morning about this

glutathione defect. I believe this glutathione deficiency is the key

problem particularly over time, and makes the patients very difficult to

manage from a detoxification standpoint. Because every time you try to

intervene and detoxify when they have this underlying defect, you actually

make them quite ill. You can actually put them in the hospital attempting

what appears to be a good detox program that works in a lot of people, but

will not work in this subset of very sick and treatment-resistant people,

which is mostly what I see.

Another little caveat to note is that I don't know if what I'm going to be

saying will generalize to all chronic fatigue syndrome. It seems like I

have a larger collection of sicker, more treatment-resistant patients.

That's kind of what I see. So when people say, " Well I did this-and-so and

that-and-so and it worked on everybody and they were well, " I never see

that. Maybe we're not looking at the same group of people. I think there

are milder forms of this disease that may very well respond to all kinds

of treatment forms.

The glutathione resistance or glutathione deficiency was first noted when

we began measuring whole blood glutathione levels and began to see these

low to low normal glutathione levels. We were also looking at functional

markers of glutathione, such as lipid peroxides. Both blood lipid

peroxides and urinary lipid peroxides, which is an endpoint functional

indicator of glutathione functionality. We're also seeing other functional

indicators of glutathione problems such as citrate elevation and alpha

ketogluterate (sp?) depression on organic acid analysis.

What was curious to me was that in many ways we were able to make progress

on just about everything that we cared to clinically measure as we applied

our therapeutic regimes--we saw a lot of people getting better--we saw a

lot of things getting better, except this glutathione. It seemed to be

extremely resistant to therapy. It was as if something was hanging on and

preventing our ability to change this system. I don't know, and I still

don't know to this day, why that is. But whatever is doing this, is a key

to this illness, I think.

This is just a slide of the degree and the reality of this glutathione

defect. Seen in red on the left, relative to control groups in blue, they

sit right at the margins of normal (although you see some that are

extremely low). They sit right at the bottom edge of normality. In

addition to this, to indicate that yes this is not only a low glutathione

functionally important, is the evidence of urinary lipid peroxides, shown

on the right, their urinary lipid peroxides are high, almost double that

of the normal population.

In addition to this, we saw extremely low serum Vitamin E levels. If you

had a glutathione defect, you might expect to see defects in holding

vitamin E in its reduced state as it's typically cycled with glutathione

between its reduced and oxidized states. And, indeed, vitamin E is very

low and it's very treatment-resistant. You can get lots of vitamin E and

not have much of an impact which I think again is an aspect of this

glutathione deficiency. If you can't recycle vitamin E, whatever you're

getting, just gets oxidized. You may also have problems with oxidizing

vitamin E in the GI tract.

We also noted some generally low red cell selenium values. But they're

even lower in white cells, specifically lymphocytes, which I think is

interesting in itself. The point being that this selenium defect may

actually be compartmentalized. That is, in some areas of the body the

selenium level might be OK, but it other areas of the body it might be

specifically depleted. I think it's extremely depleted in the white cell.

Of course, if you deplete selenium you're going to cream the glutathione

functional system. We also got interested in this low selenium from the

standpoint of the emergence in HIV disease or the discovery of a gene.

It's a glutathione-peroxidase encoding gene present in HIV which upon

rapid cycling consumes large amounts of selenium within the cell where HIV

resides. This selenium consumption effect can essentially wipe out

glutathione synthesis and then produce apoptotic cell death. So the

hypothesis is that perhaps the mechanism of CD4 depletion in HIV infection

may be involved in this selective selenium depletion of cells in which

HIV sits, and knocking out glutathione is producing apoptotic cell death.

So the fact that we were seeing selenium depletion in lymphocytes which

exceeded the selenium depletion in red cells and by other measures

suggested there might be some compartmentalized issue involving this

glutathione defect which is going to be even more problematic from a

treatment standpoint. Because what if the glutathione levels or the

selenium levels are OK in some parts of the body and then really depleted

in other parts of the body? That makes it very difficult to treat because

if you treat for the selenium defect, you might over-treat in one part of

the body just to restore another part. And it doesn't even get at the

dynamic issues involved. So we thought we were getting closer to the

problem or at least why the problem was so treatment-resistant.

To me, this is a most extraordinary paper, published by Falci, an

expert and head of NIAID and our leader in the HIV world at NIH. But he's

also a glutathione expert. And he showed in this paper, published in PNS

in 1991, that glutathione is an impressive anti-viral weapon. Under cell

conditions designed to produce log order growth in HIV, simply by raising

glutathione levels to 15 millisomething (word?), you can wipe out that

exponential growth, which is the white line, down to the yellow line,

which is the flat line. You can flat-line HIV growth simply by raising

glutathione in-vitro in the cell culture. Now 15 millisomething (word?) is

only three times physiologic. If you raise the physiologic doses, which is

5 millisomething word?), you get an intermediate line--a suppression of

HIV, but not a wipeout. By the way, this also applies to other

cytokine-induced augmention of HIV in cell cultures, such as TNF alpha and

IL-6 when injected into cell cultures also augment HIV growth, not as

well as somethingesters (?) do, but quite nicely. Again 15 ml (?)

glutathione wipes out the cytokine effect.

These two issues I thought were very important to me because it meant that

chemicals or toxins such as fourbellesters (sp?) can induce endogenous

micro-organism replication rate, especially in the presence of glutathione

deficiency. And immune-activation states can also induce the activation of

endogenous microbes in the presence of glutathione deficiency. And that

might explain why in this, quote, immune-activation state that we call

Chronic Fatigue Syndrome you see a lot of endogenous viral activation such

as EBV, CMV, HHV6, mycoplasma incognitus, chlamydia pneumonia, candida,

and on and on and on. You see the activation of this microbial ecology,

and why is this happening? It could be that it happens because cytokines

in excess stimulate these organisms, especially in the presence of

glutathione deficiency. The converse is true, however. In the presence of

good glutathione levels, it's very difficult for that to happen.

This is a diagram of what might be going on in the initial stages of this

disease, Chronic Fatigue Syndrome. Namely, some virus gets into that

person, or activates, which has one of these glutathione-peroxidase

encoding genes, producing rapid cycling production of seleno (?) proteins.

Those seleno proteins don't do much functionally, but they consume vast

quantities of selenium, anywhere from two to 16 selenium atoms per seleno

protein. Upon selenium depletion, you wipe out glutathione synthesis and

functionality, resulting in rapid viral replication, redox (?) shift

causing energy drops and detoxification failure at the cell level.

If glutathione deficiency drops low enough and redox shift rises high

enough, this cell simply dies, an apoptotic death.

[inaudible question.] I don't know. I don't know what the factors are that

govern this. It's just an important idea. If this is going on, you might

expect to see specific compartmentalized selenium deficiency in the cells

in which viruses like this sit. Now the cells that propose to cause

chronic fatigue syndrome, typically sit in the lymphocyte fraction, such

as EBV, HHV6 and so forth, and they would be expected to produce a greater

effect of selenium depletion in the white cells than other places.

Conclusions from all of this are: Glutathione has potent anti-viral

properties--if you raise the glutathione level you can stop the

replication of most any, at least, intracellular pathogen. chronic fatigue

syndrome patients are glutathione deficient. Glutathione deficiency itself

has a potent pro-viral effect. That is, not only does (high?) glutathione

levels tend to act as an anti-viral, but glutathione deficiency produces a

pro-viral effect. It can actually augment viral replication. Augment it

from the case of toxins, toxins could augment viral replication and also

cytokines themselves. So immune-activation states would itself augment

these things.

A seleno protein encoding gene would provide a significant survival

advantage to any microbial pathogen. What a great gene to have if you're a

virus. Because if you have this gene, you can't be killed. And some of the

most vicious viruses on the planet--the hemorrhagic fever virus, such as

ebola--ebola has this gene in spades. HIV has this gene in spades.

Hepatitis B and C have this gene. Other viruses are expected to have it.

HHV6, strain A, is thought to have it because it's a lytic virus. The most

interesting possibility is that this gene can be passed around from virus

to virus, especially by retroviruses. Retroviruses have the unique

capacity to insert pieces of themselves into the DNA of both human host

genomes and also into viral genomes. So HIV could actually be spawning new

and more virulent virions simply by stashing a gene like this in the next

piece of DNA it sees in which it co-habitates. And that's interesting

because HIV, HHV6 and mycoplasma incognitus all co-habitate and co-infect

exactly the same lymphocyte cell linings. Therefore, the opportunity for

transmission or sharing of this gene exists.

The reason I mention all of this to begin with is because I'm trying to

set the stage for how important it is to address this glutathione defect.

It could be THE major issue in this illness. Maybe not so much in the

beginning, but over time become the major issue. Because we're dealing

with a sub-group of people who have cellular detox failure and all that

that causes. Because if you have cell detox failure, you become a canary

to your environment. You are vulnerable to the lowest common denominator

of the toxin that you happen be be exposed to, or have. If you have

mercury in your mouth, you become mercury toxic when you get this

glutathione defect. Because a major defense, perhaps the major defense,

against mercury toxicity is in fact glutathione. If you have a toxic GI

tract--and everyone in this room has a toxic GI tract--portal circulations

are intrinsically toxic, they always have been and they always will be. If

you get a glutathione defect, then you become vulnerable to your own cell

toxicity, specifically the portal circulation.

Of course we can modulate that toxcicity by giving you a bad gut ecology,

wiping out your good flora, populate you with some bad flora and make

things even worse. But even under the best circumstances, this glutathione

defect would make it very difficult to achieve health simply by addressing

only gut ecology. Because even normal gut ecology is too toxic when you

have this problem. The point is that the glutathione defect is a central

issue in any detoxification program. You can't be looking at sources and

addressing those when you have detox failure. That's why a lot of CFIDS

patients don't do well under a lot of detoxification programs.

What we got interested in... we found out that when you give oral reduced

glutathione, it helps a little bit in some people, especially these

pressure toxic headaches they get. But when you keep raising the dose, it

actually gets sick again, and was never a very impressive response. When

we tried NAC we saw some evidence of toxcicity. In the use of NAC--I'm

concerned about high-dose NAC in this disease. I think it may be toxic.

We tried other methods to affect glutathione. Nothing seemed to be

working.

Then we got wind of this product called... it's basically undenatured whey

protein, lightly denatured to preserve the peptide action of this milk

protein. It's concentrated to about 90 percent protein and it's very, very

lightly denatured. In fact, the more lightly they denature it, the better

the action appears to be. And the more they denature it, the less active

it appears to be. In fact, if you denature it completely, down to its

constituent amino acids, it really doesn't work well at all.

People who normally have milk protein allergy seem to tolerate this, by

and large. Not 100 percent, but by and large.

This is the data from a six month study. There were eight people entered

into the study, seven of them completed the study. We got data on seven of

them. One dropped out at three months for a reason involved with the

design of the study. The first three months of the study we treated with

two packets a day, and then the second three months, half were randomized

to two packets a day and half were randomized to one packet a day. We

wanted to see if you could tell a difference clinically or by other means

between one packet a day versus two packets a day.

We did this because there was some indication that the more you treat with

this, the higher the dose, the better the effect. This is urinary lipid

peroxides combining both the two packs a day for six months, followed by

the two packs a day for three months and one pack a day for three months.

You can see there's a nice steady drop through six month in urine lipid

peroxides, which is an endpoint functional marker of glutathione. When you

segment out the two packs a day for six months group, they have a much

nicer drop. When you look at the group that goes from two packs a day to

one pack a day, you can see this nice dip where they started going back up

(in their urine lipid peroxides). Suggesting that one pack a day doesn't

work very well.

By the way, you can extend this--there are people, I've discovered since

the study was done, that do really well on three packs a day and not very

well at all on two. So clearly there is a dose response issue. Two packs a

day would probably be my recommended starting dose, but I wouldn't

hesitate to go up if if seemed like it wasn't working.

(Explains guy who dropped out of study.) The red line stops because this

is a guy who dropped out of study after three months because he had gotten

tremendous results from two packs a day. He was randomized to one pack a

day and he refused to do it, so he withdrew from study. He said, " I've got

something that helps me. Goodbye. "

There are 10 grams in a pack. [someone asks him what his source is.] I'll

talk with you later. This is a generic talk. I don't sell anything... I

don't mean to sell anything. [but we all know that Dr. Cheney was talking

about Immunocal, don't we?]

This is whole blood glutathione. This is interesting. When we looked at

whole blood glutathione, there was almost no change. There was a little

drop at month two, it was almost like the system got engaged. Glutathione

that wasn't being used was suddenly being used and the glutathione stores

actually dipped at the second month, and then they started to come up. You

can capture that at month three. And at month six it started to come up.

But overall not much change in the actual whole blood glutathione.

Suggesting to me that it isn't whole blood glutathione status that this is

affecting. It's affecting the whole glutathione system.

So what you're not seeing here... it's like you're looking at a whole sink

filled with glutathione and you're not seeing the dynamism, the

utilization of glutathione. As evidenced by dropping of the urine lipid

peroxides. Or yet, there's some other aspects of this product I don't

understand. But you can see that this group had borderline glutathione

levels. I have a feeling according to other reports that if they had

severely depleted [whole blood] glutathione levels, then you see rising

glutathione levels, if they're severely depleted. But in these marginal

cases, we just didn't see much.

[Question: What about 5 or 10 packets a day?] I'll get to that... it is an

interesting idea.

This is the exciting stuff. We wanted to see not only if this product

improved glutathione functionality, which it did, but we also wanted to

see if it knocked out micro-organisms, like the PNS article said it would.

So we measured for IgM (visa?) the inverse dilutions of IgM for chlamydia

pneumoniae. Chlamydia pneumoniae is an intracellular pathogen. It's a

common cause of hospital-acquired pneumonia. It ubiquitously infects the

population, but seems to activate under certain conditions. And if it

activates, some of the clinical conditions of this organism are chronic

sinusitis, pharyngitis, and laryngitis. But it also gets into the central

nervous system.

In a study published by a neurologist out of Vanderbilt showed that

chlyamdia pneumoniae may be a very important pathogen in multiple

sclerosis. Indeed, data they shared with me recently (and this is coming

to publication soon) showed that 80 percent of the cerebral spinal fluid

of MS patients is actively infected with this organism. Versus 15 percent

of other neurological diseases that are not MS. In a journal-published

article on neurology, aggressive treatment for chlyamdia pneumoniae

rapidly reversed an acute exacerbation of multiple sclerosis.

So we measured IgM levels for this pathogen at Vanderbilt. Most laboratory

measurements of this organism are not very good, so this is a research

grade assessment, and probably may not generalize to the run-of-the-mill

types of tests that you might get in your local labs. But IgM elevations

of 1 to 1600 (?) dilutions is evident of significant active infection with

this organism. Six months later, it just wiped it out. IgM just fell to

normal levels. It didn't really matter whether you were taking one pack a

day or two packs a day. Just wiped it out. Makes you wonder what this

might do for MS. Think about that.

We also looked at mycoplasma fermentans and mycoplasma penetrans. Both of

these pathogens have been linked to Gulf War Syndrome. They've been linked

to chronic fatigue syndrome. Again, they may be a relatively ubiquitous

mycoplasma species, intracellular, and can cause a variety of problems

when active. Again, by PCR done in Irvine, California. We were able to

show that this product also wiped out mycoplasma incognitus and penetrans.

Then we looked at HHV6. It was a little mixed here. We tested three

people.

By the way, this study was designed to do some microbial testing on

everybody, but not everything on everybody. The patients were allowed to

pick and choose depending on what we had in their chart before. We weren't

able to do everything on everybody because they were paying for this.

We did HHV6 rapid culture testing, which is a technique developed by a

company in Wisconsin. This particular culture technique uses an

intermediate (captures fiberglass?) cell line, so that you are positive

only if you are really infected, so it reduces false positives to zero.

That is, uner these conditions, all normal people are negative. You have

to do that because HHV, both A and B strains, are relatively ubiquitous.

Under these conditions, we had two positives and one negative at beginning

of study. The person on two packs a day went to zero culture (negative);

the person on one pack a day stayed positive. The person that was negative

stayed negative. Suggesting that maybe this isn't as good against viruses

as it is against bacteria, but at two packs a day it might be good against

viruses. Again, the numbers (of participants) are a bit small.

But to me, the satisfaction of this is tremendous because I'm always faced

in this disease population--well, are they sick from EBV? or are they sick

from HHV6? or are they sick from mycoplasma incognitus? or are they sick

from c pneumoniae? And the [traditional] treatment for mycoplasma and c

pneumoniae is 18 months of triple drug antibiotic therapy. And if we're

wrong on this issue, we've wiped out their gut flora and leave them a gut

ecology cripple for the rest of their lives. So now what we have is a nice

way to address almost any micro-organism that happens to be there. [using

Immunocal.] Just as the PNS article suggested.

[someone asks if there is a protocol to give people with HIV this product.

Cheney responds yes.]

Finally, how did the people feel? Their glutathione functionality

improved, though their glutathione levels were marginally improved, and

they had significant wipeout of micro-organisms. How did they feel? Five

out of six (seven?) felt significantly better. Three of those five thought

this was the best thing they had ever tried. They said it was tremendous.

In fact one dropped out of the study because he refused to stay on the

protocol at only one pack a day.

There were a couple of non-responders. But you'll notice that the two

packs a day were the best responders. There is a differential issue still

imbedded in this--namely the dose. The dose might need to be upped to see

maximum benefit in certain individual cases.