Re: Jelly - hep, complement

[Guest guest]

Thanks for the compliment. Whenever I can I stash research over

there. You or anyone else is welcome to put stuff there too. Kind of

like Ken's site, only we can all contribute. It is a little like

going to a library, when you want a particular article it is easy

for everyone to find.

This is the first time I have heard of factor H. When I think of the

coagulation system, I call it the coagulation cascade. One thing

affects another and then another, is that what you are talking

about? I'm not sure I understand Factor H yet, but in a real simple

term, does it punch a hole in the bacterial membrane thus causing

it's death? Is the cell wall the same as the cell membrane?

If they are, I thought Borrellia was Cell Wall Deficient. I am just

now trying to understand Lyme so I could be way off base.

> > Dumb question, is the factor H they talk about, heparin? I read

some

> > stuff about heparin binding to Lyme and inhibiting it. I also

just

> > found a recent study out of Japan on heparin totally clearing

> > Babesia. It's on my website in the Lyme section, along with tons

of

> > stuff about heparin and hypercoagulation. There is a whole topci

> > forum on hypercoagualtion. The address is in the links section

to

> > the left, thanks to Penny.

> >

[Guest guest]

> This is the first time I have heard of factor H. When I think of the

> coagulation system, I call it the coagulation cascade. One thing

> affects another and then another, is that what you are talking

> about?

Yes, exactly. The last componants of the cascade form or complete the

Membrane Attack Complex (MAC).

> I'm not sure I understand Factor H yet, but in a real simple

> term, does it punch a hole in the bacterial membrane thus causing

> it's death? Is the cell wall the same as the cell membrane?

No, rather the opposite, fH stops the whole complement fixation

process, and borrelia binds it to keep the MAC from forming.

The plasma membrane, cell wall, and outer membrane (present in

spirochetes and gram-negatives only) are all separate parts of the

cell envelope, which is the boundary region of the cell. Good question

regarding MAC, I dont know whether it penetrates the outer membrane

only, or the entire envelope including the wall. I think i read about

this but I forget.

> If they are, I thought Borrellia was Cell Wall Deficient. I am just

> now trying to understand Lyme so I could be way off base.

Yes, what Bowen is finding in the blood, using a technique whose

sensitivity and specificity I feel are pretty compelling (I just wish

they would/could(?) publish on it!), is almost all L-forms. Many cell

wall deficient forms of bacteria in general actually do have a thin

cell wall. However they are still resistant to normal doses of

penicillins (and sometimes to immense doses too, but not always).

Presumably this is because they place little to no reliance on the

cell walls integrity, unlike classical forms.

>

> > > Dumb question, is the factor H they talk about, heparin? I read

> some

> > > stuff about heparin binding to Lyme and inhibiting it. I also

> just

> > > found a recent study out of Japan on heparin totally clearing

> > > Babesia. It's on my website in the Lyme section, along with tons

> of

> > > stuff about heparin and hypercoagulation. There is a whole topci

> > > forum on hypercoagualtion. The address is in the links section

> to

> > > the left, thanks to Penny.

> > >

[Guest guest]

My understanding of CWDs is based entirely on my understanding of

Mycoplasma. I have been under the impression that most ABX have no

affect on Mycos because the survive inside of normal cells. Here ABX

can not reach them.

Because Mycos have no cell wall they are also not subject to ABX. I

thought in a very simple way, ABX break down the cell wall of a

typical bacteria thus causing their death. I thought the way

tetracyclines worked on Mycos was totally different. Tetracyclines

some how prevent Mycoplasma from re-entering new cells where they

will be safe from the immune system. Once locked outside they are

then an easy target for our immune system, which I believe works

just fine, IF you are talking about CWDs. I did not think these

particular ABX had any actual affect on the Myco iteslf.

Can anyone clarify this for me or fill in any missing gaps I

have.

> > > > Dumb question, is the factor H they talk about, heparin? I

read

> > some

> > > > stuff about heparin binding to Lyme and inhibiting it. I

also

> > just

> > > > found a recent study out of Japan on heparin totally

clearing

> > > > Babesia. It's on my website in the Lyme section, along with

tons

> > of

> > > > stuff about heparin and hypercoagulation. There is a whole

topci

> > > > forum on hypercoagualtion. The address is in the links

section

> > to

> > > > the left, thanks to Penny.

> > > >

[Guest guest]

Please remember, CWD, means cell wall DEFECIENT. Not that there's NO

cell wall whatsoever.

It's also my understanding that many bacteria go through various

phases. Just because it's cwd today, doesn't mean it was yesterday or

will still be tomorrow.

penny

> Because Mycos have no cell wall they are also not subject to ABX.

[Guest guest]

Penny

What Per said is true about other bacterias and fungi being capable of

mutating into a cell wall deficinet organism. A true CWD or L-form is

just that way, it didn't mutuate to get the title of CWD. When talking

about " these " forms cell wall deficient means they have NO cell wall

compared to regular bacterias. Now, has just found some research

indicating that some of these might have some minor form of a

membrane. Mycoplamsas aren't even really considered a bacteria. You

can't compare an apple and a banana.

>

> > Because Mycos have no cell wall they are also not subject to ABX.

[Guest guest]

And I'd say you're going to have to prove it to me. Mycoplasma's

still a pretty controversial field.

:-)

penny

> >

> > > Because Mycos have no cell wall they are also not subject to

ABX.

[Guest guest]

Penny,

There is tons of data on mycoplasma. If you don't believe in

Mycoplasma then I don't uderstand why you believe in Lyme. They are

very similar, and very hard to find. There are only 2 labs at the

most considered dependable when it comes to Lyme testing. There are

more then that that can test for Mycoplasma's dependably. If you

don't like the PCR/DNA test for Mycoplasma, there is also Mycoplasma

antibodies tests. The only question of Mycoplasma existing exists

amongst tradtional medicine. You know how I feel about them, since

they offered NOTHING in order to get me well. My husband just came

back positive with elevated Mycoplasma antibodies. I could keep you

reading for weeks with Mycoplasma data. I've said it several times

and I'll say it again, I'm well, targeting Mycoplasma. Believe they

exist or not. There is a posibility that they are not a problem for

you.

> > >

> > > > Because Mycos have no cell wall they are also not subject to

> ABX.

[Guest guest]

I didn't say I don't believe in mycoplasma.

But, I defintely would argue that people do not yet understand all

there is to know about mycoplasma, and they definitely don't know

how to treat it. You don't know for sure that you're well because

you killed mycoplasma directly. It may have been killed indirectly

as other infections were cleared. There's no way to tell, because

the testing isn't there. Just because you test positive on a PCR or

antibody test doesn't mean Mycoplasma's even the cause of your

illness. It might be, but there's no proof yet.

People used to think that CFS was caused by EBV (some people still

do). Just because we test positive, doesn't mean it's what's making

us sick. It could be a by product, a co-infection, or it could be

the whole shebang. No proof yet of anything.

The good news is you're better, and we can learn from that, but we

can't necessarily draw conclusions.

penny

> > > >

> > > > > Because Mycos have no cell wall they are also not subject

to

> > ABX.

[Guest guest]

Minocycline and doxy have excellent lipid solubility, ie. they

penetrate lipid membrane or correct me if i'm wrong, bio-film, also

have excellent tissue penetration/tissue uptake. Yes, with cwd, tets

have the ability to penetrate our cells, where the cwd usually are,

and stop protein synthesis, necessary for replication. Once

replication is eventually stopped, the immune system will eventually

recognize the cwd as an invader and kill them. It takes a long time.

One good thing about clarithromycin is that once synthesis is

stopped, it is irreversible, however, penetration is less than that

of the tets.

> > > > > Dumb question, is the factor H they talk about, heparin? I

> read

> > > some

> > > > > stuff about heparin binding to Lyme and inhibiting it. I

> also

> > > just

> > > > > found a recent study out of Japan on heparin totally

> clearing

> > > > > Babesia. It's on my website in the Lyme section, along

with

> tons

> > > of

> > > > > stuff about heparin and hypercoagulation. There is a whole

> topci

> > > > > forum on hypercoagualtion. The address is in the links

> section

> > > to

> > > > > the left, thanks to Penny.

> > > > >