RE: Re: Minocycline, Jelly, 4 mg and minocycline

[Guest guest]

Um, yep. My mistake. Boy, I hate math.

a

a:

4mg/Kg of body weight is the theraputic dose for mino.

For a 25lb mokkey thats about 45 mg..

And for me at 128 lbs that translates to about 230mg

SO, I wouldn't consider that low dose.

Barb

[Guest guest]

Well, Barb correctly pointed out to me that

it really was a rather high dose for the monkeys. My comment on the other issue

actually comes from a pharmaceutical company researching the use of pulsed

antibiotics including minocycline. They found that there was an optimal level,

a rather low one, where bacteria indeed do come back out.

However, I went back this morning and read

some emails I had saved. TexLyme Mom made a big point of stating that folks who

did the low dose mino were setting themselves up for a rough time. That they

would do better to follow the Roadback approach which I THINK is 100 mg of mino

every other day, so that the herx would not be so unbearable.

Meanwhile, moving quickly adding low dose

Zithromax is important. You aren’t going to get rid of borrelia or other

infections on one antibiotic alone. I really don’t see any reason for you

to not forge ahead, higher dose of mino and then in a month or two add a second

antibiotic.

I wish you had a good doctor to help. I

have found that certain docs are doing a great job in spite of the issues of

arrogance. They know enough to fine tune treatment. It’s tough to go it

alone. I am in the same boat though. I don’t have a good doctor.

a

a Yes, yes, YES, this is the kind of thing that I

am looking

for and it is VERY current too!!!! THANK YOU!!! Is what I am saying

a possibility??? Maybe! You made my day.

You said " far from mutating, come back out to play, only to find

that the antibiotic is still there and still able to kill them. "

It is really that I am wondering if something so much more off the

beaten path is happening here, like the way you stated it above.

>

> This is a curious article for a couple of reasons. One is that HIV

is

> probably not the cause of sickness in AIDS but the facilitator.

Mycoplasma

> and other opportunistic bacteria are probably what really make the

patient

> die. Thus the reason why minocycline works.

>

> But what is really curious is that these little guys were given 4

mg/kg of

> minocycline. I know, I know, they were just little monkeys. If

they weighed

> about 25 lbs. that would be about 40 mg of minocycline a day - not

a very

> high dose.

>

> Another thing that has crossed my mind - watch out - what if

Jelly's

> minocycline pill was a coated time release version and she is

cutting it up?

> Would she be getting a higher dose than she thinks all at once?

>

> Jelly, there are some good studies other than MP showing that

pulsing

> minocycline may be effective. There is an ideal point at which

bacteria get

> zapped, and it may not be the highest body concentration. One

study suggests

> that as the concentration lowers the bacteria, far from mutating,

come back

> out to play, only to find that the antibiotic is still there and

still able

> to kill them. Do not assume that any of us on this list know all

there is to

> know. Hey, if you are getting better and feel like you are herxing

STICK

> WITH IT.

>

> a Carnes

>

> http://jama.ama-assn.org/cgi/content/abstract/293/16/2003

>

>

>

> Neuroprotective and Anti-Human Immunodeficiency Virus Activity of

> Minocycline

>

> M. Zink, DVM, PhD; Uhrlaub, BS; DeWitt,

BS; Tauni

> Voelker, BS; Bullock, MS; ph Mankowski, DVM, PhD;

> Tarwater, PhD; Janice Clements, PhD; Sheila Barber, PhD

>

> JAMA. 2005;293:2003-2011.

>

> Context The prevalence of human immunodeficiency virus (HIV)

central

> nervous system (CNS) disease has not decreased despite highly

active

> antiretroviral therapy. Current antiretroviral drugs are

expensive, have

> significant adverse effects including neurotoxicity, and few cross

the

> blood-brain barrier.

>

> Objective To examine the ability of minocycline, an antibiotic

with potent

> anti-inflammatory and neuroprotective properties, to protect

against

> encephalitis and neurodegeneration using a rapid, high viral load

simian

> immunodeficiency virus (SIV) model of HIV-associated CNS disease

that

> constitutes a rigorous in vivo test for potential therapeutics.

>

> Design and Subjects Five SIV-infected pigtailed macaques were

treated with

> 4 mg/kg per day of minocycline beginning at early asymptomatic

infection (21

> days after inoculation). Another 6 macaques were inoculated with

SIV but

> remained untreated. Blood and cerebrospinal fluid (CSF) samples

were taken

> on days 7, 10, 14, 21, 28, 35, 43, 56, 70, 77, and 84, and all

macaques were

> humanely killed at 84 days after inoculation, a time that

corresponds to

> late-stage infection in HIV-infected individuals.

>

> Main Outcome Measures Blood and CSF samples were tested for viral

load by

> real-time reverse transcription-polymerase chain reaction and

levels of

> monocyte chemoattractant protein 1 were quantitated by enzyme-

linked

> immunosorbent assay. The presence and severity of encephalitis was

> determined by microscopic examination of tissues. Central nervous

system

> inflammation was further assessed by measuring infiltration and

activation

> of macrophages, activation of p38 mitogen-activated protein kinase

and

> expression of amyloid precursor protein by quantitative

> immunohistochemistry.

>

> Results Minocycline-treated macaques had less severe encephalitis

(P =

> .02), reduced CNS expression of neuroinflammatory markers (major

> histocompatibility complex class II, P = .03; macrophage marker

CD68 , P =

> .07; T-cell intracytoplasmic antigen 1, P = .03; CSF monocyte

> chemoattractant protein 1, P = .001), reduced activation of p38

> mitogen-activated protein kinase (P<.001), less axonal degeneration

> ({beta}-amyloid precursor protein, P = .03), and lower CNS virus

replication

> (viral RNA, P = .04; viral antigen, P = .04). In in vitro analysis,

> minocycline suppression of HIV and SIV replication in cultured

primary

> macrophages did not correlate with suppression of activation of

> p38-mitogen-activated protein kinase pathways, whereas suppression

in

> primary lymphocytes correlated with suppression of p38 activation.

>

> Conclusions In this experimental SIV model of HIV CNS disease,

minocycline

> reduced the severity of encephalitis, suppressed viral load in the

brain,

> and decreased the expression of CNS inflammatory markers. In vitro,

> minocycline inhibited SIV and HIV replication. These findings

suggest that

> minocycline, a safe, inexpensive, and readily available antibiotic

should be

> investigated as an anti-HIV therapeutic.

>

[Guest guest]

Jelly,

It is not just another day. That monkey

thing isn’t the only evidence that low doses, pulsed work. TexLyme Mom’s

point is that you won’t kill as much with a higher dose of minocyline but

you will have less herx. The choice is up to you.

In any case, you want to add in a second

antibiotic as soon as you can. There is fairly good evidence, in particular

from Dr. Garth Nicolson, that using one antibiotic indefinitely does not work.

All the Lyme doctors I know also agree with this.

a

Fly in the ointment, herx is more bareable down here

at my tiny

dose. Remember, highest dose of doxy won me a trip to the ER. Now if

better killing happens at lower doses then maybe this was actually a

toxic reaction to the ABX. I don't know.

Going up to 100 mgs. would likely reduce the herx according to some,

but it would be due to being out of the killing zone more, right?

The reasons RB does what they do is somewhat different then most of

us here are trying to achieve. I think they take the Mino

as a

maintenance thing. Maybe 100 mgs. is the perfect amount to shut the

little buggers up and keep them in hiding so they aren't such a

bother. Most of us here are shooting to get rid of the meds

altogether. Doing so looking into this.

> >

> > This is a curious article for a couple of reasons. One is that

HIV

> is

> > probably not the cause of sickness in AIDS but the facilitator.

> Mycoplasma

> > and other opportunistic bacteria are probably what really make

the

> patient

> > die. Thus the reason why minocycline works.

> >

> > But what is really curious is that these little guys were given

4

> mg/kg of

> > minocycline. I know, I know, they were just little monkeys. If

> they weighed

> > about 25 lbs. that would be about 40 mg of minocycline a day -

not

> a very

> > high dose.

> >

> > Another thing that has crossed my mind - watch out - what if

> Jelly's

> > minocycline pill was a coated time release version and she is

> cutting it up?

> > Would she be getting a higher dose than she thinks all at once?

> >

> > Jelly, there are some good studies other than MP showing that

> pulsing

> > minocycline may be effective. There is an ideal point at which

> bacteria get

> > zapped, and it may not be the highest body concentration. One

> study suggests

> > that as the concentration lowers the bacteria, far from

mutating,

> come back

> > out to play, only to find that the antibiotic is still there and

> still able

> > to kill them. Do not assume that any of us on this list know all

> there is to

> > know. Hey, if you are getting better and feel like you are

herxing

> STICK

> > WITH IT.

> >

> > a Carnes

> >

> > http://jama. <http://jama.ama-

assn.org/cgi/content/abstract/293/16/2003>

> ama-assn.org/cgi/content/abstract/293/16/2003

> >

> >

> >

> > Neuroprotective and Anti-Human Immunodeficiency Virus Activity of

> > Minocycline

> >

> > M. Zink, DVM, PhD; Uhrlaub, BS; DeWitt,

> BS; Tauni

> > Voelker, BS; Bullock, MS; ph Mankowski, DVM, PhD;

>

> > Tarwater, PhD; Janice Clements, PhD; Sheila Barber, PhD

> >

> > JAMA. 2005;293:2003-2011.

> >

> > Context The prevalence of human immunodeficiency virus (HIV)

> central

> > nervous system (CNS) disease has not decreased despite highly

> active

> > antiretroviral therapy. Current antiretroviral drugs are

> expensive, have

> > significant adverse effects including neurotoxicity, and few

cross

> the

> > blood-brain barrier.

> >

> > Objective To examine the ability of minocycline, an antibiotic

> with potent

> > anti-inflammatory and neuroprotective properties, to protect

> against

> > encephalitis and neurodegeneration using a rapid, high viral

load

> simian

> > immunodeficiency virus (SIV) model of HIV-associated CNS disease

> that

> > constitutes a rigorous in vivo test for potential therapeutics.

> >

> > Design and Subjects Five SIV-infected pigtailed macaques were

> treated with

> > 4 mg/kg per day of minocycline beginning at early asymptomatic

> infection (21

> > days after inoculation). Another 6 macaques were inoculated with

> SIV but

> > remained untreated. Blood and cerebrospinal fluid (CSF) samples

> were taken

> > on days 7, 10, 14, 21, 28, 35, 43, 56, 70, 77, and 84, and all

> macaques were

> > humanely killed at 84 days after inoculation, a time that

> corresponds to

> > late-stage infection in HIV-infected individuals.

> >

> > Main Outcome Measures Blood and CSF samples were tested for

viral

> load by

> > real-time reverse transcription-polymerase chain reaction and

> levels of

> > monocyte chemoattractant protein 1 were quantitated by enzyme-

> linked

> > immunosorbent assay. The presence and severity of encephalitis

was

> > determined by microscopic examination of tissues. Central

nervous

> system

> > inflammation was further assessed by measuring infiltration and

> activation

> > of macrophages, activation of p38 mitogen-activated protein

kinase

> and

> > expression of amyloid precursor protein by quantitative

> > immunohistochemistry.

> >

> > Results Minocycline-treated macaques had less severe

encephalitis

> (P =

> > .02), reduced CNS expression of neuroinflammatory markers (major

> > histocompatibility complex class II, P = .03; macrophage marker

> CD68 , P =

> > .07; T-cell intracytoplasmic antigen 1, P = .03; CSF monocyte

> > chemoattractant protein 1, P = .001), reduced activation of p38

> > mitogen-activated protein kinase (P<.001), less axonal

degeneration

> > ({beta}-amyloid precursor protein, P = .03), and lower CNS virus

> replication

> > (viral RNA, P = .04; viral antigen, P = .04). In in vitro

analysis,

> > minocycline suppression of HIV and SIV replication in cultured

> primary

> > macrophages did not correlate with suppression of activation of

> > p38-mitogen-activated protein kinase pathways, whereas

suppression

> in

> > primary lymphocytes correlated with suppression of p38

activation.

> >

> > Conclusions In this experimental SIV model of HIV CNS disease,

> minocycline

> > reduced the severity of encephalitis, suppressed viral load in

the

> brain,

> > and decreased the expression of CNS inflammatory markers. In

vitro,

> > minocycline inhibited SIV and HIV replication. These findings

> suggest that

> > minocycline, a safe, inexpensive, and readily available

antibiotic

> should be

> > investigated as an anti-HIV therapeutic.

> >

>