Re: Minocycline, Jelly, 4 mg and minocycline

[Guest guest]

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

>

> 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]

Exactly, a. Nobody knows for sure, so let's try to keep looking at things objectively. This list came about as a reaction to one person using any means necessary (including law suits) to convince the public that low dose abx was the ONLY legitimate treatment out there, so I find it doubtful that we're going to embrace a rerun of the concept without stringent questioning and/or medical documentation. The same goes for people stringently questioning Benicar, even though I personally take it every day. This article, for example, is interesting in showing the possible neuroprotective capabilities of minocycline in AIDS patients in reducing encephalitis type reactions. At the same time there are numerous studies showing just the opposite, that minocycline can induce encephlitic reactions in patients known as pseudotumer cerebri (intracranial hypertension). Both points

of view are worth considering. Likewise, it's interesting that studies on Benicar show it to be renal protective, and yet, if you've already got renal problems, it's contraindicated as a treatment. Since so much depends on what state we're in when we begin treatment and on our different abilities to metabolize drugs (i.e. the p450 pathway) it's pretty presumptuous to think we know what's going on for sure with any of these reactions. If we did, believe me, we'd all be 100% well by now. Assuming that every reaction is a herx is just irresponsible. As irresponsible as assuming that any abx will kill all bacterial infections. I will seriously consider people's experiences who I can verify are actually well. But I don't consider "well" to be dependent on all kinds of drugs or supplements or hyperbaric devices to prevent relapse. I consider well to mean our

bodies are firing on all cylinders and don't need very much in the way of assistance. penny a Carnes <pj7@...> wrote: 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 (-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]

Objectivity is extremely difficult after

the harm we have all experienced. Let’s just be objective about Jelly’s

experience as well. I have posted some ideas that MAY support her experience.

I should add that actually she may do

better with less herx on a HIGHER dose of minocyline since she is not taking

Benicar. A higher dose would kill less bacteria and thus she would FEEL better

although she would not be getting better. No one on Roadback would take the low

dose she is taking. TexLyme Mom first brought this up saying that certain folks

actually started treating their sarc with rather high doses of minocycline, not

with Benicar. I hope you see where I am going with this. Jelly may need to raise

her dose of minocycline, not to get better faster, but to reduce the herx. And,

yes, I do mean herx.

As for Benicar, I suspect MOST will have

no problem with it and even be helped. In my case it did not help me and seemed

to be causing harm. But without good longterm studies on the effect of high

dose Benicar who knows. I think being objective is often to state, “I don’t

know.” I’m sure you agree.

a

Exactly, a. Nobody knows for sure, so let's try

to keep looking at things objectively.

This list came about as a reaction to one person using any means

necessary (including law suits) to convince the public that low dose abx

was the ONLY legitimate treatment out there, so I find it doubtful that we're

going to embrace a rerun of the concept without stringent questioning

and/or medical documentation. The same goes for people stringently questioning

Benicar, even though I personally take it every day.

This article, for example, is interesting in showing the possible

neuroprotective capabilities of minocycline in AIDS patients in reducing

encephalitis type reactions. At the same time there are numerous studies

showing just the opposite, that minocycline can induce encephlitic

reactions in patients known as pseudotumer cerebri (intracranial

hypertension). Both points of view are worth considering.

Likewise, it's interesting that studies on Benicar show it to be renal

protective, and yet, if you've already got renal problems, it's contraindicated

as a treatment.

Since so much depends on what state we're in when we begin treatment

and on our different abilities to metabolize drugs (i.e. the p450 pathway) it's

pretty presumptuous to think we know what's going on for sure with any

of these reactions. If we did, believe me, we'd all be 100% well by now.

Assuming that every reaction is a herx is just irresponsible.

As irresponsible as assuming that any abx will kill all bacterial

infections.

I will seriously consider people's experiences who I can

verify are actually well. But I don't consider " well " to be dependent

on all kinds of drugs or supplements or hyperbaric devices to prevent relapse.

I consider well to mean our bodies are firing on all cylinders and don't need

very much in the way of assistance.

penny

a

Carnes <pj7@...> wrote:

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 (-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]

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]

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.

> >

>

[Guest guest]

a:

This is like dejavu.

My ansewrs are preceeded with *********

> I should add that actually she may do better with less herx on a

HIGHER dose

> of minocyline since she is not taking Benicar. A higher dose

would kill less

> bacteria and thus she would FEEL better although she would not be

getting

> better.

************** This thought- almost verbatim, is theory from the

Mr. unmentionable. It is based on the premise that the suppressive

qualities of mino are present at the higher doses (but flip-flops

minos antimicrobial properties.. i.e. saying low dose kills but high

dose does not.

There has never been anything to support this claim - and it's

a perfect example of SUBjectiviity, not objectivity.

Barb

[Guest guest]

Take a breathe Jelly- that was mis interpreted...

it's 4 milligram PER kilogram of body weight - not 4 milligram dose

total.

> >

> > 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]

I saw it:} My math skills are probably worse then a's. So it's

just another day.

> > >

> > > 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]

Thanks a, I agree as well. I will give other ABX a whirl once I

am able to tolerate a higher dose of Mino. I'm doing much better

this time on 10 mgs, then I did last time. Progress, all be it

slooooow.

> > >

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

> > >

> >

>