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Re: Lactams, glutamate transport and fatigue

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Hi Matt,

I don't recall this being discussed, and I think it's a very

significant finding. Thanks for finding it.

Yes, I am one of those who seems to respond to the beta lactams,

like Ceftin. I had a tremendous energy increase on the Ceftin.

Unfortunately, like every abx I take, it didn't last forever. :-( I

assumed it was the bacteria building resistance, but this research

suggests that perhaps something altogether different is going on,

that the Ceftin is having an effect on the central nervous system

resulting in the decrease in mental fatigue. So many drugs work for

a while, but the body adapts somehow and they lose their

effectiveness. It could be the case here.

I went back on Ceftin a few days ago, along with Zithromax. The cold

I had turned into a bronchitis that really got my chest rattling. I

couldn't shake it with the zith, but adding the Ceftin seems to be

working and yes, once again, my energy is increasing, so perhaps the

abx does both, kills and has an impact on the glutamate transport,

lessening fatigue in both ways?

I suppose the other question is this: Is there any evidence

supporting the idea that the reason our glutamate transport

expression is being suppressed in the first place, is because of the

infection, and that the antibiotic's ability to reduce the infection

causes and increase in the glutamate? Same for the elastase? Just a

wild guess. Same old chicken or the egg kind of question. :-)

penny

>

> I haven't been keeping up on the various fatigue-related boards

> recently, so I apologize if this line of reasoning has already

been

> advanced.

>

> These researchers:

>

> Ronnback L, Hansson E.

> On the potential role of glutamate transport in mental fatigue.

> J Neuroinflammation. 2004 Nov 4;1(1):22.

>

> http://tinyurl.com/cwkt3

>

> suggest that glutamate transport is related to fatigue.

>

>

>

> These researchers:

>

> Rothstein JD, Patel S, Regan MR, Haenggeli C, Huang YH,

> Bergles DE, Jin L, Dykes Hoberg M, Vidensky S, Chung DS,

> Toan SV, Bruijn LI, Su ZZ, Gupta P, Fisher PB.

> Beta-lactam antibiotics offer neuroprotection by increasing

> glutamate transporter expression.

> Nature. 2005 Jan 6;433(7021):73-7.

> PMID: 15635412

>

>

> http://tinyurl.com/7722e

>

>

> Show that glutamate transport is influenced by beta-lactams.

>

>

>

> These people:

>

> http://content.nejm.org/cgi/content/full/352/13/1376

>

>

> say, " A cautionary point illustrated by this report is that the

> beneficial effects of a given drug cannot always be attributed to

a

> single mechanism. For example, there are anecdotal claims that

> chronic fatigue syndromes respond to ceftriaxone (or other

> antibiotics) because the underlying problem is chronic Lyme

> disease. However, the study by Rothstein and colleagues1

> indicates that ceftriaxone may exert important effects on the

> central nervous system that are independent of its role as an

> antibiotic. "

>

> There is also the view, by De meirleir, that lactams inhibit

> elastase.

>

> I haven't read any of these papers yet, and won't for awhile. So

> I'm not in a position to comment in more detail.

>

> Matt

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Penny

I'm under enormous time constraints this month and literally

have only skimmed the abstracts of the sources I cited. The first

citation refers to inflammatory cytokines and their influence on

glutamate transport, so it does look, as you suggest, like the old

chicken-or-the-egg question. The tetracyclines are

anti-inflammatory and they kill off bacteria that cause the

inflammation in the first place. Obstructive sleep apnea is

pro-inflammatory and inflammation appears to aggravate apnea.

A lot of chicken-and-egg issues.

If memory serves, the narcotics are physiologically addictive

because they delay the uptake of neurotransmitters into

pre-synaptic terminals. So the narcotics extend the action of

neurotransmitters. The neurons don't like this and

down-regulate the production of the neurotransmitters, and then

you need the drugs just to achieve baseline. Perhaps neurons

eventually adapt to lactam exposure by opposing its effects. This

would predict not only that the lactams would lose potency, but

that the discontinuation of the lactams could lead to a rebound

effect, thereby aggravating the fatigue. In a sense, you'd be

addicted. But, if memory serves, the SSRIs also block uptake of

neurotransmitters, but in this case the neurons don't

compensate. You may be an early test case of this.

Did you find that your fatigue worsened when you stopped the

lactam?

Barb's been raising the issue of the addictive nature of some

antibiotics and we have some theories about how the

tetracyclines (and possibly the macrolides) might do this. Maybe

the lactams are " addictive " as well.

That last quote I gave doesn't actually say that PWCs aren't

infected, but it sort of leaves that impression. It's important that

any such conclusions be challenged for lack of evidence. I

would assume, for example, that lactams won't cause

anything that might be confused for a herxheimer reaction in

people who aren't infected. I realize that

your recoveries tend to be herx-free, but I don't think that's true

for

all PWCs.

Matt

>

> Hi Matt,

>

> I don't recall this being discussed, and I think it's a very

> significant finding. Thanks for finding it.

>

> Yes, I am one of those who seems to respond to the beta

lactams,

> like Ceftin. I had a tremendous energy increase on the Ceftin.

> Unfortunately, like every abx I take, it didn't last forever. :-( I

> assumed it was the bacteria building resistance, but this

research

> suggests that perhaps something altogether different is going

on,

> that the Ceftin is having an effect on the central nervous system

> resulting in the decrease in mental fatigue. So many drugs

work for

> a while, but the body adapts somehow and they lose their

> effectiveness. It could be the case here.

>

> I went back on Ceftin a few days ago, along with Zithromax.

The cold

> I had turned into a bronchitis that really got my chest rattling. I

> couldn't shake it with the zith, but adding the Ceftin seems to

be

> working and yes, once again, my energy is increasing, so

perhaps the

> abx does both, kills and has an impact on the glutamate

transport,

> lessening fatigue in both ways?

>

> I suppose the other question is this: Is there any evidence

> supporting the idea that the reason our glutamate transport

> expression is being suppressed in the first place, is because

of the

> infection, and that the antibiotic's ability to reduce the

infection

> causes and increase in the glutamate? Same for the

elastase? Just a

> wild guess. Same old chicken or the egg kind of question. :-)

>

> penny

>

>

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Most of the abx we use for Lyme have many non-antibiotic

properties that are known- but we really don't takl about them

too much.

Personally, if someone relapses (with Lyme) in 2 days after stopping

abx- I'd suspect some other mechanism at work (other than

wntimicrobial) - fast replicators don't bounce back that fast - and

Lyme a slow replicator.

And speaking for my self - I find the tetracycline family 'addictive "

in some ways I can't really explain well- I just know if I wean off

them I feel much better than if I try to just stop.

I wonder if some of the 'replases' people have when the cold turkey

off long term abx is disease replapse or something else. We know the

body shifts, adjusts and compensates to just about everything we do

to ourselves- so it make sense to me there's some compensatory

mechanisms that have to come into play on long term abx- and maybe-

probably- some of them are in the brain.. I know the tetracycline

family really affects my brain.. I handle those drugs like little hot

potatoes..

Barb

> >

> > Hi Matt,

> >

> > I don't recall this being discussed, and I think it's a very

> > significant finding. Thanks for finding it.

> >

> > Yes, I am one of those who seems to respond to the beta

> lactams,

> > like Ceftin. I had a tremendous energy increase on the Ceftin.

> > Unfortunately, like every abx I take, it didn't last forever. :-(

I

> > assumed it was the bacteria building resistance, but this

> research

> > suggests that perhaps something altogether different is going

> on,

> > that the Ceftin is having an effect on the central nervous system

> > resulting in the decrease in mental fatigue. So many drugs

> work for

> > a while, but the body adapts somehow and they lose their

> > effectiveness. It could be the case here.

> >

> > I went back on Ceftin a few days ago, along with Zithromax.

> The cold

> > I had turned into a bronchitis that really got my chest rattling.

I

> > couldn't shake it with the zith, but adding the Ceftin seems to

> be

> > working and yes, once again, my energy is increasing, so

> perhaps the

> > abx does both, kills and has an impact on the glutamate

> transport,

> > lessening fatigue in both ways?

> >

> > I suppose the other question is this: Is there any evidence

> > supporting the idea that the reason our glutamate transport

> > expression is being suppressed in the first place, is because

> of the

> > infection, and that the antibiotic's ability to reduce the

> infection

> > causes and increase in the glutamate? Same for the

> elastase? Just a

> > wild guess. Same old chicken or the egg kind of question. :-)

> >

> > penny

> >

> >

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Matt, this seems really important to me, and I think there's

something to it. Unfortunately, I don't know where to go with it

since I can see myself fitting both scenarios.

All I can say for sure is that it's not that I relapse badly after

going OFF the lactams. I go off the lactams because I start

relapsing. The fatigue starts coming back and they no longer seem to

work, so I stop and start something else, or take a break. I'd

always thought it was because my bugs had built resistance to the

abx, but perhaps it's just my body adapting, getting around it as

you describe. Sometimes, I notice that if I wait 6 months or so, the

abx do seem to regain some effectiveness.

But there are two important points to consider, supporting the

resistance scenario in my case.

1) There is some research that shows that resistant bacteria can

once again become susceptible to certain abx.

2) Testing shows that my bugs develop resistance easily. First time

my organisms were tested, they showed resistance to 12 of the 14 abx

they tested.

Gotta go now, but this is very interesting.

penny

> >

> > Hi Matt,

> >

> > I don't recall this being discussed, and I think it's a very

> > significant finding. Thanks for finding it.

> >

> > Yes, I am one of those who seems to respond to the beta

> lactams,

> > like Ceftin. I had a tremendous energy increase on the Ceftin.

> > Unfortunately, like every abx I take, it didn't last forever. :-

( I

> > assumed it was the bacteria building resistance, but this

> research

> > suggests that perhaps something altogether different is going

> on,

> > that the Ceftin is having an effect on the central nervous

system

> > resulting in the decrease in mental fatigue. So many drugs

> work for

> > a while, but the body adapts somehow and they lose their

> > effectiveness. It could be the case here.

> >

> > I went back on Ceftin a few days ago, along with Zithromax.

> The cold

> > I had turned into a bronchitis that really got my chest

rattling. I

> > couldn't shake it with the zith, but adding the Ceftin seems to

> be

> > working and yes, once again, my energy is increasing, so

> perhaps the

> > abx does both, kills and has an impact on the glutamate

> transport,

> > lessening fatigue in both ways?

> >

> > I suppose the other question is this: Is there any evidence

> > supporting the idea that the reason our glutamate transport

> > expression is being suppressed in the first place, is because

> of the

> > infection, and that the antibiotic's ability to reduce the

> infection

> > causes and increase in the glutamate? Same for the

> elastase? Just a

> > wild guess. Same old chicken or the egg kind of question. :-)

> >

> > penny

> >

> >

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