posted
so, neuro recommended aricept while back and i was very reluctant to try it. then when i was going to finally give it a go the $$ was over $200/mo. too much for a "lets see"
so, last appt he gave me month sample. day 2- was like a switch was turned off !!!!!!!!!!!!!
this is HUGE for me. the pain is minimal. have been able to go down to 2xday on pain meds from 3xday and pain still at 7/10 on good day. and in less than a week !!!
did notice when climbing lots o stairs my legs/gluts where screaming at me and my pain was up that night significantly. other than that i feel like this last yr has been reversed...
all from more avail. acetylcholine?????
i dont understand. anyone have any thoughts on this one???
i have always had only IgM responses. to lyme, rmsf, few others. no IgG after yr of abt. aenta denied further IV rocephin on us.
been tx for babs, bart too. no improvements. if anything all neuro worse, muscles worse and pain worse.
left knee still hurting but really feel 100% better. and this is rx used in alz. to increase amt. of acteycholine. so works by decreasing enzyme that breaks it down so more avail at nerve receptor sites...
i REALLY think this is part of the missing link in my case... but WHAT does that point to???
pain dr stumpped.. happened to see her. she tried changing cymbalta to a new rx but soon as was on lower dose day 3 the "electric shock" feeling at spine out was back so that is no-go
but, can tell in am the diff. when before take the aricept and about hr after.. i "come too"
very, very intersting and weird. got call out to neuro.
only thing i have seen assoc. with A Ch is alz. (only 33 and was high functioning RN until yr ago able to handle working 70+ hr/wk as normal) and myastenia gravis... and have been tested for lots, MS ruled out. but no MG antibody testing i can find in records.
thanks for any insight !!
oh, also low NK cells,,, 3,4,57. low neutrophils, elevated lymphocytes, disk degeneration to cervical/lumbar severe for age, cystic changes to tibia/femur of l leg, slow alpha waves. low C3. thats abotu the lab data.
-------------------- i am not a Dr. any info is only for education, suggestion or to think/research. please do not mis-intuprest as diagnostic or prescriptive, only trying to help. **
dx in 08:lyme, rmsf, bart, babs, and m.pneumonia. Posts: 422 | From TX | Registered: Oct 2008
| IP: Logged |
TerryK
Frequent Contributor (5K+ posts)
Member # 8552
posted
I'm so glad increased acetylcholine is helping you! It sure has helped me over the past 5 years.
I take a lot of supplements to boost acetylcholine and have posted about it a number of times. I found out I needed it when I was muscle testing for air hunger several years before I found out I had lyme disease. It makes the air hunger so much better.
Several years later I found an article that talks about how borrelia toxins inhibit acetylcholine. In my view, it adds to the evidence Macdonald found regarding the connection between alzheimers and spirochetes.
"The action of botulinum (as well as the toxin from the Lyme spirochete) is to prevent, through its action as a proteolytic enzyme, the release of the neurotransmitter acetylcholine."
"Dietary Supplements in Lyme Disease One of the known actions of the Lyme spirochete toxin is to diminish the release and availability of the neurotransmitter acetylcholine, a simple organic compound (see above for chemical structure). This substance is biosynthesized by the body as required in nerve activation and transmission. Supplementation by the precursors of acetylcholine synthesis would be of value to Lyme patients since they have a deficiency of this substance."
It is a very good article.
Terry
Posts: 6286 | From Oregon | Registered: Jan 2006
| IP: Logged |
Pinelady
Frequent Contributor (5K+ posts)
Member # 18524
posted
Would just taking ATP be more cost effective?
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
| IP: Logged |
Hoosiers51
Frequent Contributor (1K+ posts)
Member # 15759
posted
Glad you found something that is helping!!!
Does acetylcholine help any other symptoms besides pain and air hunger? Would it help fatigue? Muscle soreness (possibly from a longggg herx)?
Posts: 4590 | From Midwest | Registered: Jun 2008
| IP: Logged |
all i know is bout hr. after taking the dang aricept it is like i "bing !! i am here !1" careful not to over do it l...but this is amazing really. like last yr just has not happened
got of cipro/plaqunil to "See" and severe night sweats again and today feet hurt soooooooooo.... getting back on those,
only abt i am on right now anyway, ins. co. said the IV is not "medically neccessary" anymore,. geez.
called my neruo and takled to him about the HUGE change. he was stummped. was gonna do some research... just said, well...keep takingn it !!
but, we talked about the acetycholine effect has to be the underlying issue here. Was really hoping he would have some majic answer..nope.
and Hoosiers, has helped EVERYTHING but left knee pain. dont know that i will ever be rid of that. old inj/ 2 surj + several rounds of steroid inj. to knee. so -- think will be with me.
have cut down on pain meds, and ok. bit of headache today..then.. go.. oh, go put on glasses woman ! lol
-------------------- i am not a Dr. any info is only for education, suggestion or to think/research. please do not mis-intuprest as diagnostic or prescriptive, only trying to help. **
dx in 08:lyme, rmsf, bart, babs, and m.pneumonia. Posts: 422 | From TX | Registered: Oct 2008
| IP: Logged |
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Aricept works by preventing acetylcholine from being broken down via inhibiting the enzyme that does that - acetylcholinesterase.
We are making neurotransmitters all the time IF we have the nutrients to make them and usually we do (from foods and drinks).
Neurotransmitters like acetylcholine are made and help to ***transport a signal*** onto another receptor and then are broken down.
This is happening all the time at incredible (!) speeds.
During the night, we fluctuate between NREM sleep and REM sleep...about 5 times...NREM...REM...NREM...REM...and so on.
REM = random eye movement. NREM = non random eye movement.
It looks like these (NREM and REM) require melatonin and acetylcholine respectively.
In other words...melatonin then acetylcholine...melatonin...then acetylcholine.
No prob. with melatonin 'cause the body is upregulating it via breaking down tryptophan (via our defense cells). That is a good thing as melatonin is a powerful anti-oxidant.
But acetylcholine is another thing.
I personally know a lyme patient who was tested in a sleep lab and she has
NO REM SLEEP. That is not good.
Acetylcholine isn't available. Why?
Bb needs choline to MAKE one of its lipoproteins:
phosphatidylCHOLINE
(the other major lipoprotein is phosphatidylglycerol).
AND Bb looks to impact HDAC(s) which *removes* acetyl groups.
AND Bb looks to inhibit phosphate transfers.
We are making acetylcholine all the time, but
***is Bb robbing the acetyl group off OUR acetylcholine which drives it down?***
And then Bb uses the choline to make one of the lipoproteins in its cell wall?
By inhibiting the breakdown of acetylcholine (inhibit acetylcholinesterase = how Aricept works)
are we denying robbing Bb of the choline it needs? Or is there enough for both of us?
We need to look at what acetylcholine does with regards to other hormones.
"On stimulation by acetylcholine, the suprarenal medulla releases epinephrine and norepinephrine."
Would Bb then upregulate OspA which binds to our norepinephrine and epinephrine?
What need would we have then for our mAB CB2 antibody (which is made, but is defective anyway).
There are two main classes of acetylcholine receptor (AChR), *nicotinic* acetylcholine receptors (nAChR) and muscarinic acetylcholine receptors (mAChR). They are named for the ligands (binders) used to activate the receptors.
When acetylcholine binds to its receptor this happens:
Binding of acetylcholine to its receptors on the *postsynaptic cell* opens up ligand-gated sodium channels.
These allow an influx of Na+ ions, reducing the membrane potential.
Okay...Bb needs Na for its Na-ATPase which does this: ATP-ADP. And it needs NaCl for motility.
But when acetylcholine IS present, does this remove available Na from circulation and give it to US, rather than Bb? Or once again...is there enough to go around for both of us?
Acetylcholine impacts the nicotinic receptors.
and for what it's worth (couldn't get the entire abstract):
Nicotine Reduces TLR2 and NOD2, But Not TLR4- Induced NF-KappaB Activation in Mouse Spleen Macrophages.
Okay....Reducing TLR2 (that's a receptor) is important...very...as this -> making Fe available for Bb to use to grow - not to replicate, but to grow. I talked about how this happens in another post here.
If NFkB is reduces NFkB in macrophages (think of them as defense "pac men") this means inflammation goes down and pain is less.
Nicotine...I bet that got your attention...
Nicotine can be oxidised to nicotinic acid (niacin)
And niacin...get this...lowers cholesterol which happens to be the pathway Bb takes to BUILD its cell walls.
Okay...ya all know that it has been said that smokers (cigarettes) might not develop Parkinson's.
That has to do with dopamine (which is lowered by melatonin).
There is an interaction, cross-talk between dopamine (and its receptors) and acetylcholine and its nACh receptors.
Though the computer buffering (hesitations) in the youtube link drives me nuts.
Okay...so having more acetylcholine is very very beneficial, but the question remains...
will this DESTROY Bb? Or does it merely put you in remission?
Yes, I know, for many of you remission and less pain sound really really good. I understand.
Don't underestimate this pathogen. It is NOT easy to destroy.
Posts: 9481 | From Sunshine State | Registered: Mar 2001
| IP: Logged |
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Bottom line...Aricept maybe putting you in
REMISSION.
It is absolutely reducing inflammation.
Repeating:
"They determined that acetylcholine OR nicotine pretreatment resulted in a marked reduction of lipopolysaccharide-induced TNF-alpha release."
Posts: 9481 | From Sunshine State | Registered: Mar 2001
| IP: Logged |
posted
Some people asked about possible natural treatments for this. I briefly did a search online and this is what I found.
"Supplements such as choline and CDP-choline raise levels of acetylcholine. They are both available without a prescription. Choline is an essential precursor to acetylcholine, a stimulatory neurotransmitter. It also helps in the production of lipotropic agents which converts fats into useful products and aids in the production of HDL (good) cholesterol."
"Huperzine A is an extract from a club moss (Huperzia serrata) that has been used for centuries in Chinese folk medicine. Huperzine's action has been attributed to its ability to strongly inhibit acetylcholinesterase, the enzyme that breaks down acetylcholine in the synaptic cleft. Acetylcholine is involved in memory and learning. By inhibiting the enzyme that breaks it down, more acetylcholine becomes available to stimulate neurons."
"Muira puama, a Brazilian plant used for sexual enhancement, may have acetylcholinesterase inhibiting activity."
So it looks like there are at least 3 possible natural treatments. Choline, Huperzine A, and Muira puama. I am sure there are more. This is what I found in a very quick search. Just google "natural acetylcholine".
Of course...I am not a doctor so definitely do your own research on this and check with your doctor first.
-------------------- Sick since 10/2001. Tested CDC positive for Lyme 10/2008 through Quest and Igenex. Started treatment 1/2009 with LLMD. Lyme, Erichilosis, Chlamydophila Pneumoniae, Q Fever, Strep Syndrome and probably a few others I am forgetting. Posts: 451 | From Virginia | Registered: Feb 2009
| IP: Logged |
TerryK
Frequent Contributor (5K+ posts)
Member # 8552
posted
From the article: Listing 1: Dietary Supplements Increasing Acetylcholine Synthesis Improving Neurologic Function
I take choline, huperzine a, citicholine, phosphatidylcholine. Also, Vitamin B5, Vitamin B6, Vitamin C and sometimes lysine. I can't tolerate SAMe. Even taking that much may not get you to the same level as your prescription.
Terry
Posts: 6286 | From Oregon | Registered: Jan 2006
| IP: Logged |
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Aricept be *combined with* the Rx (medicinal food!) called
Axona
But it might not be as good as VCO.
Nice try though...drug company.
Neither work SEPARATELY to really get at the root of the problem.
Need to COMBINE the anti-inflammatory (Aricept) WITH the pathogen killer (Anoxa).
Over the counter, we can do the same...
OmegaBrite + VCO.
And keep pumping in probiotics.
Posts: 9481 | From Sunshine State | Registered: Mar 2001
| IP: Logged |
The Lyme Disease Network is a non-profit organization funded by individual donations. If you would like to support the Network and the LymeNet system of Web services, please send your donations to:
The
Lyme Disease Network of New Jersey 907 Pebble Creek Court,
Pennington,
NJ08534USA http://www.lymenet.org/
UBBFriend: Email this page to someone!
Printer-friendly view of this topic