[paula_w]

This is over the counter.

2010 Mar 22. [Epub ahead of print]
Effect of histamine H(2) receptor antagonism on levodopa-induced dyskinesia in the MPTP-macaque model of Parkinson's disease.

Johnston TH, van der Meij A, Brotchie JM, Fox SH.
Toronto Western Research Institute, Toronto Western Hospital, University Health Network, Toronto, Canada.

Levodopa-induced motor complications, including dyskinesia and wearing off, are troublesome side effects of treatment and impair quality of life in Parkinson's disease (PD) patients. The use of nondopaminergic agents as adjuncts to levodopa are potential options for managing these problems. Here, we asses the ability of the clinically available, selective histamine H(2) antagonist, famotidine (1, 3, and 30 mg/kg) to treat levodopa-induced dyskinesia and wearing off in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-macaque model of PD. Famotidine (3 mg/kg) increased peak activity, enhanced peak anti-parkinsonian action (1 and 3 mg/kg), and extended duration of action (3 mg/kg, by 38%) of a low dose of levodopa (compared to low dose levodopa alone). Enhancement of anti-parkinsonian actions of low dose levodopa by famotidine (3 mg/kg) was associated with only mild, nondisabling dystonia. Famotidine had no effect on the anti-parkinsonian actions of high dose levodopa (compared to high dose levodopa alone). However, famotidine (1, 3, and 30 mg/kg) had a significant effect on chorea, but not dystonia, induced by high dose levodopa (compared to high dose levodopa alone). Famotidine increased high dose levodopa-induced "good quality" on time, i.e., on time not associated with disabling dyskinesia, by up to 28% (compared to high dose levodopa alone). In conclusion, famotidine, a drug currently available for use in the clinic, can enhance the peak-dose anti-parkinsonian actions and extend total duration of action of a low dose of levodopa, without producing disabling dyskinesia. Furthermore, in combination with a higher dose of levodopa, famotidine can reduce peak-dose levodopa-induced chorea and improve the quality of on-time.

PMID: 20310030 [PubMed - as supplied by publisher]

[Jaye]

Read the conclusion (just a suggestion):

Famotidine increased high dose levodopa-induced "good quality" on time, i.e., on time not associated with disabling dyskinesia, by up to 28% (compared to high dose levodopa alone). In conclusion, famotidine, a drug currently available for use in the clinic, can enhance the peak-dose anti-parkinsonian actions and extend total duration of action of a low dose of levodopa, without producing disabling dyskinesia. Furthermore, in combination with a higher dose of levodopa, famotidine can reduce peak-dose levodopa-induced chorea and improve the quality of on-time.

Has anyone asked their doc about this, or tried it?

Jaye

[paula_w]

Originally Posted by Jaye

Read the conclusion (just a suggestion):


Has anyone asked their doc about this, or tried it?

Jaye

yeah jaye i agree and it's coming out of Toronto where various pronouncements that rule the kingdom originate.

We need to hurry and try it before they do something to make it harder for us.

[LindaH]

Thanks Paula for finding this Movement Disorders abstract! I thought the following excerpt from the full-text article was very interesting. As reported in the abstract, " Famotidine increased ‘‘good on-time’’ by 28%."
It then goes on to say, " In comparison, clinical use of the COMT inhibitor, entacapone
and MAO-B inhibitor, rasagiline, in large RCTs in advanced PD patients appear less effective.
For instance, the LARGO study27 demonstrated a significant
effect of rasagiline and entacapone on increasing
daily on-time without troublesome dyskinesia from
baseline (i.e., ‘‘good on-time’’) by 0.85 hours for both
(this equates to an increase of only 9.3%). These data
suggest that histamine H2 antagonism might be more
effective than currently available therapies to extend
good on-time..."

It sure seems to merit further studies.

[girija]

. In concl

usion, famotidine, a drug currently available for use in the clinic, can enhance the peak-dose anti-parkinsonian actions and extend total duration of action of a low dose of levodopa, without producing disabling dyskinesia. Furthermore, in combination with a higher dose of levodopa, famotidine can reduce peak-dose levodopa-induce

d chorea and improve the quality of on-time.

This is interesting, famotidine is anti-inflammatory looks like when inflammation is controlled, drugs last longer and improvement in on tim4 too
Ibuprofen study showed similar pattern,,,,,

So it is the inflammation again

[Conductor71]

Originally Posted by Jaye

Read the conclusion (just a suggestion):


Has anyone asked their doc about this, or tried it?

Jaye

I learned pretty early on not to ask about anything only in animal model stages; my neuro readily dismisses anything that has not progressed to human trial as too experimental...not as in too risky, but as in "we need more evidence".

I also learned early on to bite my tongue over this lest I blast him on how our entire diagnostic process, treatment, and prognosis is hardly based on any real qualitative or quantitative scientific standard. Apparently, observation and response to a drug is really only acceptable as a gold standard PD diagnostic process. Perhaps I overlook something, but I hate to see how the doctor's trial and error approach to treating our symptoms is any different than guiding us in wanting to try a new form of treatment? I'm sure there is more risk involved for certain approaches but for something like taking Pepcid? It must have to do with liability.

Laura

[lurkingforacure]

Originally Posted by Conductor71

I learned pretty early on not to ask about anything only in animal model stages; my neuro readily dismisses anything that has not progressed to human trial as too experimental...not as in too risky, but as in "we need more evidence".

I also learned early on to bite my tongue over this lest I blast him on how our entire diagnostic process, treatment, and prognosis is hardly based on any real qualitative or quantitative scientific standard. Apparently, observation and response to a drug is really only acceptable as a gold standard PD diagnostic process. Perhaps I overlook something, but I hate to see how the doctor's trial and error approach to treating our symptoms is any different than guiding us in wanting to try a new form of treatment? I'm sure there is more risk involved for certain approaches but for something like taking Pepcid? It must have to do with liability.

Laura

Nope, it's $$$, pure and simple. i hate to say it, but we all know it is true, at least for most docs. Read any of the books written about modern medicine and the glaring conflicts of interest and you will unfortunately see. No doc gets ANY perk for going along with someone using an OTC med. No trip to Hawaii for the family, no lush conference in Vienna all expenses paid, no lavish gifts, you see how this goes. If you doubt it, just look at how many people in this country are now on daily drugs of some kind, with more drugs for "new" disease coming out all the time. If I get up to pee more than once or twice a night, suddenly I have "overactive bladder syndrome" and need to take this new med daily for the rest of my life! Maybe I just drank too much before going to bed, how about that? Nope, I have a disease, and must be treated, daily.

I read recently the AVERAGE american is on one drug for every decade old they are...if you are fifty, you take five pills a day! Every day, forever! It makes me sick-do they have a pill for that too?

Now, we have a doc we see who is NOT like this. He doesn't agree with all we do, in fact tells us he thinks certain things are a waste of money...but he lets us do them and supports us. IF he thinks there is an actual danger to something we want to try, he will tell us, and let us know he won't be responsible (this hasn't happened yet). He is one of the rare docs I know who does not cowtow to big pharma...just wish there were more like him.

[RLSmi]

Sounds like you have a doc you can really trust.

By the way, the lowest doses used in this famotidine study, 1mg/kg and 3mg/kg, translate to 70 and 210mg for a 70kg man. I think that is way above the usual doses even in the prescription strength stuff.

[RLSmi]

Originally Posted by RLSmi

Sounds like you have a doc you can really trust.

By the way, the lowest doses used in this famotidine study, 1mg/kg and 3mg/kg, translate to 70 and 210mg for a 70kg man. I think that is way above the usual doses even in the prescription strength stuff.

The OTC Pepsid caps contain 10mg.

[HeartSong]

I discovered by accident that Pepcid helped to prolong levodopa effectiveness. I have taken it only once - last night. I took it for really bad acid reflux - half of a 10 mg tablet. I had several hours of calm and blessed relief this morning! Has anyone investigated how we can stop producing so much gastric histamine by a change in diet or other life-style change? I know that protein, particularly meat, causes the stomach to produce hydrochloric acid in order to digest it, and I think that's connected to the histamine cells in the stomach. I'm going to experiment with not eating meat for a few days and see if either my acid reflux or Parkinson's symptoms improve.