Not to mention that I am taking less than a teaspoon daily. "And, yet, it moves!"

I'm no chemist, but the argument:

"that is pretty weird since vinegar is mostly water"

doesn't, it seems to me, excuse the pun, to hold water.

A typical vinegar has 5% acetic acid. The specific density of acetic acid is 1.049, which is close enough to 1 for our purposes to not worry about distinguishing by weight and by volume figures. A dose might be 10ml. 5% of this is 0.5ml, which is approximately 0.5gm, or in the units we would normally use, 500mg.

In comparison the daily dose of rasagiline is 1mg, a typical dose of levodopa is 100mg.

My intent is not to promote vinegar. Frankly, I am sceptical. Neither is my intent to rubbish "parity checks" of the type used here, which are a perfectly reasonable first step. But, specifically, to point out that vinegar, based on the weight of its active ingredient alone, is still in the game.

John

john,
thanks for that perspective, i'll have to check your calcs when i have time.. i'm sure there are poisons where less than 1mg can kill you. but when dealing with biological compounds that you ingest, qty of molecules and half life are 2 key factors. the reason 3mg of mirapex can be just as effective as 300mg of sinemet is mirapex has a much longer half life than sinemet. same with azilect, you might not notice any affect from the 1st mg of azilect, it may take weeks for it to accumulate enough to have an affect. so it's misleading to say just 1mg has any affect. touche!

so the scientific question is what is the half life of acetic acid? is it broken down instantly in the stomach? is it like alcohol and is absorbed into the blood by the stomach wall? i can feel 1 shot of vodka but that's 40% alcohol.

i wasn't actually trying to shoot down the possibility of vinegar affecting pd. but i do use balsamic vinegar, wasn't paying attention to whether it had any affect, will have to do so.

The question is bigger than "Does vinegar impact PD?" And any question about its ability to affect our metabolism and even our general health is quickly rendered moot by a glance at the literature. Leaving PD aside for a moment:

From Johnston et al, 2006 (PMID 1785201) -
" This review examines the scientific evidence for
medicinal uses of vinegar, focusing particularly on the recent investigations supporting vinegar's role
as an antiglycemic agent. Epidemiologic studies and clinical trials were identified by a MEDLINE
title/abstract search with the following search terms: vinegar, glucose; vinegar, cancer; or vinegar,
infection. All relevant randomized or case-control trials were included in this review.....

....The chemical and organoleptic properties of vinegars are a function of the starting material and the
fermentation method. Acetic acid, the volatile organic acid that identifies the product as vinegar, is
responsible for the tart flavor and pungent, biting odor of vinegars. However, acetic acid should not be
considered synonymous with vinegar. The US Food and Drug Administration (FDA) states that
diluted acetic acid is not vinegar and should not be added to food products customarily expected to
contain vinegar.[3] Other constituents of vinegar include vitamins, mineral salts, amino acids,
polyphenolic compounds (eg, galic acid, catechin, caffeic acid, ferulic acid), and nonvolatile organic
acids (eg, tartaric, citric, malic, lactic).[4,5].....

Damn. I may have just found it. I am going to post the general background info above and then go into what just got my attention in a big way. This is cool..

I confess that I had not read the paper. It seemed to be a "lite" summary for the file. But there is a bombshell buried in it. Bear with me but do read on.

Continuing with the Johnston paper from 2006:

"Kondo and colleagues[30] reported a significant reduction in systolic blood pressure (approximately
20 mm Hg) in spontaneously hypertensive (SHR) rats fed a standard laboratory diet mixed with
either vinegar or an acetic acid solution (approximately 0.86 mmol acetic acid/day for 6 weeks) as
compared with SHR rats fed the same diet mixed with deionized water. These observed reductions in
systolic blood pressure were associated with reductions in both plasma renin activity and plasma
aldosterone concentrations (35% to 40% and 15% to 25% reductions in renin activity and aldosterone
concentrations, respectively, in the experimental vs control SHR rats). Others have reported that
vinegar administration (approximately 0.57 mmol acetic acid, orally) inhibited the renin-angiotensin
system in nonhypertensive Sprague-Dawley rats.[31]
Trials investigating the effects of vinegar ingestion on the renin-angiotensin system have not been
conducted in humans, and there is no scientific evidence that vinegar ingestion alters blood pressure
in humans. In their report, Kondo and colleagues[30] speculated that dietary acetic acid promoted
calcium absorption and thereby downregulated the renin-angiotensin system.[32] In the rat model,
acetic acid administration enhanced calcium absorption and retention[33]; moreover, in humans,
calcium absorption in the distal colon was enhanced by acetate.[34] Clearly, much work is needed to
establish whether vinegar ingestion alters calcium absorption and/or blood pressure regulation in
humans."

OK. You may as what the heck this has to do with PD? The short answer is "PLENTY". The Johnston paper was written from the prospect of cardio-protection from vinegar and made no mention of a link to PD and I am not surprised. It is not very well known and the only reason that I know anything is because of the problems that Conductor71 and I were having last year with periodic paralysis.

There is an awful lot to cover here so this is gong to be confusing, but this is important. Maybe very important.
--------------------
Dopamine-Angiotensin interactions in the basal ganglia and their relevance for Parkinson's disease. 2013 (PMID 23925977)

Hyperactivation of the local renin-angiotensin system exacerbates the inflammatory microglial response, oxidative stress, and dopaminergic degeneration, all of which are inhibited by angiotensin receptor blockers and inhibitors of angiotensin-converting enzymes. In this review we provide evidence suggesting that the renin-angiotensin system may play an important role in dopamine's mediated neuroinflammation and oxidative stress changes in Parkinson's disease. We suggest that manipulating brain angiotensin may constitute an effective neuroprotective strategy for Parkinson's disease. © 2013 Movement Disorder Society.
----------------------------------------------

The role of the central renin-angiotensin system in Parkinson's disease 2009 (PMID 19861346)

Since the discovery of a renin-angiotensin system (RAS) in the brain, several studies have linked this central RAS to neurological disorders such as ischaemia, Alzheimer's disease and depression. In the last decade, evidence has accumulated that the central RAS might also play a role in Parkinson's disease. Although the exact cause of this progressive neurodegenerative disorder of the basal ganglia remains unidentified, inflammation and oxidative stress have been suggested to be key factors in the pathogenesis and the progression of the disease. Since angiotensin II is a pro-inflammatory compound that can induce the production of reactive oxygen species due to activation of the NADPH-dependent oxidase complex, this peptide might contribute to dopaminergic cell death. In this review, three different strategies to interfere with the pathogenesis or the progression of Parkinson's disease are discussed. They include inhibition of the angiotensin-converting enzyme, blockade of the angiotensin II type 1 receptor and stimulation of the angiotensin II type 2 receptor.

----------------------------------------

And I have to go for awhile. This is getting extremely interesting.... Anyone for an entirely new treatment protocol that defines a new "gold standard"?

Lots of articles on PD and angiotensin, this one just last month from Spain:

http://www.ncbi.nlm.nih.gov/pubmed/23925977

How does this fit in with PWP who never have had high blood pressure? Wait, there are those "ranges" again: who is to say that a particular blood pressure level isn't high for a particular individual? What's high for me may not necessarily be high for anyone else. Maybe someone whose blood pressure readings have never exceeded the model of "high blood pressure" as defined by modern medicine actually may have high blood pressure for them.

Makes sense, and goes back to inflammation again. Thanks, Rick.

Regarding just what is "normal", I started this thread looking at "post-prandial hypoglycemia" and found that 1) it is low blood sugar resulting from insulin triggering a drop in glucose in the hours following a heavy carb meal and it kicks in as your level drops below about 50 and triggers alarms that produce an emergency bump up from the liver converting glucogan into glucose, OR 2) it is a response to the SPEED of fall independent of the level but is triggered as the level passes about the 70 mark and sets off a dump of stress hormones into your blood. The resulting symptoms are very much the same. This latter one makes me think of how a simple confrontation at a checkout counter can leave us drained. Very interesting.

While the response with a few exceptions has been a little underwhelming, I know that this s a tough nut to crack so I am going to forgive those of you who have failed to appreciate my Greatness, although I must warn you that when I am on that stage in Sweden (or wherever they keep that dynamite money that they will want to give me) that it will be hard to "remember the Little People". But there is yet time for redemption so, like Paul on the road to Spartacus I will trudge ahead and report when I actually have something to report.

First, there is, at least in my case, a definite improvement in my symptoms. I am sleeping better (almost ten hours last night) and I have actually gone to bed a couple of times without that panic of getting to the bed before I collapse in a puddle of assorted body fluids. I am beginning to see a more normal bedtime of 10 to 11 PM instead of 8 to 9 PM. The vinegar can put me to sleep jn the daytime, BTW. When first up I was routinely suffering with foot dystonia and cramps of the lower legs. I barely noticed anything this morning. I had one episode of screaming in my sleep on the first night of this trial but none since. I was not aware of it but my wfe tells me that it was pretty impressive. She was eventually able to awaken me (with the two dogs assistance) from her own room immediately over mine. I have only the faintest memory of doing battle with some spawn of Satan (or maybe it was my brother-in-law). I remember that it was vivid. And I think that I recall asking someone who seemed to know just when were the "naughty" dreams scheduled, but he just rolled his eyes.

I continue a habit of tending to awaken at about 2 AM in a "negative space" with that painting titled "The Nightmare" hanging above my bed and the characters from Bloom County's Binkley's Closet wandering about. I have had a couple of threats of panic attack during this period but find that simply turning on the bedside lamp keeps me awake just enough to maintain control. This is the time when your body is flooded with stress hormones as you prepare to face another day in paradise. Cortisol. Adrenaline. Noradrenaline. Commonly known. But others that are less well known. Aldosterone. Angiotensin. Runnin. These chemicals and others have the ability to reduce the biggest and baddest to whimpering shadows.

The leg cramping is more common than it was (or so I think) but it is less intense. By that I mean that rather than being a tightly focused "charlie horse" it is spread more throughout the muscle. More irritating than painful.

I usually take my first meds at 6 AM. Still do but have reduced to 1x sinemet cr 200 mg plus 1x sinemet 10/100) from twice that. I take meds every two hours and manipulate the dose but hold the spacing because that is the time frame for working with Ldopa. Stretch it to four hours without changing anything else and you are going to have trouble.

I am taking meds at 6 AM, 8, 10, Noon, 2 PM, 4, 6, and 8. Total of 2400 mg. But if you convert it to take into account the loss resulting from the controlled release formulation I am taking more like 1800 mg. I was taking 2x of the 200 mg CR each two hours until a wee ago so it was about 3000 mg or about 2000 mg. I can already tell that I can reduce it even more but I won't rush it.

The best and most encouraging change is that so long as I am being careful about missing pills or stressing out, I no longer have periods when I am"off" and feeling miserable while I wait for one more pill to give me two more hours of life. I am not experiencing "Offs" which were a daily pain just two weeks ago.

Read that last paragraph one more time. Then turn off the computer and go in search of vinegar and lets figure out if I am a lucky SOB or if we are a bunch of them. I hope for the latter.

Any way to make your vinegar trial "double blind" to remove any placebo effect ?