(I think this author is a student who suffers from IBS and is an independent researcher. Several of the SNPs identified are reported on 23andme. madelyn)

https://sites.google.com/site/annerw...ase-inhibitors


Cholinesterase inhibitors (CIs) are neurotoxins which inhibit the action of cholinesterase enzymes. The body uses cholinesterase to break down the neurotransmitter acetylcholine. Inhibition of cholinesterase interferes with the propogation of signals from the brain and central nervous system (CNS) to command various systems in the body controlled by use of acetycholine.

CIs are naturally produced by certain plants... People also produce them for use as pesticides and nerve gasses. The dangers of acute cholinesterase inhibitor poisoning are well documented (see refs [1], [11], and [14]). However, the effects of chronic low level exposure to CIs are less well documented or understood.

We are constantly exposed to low levels of CIs through the food we eat -- ... In susceptible individuals, normal levels of exposure in the diet can cause health and quality of life problems, though others eating the same diet notice no untoward effects.

I will use the term "Cholinesterase Inhibitor Sensitivity", or CIS for short, to designate those who suffer negative effects when exposed to CIs at levels found in their normal diet, but who would experience a relief of such symptoms if they were to follow a diet which sufficiently reduces their exposure. ... This term is inclusive of Nightshade Sensitivity since nightshade foods (potato, tomato, eggplant, peppers, and a few others) are the primary source of dietary CI exposure for most people...

The effects of CIS which can directly be linked to the effects of cholinesterase inhibition include intermittent and recurrent dysfunctions of muscles (spasms, cramps, twitches, muscle pain, etc.), gastrointestinal system (diarrhea, abdominal pain, etc.), poor sleep, exaggerated stress response, and anxiety (see below for more details)...

Unfortunately, the general public is unaware of this issue, and doctors are not trained to recognize or diagnose it. The effects are widespread across multiple systems, each of which is handled by a different medical specialty. A sufferer is not likely to see or investigate the overall pattern, but rather focus on whatever one issue is most disruptive at a given point in time and discuss only that issue with an appropriate medical practitioner. Tests come up negative, since neither the commands from the CNS nor the systems being controlled are at fault, and doctors don't know to suspect that the messaging between the two may be interfered with. The likely result is that it will either be treated as a psychiatric problem (such as somatoform disorder), or one of a set of chronic functional syndromes which are consistent with the reported symptoms but which have no known cause (such as IBS or dysautonomia).


There are no tests to detect CIS, though that's a dream I'm working on. The only way to know if it's CIS or not is to try the diet modification and see what happens. Note that it may take a few weeks to notice the effects, and months before all the effects go away. This is because at least some of the cholinesterase inhibiting substances, particularly the solanaceous glycoalkaloids (SGA) present in nightshade foods, build up in your tissues and are re-released slowly over time (see ref [9]).

People can't discover whether or not this would help them if they don't know about it. That is why I'm trying to collect together here what I've learned so far so that others may benefit. I hope it helps.


How do cholinesterase and cholinesterase inhibitors work?

...The most notable uses of cholinergic synapses (that is, ones using acetylcholine for transmission) are in controlling muscle contraction and the autonomic nervous system.

When an action potential arrives at the presynaptic side of a cholinergic synapse, acetylcholine is released into the synaptic cleft, and drifts over to bind to receptors on the postsynaptic side causing the desired action, such as muscle contraction. Cholinesterase breaks down the acetylcholine, clearing the receptors, allowing the postsynaptic side to relax, and resetting the synapse in preparation for the next signal.

At least, that's the way it's supposed to work. If the cholinesterase is inhibited then the release step may not work right, causing the receptors to be occupied for longer than they should be, and the postsynaptic side to get stuck in the activated state. This can cause problems...



Cholinesterase inhibitor effects


A major repercussion of this is that it increases the effective acetylcholine/dopamine (ACh/DA) ratio. When this ratio is too high, either by increased acetylcholine (ACh) tone, or decreased dopamine (DA) tone, it can cause problems. Factors which increase acetylcholine tone, such as CI levels and stress, make these problems worse. Factors which increase dopamine tone, such as exercise and positive/empowering life events make these problems better. See the "Improving Ach/DA ratio" section below for more details...

https://sites.google.com/site/annerwright/snps

SNPs potentially related to cholinesterase inhibitor sensitivity

i agree with this theory and haven't been getting dystonia here in a rehab hospital. Besides getting rid of all the surgery chemicals, the only differences in meds for me is the addition of potassium. i take nortriptyline which has anticholinergic properties. Have you searched for any relationship between acetylcholine and potassium?

Hi Paula, Sending you good vibes for a speedy recovery. I PMed you earlier with some personal recommendations for your extended rehab period.
As for potassium and acetylcholine, I have not researched that specific topic, though I know low potassium can cause leg cramps and severe muscle weakness, in addition to many other severe effects. It is a crucial component generating the electrical gradient across all membranes. On the other hand, too much potassium results in cessation of heart function.
I am reminded of Rick's post concerning potassium:

http://neurotalk.psychcentral.com/sh...t123+potassium

From wikipedia: http://en.wikipedia.org/wiki/Potassium

Potassium cations are important in neuron (brain and nerve) function, and in influencing osmotic balance between cells and the interstitial fluid, with their distribution mediated in all animals (but not in all plants) by the so-called Na+/K+-ATPase pump.[50] This ion pump uses ATP to pump three sodium ions out of the cell and two potassium ions into the cell, thus creating an electrochemical gradient over the cell membrane. In addition, the highly selective potassium ion channels (which are tetramers) are crucial for the hyperpolarization, in for example neurons, after an action potential is fired. ]
Membrane polarization
Potassium is also important in preventing muscle contraction and the sending of all nerve impulses in animals through action potentials.

Do you know if you possess the gene mutations noted in the reference?
madelyn

listing of drugs with anticholinergic effects:

http://www.health.harvard.edu/newsle...e-burden-scale

thanks madelyn. i am not sure we are thinking the same way [meaning this possible student] - i don't think it was your theory or was it?

i guess acetylcholine is important for cognition but i get a lot of relief and sleep when i lower my acetylcholine. i have a score of 6 on your scale [very informative]and may be stupid but don't care ..lol i take xanax, amantadine and nortriptyline. i am not dyskinetic and i sleep.

very interested in learning more about potassium...i was not paying full attention altho i remember rick emphasizing it. It is an electrolyte and every cell has a potassium pump.

the web pages in your link are beautifully illustrated and animated. In spite of acetylcholine's relevance to cognition,I benefit many ways from lowering it - just relaxaation for one - , just can't be a genius all the time....ha! the genius is well hidden as anyone of you who has seen me lately can testify. no speech no brain.

its a trade off but i am thinking this theory is trying to control acetylcholine through diet. that's interesting. the sensitivity would mean low acetylcholine from exposure to its enzymes that inhibit it and thus that's not a good thing for cognition.

Is this theory the same thing as the inherited genetic disorder that people often don;t know they have and anesthesia with a certain ingredient causes them to flatline and they must be brought back with artificial respirators? frannie has it , she gets sick from bug spray.

Hi Paula, this student thinks anything that causes acetylcholinesterase to be inhibited, thus resulting in increased acetylcholine, can be a very bad thing for some individuals. The student lists many foods which inhibit acetylcholinesterase leading to increased acetylcholine. Wonder if any of the preparations for cough that are used for PD have anti acetylcholine activity? Frannie must have the 3 mutations in the BCHE genes that have been associated with that reaction to anesthesia.

ok thanks i have no genes that i know about. so we do agree that acetycholine in high quantities is bad. it can get pretty confusing . thanks.