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Does TMG increase stomach acid?

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I have searched for the answer to this question using onibasu but have

found conflicting answers.

I want to increase stomach acid to help with absorption but if I take

TMG is this enough on it's own or should I add some Betaine Hcl as well?

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TMG will not do anything for stomach acid, it's different than HCI. I got them

confused also, .

Does TMG increase stomach acid?

I have searched for the answer to this question using onibasu but have

found conflicting answers.

I want to increase stomach acid to help with absorption but if I take

TMG is this enough on it's own or should I add some Betaine Hcl as well?

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Share on other sites

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>, what are acetylcholine precursors and acetylcholinesterase

>inhibitors? I'm a little confused about the relationship with TMG?

>

There is no relationship (that I'm aware of) between TMG and ACh

(acetylcholine) precursors/acetylcholinesterase (AChE) inhibitors

regarding effects on stomach acidity – I mentioned acetylcholine

elevating agents, because they enable some people to boost their

cognitive functioning (a nice bonus) as well as their stomach acidity.

I believe I may have realized why you're experiencing some confusion

regarding TMG and stomach acid. As you know, when people are

suffering from hypochlordhydria (stomach acid deficiency), a reliable

therapy involves supplementing (approx. mid-way through meals) with

betaine (or glutamic acid) HCl. HCl (as a dietary supplement is

always chelated to another molecule (e.g., betaine or glutamic

acid). Importantly, the betaine (or glutamic acid) component has no

effect on stomach ph – it just goes for the ride. This is relevant,

because betaine (anhydrous) is also known as TMG. So, if you had

someone who understood that TMG and betaine are one in the same, but

didn't understand that the reason betaine HCl supplementation is an

effective means of increasing stomach acidity is because of the HCl

moiety (and not the betaine), then they could erroneously conclude

that TMG (betaine anhydrous) can be used to decrease stomach ph.

An ACh (acetylcholine) precursor is, simply, something that converts

into acetylcholine within the body. Some examples include 1) choline

(as bitartrate, chloride, or citrate), 2) DMAE/centrophenoxine, 3)

phosphatidylcholine (a constituent of lecithin), 4) CDP-choline, and

5) alpha-GPC. The first one does not cross the BBB (blood brain

barrier) very well and is also the most likely to produce GI issues.

Four & five are less selective than the others (i.e., they increase

brain dopamine (DA) and norepinephrine (NE) concentrations as well as

ACh). Some people benefit from DA/NE increases, and others do not.

So, I can offer a few options to aid in selection: 1) take the

Braverman Nature Assessment (which provides insight into potential

neurotransmitter deficiencies/excesses), 2) read " In Search of a

Designer Brain (part 1 & 2) " by Fowkes to increase your

understanding of which neurotransmitters affect which mood/behavioral

states – this would allow you to speculate about which

neurotransmitter(s) you may want to increase, or 3) try the different

precursors, and see which one(s) best agree(s) with your system.

It is worth mentioning that some research begs the question, " Is DMAE

truly a legitimate ACh precursor? " Well, even if one were to

overlook the excessive muscle tension that results from DMAE

overdoses (a sign of cholinergic excess), any respectable biochemist

knows that Dimethylaminoethanol (DMAE) becomes trimethylaminoethanol

(choline) when it combines with an available methyl group (after

crossing the BBB).

I would use an ACh precursor over an AChE inhibitor unless

Alzheimer's dementia (or a related condition) rendered one incapable

of synthesizing ACh adequately (due to acetyltransferase

deficiency). Of course, if it weren't for un-/improperly treated

chronic mercury toxicity, Alzheimer's dementia may not exist. If

anyone knows of an Alzheimer's victim with orderly mineral transport,

please let me know.

Sincerely,

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