Terma
Member
- Joined
- May 8, 2017
- Messages
- 1,063
If it worked as expected, it could allow to increase phospholipid synthesis a little-to-moderately while blunting the acetylcholine effects, to a limited extent where another substrate/cofactor notably CDP/uridine become rate-limiting fairly quickly. Past that (ignoring acetylcholine synthesis) it goes to methylation. 275mg isn't terrible.
I would be very careful when stopping the drug because the "anticholinergic" properties (usually implied to be at the receptor level - you have to read the cyproheptadine mechanism more closely, I do not know it) effects may not guarantee anything about the acetylcholine synthesis and levels, only the receptors, so in the worst case you could get a very bad surprise if you stop cold turkey (a minority of people have had serious effects from too high choline (and uridine)).
A better bet would be to use an acetylcholine synthesis/release inhibitor than an anticholinergic that works on the receptors. Wikipedia suggests methylmercury or botulinum.
Acetylcholine - Wikipedia
I would be very careful when stopping the drug because the "anticholinergic" properties (usually implied to be at the receptor level - you have to read the cyproheptadine mechanism more closely, I do not know it) effects may not guarantee anything about the acetylcholine synthesis and levels, only the receptors, so in the worst case you could get a very bad surprise if you stop cold turkey (a minority of people have had serious effects from too high choline (and uridine)).
A better bet would be to use an acetylcholine synthesis/release inhibitor than an anticholinergic that works on the receptors. Wikipedia suggests methylmercury or botulinum.
Acetylcholine - Wikipedia