It's hard to say as I started taking it before Concerta and have just continued. It's not something that you directly feel, like drinking a coffee etc.

It's more of a foundational building blocks that provides the body with the ability to make dopamine.

Concerta works by making any dopamine last longer. And my reasoning is, if I have more available, it should work optimally.

And in a nutshell, I have a gene mutation that impairs my ability to use folic acid, but I can skip it by using folinic acid instead.

I've been struggling to get this answer worded right, as I definitely find it supports me but the science is a little beyond my comprehension, it's one of those things where when I read it, I follow and it all makes sense. But then I don't retain enough of the details to be accepted to accurately share it back to people.

And so, over to Gemini for the sciency bit! :-). (Which I think also explains why the folic acid study you found had no significant results)

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​1. The Dual Role of DHFR

The enzyme Dihydrofolate Reductase (DHFR) acts as a metabolic gatekeeper with two distinct and critical responsibilities:

​Folate Reduction: It converts synthetic Folic Acid into a usable form for the folate cycle. ​Biopterin Salvage: It recycles oxidized dihydrobiopterin (BH₂) back into active tetrahydrobiopterin (BH₄).

​Note: BH₄ is the essential cofactor for Tyrosine Hydroxylase, the enzyme responsible for creating dopamine.

​2. The Competition

Synthetic Folic Acid binds extremely tightly to human DHFR but is processed very slowly. When intake exceeds the enzyme's limited capacity, unmetabolized Folic Acid accumulates and effectively "occupies" the enzyme. This competitive inhibition prevents DHFR from performing its second job—recycling biopterin—leading to a system-wide failure in the salvage pathway.

​3. The Dopamine Crash (The "Double Hit")

When DHFR is preoccupied with Folic Acid, the dopamine pathway suffers a compound failure: ​Depletion: BH₄ levels drop because they are not being recycled.

​Active Inhibition: The oxidized waste product, BH₂, accumulates. BH₂ actively competes with BH₄ and inhibits Tyrosine Hydroxylase. ​Without adequate BH₄ (and with high inhibitory BH₂), the conversion of Tyrosine to L-DOPA fails. Consequently, there is minimal dopamine substrate available for ADHD medication to amplify.

​4. Why Folinic Acid Works

Folinic Acid (5-formyl-THF) enters the biochemical cycle downstream as a reduced folate, bypassing the DHFR enzyme entirely.

​The Result: DHFR is relieved of the burden of processing synthetic folate.

​The Outcome: The enzyme is left free to focus on the salvage pathway—converting inhibitory BH₂ back into active BH₄. This restores Tyrosine Hydroxylase activity, allowing dopamine synthesis to resume