Someone Tell Me If This Is Plausible

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Preferably someone who is knowledgable about biology and genetics, please. I am doing my best to piece together a theory, but as I forgotten most of what I used to know about biology and have very little knowledge of genetics, I may be missing something.

The Delta-F508 mutation of the CFTR gene causes a loss of phenylalanine, correct?
And without phenylalanine, it's harder to synthesize tyrosine, correct?
And with less tyrosine, it's also harder to synthesize dopamine, epinephrine, and norepinephrine, correct?
And a deficiency in those chemicals could cause ADD-like symptoms, correct?

So might carrying one copy of the Delta-F508 mutation cause ADD-like, or even autism-like, symptoms?

In my experience, it's rarely this simple.
Answers in plain English will be appreciated.

That's one way to see if you might have ADD, but talking to a doctor and seeing if any of the meds available for ADD work for you. The type of testing needed to prove your theory is cost prohibitive is cost prohibitive and only used if you are having extremely severe symptoms and meds aren't working.

Questions in plain English also appreciated
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If it's 1:30 white people (including non symptomatic carriers), then would you not expect a lot more cases of ADD than what we see at the moment?

As a tree, it's plausible, but it'd be only one in an entire forest.

My apologies about the non-plain-English question.

I don't know if this is true, but I've heard that this is widely believed in the CF community. It's the idea that carriers of a mutated gene can have very mild symptoms of CF. For example, salt cravings or a tendency toward allergies. Maybe ADD-like symptoms would be only a rare side effect of carrying Delta-F508.

No argument here. There are undoubtedly loads of potential causes for conditions like ADD and autism.