This is as I'd expect. I'd like to know if there's a dose relationship. I'll also need to see if this translates to clinical significant improvements in things like schizophrenia and CFS.

This implies a causal role. The low parasympathetic tone precedes psychosis.

It's hard to say what this tells me about my hypothesis that the 7 mg patch increases HRV. It really depends on their blood levels. The second-hand smoke machine is extremely unrealistic. They were exposed to 30 puffs of 1.8% nicotine e-juice in the first measurement interval. Assuming 150 puffs per ml, that's 3.6 mg smoked in a single 15 minute interval! I've not read the full study to confirm this calculation. Nonetheless, it's clear that these insane conditions require scrutiny. That's not even counting the fact that there's no placebo (Or even control). How am I supposed to know if this is not just an effect of being concern about inhaling e-smoke? I'm still searching for studies on low concentration of nicotine and HRV.

This confirms that thyroid function probably lacks any (direct) effect sleep. Of course, not this evidence alone, but rather this combined with "Effects of Supraphysiological Doses of Levothyroxine on Sleep in Healthy Subjects: A Prospective Polysomnography Study"

This was with a 14 mg patch. A 21 mg patch would probably reduce HRV given that a 4 mg lozenge does so.

I still expect to find enhance HRV with 7 mg. This study supports that hypothesis to an extent. That it, it shows that 14 mg may be the tipping point between increased or decreased HRV from nicotine.

Assuming a half life of two hours, I calculated a 7 mg per day patch delivers a peak dosage of around 0.8 mg. Given that a 4mg lozenge has a bioavailability of 79%, this is equivalent to a 21 mg patch.

Given that we know anything above a 7 mg patch disrupts sleep (while 7 mg enhances sleep), it's unsurprising that HRV was reduced. I expect that a 1 mg lozenge or gum would increase HRV. Given that the above citation lists the bioavailability of a 2 mg lozenge at 50%, 2 mg may also increase HRV.

Unsurprising. This supports my hypothesis that ADHD is a sleep disorder. This hypothesis should hold sound regardless of EEG. That said, I also expect to find EEG disturbance during sleep in ADHD.

I'm somewhat surprised. I was under the impression that cAMP signalled the wake phase, and cGMP signalled the sleep phase. I thus expected cGMP to increase parasympathetic tone (and therefore increase HRV)