quite the opposite, studies are quite useful (though not always correct). Btw not disagreeing with your assertion that nicotine has both CNS and SNS effects (likely mediated through NE and in the CNS by NE and DA. in this case a number of studies have looked at thyroid and nicotine, they have found no changes in thryoid levels with nicotine use. They have found it to be a metabolic stimulant through various pathways.
it is quite possible that nicotinic cholinergic receptor stimulation modulates thryoid transcription, but studies indicate that it has no direct effects on plasma thryoid levels.
as a note- this study, among others, supports your SNS/metabolic theory...
J Nutr Sci Vitaminol (Tokyo). 1990 Apr;36(2):123-30. Links
Effect of nicotine on norepinephrine turnover and thermogenesis in brown adipose tissue and metabolic rate in MSG obese mice.Yoshida T, Yoshioka K, Hiraoka N, Kondo M.
Department of Internal Medicine, Kyoto Prefectural University of Medicine, Japan.
To clarify whether nicotine stimulates the sympathetic nervous system (SNS) and thermogenesis in brown adipose tissue (BAT) and whether it promotes the resting metabolic rate (RMR), with resulting mitigation of obesity, we measured norepinephrine (NE) turnover (an indicator of SNS activity), guanosine-5'-diphosphate (GDP) binding (a thermogenic indicator), oxygen consumption in BAT, and RMR in monosodium-L-glutamate (MSG) obese and saline control mice after 2 weeks treatment with nicotine. Nicotine significantly increased NE turnover, GDP binding, oxygen consumption in BAT, and RMR, and significantly reduced body weight in MSG obese mice as well as in control mice without affecting food intake. These results suggest that nicotine stimulates NE turnover and thermogenesis in BAT, and promotes RMR, all of which contribute to the mitigation of obesity.
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