Exposure to nicotine is probably a major cause of inflammatory diseases among non-smokers.
This article assesses the hypothesis that most inflammatory diseases are conditioned responses caused by the psychoactive action of nicotine. Even in very 'light' passive smokers, the repeated nicotinic stimulation of the reward system can produce, through classical and subsequent operant conditioning, unconscious addiction to most relevant perceptions occurring simultaneously, including the artificial, non-localised sensation of pain or sickness caused by the action of nicotine on the nociceptive 'cholinergic anti-inflammatory pathway'. During nicotine abstinence and especially under stress, the brain previously addicted to this pain is compelled to reproduce it by the only method available without nicotine: causing lesions or cellular stress in one's organism, for example, by triggering intense inflammations. The author's observations and two independent studies have confirmed that nicotine withdrawal causes inflammatory crises. Furthermore, there is evidence that severe inflammations can be triggered even by almost unnoticeable exposures to nicotine, for example, by staying several minutes outdoors at a few metres from smokers. This has been clearly observed by one patient and can be deduced from theoretical considerations (sensitivity of neural pathways and cumulativeness of conditioning processes) and an animal experimental reference, and is confirmed by the fact that most inflammatory diseases affect similarly all non-smokers regardless of their apparent exposure to nicotine, despite the proven relation between nicotine withdrawal and inflammation. This sensitivity implies that the outdoors atmosphere of most densely populated urban areas represents now a serious health hazard, probably requiring the prohibition of all smokable forms of nicotine. The usual anti-smoking measures focused on closed spaces are inefficient against this danger.
Gracia
M C
MC
m.c.gracia@telefonica.net
D000109:Acetylcholine / Q000378:metabolism; D016739:Behavior, Addictive; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D008962:Models, Theoretical; D009538:Nicotine / Q000009:adverse effects*; D012907:Smoking; D014028:Tobacco Smoke Pollution
D014028:Tobacco Smoke Pollution; D009538:Nicotine; D000109:Acetylcholine