The science of smoking

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Nicotine is an insecticide. Certain plants, including tomatoes, manufacture it in their leaves to discourage bugs, which it kills by jamming the creatures’ nervous systems. It interferes with human nervous systems too and can be fatal in large doses. At lower levels, however, the effect is rather more enjoyable.

Nerve signals travel electrically but at junctions between nerve cells there are gaps, called synapses, which the signals have to jump across by converting into chemical form. These chemical messengers, called neurotransmitters, are released by the nerve cell on one side of the gap and dock on the other side with a receptor protein. Nicotine insinuates itself into this process by masquerading as a neurotransmitter called acetylcholine.

The signal passed on by the acetylcholine receptors in turn triggers the release of dopamine, another neurotransmitter, which goes on to stimulate nerve cells which seem to be involved in the sensation of pleasure.

So an influx of nicotine into the nervous system (something which a good gulp of tobacco smoke can introduce more efficiently than almost anything else) triggers a delicious rush of dopamine signals. But whereas acetylcholine is released promptly by its receptor protein and is then reabsorbed by the nerve-cell that released it, nicotine, like an ill-fitting key which jams in a lock, gets stuck, and prevents the receptor from working again for a while.

Nicotine thus has a more controlled effect than, for example, cocaine, which also works on the dopamine system but does so by preventing the re-absorption of dopamine. A cocaine high is the result of dopamine hanging around in the system, repeating its message of pleasure over and over again, whereas after the first buzz from a blast of nicotine, the stimulation declines gradually until the acetylcholine receptors switch on again.

The short-term effects of nicotine in the body, including relaxation, alertness and improved concentration, are enjoyable enough to make many people want to experience them again. But the body also adapts to regular exposure in ways that provide a physical basis for nicotine’s addictiveness.

With cocaine the link between neurological changes and addiction is clear: cocaine-users lose dopamine receptors, so come to crave the way it amplifies pleasure signals. With nicotine things are more complicated. Regular exposure to nicotine seems to increase the number of acetylcholine receptors, as the body compensates for having them shut down temporarily, but scientists are still unsure exactly how this physical change relates to nicotine addiction. Research at Brookhaven National Laboratory in New York shows that for smokers the process is further complicated by the effect of other chemicals in smoke which reduce the body’s store of an enzyme which degrades dopamine.

Whatever the details of the mechanism of addiction - genetics may play a part too - many people have come to expect a steady input of nicotine into their systems. Nicotine itself, at least at the doses delivered by cigarettes, is relatively harmless. The trouble is that cigarettes also deliver other substances into the body - such as tar and carbon monoxide - which are dangerous. It is these that increase the risks of heart disease and lung cancer: smokers die an average of 6 1/2 years before comparable non-smokers.

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