Thank you Randall for sending me Pr Molimard's ideas - this link
The nub of the argument is that nicotine is cheap and easy to manufacture and has been promoted by Drug Companies as a NRT to "assist" smokers to the profit of themselves. Governments are squandering money on something no better than placebo.
I have translated the nub of it via Google Translate....
The myth of addiction to nicotine
Ove Ferno, a Swedish chemist of the firm LEO said in an interview with the saga of the development of nicotine gum, the 1967 patent in 1978 . According to its self-observation, he was convinced that nicotine was the factor of tobacco dependence. Yet the team of Russell in London already asked questions about it . (See here)
In fact, simple observations could already doubt that nicotine alone can explain the powerful tobacco dependence:
- Usually, when a plant chemist isolates a molecule active addictive, addicts get hold fast (morphine from opium, cocaine from coca leaves, cannabis tetrahydrocannabinol, etc.).
- We know the nicotine from a century and a half, extracted, synthesized. Used as an insecticide, we have no observation of its use under addictive.
- In times of war where the tobacco quota was rare and we have no comments to add nicotine to cigarettes various leaves, wormwood, walnut etc. used as tobacco substitutes.
- Under the same conditions, no traffic nicotine has been reported.
- The pure nicotine can be obtained from chemical companies (Fluka) to 440 € per liter, which corresponds to € 1 143 would accrue to cigarettes. No "drug" is available at a price so low.
Unfortunately we do not have any medication effective enough to be a recommendation, whether the nicotine in all its forms, of bupropion (Zyban °) or varenicline (Champix °). The level of evidence of their effectiveness is very low and criticism. Doctors are prescribing formatted almost mandatory these products biased scientific literature and opinion leaders bound by conflicts of interest, and the demand of a population conditioned by the general public magazines and advertising. The role of health authorities is to provide objective information on these products, whose activity is hardly more than a placebo effect, but with financial consequences unnecessarily encumber the family budget and the Health Insurance. A serious analysis seems unable to conclude that a very low benefit / cost ratio or risk.
And a link to a second article by Jean-Pol Tassin et Marc Kirsch
Suggests that what the brain does under the influence of drugs like Cocaine, Alcohol etc does not happen in the presence of nicotine. There is something else...(read below) and therefore NRT is useless.
summary, here is the new concept of drug dependence that we proposed:
drugs decouple the noradrenergic and serotonergic neurons, they become
autonomous and hyper-reactive. The
addict is weaned so hyper-sensitive to emotions, and drug re-creating
the situation that led to the decoupling becomes a source of temporary
relief. We demonstrate this dissociation for alcohol, for morphine, heroin, amphetamine, cocaine. All these products lead to dissociation. Rest nicotine. But in fact, when we study the case of nicotine, we realize it does not produce this effect.
Nicotine does not cause this decoupling. This
explains why, for years, all animal models of nicotine are ineffective
or operate very mediocre set of amphetamine, the animal starts running,
turn nicotine, it does not move. Give amphetamine self-administration, the animal reacts very actively, with nicotine, it is very difficult. All experiments with nicotine is bad. But researchers insist, because they believe their model and believe it should apply to nicotine. They
believe that the failure does not contradict the core of their
argument, but must be related to factors annexes and secondary. So
they make hundreds of experiments to show that under certain
conditions, paying attention to certain elements, etc.., We still manage
to get a result. I think there is a bias. For
my part, I find that nicotine administration in animals does not
produce the effects predicted by the current model of addiction.
1995, Yvan Berlin to study the effect of antidepressants, is conducting
a study comparing a group of patients receiving antidepressants with a
control group who did not receive. It is based on the measurement of a metabolite in the urine. The results are unexpected in the control group, about 50 subjects, 25 had a rate of 100 and 25 have rates 50. Puzzled,
he seeks how to explain this anomaly, research bias in the recruitment
of subjects, etc.., To finally realize that there is only one parameter
that can be correlated with these results, c ' is the fact that the subjects were smokers or not. But it is not the nicotine that explains this difference in concentration. But
among the 3,000 constituents in tobacco, there are monoamine oxidase
inhibitors, MAOIs, which seem to have an important role. Berlin identifies these monoamine oxidase as the source of the effects he observed. This is the state of play when my team is at work on this issue. There
is nicotine in experimental does not work as predicted by the dominant
model, there is the simultaneous presence of nicotine in tobacco and
monoamine oxidase and the fact that tobacco is an addictive product to
potential particularly high. In the classification of addictive potential, tobacco comes first, followed by heroin, cocaine, amphetamine and alcohol, etc.. Tobacco addiction produces a rate of 22%.
So 22% of smokers are highly dependent?
In reality, it is a little more complex. 90%
of smokers are addicted, but 22% of the population, that is to say
people who have tried smoking once in their life, have become addicted. This is significant. For the alcohol, according to the studies, it is between 2 and 8%.
This addiction is not the product of nicotine alone. We tried unsuccessfully to occur with nicotine decoupling effect I mentioned. Similarly, with monoamine oxidase in isolation, decoupling does not occur. However, when the two are combined, it works.
other words, the nicotine addiction actually occurs, must be assigned
either monoamine oxidase or products that have the same action. Seeking to identify the action of MAO inhibitors, we discovered that they alter a receptor in the brain. We
modified this receiver with a very specific product that fits only on
the receiver, then we injected nicotine and this time, decoupling
occurred. So, we have a substitute product becomes effective.
alone in patch or chewing gum, does not prevent smokers to continue
smoking: 84% of people who take a patch relapse within one year, while
no patch, it is the order of 90% - the difference is minimal. Early relapses occur very quickly, within a few weeks. We
say to get that nicotine becomes a substitute effective, it must be
associated with another product that will change the receiver in
question, which in fact protects addiction. This solution is very effective on animaux3.