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Friday, 9 November 2012

The nicotine myth - down a rabbit hole!

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 [3]. 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 [4]. (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.


>>>>>>>

conclusion

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. 

Translated again....

In 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.
In 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.
In 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.
Nicotine 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.