How nicotine can be useful

plastik1912

plastik1912

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nicotine and testosterone



“For the first time, we can see that nicotine works to shuts down the estrogen production mechanism in the brain of women. We were surprised to see that this effect could be seen even with a single dose of nicotine, equivalent to just one cigarette, showing how powerful the effects of smoking are on a woman’s brain. This is a newly-discovered effect, and it’s still preliminary work. We’re still not sure what the behavioural or cognitive outcomes are; only that nicotine acts on this area of the brain, however we note that the affected brain system is a target for addictive drugs, such as nicotine”.
- Lead researcher, Associate Professor Erika Comasco (Uppsala University, Sweden).

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A dose of nicotine, equivalent to that found in a single cigarette blocks estrogen production in women’s brains. This may explain several behavioural differences in women who smoke, including why they are more resistant than men to quitting smoking. This work is presented for the first time at the ECNP Congress in Vienna.

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In 22 studies of 13,317 men, mean age 18-61years, smokers had higher mean testosterone than non-smokers (1.53nmol/L, 95% confidence interval (CI) 1.11 to 1.96) using a random effects model with inverse variance weighting. In 6 studies of 6089 women, mean age 28-62years, smoking was not clearly associated with testosterone (0.11nmol/L, 95% CI -0.08 to 0.30).

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Threshold effects were analyzed to identify the inflection point between serum cotinine and total testosterone. Indeed, a total of 7797 participants were included in our study. After adjusting for potential confounding variables, the findings indicate a positive association between serum cotinine levels and total testosterone levels (β: 0.05, 95%CI: 0.02, 0.09).

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The key enzyme in estrogen biosynthesis is aromatase (Cyp19, estrogen synthase), which catalyzes the last step of estrogen biosynthesis, aromatizing the A ring of androgens (e.g., androstenedione and testosterone) to estrone and 17β-estradiol respectively (9). Nicotine, its major metabolite cotinine, and other tobacco alkaloids were indeed found to inhibit aromatase activity in human trophoblasts, granulosa cells, and breast cancer cells, presumably through direct competitive binding to the active site of the enzyme (7,8). This mechanism has not, to date, been demonstrated in neuronal tissues either in vitro or in vivo, although aromatase is expressed in the brain, and changes in brain aromatase activity have profound effects on behavior, cognition, and response to brain injury
 

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