Nicotine brain damage in first trimester embryo

Professor Theodore A. Slotkin, a Duke Medical University toxicologist, has written a disturbing review of the destructive impact of fetal and adolescent nicotine upon the  developing animal brain. Slotkin not only teaches how nicotine hijacks and alters the trajectory of normal brain development, he shares slides of cellular damage inflicted by nicotine in the neural tube stage in rats, the embryotic stage during which the brain first begins to unfold, a stage that starts in human embryos within 3 to 4 weeks of conception.

As Slotkin points out, "the cost of tobacco-related developmental damage includes immediate perinatal events, such as spontaneous abortions, intrauterine growth retardation and perinatal deaths, and Sudden Infant Death Syndrome, but the consequences extend much further, encompassing subsequent learning disabilities, cognitive dysfunction, behavioral problems, attention deficit hyperactivity disorder, psychiatric disorders, conduct disorders, criminal behaviors and school and career failure."

In February I completed presenting 63 nicotine cessation seminars in my 28 state prisons, prisons where an average of 60% of inmates were recent slaves to nicotine. I have followed Slotkin's studies, including a frightening paper on how nicotine damages brain serotonin pathways, the neurochemical believed responsible for impulse control. I often found myself speculating on the number of audience faces that would be absent if, at crunch time, the moment prior to their crime, serotonin levels had been adequate and their rational, thinking mind had a greater degree of control over their impulsive mind.

Published in the February issue of Neurotoxicology and Teratology, Slotkin's latest paper is entitled, "If nicotine is a developmental neurotoxicant in animal studies, dare we recommend nicotine replacement therapy in pregnant women and adolescents. If you would like to read a full text PFF copy of the article let me know and I'll forward it - john@whyquit.com .

It has long been known that the nicotine molecule mimics and imitates the neurotransmitter acetylcholine by attaching to and activating certain types of acetylcholine receptors. Slotkin teaches how nicotine disrupts normal brain development by activating acetylcholine receptors early and with inappropriate intensity, before the brain neuron the receptor is attached to has had an opportunity to fully develop and properly interface with surrounding brain neurons.

According to Slotkin, "excessive stimulation of [acetylcholine receptors] by nicotine produces profound disruption at both cellular and architectural levels," with damage beginning as early as the first trimester of pregnancy.

"Fetal nicotine exposure alters the trajectory of neurodevelopment, so that defects continue to emerge over the life span," including "enhanced susceptibility to nicotine dependence and addiction in adolescence."

"It is increasingly clear that brain development extends into adolescence," but "at a lower level of activity than in the fetus or neonate." It is here that acetylcholine receptors in both the rational thinking mind and brain dopamine reward pathways were supposed to mature. But "approximately 3,000 teenagers begin smoking each day, with the majority becoming daily smokers," often with devastating developmental results -- including poor cell signaling -- that appear worse the earlier chronic smoking is initiated.

The adolescent nicotine dependent brain somehow grows or activates (upregulates) the total number of acetylcholine receptors, especially in the midbrain's reward pathways, pathways key to dependency onset, desensitization and tolerance. Slotkin cites studies, including his own, showing how "nicotine remains neurotoxic in the adolescent brain, producing persistent damage with permanent consequences," including both transient and permanent alterations to serotonin pathways.

Professor Slotkin is deeply concerned that the medical community has failed to "recognize the magnitude of the problem" or champion effective countermeasures in coming to the defense of healthy and natural fetal and youth development.

"The fact that nicotine in the adolescent brain, like the fetal brain, elicits neuronal and synaptic damage, and long-term alterations in synaptic function, means that there is likely to be a biological basis for increased susceptibility to nicotine dependence and long-term, adverse consequences during this late developmental stage. And we must not overlook the fact that the persistent changes are driven by nicotine itself, not other components of tobacco smoke; obviously this argues against the suitability of NRT for smoking cessation in this age group."

What seems to alarm Slotkin most is the fact that fetal nicotine harms, including dependency susceptibility, are compounded by adolescent nicotine damage. As Slotkin puts it, "the interaction of prenatal and adolescent nicotine goes beyond the issue of increased drug intake. At the level of neural cell damage and loss, as well as for persistent deficits in synaptic activity of cholinergic and serotonergic systems, the effects are enhanced by the double treatment."

The combination of fetal and adolescent nicotine appears to destroy protections afforded the female brain, protections the male brain did not enjoy. Where lasting neuro cell damage and behavioral deficits are normally greater in males than females after either prenatal or adolescent nicotine exposure alone, those female protections are lost upon nicotine exposure during both periods.

NRT Use During Pregnancy or Adolescence

In that nicotine is a potent neurotoxicant that adversely effects brain development and synaptic function, Slotkin is troubled by those advocating that expectant or mothers or youth use nicotine replacement products (NRT). He argues that prior to making such recommendations proponents should have to prove that doing so is not only both safe and effective, but more effective than quitting without pharmacology. Slotkin cites studies showing that NRT has not proven effective in either group. One NRT pregnancy study actually had to be discontinued after a 50% increase in adverse birth and neonatal outcomes. In a smaller study, 3 out of 21 infants showed severe neonatal morbidity and in another NRT increased the rate of congenital malformations.

While a number of harm reduction activists continue to falsely portray nicotine as being no more harmful than caffeine, Slotkin points to the fact that, "a number of animal studies of environmental tobacco smoke exposure, both in rodents and primates, point to virtually identical outcomes to those seen with nicotine alone." Those harms include neuronal and synaptic damage, cognitive dysfunction, adverse lung development, immune function and cardiorespiratory function.

As for successful smoking cessation during pregnancy or adolescence, Slotkin concludes by noting that instead of turning to interventions that have proven both unsafe and ineffective that "it is mandatory that we focus instead on non-pharmacologic interventions to achieve the important goals of smoking cessation in these groups."

Key to success with both groups is teaching them how nicotine enslaved their brain reward pathways. They need to understand how their dopamine reward and species survival event pathways quickly buried nearly all remaining memory of the beauty of life without nicotine. They need to appreciate how their limbic mind now sees smoking nicotine nearly the same as eating food, how thoughts of either tease them with dopamine "aaah" reward sensations, how doing either generate even bigger "aaah"s, and how if they wait too long prior to eating or smoking that the limbic mind's insulas will punish them with urges, anxieties and full blown craves. What they need to understand is while they cannot live without food, life will soon be be better without nicotine.

They must be made to appreciate that their addicted inner brain has been rewired (upregulation), that their dependency is as permanent as alcoholism, and that the secret to breaking free is in keeping 100% nicotine out of their bloodstream. They need to understand that when quitting they are not fighting a whole pack or even a whole cigarette but just that one powerful puff of nicotine that would, within 8-10 seconds, cause 40% of their brain's acetylcholine receptors to be occupied, generating a powerful dopamine "aaah" explosion that their mind's pay attention pathways will make nearly impossible, in the short term, to forget, that their mind would soon be begging for more.

The beauty of admitting that smoking is not just some nasty little habit but instead a true chemical addiction -- in seeing ourselves as true drug addicts in every sense -- is that it makes the rules to quitting simple. Like the alcoholic experiencing relapse after just one sip, the mind games are over. It's all or nothing. There is no figuring it out, no having our cake and eating it too. It paints a bright line in the sand, that on one side says "all" and on the other "nothing."

Looking in the mirror and seeing a true drug addict looking back destroys the need for the scores of lies our conscious thinking mind invented to explain why we had to obey the endless stream of urges, craves and anxieties flowing from our insulas. It allows us to cast aside rationalizations such as taste, boredom, flavor, pleasure, like or love. Truth is, we smoked nicotine because we had to, because a rising tide of anxieties started to hurt when we didn't. We didn't smoke because we liked smoking. We smoked because we didn't like what happened when we didn't smoke.

To learn more about nicotine dependency recovery visit and expore WhyQuit. The site is totally free, staffed entirely by volunteers, sells nothing and all offers of donations are declined. Coming home to the real you involves just one guiding principle ... no nicotine just one hour, challenge and day at a time, Never Take Another Puff!

John (Gold x8)