Working in a pre-natal clinic for the past six years, I have frequently found myself trying to convince pregnant women to quit smoking. I have always cited the usual reasons such as, low fetal birth weight, increased risk of SIDS, and as some studies suggest low cognitive ability. However, there is not much insight as to why nicotine has such detrimental affects on the developing fetal brain. A recent study in rhesus macaques preformed by Slotkin, Seidler, and Spindel spreads some light on the possible reasons smoking can increase the risk of sudden infant death syndrome in primates and the use of vitamin C to decrease these risks (Slotkin et al. 2011).
The researchers administered intravenous nicotine to pregnant macaques from day 30 of gestation to day160 at levels that would be comparable to a human female smoking 20 cigarettes a day. They then looked at the neurochemical parameters directly following birth (Slotkin et al. 2011). Nicotine caused elevations in brainstem serotonin levels and serotonin turnover, indicating hyperactivity of these pathways. The treatment also caused a deficit in cardiac norepinephrine because of a decrease in the sympathetic input. Brainstem serotonin hyperinnervation and deficit cardiac sympathetic innervations are both consistent with increased risk of hypoxia and SIDS (Slotkin et al. 2011). Examination of tissues from human infants that died of SIDS found an increase in 5HT neuron density and a decrease in 5HT receptor. These sites are involved in autonomic function, arousal, and cardio respiratory responses to physiological challenges such as hypoxia (Slotkin et al. 2011). In the macaque model when nicotine is administered prenatally, elevations in both 5HT concentration and 5HT turnover increased, indicating hyperactivity (Slotkin et al. 2011). However, researchers found co-administration of vitamin C prevented the increase 5HT turnover and decreased the in cardiac norepinephrine levels two factors believed to be liked to SIDS (Slotkin et al. 2011).
This research by no means provides a substitute for women quitting smoking while pregnant. However, it does provide a reasonable option for clinicians to consider in helping to lower the risk of SIDS in women who smoke. The research also provides some explanation of why nicotine has adverse effects on the developing brain. It is important to note that low fetal birth weight and increased risk of asthma are most commonly associated with smoking and pregnancy. This study does not address those affects nor the role vitamin C plays in influencing them.
Theodore A. Slotkin, Frederic J. Seidler, Eliot R. Spindel, Prenatal nicotine exposure in rhesus monkeys compromises development of brainstem and cardiac monoamine pathways involved in perinatal adaptation and sudden infant death syndrome: Amelioration by Vitamin C. Neurotoxicology and Teratology, Volume 33, Issue 3, May-June 2011, Pages 431-434, ISSN 0892-0362. (http://www.sciencedirect.com/science/article/pii/S0892036211000079)
It is amazing that something as simple as consuming more Vitamin C could decrease the likelihood of SIDs. In a research regarding SIDs and consumption of Vitamin C it was discovered over two hundred years ago that deficiency of Vitamin C increased the occurrence of SIDs. Fifty percent of babies born in a region within Australia were dying of SIDs. It was discovered that SIDs occurred shortly after infants received their vaccines. The infants who died were tested and found to have very low levels of Vitamin C. The article states that the infants did not have enough Vitamin C in their system to counteract the toxic effects from the vaccine. Could SIDs occur in babies whose mother smoked during their pregnancies be the same reason why SIDs occurred in babies who received vaccines? If so then this could be of clinical significance in the decrease of SIDs in women who smoke during their pregnancy.
ReplyDeleteThis also brings up the question on whether vaccines are more beneficial than harmful.
According to physiology textbooks nicotine is used as a sympathetic neurotransmitter. This made me wonder why anyone would want to smoke a cigarette that theoretically would increase sympathetic response to calm their nerves. This question turned out to be much harder to answer than I thought. There appears to be short-term and long-term mechanisms.
ReplyDeleteShort-term: Although the parasympathetic Ach can act on nAChRs expressed in the preganglionic synapses in both the sympathetic AND the parasympathetic nervous system. Since nicotine is an agonist of nACh receptors, you then get some effects that are sympathetic-mediated, and some that are parasympathetic-mediated.
Long-term: Prolonged exposure to nicotine can lead to receptor desensitization. So chronic nicotine users likely do feel more relaxed, simply because they will not respond to ACh in the same way when they are nervous.
After speaking with several professors and reading a bit online, I’ve found when nicotine is bound to cholinergic receptors it can cause a very wide range of neurotransmitters to be released depending on location, such as dopamine and serotonin-hence the good feeling/addictive properties of smoking. There is also a release of epinephrine from the adrenal medulla which causes vasoconstriction and increases HR and BP.
Reference:
Campisi, Jay, and Mark V. Reedy. "Nicotine." 18 Nov. 2011. E-mail.