The use of pharmacotherapies for smoking cessation during pregnancy

Nl, Benowitz; Da, Dempsey; Goldenberg, Renato; Hughes, Victoria; Dolan-Mullen, Patricia; Pl, Ogburn; Oncken, Cheryl; Ct, Orleans; Slotkin, T A; Hp, Whiteside; Yaffe, Sumner J.

doi:10.1136/tc.9.suppl_3.iii91

Cited by 49 publications

(33 citation statements)

References 13 publications

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“…A subsequent conference, organised in collaboration with the National Institute of Child Health and Development, explored the risks and benefits of pharmacotherapy to revise current guidelines for nicotine replacement and other approved products for pregnant and lactating women. 37 The fruits of these eVorts have been shared with the expert panel compiling the updated AHCPR guideline, and will be reflected in the revised year 2000 guideline. 36 To improve on current best practice and pave …”

Section: -28mentioning

confidence: 99%

Helping pregnant smokers quit: meeting the challenge in the next decade

Rw²,

Dc³

et al. 2001

Western Journal of Medicine

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Section: -28mentioning

confidence: 99%

Helping pregnant smokers quit: meeting the challenge in the next decade

Rw²,

Dc³

et al. 2001

Western Journal of Medicine

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“…Animal models, chiefly in rodents, have shown that nicotine is a neuroteratogen that targets neural replication and differentiation, synaptic development and synaptic activity, culminating in functional deficits and cognitive impairment that parallel the findings in offspring of smokers (Levin and Slotkin, 1998;Slotkin, 1992Slotkin, , 1999Slotkin, , 2004. Thus, although tobacco smoke contains thousands of bioactive compounds, nicotine by itself contributes significantly to fetal brain damage and its functional consequences, a factor that must be taken into account in smoking cessation strategies that utilize nicotine replacement therapy (Benowitz et al, 2000). Nicotine affects brain development because it stimulates nicotinic acetylcholine receptors (nAChRs); in the immature brain, acetylcholine, among other neurotransmitters, plays a critical neurotrophic role in determining the patterns of cell development (Lauder and Schambra, 1999;Weiss et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Effects of Prenatal Nicotine Exposure on Primate Brain Development and Attempted Amelioration with Supplemental Choline or Vitamin C: Neurotransmitter Receptors, Cell Signaling and Cell Development Biomarkers in Fetal Brain Regions of Rhesus Monkeys

Slotkin

Seidler

Qiao

et al. 2004

Neuropsychopharmacol

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Studies in developing rodents indicate that nicotine is a neuroteratogen that disrupts brain development by stimulating nicotinic acetylcholine receptors (nAChRs) that control neural cell replication and differentiation. We administered nicotine to pregnant Rhesus monkeys from gestational day 30 through 160 by continuous infusion, achieving maternal plasma levels comparable to those in smokers (30 ng/ml). Fetal brain regions and peripheral tissues were examined for nAChR subtypes, other neurotransmitter receptors, and indices of cell signaling and cell damage. Nicotine evoked nAChR upregulation, but with distinct regional disparities indicative of selective stimulatory responses. Similarly, indices of cell loss (reduced DNA), cell size and neuritic outgrowth (protein/DNA and membrane/total protein ratios) were distinct for each region and did not necessarily follow the rank order of nAChR upregulation, suggesting the involvement of additional mechanisms such as oxidative stress. We then attempted to offset the adverse effects of nicotine with standard dietary supplements known to interact with nicotine. By itself, choline elicited nicotine-like actions commensurate with its promotion of cholinergic neurotransmission. When given in combination with nicotine, choline protected some regions from damage but worsened nicotine's effects in other regions. Similarly, Vitamin C supplementation had mixed effects, increasing nAChR responses while providing protection from cell damage in the caudate, the brain region most susceptible to oxidative stress. Our results indicate that nicotine elicits neurodevelopmental damage that is highly selective for different brain regions, and that dietary supplements ordinarily thought to be neuroprotectant may actually worsen some of the adverse effects of nicotine on the fetal brain.

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“…38,49 Furthermore, nearly all benefits of brief counseling occur only in light to moderate smokers. For heavy smokers who do not respond to counseling and behavioral therapy, pharmacotherapy offers another, albeit controversial, alternative.…”

Section: Pharmacotherapiesmentioning

confidence: 99%

Smoking Cessation in Pregnancy: Why, How, and What Next…

Crawford

Tolosa²,

Goldenberg

2008

Clinical Obstetrics &Amp; Gynecology

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Smoking cessation in pregnancy has been shown to reduce low birth weight, preterm birth, and infant morbidities. The effectiveness and safety profile of current cessation approaches in pregnancy are presented. The highest cessation rates are associated with counseling and behavioral interventions. Further studies are needed to evaluate the safety and efficacy of pharmacotherapy in pregnancy including nicotine replacement therapy, bupropion and the recently approved drug Varenicline. The risks and benefits of nicotine replacement therapy in heavy smokers and bupropion are discussed. Data on fetal risk are not yet available for Varenicline.

show abstract

The use of pharmacotherapies for smoking cessation during pregnancy

Cited by 49 publications

References 13 publications

Helping pregnant smokers quit: meeting the challenge in the next decade

Helping pregnant smokers quit: meeting the challenge in the next decade

Effects of Prenatal Nicotine Exposure on Primate Brain Development and Attempted Amelioration with Supplemental Choline or Vitamin C: Neurotransmitter Receptors, Cell Signaling and Cell Development Biomarkers in Fetal Brain Regions of Rhesus Monkeys

Smoking Cessation in Pregnancy: Why, How, and What Next…

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