Smoking During Pregnancy and Infantile GI Dysregulation
Grantee: Brown University
Principal Investigator: Edmond Shenassa
Project Number: R40MC07660 (R40MC03600)
Project Date: 09/01/2004
Final Report
Smoking During Pregnancy and Infantile GI Dysregulation Final Report (PDF)
Age group(s)
- Women/Maternal
- Perinatal/Infancy (0-12 months)
Abstract
Purpose: Following MCHB's research priority IV: "Promoting the healthy development of MCH populations", we propose the first ever investigation of a physiologically plausible link between maternal smoking and infantile colic (IC). Background and significance: Intensely distressing to the infant, colic is also distressing for the caretaker. Caretakers of infants with colic have been reported as depressed, exhausted, and angry. Moreover, to the extent that caretakers of colicky infants provide fewer positive responses to their infants, colic may hinder attachment to the care-taker with serious long-term consequences. Presence of a colicky child can also adversely effect family functioning. Despite the high prevalence of colic, there is no consensus regarding its cause. Moreover, existing treatments for colic have, at best, limited efficacy in reducing infant distress. Therefore, it is important to conduct practical research to identify modifiable risk(s) for IC. Such research endeavors can be particularly beneficial to maternal and child health when they can also shed light on the pathophysiology of IC; thus, allowing development of potentially effective clinical interventions. Proposed Study: Accumulating evidence suggests exposure to cigarette smoke or its metabolites may be linked with IC. Moreover, recent studies of the gastrointestinal system provide strong, but indirect, corroborating evidence by suggesting physiologic mechanisms by which maternal smoking can be linked with the offspring's colic. This evidence can be outlined as follows: 1) smoking is linked with increased levels of plasma and intestinal motilin, and 2) higher than average levels of motilin are linked with elevated risk of IC. Although these findings from disparate fields provide a cohesive hypothesis for the physiologic mechanism linking maternal smoking with IC, the entire chain of events has not yet been examined among a single cohort, nor has the link between maternal smoking and IC been replicated in a study that simultaneously considers all sources of pre and perinatal exposure to tobacco smoke. Herein we propose to examine the chain of events within a single cohort of mothers and their infants. Discussion: Findings from the proposed investigation can have significant public health and clinical implications. The public health implications of the proposed research regard prevention IC as well as maternal smoking, particularly during and immediately after pregnancy. Prevention of colic can have a multitude of health promoting effects for both the mother and the infant. Moreover, in the U.S. alone, nearly half of all women smokers continue to smoke through their pregnancies; this amounts to about 12% of all women who give birth and over half million infants who are annually exposed to cigarette smoke prenatally. Further evidence of a link between maternal smoking and IC among offspring can provide strong additional incentive for pregnant women to quit smoking. Discovery of a link between maternal smoking, motilin, and IC would also provide preliminary support for therapeutic agents that can act as a motilin antagonists.Publications
Listed is descending order by year published.
Shenassa ED, Daskalakis C. Smoking cessation and prevention: implications of study design, research setting, and goals. In: Fong CB, ed. Smoking and Health Research Frontiers. New York, NY: Nova Science Publishers; 2007:1-8.
Morello-Frosch R, Shenassa ED. The environmental "riskscape" and social inequality: implications for explaining maternal and child health disparities. Environ Health Perspect. 2006 Aug;114(8):1150-1153.
Shenassa ED, Brown MJ. Maternal smoking and infantile gastrointestinal dysregulation: the case of colic. Pediatrics. 2004 Oct;114(4):e497-e505.
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