Home | Pregnancy Timeline | News Alerts |News Archive Jan 13, 2014
There were also no findings among male offspring."We don't yet know why this is, but possible mechanisms include sex differences in stress hormone regulation in the placenta and adaptation to prenatal environmental exposures," added Dr. Laura Stroud, first author on this study.
Mom's stress, smoking increase daughter's risk of smoking
Tobacco smoking by pregnant women has long been viewed as a public health risk because of smoking's adverse effects on the development of a fetus.
Smoking during pregnancy is linked to numerous negative outcomes, including low birth weight, sudden infant death syndrome, and increased risk for attention deficit disorder, conduct disorder, and nicotine use in offspring.
Despite this extensive literature, it is estimated that 13%-30% of women in the United States continue to smoke while pregnant.
Now, a new 40-year longitudinal study, published in Biological Psychiatry, provides strong evidence that prenatal exposure to maternal stress hormones predicts nicotine dependence later in life – but only for daughters. It also confirms previous research that babies born to moms who smoked when pregnant have an increased risk of nicotine addiction in adulthood.
"While maternal smoking during pregnancy has been shown to be an independent risk factor for nicotine dependence, we didn't really know which pathways or mechanisms were responsible. Most prior research involving biological mechanisms had been conducted in animals not humans," said Dr. Laura Stroud, first author on this study and a researcher with the Centers for Behavioral and Preventive Medicine at The Miriam Hospital in Providence, RI.
"Our study suggests that maternal smoking and high stress hormones represent a 'double-hit' in terms of increasing an offspring's risk for nicotine addiction as an adult. Because mothers who smoke are often more stressed and living in adverse conditions — these findings represent a major public health concern."
Dr. Laura Stroud, first author on this study and a researcher with the Centers for Behavioral and Preventive Medicine at The Miriam Hospital in Providence, RI.
To conduct the study, Stroud and her colleagues used data from a large, national, long-term project that began in 1959 and enrolled over 50,000 pregnant women. The offspring of those women were ultimately followed by researchers for 40 years.
For this particular project, 1,086 mothers participated, where their hormone levels (cortisol and testosterone) were measured during pregnancy and their smoking status was recorded. Their children, 649 of whom were daughters and 437 of whom were sons, were interviewed as adults and their smoking status was also recorded.
The findings revealed that in female but not male offspring, elevated prenatal cortisol exposure and exposure to maternal smoking during pregnancy were associated with increased rates of nicotine dependence as adults.
No links were found between elevated prenatal testosterone exposure and adult nicotine dependence. There were also no findings among male offspring.
"Our findings highlight the particular vulnerability of daughters to long-term adverse outcomes following maternal stress and smoking during pregnancy.
"We don't yet know why this is, but possible mechanisms include sex differences in stress hormone regulation in the placenta and adaptation to prenatal environmental exposures," added Stroud. "Also, cortisol and nicotine may affect developing male and female brains differently. Furthermore, if daughters of smoking mothers are more likely to grow up nicotine dependent, the result is dangerous cycle of intergenerational transmission of nicotine addiction."
Maternal smoking during pregnancy (MSDP) is an independent risk factor for offspring nicotine dependence (ND), but mechanisms remain unknown. We investigated prenatal glucocorticoid (cortisol) and androgen (testosterone) associations with offspring ND over 40 years and the possibility that prenatal glucocorticoids and androgens would mediate links between MSDP and offspring ND.
Participants were 1086 mother-adult offspring pairs (59% female) from the New England Family Study, a 40-year longitudinal follow-up of the Collaborative Perinatal Project. MSDP was assessed prospectively at each prenatal visit. Maternal cortisol, testosterone, and cotinine (nicotine metabolite) were assayed from third trimester maternal sera. Offspring lifetime ND was assessed via structured interview.
Significant bivariate associations emerged for: 1) MSDP/cotinine and lifetime ND; and 2) maternal cortisol and lifetime ND, for daughters only. In multivariate models, maternal cortisol and MSDP/cotinine remained significantly and independently associated with increased odds of lifetime ND of daughters. However, cortisol did not mediate the MSDP-lifetime ND relation. No associations emerged between maternal testosterone and offspring ND.
Results provide the first evidence in support of prenatal glucocorticoid programming of adult ND over 40 years in daughters only. Our study highlights two independent prenatal pathways leading to increased risk for ND in daughters: elevated prenatal glucocorticoids and MSDP/nicotine exposure. Daughter-specific effects of glucocorticoid and MSDP programming over 40 years highlight the breadth and persistence of sexually dimorphic programming effects in humans. Results do not support androgen programming of offspring ND.
The article: "Prenatal Glucocorticoids and Maternal Smoking During Pregnancy Independently Program Adult Nicotine Dependence in Daughters: A 40-Year Prospective Study" by Laura R. Stroud, George D. Papandonatos, Edmond Shenassa, Daniel Rodriguez, Raymond Niaura, Kaja Z. LeWinn, Lewis P. Lipsitt, and Stephen L. Buka (doi: 10.1016/j.biopsych.2013.07.024). The article appears in Biological Psychiatry, Volume 75, Issue 1 (January 1, 2014), published by Elsevier.
About Biological Psychiatry
Biological Psychiatry is the official journal of the Society of Biological Psychiatry, whose purpose is to promote excellence in scientific research and education in fields that investigate the nature, causes, mechanisms and treatments of disorders of thought, emotion, or behavior. In accord with this mission, this peer-reviewed, rapid-publication, international journal publishes both basic and clinical contributions from all disciplines and research areas relevant to the pathophysiology and treatment of major psychiatric disorders.
The journal publishes novel results of original research which represent an important new lead or significant impact on the field, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Reviews and commentaries that focus on topics of current research and interest are also encouraged.
Biological Psychiatry is one of the most selective and highly cited journals in the field of psychiatric neuroscience. It is ranked 4th out of 135 Psychiatry titles and 13th out of 251 Neurosciences titles in the Journal Citations Reports® published by Thomson Reuters. The 2012 Impact Factor score for Biological Psychiatry is 9.247.
Elsevier is a world-leading provider of scientific, technical and medical information products and services. The company works in partnership with the global science and health communities to publish more than 2,000 journals, including The Lancet and Cell, and 25,000 book titles, including major reference works from Mosby and Saunders. Elsevier's online solutions include ScienceDirect, Scopus, SciVal, Reaxys, ClinicalKey and Mosby's Suite, which enhance the productivity of science and health professionals, helping research and health care institutions deliver better outcomes more cost-effectively.
A global business headquartered in Amsterdam, Elsevier employs 7,000 people worldwide. The company is part of Reed Elsevier Group PLC, a world leading provider of professional information solutions in the Science, Medical, Legal and Risk and Business sectors, which is jointly owned by Reed Elsevier PLC and Reed Elsevier NV. The ticker symbols are REN (Euronext Amsterdam), REL (London Stock Exchange), RUK and ENL (New York Stock Exchange).