Association Between Maternal Smoking During Pregnancy and Severe Mental Illness in Offspring

Quinn, Patrick D.; Rickert, Martin E.; Weibull, Caroline E.; Johansson, Anna L.V.; Lichtenstein, Paul; Almqvist, Catarina; Larsson, Henrik; Iliadou, Anastasia; D’Onofrio, Brian M.

doi:10.1001/jamapsychiatry.2017.0456

Cited by 66 publications

(66 citation statements)

References 54 publications

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“…In this population study of 1.7 million Swedish offspring, maternal smoking during pregnancy was associated with an increased risk of severe mental illness in offspring. However, after comparing siblings, which accounted for all genetic and environmental confounders that make siblings similar, the relationship was weaker and no longer significant (Quinn et al, ). These findings, in combination with the results of our analysis, suggest that increased risk for the development of mental illness may be accounted for by a shared risk for both outcomes.…”

Section: Discussionmentioning

confidence: 99%

Tobacco use and psychosis risk in persons at clinical high risk

Ward

Lawson

Addington

et al. 2018

Early Intervention Psych

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Aim: To evaluate the role of tobacco use in the development of psychosis in individuals at clinical high risk. Method: The North American Prodrome Longitudinal Study is a 2-year multi-site prospective case control study of persons at clinical high risk that aims to better understand predictors and mechanisms for the development of psychosis. The cohort consisted of 764 clinical high risk and 279 healthy comparison subjects. Clinical assessments included tobacco and substance use and several risk factors associated with smoking in general population studies.Results: Clinical high risk subjects were more likely to smoke cigarettes than unaffected subjects (light smoking odds ratio [OR] = 3.0, 95% confidence interval [CI] = 1.9-5; heavy smoking OR = 4.8, 95% CI = 1.7-13.7). In both groups, smoking was associated with mood, substance use, stress and perceived discrimination and in clinical high risk subjects with childhood emotional neglect and adaption to school. Clinical high risk subjects reported higher rates of several factors previously associated with smoking, including substance use, anxiety, trauma and perceived discrimination. After controlling for these potential factors, the relationship between clinical high risk state and smoking was no longer significant (light smoking OR = 0.9, 95% CI = 0.4-2.2; heavy smoking OR = 0.3, 95% CI = 0.05-2.3). Moreover, baseline smoking status (hazard ratio [HR] = 1.16, 95% CI = 0.82-1.65) and categorization as ever smoked (HR = 1.3, 95% CI = 0.8-2.1) did not predict time to conversion.Conclusion: Persons at high risk for psychosis are more likely to smoke and have more factors associated with smoking than controls. Smoking status in clinical high risk subjects does not predict conversion. These findings do not support a causal relationship between smoking and psychosis. K E Y W O R D Sclinical high risk, psychosis, schizophrenia, substance use disorder, tobacco

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Section: Discussionmentioning

confidence: 99%

Tobacco use and psychosis risk in persons at clinical high risk

Ward

Lawson

Addington

et al. 2018

Early Intervention Psych

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“…Epidemiological studies have discovered the link between maternal cigarette smoking during pregnancy and the alteration in neurocognitive functions in the offspring (eg. schizophrenia) . Size matters, which applies well with cognitive performance.…”

Section: Maternal Cigarette Smoking and Neurocognitive Outcomesmentioning

confidence: 95%

What lessons have we learnt about the impact of maternal cigarette smoking from animal models?

Chan

Oliver

Chen

2019

Clin Exp Pharma Physio

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Maternal first‐ or second‐hand tobacco smoking during pregnancy is still common albeit that the detrimental effects to the unborn child are well known. Maternal tobacco cigarette smoking can affect multiple organ systems in the offspring, rendering them at increased risk of various conditions throughout life (eg. intrauterine underdevelopment, asthma, substance abuse, diabetes). However, this review will only focus on its impact on the brain and the related molecular changes in the offspring based on evidence from animal studies. Although epidemiological studies have identified the associations between maternal cigarette smoke exposure (SE) and brain disorders, animal models can help identify the underlying mechanisms and test interventions. Human studies have found that maternal SE is closely linked to small brain size and changes in brain structure and associated with a high risk of cognitive defects. Animal models suggest that this may be due to increased brain oxidative stress and inflammation during the neonatal period, leading to increased brain cell apoptosis in adulthood. There is a distinct gender bias of such impacts, where male offspring are more affected than females. Female offspring seem to have developed the adaptation by increasing endogenous antioxidant levels. Indeed, animal studies have shown that using antioxidant supplementation during pregnancy can improve neurological outcomes in male offspring, however, the efficacy in humans is yet to be confirmed. Furthermore, some animal studies suggested nicotine as the key player in intrauterine underdevelopment due to maternal SE, while human clinical trials using nicotine replacement therapy do not support this mechanism. This review will discuss the possible reasons.

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“…The Quinn et al 1 results are relatively convincing. The SDP-SMI association is substantially attenuated with measured confounders and discordant cousin pairs.…”

mentioning

confidence: 89%

“…When, as in Quinn et al, 1 the exposure outcome relationship is substantially attenuated in co-relative pairs, one can be relatively confident that familial confounders are at work, so that causal processes alone cannot explain the findings. However, when the association does not attenuate in co-relative designs, more caution is needed.…”

mentioning

confidence: 90%