Prenatal teratogens and the development of adult mental illness

Watson, Jennifer Bunn; Mednick, Sarnoff A.; Huttunen, Matti; Wang, Xueyi

doi:10.1017/s0954579499002151

Cited by 211 publications

(139 citation statements)

References 6 publications

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“…Lifetime maternal PTSD symptoms have also been shown to dosedependently associate with offspring PTSD symptoms in the general population (Roberts et al, 2012). Comparable findings have been observed in studies of offspring prenatally exposed to nuclear and natural disaster, where offspring of affected parents exhibited greater rates of depression and attention deficit hyperactivity disorder symptoms (Watson et al, 1999;Huizink et al, 2007).…”

Section: Clinical Observations and Significancementioning

confidence: 89%

Intergenerational Transmission of Stress in Humans

Bowers

Yehuda

2015

Neuropsychopharmacol

409

269

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The hypothesis that offspring are affected by parental trauma or stress exposure, first noted anecdotally, is now supported empirically by data from Holocaust survivor offspring cohorts and other populations. These findings have been extended to less extreme forms of stress, where differential physical, behavioral, and cognitive outcomes are observed in affected offspring. Parental stress-mediated effects in offspring could be explained by genetics or social learning theory. Alternatively, biological variations stemming from stress exposure in parents could more directly have an impact on offspring, a concept we refer to here as 'intergenerational transmission', via changes to gametes and the gestational uterine environment. We further extend this definition to include the transmission of stress to offspring via early postnatal care, as animal studies demonstrate the importance of early maternal care of pups in affecting offsprings' long-term behavioral changes. Here, we review clinical observations in offspring, noting that offspring of stress-or trauma-exposed parents may be at greater risk for physical, behavioral, and cognitive problems, as well as psychopathology. Furthermore, we review findings concerning offspring biological correlates of parental stress, in particular, offspring neuroendocrine, epigenetic, and neuroanatomical changes, in an attempt to determine the extent of parental stress effects. Although understanding the etiology of effects in offspring is currently impeded by methodological constraints, and limitations in our knowledge, we summarize current information and conclude by presenting hypotheses that have been prompted by recent studies in the field.

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Section: Clinical Observations and Significancementioning

confidence: 89%

Intergenerational Transmission of Stress in Humans

Bowers

Yehuda

2015

Neuropsychopharmacol

409

269

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“…In addition, traumatic events not involving abuse, such as parental loss early in life, are associated with developing major depression, anxiety disorders, and schizophrenia in adulthood (Agid et al, 1999;Kendler et al, 1992). Even prenatal stress, because of infection, malnutrition, or maternal psychological stress, is a significant risk factor for developing mental illness in adulthood (Brown et al, 2000(Brown et al, , 2004St Clair et al, 2005;Stein et al, 2009;Watson et al, 1999). In women with major depression, childhood abuse is correlated with smaller hippocampal volume, suggesting long-lasting effects of developmental experience on hippocampal structure in humans (Vythilingam et al, 2002).…”

Section: Effects Of Early-life Experiences On Adult Neurogenesis and mentioning

confidence: 99%

Adult Neurogenesis and Mental Illness

Schoenfeld

Cameron

2014

Neuropsychopharmacol

162

108

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Several lines of evidence suggest that adult neurogenesis, the production of new neurons in adulthood, may play a role in psychiatric disorders, including depression, anxiety, and schizophrenia. Medications and other treatments for mental disorders often promote the proliferation of new neurons; the time course for maturation and integration of new neurons in circuitry parallels the delayed efficacy of psychiatric therapies; adverse and beneficial experiences similarly affect development of mental illness and neurogenesis; and ablation of new neurons in adulthood alters the behavioral impact of drugs in animal models. At present, the links between adult neurogenesis and depression seem stronger than those suggesting a relationship between new neurons and anxiety or schizophrenia. Yet, even in the case of depression there is currently no direct evidence for a causative role. This article reviews the data relating adult neurogenesis to mental illness and discusses where research needs to head in the future.

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“…It has been reported, for example, that the prevalence of depression was increased in children prenatally exposed to the earthquake in Tangshan, China, in 1976. 156 In rat studies, PS has been reported to result in developmental abnormalities that may have long-term detrimental consequences for brain functioning and may lead to increased susceptibility to psychopathology, including depression, in adulthood. 157,158 Prenatal stressors such as repeated saline injections, daily restraint stress, or crowding (for review see Kofman, 126 Maccari et al 135 ) have been associated with several deficits in the offspring, such as reduced birth weight, increased infant morbidity, locomotor and cognitive retardation, circadian abnormalities and sleep disturbances, alterations in sexual or social behavior, and learning deficits.…”

Section: Stressmentioning

confidence: 99%

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

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In recent years, the term serotonergic vulnerability (SV) has been used in scientific literature, but so far it has not been explicitly defined. This review article attempts to elucidate the SV concept. SV can be defined as increased sensitivity to natural or experimental alterations of the serotonergic (5-HTergic) system. Several factors that may disrupt the 5-HTergic system and hence contribute to SV are discussed, including genetic factors, female gender, personality characteristics, several types of stress and drug use. It is explained that SV can be demonstrated by means of manipulations of the 5-HTergic system, such as 5-HT challenges or acute tryptophan depletion (ATD). Results of 5-HT challenge studies and ATD studies are discussed in terms of their implications for the concept of SV. A model is proposed in which a combination of various factors that may compromise 5-HT functioning in one person can result in depression or other 5-HT-related pathology. By manipulating 5-HT levels, in particular with ATD, vulnerable subjects may be identified before pathology initiates, providing the opportunity to take preventive action. Although it is not likely that this model applies to all cases of depression, or is able to identify all vulnerable subjects, the strength of the model is that it may enable identification of vulnerable subjects before the 5-HT related pathology occurs. Molecular Psychiatry ( Keywords: serotonin; mood disorders; stress; genetics; sex; tryptophan Involvement of serotonin in depressionMood disorders are one of the most prevalent forms of mental illness. 1 According to the DSM-IV, the lifetime risk for major depressive disorder is between 10 and 25% for women and between 5 and 12% for men. 2 Depression has been studied intensively during the last few decades, but the psychological and neurobiological determinants of depression have not yet been precisely defined. Although several factors are known to contribute to the etiology of depression, it is not clear how these factors cause depression, and why some subjects become depressed while others remain unaffected. In terms of biological factors in the etiology of depression, there are several hypotheses. These include neurotransmitter dysfunctions (serotonin, 5-HT; dopamine, DA; norepinephrine, NE); dysregulations in hypothalamic-pituitary-adrenal (HPA) axis activity; and immune system imbalance. The aim of this article is not to discuss all of these hypotheses in detail, but to evaluate the role that serotonin may play within these hypothesized mechanisms.It is widely accepted that diminished serotonergic (5-HTergic) function is involved in the onset and course of depression. 3,4 The 5-HTergic system is a large and complex system. Although nearly all cell bodies of 5-HTergic neurons are located in the raphe nuclei in the brain stem, the axons of these neurons innervate almost the entire brain. The actions of 5-HT are mediated by 16 types and subtypes of receptors. 5 As the 5-HTergic system is assumed to be a modulatory system, the exact func...

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Prenatal teratogens and the development of adult mental illness

Cited by 211 publications

References 6 publications

Intergenerational Transmission of Stress in Humans

Intergenerational Transmission of Stress in Humans

Adult Neurogenesis and Mental Illness

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

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