Prenatal stress (or prenatal maternal stress) is exposure of an expectant mother to psychosocial or physical stress, which can be caused by daily life events or by environmental hardships. [1] [2] This psychosocial or physical stress that the expectant mother is experiencing has an effect on the fetus. According to the Developmental Origins of Health and Disease (DOHaD), a wide range of environmental factors a woman may experience during the perinatal period can contribute to biological impacts and changes in the fetus that then causes health risks later in the child's life. [3]
Health risks include impaired cognitive development, low birth weight, and risk of mental disorders in the offspring. [2]
Studies have been conducted longitudinally in order to explore the way that prenatal stress impacts the fetus and its development. These studies took place over the course of the pregnancy and months after in order to collect the data necessary. The stress of the mothers was assessed using self-questionnaires like the Perceived Stress Scale (PSS) [4] [5] and the Patient Health Questionnaire-8 (PHQ8). [5]
While focusing on the stress of the mothers during the pregnancy, researchers also focused on the hypothalamic-pituitary adrenal axis (HPA axis) which is a set of glucocorticoid feedback interactions through the mother to the placenta and then to the fetus. [5] By focusing on the HPA axis, researchers can see how prenatal stress affects fetal development.
Some research includes studies like McKenna et al. suggesting that the idea of pregnancy can cause an increased risk of psychopathology and these exposures during gestation impacts epigenetic. [3] The mother's usage of selective serotonin repute inhibitors (SSRIs) was observed while the epigenetic age of the child was calculated through fetal umbilical cord blood. [3]
Saboory et al. found that prenatal psychosocial stress can cause delays in child growth and development through assessing the child's weight, height and head circumference every two months after they were born. [4] They also assessed the child's cognitive development through the use of the Ages and Stages Questionnaire (ASQ). [4]
Another study, Brannigan et al. focused on how prenatal stress contributes to personality disorders by looking at children decades later born from mothers who spent time in a mental health clinic in Finland. [6]
This research all found negative correlations between prenatal stress and the child's development.
Stress during the development of the fetus can be inherited and change the gene expression in the fetus. [7] This change is an epigenetic change that modifies but does not affect the building of the DNA sequence. This modification will affect whether the gene is turned off or on and will lead to Transgenerational Stress Inheritance. [8]
One of the pathways that has been studied is the inheritance of disrupted heterochromatin. Heterochromatin is important in many functions of the cell mostly in gene regulation. During high levels of stress during pregnancy dATF-2, which is required for formation of heterochromatin, will phosphorylate and disrupt the formation. This will lead to the release of dATF-2 from the heterochromatin, which then can be inherited in offspring. [9]
Another pathway that prenatal stress can interfere with fetal development is telomere length. [10] A telomere is a structure of repetitive DNA sequences that can be found at the end of chromosomes. They are made up of the same short DNA sequence that is repeated multiple times and serve to protect the ends of chromosomes so they do not become damaged. [11] Another function of telomeres is to allow chromosomes to properly function in the process of replication. However, each time a cell divides, the telomeres loses length and becomes shorter. After repeated replications they will eventually become so short that the cell is unable to divide any further and the cell will die. [10] When offspring are exposed to prenatal distress during development it can affect the length of the offspring's telomeres, more specifically it can result in shortened telomeres. [12] Shortened telomeres have been linked to multiple issues including shortened lifespan and increased risk of diseases. [13] Typically, telomeres shorten substantially with increasing age, and telomere length is thus a bioindicator of aging. However, prenatal stress puts offspring at an increased state of vulnerability by shortening the telomeres and leaving less room for shortening as the offspring continue to age. [12]
A study by Sandman and Davis [14] shows that the timing of prenatal stress is crucial to understanding how prenatal stress affects prenatal and postnatal development. Cortisol is often used to measure stress as it is a hormone that is released during stressful events. If an expectant mother is experiencing a stressful event such as income insecurity or being a teenage mother, cortisol is secreted as a result. [15] However, as demonstrated by Sandman and Davis, the timing of cortisol release can sometimes have a harmful effect on development and sometimes not depending on when in pregnancy stress is experienced. [14] Prenatal stress can increase the likelihood of maternal and endocrinological problems. Prenatal stress can even cause the embryo to arrive earlier than expected.
Sandman and Davis studied "125 full- term infants at 3, 6, and 12 months of age" [14] to determine the effects of maternal cortisol timing differences on development. They found that "exposure to elevated concentrations of cortisol early in gestation was associated with a slower rate of development over the 1st year and lower mental development scores at 12 months" and "elevated levels of maternal cortisol late in gestation were associated with accelerated cognitive development and higher scores at 12 months". [14] Overall, cortisol's effects on infant cognitive development are dependent upon the timing of cortisol release. [14] Furthermore, prenatal stress can have an effect on fetal development by causing obesity, diabetes, cardiovascular disease, and other problems.
Poor eating habits and lack of physical activity are not the only contributing factors to prenatal stress on the baby. Stress on the mother during pregnancy can lead to issues in cognitive development, social development and more. [16] A great deal of brain development happens during the fetal period in pregnancy and the progress happens rapidly in this stage. [17] Since there is such a large amount of growth occurring during this time-period in the child's life, there are a lot of outside factors in the environment that can affect this development. [17] These outside factors could be anything from poor nutrition, excess cortisol levels or even genetic influences. The fetus's development can be impacted through the level of the placenta, and there is evidence to show how prenatal stress can have consequences on the placenta and in turn the fetus during pregnancy. [16]
The resulting effects can impact many different areas of the developing child's brain, such as the hypothalamus, corpus callosum, amygdala, hippocampus, and cerebellum. Animal studies have shown that prenatal stress may result in reduced hippocampus volumes and amygdala nuclei volumes, both of which may have a negative impact on memory. [18] There is indirect evidence to suggest that prenatal stress could alter the size and morphology of the corpus callosum, and it is known that alterations in the corpus callosum are observed in autism, ADHD, and schizophrenia. [18] Furthermore, alterations to the cerebellum may also be involved in autism, ADHD, and schizophrenia, and prenatal stress may also play a role in altering the physiology of the cerebellum. Studies done in rats have shown that prenatal stress may affect the size and number of granule cells in the cerebellum, as well as cause an increase in the number of Purkinje cells. [18] Also shown in rats, there is evidence to suggest that prenatal stress can result in the feminization of males by reducing the volume one of the hypothalamic nuclei that is involved in the sexual behavior of males. [18]
These impacts have mostly been noted in animal studies because of the concerns that surround human studies with prenatal stress. [16] The ethical concerns with human studies and prenatal stress have led to little to no studies showing the direct impacts stress can have on fetal development, and it has shown to be difficult to draw inferences and connections between the animal studies and human pregnancies. [16] It has been suggested that one way to monitor the impact of stress on the infant's development is through the mother's exposure to natural disasters. There has been some research analyzing how natural disasters such as hurricanes can affect fetal development when the mother is exposed during pregnancy. [19] This research showed that there were impacts psychologically on the children who were exposed to this type of stress in the womb, in terms of increased risk for developing childhood psychopathologies. [19] Natural disaster research like this has shown the effects of stress on pregnancy without the issues that surround human research and is able to show results within humans instead of drawing from other animals.
Prenatal distress has been shown to increase the risk that the offspring will develop a mental disorder as well as the severity of some symptoms. Typical disorders that are increased due to prenatal distress include autism, the severity of ADHD, and the development of mood disorders. [20] Prenatal stress disrupts multiple developmental systems within the individual carrying offspring. One of the disrupted processes is hormone production. Maternal exposure to excess dihydrotestosterone, progestin, and norethindrone have been linked to a higher risk of offspring developing ASD. [21] A 2008 study found that children whose mothers experienced moderate to severe stress during their pregnancy tended to develop symptoms that more frequently fell on the severe side of the ADHD severity spectrum. This distinction was made in comparison to those with ADHD whose mothers were not exposed to prenatal stressors. [22] This increased development of ADHD from heightened prenatal distress can be due to many factors, one of the more popular and founded claims being the neurological development of the offspring. Exposure to stress during the process of pregnancy affects fetal brain development and predisposes offspring to the development of a multitude of mental disorders. [23] Many studies have found that there is an association between ADHD and lessened functioning within the prefrontal cortex (PFC). This area of the brain plays a crucial role in attention regulation as well as behavioral and emotional control. The PFC right hemisphere in particular has been linked to decreased size in individuals who have ADHD. [24] This is notable due to the important role of the PFC right hemisphere which is behavioral inhibition, a common struggle for individuals with ADHD. Prenatal distress has also been linked to the development of mood disorders such as depression or anxiety. A 2019 study found that prenatal distress, specifically during the first 20 weeks of gestation, was linked to higher mood dysregulation and lower grey matter (GM) volume. [25] The lessening of grey matter volume is a detrimental loss because of the multitude of functions that this structure is essential for. Grey matter is found throughout the central nervous system and is crucial for motor function, memory, and emotions. [26] The reduction of GM volume is impactful in many negative ways which is another contributing factor that can lead to the development of mental disorders in children that experience in utero stress.
Prenatal stress has increased as a result of the recent changes caused by the COVID-19 pandemic. Researchers are attempting to determine how the pandemic relates to prenatal stress, why so many women are experiencing stress and anxiety, and how these issues can be avoided. Researchers conducted a study by developing a questionnaire for pregnant women that included age, sex, race, health insurance status, financial status, any pregnancy risks, medical conditions, treatments, doctor's appointments, how many appointments were canceled due to COVID-19, and stress levels on a scale of mild, moderate, and severe. Three-quarters of the research participants were white or non-Hispanic, according to the questionnaire. There were 280 women who reported mild cases, 170 who reported moderate cases, and 171 who reported severe cases. Following the questionnaire, researchers discovered that mothers were experiencing high levels of anxiety and stress because they were afraid of contacting the covid virus and having the virus affect their fetus, having one person in the delivery room, and making online appointments without being checked in person. As a result, researchers proposed that there should be in-person engagement for the mother, information provided to the mother about COVID-19 and the protocols to reduce the risk of contacting it, and consistent check-in appointments to check the mother's mental health status. [27]
Pups that underwent prenatal stress showed lower plasma testosterone when compared to the control pups. This is caused by the disruption of prenatal development which did not allow the complete masculinization of the prenatally stressed pups’ central nervous system. In humans, prenatal stress affects development differently in boys and girls. Males may exhibit less masculine characteristics as a result of prenatal stress, whereas females may exhibit less feminine characteristics. Prenatal stress, on the other hand, can have serious consequences for both genders. [28]
Particularly in the striatum of the prenatally stressed male pups showed an increase in vanilmandelic acid, dopamine, serotonin, 5-hydroxyindoleacetic acid which all can affect sexual behavior. The prenatally stressed male pups showed a significant latency in mounting behavior when compared to controls. [29]
When performing the radial arm maze task, prenatally stressed male rats showed a greater increase in dopamine than prenatally stressed females, which is thought to facilitate impairment in the males but improve female performance. Females who were prenatally stressed also had an effect on corticosterone secretion.
Being prenatally stressed increased the anxiety response of the female rats. Yet, it had no effect on the males. [30]
Prenatal stress inhibits the masculinization of the male brain by inhibiting the growth of the sexually cluster of cells of the preoptic area. Prenatal stress does have an effect on brain sexual differentiation after measuring the volume of the sexually dimorphic nucleus of the preoptic area of both female and males in the control and stressed groups.
Previous studies found that a decrease in testosterone is seen in pups of prenatally stressed mothers. Authors suggest this may cause the reduced in the sexually dimorphic nucleus of the preoptic area and says it is similar to the effects of neonatal castration. Also, stressed males had larger sexually dimorphic nucleus of the preoptic area at birth, but then at 20 and 60 days are found to only have 50% of the volume of the control males. Whereas control males are two times larger than control females on days 20 and 60, but the stressed males show no statistical difference to control females on respective days. These findings show support that the male brain is not showing the expected sexual dimorphism when prenatally stressed. [31]
Another study led by Kerchner et al. investigated the volume of the medial amygdala and the two compartments posterodorsal and the posteroventral in mice that also were prenatally stressed. Posterodorsal is thought to show organizational and activational effects from gonadal steroids. The medial amygdala for the control and stressed males was 85% larger than females with the males (stressed and control) resembling each other.
To look for specific regions within the medial amygdala that may have been affected, data showed that both the posterodorsal and posteroventral, all male groups were larger in volume than the females, but male groups did not significantly differ from each other. This study confirmed that the medial amygdala is sexually dimorphic; the males are larger than the females.
The posterodorsal and posteroventral were shown to be sexually dimorphic too. The writer suggested that these areas may act similarly to sexually dimorphic nucleus of the preoptic area in response to testosterone, but prenatal stress did not show an effect on the medial amygdala as it does on the sexually dimorphic nucleus of the preoptic area. Also, the posteroventral was 40% larger in control males than females. These results were thought to be caused by the sensitive period of the medial amygdala which is in the first days after birth. The medial amygdala, posterodorsal and posteroventral all show to be resistant against demasculinization from prenatal stress. [32]
A longitudinal study done on prenatal stress and gender roles showed that prenatal stress only plays a small part in the gender roles the offspring takes on and mentions it has more to do with older siblings, maternal use of alcohol and/or tobacco, maternal education, and the observance or teaching of “traditional sex roles” from the parents. [33]
Prenatal stress and negative mood during pregnancy has been shown to increase the risk for poor childbirth outcomes and postnatal maternal mood problems. Prenatal distress can interfere with the mother-infant attachment and child development outcomes. [34] [35] Despite the clear association between prenatal stress and child outcomes, women do not receive screening, prevention, or treatment for mood or stress concerns. [36] [37]
It is essential to examine interventions that aim to reduce anxiety, depression, and stress during pregnancy. Mindfulness-based stress reduction has been demonstrated to reduce anxiety and depression for people with stress-related and chronic medical conditions. [38]
One pilot study shows promise for the potential of a mindfulness-based intervention to reduce negative affect and anxiety of women during pregnancy. Based out of the California Pacific Medical Center Research Institute, investigators Dr. Cassandra Vieten and Dr. John Astin conducted a wait-list control pilot study that tested a group-based mindfulness intervention. There were 31 women enrolled in the study: 13 women were assigned to the intervention and 18 women were assigned to the control group.
Measures of anxiety, negative affect, positive affect, depression, mindfulness, perceived stress, and affect regulation were taken before intervention or control was assigned and after the intervention or control was completed. Measures were repeated at a follow-up visit 3 months after the intervention or control was completed. The investigators found a significant decrease in anxiety (p<.05) and negative affect (p <.04) in women who completed the mindfulness based intervention, but not a significant decrease in depression, positive affect, mindfulness, affect regulation, and perceived stress.
These results suggest that mindfulness intervention during pregnancy reduce anxiety and negative affect of mothers. This study is a promising start to the potential impact that mindfulness based interventions could have on reducing prenatal stress, and thereby improving child outcomes. [39]
The relationship between biology and sexual orientation is a subject of on-going research. While scientists do not know the exact cause of sexual orientation, they theorize that it is caused by a complex interplay of genetic, hormonal, and environmental influences. Hypotheses for the impact of the post-natal social environment on sexual orientation, however, are weak, especially for males.
The hypothalamic–pituitary–adrenal axis is a complex set of direct influences and feedback interactions among three components: the hypothalamus, the pituitary gland, and the adrenal glands. These organs and their interactions constitute the HPA axis.
Environmental toxicants and fetal development is the impact of different toxic substances from the environment on the development of the fetus. This article deals with potential adverse effects of environmental toxicants on the prenatal development of both the embryo or fetus, as well as pregnancy complications. The human embryo or fetus is relatively susceptible to impact from adverse conditions within the mother's environment. Substandard fetal conditions often cause various degrees of developmental delays, both physical and mental, for the growing baby. Although some variables do occur as a result of genetic conditions pertaining to the father, a great many are directly brought about from environmental toxins that the mother is exposed to.
Prenatal development includes the development of the embryo and of the fetus during a viviparous animal's gestation. Prenatal development starts with fertilization, in the germinal stage of embryonic development, and continues in fetal development until birth.
The sexually dimorphic nucleus (SDN) is an ovoid, densely packed cluster of large cells located in the medial preoptic area (POA) of the hypothalamus which is believed to be related to sexual behavior in animals. Thus far, for all species of mammals investigated, the SDN has been repeatedly found to be considerably larger in males than in females. In humans, the volume of the SDN has been found to be 2.2 times as large in males as in females and to contain 2.1 times as many cells. The human SDN is elongated in females and more spherical in males. No sex differences have been observed in the human SDN in either cell density or mean diameter of the cell nuclei. The volume and cell number of the human SDN considerably decreases with age, although the decrease in cell number is both sex and age-specific. In males, a substantial decrease in the cell number of the human SDN was observed between the age of 50–60 years. Cell death was more common in females than males, especially among those older than 70 years of age. The SDN cell number in females can drop to 10-15% of that found in early childhood.
The preoptic area is a region of the hypothalamus. MeSH classifies it as part of the anterior hypothalamus. TA lists four nuclei in this region,.
Metabolic imprinting refers to the long-term physiological and metabolic effects that an offspring's prenatal and postnatal environments have on them. Perinatal nutrition has been identified as a significant factor in determining an offspring's likelihood of it being predisposed to developing cardiovascular disease, obesity, and type 2 diabetes amongst other conditions.
Vivette Glover is a British Professor of Perinatal Psychobiology at Imperial College London. She studies the effects of stress in pregnancy on the development of the fetus and child.
Sexual orientation is an enduring pattern of romantic or sexual attraction to persons of the opposite sex or gender, the same sex or gender, or to both sexes or more than one gender, or none of the aforementioned at all. The ultimate causes and mechanisms of sexual orientation development in humans remain unclear and many theories are speculative and controversial. However, advances in neuroscience explain and illustrate characteristics linked to sexual orientation. Studies have explored structural neural-correlates, functional and/or cognitive relationships, and developmental theories relating to sexual orientation in humans.
Prenatal cocaine exposure (PCE), theorized in the 1970s, occurs when a pregnant woman uses cocaine and thereby exposes her fetus to the drug. Babies whose mothers used cocaine while pregnant supposedly have increased risk of several different health issues during growth and development.
The hormonal theory of sexuality holds that, just as exposure to certain hormones plays a role in fetal sex differentiation, such exposure also influences the sexual orientation that emerges later in the individual. Prenatal hormones may be seen as the primary determinant of adult sexual orientation, or a co-factor with genes, biological factors and/or environmental and social conditions.
Prenatal memory, also called fetal memory, is important for the development of memory in humans. Many factors can impair fetal memory and its functions, primarily maternal actions. There are multiple techniques available not only to demonstrate the existence of fetal memory but to measure it. Fetal memory is vulnerable to certain diseases so much so that exposure can permanently damage the development of the fetus and even terminate the pregnancy by aborting the fetus. Maternal nutrition and the avoidance of drugs, alcohol and other substances during all nine months of pregnancy is important to the development of the fetus and its memory systems. The use of certain substances can entail long-term permanent effects on the fetus that can carry on throughout their lifespan.
Developmental Origins of Health and Disease is an approach to medical research factors that can lead to the development of human diseases during early life development. These factors include the role of prenatal and perinatal exposure to environmental factors, such as undernutrition, stress, environmental chemical, etc. This approach includes an emphasis on epigenetic causes of adult chronic non-communicable diseases. As well as physical human disease, the psychopathology of the foetus can also be predicted by epigenetic factors.
Parental experience, as well as changing hormone levels during pregnancy and postpartum, cause changes in the parental brain. Displaying maternal sensitivity towards infant cues, processing those cues and being motivated to engage socially with her infant and attend to the infant's needs in any context could be described as mothering behavior and is regulated by many systems in the maternal brain. Research has shown that hormones such as oxytocin, prolactin, estradiol and progesterone are essential for the onset and the maintenance of maternal behavior in rats, and other mammals as well. Mothering behavior has also been classified within the basic drives.
Endocrinology of parenting has been the subject of considerable study with focus both on human females and males and on females and males of other mammalian species. Parenting as an adaptive problem in mammals involves specific endocrine signals that were naturally selected to respond to infant cues and environmental inputs. Infants across species produce a number of cues to inform caregivers of their needs. These include visual cues, like facial characteristics, or in some species smiling, auditory cues, such as vocalizations, olfactory cues, and tactile stimulation. A commonly mentioned hormone in parenting is oxytocin, however many other hormones relay key information that results in variations in behavior. These include estrogen, progesterone, prolactin, cortisol, and testosterone. While hormones are not necessary for the expression of maternal behavior, they may influence it.
Maternal fetal stress transfer is a physiological phenomenon in which psychosocial stress experienced by a mother during her pregnancy can be transferred to the fetus. Psychosocial stress describes the brain's physiological response to perceived social threat. Because of a link in blood supply between a mother and fetus, it has been found that stress can leave lasting effects on a developing fetus, even before a child is born. According to recent studies, these effects are mainly the result of two particular stress biomarkers circulating in the maternal blood supply: cortisol and catecholamines.
Changing hormone levels during pregnancy and postpartum as well as parental experience cause changes in the parental brain. Both the father and mother undergo distinct biological changes as they transition to parents, but the changes that occur in the paternal brain are not as well studied. Similar to the changes that occur in the maternal brain, the same areas of the brain are activated in the father, and hormonal changes occur in the paternal brain to ensure display of parenting behavior. In only 5% of mammalian species, including humans, the father plays a significant role in caring for his young. Paternal caregiving has independently evolved multiple times in mammals, and can appear in some species under captivity.
Epigenetics of anxiety and stress–related disorders is the field studying the relationship between epigenetic modifications of genes and anxiety and stress-related disorders, including mental health disorders such as generalized anxiety disorder (GAD), post-traumatic stress disorder, obsessive-compulsive disorder (OCD), and more. These change can lead to transgenerational stress inheritance.
Fetal programming, also known as prenatal programming, is the theory that environmental cues experienced during fetal development play a seminal role in determining health trajectories across the lifespan.
COVID-19 impact on pregnant women is the prenatal maternal stress that COVID-19 places the fetus and on the expectant mother. This impact can include psychosocial or physical stress caused by daily life events or by environmental hardships. Mental health issues, such as maternal depression, affect 10-20% of women and are linked to a variety of negative child outcomes. Prenatal stress has been demonstrated to affect the critical development stages in postnatal life that persist throughout adulthood. Health risks include impaired cognitive development, low birth weight, and risk of mental disorders in the offspring. Epigenetics may also be associated with the biological processes involved in prenatal stress, possibly leading to fetal programming.
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