What she has been through is a wonderful experience.
26 Kasım 2010 Cuma
Brain brain brain.. What does it do really?
I believe everyone should watch the following video to gain a perspective for the title of this post:
31 Ekim 2010 Pazar
Attachment Theory - briefly
I would like to talk about attachment theory briefly.
“Attachment theory is a psychological, evolutionary, and ethological theory concerning relationships between humans. The most important tenet of attachment theory is that a young child needs to develop a relationship with at least one primary caregiver for social and emotional development to occur normally. The theory was formulated by psychiatrist and psychoanalyst John Bowlby.” (source: Wikipedia)
Some basic notions are:
Imprinting: it is a sudden, biologically primed behavior; it is innate (e.g., ducks)
Attachment: it is a strong emotional bond between caregiver and infant; it is not innate, it is learned
Secure: critical element for a secure environment is not simply food, it is contact comfort and attuned caregiver.
Attachment: it is a strong emotional bond between caregiver and infant; it is not innate, it is learned
Secure: critical element for a secure environment is not simply food, it is contact comfort and attuned caregiver.
The developmental process for the attachment is as follows:
*indiscriminate attachment (0 – 3 months) – care-eliciting behavior directed toward any human
*discriminate attachment (3 – 7 months) – directed toward familiar caregivers
*specific attachment (begins 7 months) – directed toward most familiar primary caregiver (PCG)
*stranger anxiety (6 – 18 months) – distressed in contact with unfamiliar people
*separation anxiety (8 months – 2, 3 yrs) – stressed when separated from primary caregiver (PCG)
*discriminate attachment (3 – 7 months) – directed toward familiar caregivers
*specific attachment (begins 7 months) – directed toward most familiar primary caregiver (PCG)
*stranger anxiety (6 – 18 months) – distressed in contact with unfamiliar people
*separation anxiety (8 months – 2, 3 yrs) – stressed when separated from primary caregiver (PCG)
While assessing the types of attachment, which is measured by “strange situation”, mother (PCG) and the child are together in an unfamiliar, novel room with toys. At one point in time, a stranger enters, then after a while the mother leaves and then the mother returns. What is observed here is what the child does in each change. There are four possibilities of behavior:
1) If the child is secure, he explores, is curious about situation and stranger; feels distress when mother leaves; recovers and returns to play; then exhibits joy when mother(PCG) returns.
(Securely attached child has a secure attachment with his father, he is resilient, competent and has high self-esteem. He will have good social adjustment with peers, advanced cognitive development such as school success, curiosity and self-reliance. He will become a healthy adult; he will be able to love and have sexual relationships.)
2) If the child is anxious-resistant, he is fearful, clings to mother, does not explore; distressed when mother leaves, but is not soothed when she returns; resists her attention.
3) If the child is anxious-avoidant, the child has minimal interaction with mother, stranger and toys; he is not distressed when mother leaves; does not seek contact or comfort when she returns.
4) If the child is disorganized-disoriented, he engages in contradictory behaviors toward mother, stranger, toys; he does not fully engage with anyone or anything; he engages in stereotyped rocking; disoriented, dazed when mother leaves; helpless effort to elicit soothing (indicator of abused child).
There are some mental representations of attachment;
- Internal working models of “care” and “care-givers” are formed,
- The attachment in childhood forms basis of sense of self and expectations for close relations with others in the future.
- If the caregiver is consistent, reliable, attuned and soothing, then the infant will say “I’m worthy, lovable, loved, competent; care-givers are loving”
- If the caregiver is inconsistent, withholding and abusive, then the infant will say “I’m unworthy, unlovable, defective, unloved; care-givers are unloving”
As we can see, the way primary caregiver treats the child is very important. It is obvious that it shapes one's adult personality; therefore, it is a very important issue. It should not be forgotten that the biology has not changed through centuries; infants were helpless then when they are born, and they are still. The caregiver should absolutely respond to him rather than ignoring, neglecting or refusing him. However the person beside treats him, he becomes attached to that person in some way but of course the nature of the attachment changes. There may of course be some differences in attachment quality based on patterning of care and the organization of attachment behavior, but if there is no attachment, it is a serious problem. There must also be love, acceptance and trust in the relationship with the infant.
sources: Lecture notes of "Introduction to Psychology"
The book "The Science of Mind and Behavior", Passer & Smith, 3rd edition,
The book "The Science of Mind and Behavior", Passer & Smith, 3rd edition,
Workshop with Alan Sroufe (23rd and 24th of October)
Why Is the Fetus So Vulnerable to the Environment?
This is something that I found on 'psychology today', I did not just write down the link because I wanted to underline some part of it. I hope it will give some idea about the vulnerability of the fetus.
Nine months of vulnerability
Here's a young woman named Kate at a party with her husband on the Upper West Side in Manhattan. She's twenty-five years old, a teacher happily married to an attorney, and she wants children. It's someone's birthday party, a happy occasion, and Kate has been sipping vodka tonics one after the other and enjoying herself.
Although she doesn't know it yet, Kate is pregnant. The embryo is just beginning the second week of gestation. In 35 or 36 weeks she'll have a baby boy, and soon after birth the baby will have physical problems, mental problems, and an unpredictable future.
Some women can do heavy drinking during early pregnancy and nothing much happens to the child they carry. Kate isn't one of those women. The embryo in her uterus is vulnerable to a sudden increase in blood alcohol. Or maybe Kate's body detoxifies alcohol too slowly. We don't know the mechanisms for individual vulnerabilities. Kate's child, the child she yearns to have, will be diagnosed with fetal alcohol syndrome, including a related cardiac defect and mental deficits.
The placenta is the organ that acts as the interface between the mother and the developing embryo or fetus. Although the placenta acts as a filter and detoxifying system, its efficiency differs from one woman to the next and we don't yet understand the details of the differences.
For the developing embryo, ethyl alcohol (ethanol, the alcohol we drink), usually passes through the placenta intact. Ethanol is an environmental toxic chemical--with embryo damage caused not by air pollution, water pollution, or food pollution, but by a woman aware or not yet aware that she's pregnant, for example, a woman drinking too much at an innocent birthday party.
Yes, it's insidious, and it's unfortunate that we started being serious about this problem only a few decades ago.
Let's consider wine. I like wine, especially Italian wine, maybe because I once lived in Italy. Wine is important in Italy, and the custom in rural towns and villages is to drink moderate amounts of wine with meals every day. Binge drinking is rare, except among the young and in cities. But binge drinking is not the only way alcohol can be dangerous for an embryo or fetus.
One of the oldest parts of Italy is Rome and the area around Rome, the region called Lazio. In the region of Lazio 62 percent of women drink alcohol prior to pregnancy and 53 percent during pregnancy. Twelve percent of pregnant women in Lazio drink 7 or more drinks a week. Some Italian women who ordinarily don't drink regularly start drinking during pregnancy because of a popular belief in Italy that moderate alcohol has benevolent effects during pregnancy.
So is it harmful to the fetus? Yes, it's harmful to the fetus. Currently, 3.5 percent of the children in Lazio have the markers of fetal alcohol spectrum disorder (FASD). That's the highest prevalence of FASD in the Western world and more than 3 times the prevalence in the United States.
Prenatal developmental damage by alcohol is an example of the high vulnerability of the embryo and fetus to chemical impacts. Toxicologists estimate that during the nine months of gestation, the developing fetus is about 100 times more vulnerable to environmental impacts than children or adults. There are good biological reasons for this vulnerability, and a look at the reasons helps us understand some important features of development.
The human egg cell (ovum) is the largest cell in the body, on average 145 microns in diameter (average human hair width is 100 microns, or 0.1 millimeters), which means the egg cell is visible to the naked eye. The ovum is about 15 times larger than ordinary cells such as skin cells and liver cells, but it's still no larger than a dot, smaller than the period at the end of this sentence. The profound glory of human reproduction, the wonder of wonders, is that under the right circumstances and during about 277 days, this biological dot is capable of turning itself into a 7-pound infant ready to scream at you to look smart and give it some food and attention.
Fetal development is a consequence of cascades of biochemical reactions, cascades of geneexpression, cellular movements, tissue formation, and organ construction. A cascade is a succession of sequentially interdependent events, each event both triggered by the event preceding it and itself acting as a trigger for the next event. Human development from conception to birth involves many thousands of cascades, sequences of events with specific vulnerabilities at specific times -- and the possibility for several vulnerabilities at any single time.
The whole developmental mix of cascades moves forward by both internal triggers and triggering by interactions with the local cellular environment. So the first important cause of prenatal vulnerability is complexity: the sheer complexity at many levels of prenatal development means that an enormous number of different and important process points are available for disruptive impacts.
Another important cause of prenatal vulnerability is pace, the high rate of cellular proliferation necessary to transform a single microscopic cell (the fertilized ovum) into a six- or seven-pound newborn infant that consists of trillions of cells specialized and arranged to constitute the human body externally and internally -- albeit in the small of the infant. It's estimated that in the human developing prenatal brain and nervous system about 250,000 new neurons are generated each minute at the peak of cell proliferation during gestation. The high rate of cell proliferation means a high rate of metabolism, a high rate of chemical synthesis, a high rate of cellular rearrangements and migrations, a high rate of conversion of maternal nutrients into fetal cells and tissues, and so on. In prenatal development, everything is happening rapidly, and the consequence is that if any specific process has its rate changed up or down by an unscheduled impact with the local environment, the consequence may be anything from a subtle bending of development in one direction or another to a lethal corruption that kills the embryo or fetus.
The third major cause of the vulnerability of prenatal development involves size and simple physics. If a small permeable mass--for example, a cluster of cells--is exposed to a chemical, that chemical can reach all parts of the mass quickly by simple random diffusion. With larger masses, the diffusion time to reach all parts increases dramatically. But as late as the 6th week of gestation, the human embryo is still only a quarter of an inch in length, has no developed circulatory system, and any freely permeating chemical that gets into the embryo by any route will quickly diffuse throughout the embryo to impact every embryonic cell.
Throughout the embryonic period, until the 10th week of gestation, the situation is not much better. At the 10th week, when we begin to call the developing embryo a "fetus", we're dealing with an embryo/fetus about two inches in length, indeed recognizable as a vaguely human form, but still small enough for simple diffusion to quickly distribute any permeating chemical entity throughout its body.
Small size facilitating distribution by simple diffusion is one of the reasons the early weeks of prenatal development are so vulnerable to certain chemical impacts. The other important reason is that the effects of impacts on the early part of development can be multiplied as the cascades of development proceed.
For example, there is mounting evidence that a critical window of vulnerability for fetal alcohol spectrum disorder occurs very early--during and shortly after the blastocyst stage--and that the impact of alcohol is on early gene expression in the developing embryo. Given this evidence, the most reasonable assumption is that concentrations of alcohol too low to produce gross morphological disruptions may cause subtle and yet unknown changes in the connections between nerve cells in the developing brain. There is certainly evidence of troubles in cognitive performance of children whose mothers drank only moderate amounts of alcohol during pregnancy.
[Parts of the above text are adapted from More Than Genes: What Science Can Tell Us About Toxic Chemicals, Development, and the Risk to Our Children. Author: Dan Agin. Oxford University Press, 2009
here is the link:
http://www.psychologytoday.com/blog/more-genes/200911/more-genes-ii-why-is-the-fetus-so-vulnerable-the-environment
Although she doesn't know it yet, Kate is pregnant. The embryo is just beginning the second week of gestation. In 35 or 36 weeks she'll have a baby boy, and soon after birth the baby will have physical problems, mental problems, and an unpredictable future.
Some women can do heavy drinking during early pregnancy and nothing much happens to the child they carry. Kate isn't one of those women. The embryo in her uterus is vulnerable to a sudden increase in blood alcohol. Or maybe Kate's body detoxifies alcohol too slowly. We don't know the mechanisms for individual vulnerabilities. Kate's child, the child she yearns to have, will be diagnosed with fetal alcohol syndrome, including a related cardiac defect and mental deficits.
The placenta is the organ that acts as the interface between the mother and the developing embryo or fetus. Although the placenta acts as a filter and detoxifying system, its efficiency differs from one woman to the next and we don't yet understand the details of the differences.
For the developing embryo, ethyl alcohol (ethanol, the alcohol we drink), usually passes through the placenta intact. Ethanol is an environmental toxic chemical--with embryo damage caused not by air pollution, water pollution, or food pollution, but by a woman aware or not yet aware that she's pregnant, for example, a woman drinking too much at an innocent birthday party.
Yes, it's insidious, and it's unfortunate that we started being serious about this problem only a few decades ago.
Let's consider wine. I like wine, especially Italian wine, maybe because I once lived in Italy. Wine is important in Italy, and the custom in rural towns and villages is to drink moderate amounts of wine with meals every day. Binge drinking is rare, except among the young and in cities. But binge drinking is not the only way alcohol can be dangerous for an embryo or fetus.
One of the oldest parts of Italy is Rome and the area around Rome, the region called Lazio. In the region of Lazio 62 percent of women drink alcohol prior to pregnancy and 53 percent during pregnancy. Twelve percent of pregnant women in Lazio drink 7 or more drinks a week. Some Italian women who ordinarily don't drink regularly start drinking during pregnancy because of a popular belief in Italy that moderate alcohol has benevolent effects during pregnancy.
So is it harmful to the fetus? Yes, it's harmful to the fetus. Currently, 3.5 percent of the children in Lazio have the markers of fetal alcohol spectrum disorder (FASD). That's the highest prevalence of FASD in the Western world and more than 3 times the prevalence in the United States.
Prenatal developmental damage by alcohol is an example of the high vulnerability of the embryo and fetus to chemical impacts. Toxicologists estimate that during the nine months of gestation, the developing fetus is about 100 times more vulnerable to environmental impacts than children or adults. There are good biological reasons for this vulnerability, and a look at the reasons helps us understand some important features of development.
The human egg cell (ovum) is the largest cell in the body, on average 145 microns in diameter (average human hair width is 100 microns, or 0.1 millimeters), which means the egg cell is visible to the naked eye. The ovum is about 15 times larger than ordinary cells such as skin cells and liver cells, but it's still no larger than a dot, smaller than the period at the end of this sentence. The profound glory of human reproduction, the wonder of wonders, is that under the right circumstances and during about 277 days, this biological dot is capable of turning itself into a 7-pound infant ready to scream at you to look smart and give it some food and attention.
Fetal development is a consequence of cascades of biochemical reactions, cascades of geneexpression, cellular movements, tissue formation, and organ construction. A cascade is a succession of sequentially interdependent events, each event both triggered by the event preceding it and itself acting as a trigger for the next event. Human development from conception to birth involves many thousands of cascades, sequences of events with specific vulnerabilities at specific times -- and the possibility for several vulnerabilities at any single time.
The whole developmental mix of cascades moves forward by both internal triggers and triggering by interactions with the local cellular environment. So the first important cause of prenatal vulnerability is complexity: the sheer complexity at many levels of prenatal development means that an enormous number of different and important process points are available for disruptive impacts.
Another important cause of prenatal vulnerability is pace, the high rate of cellular proliferation necessary to transform a single microscopic cell (the fertilized ovum) into a six- or seven-pound newborn infant that consists of trillions of cells specialized and arranged to constitute the human body externally and internally -- albeit in the small of the infant. It's estimated that in the human developing prenatal brain and nervous system about 250,000 new neurons are generated each minute at the peak of cell proliferation during gestation. The high rate of cell proliferation means a high rate of metabolism, a high rate of chemical synthesis, a high rate of cellular rearrangements and migrations, a high rate of conversion of maternal nutrients into fetal cells and tissues, and so on. In prenatal development, everything is happening rapidly, and the consequence is that if any specific process has its rate changed up or down by an unscheduled impact with the local environment, the consequence may be anything from a subtle bending of development in one direction or another to a lethal corruption that kills the embryo or fetus.
The third major cause of the vulnerability of prenatal development involves size and simple physics. If a small permeable mass--for example, a cluster of cells--is exposed to a chemical, that chemical can reach all parts of the mass quickly by simple random diffusion. With larger masses, the diffusion time to reach all parts increases dramatically. But as late as the 6th week of gestation, the human embryo is still only a quarter of an inch in length, has no developed circulatory system, and any freely permeating chemical that gets into the embryo by any route will quickly diffuse throughout the embryo to impact every embryonic cell.
Throughout the embryonic period, until the 10th week of gestation, the situation is not much better. At the 10th week, when we begin to call the developing embryo a "fetus", we're dealing with an embryo/fetus about two inches in length, indeed recognizable as a vaguely human form, but still small enough for simple diffusion to quickly distribute any permeating chemical entity throughout its body.
Small size facilitating distribution by simple diffusion is one of the reasons the early weeks of prenatal development are so vulnerable to certain chemical impacts. The other important reason is that the effects of impacts on the early part of development can be multiplied as the cascades of development proceed.
For example, there is mounting evidence that a critical window of vulnerability for fetal alcohol spectrum disorder occurs very early--during and shortly after the blastocyst stage--and that the impact of alcohol is on early gene expression in the developing embryo. Given this evidence, the most reasonable assumption is that concentrations of alcohol too low to produce gross morphological disruptions may cause subtle and yet unknown changes in the connections between nerve cells in the developing brain. There is certainly evidence of troubles in cognitive performance of children whose mothers drank only moderate amounts of alcohol during pregnancy.
[Parts of the above text are adapted from More Than Genes: What Science Can Tell Us About Toxic Chemicals, Development, and the Risk to Our Children. Author: Dan Agin. Oxford University Press, 2009
here is the link:
http://www.psychologytoday.com/blog/more-genes/200911/more-genes-ii-why-is-the-fetus-so-vulnerable-the-environment
Androgen Insensitivity Syndrome
Androgen insensitivity syndrome (AIS) is a condition that results in the partial or complete inability of the cell to respond to androgens. The unresponsiveness of the cell to the presence of androgenic hormones can impair or prevent the masculinization of male genitalia in the developing fetus, as well as the development of male secondary sexual characteristics at puberty, but does not significantly impair female genital or sexual development. As such, the insensitivity to androgens is only clinically significant when it occurs in genetic males (i.e. individuals with a Y chromosome, or more specifically, an SRY gene).
AIS is divided into three categories that are differentiated by the degree of genital masculinization: complete androgen insensitiviy syndrome (CAIS) is indicated when the external genitelia is that of a normal female, mild androgen insensitivity syndrome (MAIS) is indicated when the external genitelia is that of a normal male, and partial androgen insensitivity syndrome (PAIS) is indicated when an external genitelia is partially, but not fully masculinized.
Androgen insensitivity syndrome is the largest single entity that leads to 46, XY undermasculinization.
source: http://en.wikipedia.org/wiki/Androgen_insensitivity_syndrome
From the lecture:
Sexual differentiation occurs during the embryonic stage of prenatal development. Before differentiation, we are the same; every embryo has female characteristics by default. Genetic activity on Y sex chromosome causes the testes to begin to differentiate. Once testes develop, they produce androgens (male sex hormones). The most important sex hormone is testosterone which promotes growth of male sexual characteristics and sperm. Ovaries differentiate if Y chromosome is absent. By 4 months, distinct external genital structures are formed.
In absence of androgens, female reproduction system develops (initial undifferentiated structures). Therefore an embryo with a pair of XY chromosomes should be exposed to androgens in order to be able to develop as a male. If the embryo is not exposed to androgens, female develops however the chromosome structure is.
Here are some pictures about androgen insensitivity syndrome:
AIS is divided into three categories that are differentiated by the degree of genital masculinization: complete androgen insensitiviy syndrome (CAIS) is indicated when the external genitelia is that of a normal female, mild androgen insensitivity syndrome (MAIS) is indicated when the external genitelia is that of a normal male, and partial androgen insensitivity syndrome (PAIS) is indicated when an external genitelia is partially, but not fully masculinized.
Androgen insensitivity syndrome is the largest single entity that leads to 46, XY undermasculinization.
source: http://en.wikipedia.org/wiki/Androgen_insensitivity_syndrome
From the lecture:
Sexual differentiation occurs during the embryonic stage of prenatal development. Before differentiation, we are the same; every embryo has female characteristics by default. Genetic activity on Y sex chromosome causes the testes to begin to differentiate. Once testes develop, they produce androgens (male sex hormones). The most important sex hormone is testosterone which promotes growth of male sexual characteristics and sperm. Ovaries differentiate if Y chromosome is absent. By 4 months, distinct external genital structures are formed.
In absence of androgens, female reproduction system develops (initial undifferentiated structures). Therefore an embryo with a pair of XY chromosomes should be exposed to androgens in order to be able to develop as a male. If the embryo is not exposed to androgens, female develops however the chromosome structure is.
Here are some pictures about androgen insensitivity syndrome:
Caster Semenya:
Mokgadi Caster Semenya (born 7 January 1991) is a South African middle-distance runnerand world champion. Semenya won gold in the women's 800 metres at the 2009 World Championships with a time of 1:55.45 in the final.
Following her victory at the 2009 World Championships, questions were raised about whether Semenya has an physical condition that might give her an unfair advantage over other female racers. She was withdrawn from international competition until 6 July 2010 when the IAAF cleared her to return to competition. In 2010, the British magazine New Statesman included Semenya in its list "The World's 50 Most Influential Figures 2010".
Effects of Prenatal Social Stress on Offspring Development
This is an article that I found in our school library's database and that I have been reading. At first I thought of sharing some of the information but since it is not a long article, I decided to share all the article here. Please enjoy.
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ABSTRACT—In nonhuman mammals, the social environment in which pregnant females live is critical for their offsprings’ brain development, endocrine state, and social and sexual behavior later in life. Social instability during pregnancy generally brings about a behavioral and neuroendocrine masculinization in daughters and a less pronounced expression of male-typical traits in sons. We favor the hypothesis that such behavioral effects of prenatal social stress are not necessarily "pathological" (nonadaptive) consequences of adverse social conditions. Rather, pregnant mothers could be adjusting their offspring to their environment in an adaptive way.
Ontogeny is the development of an individual from the moment the egg is fertilized until death. Most research on behavioral ontogeny has focused on the early postnatal phase, probably because socialization and learning processes are thought to play their most important role during this time. However, there is growing evidence that environmental influences before birth also have impact on the individual’s development later in life (de Weerth, Buitelaar, & Mulder, 2005). In particular, stressors acting on the mother during pregnancy can have distinct and long-term effects on behavior, reproductive functions, and the immune, neuroendocrine and autonomic systems of her offspring (de Kloet, Sibug, Helmerhorst, & Schmidt, 2005). In most experimental studies on the effects of prenatal stress, pregnant female animals have been subjected to nonsocial stressors (e.g., bright light, restraint). Interpretation of these studies is difficult, because such artifical stressors typically do not occur in those animals’ natural environments (Kaiser & Sachser, 2005). In their natural habitats, animals have to cope with a variety of stressors that depend on their ecological niche. They have to adjust to the physical environment (e.g., weather) and to the biotic world that surrounds them (e.g., predators, food shortage). A major part of an individual’s biotic environment consists of other members of the same species, which can be defined as that individual’s ‘‘social world.’’ In fact, a majority of human and animal daily expectations, motivations, and behaviors are directed toward encounters with conspecifics. On the one hand, this social world can support welfare and health (e.g., through the effects of social support). On the other hand, it can result in severe stress, eventually leading to disease and even death (e.g., in the case of social defeat, social instability, or crowding; von Holst, 1998). Thus, the social environment represents a very influential stressor, which, during pregnancy, can be crucial for the development of the offspring (Kaiser & Sachser, 2005).
EFFECTS OF THE PRENATAL SOCIAL ENVIRONMENT ON OFFSPRING DEVELOPMENT AND BEHAVIOR
Animal Studies
The most comprehensive insights from studies of nonhuman animals regarding prenatal social influences on offspring development have been derived from studies in guinea pigs (Kaiser & Sachser, 2005). For example, when compared to daughters whose mothers had lived in a stable social environment during pregnancy (that is, group composition was kept constant, with one male and five females), female guinea pigs whose mothers had lived in an unstable social environment (every third day, two females from different groups were exchanged) showed conspicuous behavioral masculinization (e.g., displaying high levels of male-typical courtship behavior) later in life, increased testosterone concentrations, and a maletypical distribution pattern of androgen receptors in parts of the limbic system (Kaiser, Kruijver, Swaab, & Sachser, 2003).
Compared to male guinea pigs whose mothers had lived in a stable social environment, those whose mothers had lived in an unstable social environment during pregnancy showed behavioral infantilization (e.g., displaying behavioral patterns usually shown only by very young male guinea pigs, such as sitting in close bodily contact), delayed development of the adrenocortical system, and down-regulation of androgen receptor expression in the limbic system (Kaiser, Kruijver, Straub, Sachser, & Swaab, 2003).
Studies of prenatal social influences on offspring development have been conducted only in a few other species (e.g., mice, rats, squirrel monkeys). Although a variety of different social stressors have been applied in these experiments (e.g., crowding, social confrontation, changing group membership), a common characteristic of all approaches is the induction of social instability. In general, under such conditions, the number of interactions with conspecifics increases and the predictability and controllability of social encounters dramatically decline. Interestingly, modern stress research shows that, in animals as well as in humans, situations of uncertainty or unpredictability are a major source of stress responses (von Holst, 1998).
When all experimental studies on prenatal social stress are compared, some general conclusions can be drawn: Female offspring show a masculinization of behavior, endocrine state, and brain development. Male offspring show a less pronounced expression of male-typical traits (e.g., demasculinization, feminization) and/or a delay in development. In addition, there are some indications that both sexes might have a more or less severe impairment of reproductive functions (cf., Kaiser & Sachser, 2005).
Human Studies
The long-lasting effects of prenatal stress on offspring are also well known in humans: Children of mothers who were stressed during pregnancy develop higher risk of different diseases (including cardiovascular illness and diabetes) and may experience physical and cognitive developmental delays (e.g., Huizink, Mulder, & Buitelaar, 2004; Wadhwa, 2005). However, only limited data concerning the effects of social stressors during pregnancy on human offspring later in life are available. Those few studies, however, point to distinct effects on behavioral and physiological development. For instance, family discord during pregnancy leads to behavioral disturbances in children, and such children are more likely to develop psychopathological disorders such as autism (Ward, 1990; unfortunately, it is not mentioned whether this finding is controlled for postnatal effects). Similarly, moderate to severe stressors combined with low levels of social support during pregnancy reduce children’s head circumference at birth, pointing to the effects of prenatal stress on brain development (Glynn & Sandman, 2006). Children whose mothers experienced high levels of daily hassles and pregnancy-specific anxiety show lower mental and motor developmental scores at 8 months of age after correcting for postnatal stress (Buitelaar, Huizink, Mulder, Robles de Medina, & Visser, 2003).
EFFECTS OF PRENATAL SOCIAL STRESS: PATHOLOGY OR ADAPTATION?
Researchers typically interpret the characteristic traits of individuals who were exposed to adverse environmental stimuli (stressors) during pregnancy as deviations from some standard considered optimal, and phenotypic differences in offspring are frequently called pathological. Alternatively, and in accordance with current evolutionary theory, these traits might also represent adaptive maternal effects; that is, the offspring’s fitness is enhanced by maternal adjustments to the current environmental conditions.
Adaptation through maternal effects—that is, control and/or modulation of the offspring’s phenotype—has become a key concept in modern evolutionary biology (see, e.g., Groothuis, Mu¨ ller, von Engelhardt, Carere, & Eising, 2005; Mousseau & Fox, 1998) and numerous studies to reveal the mechanism underlying these phenomena are currently underway. Particular maternal hormonal responses to environmental stimuli represent a potential tool by which development of offspring can be influenced. Indeed, in different bird species, mothers’ deposition of androgens into the yolk of their eggs varies with environmental factors or social conditions, and experimental studies have shown effects of enhanced androgen levels on offspring traits such as competitiveness or growth (Groothuis, Mu¨ ller, von Engelhardt, Carere, & Eising, 2005). Results of two recent studies in wild spotted hyenas and guinea pigs suggest that prenatal androgen exposure can adaptively influence offspring phenotype (in terms of aggression, sexual behavior, and testosterone responsiveness to social challenge) regularly in mammals as well (Dloniak, French,&Holekamp, 2006; Kemme, Kaiser,& Sachser, 2007). If such traits result in enhancement of fitness parameters such as social dominance or reproductive benefits, we can speak of an adaptive phenotype.
Possible Benefits of Altered Phenotypes
The questions arise: What is the benefit of being a masculinized daughter? And what is the benefit for sons who show less pronounced expression of male-typical traits and/or a delay in development?
Consider the case of fluctuations in the density of natural populations of mammals. Under high-density conditions, social instability is a common trait, whereas low population densities are characterized by stable social situations (von Holst, 1998). Hence, different pregnant females may experience very different degrees of social stability in their natural habitats. If a pregnant female living in a high-density population has the possibility of preprogramming her daughters in such a way that they will gain maximum reproductive success in that high-density situation, it would seem reasonable for her to masculinize them in order to make them more robust and/or more competitive. These and other masculine traits facilitate the attainment of dominant social positions, which in turn help to defend important resources such as food and shelter (which are scarce in highdensity situations) more efficiently. However, frequently a characteristic feature of masculinized females is impairment of reproductive function later in life (Kaiser & Sachser, 2005). Thus, under high-density conditions, there is likely to be a tradeoff between the benefits of a behaviorally and endocrinologically masculinized phenotype and the costs of decreased reproductive success. Although decreased reproductive success might seem inconsistent with the idea of enhanced fitness, under such conditions, masculinized females might fare better than nonmasculinized females; the latter may often fail to reproduce at all because of lower social status that prevents access to resources necessary for reproduction. Under low-density conditions, however, sufficient resources are available and competitive abilities are less important. Under such conditions, it would seem more beneficial to invest time and energy in reproductive effort rather than to build and maintain a male-typical phenotype for defending resources. Thus, under low-density conditions, reproductive success would be higher in nonmasculinized females than in masculinized ones (Kaiser & Sachser, 2005).
The argument is similar for sons. Around the time of sexual maturity, they can find themselves in different situations. Consider a low-density condition with only a few males of the same age and some females present. In such a situation, the best strategy to maximize reproductive success would be to fight for the access to a copulation partner, because usually the winners will mate. Under such conditions, mothers will maximize their own fitness if they program their sons prenatally in a way that maximizes the timely expression of male-typical traits. In contrast, when animals live at high densities in large, age-graded populations, a different situation exists: Under such conditions, in many species, high-ranking (alpha) males almost exclusively sire all the offspring. Remarkably, males usually do not attain an alpha position until well beyond the age of sexual maturity (e.g., mandrills; Setchell, Charpentier, & Wickings, 2005). A male born in a high-density population should avoid agonistic encounters at too early an age, because this will not result in reproductive success. By neither signaling sexual interest in females nor displaying other signs of sexual maturity, a pubescent male is less likely to be attacked by the alpha males. This strategy should change, however, around the time of social maturity in order to attain the alpha position that is required for reproductive success. Thus, under conditions of high density, mothers may provide their sons with a more adaptive reproductive strategy by programming them prenatally in a way that delays development and/or diminishes expression of maletypical traits until social maturity is attained (Kaiser & Sachser, 2005).
Currently, much experimental animal research is being conducted to test such hypotheses on the adaptive value of prenatal maternal programming (Dloniak, French, & Holekamp, 2006; Kemme, Kaiser, & Sachser, 2007).
Human Studies
Similar arguments for the adaptive value of the response to prenatal-stress effects in humans have been put forward. For example, Bateson et al. (2004) hypothesize that a period of starvation during pregnancy tells the developing fetus that food is probably going to be scarce in the future. Babies of such mothers often show small body weight and correspondingly modified metabolism. These traits are not necessarily pathological, inasmuch as they help the baby to cope with environments of low food availability. The proposed mechanism for these persistent effects into adulthood involves alteration in set points for various aspects of basic metabolism (e.g., glucoregulation, adiposity, and blood pressure; Roseboom, de Rooij, & Painter, 2006).
For ethical reasons, in humans it is not feasible to experimentally manipulate hormonal levels during early development or exposure to stress in pregnant mothers. Nevertheless, good evidence that the behavioral phenotype of daughters can be shaped by prenatal androgens does exist. For example, girls with congenital adrenal hyperplasia (an autosomal recessive disorder that causes elevated adrenal androgens) are exposed to elevated androgen concentrations during fetal development, and this results in a masculinized phenotype—revealed, for example, by increased rough-and-tumble play (Hines, 2006). Other evidence shows that androgen levels in women can be affected by environmental situations: Testosterone concentrations increase, for example, in periods of high-intensity exercise (Bergeron et al., 1991). We therefore propose that androgen concentrations in pregnant women may change as a result of environmental factors and that these changed androgen concentrations may influence fetal central-nervous-system differentiation during early development, thereby shaping the behavioral phenotype of the offspring later in life. Whether or not this specific phenotype represents an adaptive adjustment to the environmental conditions under which the mother has lived during pregnancy remains to be determined.
CONCLUSION
Studies of animals and humans clearly show that severe stressors acting upon a pregnant female can have profoundly negative effects on the later development and health of her offspring. In such cases, prenatal stress results in pathology and no discussion about adaptive function seems appropriate. Recent experimental animal studies of prenatal stress, when considered from an evolutionary perspective, draw attention to an additional
This article:
By: Kaiser, Sylvia; Sachser, Norbert. Current Directions in Psychological Science (Wiley-Blackwell), Apr2009, Vol. 18 Issue 2, p118-121, 4p; DOI: 10.1111/j.1467-8721.2009.01620.x
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ABSTRACT—In nonhuman mammals, the social environment in which pregnant females live is critical for their offsprings’ brain development, endocrine state, and social and sexual behavior later in life. Social instability during pregnancy generally brings about a behavioral and neuroendocrine masculinization in daughters and a less pronounced expression of male-typical traits in sons. We favor the hypothesis that such behavioral effects of prenatal social stress are not necessarily "pathological" (nonadaptive) consequences of adverse social conditions. Rather, pregnant mothers could be adjusting their offspring to their environment in an adaptive way.
Ontogeny is the development of an individual from the moment the egg is fertilized until death. Most research on behavioral ontogeny has focused on the early postnatal phase, probably because socialization and learning processes are thought to play their most important role during this time. However, there is growing evidence that environmental influences before birth also have impact on the individual’s development later in life (de Weerth, Buitelaar, & Mulder, 2005). In particular, stressors acting on the mother during pregnancy can have distinct and long-term effects on behavior, reproductive functions, and the immune, neuroendocrine and autonomic systems of her offspring (de Kloet, Sibug, Helmerhorst, & Schmidt, 2005). In most experimental studies on the effects of prenatal stress, pregnant female animals have been subjected to nonsocial stressors (e.g., bright light, restraint). Interpretation of these studies is difficult, because such artifical stressors typically do not occur in those animals’ natural environments (Kaiser & Sachser, 2005). In their natural habitats, animals have to cope with a variety of stressors that depend on their ecological niche. They have to adjust to the physical environment (e.g., weather) and to the biotic world that surrounds them (e.g., predators, food shortage). A major part of an individual’s biotic environment consists of other members of the same species, which can be defined as that individual’s ‘‘social world.’’ In fact, a majority of human and animal daily expectations, motivations, and behaviors are directed toward encounters with conspecifics. On the one hand, this social world can support welfare and health (e.g., through the effects of social support). On the other hand, it can result in severe stress, eventually leading to disease and even death (e.g., in the case of social defeat, social instability, or crowding; von Holst, 1998). Thus, the social environment represents a very influential stressor, which, during pregnancy, can be crucial for the development of the offspring (Kaiser & Sachser, 2005).
EFFECTS OF THE PRENATAL SOCIAL ENVIRONMENT ON OFFSPRING DEVELOPMENT AND BEHAVIOR
Animal Studies
The most comprehensive insights from studies of nonhuman animals regarding prenatal social influences on offspring development have been derived from studies in guinea pigs (Kaiser & Sachser, 2005). For example, when compared to daughters whose mothers had lived in a stable social environment during pregnancy (that is, group composition was kept constant, with one male and five females), female guinea pigs whose mothers had lived in an unstable social environment (every third day, two females from different groups were exchanged) showed conspicuous behavioral masculinization (e.g., displaying high levels of male-typical courtship behavior) later in life, increased testosterone concentrations, and a maletypical distribution pattern of androgen receptors in parts of the limbic system (Kaiser, Kruijver, Swaab, & Sachser, 2003).
Compared to male guinea pigs whose mothers had lived in a stable social environment, those whose mothers had lived in an unstable social environment during pregnancy showed behavioral infantilization (e.g., displaying behavioral patterns usually shown only by very young male guinea pigs, such as sitting in close bodily contact), delayed development of the adrenocortical system, and down-regulation of androgen receptor expression in the limbic system (Kaiser, Kruijver, Straub, Sachser, & Swaab, 2003).
Studies of prenatal social influences on offspring development have been conducted only in a few other species (e.g., mice, rats, squirrel monkeys). Although a variety of different social stressors have been applied in these experiments (e.g., crowding, social confrontation, changing group membership), a common characteristic of all approaches is the induction of social instability. In general, under such conditions, the number of interactions with conspecifics increases and the predictability and controllability of social encounters dramatically decline. Interestingly, modern stress research shows that, in animals as well as in humans, situations of uncertainty or unpredictability are a major source of stress responses (von Holst, 1998).
When all experimental studies on prenatal social stress are compared, some general conclusions can be drawn: Female offspring show a masculinization of behavior, endocrine state, and brain development. Male offspring show a less pronounced expression of male-typical traits (e.g., demasculinization, feminization) and/or a delay in development. In addition, there are some indications that both sexes might have a more or less severe impairment of reproductive functions (cf., Kaiser & Sachser, 2005).
Human Studies
The long-lasting effects of prenatal stress on offspring are also well known in humans: Children of mothers who were stressed during pregnancy develop higher risk of different diseases (including cardiovascular illness and diabetes) and may experience physical and cognitive developmental delays (e.g., Huizink, Mulder, & Buitelaar, 2004; Wadhwa, 2005). However, only limited data concerning the effects of social stressors during pregnancy on human offspring later in life are available. Those few studies, however, point to distinct effects on behavioral and physiological development. For instance, family discord during pregnancy leads to behavioral disturbances in children, and such children are more likely to develop psychopathological disorders such as autism (Ward, 1990; unfortunately, it is not mentioned whether this finding is controlled for postnatal effects). Similarly, moderate to severe stressors combined with low levels of social support during pregnancy reduce children’s head circumference at birth, pointing to the effects of prenatal stress on brain development (Glynn & Sandman, 2006). Children whose mothers experienced high levels of daily hassles and pregnancy-specific anxiety show lower mental and motor developmental scores at 8 months of age after correcting for postnatal stress (Buitelaar, Huizink, Mulder, Robles de Medina, & Visser, 2003).
EFFECTS OF PRENATAL SOCIAL STRESS: PATHOLOGY OR ADAPTATION?
Researchers typically interpret the characteristic traits of individuals who were exposed to adverse environmental stimuli (stressors) during pregnancy as deviations from some standard considered optimal, and phenotypic differences in offspring are frequently called pathological. Alternatively, and in accordance with current evolutionary theory, these traits might also represent adaptive maternal effects; that is, the offspring’s fitness is enhanced by maternal adjustments to the current environmental conditions.
Adaptation through maternal effects—that is, control and/or modulation of the offspring’s phenotype—has become a key concept in modern evolutionary biology (see, e.g., Groothuis, Mu¨ ller, von Engelhardt, Carere, & Eising, 2005; Mousseau & Fox, 1998) and numerous studies to reveal the mechanism underlying these phenomena are currently underway. Particular maternal hormonal responses to environmental stimuli represent a potential tool by which development of offspring can be influenced. Indeed, in different bird species, mothers’ deposition of androgens into the yolk of their eggs varies with environmental factors or social conditions, and experimental studies have shown effects of enhanced androgen levels on offspring traits such as competitiveness or growth (Groothuis, Mu¨ ller, von Engelhardt, Carere, & Eising, 2005). Results of two recent studies in wild spotted hyenas and guinea pigs suggest that prenatal androgen exposure can adaptively influence offspring phenotype (in terms of aggression, sexual behavior, and testosterone responsiveness to social challenge) regularly in mammals as well (Dloniak, French,&Holekamp, 2006; Kemme, Kaiser,& Sachser, 2007). If such traits result in enhancement of fitness parameters such as social dominance or reproductive benefits, we can speak of an adaptive phenotype.
Possible Benefits of Altered Phenotypes
The questions arise: What is the benefit of being a masculinized daughter? And what is the benefit for sons who show less pronounced expression of male-typical traits and/or a delay in development?
Consider the case of fluctuations in the density of natural populations of mammals. Under high-density conditions, social instability is a common trait, whereas low population densities are characterized by stable social situations (von Holst, 1998). Hence, different pregnant females may experience very different degrees of social stability in their natural habitats. If a pregnant female living in a high-density population has the possibility of preprogramming her daughters in such a way that they will gain maximum reproductive success in that high-density situation, it would seem reasonable for her to masculinize them in order to make them more robust and/or more competitive. These and other masculine traits facilitate the attainment of dominant social positions, which in turn help to defend important resources such as food and shelter (which are scarce in highdensity situations) more efficiently. However, frequently a characteristic feature of masculinized females is impairment of reproductive function later in life (Kaiser & Sachser, 2005). Thus, under high-density conditions, there is likely to be a tradeoff between the benefits of a behaviorally and endocrinologically masculinized phenotype and the costs of decreased reproductive success. Although decreased reproductive success might seem inconsistent with the idea of enhanced fitness, under such conditions, masculinized females might fare better than nonmasculinized females; the latter may often fail to reproduce at all because of lower social status that prevents access to resources necessary for reproduction. Under low-density conditions, however, sufficient resources are available and competitive abilities are less important. Under such conditions, it would seem more beneficial to invest time and energy in reproductive effort rather than to build and maintain a male-typical phenotype for defending resources. Thus, under low-density conditions, reproductive success would be higher in nonmasculinized females than in masculinized ones (Kaiser & Sachser, 2005).
The argument is similar for sons. Around the time of sexual maturity, they can find themselves in different situations. Consider a low-density condition with only a few males of the same age and some females present. In such a situation, the best strategy to maximize reproductive success would be to fight for the access to a copulation partner, because usually the winners will mate. Under such conditions, mothers will maximize their own fitness if they program their sons prenatally in a way that maximizes the timely expression of male-typical traits. In contrast, when animals live at high densities in large, age-graded populations, a different situation exists: Under such conditions, in many species, high-ranking (alpha) males almost exclusively sire all the offspring. Remarkably, males usually do not attain an alpha position until well beyond the age of sexual maturity (e.g., mandrills; Setchell, Charpentier, & Wickings, 2005). A male born in a high-density population should avoid agonistic encounters at too early an age, because this will not result in reproductive success. By neither signaling sexual interest in females nor displaying other signs of sexual maturity, a pubescent male is less likely to be attacked by the alpha males. This strategy should change, however, around the time of social maturity in order to attain the alpha position that is required for reproductive success. Thus, under conditions of high density, mothers may provide their sons with a more adaptive reproductive strategy by programming them prenatally in a way that delays development and/or diminishes expression of maletypical traits until social maturity is attained (Kaiser & Sachser, 2005).
Currently, much experimental animal research is being conducted to test such hypotheses on the adaptive value of prenatal maternal programming (Dloniak, French, & Holekamp, 2006; Kemme, Kaiser, & Sachser, 2007).
Human Studies
Similar arguments for the adaptive value of the response to prenatal-stress effects in humans have been put forward. For example, Bateson et al. (2004) hypothesize that a period of starvation during pregnancy tells the developing fetus that food is probably going to be scarce in the future. Babies of such mothers often show small body weight and correspondingly modified metabolism. These traits are not necessarily pathological, inasmuch as they help the baby to cope with environments of low food availability. The proposed mechanism for these persistent effects into adulthood involves alteration in set points for various aspects of basic metabolism (e.g., glucoregulation, adiposity, and blood pressure; Roseboom, de Rooij, & Painter, 2006).
For ethical reasons, in humans it is not feasible to experimentally manipulate hormonal levels during early development or exposure to stress in pregnant mothers. Nevertheless, good evidence that the behavioral phenotype of daughters can be shaped by prenatal androgens does exist. For example, girls with congenital adrenal hyperplasia (an autosomal recessive disorder that causes elevated adrenal androgens) are exposed to elevated androgen concentrations during fetal development, and this results in a masculinized phenotype—revealed, for example, by increased rough-and-tumble play (Hines, 2006). Other evidence shows that androgen levels in women can be affected by environmental situations: Testosterone concentrations increase, for example, in periods of high-intensity exercise (Bergeron et al., 1991). We therefore propose that androgen concentrations in pregnant women may change as a result of environmental factors and that these changed androgen concentrations may influence fetal central-nervous-system differentiation during early development, thereby shaping the behavioral phenotype of the offspring later in life. Whether or not this specific phenotype represents an adaptive adjustment to the environmental conditions under which the mother has lived during pregnancy remains to be determined.
CONCLUSION
Studies of animals and humans clearly show that severe stressors acting upon a pregnant female can have profoundly negative effects on the later development and health of her offspring. In such cases, prenatal stress results in pathology and no discussion about adaptive function seems appropriate. Recent experimental animal studies of prenatal stress, when considered from an evolutionary perspective, draw attention to an additional
hypothesis: that variation in behavioral phenotype brought about by prenatal stressors may represent an adaptation to the prevailing environmental situation. From this point of view, deviations from the behavioral and physiological standard, such as masculinized daughters and infantilized sons, should not be regarded as pathological but may rather be seen as representing adaptations to the offspring’s likely environment. It is timely and exciting to test whether some of the individual variation among members of our species might not reflect the action of similar, and perhaps now vestigial, processes. Accordingly the central hypothesis is this: We share the same mechanisms with nonhuman mammals that allow infants to be preadapted to the world their mothers live in during pregnancy. In particular, we assume that the environment in which a pregnant woman lives affects her endocrine state, which in turn influences fetal brain development, thereby adapting the infant’s behavior and physiology to cope successfully with the challenges of the environmental niche of the mother. If so, children of mothers who have lived in a stable social situation during pregnancy will cope better with conditions of social stability later in life than will children whose mothers have lived under unstable social conditions. However, children whose mothers have lived under unstable social conditions during pregnancy might cope better with conditions of social instability later in life than might children of mothers who have lived in stable social situations. Future studies are required to test these hypotheses.
This article:
By: Kaiser, Sylvia; Sachser, Norbert. Current Directions in Psychological Science (Wiley-Blackwell), Apr2009, Vol. 18 Issue 2, p118-121, 4p; DOI: 10.1111/j.1467-8721.2009.01620.x
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