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This pioneering study looks at the effects of prenatal testosterone on postnatal development and behavior. Hormonal effects on behavior have long been studied in animals; the unique contribution of this book is to suggest a connection between human fetal hormones and later behavior. It details for the first time testosterone's effect on social and language development, opening a new avenue of research for cognitive neuroscience. The authors look at samples of amniotic fluid taken during amniocentesis at 16 weeks' gestation, and relate the fetal level of testosterone (which is present in fetuses of both sexes, although in different quantities) to behavior at ages 1, 2, and 4 years. They argue that the amniotic fluid provides a window into the child's past -- a chemical record of that child's time in the womb -- that allows informed prediction about the child's future brain, mind, and behavior. This is not the retrospective speculation of psychoanalysis, they point out, but an opportunity to study development prospectively and trace developmental precursors and causes of later cognition. The study suggests that prenatal levels of testosterone affect a range of later behaviors in children, from the inclination to make eye contact with others to the size of the vocabulary. It also suggests that prenatal testosterone level may be related to the development of typically "masculine" and "feminine" behaviors. The study's ongoing research explores whether fetal testosterone has any link with the risk of developing autism. Connecting endocrinology and psychology, the authors propose that there is a biological component to behaviors often thought to be produced by the social environment.
Amniotic liquid --- Fetus --- Testosterone --- Child Development --- Fetal Development --- Embryonic Development --- Embryonic and Fetal Development --- Testosterone Congeners --- Human Development --- Androstenols --- Reproduction --- Morphogenesis --- Androstenes --- Growth and Development --- Behavior and Behavior Mechanisms --- Gonadal Steroid Hormones --- Psychiatry and Psychology --- Reproductive Physiological Processes --- Gonadal Hormones --- Androstanes --- Physiological Processes --- Hormones --- Reproductive Physiological Phenomena --- Steroids --- Physiological Phenomena --- Polycyclic Compounds --- Reproductive and Urinary Physiological Phenomena --- Hormones, Hormone Substitutes, and Hormone Antagonists --- Phenomena and Processes --- Chemicals and Drugs --- Gynecology & Obstetrics --- Medicine --- Health & Biological Sciences --- Analysis --- Growth --- Testosterone. --- Analysis. --- Growth. --- Reproductive Physiologic Concepts --- Reproductive Physiological Phenomenon --- Reproductive Physiological Process --- Reproductive Physiological Concepts --- Concept, Reproductive Physiologic --- Concept, Reproductive Physiological --- Concepts, Reproductive Physiologic --- Concepts, Reproductive Physiological --- Phenomena, Reproductive Physiological --- Phenomenon, Reproductive Physiological --- Physiologic Concept, Reproductive --- Physiologic Concepts, Reproductive --- Physiological Concept, Reproductive --- Physiological Process, Reproductive --- Physiological Processes, Reproductive --- Process, Reproductive Physiological --- Processes, Reproductive Physiological --- Reproductive Physiologic Concept --- Reproductive Physiological Concept --- Hormones, Substitutes, Antagonists --- Physiology, Reproductive and Urinary --- Reproductive and Urinary Physiological Phenomenon --- Reproductive and Urinary Physiology Concepts --- Reproductive and Urinary Physiology Phenomenon --- Reproductive and Urinary Tract Physiological Concepts --- Reproductive and Urinary Tract Physiological Phenomena --- Reproductive and Urinary Tract Physiological Phenomenon --- Reproductive and Urinary Tract Physiology --- Reproductive and Urinary Physiology --- Reproductive and Urinary Physiology Phenomena --- Compounds, Polycyclic --- Physiological Concepts --- Physiological Phenomenon --- Physiological Process --- Concept, Physiological --- Concepts, Physiological --- Phenomena, Physiological --- Phenomenas, Physiological --- Phenomenon, Physiological --- Physiological Concept --- Process, Physiological --- Processes, Physiological --- Catatoxic Steroids --- Steroids, Catatoxic --- Hormone --- Hormone Receptor Agonists --- Agonists, Hormone Receptor --- Receptor Agonists, Hormone --- Hormones, Gonadal --- Sex Hormones --- Sex Steroid Hormones --- Hormones, Gonadal Steroid --- Hormones, Sex Steroid --- Steroid Hormones, Gonadal --- Steroid Hormones, Sex --- Development and Growth --- Human Reproductive Index --- Human Reproductive Indexes --- Reproductive Period --- Human Reproductive Indices --- Index, Human Reproductive --- Indexes, Human Reproductive --- Indices, Human Reproductive --- Period, Reproductive --- Periods, Reproductive --- Reproductive Index, Human --- Reproductive Indices, Human --- Reproductive Periods --- Development, Human --- Anabolic Steroids --- Androgen Analogs --- Androgen Analogues --- Androgens, Synthetic --- Synthetic Androgens --- Analogs, Androgen --- Analogues, Androgen --- Steroids, Anabolic --- Prenatal Programming --- Embryo and Fetal Development --- Programming, Prenatal --- 17-beta-Hydroxy-4-Androsten-3-one --- 17-beta-Hydroxy-8 alpha-4-Androsten-3-one --- 8-Isotestosterone --- AndroGel --- Androderm --- Andropatch --- Androtop --- AstraZeneca Brand of Testosterone --- Auxilium Pharmaceuticals Inc. Brand of Testosterone --- Bartor Brand of Testosterone --- CEPA Brand of Testosterone --- Dr. Kade Brand of Testosterone --- Faulding Brand of Testosterone --- Ferring Brand of Testosterone --- GlaxoSmithKline Brand of Testosterone --- Hauck Brand of Testosterone --- Histerone --- Ortho Brand of Testosterone --- Paladin Brand of Testosterone --- Pasadena Brand of Testosterone --- Schering Brand of Testosterone --- SmithKline Beecham Brand of Testosterone --- Solvay Brand of Testosterone --- Sterotate --- Sustanon --- Testim --- Testoderm --- Testolin --- Testopel --- Testosterone Sulfate --- Ulmer Brand of Testosterone --- Unimed Brand of Testosterone --- Watson Brand of Testosterone --- 17 beta Hydroxy 4 Androsten 3 one --- 17 beta Hydroxy 8 alpha 4 Androsten 3 one --- 8 Isotestosterone --- Embryonic Programming --- Post-implantation Embryo Development --- Postnidation Embryo Development --- Postnidation Embryo Development, Animal --- Pre-implantation Embryo Development --- Prenidation Embryo Development, Animal --- Embryo Development --- Embryogenesis --- Postimplantation Embryo Development --- Preimplantation Embryo Development --- Development, Embryo --- Development, Embryonic --- Development, Postnidation Embryo --- Embryo Development, Post-implantation --- Embryo Development, Postimplantation --- Embryo Development, Postnidation --- Embryo Development, Pre-implantation --- Embryo Development, Preimplantation --- Embryonic Developments --- Embryonic Programmings --- Post implantation Embryo Development --- Pre implantation Embryo Development --- Embryo, Mammalian --- Embryo, Nonmammalian --- Fetal Growth --- Fetal Programming --- Development, Fetal --- Fetal Programmings --- Growth, Fetal --- Infant Development --- Development, Child --- Development, Infant --- Fetal growth --- Intrauterine growth --- Liquor amnii --- growth & development --- Hydroxyandrostenes --- Endocrine Disruptors --- Hydrocarbons, Cyclic --- Endocrine Glands --- Developmental Biology --- Epigenesis, Genetic --- Psychology, Developmental --- Beginning of Human Life --- Psychology, Child --- Androgens --- Body fluids --- Embryology --- Pregnancy --- Humans --- NEUROSCIENCE/General
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There is extensive evidence from animal models that gonadal steroids, produced in fetal and neonatal life, act on the developing organism to produce sex differences far beyond the reproductive system. That early gonadal steroid exposure also plays an important role in human development is supported by studies of individuals with disorders of sex determination and differentiation. It is much less clear whether normal variation in gonadal steroid exposure predicts sexually dimorphic health outcomes or within-sex variation. This is largely due to challenges related to the assessment of gonadal steroid exposure in the developing fetus and neonate. Regarding the prenatal period, serial measurements of serum hormone levels in the fetus, for use in studies of later development, are not possible for ethical reasons. Researchers have measured hormones in maternal blood, umbilical cord blood, and amniotic fluid; used putative anthropometric indices such as the relative lengths of the 2nd and 4th digits (2D:4D); evaluated common variants in genes related to hormone production, transport, and metabolism; and examined development in opposite sex twins and the offspring of mothers with hyperandrogeny. Each of these approaches has particular strengths and notable weaknesses. Regarding the neonatal period, serial measurements in serum are often impractical for studies of typical development. Salivary hormone assays, frequently used in studies of older children and adults, have not been extensively investigated in neonates. The most appropriate timing for testing is also open to debate. Early work suggested that testosterone levels in males begin to rise after the first postnatal week, peak around the 3rd to 4th months of life, and then drop back to very low levels by 1 year. However a more recent study of 138 infants did not demonstrate this pattern. Testosterone was highest on the day of birth and gradually dropped over the first 6 months. Even less is known about patterns of early estrogen exposure, though highly sensitive bioassays indicated that sex differences are present in early childhood. In addition, the design and interpretation of studies may be impacted by widespread acceptance of conceptual frameworks that are not well-supported empirically. For example, many researchers presume that the free hormone hypothesis, which states that unbound hormone is more readily diffusible into tissues and thus a better measure of actual exposure, is true. However this hypothesis has been challenged on multiple grounds. A second example: it is generally accepted that masculinization of the human brain is primarily mediated by the androgen receptor (in contrast to rodents where the estrogen receptor plays a major role), in part because chromosomal males with complete androgen insensitivity generally espouse a female gender identity. However this is not always the case, and other sexually dimorphic outcomes have not been carefully assessed in CAIS. The aim of this research topic is to gather together experimental and review papers which address the diverse challenges in assessing prenatal and neonatal gonadal steroid exposure for studies of human development with the expectation that this will allow more critical appraisal of existing studies, identify critical research gaps, and improve the design of future studies.
Endocrinology. --- minipuberty --- Testosterone --- androgen receptor --- digit ratio --- prenatal --- sexual differentiation --- umbilical cord blood --- Opposite-sex twins --- Saliva --- Hypogonadism
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There is extensive evidence from animal models that gonadal steroids, produced in fetal and neonatal life, act on the developing organism to produce sex differences far beyond the reproductive system. That early gonadal steroid exposure also plays an important role in human development is supported by studies of individuals with disorders of sex determination and differentiation. It is much less clear whether normal variation in gonadal steroid exposure predicts sexually dimorphic health outcomes or within-sex variation. This is largely due to challenges related to the assessment of gonadal steroid exposure in the developing fetus and neonate. Regarding the prenatal period, serial measurements of serum hormone levels in the fetus, for use in studies of later development, are not possible for ethical reasons. Researchers have measured hormones in maternal blood, umbilical cord blood, and amniotic fluid; used putative anthropometric indices such as the relative lengths of the 2nd and 4th digits (2D:4D); evaluated common variants in genes related to hormone production, transport, and metabolism; and examined development in opposite sex twins and the offspring of mothers with hyperandrogeny. Each of these approaches has particular strengths and notable weaknesses. Regarding the neonatal period, serial measurements in serum are often impractical for studies of typical development. Salivary hormone assays, frequently used in studies of older children and adults, have not been extensively investigated in neonates. The most appropriate timing for testing is also open to debate. Early work suggested that testosterone levels in males begin to rise after the first postnatal week, peak around the 3rd to 4th months of life, and then drop back to very low levels by 1 year. However a more recent study of 138 infants did not demonstrate this pattern. Testosterone was highest on the day of birth and gradually dropped over the first 6 months. Even less is known about patterns of early estrogen exposure, though highly sensitive bioassays indicated that sex differences are present in early childhood. In addition, the design and interpretation of studies may be impacted by widespread acceptance of conceptual frameworks that are not well-supported empirically. For example, many researchers presume that the free hormone hypothesis, which states that unbound hormone is more readily diffusible into tissues and thus a better measure of actual exposure, is true. However this hypothesis has been challenged on multiple grounds. A second example: it is generally accepted that masculinization of the human brain is primarily mediated by the androgen receptor (in contrast to rodents where the estrogen receptor plays a major role), in part because chromosomal males with complete androgen insensitivity generally espouse a female gender identity. However this is not always the case, and other sexually dimorphic outcomes have not been carefully assessed in CAIS. The aim of this research topic is to gather together experimental and review papers which address the diverse challenges in assessing prenatal and neonatal gonadal steroid exposure for studies of human development with the expectation that this will allow more critical appraisal of existing studies, identify critical research gaps, and improve the design of future studies.
Endocrinology. --- minipuberty --- Testosterone --- androgen receptor --- digit ratio --- prenatal --- sexual differentiation --- umbilical cord blood --- Opposite-sex twins --- Saliva --- Hypogonadism
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There is extensive evidence from animal models that gonadal steroids, produced in fetal and neonatal life, act on the developing organism to produce sex differences far beyond the reproductive system. That early gonadal steroid exposure also plays an important role in human development is supported by studies of individuals with disorders of sex determination and differentiation. It is much less clear whether normal variation in gonadal steroid exposure predicts sexually dimorphic health outcomes or within-sex variation. This is largely due to challenges related to the assessment of gonadal steroid exposure in the developing fetus and neonate. Regarding the prenatal period, serial measurements of serum hormone levels in the fetus, for use in studies of later development, are not possible for ethical reasons. Researchers have measured hormones in maternal blood, umbilical cord blood, and amniotic fluid; used putative anthropometric indices such as the relative lengths of the 2nd and 4th digits (2D:4D); evaluated common variants in genes related to hormone production, transport, and metabolism; and examined development in opposite sex twins and the offspring of mothers with hyperandrogeny. Each of these approaches has particular strengths and notable weaknesses. Regarding the neonatal period, serial measurements in serum are often impractical for studies of typical development. Salivary hormone assays, frequently used in studies of older children and adults, have not been extensively investigated in neonates. The most appropriate timing for testing is also open to debate. Early work suggested that testosterone levels in males begin to rise after the first postnatal week, peak around the 3rd to 4th months of life, and then drop back to very low levels by 1 year. However a more recent study of 138 infants did not demonstrate this pattern. Testosterone was highest on the day of birth and gradually dropped over the first 6 months. Even less is known about patterns of early estrogen exposure, though highly sensitive bioassays indicated that sex differences are present in early childhood. In addition, the design and interpretation of studies may be impacted by widespread acceptance of conceptual frameworks that are not well-supported empirically. For example, many researchers presume that the free hormone hypothesis, which states that unbound hormone is more readily diffusible into tissues and thus a better measure of actual exposure, is true. However this hypothesis has been challenged on multiple grounds. A second example: it is generally accepted that masculinization of the human brain is primarily mediated by the androgen receptor (in contrast to rodents where the estrogen receptor plays a major role), in part because chromosomal males with complete androgen insensitivity generally espouse a female gender identity. However this is not always the case, and other sexually dimorphic outcomes have not been carefully assessed in CAIS. The aim of this research topic is to gather together experimental and review papers which address the diverse challenges in assessing prenatal and neonatal gonadal steroid exposure for studies of human development with the expectation that this will allow more critical appraisal of existing studies, identify critical research gaps, and improve the design of future studies.
Endocrinology. --- minipuberty --- Testosterone --- androgen receptor --- digit ratio --- prenatal --- sexual differentiation --- umbilical cord blood --- Opposite-sex twins --- Saliva --- Hypogonadism --- minipuberty --- Testosterone --- androgen receptor --- digit ratio --- prenatal --- sexual differentiation --- umbilical cord blood --- Opposite-sex twins --- Saliva --- Hypogonadism
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