5
Hormonal Mediation of Physiological and Behavioral Processes That Influence Fertility

Judy L. Cameron

This chapter reviews the complex and diverse roles that hormones play in mediating the physiological and behavioral processes that influence human fertility. Much of the focus is on hormones of the reproductive axis, which mediate the physiological processes governing fertility and provide powerful modulation of sexual behavior. Secretion of these hormones changes over the life span. Reproductive hormones are secreted in surprisingly high levels in prenatal development and at this time help set the stage for later development of normal reproductive physiology and behavior in adulthood. There is then a period of childhood quiescence, when the reproductive axis is essentially “turned off”, followed by a cascade of hormonal changes that occur with puberty. In males, reproductive hormone secretion is rather stable in the adult years, with a slow decline in levels occurring with aging. In contrast, much greater fluxes in hormone secretion occur throughout adulthood in women, with large changes in hormone secretion occurring over the course of each menstrual cycle, followed by a period of irregular hormone secretion during the transition to menopause and ultimately a marked decline in reproductive hormone levels in the postmenopausal period. Understanding the changes in reproductive hormone secretion across the life span has implications for the design of biodemographic studies with regard to how and when reproductive function and sexual behavior are assessed and understanding the factors that influence these measures.

Many lifestyle choices and life events can modulate activity of the reproductive axis and thus impact significantly on both reproductive physiology and behavior. In the modern world, pharmacological modulation of repro-



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Offspring: Human Fertility Behavior in Biodemographic Perspective 5 Hormonal Mediation of Physiological and Behavioral Processes That Influence Fertility Judy L. Cameron This chapter reviews the complex and diverse roles that hormones play in mediating the physiological and behavioral processes that influence human fertility. Much of the focus is on hormones of the reproductive axis, which mediate the physiological processes governing fertility and provide powerful modulation of sexual behavior. Secretion of these hormones changes over the life span. Reproductive hormones are secreted in surprisingly high levels in prenatal development and at this time help set the stage for later development of normal reproductive physiology and behavior in adulthood. There is then a period of childhood quiescence, when the reproductive axis is essentially “turned off”, followed by a cascade of hormonal changes that occur with puberty. In males, reproductive hormone secretion is rather stable in the adult years, with a slow decline in levels occurring with aging. In contrast, much greater fluxes in hormone secretion occur throughout adulthood in women, with large changes in hormone secretion occurring over the course of each menstrual cycle, followed by a period of irregular hormone secretion during the transition to menopause and ultimately a marked decline in reproductive hormone levels in the postmenopausal period. Understanding the changes in reproductive hormone secretion across the life span has implications for the design of biodemographic studies with regard to how and when reproductive function and sexual behavior are assessed and understanding the factors that influence these measures. Many lifestyle choices and life events can modulate activity of the reproductive axis and thus impact significantly on both reproductive physiology and behavior. In the modern world, pharmacological modulation of repro-

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Offspring: Human Fertility Behavior in Biodemographic Perspective ductive hormone levels is common. Large numbers of women take exogenous hormones in the form of contraceptives, and even greater numbers of women are given estrogen replacement therapy in the postmenopausal period. A more limited but rapidly expanding subset of individuals consume steroid hormones to regulate body strength and endurance, particularly individuals who participate in competitive sports. And with the more widespread consumption of foods that contain phytoestrogens, environmental exposure to hormones is becoming an issue of greater importance. A variety of events that occur over the course of a normal life can also significantly influence activity of the reproductive axis. Pregnancy and lactation are associated with profound changes in the functioning of the reproductive axis, fertility, sexual behavior, and maternal behavior. Common life stresses, including metabolic stresses associated with undernutrition or the increased energy expenditure of participation in chronic vigorous exercise can suppress the activity of the reproductive axis. And psychosocial stresses provide an even more common inhibition to the reproductive axis. Even if reproductive hormone secretion is maintained, these life events can markedly alter circulating levels of reproductive hormones and thus influence fertility and sexual behavior. Biodemographic studies need to track lifestyle choices and life events to allow an accurate conceptualization of factors influencing fertility outcomes in human relationships. Lastly, it is important to keep in mind that there are dramatic individual differences in normal circulating levels of reproductive hormones, the amount of hormone needed to maintain normal reproductive physiology and sexual behavior, and the sensitivity of individuals to the various forms of stress-induced reproductive dysfunction. We are just beginning the daunting task of elucidating the systems in the brain that underlie these individual differences. However, it is likely that the task of understanding the role that individual differences play in contributing to fertility outcomes will be even more complex. HORMONES INFLUENCING REPRODUCTIVE FUNCTION AND BEHAVIOR Physiological Regulation by Reproductive Hormones This section provides an overview of the hormones that comprise the reproductive axis, how they are regulated and secreted, and their physiological actions in the body (for more detailed information see Steiner and Cameron, 1989; and Griffin and Ojeda, 2000). Particular attention is given to issues that influence the types of measurements made in the field of biodemography. Although many people think of reproductive function as a bodily func-

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Offspring: Human Fertility Behavior in Biodemographic Perspective tion governed by endocrine organs of the pelvis, testes, and ovaries, specialized neurons in the brain and hormones secreted by the “master endocrine organ,” the pituitary, located just beneath the brain, play critical roles in governing reproductive function (see Figure 5-1). Not only do the brain and pituitary coordinate and provide the “central drive” to the reproductive axis throughout life, the brain is also the primary site where environmental factors that modulate reproductive function act. The region of the brain involved in the regulation of reproductive function as well as many of the body’s other basic homeostatic functions (i.e., control of food intake, growth, response to stress, water balance, metabolic rate) is the hypothalamus. The hypothalamus sits at the base of the brain and is connected by a specialized portal blood system to the pituitary, just below. A population of specialized neurons in the hypothalamus produce the neurotransmitter, gonadotropin-releasing hormone (or GnRH, named for its ability to release the hormones in the pituitary that provide trophic support to the ovaries and testes—the gonadotropins— luteinizing hormone, LH and follicle-stimulating hormone, FSH). GnRH travels via the portal capillaries to the anterior pituitary, where it stimulates the synthesis and release of the pituitary hormones, LH and FSH. Many neurotransmitter systems from the brainstem, limbic system, and other areas of the hypothalamus convey information to GnRH neurons (Kordon et al., 1994). These afferent systems include neurons that contain neurotransmitters that are generally stimulatory to GnRH neurons, such as norepinephrine, dopamine, serotonin, glutamate, neuropeptide Y, and galanin, as well as neurotransmitters that are generally inhibitory to GnRH neurons, such as gamma aminobutyric acid (GABA), endogenous opiate peptides, and the central hypothalamic hormone that governs the adrenal axis, corticotropin-releasing hormone (CRH). Importantly, both in normal physiological conditions and in response to environmental signals (such as changes in nutrition, exercise, and psychosocial stress) the activity of the reproductive axis is changed by modulation of the neural inputs into GnRH neurons. For example, various forms of stress can lead to a suppression of reproductive function by acting to increase inhibitory drive to GnRH neurons by increasing either ß-endorphin or CRH input into the GnRH neuronal system (Feng et al., 1991; Norman and Smith, 1992). Decreased firing of GnRH neurons leads to less GnRH stimulation of pituitary LH and FSH release and thus less stimulation of ovarian and testicular function. It is also important to understand that changes in neuronal function in a number of neurological and psychiatric diseases can be associated with alterations in both reproductive physiology and behavior. For example, changes in both reproductive function and sexual behavior are commonly reported by patients suffering from depression, anxiety disorders, and obsessive-compulsive disorders (Clayton, 2002; Shabsigh et al., 2001). The

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Offspring: Human Fertility Behavior in Biodemographic Perspective FIGURE 5-1 Schematic diagram of the hypothalamic-pituitary-gonadal axis. Interrelationships between hormones and neurotransmitters are shown as stimulatory (+) or inhibitory (–).

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Offspring: Human Fertility Behavior in Biodemographic Perspective drugs used to treat these disorders have the potential to impact reproductive function because they can affect neural input into GnRH neurons as well as treat neurotransmitter imbalances in higher cortical areas (Clayton, 2002; Montgomery et al., 2002). GnRH is a small 10 amino acid peptide that is rapidly metabolized, so although it reaches the pituitary in adequate concentrations to stimulate the synthesis and secretion of LH and FSH, it is usually not detectable in the peripheral circulation. However, GnRH can be given systemically to stimulate activity of the reproductive axis in a number of situations where reproductive function is suppressed. In such circumstances it is important to provide GnRH in a “pulsatile” fashion (a pulse every 1 to 3 hours), in that continuous administration of GnRH will down-regulate pituitary GnRH receptors and lead to a suppression of pituitary LH and FSH release, rather than a stimulation of release (Belchetz et al., 1978). However, as one can imagine, administration of pulses of GnRH is difficult and inconvenient, usually requiring the patient to have an in-dwelling subcutaneous catheter and wear an electronic pump. Thus, restoration of normal reproductive function in individuals in which normal activity of the reproductive axis is compromised can be a fairly arduous undertaking. The converse situation, where the reproductive axis is active at an inappropriate time, such as in cases of precocious puberty, is much more easily resolved by giving a long-acting GnRH-analog (many orally active forms are available) that will provide continuous activity at the pituitary, down regulate GnRH receptors, and thus essentially shut off pituitary LH and FSH synthesis and secretion and all functions of the reproductive axis downstream from the pituitary (Moghissi, 1990). LH and FSH are glycoprotein hormones originally named for their action at the level of the ovary in the female, but the same hormones are produced in the male and govern testicular function (Griffin and Ojeda, 2000; Steiner and Cameron, 1989). The gonadotropins are released into the peripheral bloodstream and act at cells that have specific LH and FSH receptors, primarily at the gonads. In the male, LH binds to testicular cells (Leydig cells) and stimulates the synthesis and secretion of testosterone. FSH binds to Sertoli cells in the seminiferous tubules and along with testosterone stimulates the process of spermatogenesis. In the female, FSH acts on ovarian follicles to stimulate their growth and the production of estrogen. LH acts on the fully developed follicle to stimulate ovulation and then to support the function of the transient endocrine tissue formed during the last 2 weeks of each menstrual cycle, the corpus luteum (see Figure 5-2 for an overview of hormonal changes during the female menstrual cycle). The corpus luteum secretes both estrogen and progesterone, which play a critical role in preparing the uterine endometrium for implantation of a developing embryo should fertilization occur. Not surprisingly, in that both LH

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Offspring: Human Fertility Behavior in Biodemographic Perspective FIGURE 5-2 Diagrammatic representation of changes in plasma levels of estradiol, progesterone, LH, FSH, and portal levels of GnRH over the human menstrual cycle. and FSH secretion are stimulated by GnRH, both hormones are released into the bloodstream in a pulsatile manner, at rates of about one pulse every 2 to 3 hours in males and at rates that vary in females from one pulse every hour to one pulse every 8-12 hours at various stages of the menstrual cycle (Soules et al., 1984; see Figure 5-3). The pulsatile nature of LH and FSH secretion can be a confound when hormone measures are collected as part of large population studies, in that a single blood sample may be collected when hormone levels are at the peak or nadir of a pulse; thus, variation

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Offspring: Human Fertility Behavior in Biodemographic Perspective FIGURE 5-3 Examples of the pulsatile pattern of LH secretion in a woman during the late follicular phase (A) and midluteal phase (B) of the menstrual cycle. Steroid hormone levels on the day of each study are indicated on each graph. Note the dramatic slowing of pulsatile LH secretion as a result of gonadal steroid hormone negative feedback during the luteal phase. (Redrawn from Soules et al., 1984.)

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Offspring: Human Fertility Behavior in Biodemographic Perspective within an individual can be great, making it difficult to detect group differences or changes in hormone levels in response to environmental or social conditions. The gonadal steroid hormones are produced in a common synthetic pathway, all of them derived from the same precursor, cholesterol. Although androgens are commonly thought of as male hormones, they are produced in both the male and the female, and likewise the female hormone, estrogen, is present in the male and the female. In males, testosterone produced by the Leydig cells of the testes can act at its target tissues by binding to testosterone receptors, or first being converted to a more potent androgen, dihydrotestosterone, by the enzyme 5 α-reductase, or by being converted to estrogen by the enzyme aromatase and acting by binding to estrogen receptors. In females the pathway for estradiol production involves an intermediate step of androgen production, and thus the ovary is a source of low levels of androgens, principally androstenedione. The body produces three forms of estrogen: estradiol, which is the principal form of estrogen produced by the ovary; estrone; and estriol, which is produced predominantly by aromatization of androgens in peripheral fat tissue. Estriol production is thus related to body fat composition and is an important source of estrogen in the postmenopausal woman, once production of estradiol by the ovaries has ceased. Steroid hormones primarily travel through the bloodstream bound to proteins (>70 percent bound). In conditions where there is a change in the concentration of binding proteins in the circulation (i.e., with long-term changes in nutritional status, changes in either the level of energy availability or the ratio of protein to carbohydrate consumed; pregnancy, liver disease), the amount of steroid hormone in the circulation and its delivery to tissues are also affected. Assay procedures are generally available to measure both free and total (free + protein bound) steroid hormone concentrations in the blood, and it is important to distinguish between these. The gonadal steroid hormones have important actions in a number of reproductive tissues. In the male, testosterone acts to stimulate development of male secondary sexual characteristics, including enlargement of the penis and testes, increased muscle mass, deepening of the voice, and stimulation of adult hair growth patterns. In the ovaries, estrogen acts to stimulate proliferation of follicular cells and maturation of the oocyte, preparing it for ovulation. At the uterus, estrogen acts during both the follicular and luteal phases of the menstrual cycle to stimulate development of the uterine lining and prepare it for implantation of a fertilized ovum. During the late follicular phase, rising levels of estrogen also act on the cervical mucosa to stimulate the elaboration of a thin, watery mucus that is amenable to sperm penetration. At the breast, estrogen stimulates development at puberty and further development during pregnancy and plays an important role in stimu-

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Offspring: Human Fertility Behavior in Biodemographic Perspective lating milk production during lactation. Estrogen receptors are also found in many other organs, including bone, pancreas, fat, and blood vessels. Progesterone is secreted in large quantities during the last 2 weeks of each menstrual cycle. Under the influence of progesterone, the uterine glands in the endometrium enter a secretory phase and produce large amounts of glycogen, which provides nutritional support for early development of an embryo. Withdrawal of progesterone at the end of the luteal phase leads to shedding of the uterine endometrium and menses, which marks the termination of one menstrual cycle and the initiation of the next cycle. Progesterone also acts at the cervix to thicken cervical mucus, making it hostile to sperm penetration, and at the breast in late pregnancy working in concert with estrogen to prepare for lactation. All three gonadal steroid hormones also act at receptors in the brain, as will be discussed in more detail in the section below. One of the actions of these hormones in the brain is to provide feedback regulation to the hypothalamic GnRH neurons and the pituitary gonadotropin-secreting cells. Steroid hormone secretion is relatively stable in the adult years in males, although it must be remembered that the gonadotropins and testosterone are secreted in a pulsatile fashion. However, in the female there are marked changes in the circulating concentrations of gonadotropins and gonadal steroid hormones across the menstrual cycle (Erickson, 1978; Figure 5-2). The menstrual cycle is commonly divided into two phases, each of which is approximately 2 weeks in length. The first 2 weeks constitute the follicular phase. During this time small groups of ovarian follicles, each of which is a layer of cells surrounding an ovum, are developing and maturing, and as they do so under the trophic influence of FSH and LH, they secrete increasing concentrations of estradiol. Thus, over this 2-week time span, estradiol levels are very low during the first week and then increase exponentially in the second week. The rising secretion of estradiol by a fully developed follicle provides a positive feedback signal to the brain and pituitary, resulting in a massive release of LH and FSH at midcycle, and this “surge” of gonadotropins triggers ovulation, so that the mature follicle bursts and the ovum is released into the nearby fallopian tube and can travel to the uterus. The follicular cells that surrounded the developing ovum reorganize into a transient endocrine tissue, the corpus luteum, which produces both estradiol and progesterone in the last 2 weeks of the cycle, the luteal phase. Unless pregnancy occurs, the corpus luteum spontaneously regresses after about 2 weeks, and the withdrawal of progesterone support to the uterine lining leads to menstruation, which marks the beginning of a new cycle. Population studies that track reproductive hormone secretion must take these rather marked cyclic fluctuations in hormone levels into account in order to adequately examine how changes in hormone secretion in females

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Offspring: Human Fertility Behavior in Biodemographic Perspective of reproductive age are linked to fertility outcomes, behavior, or environmental conditions. Measurement of reproductive hormone levels in large field studies can be a challenge. Many of these studies are conducted at some distance from medical or laboratory facilities, where collection of blood samples, centrifugation of the samples to collect plasma, and immediate transfer to frozen storage to prevent deterioration of hormones are not possible. Fortunately, considerable advances have been made in the last decade in the development of techniques for measuring reproductive hormone levels in more easily obtainable body—fluids, saliva and urine (Campbell, 1994; Ellison, 1994; Lasley et al., 1994; Lasley and Shidleler, 1994). Improvement of the sensitivity of assay methods makes it possible to detect the low levels of hormones that are present in these fluids (Clough et al., 1992; Ellison, 1988; Stanczyk et al., 1980;). Moreover, development of collection and storage techniques that can be utilized in remote areas of the world (Lipson and Ellison, 1989; Young and Bermes, 1986) has facilitated the study of the relationship between activity of the reproductive axis and many other parameters measured in demographic population studies. Salivary samples can reflect acute changes in plasma hormone levels, while urinary measures provide an integrated assessment of steroid hormone secretion over a number of hours. Salivary samples are useful for detection of gonadal steroid hormones. Salivary steroid hormone levels reflect the levels of free hormone present in the blood (i.e., steroid that is not bound to plasma proteins). Saliva can be easily collected at frequent intervals and can be stored at room temperature for several weeks without significant deterioration of hormones. However, it is not useful for measurement of the gonadotropins, LH and FSH, and will not provide an index of changes in plasma protein levels that may be responsible for changes in free steroid hormone concentrations. Gonadotropin metabolites, as well as steroid hormones, can be measured in urine samples. And urine is particularly useful for the early detection of human chorionic gonadotropin, a placental hormone that serves as a useful indicator of early pregnancy (Canfield and O’Connor, 1991). Behavioral Regulation by Reproductive Hormones Sexual behavior can be divided into distinct aspects, in both males and females, which include attractiveness, sexual desire, arousal, orgasm, and reinitiation. Here we will not focus on detailed information about how each of these sexual behaviors is influenced by hormones but rather on two broad areas—sexual desire and sexual behavior. There is evidence that most aspects of sexual behavior, particularly in males, are influenced by gonadal steroid hormones. Steroid hormone receptors are abundant in the brain. Classical estrogen receptors (now called estrogen α-receptors) are

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Offspring: Human Fertility Behavior in Biodemographic Perspective strongly concentrated in the hypothalamus but are also found in areas of the brain with strong connections to the hypothalamus (Simerly et al., 1990). More recently, a second form of estrogen receptor (estrogen ß-receptors) was identified and found to be present throughout the rostralcaudal extent of the brain, including the cerebral cortex (Shughrue et al., 1997). Specific receptors for progesterone are induced by estrogen in hypothalamic regions of the brain, and there is also some evidence for constitutive expression of progesterone receptors (Bethea et al., 1992). Androgen receptor mapping studies have shown considerable overlap in the distribution of androgen and estrogen receptors throughout the brain (Michael et al., 1995; Simerly et al., 1990). Our discussion here will focus on the effects of gonadal steroid hormones on sexual behaviors, although there is evidence that they modulate a variety of other behaviors (Cameron, 2001). Recognition of an important link between sexual behavior and hormones arose originally from the finding that castration of adult males often results in diminished sexual activity and erectile difficulty (Luttge, 1971). In hypogonadal or castrated men, withdrawal of testosterone has been reported to result in a rapid decrease in sexual interest and activity that is reinstated with testosterone replacement (Davidson et al., 1982; Kwan et al., 1983). There are similar findings in nonhuman primate species, such that as the breeding season comes to an end and the annual cycle of testicular regression occurs, male sexual activity falls off sharply (Gordon et al., 1976). However, there is also clear evidence of tremendous variability among individuals in the rate of loss of sexual activity and the degree of diminution of sexual activity with loss of testosterone. The 1959 study by Bremer followed 244 men castrated for medical reasons and found that a third of them retained sexual interest and activity for over a year, some for up to 10 years. Similarly, in male macaques castration has been associated with a gradual reduction but not an elimination of male sexual behavior (Michael and Wilson, 1974; Phoenix et al., 1973). In normal men there is no correlation between testosterone levels and individual differences in sexual desire or behavior (Schiavi and White, 1976). This finding supports the concept that there is a threshold for testosterone actions on sexual behavior in males over which no further effects of testosterone are apparent (Meston and Frohlich, 2000). Studies in macaques suggest that other social factors interact with circulating testosterone concentrations to impact on sexual behavior. Wallen (1999) showed that suppression of testicular hormones decreased sexual activity in low-ranking male monkeys but that sexual behavior in high-ranking males was not measurably affected. In women the factors regulating sexual desire and activity, and the role that hormones play in this regard, are even less well understood. Studies of surgical ovariectomy generally report that these women have a decrease in sexual desire from presurgical levels (Dennerstein et al., 1977; Lieblum et

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Offspring: Human Fertility Behavior in Biodemographic Perspective communication between the fields of demography and biomedical sciences, such that methodologies are well understood, where possible similar measurements are made and at the least complexities understood by examining individuals are considered in the design of demographic studies. But it is also important that the information flow go in the opposite direction, so that the field of demography can play a larger role in guiding biomedical scientists toward interesting questions for detailed study. There are a number of areas in need of further investigation to fully understand the role that hormones play in fertility outcomes. In many areas, studies with more frequent measurements are needed to more accurately assess the hormonal function that may underlie physiology and behavior. In a number of areas there is also a need for more accurate quantification of other measures. For example, in the case of assessing the actual role of undernutrition on fertility in much of the developing world, more accurate measures of the level of nutritional intake and the duration of the undernourished period would help sort out why there seems to be disagreement between demographers and biomedical scientists as to whether energetic status is an important regulator of reproductive ecology. A stronger recognition of the tremendous role that individual differences play in both reproductive physiology and behavior is needed to accurately design and interpret studies. This is true in terms of both normal functioning and reactions to various stresses and environmental conditions. Measurement of a greater number of variables in a given study is going to be essential to fully understand the interactions between hormones and other variables, such as dominance, temperament, and stress sensitivity, in determining both reproductive physiology and behavior. In the end, achieving this complex understanding will likely require a multidisciplinary approach—teams of investigators with different backgrounds working together to design studies that take into account the nuances of physiology, psychology, and population biology. REFERENCES Adams, D.B., A.R. Gold, and A.D. Burt 1997 Rise in female-initiated sexual activity at ovulation and its suppression by oral contraceptives. The New England Journal of Medicine 299:1145-1150. al Bustan, M.A., N.F. el Tomi, M.F. Faiwalla, and V. Manav 1995 Maternal sexuality during pregnancy and after childbirth in Muslim Kuwaiti women. Archives of Sexual Behavior 24:207-215. Alder, E.M., A. Cook, D. Davidson, C. West, and J. Bancroft 1986 Hormones, mood and sexuality in lactating women. British Journal of Psychiatry 148:74-79. Aono, T., T. Kinugasa, T. Yamamoto, A. Miyake, and K. Kuracki 1975 Assessment of gonadotropin secretion in women with anorexia nervosa. Acta Endocrinologica (Copenhagen) 80:630-641.

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Offspring: Human Fertility Behavior in Biodemographic Perspective Bachmann, G.A., and S.R. Leiblum 1991 Sexuality in sexagenarian women. Maturitas 13:43-50. Bachmann, G.A., S.R. Leiblum, B. Sandler, W. Ainsley, R. Narcesian, R. Shelden, and H.N. Hymans 1985 Correlates of sexual desire in post-menopausal women. Maturitas 7:211-216. Bancroft, J., D. Sanders, D. Davidson, and P. Warner 1983 Mood, sexuality, hormones and the menstrual cycle. III. Sexuality and the role of androgens. Psychosomatic Medicine 45:509-516. Bain, J. 2001 Andropause: Testosterone replacement therapy for aging men. Canadian Family Physician 47:91-97. Barraclough, C., and J. Leathem 1954 Infertility induced in mice by a single injection of testosterone propionate. Proceedings of the Society for Experimental Biology and Medicine 85:673-674. Baum, M.J., B.J. Everitt, J. Herbert, and E.B. Keverne 1977 Hormonal basis of proceptivity and receptivity in female primates. Archives of Sexual Behavior 6:173-192. Belchetz, P.E., T.M. Plant, Y. Nakai, E.J. Keogh, and E. Knobil 1978 Hypophysial responses to continuous and intermittent delivery of hypothalamic gonadotropin-releasing hormone. Science 202:631-633. Belsky, J., L. Steinberg, and P. Draper 1991 Childhood experience, interpersonal development and reproductive strategy: An evolutionary theory of socialization. Child Development 62:671-675. Berga, S.L., T.L. Daniels, and D.E. Giles 1997 Women with functional hypothalamic amenorrhea but not other forms of anovulation display amplified cortisol concentrations. Fertility and Sterility 67:1024-1030. Berga, S.L., T.L. Loucks, and J.L. Cameron 2001 Endocrine and chronobiological effects of fasting in women. Fertility and Sterility 75:926-932. Berga, S.L., A.B. Loucks, W.G. Rossmanith, L.M. Kettel, G.A. Laughlin, and S.S. Yen 1991 Acceleration of luteinizing hormone pulse frequency in functional hypothalamic amenorrhea by dopaminergic blockade. Journal of Clinical Endocrinology and Metabolism 72:151-156. Berga, S.L., J.F. Mortola, L. Girton, B. Suh, G. Laughlin, P. Pham, and S.S. Yen 1989 Neuroendocrine aberrations in women with functional hypothalamic amenorrhea. Journal of Clinical Endocrinology and Metabolism 68:301-308. Bethea, C.L., W.H. Fahrenbach, S.A. Sprangers, and F. Freesh 1992 Immunocytochemical localization of progestin receptors in monkey hypothalamus: Effect of estrogen and progestin. Endocrinology 130:895-905. Bhalla, M., and J.R. Shrivatava 1974 A prospective study of the age of menarche in Kampur girls. Indian Pediatrics 11:487-493. Biederman, J., R.J. Baldessarini, J.S. Harmatz, T.M. Rivinus, G.W. Arana, D.B. Herzog, and U. Schildkrout 1986 Heterogeneity in anorexia nervosa. Biological Psychiatry 21:2113-216. Bongaarts, J. 1980 Does malnutrition affect fecundity? A summary of evidence. Science 208:564-569. Bonsall, R.W., D. Zumpe, and R.P. Michael 1978 Menstrual cycle influences on operant behavior of female rhesus monkeys. Journal of Comparative Physiological Psychology 92:846-855.

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