The Princeton Guide to Evolution

VII.2

Evolution of Hormones and Behavior

Ellen D. Ketterson, Jonathan W. Atwell, and Joel W. McGlothlin

OUTLINE

1. Hormonal mechanisms and phenotypic variation

2. Hormones and phenotypic integration

3. Hormones and microevolution

4. Hormones and macroevolution

5. Summary and future directions

Early evolutionary biologists often focused on either genes or visible phenotypes while neglecting the myriad developmental and physiological mechanisms that link them. Recently, evolutionary biologists have become more interested in these mechanisms and have come to appreciate the role they play in the evolutionary process. This chapter focuses on a major class of physiological mechanisms—hormones—and discusses a few of the many ways that understanding hormonal mechanisms can enrich our understanding of evolution. Although the discussion is biased toward vertebrate animals and those mechanisms that mediate behavior, the same principles apply to other taxa and to other complex phenotypes.

GLOSSARY

Activational Effect. The effect of a hormone that fluctuates with circulating hormone levels and is often reversible (i.e., not permanent, as with organizational effects).

Challenge Hypothesis. The concept that the arrival of an aggressive intruder induces a hormonal response, often an elevation in testosterone, in the animal on which it intrudes. Similar to an immune response to a pathogen, which can prepare an organism for subsequent encounters with the pathogen, the hormonal response to an aggressive challenge is hypothesized to induce physiological preparation for future intrusions.

Correlational Selection. Selection that arises when traits interact in their effects on fitness; may act over time to assemble groups of traits that work well together, including hormone-mediated suites.

Hormonal Pleiotropy. Coordination of a suite of correlated or co-occurring traits by a common underlying hormonal mechanism.

Hormone. A chemical messenger molecule that is released from specialized glands or cells into the circulation and regulates a biological response at target cells or tissues.

Hormone-Mediated Suite. A group of traits that are correlated owing to the influence of a hormone.

Hormone-Mediated Trait. Phenotype affected by the action of a hormone.

Organizational Effect. Developmental effect of a hormone occurring early in life, including prenatal; usually irreversible and often involves a specific sensitive period.

Phenotypic Engineering. An experimental approach used to assess the adaptive value of a trait or traits by manipulating individual phenotypes (e.g., experimentally altering hormone levels and measuring behavioral, performance, and/or fitness consequences).

Phenotypic Integration. Patterns of correlation or interdependence among different parts of the phenotype; can be mediated by common underlying hormonal mechanisms of trait expression or development.

Phenotypic Plasticity. The capability to express more than one phenotype for a given genotype, often mediated by hormonal mechanisms. This may occur at many timescales.

Receptor. A protein on the surface or interior of a cell that binds to a hormone, leading to modulation of cellular functioning (e.g., activation/inhibition of gene transcription or second messenger networks).

Target. Tissues or cells whose function is influenced by the action of a hormone owing to the presence of hormone receptor proteins.

Trade-off. The situation that occurs when two traits (often components of fitness, e.g., mating effort versus parental effort) cannot be simultaneously maximized because the expression of each comes at the expense of the other.

1. HORMONAL MECHANISMS AND PHENOTYPIC VARIATION

What Are Hormones?

Hormones are classically defined as chemical signals produced in specialized glands and carried throughout the rest of the body by the circulatory system. They function by binding to receptor proteins located within or on the surface of the cells of target tissues, leading to altered cell physiology or changes in gene expression. The resulting hormone-mediated changes in target cells and tissues underlie variation in a diverse array of phenotypes, including physiology, morphology, and behavior.

Many kinds of molecules can act as hormones. In animals, two of the largest and best-studied classes are peptide (or protein) and steroid hormones. Peptides are composed of chains of amino acids and usually interact with receptors on the cell membrane, typically activating second messenger systems that trigger cascading reactions within the cell. Steroid hormones are synthesized from cholesterol and tend to bind to intracellular receptors, which then directly or indirectly regulate gene expression. Examples of protein hormones relevant to behavior include prolactin, arginine vasopressin, and melanocortin, and examples of relevant steroid hormones include estrogens, androgens (e.g., testosterone), and glucocorticoids (e.g., cortisol and corticosterone).

Neurotransmitters, such as dopamine or serotonin, usually act at neural synapses to enable neural transmission and are thus often considered as a separate class of chemical messengers. However, recent studies blur the distinction between hormones and neurotransmitters. Classical hormones such as estrogen can be synthesized in the brain and act locally and instantaneously to modulate behavior, much like a neurotransmitter. Similarly, epinephrine (adrenaline) is produced by the adrenal glands and can influence behavior both as a neurotransmitter and as a classical hormone in non-neural tissues. Further, tissues not traditionally considered endocrine glands are known to secrete hormones; for example, the liver produces insulin-like growth factor (IGF-1), a peptide hormone linked to variation in vertebrate life history and behavior.

Organizational and Activational Effects of Hormones

Hormonal influences that occur as part of developmental processes are referred to as organizational effects and often persist throughout the life of the animal. For example, although male and female genomes are nearly identical, minor differences (i.e., a single gene or chromosome determining sex) can give rise to striking dissimilarities in sexual phenotypes because of the organizational action of hormones during early development. Within-sex polymorphisms can also be associated with organizational hormonal differences (e.g., “sneaker” males in fish, and plumage color polymorphisms in songbirds). The hormonal environment that an embryo experiences during sensitive phases of development is often influenced by its mother’s hormonal state. Female birds deposit hormones in yolk that affect embryonic development and the behavior of hatchlings; female mammals provide a uterine hormonal environment that can influence the behavioral development of offspring before birth.

Hormonal influences on phenotype that fluctuate with hormone levels are known as activational effects. Activational effects of hormones often underlie reversible changes, such as behavioral flexibility in response to changes in the physical or social environment. Some within-sex polymorphisms in insects, lizards, and other groups are activational in nature, allowing, for example, males to alternate between territorial and satellite strategies depending on the situation.

Sites and Modes of Hormone Action

For behavioral traits, the target tissues of hormone action are often located in the central nervous system. These targets include the brain and spinal cord, which are sensitive to both organizational and activational effects of hormones. Other target tissues relevant to behavior include structures related to social interactions (e.g., a cock’s comb, which responds to androgens) or locomotion. For physiological traits, hormones may affect a wide variety of target tissues to influence metabolism, biological rhythms, and immune function.

Importantly, variation in the density or location of hormone receptors among the cells of target tissues can determine the phenotypic response to a hormone. Receptor location and density are known to vary dynamically during development, between sexes, between seasons, and over short timescales in adulthood. An example involving sex role reversal can be seen in the African black coucal, a bird species in which “traditional” sex roles are reversed. In the black coucal, females sing, fight, and compete with one another for mates, while males incubate eggs and care for the young. Cornelia Voigt and colleagues have shown that although male black coucals have much higher testosterone levels during breeding, the density of androgen receptors in key brain regions is much lower in males than in females, apparently facilitating the observed “reversal” in sexual behavior.

Hormonal Cascades

Hormones rarely act alone. Many exist as part of a hormonal axis or cascade, in which the synthesis or release of one hormone is itself modulated by another hormone, usually one produced in another part of the body. The hypothalamic-pituitary-gonadal (HPG) endocrine axis is a classic example. The HPG axis is initiated by a peptide hormone, gonadotropin-releasing hormone (GnRH), that is released from the hypothalamus in the brain and acts on the pituitary gland situated directly below the brain, prompting it to release luteinizing hormone (LH) and follicle stimulating hormone (FSH). LH subsequently modulates the release of steroid hormones (androgens or estrogens) by the gonads (the testes or ovaries). Gonadal hormones may in turn cause negative feedback, downregulating the release of hormones earlier in the pathway to suppress the activity of the axis. Events that regulate the initial release of GnRH from the hypothalamus, which may involve other hormones or neuropeptides, are less completely understood and are the subject of active research.

As demonstrated by the HPG axis, the circulating concentration of any given hormone signal may be regulated at multiple points in a hormonal cascade, resulting in highly flexible hormonal systems. Adding even more complexity, hormonal axes often interact with one another. For example, the hypothalamic-pituitary-adrenal (HPA) axis, which functions in response to acute and chronic stress, interacts in complex ways with the HPG axis. Interactions between these two axes allow animals not only to modulate reproductive effort in response to stressors but also to modulate their sensitivity to stressors in response to reproductive state. As an example, responsiveness of the HPA axis to stressors can decline with age, allowing older individuals to invest relatively more in reproduction at a potential cost to investment in self-maintenance (e.g., growth or immunity).

Sources of Variation in Hormone-Mediated Phenotypes

Hormone-mediated behaviors often show noticeable variation within and among natural populations. Variation in hormone signal concentrations or hormone receptor distributions in target tissues are the most obvious determinants of this variation, but additional layers of complexity are almost always present. The activity of certain hormones is influenced by the presence of hormone-binding proteins, which may facilitate or inhibit the delivery of the hormone to target tissues, depending on the relative binding affinities of the hormone for the binding protein and the target hormone receptor. Similarly, metabolizing enzymes can act to alter hormone signal concentrations over time by affecting their half-life in the circulation or their conversion to related hormones that are active in different tissues. Testosterone, for example, is often converted to a form of estrogen in the brain, where it then binds to estrogen receptors to alter gene transcription.

Adding to the complexity of characterizing hormonal regulation of behavior is that this regulation is not unidirectional: behavioral experiences can also alter levels of hormones and their receptors. Thus, hormones influence behavior, but behavior also influences hormones. One example of behavioral effects on hormone levels is the challenge hypothesis. First proposed by John Wingfield, this hypothesis predicts that animals will respond to an aggressive challenge with an increase in testosterone. This prediction has been borne out in a wide array of vertebrate taxa and has even been applied to insects that respond to an aggressive challenge with an increase in juvenile hormone.

Of particular interest to evolutionary biologists is the possibility that individual variation in hormone-mediated phenotypes has a genetic basis and may thus serve as the raw material of evolution. Although studies quantifying heritable genetic variation in hormone levels or hormone-mediated traits are rare, it is clear from both artificial selection and pedigree studies that such variation does exist. Just as often, however, individual variation in hormones and hormonally mediated phenotypes may reflect environmental variation. Cues such as temperature, photoperiod, and food availability can alter phenotypes through the action of hormones. In these cases, hormones serve to mediate phenotypic plasticity—that is, to create different phenotypes from a single genotype. Birds fatten before they migrate, and become active at night rather than during the day, hamsters hibernate in winter, and many temperate-zone organisms breed when the days are long. These seasonal changes in phenotypic expression are examples of phenotypic plasticity modulated by the environment, and all have been shown to have a hormonal basis that responds to day length. Hormone-mediated plasticity can also facilitate shorter-term changes in behavior, for example, when a spike in adrenaline or glucocorticoids modulates “fight-or-flight” behavior in stressful situations. The role of hormones in facilitating plastic responses to variable environments is also likely to have a genetic basis that can evolve in response to selection. Thus, studying hormonal mechanisms may provide particular insight into how populations adapt to environmental change.

2. HORMONES AND PHENOTYPIC INTEGRATION

Hormonal Pleiotropy and Phenotypic Integration

Another reason that hormones are of interest to evolutionary biologists is their ability to influence the expression of suites of correlated traits. This property means that hormones are well suited to act as a physiological mechanism underlying phenotypic integration, the pattern of correlation among an organism’s different traits. By analogy to genetic pleiotropy, the term used to describe the effect of an individual gene on multiple traits, an individual hormone’s influences on multiple traits may also be thought of as a form of pleiotropy. The classic example of hormonal pleiotropy is testosterone, which has been experimentally and observationally linked to many behavioral, morphological, and physiological processes, including aggression, parental care, ornament expression, and immune function. Like genetic pleiotropy, this shared mechanism may result in trade-offs (e.g., between aggression and parental care).

Phenotypic integration interests evolutionary biologists for two reasons. First, when traits are genetically correlated with one another, they cannot evolve independently; selection acting on one trait will lead to evolutionary change in correlated traits as a by-product. Second, patterns of phenotypic integration often represent adaptive solutions to problems posed by an organism’s environment. Ultimately, traits may be correlated because they work well together, and selection has favored mechanisms that cause their expression to be coordinated.

There are many examples of suites of traits that foster survival and reproduction more effectively when they are expressed in a coordinated fashion. Cryptic appearance, for example, is more likely to reduce predation if it is coupled with cryptic behavior. Bright colors may be more attractive to potential mates when associated with loud or complex and engaging displays. Infected animals may be more likely to survive an infection if they run a fever and become lethargic and anorexic. Each of these examples demonstrates how coexpression of behavior, physiology, and morphology can achieve adaptive solutions to problems such as avoiding predation, attracting a mate, or recovering from infection, and each may involve regulation by hormonal mechanisms.

Examples of associations among traits orchestrated by hormones to produce complex phenotypes come from a wide array of organisms, including beetles, butterflies, crickets, lizards, rodents, and songbirds. One theme that emerges is that hormones often act as mechanistic links in trade-offs in life histories. For example, allocation of time and energy to parenting can be in conflict with time and energy allocated to mating, reproduction, and self-maintenance. A common regulatory mechanism like a hormone may allow organisms to plastically adjust multiple traits in a coordinated fashion, allowing changes in allocation over short periods within a lifetime or over environments that vary in space and time.

Hormones and Correlated Evolution

As both integrators of multiple traits and environmentally sensitive links between genotype and phenotype, hormonal mechanisms are uniquely situated to play a particularly important role in shaping the evolution of complex traits. For example, selection of one trait in a hormone-mediated suite (e.g., aggressive behavior) could lead to correlated responses in other traits (e.g., parental behavior) owing to an altered profile of a shared hormonal mechanism (e.g., testosterone). Because of this potential to cause evolutionary change in traits that may not be directly favored by natural selection, hormones are often considered to act as evolutionary constraints. In extreme cases, such as when a hormone-mediated trait is under very strong selection, it is theoretically possible for maladaptive changes to occur in correlated traits. At the other extreme, however, hormone-mediated correlations can cause adaptation to proceed more quickly if selection favors simultaneous changes in many traits.

From another perspective, hormone-mediated suites of traits may be seen as adaptations that have been assembled by natural selection. When traits function together as a group, they are often subject to a type of natural selection called correlational selection. Such selection occurs when traits interact in their effects on fitness, as, for example, when the probability of surviving or reproducing depends less on the value of a single trait than on whether the values of two traits match. Thus, sexual ornaments may be advantageous only when coexpressed with large body size, and mismatches of ornament and body size could be detrimental. Correlational selection is likely to be common in nature, and although perhaps understudied in relation to other forms of selection, a few demonstrations in the wild have been reported, including a study of antipredator behavior and color patterns in garter snakes by Edmund Brodie III, and our own work involving body size and color patterns in dark-eyed juncos.

Evidence suggests that such hormone-mediated correlations may facilitate adaptation and diversification, allowing simultaneous shifts for groups of traits that are favored together in a new or changing environment. Comparative studies reveal that hormonal mechanisms and hormone-mediated phenotypic integration are highly conserved across taxa and over long evolutionary timescales. For example, the HPG axis described earlier is incredibly similar in most vertebrates, as are the types of traits regulated by the androgens it produces. However, studies of closely related species and populations also reveal that certain phenotypes can sometimes become dissociated from the systemic effects of hormone signal levels (e.g., via changes in receptor densities in a target tissue). For example, although many species of songbirds show decreases in parental care in response to testosterone, closely related species sometimes show insensitivity to testosterone. This insensitivity seems to be an evolved response to other aspects of the species’ life history or environment, such as breeding season length. Such evolutionary change in the makeup of hormone-mediated suites is likely driven by shifts in the strength or direction of correlational selection, which may be caused by environmental change or colonization of a new habitat.

Ongoing research aims to more precisely understand the role that hormonal mechanisms play in both evolution within populations (i.e., microevolution) and large-scale patterns of evolutionary history (i.e., macroevolution). We discuss each in turn in the following sections.

3. HORMONES AND MICROEVOLUTION

Of deep interest to biologists studying microevolution are the relationships among phenotypes, environmental conditions, and fitness, including the mechanisms that generate and maintain variation within populations and lead to phenotypic changes within populations and among closely related populations. In recent decades, both experimental and observational studies have begun to characterize the evolutionary dynamics of hormonal mechanisms and hormone-mediated phenotypes in natural systems.

Phenotypic Engineering

One approach to establishing how selection operates on hormonal variation is to employ phenotypic engineering. By manipulating hormone levels or receptor-binding properties with pharmacological agents, it is possible to modify phenotypes and measure the resultant fitness consequences in field studies of free-living animals. This approach has been employed successfully to investigate the fitness consequences of elevated or reduced hormone levels in several natural systems.

Our own work (involving many collaborators over several decades) on dark-eyed juncos, a species of songbird, is an example of this approach. In these studies, testosterone implants were used to elevate hormone levels of male juncos to naturally high levels throughout the breeding season to document behavioral and physiological responses as well as to measure survival and reproductive success. Relative to controls, high-testosterone males sang more often and had higher mating success. The benefits of higher testosterone were accompanied by costs, however. Testosterone led to higher levels of stress hormones (corticosterone), suppressed immune activity, and decreased survival. These experimental results demonstrated that opposing selective forces (survival costs versus reproductive benefits) may act on testosterone and its associated traits. Similar phenotypic engineering approaches have been employed in several other systems, including amphibians, reptiles, and other birds.

Natural Variation and Fitness in the Wild

Despite the power of hormonal manipulations to experimentally demonstrate hormonal mechanisms and trade-offs, one limitation is that manipulations may obscure natural variation in hormones and hormone-mediated phenotypes as exhibited in nature. Natural variation among individuals, which may occur in hormone levels, receptor densities, or other aspects of hormone pathways, is required for selection to operate on suites of hormone-mediated traits.

Several recent studies of natural populations have found correlations between natural variation in hormone levels and both phenotypes and components of fitness. Examples of such covariation measured in wild populations include our own work examining testosterone, aggression, and parental behavior in juncos, as well as Maria Thaker’s work on corticosterone, a glucocorticoid stress hormone, and predator escape behaviors in tree lizards. Several recent studies have shown relationships between corticosterone and survival or reproductive success in the wild. Taken together, these results indicate that hormone-mediated traits are often the targets of selection and that understanding the causes and consequences of natural variation in hormone pathways can be informative for understanding the evolution of natural populations.

Artificial Selection

Artificial selection studies conducted in the laboratory have also provided insight into the evolutionary importance of coordinating hormonal mechanisms. Animal breeders have known for centuries that selecting particular behavioral or morphological traits brings along suites of correlated phenotypes. Contemporary scientists have selected for specific behavioral traits or hormone levels and quantified the observed changes. For example, Kees van Oers and colleagues selected for “fast” and “slow” exploratory boldness behavior in male great tits (songbirds) and found correlated responses in testosterone and immune function in just a handful of generations. Similarly, when Suzanne Mills and colleagues selected on immune function in voles, they found it led to correlated responses in testosterone levels.

Such artificial selection studies reveal substantial heritable genetic variation in hormonal mechanisms, which could provide the raw material for selection to shape hormone-mediated phenotypes over short-term evolutionary timescales. Artificial selection studies also demonstrate the types of integrated evolutionary responses that may be expected for hormone-mediated suites in the wild.

Population Divergence in Hormone-Mediated Suites

Another approach to characterizing the microevolutionary dynamics of hormone-mediated traits is to examine variation in hormonal mechanisms among closely related populations. Comparing tropical versus temperate populations of the same species, for example, has revealed that hormonal profiles may differ dramatically within a species across environments, accompanied by correlated changes in life history and behavior. One such example comes from Brent Horton and colleagues, who recently showed that orange-crowned warblers breeding in Alaska exhibit higher early-peak and much more seasonally variable testosterone levels across the breeding season when compared with a population of the same species breeding off the coast of Southern California. Similarly, studies of urban versus wildland populations of the same species revealed that phenotypic divergence in hormone levels and hormone-mediated suites can occur over just a few generations in response to novel or changing environments. In some cases, major behavioral shifts may be required for population persistence in a novel or altered environment, and hormonal responses may accommodate and coordinate such behavioral change. “Common garden” studies of hormonal, behavioral, morphological, and physiological variation—in which individuals from different populations are raised under identical environmental conditions—have indicated that both phenotypic plasticity and genetic differences may underlie hormonally mediated variation among recently diverged populations. As examples, two distinct studies of urban versus wildland songbirds by Jesko Partecke (European blackbirds in Germany) and our research group (dark-eyed juncos in Southern California) have found that short-term elevation of stress hormones (i.e., corticosterone) in response to capture and handling was reduced in recently established urban songbird populations, and these differences persisted, in part, in subsequent common garden studies—indicating that both rapid evolution and phenotypic plasticity likely play a role in hormonal and behavioral divergence in these systems.

4. HORMONES AND MACROEVOLUTION

To study the long-term evolutionary significance of hormonal mechanisms, evolutionary biologists use the comparative method, studying patterns of diversity across taxa to make inferences about the origins and rates of diversification of endocrine systems and hormone-mediated traits. Such studies have revealed that molecules that act as hormones are relatively few in number and phylogenetically ancient. For example, several families of hormones, including vasopressin-oxytocin family peptides, gonadotropin-releasing peptides, and steroids such as androgens and estrogens are present in and serve similar regulatory functions across nearly all studied vertebrate taxa with only minor modifications in their molecular structure. We detail just two of the many examples of how the comparative approach has informed us about the role of hormones in macroevolutionary patterns.

Evolution of Hormones and Their Receptors

Because hormone-mediated phenotypes emerge from interactions between hormones and receptors, one particularly interesting question is, How do hormone-receptor molecules evolve to serve new functions? An example can be found in work by Joseph Thornton and colleagues on two classes of steroid hormones, mineralocorticoids and glucocorticoids. Each class of hormones plays key roles in electrolyte balance and in metabolic responses to stressors, respectively, and each has its own class of receptor, the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR). Both receptors act as transcription factors that bind to different regions of DNA. Comparative evidence by Thornton’s group indicates that the genes that code for MR and GR arose through gene duplication. By comparing the sequences for MR and GR along different fish and tetrapod lineages, scientists have succeeded in re-creating the sequence of the ancestral corticoid receptor that preceded present-day MR and GR by 450 million years. By synthesizing the ancestral receptor in the lab and studying its ability to bind with extant hormones, they were able to show how sequential changes in the amino acid sequence of both classes of receptors affected their ability to bind with both ancient and more modern forms of their hormones. This unique experimental twist on the comparative approach has revealed not only how strongly form, function, and mechanisms of action of hormones are conserved, but also how evolutionary innovation has proceeded across distant taxa over vast timescales.

Comparative Studies of Hormones, Behavior, and Life History

The diversity of behavioral traits and complex phenotypes among closely related species has also been the subject of studies aiming to understand the physiological mechanisms underlying more recent evolution. Several such studies have revealed that relatively minor variations in neuroendocrine mechanisms underlie major behavioral and life history differences among closely related species. For example, a series of studies by Larry Young and colleagues on prairie voles, which are among the few percent of socially monogamous mammals, showed that vasopressin receptor gene expression in the brain’s reward circuitry is greater in prairie voles versus nonmonogamous vole species. Furthermore, Young’s group found that males of nonmonogamous vole species could be induced to express monogamous-like behavior simply by overexpressing the vasopressin receptor gene in this same brain area. Similarly, studies of closely related songbird species by James Goodson and colleagues showed that different patterns of neuropeptide activation of social brain nuclei underlie striking differences in social systems (e.g., territorial versus gregarious).

5. SUMMARY AND FUTURE DIRECTIONS

Hormonal mechanisms regulate the coordinated expression of multiple behavioral, physiological, and morphological phenotypes in ways that often seem to optimize individual fitness in the face of conflicting demands. Hormones are of particular interest to evolutionary biologists because they have pleiotropic effects and can modulate both genetic and plastic responses to environmental change for suites of traits. Although hormonal mechanisms themselves are quite conserved across taxa, specific traits and trade-offs mediated by these mechanisms show wide diversity across the animal kingdom. Artificial selection experiments and studies of evolution within and among natural populations have revealed the potential for hormone-mediated suites to evolve rapidly.

Despite a growing understanding of the role of hormones in the evolution of behavior and other complex phenotypes, there is still much to learn. For example, we know little about how readily hormone-mediated correlations may be assembled and dismantled by natural selection. Similarly, it is unclear whether hormonal mechanisms are more likely to limit or facilitate adaptation. Emerging experimental approaches in behavioral neuroendocrinology as well as continued development of genomic and bioinformatic tools should lead to a better understanding of the mechanisms by which hormones influence evolutionary change and phenotypic plasticity, and serve to produce a clearer picture of the evolutionary history of endocrine systems.

The principles described here may have practical applications. A few areas in which the intersection between hormones and evolution may provide insight include adaptation of natural populations to anthropogenic environmental change, host-pathogen dynamics including human disease, and the effects of endocrine-disrupting chemicals in the environment.

A key message of this chapter is that both the plastic responses of organisms and the genetic evolution of populations are not likely to involve single traits in isolation but rather correlated suites of traits that are often under hormonal regulation. Such hormonal mechanisms have likely evolved to successfully coordinate multiple behavioral, morphological, and physiological traits, but once established, may influence the evolutionary trajectory of populations. Thus, hormonal mechanisms have the potential to play a fundamental role in limiting or facilitating patterns of diversification of behavior and other complex traits. Understanding this role can provide unique insights into both contemporary microevolutionary processes and historical macroevolutionary patterns.