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The placebo effect in the immune and endocrine system is basically a conditioned response, whereby classical conditioning plays a key role. Conditioned immunosuppression affects a number of immune mediators, like interleukin-2 and interferon-gamma. Some negative allergic reactions may be induced by the administration of nocebos. The responses of some hormones, like insulin, growth hormone, and cortisol, have been successfully conditioned. In addition, the hypothalamus-pituitary-adrenal axis may represent an important system in placebo and nocebo responsiveness.

In this chapter we provide an overview of recent research on the biopsychological correlates of implicit motives. We review evidence for a role of gonadal steroids (testosterone and estradiol) as well as stress axis activation in power motivation arousal and satisfaction/frustration, summarize recent research on the role of progesterone and affiliation motivation, and discuss a possible role for arginine–vasopressin in achievement motivation. We also present findings from brain imaging work that indicate that the needs for power, affiliation, and achievement modulate activity in a core motivational circuit consisting of striatum, amygdala, orbitofrontal cortex, and insula when nonverbal social incentives are processed.

This essay describes neurobiological and neuroendocrine mechanisms that are implicated in human caregiving. Anatomical and biochemical systems that first appeared in the evolutionary transition from reptiles to mammals allowed the emergence of mammalian sociality. Human behaviors are characterized by symbiotic and reciprocal interactions, which are necessary for successful caregiving. The autonomic nervous system, and especially the mammalian changes in the parasympathetic system, provides an essential neural platform for social behavior. Especially critical to coordinating the features of positive sociality are neuropeptides including oxytocin and vasopressin. These neuropeptides modulate the mammalian autonomic nervous system to foster the expression of social behaviors and, when adaptive, defensive behaviors. Oxytocin, the same peptide that regulates various aspects of mammalian reproduction including birth, lactation and maternal behavior, is also involved in the beneficial and reciprocal effects of caregiving on physiology, behavior and health.

This chapter reviews epidemiologic studies on metabolic and hormonal predictors of obesity. It focuses primarily on prospective cohort studies, first discussing metabolic predictors, including resting metabolic rate (RMR), respiratory quotient (RQ), and insulin sensitivity, and then examining studies of hormonal predictors (such as ghrelin, leptin, and adiponectin) of obesity. For inflammatory cytokines, the chapter reviews recent prospective studies on C-reactive protein (CRP) and fibrinogen. Finally, it discusses the relationship between the stress hormone cortisol and adiposity.

Endocrine systems play an important role in development, and in maintaining normal health. The hypothalamic–pituitary–adrenal (HPA) axis is one plausible pathway as it may be related to frailty, cognitive decline and cardiometabolic disturbances. The natural history of cortisol responsiveness is not well described but adaptation to chronic stressors may result in reduced diurnal variability. Observational evidence suggests that life course stressors, both physical and psychological, may have long term influences on the HPA axis. Intervention studies have suggested that these patterns are reversible. Our meta-analyses have found that reduced cortisol diurnal variability was the most consistent predictor of worse physical performance and worse cognition on tests of fluid capability. These results provide evidence for the role of the HPA axis in age-related decline. Future research needs to examine longitudinal changes in HPA dynamics and the potential role of the HPA axis in targeting or monitoring public health interventions.

The adrenal cortex secretes a wide range of steroids. Nearly all attention has been focused on the role in brain damage of cortisol (or corticosterone, its counterpart in some species). Only recently have the powerful effects on neural function of other adrenal-derived steroids been recognised. The secretion of cortisol is highly labile. There are marked diurnal variations: highest levels coincide with the start of activity, irrespective of when that occurs (e.g. in the early morning in humans, but at the start of the night in rats and other nocturnal species).

This chapter describes fear and its neuroendocrine regulation. It specifically highlights the role of elevated cortisol and corticotropin-releasing hormone (CRH) in the regulation of fear responses, placing a particular emphasis on the central nucleus of the amygdala and the bed nucleus of the stria terminalis. It starts with a discussion of the central motive state of fear and its biological basis. It then discusses the neural circuitry that underlies the perception of fearful events and fear-related behaviors. Next, it presents a description of the neuroendocrine basis of fear and a discussion of glucocorticoids and CRH in sustaining fear-related behaviors. Moreover, it evaluates the role of norepinephrine and epinephrine in facilitating responses to and memory of aversive events. It is showed that neuropeptides such as CRH chemically code the sense of fear that is sustained by elevated cortisol and that may underlie the excessively shy, fearful child's hyperexcitable central state.

This chapter presents the data that adrenocortical activity is an important factor mediating the child's internal social milieu. The results show that rat pups may “internalize” the results of early maternal regulation, encoded as information about how easy or difficult it is to activate stress-sensitive systems in adulthood. Discussion on attachment, temperament and adrenocortical function is also provided. Even though only a few studies on attachment and cortisol in humans have been conducted, it is probably that thresholds for adrenocortical function are influenced by early mother-child interactions. The most consistent result observed is that infants with disorganized attachments display larger cortisol responses to the Strange Situation than do those with organized attachments. It can be concluded that there are at least two pathways to hyperactivity of the adrenocortical system: (1) innate constitutional differences (temperament) and (2) less than optimal mother-infant interactions early in life.

This chapter looks at how environmental factors—such as parenting, abuse, poverty, head injury, birth complications, nutrition, toxins, and a variety of other factors—can contribute to psychopathy. As discussed in Chapter 2, these factors have the ability to change gene transcription, or the way in which a gene's DNA sequence produces proteins. This may, in turn, alter neurochemical signaling mechanisms or the way that the brain develops. Environmental factors can also alter levels of neurochemicals such as hormones. For example, trauma or chronic stress can alter cortisol levels and thus change the way the brain responds to stress in the future. Finally, environmental influences in the womb or in early childhood can alter the way that the brain develops, leading to differences in structure and functioning.

Although ECT was developed as a treatment for schizophrenia, its ease of use, its safety, and the lack of effective treatments for many psychiatric conditions encouraged experimentation with this therapy to treat other disorders. These explorations define a cluster of conditions— acute and chronic psychosis, psychiatric disorders in pregnancy and the postpartum period, and intractable seizure disorders—in which ECT has a clinical role. Strongly held beliefs (delusions), abnormal sensory experiences (hallucinations, illusions) that are not based upon reality, and beliefs that others are paying special attention or plotting harm to the subject (paranoid thoughts) impair social functioning and disrupt family life. Thought disorders are the central peculiarity of schizophrenia but are also frequently found in patients with depression, mania, toxic states, and brain disorders. Regardless of the cause or the associated signs and symptoms, treatment can reduce the psychosis. This benefit is often given small notice, however, because ECT is widely regarded as an antidepressant, not an antipsychotic, treatment. The relief of psychosis afforded by ECT varies with the underlying condition. Disorders in thought in patients with depression or mania are readily relieved. Indeed, the more severe form of psychotic depression is relieved more rapidly than nonpsychotic depression. When ECT is used to treat patients with malignant catatonia and delirium, the psychosis is relieved at the same time as the toxic state. When psychosis dominates the clinical condition without other features, schizophrenia is the usual diagnosis. For acute schizophrenia dominated by the positive symptoms of paranoia, catatonia, or excitement, ECT is quite helpful. It is not helpful for the chronic varieties dominated by passivity and withdrawal, the negative signs of the illness. The clinical approach to the diagnosis of a psychotic condition is to exclude other causes for psychosis first and reserve the label “schizophrenia” for the residue of “not otherwise diagnosed” psychotic conditions. While we are able to ameliorate the psychoses in mood disorders and toxic states, palliation and symptom reduction are the best that we can offer other psychotic patients. Electroconvulsive therapy and insulin coma therapy were the main treatments for psychosis at the time when Thorazine and other new antipsychotic drugs were introduced in the 1950s.

This chapter describes the various methods used for quantifying concentrations of circulating hormones and thus assessing endocrine function. The paradigm of feedback regulation (for example, of the hypothalamic-pituitary-target gland axis) is central to this assessment of endocrine status. Any disruption in such an axis can cause alterations in trophic and target hormone pairs. High concentration of a target gland hormone coupled with low concentration of the corresponding trophic hormone (e.g., pituitary hormone) suggests autonomous secretion by the target endocrine organ, as is typical in primary hyperthyroidism, e.g., high thyroxine (T4), suppressed thyroid stimulating hormone (TSH). Elevated concentrations of both members of a hormone pair usually indicate autonomous secretion of the trophic hormone, either from the normal site or from a tumor in an “ectopic” (extraglandular) location. For example, excess cortisol production driven by a high plasma adrenocorticotropic hormone (ACTH) level may be due to the secretion of pituitary ACTH or secretion of ACTH by lung tumors. Alternatively, the combined elevation of trophic and target endocrine gland hormones can result from resistance to the action of the target endocrine gland hormone e.g., elevated luteinizing hormone (LH) and testosterone in androgen resistance. Autonomous hypersecretion of the trophic hormone typically results in clinical evidence of target gland hormone excess, whereas resistance to the target gland hormone leads to manifestations of hormone deficiency. Hormones circulating in the plasma were first detected by in vivo bioassays, in which plasma or extracts of plasma were injected into animals and biological responses were measured. Unfortunately, most in vivo bioassays lack the precision, sensitivity, and specificity required to measure the low concentrations of many hormones in plasma, and the assays are cumbersome and impractical for routine use in clinical chemistry laboratories. Great progress in measuring plasma hormone concentrations came with the development of radioimmunoassays (RIAs) in the late 1950s. An unknown concentration of hormone in plasma is estimated by allowing competition with a labeled hormone or analog for specific binding sites on an antibody.

Chapter 7 considers stress as a modulator of adolescent development. It starts with an overview of the key hormones in the hypothalamic–pituitary–adrenal (HPA) axis and describes responses of the HPA axis and the sympathetic nervous system to stress. The HPA stress response is somewhat different in adolescents compared with adults; adolescents often show heightened stress reactivity and a protracted recovery period after psychological stressors compared to adults. The chapter then reviews research on chronic stress-induced anatomical and functional changes in the hippocampus, prefrontal cortex, and amygdala, three brain regions involved in regulation of the HPA axis and modulation of stress responses. Stress-induced changes in these brain regions include dendritic complexity of pyramidal cells, attenuated long-term potentiation, attention deficits, and changes in fear and depressive-like behaviors; these changes may be long-lasting. The perfect storm alludes to the alignment of three features of adolescence that together may render the adolescent brain especially vulnerable to effects of chronic stress: (a) The quality and quantity of stressors is different during adolescence than in adulthood; (b) stress reactivity is higher during adolescence; and (c) the hippocampus, prefrontal cortex, and amygdala are sensitive to stress hormones and are still developing during adolescence. However, the developing adolescent brain may be more resilient to insult, more responsive to interventions, and more buffered by social support systems.

Memory consolidation processes can be highly selective. For example, negative emotional aspects of events tend to be consolidated more readily than other, more neutral, aspects. This chapter discusses evidence that the sleeping brain provides an ideal environment for memory consolidation, and that active, as opposed to passive, sleep-based consolidation processes are particularly important in explaining why emotional memories are retained so well. I also review evidence that elevated levels of stress hormones (cortisol, norepinephrine), particularly during the time of the initial experience, support downstream emotional memory consolidation. The chapter then proposes a working model that describes why arousal and stress at encoding may set the stage for sleep to etch emotional memories in the brain on a long-lasting basis and presents recent data to support this model. However, in addition to promoting the consolidation and stabilization of emotional memories, evidence suggests that sleep and stress also transform memories—in both adaptive and maladaptive ways. Memory for negative emotional experiences, while adaptive in general, can also contribute to the etiology and perpetuation of clinical conditions such as depression and anxiety. Thus, I argues that it is possible to have “too much of a good thing” and suggests ways that the transformative nature of stress and sleep might be used to restructure maladaptive memories in the clinic.

This chapter discusses hormones in relation to psychopathy. Hormones are chemical messengers that travel through the bloodstream and bind to receptors in the brain and body. When hormones bind to receptors in the brain, they can affect the functioning of brain regions. Hence, hormones can be thought of as an intermediate step between genetic or environmental factors and brain functioning. In addition, hormone systems are highly sensitive to environmental and psychological factors such as stress. The chapter specifically studies two primary hormones that have been associated with psychopathy—cortisol and testosterone. Cortisol and testosterone have been associated with several features that are observed in psychopathy, including blunted stress reactivity, fearlessness, aggression, and stimulation seeking.

This chapter turns to the latest diagnosis of the problem that early intervention aims to address, focusing on the quality of parenting and infant brain development. It explores how brain claims came to define and propel to the fore early intervention in how mothers bring up their children as a logical expression of social investment models of social policy. The chapter also looks at the use and misuse of developmental neuroscience and of evidence for the early years being formative, to open to question the detail of the five key biologised motifs — critical periods, maternal attunement, synaptic density, cortisol and the prefrontal cortex — that are mobilised to make the case for intervention in the parenting of young, disadvantaged and marginalised mothers.

The spontaneous way in which people often come to feel the emotions of others is largely thought to explain empathy, including the ability to understand others, feel their emotions, and be motivated to help them. However, there are many occasions in which people feel empathy but do not help. Moreover, people sometimes report an urge to help that is not preceded by feelings of empathy or sympathy. Our work seeks to resolve this empathy–altruism divide by dissociating the neural mechanisms for recognizing and resonating with another’s state from the mechanisms that motivate us to act. Our integrative theory and data predict that people will feel with and help others when they attend to their state as long as their own needs are not compromised in so doing. However, overwhelming emotion or a fear for one’s own safety or effectiveness will inhibit helping while physiological arousal and activation can actually motivate aid in situations of immediate need without passing through any feelings of empathy or sympathy. Here we outline a research agenda that is theoretically grounded in interdisciplinary models of empathy and altruism.

The placebo effect in the immune and endocrine system is basically a conditioned response, whereby classical conditioning plays a key role. Conditioned immunosuppression affects a number of immune mediators, like interleukin-2 and interferon-gamma. Some negative allergic reactions may be induced by the administration of nocebos. The responses of some hormones, like insulin, growth hormone, and cortisol, have been successfully conditioned. In addition, the hypothalamus–pituitary–adrenal axis may represent an important system in placebo and nocebo responsiveness. Overall, the findings within the domain of the immune and endocrine system provide compelling evidence that conscious expectation is not always necessary for a placebo response to occur, and unconscious Pavlovian conditioning may represent the main mechanism.

A growing body of research shows that people’s family environments have potent effects on the body’s stress physiology. This chapter provides an overview of the links between family relationships in everyday life and cortisol, the body’s primary stress hormone. Key findings linking marital relationships to cortisol production are reviewed, as well as how family relationships impact children’s cortisol; the chapter focuses primarily on key findings from the past five years. The final section covers cutting-edge work that attempts to answer critical mechanistic questions of how family relationships “get under the skin” to affect cortisol production and, ultimately, physical health. The chapter concludes with a discussion of emerging research that seeks to investigate family relationships, stress physiology, and health outcomes in concert in order to clarify stress–health links.

By virtue of more problem driven rather than discipline driven, integrated research methods and theories both anthropologists and psychologists are elucidating the neuro-hormonal processes underlying brain architecture and the degree to which breastmilk constituents and the conditions, circumstances and social contexts within which primate infants are raised influences their cognition and temperament.

Distress is associated with both increased and decreased food intake, with eating less being the typical and predominant response. Distress is normally associated with physiological reactions that are designed to prepare the individual for a fight or flight response, thereby suppressing feelings of hunger. However, so-called emotional eaters show the atypical response to distress of eating similar or larger amounts of food. The present chapter explores possible causes of distress-induced emotional eating in terms of mechanisms and etiology. Possible mechanisms that are discussed are stress-induced hunger, interoceptive awareness, alexithymia, and changes in the stress responses of the hypothalamic–pituitary–adrenal (HPA) axis (cortisol). Etiology, that is, the emergence of emotional eating in adolescence will be examined by presenting studies on increases in emotional eating in association with inadequate parenting and depressive feelings in interaction with genetic vulnerability (the dopamine D2 receptor gene (DRD2) or serotonin transporter gene (SCL6A4/5-HTT)). Finally, emotional eating as a mediator between depression and both body mass index and weight gain will be examined and suggestions for obesity interventions and future research will be given.