Psychiatric disorders are complex and multifaceted conditions that profoundly impact various aspects of an individual’s life. Although the neurobiology of these disorders is not fully understood, extensive research suggests intricate interactions between genetic factors, changes in brain structure, disruptions in neurotransmitter pathways, as well as environmental influence.

In the case of psychotic disorders, such as schizophrenia, strong genetic components have been identified as a key feature in the development of psychosis. Moreover, alterations in dopamine function and structural brain changes that result in volume loss seem to be pervasive in people affected by these disorders. Meanwhile, mood disorders, including major depressive disorder and bipolar disorder, are characterized by disruptions in neurotransmitter systems responsible for mood regulation, such as serotonin, norepinephrine, and dopamine. Anxiety and personality disorders also exhibit neurotransmitter dysfunction and neuroanatomical changes, in addition to showing a genetic overlap with mood and psychotic disorders.

Understanding the underlying mechanisms in the pathophysiology of these conditions is of paramount importance and involves integrating findings from various research areas, including at the molecular and cellular levels. This brief overview aims to highlight some of the important developments in our current understanding of psychiatric disorders. Future research should aim to incorporate a comprehensive approach to further unravel the complexity of these disorders and pave the way for targeted therapeutic strategies and effective treatments to improve the lives of individuals afflicted by them.

The environment represents a central research object in the Developmental Origins of Health and Disease (DOHaD) and related fields such as epigenetics. This chapter discusses how DOHaD researchers operationalise and measure environments in and through their research practices to produce knowledge on how environmental experiences relate to health outcomes over the lifecourse. While DOHaD researchers discursively acknowledge the complexity of lived environments, we identify some of the current challenges to put this complexity into research practice, often resulting in reductionist accounts of the dynamic nature of human experiences. By proposing the term ’doing environments,’ we emphasise how practices to enact environments for scientific inquiry are products of decisions and negotiation processes that need careful consideration on what social and political consequences these ’doings’ might have and for whom. To that end, we aim to lay the ground for interdisciplinary conversations to engage in critical reflections about the social and political dimensions of doing environments in DOHaD research.

This chapter explores the relationship between climate distress – particularly fear and sadness about climate change – and clinical-level psychiatric symptoms in children and young people, focusing on pediatric anxiety and depression. In response to societal tendencies to under- or overplay the mental health risks of climate emotional impacts, it describes the spectrum of healthy and unhealthy pediatric anxiety and depression, the role that chronic stress and direct climate impacts play on child and adolescent brain development and clinical syndromes, and the ways that responding emotionally to climate change can influence youth identity development and emotional strength. The chapter provides a template for how to assess young people’s climate emotions clinically, offering several detailed case descriptions to illustrate how stress, psychopathology, psychological and brain development, and climate emotions can weave together to influence the sum of a young person’s presentation. As parents’ and other adults’ responses play a key role in whether these emotions evolve to a clinical level, it also suggests some best practices for interacting with climate-distressed youth to minimize poor clinical outcomes.

There is no consensus for the concept of treatment-resistant depression (TRD). Although some authors argue considering TRD a depression subtype is not supported by evidence, its impact on the individual and society is clear. This chapter discusses the concept of TRD, presents evidence about its neurobiology, pharmacological interventions, and describes drugs currently under investigation. Among the pharmacological strategies to manage TRD, guidelines include increasing the antidepressant dose, switching to another new antidepressant, combining two or more antidepressants, and augmentation of the current medication. Several new components have been investigated for TRD targeting, for instance, the glutamatergic system, inflammatory system, the opioid system, the cholinergic system, dopaminergic system, and neurotrophin signaling. Finally, machine-learning techniques using clinical and neurobiological data provide promising information about treatment outcomes prediction that could change the current approach to a more personalized one.

Eating disorders are complex and serious illnesses that can result in physical and psychiatric comorbidities, medical emergencies and progressive health consequences. Although general psychiatrists may be called upon to assist in emergencies or differential diagnoses, training in this area has been limited. The author attempts to fill the gap by providing a summary of the most recent advances in the field of eating disorders in this chapter to help orient trainees and general psychiatrists. This chapter provides an overview of the most recent changes to the DSM-5 and ICD-11 diagnostic categories for eating disorders, as well as their epidemiology, aetiology and treatment, including the management of complications and life-threatening medical emergencies.

The chapter summarises recent advances in the genetic and neurobiological understanding of eating disorders, as well as emerging new research. These scientific advances have the potential to contribute to the development of new, more-effective eating disorder treatments in the future.

Adverse childhood experiences (ACEs), including family dysfunction as well as abuse and neglect, have enduring effects on development. Research across diverse populations documents that ACEs are prevalent and cumulative, influencing children’s developing mental, emotional, and physical systems that affect long-term physical and mental health, social relationships, and parenting attitudes and behaviors. Protective and compensatory experiences (PACEs), including nurturing relationships and stable, supportive environments, can mitigate the effects of ACEs, disrupting the intergenerational transmission of adversity. In this chapter, we summarize the effects of ACEs on neurobiological, cognitive, social, and emotional development. Next, we discuss the effects of cumulative protective experiences and the introduce the concept of Balanced Parenting to promote resilience in the face of adversity. We include examples of how parents and other caregivers can effectively parent children with a history of ACEs at different developmental stages, and conclude with a discussion of new directions for research and practice.

This chapter is intended to provide a neurobiologically based framework to understand the behavioral problems seen in PWS. These abnormalities are as a direct result of the loss of function of chromosome 15q11-13. The main brain abnormalities in PWS arise from a dysfunction of areas of higher functioning such as the hypothalamus, insula, orbitofrontal, and anterior cingulate cortices. Additionally, there is abnormal functioning of the serotonin, dopamine, and norepinephrine systems. These dysfunctions collectively lead to the failure of the response monitoring or model-based learning function of the brain. Inadequate or impaired functioning of the response monitoring system in patients with PWS leads to multiple issues including impulsivity and response perseveration. Finally, in place of utilizing the response monitoring system, patients with PWS resort to habit-based learning, which leads to inflexibility. Reminding ourselves of the complex neurobiology that drives our patients and loved ones with PWS might lead to better tolerance for their maladaptive behaviors and more useful management strategies.

This chapter introduces a rationale for a YA Temperament Based Therapy with Support version of treatment. In YATBT-S, parents are primary “Supports,” or the “S” in TBT-S. This chapter addresses concepts unique to young adult development, including a model for parental involvement specifically tailored for the YA life stage. It addresses why parents need to be included in treatment for YA with AN. Components of YA developmental stages and forms of parental assistance are outlined to establish a collaborative, interdependent treatment model.

For those with anorexia nervosa, it is (1) not a “natural” or dominant brain response to eating like those without AN. (2)It is difficult to trust what and when to eat. (3) It is not typical to experience pleasure in eating a variety of foods. (4) Eating is anxiety provoking. Not eating appears to reduce anxiety. Individuals with AN tend to experience reduced sensitivity to reward and increased sensitivity to punishment. Altered sensitivity to reward and punishment is observed in those with AN, for both food and general rewards/losses and thus suggests a broader deficit in reward processing. Hunger does not increase reward sensitivity in AN, suggesting a deficit in translating physiological signals to motivated behavior, and explaining why individuals with AN can restrict food despite starvation. Altered reward processing may be why we see low motivation for recovery and anhedonia. Decreased brain response to reward in the cognitive circuitry in AN is associated with elevated anxiety, suggesting a brain basis for coding food as risky.

Studies show that eating disorders tend to run in families. This suggests genes contribute to eating disorders. Genes cause traits. Several studies show people with eating disorders share traits that existed before the disorder, and they appear to contribute toward maintaining the disorder. For example perfectionism, obsessionality, high achievement orientation, and anxiety are common AN traits. Brain imaging studies show differences in the parts of the brain involved in eating in individuals with eating disorders compared with those who do not have eating disorders. Together, research shows there are strong genetic and neurobiological causes of eating disorders.