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This study explores the social, biological, and genetic determinants of depression in later life. It adds complexity to the idea that later life depression is a natural outgrowth of vascular impairment, antagonistic pleiotropy, or compromised neuroanatomical structures, arguing instead for the importance of education as a fundamental cause.

The study uses the NAS-NRC Twin Registry of World War II Veterans. The use of twins permits the exploration of gene-environment interplay. A recent survey instrument associated with the registry contains numerous indicators of health, including a measure of depression.

The results show that education has a strong negative relationship with depression among those in their 70s and early 80s. Although this relationship is partly explained by lower rates of cardiovascular disease and diabetes among the well-educated, the relationship between education and many common physical illnesses is quite small. Most people of this age experience at least one chronic illness. The relationship between education and depression is explained, instead, by how education reduces impairments in activities of daily living. These impairments are not an inevitable outgrowth of declining health. The well-educated are better able to moderate the impact of poor health on daily functioning. Moreover, the well-educated are able to avoid the otherwise strong genetic risks for depression in later life. Gene × environment models show a high heritability for later life depression on average, but also reveal that this heritability declines with increasing education. Among those with a four-year college degree, the heritability of depression is very small.

These patterns are interpreted in light of compensatory gene × environment interactions, which emphasize the importance of especially enriched environments for overcoming genetic risk.

Genetic risk for depressive disorders is poorly understood despite consistent suggestions of a high heritable component. Most genetic studies have focused on risk associated with single variants, a strategy which has so far only yielded small (often non-replicable) risks for depressive disorders. In this paper we argue that more substantial risks are likely to emerge from genetic variants acting in synergy within and across larger neurobiological systems (polygenic risk factors). We show how knowledge of major integrated neurobiological systems provides a robust basis for defining and testing theoretically defensible polygenic risk factors. We do this by describing the architecture of the overall stress response. Maladaptation via impaired stress responsiveness is central to the aetiology of depression and anxiety and provides a framework for a systems biology approach to candidate gene selection. We propose principles for identifying genes and gene networks within the neurosystems involved in the stress response and for defining polygenic risk factors based on the neurobiology of stress-related behaviour. We conclude that knowledge of the neurobiology of the stress response system is likely to play a central role in future efforts to improve genetic prediction of depression and related disorders.

Heritability studies attempt to estimate the contribution of genes (vs. environments) to variation in phenotypes (or outcomes of interest) in a given population at a given time. This chapter scrutinizes heritability studies of adverse health phenotypes, emphasizing flaws that have become more glaring in light of recent advances in the life sciences and manifest most visibly in epigenetics.

Drawing on a diverse body of research and critical scholarship, this chapter examines the veracity of methodological and conceptual assumptions of heritability studies.

The chapter argues that heritability studies are futile for two reasons: (1) heritability studies suffer from serious methodological flaws with the overall effect of making estimates inaccurate and likely biased toward inflated heritability, and, more importantly (2) the conceptual (biological) model on which heritability studies depend – that of identifiably separate effects of genes versus the environment on phenotype variance – is unsound. As discussed, contemporary bioscientific work indicates that genes and environments are enmeshed in a complex (bidirectional, interactional), dynamic relationship that defies any attempt to demarcate separate contributions to phenotype variance. Thus, heritability studies attempt the biologically impossible. The emerging research on the importance of microbiota is also discussed, including how the commensal relationship between microbial and human cells further stymies heritability studies.

Understandably, few sociologists have the time or interest to be informed about the methodological and theoretical underpinnings of heritability studies or to keep pace with the incredible advances in genetics and epigenetics over the last several years. The present chapter aims to provide interested scholars with information about heritability and heritability estimates of adverse health outcomes in light of recent advances in the biosciences.

This chapter compares interdisciplinary research that engages genomic science from economics, political science, and sociology. It describes, compares, and evaluates concepts and research findings from new and rapidly developing research fields, and develops a conceptual taxonomy of the social environment.

A selection of programmatic and empirical articles, published mostly since 2008 in leading economics, political science, and sociology journals, were analyzed according to (a) the relationship they pose between their discipline and genomic science, (b) the specific empirical contributions they make to disciplinary research questions, and (c) their conceptualization of the “social environment” as it informs the central problematique of current inquiry: gene-environment interaction.

While all three of the social science disciplines reviewed engage genomic science, economics and political science tend to engage genomics on its own terms, and develop genomic explanations of economic and political behavior. In contrast, sociologists develop arguments that for genomic science to advance, the “environment” in gene-environment interaction needs better theorization and measurement. We develop an approach to the environment that treats it as a set of measurable institutional (rule-like) arrangements, which take the forms of neighborhoods, families, schools, nations, states, and cultures.

Interdisciplinary research that combines insights from the social sciences and genomic science should develop and apply a richer array of concepts and measures if gene-environment research – including epigenetics – is to advance.

This chapter provides a critical review and redirection of three rapidly developing areas of interdisciplinary research on gene-environment interaction and epigenetics.

Sex and gender are regarded as critical structural determinants of mental health and mental illness. Mental illness is a complex phenomenon, and risky behaviour and substance use commonly occur simultaneously or subsequent to one another. A gendered vulnerability in biological, environmental, and behavioural risk factors has been registered in the development and escalation of mental illness. Studies have found that women who use drugs experience greater physical and mental health repercussions than men. Women who use drugs present higher rates of depression and anxiety, suicidal tendencies, isolation and general psychological distress. This chapter addresses the most common mental illnesses associated with women who use drugs: depression, anxiety, trauma-related disorders, and eating disorders.

This study evaluates cross-national differences in public beliefs about the causes of health and the role of these beliefs in shaping attitudes regarding health policy.

The study uses data from the 2011 International Social Survey Program, which includes questions on health and health care, asked in 29 countries. Respondents were asked about four specific causes of poor health (i.e., genes, behavior, the environment, and poverty). Respondents were also asked about their attitudes regarding three aspects of health policy: their support for government-provided care, the perceived fairness of income disparities in medical treatment, and their support for providing health care to noncitizens.

The study has three findings. First, the study reveals the global reach of a multicausal view. The four beliefs about the causes of poor health are positively correlated in all countries. However, there is considerable cross-national variation in the average support for specific causes. Although in some countries proximate causes, such as genes, are endorsed more frequently than distal causes, such as poverty, this is by no means a uniform pattern. Support for genetic causes is high, but genetic reductionism is rare. Second, the study reveals that health beliefs are fundamentally political beliefs. The single most important determinant of beliefs about the causes of health is the country in which the respondent resides, exceeding in influence religion, education, and even personal experiences with health and health care. Third, the study reveals that the political connotations of health beliefs vary between countries, especially beliefs regarding genes. In general, those who endorse behavioral arguments favor less government involvement in health care and are more accepting of income disparities in the quality of care. Those who endorse the environment and poverty, meanwhile, tend to support a stronger role of government. Yet, the magnitude of these associations varies and, in the case of genetic arguments, even the direction of the association varies. Genetic arguments are frequently associated with support for a stronger role of government, but genetic arguments also are occasionally associated with support for the exclusion of noncitizens from the health care system.

International survey research is valuable for exploring the scope of patterns revealed in a limited set of countries, but it is difficult to pinpoint the source of cross-national differences.

The study demonstrates the importance of national context in shaping health beliefs, as well as the role of beliefs regarding the causes of health in setting the stage for public receptivity to government-provided care. The study also illustrates the value of thinking about beliefs about genes as reflecting larger projects of biocitizenship, at least in some countries.

The aim of this paper is to provide an overview of the dominant approaches used to explain causes of challenging behaviour.

This paper is the second in a two‐part series. It presents the causes of challenging behaviour according to the three theoretical approaches that have dominated the literature: applied behaviour analysis; biological factors; and psychiatric disorders.

It is apparent that the causes of challenging behaviour are likely to be complex and involve multiple factors. The approaches that have dominated the literature focus on single causes and do not explore possible interactions between various causes. Given the shortcomings of existing approaches, a fourth approach, the biopsychosocial model, is proposed as an alternative model to explain the causes of challenging behaviour.

This paper is the most recent of only a few providing an overview of the various approaches that seek to explain the causes of challenging behaviour.

The combination of heightened emphasis on risk and its management in mental health, the precautionary principle, the idea of genetic susceptibility, advances in screening technology, and the promise of preventive pharmaceutical intervention is highly potent, especially in a world in which preventive prescription of psychiatric medication has become routine. Psychiatric professionals are given the obligation of governing, and being governed, in the name of risk, and in a political and public sphere suffused by the dread of insecurity. But there are risks in seeking to govern risk in a biological age. In this paper Nikolas Rose argues that the public, politicians and professionals alike might do better to refuse the demands of risk, and learn to live with uncertainty.