Search results

This paper aims to provide a brief and accessible introduction to genetics and epigenetics for forensic practitioners. It provides two primers which define key genetic concepts and explain what epigenetic mechanisms actually are. The primers are provided alongside sections that focus on genetic research relevant to forensic practice, with a range of key messages that support the call to contextualise harmful behaviour and build better awareness of gene-environment relationships.

This is an opinion paper.

Select and seminal studies from the genetic literature that have forensic practice relevance are cited. These include studies from candidate gene research and epigenetic research. They highlight a number of key themes, including the way neurodevelopment and behaviour are contextually adjusted to fit certain environments, with epigenetic changes being an underpinning biological mechanism that facilitates this.

This article aims to introduce forensic practitioners to basic concepts in genetics and epigenetics so that they are able to engage with the relevant literature and understand the far-reaching implications for forensic practice.

It is becoming increasingly useful for forensic practitioners to appreciate how life experiences are encoded into biology through epigenetics. This paper highlights the potential of genetic and epigenetic research to provide major contributions to real-world practice in the coming years. It provides a modern biopsychosocial perspective on harmful behaviour and helps deepen the understanding of our efforts to support behaviour change. It offers ways to think of social and rehabilitative initiatives in biological terms.

This paper is one of few modern texts that focusses on the relevance of genetic and epigenetic research in applied forensic practice. It aims to introduce relevant concepts in an accessible manor. It intends to introduce biologically informed ways of understanding harmful behaviour within context and with attention to its function. It contributes to a de-pathologising narrative.

The purpose of this review is to provide a comprehensive summary, for both experts and non‐experts, of new findings on interactions among diet, genes, and exercise in determining the risk for chronic disease.

The present review focuses on the key role of exercise in modulating the ratio of muscle fiber types and the resulting effects on overall health.

Exercise and a diet rich in omega‐3 (n‐3) fatty acids modulate human gene expression and lower the risk for chronic disease. Emerging evidence, synthesized here, shows that a family of gene regulatory proteins, the PPAR (peroxisome proliferator‐activated receptor) transcription factor family, regulates the synthesis of human muscle fibers and thereby affects glucose metabolism and the risk for obesity, diabetes, and heart disease. Dietary fatty acids, in particular n‐3 polyunsaturated fatty acids, act on PPAR family members, and thereby enhance the synthesis of specific muscle fiber types. Human muscle fibers contain a heterogeneous mix of slow‐oxidative, fast‐oxidative, and fast‐glycolytic muscle fibers. At the extremes of the spectrum, low‐oxidative fibers, important for endurance activities, rely on a complete oxidation of sugars as well as fats for energy, and are associated with high insulin sensitivity. In contrast, fast‐glycolytic fibers, important for short, intense exercise, predominantly use a quick, but only partial breakdown of sugars (glycolysis) for energy. Not surprisingly, sprinters have more fast‐glycolytic fibers, while endurance athletes have more slow‐oxidative fibers. The relative ratio of these different fiber types, in part genetically fixed and in part respondent to diet and exercise, determines not only what type of activities an individual performs best, but also affects the risk for chronic disease. Recent research has identified correlations between muscle fiber type and PPAR type as well as between even modest levels of endurance training and a lowering of the risk for insulin resistance, obesity, diabetes, and heart disease.

This review synthesizes recently discovered mechanisms into a framework supporting the conclusion that even moderate levels of endurance exercise, combined with a sufficient intake of n‐3 fatty acids, lower the risk for chronic disease.

This article provides accessible and comprehensive information to researchers, nutritionists, and consumers who are interested in using lifestyle management (such as exercise and diet) to lower the risk for chronic disease.

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.

The chapter analyses the re-emergence of gene editing as an object of policy attention at the European Union (EU) level. Editing the genome of plants and/or animals has been a rather controversial component of all EU policies on agricultural biotechnology since the late 1980s. The chapter examines in detail the various initiatives that have been assumed for the regulation of gene editing at the EU level. Since the first political and legislative attempts, the field has been revolutionized with the development of the CRISPR-Cas9 system, which is comparatively much easier to design, produce, and use. Beyond the pure, safety-driven scientific questions, gene editing, in its contemporary form, raises a series of ethical and regulatory questions that are discussed in the context of the legal options and competences of the EU legislators. Special attention is paid to questions about the legal status of gene editing in Europe and the adequacy of the current GMO framework to deal with all the challenges associated with the latest scientific developments in the field of gene editing with a special focus on gene drive. Given the ongoing discussions regarding the ethical tenets of gene editing, the chapter investigates the question on whether there is a need to shape an EU-wide “intervention” that will address the complex and dynamic socio-ethical challenges of gene editing and puts forward a series of proposals for the framing of an inclusive framework that will be based on the need to re-enforce public trust in the EU governance of emerging technologies.

Genetic engineering offers an opportunity to improve aspects of the agronomic performance, resistance to pests and pathogens and end use quality of crops by inserting specific genes. Discusses the basic principles and procedures of plant genetic engineering, including the use of particle bombardment for delivery of genes into regenerable tissues. Also discusses how this technology can be used to alter the level (up or down‐regulation) or pattern of expression of endogenous genes, or to insert novel activities or properties by inserting genes from other sources (other plants, animals or microbes). Finally, describes work in progress in our own laboratories on the improvement of the bread‐ making quality of wheat by manipulating the amount and composition of the HMW subunits of glutenin.

Discusses applications of genetic engineering including some which are already used commercially. Outlines some of the technical complexities of gene transfer in plants. Touches on the regulation of gene transfer technology.

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.