Qatari intersections with global genetics research and discourse

Currently, there is no consensus regarding services required to help families with consanguineous marriages manage their increased genetic reproductive risk. Genetic services for communities with a preference for consanguineous marriage in the UK remain patchy, often poor. Receiving two disparate explanations of the cause of recessive disorders (cousin marriage and recessive inheritance) leads to confusion among families. Further, the realisation that couples in non-consanguineous relationships have affected children leads to mistrust of professional advice. British Pakistani families at-risk for recessive disorders lack an understanding of recessive disorders and their inheritance. Such an understanding is empowering and can be shared within the extended family to enable informed choice. In a three-site qualitative study of British Pakistanis, we explored family and health professional perspectives on recessively inherited conditions. Our findings suggest, firstly, that family networks hold strong potential for cascading genetic information, making the adoption of a family-centred approach an efficient strategy for this community. However, this is dependent on provision of high-quality and timely information from health care providers. Secondly, families' experience was of ill-coordinated and time-starved services, with few having access to specialist provision from Regional Genetics Services; these perspectives were consistent with health professionals' views of services. Thirdly, we confirm previous findings that genetic information is difficult to communicate and comprehend, further complicated by the need to communicate the relationship between cousin marriage and recessive disorders. A communication tool we developed and piloted is described and offered as a useful resource for communicating complex genetic information.

Discourses of Globalisation and Values Education, the 34th book in the 36-volume book series Globalisation, Comparative Education and Policy Research, analyses major discourses of effective and engaging learning environments for teaching values education globally in schools. The main aim of this monograph is to offer a new insight into understanding of the nexus between ideology, the state, and values education in schools.

This chapter uses the example of consanguineous marriages to illustrate how risk for offspring with genetic disease has become a focal concern in the governance of the health of populations, and to explore some local responses to the scientific discourse of genetic risk in cousin marriages. It first outlines the principles of Mendelian genetics that underpin clinical assessments of risk for single gene conditions as backdrop for the analysis of divergences between scientific and local understandings of genetic risk. It considers similarities and differences between public and policy discourses about the health risks of consanguineous marriage in Europe, where such marriages are rare, and in the Middle East, where such marriages are more common. In Europe, the issue is bound into discourses concerning the non-integration of immigrant-origin minorities; across the Gulf States, consanguineous marriage seems to have become a proxy for genetic risk, its identification and management associated with modernity. It then explores some consistent disconnects between scientific understandings of causality and risk for recessive disease across these contexts. It notes, locally, the common invocation of environmental and spiritual factors and the equation of genes with blood, the influence of patrilineal kinship, and the ambiguities of the concept of being a ‘carrier’ and of probabilistic risk assessments. The chapter shows how scientific and local ideas about risk perception and management evolve alongside and relation to one other, sometimes with clinically significant consequences for families and for health services.

In this paper the term 'globalisation' means the international integration of nationally organised markets in conjunction with increasing cross-country flows of factors of production. According to this globalisation has been under way for centuries. Globalisation is not a completely autonomous, not even a solely market driven process. Historically, it is for the most part determined by decisions of nation states. In times of globalisation speeding up, typically social and political debates start about the driving forces, extent and impact of globalisation. Already two centuries ago, globalisation has been discussed in a similar way as today. Initially, there is a debate about the organisation of the foreign trade regime. Because change of social and economic structures is an integral part of globalisation, the debate about the impact of structural change is constituent in globalisation discourses. Winners and losers of the structural change try to improve their social position through foreign trade policy. These two levels of globalisation discourses are usually distorted by the argument that globalisation and the induced change of societal structures provoke adverse effects on the prevailing system of values. Because of this the globalisation discourse becomes a matter of emotion and disproportionately complex. The paper demonstrates the three levels of a typical globalisation discourse by using three examples. First, the actual globalisation discourse will be discussed. Second, in Germany at the beginning of the 20th century globalisation has been hotly debated under the heading "agrarian versus industrial state". Third, the typical globalisation discourse can also be outlined by the dispute about the reform policy in Prussia in the early 19th century.

The “obesogenic environment” does not affect all children equally. Diminished opportunities for physical activity in daily life and increasing availability and declining cost of calorie-dense foods are primary culprits in the obesity epidemic. But there is more to obesity than the environment. Even children raised together in the same family may experience diverging trajectories of body mass.1 The fact that children confronted with similar environmental circumstances experience disparate outcomes has been attributed to genetic factors.2 And family-based and molecular genetic methods indicate substantial genetic contributions to obesity etiology.3 But just what these genetic factors are and just how they contribute to individual differences in response to the obesogenic environment remains, if not entirely a mystery, an enduring puzzle.4 Solving this puzzle is a public health priority. There is no going back to a world in which calories are scarce and obtaining them is physically demanding. And governments and their publics have shown little enthusiasm for regulations restricting access to palatable, calorie dense foods. Policies and public health messaging that reframe health-behavior decision-making provide a population-level approach to promoting healthier diets and more active lifestyles.5 Complementary practices are needed to that can more directly address the most vulnerable individuals, preferably early in life, before obesity develops. Rapid growth in the first months and years of life is associated with increased obesity risk across the life course.6 Genome-wide association studies (GWAS) have discovered common genetic variants that predispose to higher adult body-mass index.7 These variants contribute to the etiology of obesity partly by increasing the rate of growth in childhood.8 The next step in translating these discoveries to develop interventions that can prevent obesity is to identify mediating mechanisms that connect the DNA sequence a child inherits with the rapid growth trajectory that places them at risk for obesity and its adverse health consequences. In this issue of JAMA Pediatrics, articles by Jaarsveld and colleagues and Llewellyn and colleagues suggest one such mechanism: individual differences in satiety responsiveness during childhood. Specifically, these studies suggest that diminished satiety responsiveness is a conduit through which genetic risk accelerates weight gain in early life, contributing to obesity pathogenesis. The study by Jaarsveld and colleagues examined longitudinal associations between infant satiety- and food-responsiveness and weight gain in a sample of 228 same-sex dizygotic twin pairs followed from birth through age 15 months. Satiety- and food-responsiveness were measured for the first three months of life, when all children were exclusively breast-fed. The twins were selected from a larger cohort on the basis of high within-pair discordance in appetite measures. The researchers then conducted a co-twin control analysis to test whether infant appetite phenotypes predicted the rate of weight gain. The co-twin control analysis asked whether the twin with the higher appetite gained more weight than their co-twin with the lower appetite. The co-twin design rules out confounding by any factors that influence both appetite and weight gain and are shared by twins in a family. For example, constitution of the breast milk, the feeding environment, and maternal biases in reporting on appetite are all controlled. Within this design, the researchers found that the twin with the greater appetite—lower satiety responsiveness, higher food responsiveness—gained weight more rapidly. Appetite was not related to weight at birth. From birth, differences emerged quickly; by age three months the twin with the higher appetite was already heavier. This finding parallels what has been observed for the genetic risks discovered in GWAS of obesity phenotypes. Those genetic risks show little influence on birth weight,9 but they do influence the rate of growth during the first months of life.10 The study by Llewellyn and colleagues directly examined relationships among genetic risk for obesity, satiety responsiveness, and body mass index and waist circumference standard deviation scores) in a sample of over 2,000 unrelated children selected from a larger twin cohort. Children were genotyped for 28 obesity-associated variants identified in previous genome-wide association studies of obesity phenotypes. These variants were then combined to produce a continuous index of genetic risk for each child—their “genetic risks score.” Children with higher genetic risk scores exhibited reduced satiety responsiveness and had higher body mass index and waist circumference relative to age-peers with lower genetic risk scores. Statistical tests indicated that small portions of the genetic associations with adiposity measures were mediated through reduced satiety responsiveness. Intriguingly, the genetic risk mediated through satiety responsiveness was not fully explained by the FTO locus, which had previously been linked with appetite phenotypes.11 These findings argue for an expansion of the program of appetite and obesity research focused on the FTO gene to consider a polygenic approach12 that examines profiles of genetic risks across the genome. In suggesting infant and early childhood satiety responsiveness as a mediator of polygenic risk for obesity, these studies highlight an important translational application of genetic discoveries: To identify intermediate phenotypes in disease pathogenesis that can serve as targets for intervention and/or provide guidance as to when in development and with whom to intervene.13 In this case, findings suggest that a mother’s report on her child’s appetite may be informative in identifying children especially vulnerable to developing obesity. The link between appetite and polygenic risk for obesity suggests that children identified in this way may be responsive to preventative interventions that promote healthy lifestyle practices; observation studies indicate that polygenic risk for obesity is amplified by poor diet14 and can be mitigated by active lifestyle.15 Whether maternal reports of eating behaviors are sufficiently sensitive and specific to identify individuals who can benefit from preventative interventions and whether interventions prove as effective with genetically at risk individuals as observational studies suggest are topics for further research. In parallel to exploratory intervention studies, a number of more basic questions should be answered to clarify the translational significance of findings for infant and childhood satiety responsiveness. First, what are the long-term consequences of individual differences in appetite in infancy and early childhood? Studies are needed that follow children from early life into adolescence and adulthood to test whether appetite measured in infancy and childhood is predictive of later obesity. Second, at what point during development are individual differences in appetite established and how do changes in appetite relate to changes in obesity risk? Studies that include repeated measures of appetite and weight during infancy and childhood are needed to determine when differences in appetite first manifest, how stable these differences are over time, and whether diminishment or increase in appetite predicts corresponding changes in weight. Third, do these findings generalize to non-European populations? Studies are needed to test replication of these findings in cohorts other ethnic groups. Stepping back from the specific case of appetite and obesity, these studies highlight an interdisciplinary approach to pediatrics research that has potential to inform prevention and treatment not just for obesity, but for a range of common chronic health problems that begin to develop during childhood. The sequencing of the human genome unleashed a flood of genetic discovery research. These studies have mostly focused on taking increasingly sophisticated measurements of genomes in ever-larger samples of individuals, almost all of whom are adults. To realize the translational potential of these discovery studies, research is needed that applies genetic discoveries to investigate disease processes early in life. Many investigators have been disappointed by the small effect-sizes observed for GWAS discovered risk variants. And funders are drained from the high costs of generating the data to support the initial discovery studies. Both groups should take another look at the opportunities now available. The true effect-sizes of GWAS discoveries cannot be known until we understand how genetic risks contribute to pathogenesis. And conducting the research to generate this understanding need not be cost prohibitive. Measuring genomes gets cheaper by the day. Longitudinal studies of population-representative samples that capture high quality measures of developmental phenotypes for conditions ranging from obesity and asthma to behavioral and emotional problems already exist. What is needed is the creativity, the will, and the resources to put these rich databases to work to achieve the next generation of advances in genetics and health science.

Attention deficit hyperactivity disorder (ADHD) is not only highly prevalent, persistent and impairing but also is one of the most heritable of all psychiatric disorders. As a result, ADHD has been the focus of considerable genetic research. The results of recent genetic studies are reviewed with a focus on the emerging picture and future trends. ADHD appears to be a complex disorder in which multiple genetic and environmental risks contribute to a quantitative trait. At the same time, there is growing evidence that in a proportion of cases, individually rare variants such as copy number variants may play an important causal role. The more genetic risks, both common and rare, the more extreme the trait. With increasing samples and advanced genetic methods, single nucleotide polymorphism (SNPs) and copy number variants (CNVs) conferring risk for ADHD are being identified. Further study will be required before we can understand the causal significance of these findings. Increased sample size is an urgent necessity if we are to discover potentially causal variants. Non-behavioral markers of genetic risk known as endophenotypes could also play a role in parsing the phenotypic and genetic heterogeneity of ADHD as they have in other complex disorders. Genetic studies in ADHD hold the potential for refined nosology, more precise diagnosis, and differential diagnosis, improved early identification leading to novel intervention strategies and identification of innovative targets for therapeutics based on a precise understanding of disease mechanism.

This article examines the interaction between human population genetics and the reconstruction of national identities and histories. Since the first use of mitochondrial DNA analysis of human origins in 1987, scientific research on population history using genetic technologies, or genetic history studies, has flourished, engaging with diverse politics of social identity and national belonging across the globe. Previous scholars have stated that a distinct feature of genetic history studies is the globalized research and commercial network enabled by technological innovations and social transformations during the 1990s. This paper contributes further to this literature by analyzing how local geneticists became part of the global research network and how globalization at large—e.g., economic liberalization and the rise of multiculturalism—functioned in the development of genetic history studies in South Korea. By focusing on a leading population geneticist, Kim Wook and his genetic origin research on Koreans, I will show the role that Korean geneticists had in reconfiguring Korean national identity—from an ethnically homogeneous group to an ethnically diverse one—while their research practices, questions, and methods were inspired and supported by domestic globalization policies and discourses and a transnational network of genetic history studies. I will also reveal the essential, albeit equivocal, part genetic knowledge played in the debate on national belonging in this county.

BackgroundApolipoprotein-E (APOE) genetic testing for Alzheimer’s disease is becoming more important as clinical trials are increasingly targeting individuals carrying APOE-ε4 alleles. Little is known about the interest in finding out one’s genetic risk for Alzheimer’s disease in the general population. Our objective was to examine this in a sample of cognitively normal (CN) adults within a population-based online research registry with the goal to implement APOE-ε4 status for trial recruitment.MethodsAn online survey was completed by 442 CN participants between the age of 49 and 75 years (56% female) from the Dutch Brain Research Registry. The survey assessed interest in participation in research into, and disclosure of, genetic risk for dementia. The survey assessed interest in participation in research into, and disclosure of, genetic risk for dementia and knowing their genetic risk in different hypothetical risk scenarios (10%, 30%, and 50% genetic risk for dementia at age 85, corresponding to APOEε2/ε2 or ε2/ε3, APOEε3/ε4 or ε2ε4, and APOE-ε4/ε4 genotypes). Cochran’s Q and post hoc McNemar tests were used to analyse differences in frequencies across scenarios.ResultsMost participants were interested in participating in research into and disclosure of their genetic risk (81%). The most reported reason was to contribute to scientific research (94%). Interest was higher in males, whilst lower-educated participants were more often undecided. When provided with different risk scenarios, interest in knowing their risk was somewhat higher in the scenarios with higher risk, i.e. in the 50% (79%) compared to the 10% scenario (73%;χ2(2) = 7.98; p = .005). Most individuals expected they would share their genetic risk with close relatives (77–89%), would participate in medication trials (79–88%), and would make long-term arrangements, e.g. retirement, health care, will (69–82%), with larger proportions for scenarios with higher hypothetical genetic risk.ConclusionsOur findings indicate that the vast majority of CN adults participating in a research registry expresses interest in AD genetic risk research and disclosure. Interest in genetic risk disclosure is higher in scenarios corresponding to the APOE-ε4 genotype. This suggests APOE-ε4 screening within an online research registry is potentially a well-received method to accelerate inclusion for trials.

A Labour MP has called for a public debate on the genetic risks of marriages between first cousins in Britain's Pakistani community, after reports of an unusually high rate of...

Globalization has become one of the most influential forces shaping political and social policies in Indonesia, producing both opportunities and challenges for national sovereignty, governance, and cultural identity. This research aims to analyze how globalization influences Indonesia’s political and social policies and to examine the extent to which Indonesia demonstrates agency in responding to global pressures. Employing a qualitative research design, the study was conducted from June to August 2025 in Jakarta, Yogyakarta, and Bandung, with data collected through in-depth interviews, focus group discussions, and document analysis. Findings reveal that globalization has strongly influenced political reforms such as decentralization, democratization, and human rights policies, while also shaping social policies in education, cultural preservation, and social welfare. At the same time, Indonesia demonstrates a dual and hybrid approach, selectively adopting global norms while maintaining national priorities and local identity. Globalization has also generated paradoxical effects, fostering openness and innovation while simultaneously stimulating cultural resistance, social inequality, and identity reassertion. The study concludes that Indonesia exemplifies adaptive globalization, negotiating global pressures with local values and strategic interests. This research contributes theoretically by integrating political and social perspectives in the globalization discourse and practically by providing insights for policymakers to design inclusive, culturally sensitive, and context-responsive policies.

Genome-wide hypothesis-free discovery methods have identified loci that are associated with heavy smoking in adulthood. Research is needed to understand developmental processes that link newly discovered genetic risks with adult heavy smoking. To test how genetic risks discovered in genome-wide association studies of adult smoking influence the developmental progression of smoking behavior from initiation through conversion to daily smoking, progression to heavy smoking, nicotine dependence, and struggles with cessation. A 38-year, prospective, longitudinal study of a representative birth cohort. The Dunedin Multidisciplinary Health and Development Study of New Zealand. The study included 1037 male and female participants. We assessed genetic risk with a multilocus genetic risk score. The genetic risk score was composed of single-nucleotide polymorphisms identified in 3 meta-analyses of genome-wide association studies of smoking quantity phenotypes. Smoking initiation, conversion to daily smoking, progression to heavy smoking, nicotine dependence (Fagerström Test of Nicotine Dependence), and cessation difficulties were evaluated at 8 assessments spanning the ages of 11 to 38 years. Genetic risk score was unrelated to smoking initiation. However, individuals at higher genetic risk were more likely to convert to daily smoking as teenagers, progressed more rapidly from smoking initiation to heavy smoking, persisted longer in smoking heavily, developed nicotine dependence more frequently, were more reliant on smoking to cope with stress, and were more likely to fail in their cessation attempts. Further analysis revealed that 2 adolescent developmental phenotypes-early conversion to daily smoking and rapid progression to heavy smoking-mediated associations between the genetic risk score and mature phenotypes of persistent heavy smoking, nicotine dependence, and cessation failure. The genetic risk score predicted smoking risk over and above family history. Initiatives that disrupt the developmental progression of smoking behavior among adolescents may mitigate genetic risks for developing adult smoking problems. Future genetic research may maximize discovery potential by focusing on smoking behavior soon after smoking initiation and by studying young smokers.

The world can be characterized by dynamics of acceleration. The African population will double during the next three decades; global urban infrastructures will double by 2050; to stay below the 2 °C guardrail and to avoid dangerous climate change, emissions need to peak by 2020 and be reduced to zero by 2050; The decisions of states, firms and political actors during the next one or two decades will create very long-term path dependencies in the emerging global society. Acceleration, path dependencies and very long-term impacts of current decisions need to be taken into account in Global Cooperation Research. The Kate Hamburger Kolleg / Centre for Global Cooperation Research therefore brought together scenario experts, integrated assessment scholars and science fiction authors with global cooperation researchers. All of them agreed that shaping the future, organizing transformation processes towards sustainability and investing in global cooperation to make globalization work for all means building on new narratives about possible futures. Narratives are about imagination, creativity, innovation, diversity. Without transformative narratives, we cannot go beyond incremental changes. This Global Dialogues publication builds important bridges between scholars from very different disciplines which can help us to merge the knowledge of future scenario thinkers and pioneers of global cooperation research. (from the Preface)

The notion of interculturality is complex and polysemous in global research and education. Considering the turbulent times that the world has experienced in recent years, it is increasingly important to confront and enrich this significant scientific notion to make it more inclusive and epistemologically diverse. This paper has two main objectives. First, it reviews the current state of the global literature on the notion of interculturality in education published in English, observing how different ideologies occupy the field—from dominating voices to ‘minor’ ones which are more glocalized (global + local). On the basis of this review calling for more ‘minor’ voices to be heard, the core of the paper is based on the analysis of discussions between Chinese students at a specific institution of higher education (a ‘minority-serving institution’ or Minzu University) in China, where students from the 56 different Minzu groups of China live, study and cooperate together. The glocal ideology of Minzu (often mistranslated as ‘ethnic’ in English), a form of interculturality, is specific to this context and has not been systematically researched. Three groups of students with different ‘Minzu/ethnic’, linguistic and study profiles were paired together to discuss what interculturality could mean and entail. Three interrelating layers of discourses were identified through a dialogical discourse analysis of what the students co-constructed together: glocality, politics and philosophy of life for all. In general, the students demonstrated a nuanced understanding of interculturality that intersected partly with global academic discourses of interculturality. Their insights contributed advanced reflections and critical thoughts on the notion, highlighting the need for a collaborative and innovative approach to its understanding and utilization.

ABSTRACTIntroductionProstate cancer is the second most common cancer worldwide, and there is no national prostate cancer screening programme in the United Kingdom. Men of African ancestry are twice as likely to be diagnosed as men of European ancestry and are diagnosed at a younger age. Despite this, Black men are under‐represented in seeking advice about prostate cancer symptoms, screening and genetic research. There is increasing research focused on targeted prostate cancer screening, using genetic testing to guide screening by identifying those at highest risk, but this could only be considered if people of all ethnicities would accept this approach. It is vital to diagnose prostate cancer early, when it is curable. We wanted to identify the barriers to engagement with prostate cancer genetic research to increase participation from those at highest risk.MethodsWe conducted two community discussion groups, each attended by 30–35 Black men and their families. We conducted interviews with three Black community champions who have a lived experience of prostate cancer. Thematic analysis was performed on the transcripts. We used a participatory approach to develop our themes with members of the community, two of whom are co‐authors on this paper.ResultsThemes were grouped as barriers or facilitators to engagement with prostate cancer genetic risk services. Barriers included GP reluctance to perform prostate‐specific antigen (PSA) testing, cultural inhibition around discussing prostate cancer and family history, fear of rectal examination, fear of cancer diagnosis and lack of trust in the healthcare system, no awareness about the role of genetics in prostate cancer risk assessment, negative connotations of genetic testing (e.g., genetic modification) and genetic data being used inappropriately. Facilitators were family and community support, the sharing of experiences, good communication with doctors, raised prostate cancer awareness, genetic risk assessment to guide the need for screening and facilitate early diagnosis, improving future outcomes for prostate cancer in the Black community through engaging with genetic research and assurance that there are regulations in place to protect genetic and personal data with guidance around when genetic results must be disclosed.ConclusionsUnderstanding barriers and facilitators can guide recommendations for health services to improve access and uptake within the Black community and improve representation in genetic research. Better representation will support improvements in cancer outcomes and understanding of the genetic risk of prostate cancer in the Black community.Patient or Public ContributionWe initially attended community prostate cancer awareness events to speak to members of the community. We established trusted and two‐way relationships with Black ‘community champions’ who lead support groups in the Black community and often have a lived experience of prostate cancer. We were invited to attend their support groups to deliver awareness talks and address concerns about prostate cancer risk and screening. We then conducted discussion groups and collected data. Our analysis was conducted in partnership with our community champions. Our findings are described in this paper, with their co‐authorship. We have also disseminated our findings in a co‐produced newsletter to feed back our findings to the community members, who gave us their time. We have also shared information at a stakeholder day, attended by 65 individuals from the community, where we also planned future work. We have reimbursed participants for their time, which is in line with NIHR guidance. As described above, patient and public involvement has been the guiding principle throughout this project.

Recognition in global politics is not only earned through institutions or capabilities; it is narrated into being. This article investigates how the European Union (EU) is framed as a technological actor in global discourse, focusing on the symbolic dynamics of discursive recognition. Defined as a performative process through which legitimacy and agency are constructed in elite narratives, recognition is examined here through a mixed‐methods analysis of 148 Foreign Policy articles from January 2010 to March 2025. The paper introduces a two‐dimensional typology that maps how the EU is positioned along axes of regulatory authority and innovation capability. Findings indicate a significant shift in narrative patterns: early portrayals emphasised the EU's regulatory dominance but highlighted its technological shortfalls, whilst more recent discourse presents regulation as a competitive advantage and acknowledges the EU's growing presence in emerging tech domains. Although the EU is not yet fully recognised as a technological superpower, its symbolic profile has become increasingly multifaceted and contested. The analysis underscores how, in fragmented governance environments, power is exercised not only through policies and platforms, but through stories that travel, making recognition a vital, relational resource in shaping global technological influence.