Economic And Social Preference
Introduction
Section titled “Introduction”Economic and social preferences encompass the diverse ways individuals make choices, interact with others, and respond to incentives within economic and social contexts. These preferences include traits such as risk tolerance, impulsivity, altruism, trust, fairness, cooperation, and political orientation. They are fundamental to understanding human behavior, influencing decisions ranging from personal finance and career paths to social interactions and civic engagement. The variability in these preferences across individuals is a subject of extensive research, exploring both environmental and biological influences.
Biological Basis
Section titled “Biological Basis”Like many complex human characteristics, economic and social preferences are considered to have a biological basis, with genetic factors contributing to individual differences. Research into common traits suggests that genetic variations, particularly single nucleotide polymorphisms (SNPs), can be associated with these behavioral tendencies.[1] These preferences are typically polygenic, meaning they are influenced by many genes, each contributing a small effect, rather than a single gene dictating a specific preference. The biological mechanisms often involve complex neural circuits in the brain associated with reward processing, decision-making, emotional regulation, and social cognition, influenced by neurotransmitter systems.
Clinical Relevance
Section titled “Clinical Relevance”While not diseases themselves, extreme manifestations or certain profiles of economic and social preferences can have implications for mental health and well-being. For instance, extreme risk-taking or impulsivity might be associated with certain behavioral disorders, while atypical social preferences could relate to conditions affecting social interaction. Understanding the underlying genetic and biological factors could potentially offer insights into vulnerabilities or resilience to conditions like depression, which has been a focus of genetic studies.[2]
Social Importance
Section titled “Social Importance”The study of economic and social preferences holds significant social importance. Insights into their genetic underpinnings can enhance our understanding of human diversity in decision-making, contributing to fields like behavioral economics, sociology, and political science. Such knowledge can inform public policy, educational strategies, and interventions aimed at promoting well-being and fostering cooperative societies. Recognizing the multifaceted nature of these preferences, including their genetic components, allows for a more nuanced appreciation of individual differences and the factors shaping societal outcomes.
Limitations
Section titled “Limitations”Research into the genetic architecture of economic and social preference, while shedding light on heritable components, faces several inherent limitations that warrant careful consideration when interpreting findings. These challenges stem from the complex nature of the traits themselves, the methodologies employed in genetic studies, and the broad scope of influences on human behavior.
Methodological and Statistical Constraints
Section titled “Methodological and Statistical Constraints”The ability to robustly identify specific genetic associations with economic and social preference is significantly hampered by statistical power issues. Studies, even those with thousands of participants, are often underpowered to detect individual single nucleotide polymorphisms (SNPs) given that these traits are highly polygenic, with each common SNP contributing only a very small fraction to the overall variance . Such effects can influence choices related to career, education, and lifestyle, thereby affecting economic standing and social engagement. Similarly, theRAB30 gene, with variant rs11233413 , is vital for intracellular transport and protein secretion, processes critical for neuronal communication and immune function.[3] Variations here might alter the efficiency of these cellular functions, potentially influencing an individual’s stress resilience and social adaptability, which are valuable traits in both personal and professional spheres.
Other variants contribute to differences in neural development and sensory processing. The rs500454 variant, located near SEMA3C and EIF4EP4, could influence axon guidance and protein synthesis regulation, respectively, impacting neural circuit formation and overall brain function.[4] These biological underpinnings are fundamental to cognitive abilities like learning and decision-making, which have direct implications for educational attainment and economic productivity. Furthermore, variants like rs41418949 in NETO1, a gene critical for synaptic function, might affect memory, emotional regulation, and learning capacity, shaping an individual’s aptitude for complex tasks and social interactions. Genetic variations in NKAIN2 and the long non-coding RNA RNF217-AS1, exemplified by rs9398764 , could affect neuronal excitability and gene expression, influencing aspects like attention, mood, and sensory perception.[5] These factors are crucial for effective social integration and performance in various economic roles.
Further influencing a wide range of cellular functions are variants in non-coding regions and genes involved in regulatory or structural roles. The region encompassing LINC02063 and LINC02114, with variants like rs6555263 , rs6555264 , and rs6894281 , involves long intergenic non-coding RNAs that regulate gene expression, potentially affecting developmental processes and stress responses.[6] Such regulatory impacts can contribute to variations in health and resilience, impacting an individual’s ability to maintain employment and contribute to society. Variants within or near pseudogenes like TUBBP11 and SSX2IPP1, including rs10937540 , rs6775909 , rs7628767 , rs9821642 , rs9820695 , and rs4856162 , as well as RAP1BP2, can indirectly influence cellular structure and signaling, affecting physical health and cognitive flexibility. The RGS6 gene, with variant rs4902960 , modulates G-protein coupled receptor signaling, impacting cardiovascular health and emotional stability, which are vital for sustained well-being and productivity.[7] Lastly, the rs436000 variant between GCFC2 and SUCLA2P2could affect gene transcription and metabolic efficiency, influencing an individual’s overall physiological robustness and disease susceptibility, thereby impacting healthcare costs and economic participation.
The researchs context does not contain information regarding the classification, definition, and terminology of ‘economic and social preference’.
Genetic Predisposition
Section titled “Genetic Predisposition”Economic and social preference is influenced by a complex interplay of genetic factors. Genome-wide association studies (GWAS) have identified numerous inherited variants, or single nucleotide polymorphisms (SNPs), that contribute to traits closely related to economic and social preferences, such as subjective well-being, depressive symptoms, neuroticism, and specific temperament scales like Harm Avoidance and Reward Dependence.[8] These studies often employ multi-trait analysis of genome-wide association summary statistics to uncover the genetic architecture underlying such complex phenotypes.[9] The trait is largely polygenic, meaning it is influenced by many genes, each contributing a small effect, rather than a single gene.[9] Furthermore, research on temperament scales indicates sex differences in the source of genetic variation for certain traits, implying that partly different genetic factors explain variance in males and females.[10] This suggests the presence of complex gene-gene interactions or sex-specific genetic effects that modulate the expression of economic and social preferences.
Environmental and Societal Influences
Section titled “Environmental and Societal Influences”Beyond genetic factors, economic and social preferences are significantly shaped by environmental and societal influences. The existence of research entities like the Center for Economic and Social Research and the Social Science Genetic Association Consortium (SSGAC) underscores the critical role of socioeconomic factors in understanding these preferences.[9] These factors encompass a broad spectrum of societal conditions, including cultural norms, educational systems, and economic opportunities, which collectively influence an individual’s decision-making and preferences within social and economic contexts. The SSGAC’s focus on “social-scientific outcomes” further highlights the importance of these broader environmental and social contexts in shaping human behavior and well-being.[8]
Gene-Environment Interaction
Section titled “Gene-Environment Interaction”The expression of genetic predispositions for economic and social preferences is not deterministic but is dynamically modulated by environmental factors through gene-environment interactions. These interactions occur when genetic variants modify an individual’s susceptibility or response to specific environmental triggers, or when environmental factors influence how genetic predispositions are expressed.[11] For instance, the concept of an “additive genetic effect” in studies of temperament scales acknowledges a baseline genetic contribution that can be further influenced by an individual’s environment, leading to diverse phenotypic outcomes in economic and social behaviors.[10] Understanding this complex interplay is crucial for a comprehensive view of how economic and social preferences develop.
Genetic Architecture of Economic and Social Preferences
Section titled “Genetic Architecture of Economic and Social Preferences”Economic and social preferences are complex traits characterized by a highly polygenic genetic architecture, meaning that variation in these traits is influenced by a multitude of genetic variants, each contributing a small effect.[12] Studies have shown that the heritable variation for these preferences is explained by many genes, rather than a few genes with large individual impacts.[12]Specifically, individual single nucleotide polymorphisms (SNPs) are understood to explain only a minor fraction of the overall variance, with true associations between common SNPs and economic and political phenotypes likely having very small effect sizes.[12] This complex architecture, shaped by evolutionary forces such as mutation, genetic drift, and natural selection, dictates the challenges in identifying specific genetic variants associated with these traits.[12] The molecular-genetic-based estimates of heritability for economic and social preferences largely align with estimates derived from traditional twin studies, confirming a significant genetic component to these behaviors.[12] This polygenic nature implies that while genes play a role, their influence is distributed across the genome, with no single SNP typically achieving conventional genome-wide significance thresholds.[12] Furthermore, the concept of pleiotropy, where a single genetic marker can influence multiple distinct traits, is relevant in understanding the broader biological implications of these genetic findings.[12]
Molecular and Cellular Foundations
Section titled “Molecular and Cellular Foundations”The genetic variants influencing economic and social preferences are hypothesized to operate through intricate molecular and cellular pathways, although specific details for these preferences are not extensively elucidated in current research.[12] Genetic associations are expected to eventually shed light on the underlying biological processes, which would involve critical biomolecules such as proteins, enzymes, receptors, hormones, and transcription factors.[12] These biomolecules are integral to cellular functions and metabolic processes, forming regulatory networks that translate genetic information into physiological and behavioral outcomes. Understanding these pathways could lead to new theoretical constructs that are more aligned with the underlying biology of concepts like “risk aversion” or “patience”.[12]
Neurobiological Correlates of Behavior
Section titled “Neurobiological Correlates of Behavior”At the tissue and organ level, the genetic influences on economic and social preferences ultimately manifest through neurobiological mechanisms, primarily within the brain. While specific brain regions or neural circuits are not detailed, the observable behavioral traits associated with these preferences are a direct consequence of complex neural processing.[12] Genetic variations, through their impact on molecular and cellular pathways, can subtly alter neural function, affecting how individuals perceive, evaluate, and respond to economic and social stimuli.[12] Such modifications in neural activity contribute to the systemic consequences observed in various behaviors and decision-making processes, underscoring the interconnectedness of genetic predisposition and behavioral expression.
Developmental Context and Environmental Interactions
Section titled “Developmental Context and Environmental Interactions”The development of economic and social preferences is a complex process influenced by the interplay between an individual’s genetic makeup and their environment. Genetic factors, while stable, interact with environmental cues throughout development, shaping the expression of these preferences.[12] The presence of gene-environment interactions further complicates the study of these traits, requiring sophisticated analytical approaches to disentangle their respective contributions.[12] Understanding how these genetic influences unfold over an individual’s lifespan, from early developmental stages to mature decision-making, is crucial for comprehending the full scope of their impact on behaviors and outcomes.
Population Studies
Section titled “Population Studies”Understanding the population-level dynamics of economic and social preferences relies heavily on large-scale cohort studies that track individuals over extended periods, providing crucial longitudinal data. Major initiatives such as the Atherosclerosis Risk in Communities (ARIC) study, which recruited over 15,000 middle-aged participants across four US communities, and the Cardiovascular Health Study (CHS), enrolling nearly 6,000 individuals aged 65 and older, exemplify this approach by collecting comprehensive health, lifestyle, and demographic information over decades.[13] Similarly, the Framingham Heart Study (FHS), with its Original cohort from 1948 and Offspring cohort from 1971, offers a unique multi-generational perspective, allowing researchers to investigate temporal patterns and the influence of generational factors on various traits, including those potentially related to preferences.[14] These studies often involve repeated examinations, with FHS cohort 1 undergoing 28 visits and CHS 22 examinations, enabling the capture of dynamic changes in health outcomes, behaviors, and potentially evolving social and economic preferences over the life course.[14] Beyond US cohorts, European studies like the Rotterdam Study (RS), which recruited nearly 8,000 participants aged 55 or older, and the Study of Health in Pomerania (SHIP), also contribute significantly to this global understanding by providing data from distinct demographic and geographic contexts.[15]These extensive cohorts are critical for genetic epidemiological programs, where they facilitate the collection of fasting blood samples, biochemical and physiological measurements, and detailed questionnaire data on medical history, lifestyle, and environmental exposures, all following standardized protocols.[16] The integration of such rich, longitudinal datasets is fundamental for identifying factors that shape complex human traits, including economic decision-making and social interactions, by observing their prevalence and incidence over time within diverse adult populations.
Population Diversity and Geographic Variations
Section titled “Population Diversity and Geographic Variations”Investigations into economic and social preferences benefit immensely from cross-population comparisons, which highlight ancestry differences and geographic variations in these complex traits. Studies conducted in geographically isolated populations, such as the CROATIA-Vis and CROATIA-Korčula cohorts, involving over 1,000 and nearly 1,000 Croatians respectively, offer unique insights into population-specific effects due to their distinct genetic and environmental homogeneity.[16] These island populations, contrasted with a cohort from a larger city like Split, allow for the examination of how genetic background and localized environmental exposures might influence preferences and health outcomes, including susceptibility to infectious diseases.[17] International collaborations further broaden this perspective, with research efforts spanning institutions in Australia, New Zealand, the Netherlands, and various locations across the United States, indicating a global endeavor to understand traits across diverse ethnic and cultural landscapes.[18] However, methodological considerations regarding population representativeness are crucial, as demonstrated by studies where specific demographic groups, such as African American participants from the ARIC and CHS cohorts, were excluded from certain analyses.[13] Such exclusions can limit the generalizability of findings, underscoring the importance of including diverse ancestries to fully capture the spectrum of human variation in preferences and their underlying factors. The careful recruitment of adult individuals from communities, irrespective of specific phenotypes, ensures a foundational understanding of population-wide distributions, while also necessitating explicit consideration of potential generation confounders in multi-cohort analyses, as addressed by analyzing Framingham Heart Study cohorts separately.[14]
Epidemiological Associations and Methodological Rigor
Section titled “Epidemiological Associations and Methodological Rigor”Epidemiological studies are pivotal for identifying the prevalence patterns, incidence rates, and demographic and socioeconomic correlates of various traits, including those that might influence economic and social preferences. Research often employs sophisticated statistical models, such as logistic regression for binary outcomes and linear regression for ordinal variables, to discern associations between genetic variants and complex traits or disease risks.[17]A critical aspect of these analyses involves robust adjustments for confounding factors, including demographic variables like age and gender, and socioeconomic status, which can be quantified through metrics like material possessions (e.g., plumbing, heating, phone, computer) and years of schooling.[17] These socioeconomic variables are typically transformed into categorical data to better capture their influence, while missing data are carefully imputed based on cohort, gender, and age group to maintain statistical power and validity.[17] Furthermore, study designs prioritize ethical considerations, with all participants providing informed consent and protocols adhering to guidelines such as the Declaration of Helsinki.[16]The rigor of these methodologies extends to sample size, with many studies pooling data from thousands of participants, and to accounting for population structure and familial relatedness through methods like kinship matrix calculations, ensuring that observed associations are not spurious.[17] While large sample sizes and comprehensive adjustments enhance the generalizability of findings, the ability to replicate results in independent study samples, such as using AGES and WGHS cohorts for kidney function studies, is fundamental to confirming epidemiological associations and establishing their broader population-level implications.[13]
Ethical Foundations of Genetic Information
Section titled “Ethical Foundations of Genetic Information”The study of genetic variants associated with complex traits like ‘economic and social preference’ raises significant ethical questions regarding the use and interpretation of such sensitive information. A cornerstone of ethical genetic research and application is informed consent, ensuring individuals fully understand the implications of genetic testing, including potential psychological impacts and the scope of data sharing. The research itself highlights the importance of this, noting that data availability is restricted due to privacy regulations and the informed consent of participants.[19]Beyond consent, robust privacy protections are paramount to prevent genetic discrimination. Information about an individual’s genetic predisposition for ‘economic and social preference’ could potentially be misused in areas such as employment, insurance, or even social profiling, leading to unfair treatment or stigmatization. The potential for such data to influence reproductive choices also presents a complex ethical dilemma, as individuals might face pressure to select for or against certain genetic predispositions, blurring lines between health and desirability.
Societal Implications and Equity Concerns
Section titled “Societal Implications and Equity Concerns”The social implications of understanding the genetic underpinnings of ‘economic and social preference’ are profound, potentially exacerbating existing societal inequalities. Stigmatization could arise if certain genetic profiles are deemed “less desirable,” impacting self-perception and social acceptance. This research, involving departments of economics and sociology, inherently bridges genetic findings with social structures, underscoring the potential for socioeconomic factors to interact with genetic information, influencing perceptions of individual worth or capability.[8] Furthermore, the availability and interpretation of genetic testing for such traits could lead to new forms of health disparities or deepen existing ones, particularly concerning access to advanced genetic counseling and interventions. Vulnerable populations, already facing systemic disadvantages, might be disproportionately affected by the implications of such genetic information, whether through lack of access to beneficial applications or increased exposure to discriminatory practices. Equitable resource allocation in the context of genetic technologies becomes critical to ensure that these advancements do not widen the gap between those who can leverage genetic insights and those who cannot, requiring a global health perspective to address disparities across different cultural and economic contexts.
Policy, Regulation, and Research Integrity
Section titled “Policy, Regulation, and Research Integrity”Effective policy and regulation are essential to navigate the ethical complexities arising from genetic studies of ‘economic and social preference’. This includes developing comprehensive genetic testing regulations that govern how such tests are offered, interpreted, and utilized, alongside stringent data protection measures to safeguard highly sensitive genetic information. The studies themselves emphasize the necessity of ethical approval and consent to participate, highlighting the existing frameworks for research ethics.[20] Establishing clear clinical guidelines is crucial for practitioners to ethically counsel individuals about genetic predispositions for complex traits, ensuring that information is presented accurately and without undue influence or predictive certainty. Beyond individual data, the broader research landscape requires robust frameworks for research ethics that address the societal impact of findings, particularly when dealing with traits that could be misinterpreted or misused to reinforce social biases. These regulatory and ethical guidelines must evolve continually to keep pace with scientific advancements and address emerging challenges in the responsible application of genetic knowledge.
Key Variants
Section titled “Key Variants”Frequently Asked Questions About Economic And Social Preference
Section titled “Frequently Asked Questions About Economic And Social Preference”These questions address the most important and specific aspects of economic and social preference based on current genetic research.
1. Why am I so bad at saving money compared to my friends?
Section titled “1. Why am I so bad at saving money compared to my friends?”Your approach to money, including traits like impulsivity or risk tolerance, has a biological basis, with genetic factors contributing to individual differences. These preferences are polygenic, meaning many genes with small effects influence them. Your brain’s reward processing and decision-making circuits, shaped by your genes, play a role in your financial choices, potentially differing from your friends’.
2. My sibling is super generous, but I’m not. Why the difference?
Section titled “2. My sibling is super generous, but I’m not. Why the difference?”Individual differences in traits like altruism are partly influenced by genetics. While you share many genes with your sibling, variations in specific genetic markers can contribute to different levels of generosity. Environmental factors and unique life experiences also play a significant role in shaping these preferences, even within families.
3. Why do some people trust strangers easily, but I don’t?
Section titled “3. Why do some people trust strangers easily, but I don’t?”Trust is a complex social preference with a genetic component. Differences in your genetic makeup can influence the neural circuits in your brain responsible for social cognition and emotional regulation, leading to varying levels of inherent trust. Your personal experiences and environment also heavily shape how much you trust others.
4. Is it true that my political views are partly genetic?
Section titled “4. Is it true that my political views are partly genetic?”Yes, research suggests that political orientation, like other social preferences, has a biological basis with genetic factors contributing to individual differences. These are polygenic traits, influenced by many genes, each with a small effect. However, environmental factors and personal experiences also play a crucial role in shaping your political views.
5. Can I really change how risky I am with decisions?
Section titled “5. Can I really change how risky I am with decisions?”While your inherent risk tolerance has a genetic basis, it’s not entirely fixed. Your genes influence your brain’s decision-making and reward processing. However, these genetic predispositions interact with your environment and experiences. With conscious effort, new experiences, and learned strategies, you can certainly modify your approach to risk over time.
6. Why do I sometimes make impulsive choices even when I know better?
Section titled “6. Why do I sometimes make impulsive choices even when I know better?”Impulsivity is influenced by complex neural circuits in your brain related to reward processing and decision-making, which have a genetic basis. Even when you understand the consequences, these biological underpinnings can make it harder to resist immediate gratification. Environmental factors like stress or lack of sleep can also amplify these tendencies.
7. Does my family history affect how much I value fairness?
Section titled “7. Does my family history affect how much I value fairness?”Yes, preferences like fairness are considered to have a biological basis, with genetic factors contributing to how strongly individuals value them. While your family environment certainly shapes your understanding of fairness, your genetic inheritance also plays a part in your intrinsic inclination towards equitable outcomes, contributing to individual differences.
8. Why are some people naturally better cooperators than me at work?
Section titled “8. Why are some people naturally better cooperators than me at work?”Cooperation is a social preference that research shows has a genetic component, influencing individual differences. Your genetic makeup can affect the neural circuits involved in social cognition and interaction, making some people more predisposed to cooperative behaviors. However, workplace culture and personal incentives also strongly shape how you collaborate.
9. Could extreme risk-taking affect my mental well-being?
Section titled “9. Could extreme risk-taking affect my mental well-being?”Yes, extreme manifestations of preferences like risk-taking can have implications for your mental health. While not a disease itself, excessive risk-taking or impulsivity can be associated with certain behavioral disorders. Understanding these underlying biological factors can offer insights into vulnerabilities or resilience to such conditions.
10. Does my ethnic background influence my trust levels?
Section titled “10. Does my ethnic background influence my trust levels?”Research into genetic influences on preferences like trust has often focused on specific populations, such as those of European ancestry. While genetic factors play a role, the transferability of specific genetic associations and heritability estimates across different ancestries is still being investigated. Environmental and cultural factors unique to ethnic backgrounds also significantly shape trust levels.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Eriksson N, et al. “Web-based, participant-driven studies yield novel genetic associations for common traits.” PLoS Genet, vol. 6, no. 6, 2010, p. e1000993.
[2] Otowa T, et al. “The First Pilot Genome-Wide Gene-Environment Study of Depression in the Japanese Population.” PLoS One, vol. 11, no. 8, 2016, p. e0160244.
[3] Soler Artigas, M, et al. “Genome-wide association and large-scale follow up identifies 16 new loci influencing lung function.” Nat Genet, 2011.
[4] Jiang, Y, et al. “Propensity score-based nonparametric test revealing genetic variants underlying bipolar disorder.” Genet Epidemiol, 2012.
[5] Kraja, AT, et al. “A bivariate genome-wide approach to metabolic syndrome: STAMPEED consortium.” Diabetes, 2011.
[6] Wilk, JB, et al. “Framingham Heart Study genome-wide association: results for pulmonary function measures.” BMC Med Genet, 2007.
[7] Stokowski, RP, et al. “A genomewide association study of skin pigmentation in a South Asian population.” Am J Hum Genet, 2007.
[8] Okbay, A et al. “Genetic variants associated with subjective well-being, depressive symptoms, and neuroticism identified through genome-wide analyses.”Nat Genet, 2016.
[9] Turley, Patrick, et al. “Multi-trait analysis of genome-wide association summary statistics using MTAG.” Nature Genetics, vol. 49, no. 12, 2017, pp. 1731-1735.
[10] Verweij, K. J., et al. “A genome-wide association study of Cloninger’s temperament scales: implications for the evolutionary genetics of personality.” Biological Psychology, vol. 85, no. 1, 2010, pp. 126-132.
[11] Figueroa, Joshua D., et al. “Genome-wide association study identifies multiple loci associated with bladder cancer risk.”Human Molecular Genetics, vol. 23, no. 5, 2014, pp. 1387-1394.
[12] Benjamin, Daniel J., et al. “The genetic architecture of economic and political preferences.” Proceedings of the National Academy of Sciences 109.20 (2012): 8026-8031.
[13] Kottgen, A et al. “Multiple loci associated with indices of renal function and chronic kidney disease.”Nat Genet, 2009.
[14] He, L et al. “Pleiotropic Meta-Analyses of Longitudinal Studies Discover Novel Genetic Variants Associated with Age-Related Diseases.” Front Genet, 2016.
[15] Gottlieb, DJ et al. “Novel loci associated with usual sleep duration: the CHARGE Consortium Genome-Wide Association Study.” Mol Psychiatry, 2015.
[16] Lauc, G et al. “Loci associated with N-glycosylation of human immunoglobulin G show pleiotropy with autoimmune diseases and haematological cancers.”PLoS Genet, 2013.
[17] Gelemanovic, A et al. “Genome-Wide Meta-Analysis Identifies Multiple Novel Rare Variants to Predict Common Human Infectious Diseases Risk.” Int J Mol Sci, 2023.
[18] Jensen, RA et al. “Genome-wide association study of retinopathy in individuals without diabetes.”PLoS One, 2013.
[19] Pardo, L. M. “Genome-Wide Association Studies of Multiple Keratinocyte Cancers.” PLoS One, vol. 12, no. 1, 12 Jan. 2017, p. e0169229.
[20] Graham, P. S., et al. “Genome-wide association studies for diabetic macular edema and proliferative diabetic retinopathy.”BMC Medical Genetics, vol. 19, no. 1, 9 May 2018, p. 70.