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Advances in molecular genetics have led to the exponential growth of the direct-to-consumer genetic testing industry, resulting in the assembly of massive privately owned genetic databases. This article explores the potential impact of this new data type on the field of marketing. Drawing on findings from behavioral genetic research, the authors propose a framework that incorporates genetic influences into existing consumer behavior theory and use it to survey potential marketing uses of genetic data. Applications include business strategies that rely on genetic variants as bases for segmentation and targeting, creative uses that develop consumers’ sense of community and personalization, use of genetically informed study designs to test causal relations, and refinement of consumer theory by uncovering biological mechanisms underlying behavior. The authors further evaluate ethical challenges related to autonomy, privacy, misinformation, and discrimination that are unique to the use of genetic data and are not sufficiently addressed by current regulations. They conclude by proposing an agenda for future research.

Humans survive and thrive through social exchange. Yet, social dependency also comes at a cost. Perceived social isolation, or loneliness, affects physical and mental health, cognitive performance, overall life expectancy, and increases vulnerability to Alzheimer’s disease-related dementias. Despite severe consequences on behavior and health, the neural basis of loneliness remains elusive. Using the UK Biobank population imaging-genetics cohort (n = ~40,000, aged 40–69 years when recruited, mean age = 54.9), we test for signatures of loneliness in grey matter morphology, intrinsic functional coupling, and fiber tract microstructure. The loneliness-linked neurobiological profiles converge on a collection of brain regions known as the ‘default network’. This higher associative network shows more consistent loneliness associations in grey matter volume than other cortical brain networks. Lonely individuals display stronger functional communication in the default network, and greater microstructural integrity of its fornix pathway. The findings fit with the possibility that the up-regulation of these neural circuits supports mentalizing, reminiscence and imagination to fill the social void., Here, using pattern-learning analyses of structural, functional, and diffusion brain scans in ~40,000 UK Biobank participants, the authors provide population-scale evidence that the default network is associated with perceived social isolation.

Research in the field of multisensory perception shows that what we hear can influence what we see in a wide range of perceptual tasks. It is however unknown whether this extends to the visual perception of risk, despite the importance of the question in many applied domains where properly assessing risk is crucial, starting with financial trading. To fill this knowledge gap, we ran interviews with professional traders and conducted three laboratory studies using judgments of financial asset risk as a testbed. We provide evidence that the presence of ambient sound impacts risk perception, possibly due to the combination of facilitatory and synesthetic effects of general relevance to the perception of risk in many species as well as humans. We discuss the implications of our findings for various applied domains (e.g., financial, medical, and military decision-making), and raise new questions for future research.

The second-to-fourth digit ratio (2D:4D) has been associated with sexual dimorphism, with a lower 2D:4D in males. A large body of research has relied on the 2D:4D as a proxy for prenatal androgen exposure, and includes reports of relationships between 2D:4D and a wide range of human traits. Here, we examine the validity of the 2D:4D proxy by studying the association between 2D:4D and classical Congenital Adrenal Hyperplasia (CAH) due to 21-hydroxylase deficiency, a condition characterized by excessive prenatal exposure to androgens during most of the gestational period. To this end, we retrospectively examine 513 serial radiographs of the left hand obtained clinically in 90 youth with classical CAH (45 female) and 70 control youth (31 female). Replicating previous reports, we observe associations of the 2D:4D with sex (lower 2D:4D in males) and age (increase of 2D:4D through development). However, we find no evidence for differences in 2D:4D between CAH and controls (full sample: β = −0.001 (−0.008, 0.006)]; females: β = −0.004 [−0.015, 0.007]; males: β = 0.001, [−0.008, 0.011]). Although our findings do not rule out a small association between the 2D:4D and CAH, they cast doubt on the usefulness of the 2D:4D as a biomarker for prenatal androgen exposure in behavioral research.

Economic preferences may be shaped by exposure to sex hormones around birth. Prior studies of economic preferences and numerous other phenotypic characteristics use digit ratios (2D : 4D), a purported proxy for prenatal testosterone exposure, whose validity has recently been questioned. We use direct measures of neonatal sex hormones (testosterone and oestrogen), measured from umbilical cord blood ( n = 200) to investigate their association with later-life economic preferences (risk preferences, competitiveness, time preferences and social preferences) in an Australian cohort (Raine Study Gen2). We find no significant associations between testosterone at birth and preferences, except for competitiveness, where the effect runs opposite to the expected direction. Point estimates are between 0.05–0.09 percentage points (pp) and 0.003–0.14 s.d. We similarly find no significant associations between 2D : 4D and preferences ( n = 533, point estimates 0.003–0.02 pp and 0.001–0.06 s.d.). Our sample size allows detecting effects larger than 0.11 pp or 0.22 s.d. for testosterone at birth, and 0.07 pp or 0.14 s.d. for 2D : 4D ( α = 0.05 and power = 0.90). Equivalence tests show that most effects are unlikely to be larger than these bounds. Our results suggest a reinterpretation of prior findings relating 2D : 4D to economic preferences, and highlight the importance of future large-sample studies that permit detection of small effects.

The second-to-fourth digit ratio (2D:4D) has been associated with sexual dimorphism, with a lower 2D:4D in males. A large body of research has relied on the 2D:4D as a proxy for prenatal androgen exposure, and includes reports of relationships between 2D:4D and a wide range of human traits. Here, we examine the validity of the 2D:4D proxy by studying the association between 2D:4D and classical Congenital Adrenal Hyperplasia (CAH) due to 21-hydroxylase deficiency, a condition characterized by excessive prenatal exposure to androgens during most of the gestational period. To this end, we retrospectively examine serial radiographs of the left hand obtained clinically in 91 youth with classical CAH (49.5% female) and 70 control youth (44.3% female). Replicating previous reports, we observe associations of the 2D:4D with sex (lower 2D:4D in males), age (increase of 2D:4D through development) and ethnicity (lower 2D:4D in Hispanic individuals). However, we find no evidence for differences in 2D:4D between CAH and controls (full sample: □ = 0.0003 [-0.007, 0.008]; females: □ = −0.004 [-0.015, 0.007]; males: □ = 0.003, [-0.007, 0.013]). Although our findings do not rule out a small association between the 2D:4D and CAH, they cast doubt on the usefulness of the 2D:4D as a biomarker for prenatal androgen exposure in behavioral research.

The ratio of length between the second and fourth fingers (2D:4D) is commonly used as an indicator of prenatal sex hormone exposure. Several approaches have been used to try to validate the measure, including examining 2D:4D in people with congenital adrenal hyperplasia (CAH), a suite of conditions characterised by elevated adrenal androgen production secondary to defective steroidogenesis. We present a systematic review and meta-analysis that examines the relationship between these two variables. Twelve articles relating to nine CAH cohorts were identified, and 2D:4D comparisons have been made between cases and controls in eight of these cohorts. Altogether, at least one 2D:4D variable has been compared between n = 251 females with CAH and n = 358 unaffected females, and between n = 108 males with CAH and n = 204 unaffected males. A previous meta-analysis (Hönekopp and Watson, 2010) reported lower right hand (R2D:4D) and left hand (L2D:4D) digit ratios in patients with CAH relative to sex-matched controls. Our meta-analysis showed the same pattern, with medium effect sizes for R2D:4D and small effect sizes for L2D:4D. Differences of small magnitude were also observed for M2D:4D, and no significant effects were observed for D[R-L]. Notably, the only effects that remained statistically significant when stratified by sex were R2D:4D in males and L2D:4D in females, and the average effect size had reduced by 46.70% since the meta-analysis of Hönekopp and Watson (2010). We also found that individual comparisons in this literature were considerably underpowered, and that patterns of sexual dimorphism in 2D:4D were similar in CAH samples as in typically developing populations. Findings are discussed in relation to the prenatal androgen hypothesis as well as alternative explanations.

In nonhumans, the sex steroid testosterone regulates reproductive behaviors such as fighting between males and mating. In humans, correlational studies have linked testosterone with aggression and disorders associated with poor impulse control, but the neuropsychological processes at work are poorly understood. Building on a dual-process framework, we propose a mechanism underlying testosterone’s behavioral effects in humans: reduction in cognitive reflection. In the largest study of behavioral effects of testosterone administration to date, 243 men received either testosterone or placebo and took the Cognitive Reflection Test (CRT), which estimates the capacity to override incorrect intuitive judgments with deliberate correct responses. Testosterone administration reduced CRT scores. The effect remained after we controlled for age, mood, math skills, whether participants believed they had received the placebo or testosterone, and the effects of 14 additional hormones, and it held for each of the CRT questions in isolation. Our findings suggest a mechanism underlying testosterone’s diverse effects on humans’ judgments and decision making and provide novel, clear, and testable predictions.

A critical component of both economic and perceptual decision making under uncertainty is the belief-formation process. However, most research has studied belief formation in economic and perceptual decision making in isolation. One reason for this separate treatment may be the assumption that there are distinct psychological mechanisms that underlie belief formation in economic and perceptual decisions. An alternative theory is that there exists a common mechanism that governs belief formation in both domains. Here, we test this alternative theory by combining a novel computational modeling technique with two well-known experimental paradigms. We estimate a drift-diffusion model (DDM) and provide an analytical method to decode prior beliefs from DDM parameters. Subjects in our experiment exhibit strong extrapolative beliefs in both paradigms. In line with the common mechanism hypothesis, we find that a single computational model explains belief formation in both tasks and that individual differences in belief formation are correlated across tasks. Data, as supplemental material, are available at http://dx.doi.org/10.1287/mnsc.2016.2453 . This paper was accepted by Yuval Rottenstreich, judgment and decision making.

Previous research points to the heritability of risk-taking behaviour. However, evidence on how genetic dispositions are translated into risky behaviour is scarce. Here, we report a genetically-informed neuroimaging study of real-world risky behaviour across the domains of drinking, smoking, driving, and sexual behaviour, in a European sample from the UK Biobank (N= 12,675). We find negative associations between risky behaviour and grey matter volume (GMV) in distinct brain regions, including amygdala, ventral striatum, hypothalamus, and dorsolateral prefrontal cortex (dlPFC). These effects replicate in an independent sample recruited from the same population (N=13,004). Polygenic risk scores for risky behaviour, derived from a genome-wide association study in an independent sample (N=297,025), are inversely associated with GMV in dlPFC, putamen, and hypothalamus. This relation mediates ~2.2% of the association between genes and behaviour. Our results highlight distinct heritable neuroanatomical features as manifestations of the genetic propensity for risk taking.One Sentence SummaryRisky behaviour and its genetic associations are linked to less grey matter volume in distinct brain regions.

The capacity to infer others' mental states (known as ‘mind reading’ and ‘cognitive empathy’) is essential for social interactions across species, and its impairment characterizes psychopathological conditions such as autism spectrum disorder and schizophrenia. Previous studies reported that testosterone administration impaired cognitive empathy in healthy humans, and that a putative biomarker of prenatal testosterone exposure (finger digit ratios) moderated the effect. However, empirical support for the relationship has relied on small sample studies with mixed evidence. We investigate the reliability and generalizability of the relationship in two large-scale double-blind placebo-controlled experiments in young men ( n = 243 and n = 400), using two different testosterone administration protocols. We find no evidence that cognitive empathy is impaired by testosterone administration or associated with digit ratios. With an unprecedented combined sample size, these results counter current theories and previous high-profile reports, and demonstrate that previous investigations of this topic have been statistically underpowered.

The impact of testosterone on decision-making is a growing literature, with several reports of economically relevant outcomes. Similar to Wibral et al. (2012), we investigate the effects of exogenous testosterone administration on deception in a double-blind placebo controlled study. Participants (N = 242) were asked to roll a die in private and were paid according to their reported roll, which creates the opportunity to lie about the outcome to increase earnings. We find evidence for self-serving lying in both treatment and control groups and a statistically insignificant negative effect (d = −0.17, 95% CI[−0.42, 0.08]) indicating more honest behavior (i.e., lower reports) following testosterone administration. Although insignificant, the direction was the same as in the Wibral et al. study, and the meta-analytic effect of the two studies demonstrates lower reporting (i.e., more honesty) following testosterone (vs. placebo) administration, significant at the 0.05 level (d = −0.27, 95% CI[−0.49, −0.06]). We discuss how our results and methodology compare with Wibral et al. and identify potential causes for differences in findings. Finally, we consider several plausible connections between testosterone and lying that may be further investigated using alternative methodologies.

Loss aversion is a well-known behavioral regularity in financial decision making, describing humans' tendency to overweigh losses compared to gains of the same amount. Recent research indicates that stress and associated hormonal changes affect loss aversion, yet the underlying neuroendocrine mechanisms are still poorly understood. Here, we investigated the causal influence of two major stress neuromodulators, cortisol and noradrenaline, on loss aversion during financial decision making. In a double-blind, placebo-controlled between-subject design, we orally administered either the α2-adrenergic antagonist yohimbine (increasing noradrenergic stimulation), hydrocortisone, both substances, or a placebo to healthy young men. We tested the treatments' influence on a financial decision-making task measuring loss aversion and risk attitude. We found that both drugs combined, relative to either drug by itself, reduced loss aversion in the absence of an effect on risk attitude or choice consistency. Our data suggest that concurrent glucocorticoid and noradrenergic activity prompts an alignment of reward- with loss-sensitivity, and thus diminishes loss aversion. Our results have implications for the understanding of the susceptibility to biases in decision making.

The history of humankind is an epic of cooperation, which is ubiquitous across societies and increasing in scale. Much human cooperation occurs where it is risky to cooperate for mutual benefit because successful cooperation depends on a sufficient level of cooperation by others. Here we show that arginine vasopressin (AVP), a neuropeptide that mediates complex mammalian social behaviors such as pair bonding, social recognition and aggression causally increases humans’ willingness to engage in risky, mutually beneficial cooperation. In two double-blind experiments, male participants received either AVP or placebo intranasally and made decisions with financial consequences in the “Stag hunt” cooperation game. AVP increases humans’ willingness to cooperate. That increase is not due to an increase in the general willingness to bear risks or to altruistically help others. Using functional brain imaging, we show that, when subjects make the risky Stag choice, AVP down-regulates the BOLD signal in the left dorsolateral prefrontal cortex (dlPFC), a risk-integration region, and increases the left dlPFC functional connectivity with the ventral pallidum, an AVP receptor-rich region previously associated with AVP-mediated social reward processing in mammals. These findings show a previously unidentified causal role for AVP in social approach behavior in humans, as established by animal research.

The neurohormone oxytocin (OT) has been one the most studied peptides in behavioural sciences over the past two decades. Primarily known for its crucial role in labour and lactation, a rapidly growing literature suggests that intranasal OT (IN-OT) may also play a role in the emotional and social lives of humans. However, the lack of a convincing theoretical framework explaining the effects of IN-OT that would also allow the prediction of which moderators exert their effects and when has raised healthy skepticism regarding the robustness of human behavioural IN-OT research. Poor knowledge of the exact pharmacokinetic properties of OT, as well as crucial statistical and methodological issues and the absence of direct replication efforts, may have lead to a publication bias in the IN-OT literature, with many unpublished studies with null results remaining buried in laboratory drawers. Is there a file drawer problem in IN-OT research? If this is the case, it may also be true in our own laboratory. The present study aims to answer this question, document the extent of the problem and discuss its implications for OT research. For eight studies (including 13 dependent variables overall, as assessed through 25 different paradigms) performed in our laboratory between 2009 and 2014 on 453 subjects, the results obtained were too often not those that were expected. Only five publications emerged from our studies and only one of these reported a null finding. After realising that our publication portfolio has become less and less representative of our actual findings and because the nonpublication of our data might contribute to generating a publication bias in IN-OT research, we decided to retrieve these studies from our drawer and encourage other laboratories to do the same.

People often rely on intuitive judgments at the expense of deliberate reasoning, but what determines the dominance of intuition over deliberation is not well understood. Here, we employed a psychopharmacological approach to unravel the role of two major endocrine stress mediators, cortisol and noradrenaline, in cognitive reasoning. Healthy participants received placebo, cortisol (hydrocortisone) and/or yohimbine, a drug that increases noradrenergic stimulation, before performing the cognitive reflection test (CRT). We found that cortisol impaired performance in the CRT by biasing responses toward intuitive, but incorrect answers. Elevated stimulation of the noradrenergic system, however, had no effect. We interpret our results in the context of the dual systems theory of judgment and decision making. We propose that cortisol causes a shift from deliberate, reflective cognition toward automatic, reflexive information processing.

Heavy alcohol consumption can have significant deleterious neural consequences, including brain atrophy, neuronal loss, poorer white matter fiber integrity, and cognitive decline. However, the effects of light-to-moderate alcohol consumption on brain structure remain unclear. Here, we examine the associations between alcohol intake and brain structure using multimodal imaging data from 36,678 generally healthy middle-aged and older adults from the UK Biobank, controlling for numerous potential confounds. We find negative associations between alcohol intake and global gray matter volume (GMV) and white matter volume (WMV), which become stronger as intake increases. An examination of the associations between alcohol intake and 139 regional GMV imaging-derived phenotypes (IDPs) and 375 WM microstructure IDPs yielded 304 (59.1%) significant findings, including 125 GMV IDPs that are spread across the brain and 179 WM microstructure IDPs across multiple tract regions. In general, findings comport with the existing literature. However, a daily alcohol intake of as little as one to two units – 250 to 500 ml of a 4% beer or 76 to 146 ml of a 13% wine – is already associated with GMV deficits and altered WMV microstructure, placing moderate drinkers at risk.One Sentence SummaryModerate alcohol intake, consuming one or more daily alcohol units, has adverse effects on brain health.