A tactical retreat? Conceptualising the dynamics of European grocery retail divestment from East Asia

The internationalisation of the firm is a highly dynamic process, in which periods of investment and expansion intermingle with periods of divestment and retrenchment. Academic research to date has focused on identifying the reasons for and the processes of divestment. Empirical studies either evidence generic pressures or provide case studies of specific incidents. There few longitudinal studies of international divestment, consequently the dynamic interactions between host market, home market and firm level factors, and how the institutional context changes over time is underplayed. This paper seeks to rectify this gap in our understanding. We explore the rationale and evolving dynamics of European grocery retail divestment in East Asia over a thirty year period. Taking an inductive approach and drawing on analysis of contemporary narratives drawn from company documentation, trade journals, newsfeeds and market reports, three phases can be identified characterised by specific factors and combinations of factors which intersect to provide the key pressures and stimuli for divestment. We conclude that at different time periods, different internal and external contextual influences manifest themselves through different priorities within the firm’s strategy - marked by a switch from local (host) market, to regional, to global firm-centric considerations. Longitudinal analyses allow a greater recognition of this dynamic interplay of factors, and the changes in these relationships, and provides a more nuanced understanding of the international divestment process

The association between cognitive ability and body mass index: A sibling-comparison analysis in four longitudinal studies

BACKGROUND: Body mass index (BMI) and obesity rates have increased sharply since the 1980s. While multiple epidemiologic studies have found that higher adolescent cognitive ability is associated with lower adult BMI, residual and unobserved confounding due to family background may explain these associations. We used a sibling design to test this association accounting for confounding factors shared within households. METHODS AND FINDINGS: We used data from four United States general youth population cohort studies: the National Longitudinal Study of Youth 1979 (NLSY-79), the NLSY-79 Children and Young Adult, the NLSY 1997 (NLSY-97), and the Wisconsin Longitudinal Study (WLS); a total of 12,250 siblings from 5,602 households followed from adolescence up to age 62. We used random effects within-between (REWB) and residualized quantile regression (RQR) models to compare between- and within-family estimates of the association between adolescent cognitive ability and adult BMI (20 to 64 years). In REWB models, moving from the 25th to 75th percentile of adolescent cognitive ability was associated with -0.95 kg/m2 (95% CI = -1.21, -0.69) lower BMI between families. Adjusting for family socioeconomic position reduced the association to -0.61 kg/m2 (-0.90, -0.33). However, within families, the association was just -0.06 kg/m2 (-0.35, 0.23). This pattern of results was found across multiple specifications, including analyses conducted in separate cohorts, models examining age-differences in association, and in RQR models examining the association across the distribution of BMI. Limitations include the possibility that within-family estimates are biased due to measurement error of the exposure, confounding via non-shared factors, and carryover effects. CONCLUSIONS: The association between high adolescent cognitive ability and low adult BMI was substantially smaller in within-family compared with between-family analysis. The well-replicated associations between cognitive ability and subsequent BMI may largely reflect confounding by family background factors

Weakening of the cognition and height association from 1957 to 2018: Findings from four British birth cohort studies

BACKGROUND: Taller individuals have been repeatedly found to have higher scores on cognitive assessments. Recent studies have suggested that this association can be explained by genetic factors, yet this does not preclude the influence of environmental or social factors that may change over time. We thus tested whether the association changed across time using data from four British birth cohorts (born in 1946, 1958, 1970, and 2001). METHODS: In each cohort height was measured and cognition via verbal reasoning, vocabulary/comprehension, and mathematical tests; at ages 10/11 and 14/17 years (N=41,418). We examined associations between height and cognition at each age, separately in each cohort, and for each cognitive test administered. Linear and quantile regression models were used. RESULTS: Taller participants had higher mean cognitive assessment scores in childhood and adolescence, yet the associations were weaker in later (1970 and 2001) cohorts. For example, the mean difference in height comparing the highest with lowest verbal cognition scores at 10/11 years was 0.57 SD (95% CI = 0.44-0.70) in the 1946 cohort, yet 0.30 SD (0.23-0.37) in the 2001 cohort. Expressed alternatively, there was a reduction in correlation from 0.17 (0.15-0.20) to 0.08 (0.06-0.10). This pattern of change in the association was observed across all ages and cognition measures used, was robust to adjustment for social class and parental height, and modeling of plausible missing-not-at-random scenarios. Quantile regression analyses suggested that these differences were driven by differences in the lower centiles of height, where environmental influence may be greatest. CONCLUSIONS: Associations between height and cognitive assessment scores in childhood-adolescence substantially weakened from 1957-2018. These results support the notion that environmental and social change can markedly weaken associations between cognition and other traits. FUNDING: DB is supported by the Economic and Social Research Council (grant number ES/M001660/1); DB and LW by the Medical Research Council (MR/V002147/1). The Medical Research Council (MRC) and the University of Bristol support the MRC Integrative Epidemiology Unit [MC_UU_00011/1]. NMD is supported by an Norwegian Research Council Grant number 295989. VM is supported by the CLOSER Innovation Fund WP19 which is funded by the Economic and Social Research Council (award reference: ES/K000357/1) and Economic and Social Research Council (ES/M001660/1). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

Little genomic support for Cyclophilin A-matrix metalloproteinase-9 pathway as a therapeutic target for cognitive impairment in APOE4 carriers

Therapeutic targets for halting the progression of Alzheimer’s disease pathology are lacking. Recent evidence suggests that APOE4, but not APOE3, activates the Cyclophilin-A matrix metalloproteinase-9 (CypA-MMP9) pathway, leading to an accelerated breakdown of the blood–brain barrier (BBB) and thereby causing neuronal and synaptic dysfunction. Furthermore, blockade of the CypA-MMP9 pathway in APOE4 knock-in mice restores BBB integrity and subsequently normalizes neuronal and synaptic function. Thus, CypA has been suggested as a potential target for treating APOE4 mediated neurovascular injury and the resulting neuronal dysfunction and degeneration. The odds of drug targets passing through clinical trials are greatly increased if they are supported by genomic evidence. We found little evidence to suggest that CypA or MMP9 affects the risk of Alzheimer’s disease or cognitive impairment using two-sample Mendelian randomization and polygenic risk score analysis in humans. This casts doubt on whether they are likely to represent effective drug targets for cognitive impairment in human APOE4 carriers

Investigating how the accuracy of teacher expectations of pupil performance relate to socioeconomic and genetic factors

Teacher expectations of pupil ability can influence educational progression, impacting subsequent streaming and exam level. Systematic discrepancies between teacher expectations of pupil achievement may therefore have a detrimental effect on children’s education. Associations between socioeconomic and demographic factors with teacher expectation accuracy have been demonstrated, but it is not known how teacher expectations of achievement may relate to genetic factors. We investigated these relationships using nationally standardized exam results at ages 11 and 14 from a UK longitudinal cohort study. We found that teacher expectation of achievement was strongly correlated with educational test scores. Furthermore, the accuracy of teacher expectation was patterned by pupil socioeconomic background but not teacher characteristics. The accuracy of teacher expectation related to pupil’s genetic liability to education as captured by a polygenic score for educational attainment. Despite correlation with the polygenic score, we found no strong evidence for genomewide SNP heritability in teacher reporting accuracy

Polygenic and socioeconomic risk for high body mass index:69 years of follow-up across life

Genetic influences on body mass index (BMI) appear to markedly differ across life, yet existing research is equivocal and limited by a paucity of life course data. We thus used a birth cohort study to investigate differences in association and explained variance in polygenic risk for high BMI across infancy to old age (2-69 years). A secondary aim was to investigate how the association between BMI and a key purported environmental determinant (childhood socioeconomic position) differed across life, and whether this operated independently and/or multiplicatively of genetic influences. Data were from up to 2677 participants in the MRC National Survey of Health and Development, with measured BMI at 12 timepoints from 2-69 years. We used multiple polygenic indices from GWAS of adult and childhood BMI, and investigated their associations with BMI at each age. For polygenic liability to higher adult BMI, the trajectories of effect size (β) and explained variance (R2) diverged: explained variance peaked in early adulthood and plateaued thereafter, while absolute effect sizes increased throughout adulthood. For polygenic liability to higher childhood BMI, explained variance was largest in adolescence and early adulthood; effect sizes were marginally smaller in absolute terms from adolescence to adulthood. All polygenic indices were related to higher variation in BMI; quantile regression analyses showed that effect sizes were sizably larger at the upper end of the BMI distribution. Socioeconomic and polygenic risk for higher BMI across life appear to operate additively; we found little evidence of interaction. Our findings highlight the likely independent influences of polygenic and socioeconomic factors on BMI across life. Despite sizable associations, the BMI variance explained by each plateaued or declined across adulthood while BMI variance itself increased. This is suggestive of the increasing importance of chance ('non-shared') environmental influences on BMI across life

Population phenomena inflate genetic associations of complex social traits

Heritability, genetic correlation, and genetic associations estimated from samples of unrelated individuals are often perceived as confirmation that genotype causes the phenotype(s). However, these estimates can arise from indirect mechanisms due to population phenomena including population stratification, dynastic effects, and assortative mating. We introduce these, describe how they can bias or inflate genotype-phenotype associations, and demonstrate methods that can be used to assess their presence. Using data on educational achievement and parental socioeconomic position as an exemplar, we demonstrate that both heritability and genetic correlation may be biased estimates of the causal contribution of genotype. These results highlight the limitations of genotype-phenotype estimates obtained from samples of unrelated individuals. Use of these methods in combination with family-based designs may offer researchers greater opportunities to explore the mechanisms driving genotype-phenotype associations and identify factors underlying bias in estimates