The 100-Year Life and the New Family Law

This draft book chapter, prepared as part of a symposium on The 100-Year Life by Linda Gratton and Andrew Scott, reflects on the future of family law in an era of longer lives. Our analysis leads us to conclude that the 100-year life is indeed likely to have an impact on the nature, scope, and definition of family law, but that families will continue to function as the primary setting for intimacy and for caregiving and caretaking, whatever form those families take. Further, the importance to both individual and social welfare of family support throughout life points to a need for reform of current family law doctrine. The impact of longer life on doctrines regulating the relationship of parents and minor children is likely to be modest, but doctrinal and policy reforms will be needed to support individuals in following their preferences for intimacy and security in old age – as will reforms to the minimal role of the state in promoting security for individuals in different family forms and of differing socioeconomic status. We suggest general goals for law reform and offer specific proposals

Family Law for the One-Hundred-Year Life

Family law is for young people. To facilitate child rearing and help spouses pool resources over a lifetime, the law obligates parents to minor children and spouses to each other. Family law’s presumption of young, financially interdependent, conjugal couples raising children privileges one family form — marriage — and centers the dependency needs of children. This age myopia fundamentally fails older adults. Families are essential to flourishing in the last third of life, but the legal system offers neither the family forms many older adults want nor the support of family care older adults need. Racial and economic inequities, accumulated across lifetimes, exacerbate these problems. Family law’s failures are particularly pressing in light of a tectonic demographic shift underway in our society: Americans are living longer, with half of all five-year-olds today projected to live more than one hundred years. The proportion of older adults as a percentage of our population is also rapidly growing and will soon surpass that of minor children. This Article argues that family law must adapt to the new old age. At a conceptual level, family law should address the interests and needs of families across the life span, not just those of younger people. And it must reflect three core commitments: centering the autonomy interests of older persons, addressing structural inequities, and ensuring that legal mechanisms are efficient and accessible. This conceptual shift leads to a series of practical reforms to laws governing family formation and family support. The interests of older adults will be better served if they have access to a broader array of family forms and can easily customize these family relationships. We thus propose reforms that decenter marriage as the primary option and make it easier to opt into and out of legal obligations. To support the familial caregiving that is essential to wellbeing, we propose a set of reforms to federal, state, and local laws that would provide economic relief and other support to family caregivers. By offering pluralistic family forms, better support for familial caregiving, and an appreciation of the legal implications of the centrality of relationships in the last third of life, this Article charts a path for family law for the one-hundred-year life

Leading Through Learning: Using Evolutionary Learning to Develop, Implement, and Improve Strategic Initiatives

Equitably educating students requires effective differentiation of services based on students’ strengths and needs. Doing so reliably at scale is difficult given the diversity of students and contexts in our public school systems and the diversity of needs created by historical and institutionalized discrimination against people of color, immigrants, and other populations. Still, a number of systems and organizations have succeeded in advancing equity at scale. They have done so by finding new ways to design, lead, and manage their operations and engage internal and external stakeholders – in our language, new ways to govern2 their work. Cutting across these promising governance practices are adult and student learning systems that provide transparency into how school leaders actually lead, teachers actually teach, and students actually learn day to day, school by school, classroom by classroom, and lesson by lesson. This combination of transparency, experimentation, and broad participation and knowledge sharing reveals effective ways to serve individual and groups of students, severing deeply entrenched links between student background, access to opportunity, and learning outcomes

“I just want to be skinny.”: A content analysis of tweets expressing eating disorder symptoms

There is increasing concern about online communities that promote eating disorder (ED) behaviors through messages and/or images that encourage a “thin ideal” (i.e., promotion of thinness as attractive) and harmful weight loss/weight control practices. The purpose of this paper is to assess the content of body image and ED-related content on Twitter and provide a deeper understanding of EDs that may be used for future studies and online-based interventions. Tweets containing ED or body image-related keywords were collected from January 1-January 31, 2015 (N = 28,642). A random sample (n = 3000) was assessed for expressions of behaviors that align with subscales of the Eating Disorder Examination (EDE) 16.0. Demographic characteristics were inferred using a social media analytics company. The comprehensive research that we conducted indicated that 2,584 of the 3,000 tweets were ED-related; 65% expressed a preoccupation with body shape, 13% displayed issues related to food/eating/calories, and 4% expressed placing a high level of importance on body weight. Most tweets were sent by girls (90%) who were ≤19 years old (77%). Our findings stress a need to better understand if and how ED-related content on social media can be used for targeting prevention and intervention messages towards those who are in-need and could potentially benefit from these efforts.</div

Weak-Singlet Fermions: Models and Constraints

We employ data from precision electroweak tests and collider searches to derive constraints on the possibility that weak-singlet fermions mix with the ordinary Standard Model fermions. Our findings are presented within the context of a theory with weak-singlet partners for all ordinary fermions and theories in which only third-generation fermions mix with weak singlets. In addition, we indicate how certain results can be applied more widely in theories containing exotic fermions.Comment: 29 pages, 12 figures; added 1 reference, expanded introductio

Extra embryos: The ethics of cryopreservation in Ecuador and elsewhere

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73714/1/ae.2007.34.1.181.pd

Contribution of copy number variants to schizophrenia from a genome-wide study of 41,321 subjects

Copy number variants (CNVs) have been strongly implicated in the genetic etiology of schizophrenia (SCZ). However, genome-wide investigation of the contribution of CNV to risk has been hampered by limited sample sizes. We sought to address this obstacle by applying a centralized analysis pipeline to a SCZ cohort of 21,094 cases and 20,227 controls. A global enrichment of CNV burden was observed in cases (OR=1.11, P=5.7×10−15), which persisted after excluding loci implicated in previous studies (OR=1.07, P=1.7 ×10−6). CNV burden was enriched for genes associated with synaptic function (OR = 1.68, P = 2.8 ×10−11) and neurobehavioral phenotypes in mouse (OR = 1.18, P= 7.3 ×10−5). Genome-wide significant evidence was obtained for eight loci, including 1q21.1, 2p16.3 (NRXN1), 3q29, 7q11.2, 15q13.3, distal 16p11.2, proximal 16p11.2 and 22q11.2. Suggestive support was found for eight additional candidate susceptibility and protective loci, which consisted predominantly of CNVs mediated by non-allelic homologous recombination

Age at first birth in women is genetically associated with increased risk of schizophrenia

Prof. Paunio on PGC:n jäsenPrevious studies have shown an increased risk for mental health problems in children born to both younger and older parents compared to children of average-aged parents. We previously used a novel design to reveal a latent mechanism of genetic association between schizophrenia and age at first birth in women (AFB). Here, we use independent data from the UK Biobank (N = 38,892) to replicate the finding of an association between predicted genetic risk of schizophrenia and AFB in women, and to estimate the genetic correlation between schizophrenia and AFB in women stratified into younger and older groups. We find evidence for an association between predicted genetic risk of schizophrenia and AFB in women (P-value = 1.12E-05), and we show genetic heterogeneity between younger and older AFB groups (P-value = 3.45E-03). The genetic correlation between schizophrenia and AFB in the younger AFB group is -0.16 (SE = 0.04) while that between schizophrenia and AFB in the older AFB group is 0.14 (SE = 0.08). Our results suggest that early, and perhaps also late, age at first birth in women is associated with increased genetic risk for schizophrenia in the UK Biobank sample. These findings contribute new insights into factors contributing to the complex bio-social risk architecture underpinning the association between parental age and offspring mental health.Peer reviewe

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

GWAS Meta-Analysis of Suicide Attempt: Identification of 12 Genome-Wide Significant Loci and Implication of Genetic Risks for Specific Health Factors

Objective: Suicidal behavior is heritable and is a major cause of death worldwide. Two large-scale genome-wide association studies (GWASs) recently discovered and crossvalidated genome-wide significant (GWS) loci for suicide attempt (SA). The present study leveraged the genetic cohorts from both studies to conduct the largest GWAS metaanalysis of SA to date. Multi-ancestry and admixture-specific meta-analyses were conducted within groups of significant African, East Asian, and European ancestry admixtures. Methods: This study comprised 22 cohorts, including 43,871 SA cases and 915,025 ancestry-matched controls. Analytical methods across multi-ancestry and individual ancestry admixtures included inverse variance-weighted fixed-effects meta-analyses, followed by gene, gene-set, tissue-set, and drug-target enrichment, as well as summary-data-based Mendelian randomization with brain expression quantitative trait loci data, phenome-wide genetic correlation, and genetic causal proportion analyses. Results: Multi-ancestry and European ancestry admixture GWAS meta-analyses identified 12 risk loci at p values &lt;5×10-8. These loci were mostly intergenic and implicated DRD2, SLC6A9, FURIN, NLGN1, SOX5, PDE4B, and CACNG2. The multi-ancestry SNP-based heritability estimate of SA was 5.7% on the liability scale (SE=0.003, p=5.7×10-80). Significant brain tissue gene expression and drug set enrichment were observed. There was shared genetic variation of SA with attention deficit hyperactivity disorder, smoking, and risk tolerance after conditioning SA on both major depressive disorder and posttraumatic stress disorder. Genetic causal proportion analyses implicated shared genetic risk for specific health factors. Conclusions: This multi-ancestry analysis of suicide attempt identified several loci contributing to risk and establishes significant shared genetic covariation with clinical phenotypes. These findings provide insight into genetic factors associated with suicide attempt across ancestry admixture populations, in veteran and civilian populations, and in attempt versus death.</p