No double trouble: How to reopen the economy.

This policy introduces a measure of choice, consonant with our culture. Those younger than 65 can make their own personal tradeoffs between heath and livelihood, while older people, knowing that the virus will be spreading more quickly through the population will be even more cautious, thus preventing their early deaths. We return decisions to people while ensuring that the sum total of decisions does not overwhelm our hospitals. One felicitous result of this policy is that the virus will spread more quickly through the healthier population. This means that when the elderly re-engage in social life they will encounter fewer rather than more infected people reducing the likelihood that they will become sick and die themselves. Ironically, the best way to protect seniors is to let the virus spread in a controlled fashion among those who are not

Pandemic lockdown must fail: Save lives without crippling the economy

In the following working paper, I want to make a plea for what I am calling a “reverse quarantine”—quarantining people who are over 65 (who number 52 million), before they get sick. We need to complement this policy with federally funded and locally organized efforts to support seniors in place, drawing on the wellsprings of American pragmatism, the capacity to respond in emergencies, American volunteerism, and neighbor-to-neighbor assistance. We can’t turn quarantine into imprisonment. We must work as hard as we can to create a psychological sense of community at a moment when, paradoxically, social distancing is driving us apart. This may be utopian, but in the presence of disaster, hope can be motivating. Why do this? If the elderly stay in place this will both reduce deaths, as seniors are the most vulnerable, and reduce the number of people who can transmit the infection. We reduce the total burden on the health system. With the burden eased, we can let the virus spread more quickly, knowing that we have the hospital beds and equipment to help them. This would shorten the economic downturn leading to fewer business bankruptcies. After all, within the year, everyone who can be infected will be. The challenge that bedevils and threatens us, should we find no resolution, is to match pacing with the requisite supply of beds. In this note I provide the data and its analysis to back up this argument, to the best of my ability. I hope the latter was up to the task. This note is organized into six sections. In the first section, I introduce the HS and reproduce within the limits of my Excel modeling tools, their projection. In the second, I argue that social distancing will in all likelihood fail. We will have few of its benefits and most of its costs. In the third, I draw on a long theoretical tradition that connects long bouts of unemployment to deaths. I suggest that if social distancing provokes a long economic downturn, between 28,000 and 68,000 people will die in the years following the crisis. In the fourth, I briefly describe the Chinese and South Korean strategies for coping with the crisis. I argue that their successes are based on their distinctive culture and politics. We can’t use them here. In the fifth, I use a range of data sources, starting with HS, to estimate how many beds are “released” by quarantining seniors. I estimate that we can reduce the number of new beds we must build or re-purpose by over a million if we quarantine the elderly, decrease the length of stay in non-ICU beds, and repurpose current hospital beds. This may be an overestimate—a best case scenario—but I believe that the estimate is within an order of magnitude correct. In the sixth, I outline the rudiments of an American plan for tackling the crisis acknowledging that it may be still-born, with so little time left. It combines a war-economy with local initiative. I end with a plea that we expand the discourse about the crisis beyond the language and frameworks of the public health discipline. We need the voices of engineers, business leaders, economists and project managers. If we ever needed a “systems view,” it is now

Ideas in Philanthropic Field-Building: Where They Come From and How They Are Translated Into Actions

Discusses how grantmakers can contribute to their fields by identifying promising ideas and translating them into successful program initiatives. Part of the series Practice Matters: The Improving Philanthropy Project

Ideas in Philanthropic Field Building: Where They Come from and How They Are Translated into Actions - Executive Summary

Ideas are often the currency of philanthropy. Ideas animate fields of philanthropic endeavor. Ideas can constitute "forces" in field building that determine a field's direction. This paper examines the sources of ideas that program professionals in foundations draw from to create programs and influence fields of philanthropic interest. It also provides guidance about how foundation program staff can identify powerful and useful ideas and apply these to the work of philanthropy

Ideas in Philanthropic Field Building: Where They Come from and How They Are Translated into Actions - Discussion Guide

This discussion guide contains four sets of questions designed to help foundation program staff examine their own practices for identifying and assessing the viability of ideas for foundation investments and field building. The questions are excerpted from the paper, Ideas in Philanthropic Field Building: Where They Come From and How They Are Translated into Actions, and included here for the convenience of readers who wish to use them for individual study or group discussion purposes

Calculating Life and Death in a Time of Covid

The current pandemic makes us feel helpless. We can respond to its predation pragmatically but its silent march through the population promotes dread. Our helplessness undermines our belief in our culture as the source of our self-esteem and felt significance. One response to our experience of helplessness is the omnipotent stance, the idea that we can master the virus, stop it in its tracks, command one another to comply with injunctions and wreak a path of destruction by devastating the economy. Omnipotence promotes magical thinking. In the service of defeating death, we ignore actual suffering; deaths of despair and deaths in nursing homes. There is an antidote to omnipotence: Look at our situation objectively, acknowledge its gravity, use our moral compass to assess impossible choices, and the tradeoffs they impose, and draw on our pragmatism and inventiveness to relax the tradeoffs. A model that Wharton school researchers developed provides a framework for looking at our situation objectively. It posits a tradeoff between deaths and livelihoods should we fully reopen the economy. Three estimates of the value of lives- the value of a “statistical life,” the value of a statistical life-year and the value of a life based on highway fatalities,--together suggest to this author that we should fully reopen, with the precondition that we take six steps to protect seniors and hospital surge capacity. To arrive at such a choice we must navigate the moral terrain of sacrificing lives so that others may flourish. This entails examining our thoughts and feelings in response to the moral dilemmas we encounter. The paper is divided into five sections. The first introduces the paper. The second explores the theme of omnipotence. The third examines the role of culture in our battle against the death. The fourth takes us beyond omnipotence. It does this by calculating life and death so that we can ground our moral reasoning and feeling in an objective understanding of our situation. The fifth section is an appendix that provides additional information

Strategic Leadership Perspective

The project purpose was to identify the program constraints through cause and effect linkages, determine whether the root causes identified had program benefits and identify the driving causes of undesirable effects through Method of Synchronization: Articulation Interdependency Process Flow of Information Sense of Urgency/Prioritization Furthermore, we wanted to enlarge our perspective from a process mindset to a whole systems perspective looking at the systems that comprise JCIPE and how the systems are interconnected and interdependent and affect the purpose of the organization. Our overview led us to analyze possible physical, policy or cultural constraints that impose upon the JCIPEs success and drove us to our search using sufficient cause thinking to identify potential root causes. Using Theory of Constraint tools: Undesirable Effects, Current Reality Tree and Evaporating Cloud, we determined assumptions and used interpolations to narrow our scope to arrive at a likely root cause

Hundreds of variants clustered in genomic loci and biological pathways affect human height

Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits, but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait. The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P < 0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways.

NRXN3 Is a Novel Locus for Waist Circumference: A Genome-Wide Association Study from the CHARGE Consortium

Central abdominal fat is a strong risk factor for diabetes and cardiovascular disease. To identify common variants influencing central abdominal fat, we conducted a two-stage genome-wide association analysis for waist circumference (WC). In total, three loci reached genome-wide significance. In stage 1, 31,373 individuals of Caucasian descent from eight cohort studies confirmed the role of FTO and MC4R and identified one novel locus associated with WC in the neurexin 3 gene [NRXN3 (rs10146997, p = 6.4×10−7)]. The association with NRXN3 was confirmed in stage 2 by combining stage 1 results with those from 38,641 participants in the GIANT consortium (p = 0.009 in GIANT only, p = 5.3×10−8 for combined analysis, n = 70,014). Mean WC increase per copy of the G allele was 0.0498 z-score units (0.65 cm). This SNP was also associated with body mass index (BMI) [p = 7.4×10−6, 0.024 z-score units (0.10 kg/m2) per copy of the G allele] and the risk of obesity (odds ratio 1.13, 95% CI 1.07–1.19; p = 3.2×10−5 per copy of the G allele). The NRXN3 gene has been previously implicated in addiction and reward behavior, lending further evidence that common forms of obesity may be a central nervous system-mediated disorder. Our findings establish that common variants in NRXN3 are associated with WC, BMI, and obesity

Identification, Replication, and Fine-Mapping of Loci Associated with Adult Height in Individuals of African Ancestry

Adult height is a classic polygenic trait of high heritability (h2 ∼0.8). More than 180 single nucleotide polymorphisms (SNPs), identified mostly in populations of European descent, are associated with height. These variants convey modest effects and explain ∼10% of the variance in height. Discovery efforts in other populations, while limited, have revealed loci for height not previously implicated in individuals of European ancestry. Here, we performed a meta-analysis of genome-wide association (GWA) results for adult height in 20,427 individuals of African ancestry with replication in up to 16,436 African Americans. We found two novel height loci (Xp22-rs12393627, P = 3.4×10−12 and 2p14-rs4315565, P = 1.2×10−8). As a group, height associations discovered in European-ancestry samples replicate in individuals of African ancestry (P = 1.7×10−4 for overall replication). Fine-mapping of the European height loci in African-ancestry individuals showed an enrichment of SNPs that are associated with expression of nearby genes when compared to the index European height SNPs (P<0.01). Our results highlight the utility of genetic studies in non-European populations to understand the etiology of complex human diseases and traits