Harming animals and massacring humans: Characteristics of public mass and active shooters who abused animals. Arnold Arluke, Adam Lankford, Eric Madfis. Behavioral Sciences and the Law , https://doi.org/10.1002/bsl.2385
Abstract: Researchers have extensively studied the tendency of certain violent criminals to hurt or torture animals, primarily focusing on domestic abusers and serial killers. However, little is known about the extent or nature of prior animal abuse among active shooters and public mass shooters. Public mass and active shooters essentially represent a single offender type: they are people who commit rampage attacks in public places and attempt to harm multiple victims beyond a single target. The only difference is that “mass” shootings are traditionally defined as cases resulting in the death of four or more victims, while “active” shootings have no minimum threshold. This study aimed to identify all publicly reported cases of active and mass shooters who engaged in animal cruelty, describe the nature of their violence toward animals and humans, and examine how they differ from other perpetrators without this history. Overall, this study found 20 cases of offenders with a publicly reported history of animal abuse. Comparisons between offenders with and without this history indicated that animal‐abusing offenders were more likely to be young and White, less likely to die at the crime scene, and more likely to kill and wound a large number of victims. While this finding supports the idea that animal abuse might be a warning sign for a small but deadly minority of mostly youthful offenders, it is likely not a robust signal of future shooters in general because animal abuse is rarely reported in this population of offenders at large.
Bipartisan Alliance, a Society for the Study of the US Constitution, and of Human Nature, where Republicans and Democrats meet.
Sunday, October 14, 2018
We discovered hundreds of genes that, when their activity is enhanced, suppressed, or turned off, lengthen life & enhance health under laboratory conditions; does this support George Williams’ 1957 paper aobut antagonistic pleiotropy hypothesis of aging?
Is Antagonistic Pleiotropy Ubiquitous in Aging Biology? Steven N Austad Jessica M Hoffman. Evolution, Medicine, and Public Health, eoy033, https://doi.org/10.1093/emph/eoy033
Abstract: George Williams’ 1957 paper developed the antagonistic pleiotropy hypothesis of aging, which had previously been hinted at by Peter Medawar. Antagonistic pleiotropy, as it applies to aging, hypothesizes that animals possess genes that enhance fitness early in life but diminish it in later life and that such genes can be favored by natural selection because selection is stronger early in life even as they cause the aging phenotype to emerge. No genes of the sort hypothesized by Williams were known sixty years ago, but modern molecular biology has now discovered hundreds of genes that, when their activity is enhanced, suppressed, or turned off, lengthen life and enhance health under laboratory conditions. Does this provide strong support for Williams’ hypothesis? What are the implications of Williams’ hypothesis for the modern goal of medically intervening to enhance and prolong human health? Here we briefly review the current state of knowledge on antagonistic pleiotropy both under wild and laboratory conditions. Overall, whenever antagonistic pleiotropy effects have been seriously investigated, they have been found. However, not all trade-offs are directly between reproduction and longevity as is often assumed. The discovery that antagonistic pleiotropy is common if not ubiquitous implies that a number of molecular mechanisms of aging may be widely shared among organisms and that these mechanisms of aging can be potentially alleviated by targeted interventions.
Topic: aging phenotype genes longevity molecular biology reproductive physiological process pleiotropism elderly
Abstract: George Williams’ 1957 paper developed the antagonistic pleiotropy hypothesis of aging, which had previously been hinted at by Peter Medawar. Antagonistic pleiotropy, as it applies to aging, hypothesizes that animals possess genes that enhance fitness early in life but diminish it in later life and that such genes can be favored by natural selection because selection is stronger early in life even as they cause the aging phenotype to emerge. No genes of the sort hypothesized by Williams were known sixty years ago, but modern molecular biology has now discovered hundreds of genes that, when their activity is enhanced, suppressed, or turned off, lengthen life and enhance health under laboratory conditions. Does this provide strong support for Williams’ hypothesis? What are the implications of Williams’ hypothesis for the modern goal of medically intervening to enhance and prolong human health? Here we briefly review the current state of knowledge on antagonistic pleiotropy both under wild and laboratory conditions. Overall, whenever antagonistic pleiotropy effects have been seriously investigated, they have been found. However, not all trade-offs are directly between reproduction and longevity as is often assumed. The discovery that antagonistic pleiotropy is common if not ubiquitous implies that a number of molecular mechanisms of aging may be widely shared among organisms and that these mechanisms of aging can be potentially alleviated by targeted interventions.
Topic: aging phenotype genes longevity molecular biology reproductive physiological process pleiotropism elderly
Strong discrepancy between stated and revealed behavior: given a natural setting, people may actually behave inconsistently with the way in which they otherwise “brand” themselves; this is a big problem for predictability of survey answers
Why (field) experiments on unethical behavior are important: Comparing stated and revealed behavior. Yonas Alema et al. Journal of Economic Behavior & Organization, https://doi.org/10.1016/j.jebo.2018.08.026
Highlights
• Field experiment on unethical behavior.
• Comparison of stated behavior and revealed behavior.
• Experiment induces reciprocity and guilt in two treatments.
• Result 1: strong discrepancy between stated and revealed behavior.
• Result 2: inducing reciprocity and guilt reduces unethical behavior compared to control.
Abstract: Understanding unethical behavior is essential to many phenomena in the real world. We carry out a field experiment in a unique setting that varies the levels of reciprocity and guilt in an ethical decision. A survey more than one year before the field experiment allows us to compare at the individual level stated unethical behavior with revealed behavior in the same situation in the field. Our results indicate a strong discrepancy between stated and revealed behavior, regardless of the specific treatment in the field experiment. This suggests that, given a natural setting, people may actually behave inconsistently with the way in which they otherwise “brand” themselves. Our findings raise caution about the interpretation of stated behavioral measures commonly used in research on unethical behavior. In addition, we show that inducing reciprocity and guilt leads to a decrease in unethical behavior.
Highlights
• Field experiment on unethical behavior.
• Comparison of stated behavior and revealed behavior.
• Experiment induces reciprocity and guilt in two treatments.
• Result 1: strong discrepancy between stated and revealed behavior.
• Result 2: inducing reciprocity and guilt reduces unethical behavior compared to control.
Abstract: Understanding unethical behavior is essential to many phenomena in the real world. We carry out a field experiment in a unique setting that varies the levels of reciprocity and guilt in an ethical decision. A survey more than one year before the field experiment allows us to compare at the individual level stated unethical behavior with revealed behavior in the same situation in the field. Our results indicate a strong discrepancy between stated and revealed behavior, regardless of the specific treatment in the field experiment. This suggests that, given a natural setting, people may actually behave inconsistently with the way in which they otherwise “brand” themselves. Our findings raise caution about the interpretation of stated behavioral measures commonly used in research on unethical behavior. In addition, we show that inducing reciprocity and guilt leads to a decrease in unethical behavior.
Antisocial behavior is heritable, but heritability varies by subtype and age; adversity predicts antisocial behavior directly & moderates genetic effects; we need genome-wide association studies of antisocial behavior with larger sample sizes
Genetic influences on antisocial behavior: recent advances and future directions. Arianna M Gard, Hailey L Dotterer, Luke W Hyde. Current Opinion in Psychology, Volume 27, June 2019, Pages 46-55, https://doi.org/10.1016/j.copsyc.2018.07.013
Highlights
• The heterogeneity of antisocial behavior needs to be considered in genetic studies.
• Antisocial behavior is heritable, but heritability varies by subtype and age.
• Adversity predicts antisocial behavior directly and moderates genetic effects.
• Genome-wide association studies of antisocial behavior with larger sample sizes are needed.
• Polygenic risk scores may capture cumulative genetic effects on antisocial behavior.
• Neurogenetics links genes to behavior via the brain.
Abstract: Understanding the etiology of antisocial behavior (i.e. violence, criminality, rule-breaking), is essential to the development of more effective prevention and intervention strategies. We provide a summary of the genetic correlates of antisocial behavior, drawing upon findings from behavioral, molecular, and statistical genetics. Across methodologies, our review highlights the centrality of environmental moderators of genetic effects, and how behavioral heterogeneity in antisocial behavior is an important consideration for genetic studies. We also review novel analytic techniques and neurogenetic approaches that can be used to examine how genetic variation predicts antisocial behavior. Finally, to illustrate how findings may converge across approaches, we describe pathways from genetic variability in oxytocin signaling to subtypes of antisocial behavior.
Highlights
• The heterogeneity of antisocial behavior needs to be considered in genetic studies.
• Antisocial behavior is heritable, but heritability varies by subtype and age.
• Adversity predicts antisocial behavior directly and moderates genetic effects.
• Genome-wide association studies of antisocial behavior with larger sample sizes are needed.
• Polygenic risk scores may capture cumulative genetic effects on antisocial behavior.
• Neurogenetics links genes to behavior via the brain.
Abstract: Understanding the etiology of antisocial behavior (i.e. violence, criminality, rule-breaking), is essential to the development of more effective prevention and intervention strategies. We provide a summary of the genetic correlates of antisocial behavior, drawing upon findings from behavioral, molecular, and statistical genetics. Across methodologies, our review highlights the centrality of environmental moderators of genetic effects, and how behavioral heterogeneity in antisocial behavior is an important consideration for genetic studies. We also review novel analytic techniques and neurogenetic approaches that can be used to examine how genetic variation predicts antisocial behavior. Finally, to illustrate how findings may converge across approaches, we describe pathways from genetic variability in oxytocin signaling to subtypes of antisocial behavior.