The Dark Side of Morality: Group Polarization and Moral Epistemology

This article argues that philosophers and laypeople commonly conceptualize moral truths or justified moral beliefs as discoverable through intuition, argument, or some other purely cognitive or affective process. It then contends that three empirically well-supported theories all predict that this ‘Discovery Model’ of morality plays a substantial role in causing social polarization. The same three theories are then used to argue that an alternative ‘Negotiation Model’ of morality—according to which moral truths are not discovered but instead created by actively negotiating compromises—promises to reduce polarization by fostering a progressive willingness to ‘work across the aisle’ to settle moral issues cooperatively. This article then examines potential methods for normatively evaluating polarization, arguing there are prima facie reasons to favor the Negotiation Model over the Discovery Model based on their hypothesized effects on polarization. Finally, I outline avenues for further empirical and philosophical research

Derivation of Morality from Prudence

This chapter derives and refines a novel normative moral theory and descriptive theory of moral psychology--Rightness as Fairness--from the theory of prudence defended in Chapter 2. It briefly summarizes Chapter 2’s finding that prudent agents typically internalize ‘moral risk-aversion’. It then outlines how this prudential psychology leads prudent agents to want to know how to act in ways they will not regret in morally salient cases, as well as to regard moral actions as the only types of actions that satisfy this prudential interest. It then uses these findings to defend a new derivation of my (2016) theory of morality, Rightness as Fairness, showing how the derivation successfully defends Rightness as Fairness against a variety of objections. The chapter also details how this book’s theory helps to substantiate the claim that Rightness as Fairness unifies a variety of competing moral frameworks: deontology, consequentialism, contractualism, and virtue ethics. Finally, the chapter shows how Chapter 2’s theory of prudence entails some revisions to Rightness as Fairness, including the adoption of a series of Rawlsian original positions to settle moral and social-political issues under ideal and nonideal circumstances—thus entailing a unified normative and descriptive psychological framework for prudence, morality, and justice

The P2P Simulation Hypothesis and Meta-Problem of Everything

David. J. Chalmers examines eleven possible solutions to the meta-problem of consciousness, ‘the problem of explaining why we think that there is a problem of consciousness.’ The present paper argues that Chalmers overlooks an explanation that he has otherwise taken seriously, and which a number of philosophers, physicists, and computer scientists have taken seriously as well: the hypothesis that we are living in a computer simulation. This paper argues that a particular version of the simulation hypothesis is at least as good of a solution to the meta-problem of consciousness as many explanations Chalmers considers, and may even be a better one—as it may be the best solution to a much broader meta-philosophical problem: the ‘meta-problem of everything’, the problem of explaining why our world has the quantum-mechanical, relativistic, and philosophical features it does

Why explicit performance bonds are absent from employment contracts

Contains bibliographical references (p. 19-20)

Neurofunctional Prudence and Morality: A Philosophical Theory

This book outlines a unified theory of prudence and morality that merges a wide variety of findings in behavioral neuroscience with philosophically sophisticated normative theorizing. Chapter 1 lays out the emerging behavioral neuroscience of prudence and morality. Chapter 2 then outlines a new theory of prudence as fairness to oneself across time. Chapter 3 then derives a revised version of my 2016 moral theory--Rightness as Fairness--from this theory of prudence, showing how the theory of prudence defends Rightness as Fairness against various critiques and unifies prudence, morality, and justice. Chapter 4 then argues that this theory explains a variety of normative philosophical and empirical neuroscientific phenomena better than alternatives. Finally, Chapter 5 responds to potential objections and explores future research avenues

Nonideal Justice as Nonideal Fairness

This article argues that diverse theorists have reasons to theorize about fairness in nonideal conditions, including theorists who reject fairness in ideal theory. It then develops a new all-purpose model of ‘nonideal fairness.’ §1 argues that fairness is central to nonideal theory across diverse ideological and methodological frameworks. §2 then argues that ‘nonideal fairness’ is best modeled by a nonideal original position adaptable to different nonideal conditions and background normative frameworks (including anti-Rawlsian ones). §3 then argues that the parties to the model have grounds to seek a variety of remedial social, legal, cultural, and economic ‘nonideal primary goods’ for combating injustice, as well as grounds to distribute these goods in an equitable and inclusive manner. Finally, I illustrate how the model indexes the nonideal primary goods it justifies to different nonideal contexts and background normative frameworks, illustrating why diverse theorists should find the model and its output principles attractive

Impaired Cleavage of Preproinsulin Signal Peptide Linked to Autosomal-Dominant Diabetes

Recently, missense mutations upstream of preproinsulin’s signal peptide (SP) cleavage site were reported to cause mutant INS gene-induced diabetes of youth (MIDY). Our objective was to understand the molecular pathogenesis using metabolic labeling and assays of proinsulin export and insulin and C-peptide production to examine the earliest events of insulin biosynthesis, highlighting molecular mechanisms underlying β-cell failure plus a novel strategy that might ameliorate the MIDY syndrome. We find that whereas preproinsulin-A(SP23)S is efficiently cleaved, producing authentic proinsulin and insulin, preproinsulin-A(SP24)D is inefficiently cleaved at an improper site, producing two subpopulations of molecules. Both show impaired oxidative folding and are retained in the endoplasmic reticulum (ER). Preproinsulin-A(SP24)D also blocks ER exit of coexpressed wild-type proinsulin, accounting for its dominant-negative behavior. Upon increased expression of ER–oxidoreductin-1, preproinsulin-A(SP24)D remains blocked but oxidative folding of wild-type proinsulin improves, accelerating its ER export and increasing wild-type insulin production. We conclude that the efficiency of SP cleavage is linked to the oxidation of (pre)proinsulin. In turn, impaired (pre)proinsulin oxidation affects ER export of the mutant as well as that of coexpressed wild-type proinsulin. Improving oxidative folding of wild-type proinsulin may provide a feasible way to rescue insulin production in patients with MIDY

Estrogens promote misfolded proinsulin degradation to protect insulin production and delay diabetes

Summary: Conjugated estrogens (CE) delay the onset of type 2 diabetes (T2D) in postmenopausal women, but the mechanism is unclear. In T2D, the endoplasmic reticulum (ER) fails to promote proinsulin folding and, in failing to do so, promotes ER stress and β cell dysfunction. We show that CE prevent insulin-deficient diabetes in male and in female Akita mice using a model of misfolded proinsulin. CE stabilize the ER-associated protein degradation (ERAD) system and promote misfolded proinsulin proteasomal degradation. This involves activation of nuclear and membrane estrogen receptor-α (ERα), promoting transcriptional repression and proteasomal degradation of the ubiquitin-conjugating enzyme and ERAD degrader, UBC6e. The selective ERα modulator bazedoxifene mimics CE protection of β cells in females but not in males. : Estrogens prevent diabetes in women, but the mechanism is poorly understood. Xu et al. report that estrogens activate the endoplasmic-reticulum-associated protein degradation pathway, which promotes misfolded proinsulin degradation, suppresses endoplasmic reticulum stress, and protects insulin secretion in mice and in human pancreatic β cells. Keywords: estrogens, beta cell, islet, endoplasmic reticulum stress, proinsulin misfolding, diabetes, bazedoxifene, sex dimorphism, ERAD, SER