I work in areas of formal epistemology, philosophy of mathematics, decision theory, and am increasingly interested in issues of social epistemology and collective action, both as they relate to my earlier areas and in other ways. I’ve done work on various paradoxes of the infinite in probability and decision theory, on the foundations of Bayesianism, on the social epistemology of mathematics, and written one weird paper using metaphysics to derive conclusions about physics. Links of Interest: My research website including links and descriptions to most of my papers. My appearance (in 2015) on Julia Galef’s “Rationally Speaking” podcast, discussing Newcomb’s Paradox, its connection to other issues in decision theory and free will, and what I call a “tragedy of rationality”. A discussion (from 2011) with Jonathan Weisberg about the role of accuracy in constraining beliefs and probabilities, and their connection, on Philosophy TV. The idea of this discussion eventually became my Dr. Truthlove paper in Nous (paper available from Philosophers’ Annual - 10 Best Papers of 2015) My paper “Decision Theory without Representation Theorems”, at the open access journal Philosophers’ Imprint. My old blog, Antimeta, which I ran for several years in graduate school, discussing issues in philosophy of mathematics, probability, and occasionally metaphysics. My posts from the period 2005-2009 on Brian Weatherson’s blog, Thoughts, Arguments, and Rants.
It may seem odd to assert that patient brooding and waiting for imaginative validation is the proper way of doing science; after all, most professional scientists and philosophers believe that the essence of science is ‘evidence’ derived from observations and experiments, synthesized by some kind of logical and rational method. But personal experience, history and theoretical considerations all suggest that a prolonged state of ‘patient brooding’ is the hallmark and prerequisite of ‘deep science’; a practical necessity for the most creative and significant breakthroughs.
The currently prevailing theory of a transmissible cancer cell lineage in Tasmanian devils was based on the discovery of apparently identical chromosomal aberrations in facial tumors of several animals. New findings of facial tumors that have no detectable cytogenetic similarities to previously published cancer karyotypes and the recent detection of varying portions of chromosome Y in all tumor cell lines of male devils (but none in tumors of females) cast doubt on the theory of a cancer transplant. Thus, I propose an alternative scenario in which similar chromosomal and genetic aberrations in individual cancers are a consequence of the low genetic diversity in populations of the Tasmanian devil resulting in a unique telomere length profile. Critically short telomeres on certain chromosome ends lead to chromosome-specific fusions and the activation of species-specific transposable elements that cause the observed karyotypic and molecular convergence. This new concept can explain the existence of genetic signs of tumor clonality within a population despite the independent origin of each facial cancer in these cancer-prone animals.
Twitter backchannels are increasingly popular at medical conferences. A variety of user groups, including healthcare providers and third party entities (e.g., pharmaceutical or medical device companies) use these backchannels to communicate with one another. These backchannels are unregulated and can allow third party commercial entities to exert an equal or greater amount of influence than healthcare providers. Third parties can use this influence to promote their products or services instead of sharing unbiased, evidence-based information. In the #MICEproject we quantified the influence that third party commercial entities had in 13 major medical conferences.
Upon re-examination of large telomere datasets from healthy human populations, a downward secular trend in telomere length at birth was found. The authors theorized that relatively recent environmental stresses to female germ cells could have driven the observed intergenerational telomere erosion; otherwise, these trends would have pushed populations into pathological telomere length ranges within a few centuries. Strangely, the authors decided to disregard an 11-year-old theory of telomere-driven macroevolution that is based on progressive intergenerational telomere loss as the driving force behind species extinction and speciation. Additionally, Holohan and colleagues introduced a “new” interpretation of the old-father-long-telomered-offspring effect, namely as a consequence of intergenerational telomere erosion in the female lineage. Yet, an identical theoretical model has been published twice, several years before. To distinguish between a temporary trend caused by environmental pollution and a general evolutionary mechanism of intergenerational telomere erosion, we urgently need telomere length data from multigenerational studies on mammals with a short generation-time.
Background Autophagy is central to health, and a decline in autophagy from the youthful, healthy state correlates with disease and aging. Among the diseases in which a decline in autophagy is prominent are neurological and neuroimmune disorders, such as Alzheimer’s and Parkinson’s. Psychiatric disorders are characterized almost universally by increased inflammation and oxidative stress, which are negatively related to levels of autophagy. Treatments designed to restore or increase autophagy may have efficacy in psychiatric disorders such as depression, bipolar disorder, and schizophrenia. Findings Recent research has found that many psychoactive drugs in several different classes, such as anti-psychotics, tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), and lithium, strongly promote autophagy in neurons. Other diverse interventions, such as rapamycin, trehalose, and exercise, have been shown to have antidepressant effects in animals and sometimes in humans. Most drugs used in other areas of medicine do not activate autophagy. The case is made in this paper that autophagy may play a central role in the mechanism of action of these drugs and interventions through direct effects on autophagy as well as concomitant lowering of levels of inflammation and oxidative stress. Conclusions Many drugs used in the treatment of psychiatric illnesses activate autophagy, and this may be their central mechanism of action, which lends new insight into the pathogenesis of mental illness and to potential new therapies for them.