Volume 24, Number 1, Winter
O’Shaughnessy advocates an account of inner awareness (in the sense of the present series of articles) that I would categorize as a remembrance theory. Accordingly, as the consciousness stream is proceeding, one is normally acquiring without any occurrent conceptual awareness of one’s experiences, thus silently and automatically, a latent knowledge of these experiences that can subsequently provide experiential remembrances of them. It is these remembrances that are proposed to be one’s inner awareness of one’s experiences: occurrent non-inferential conceptual awarenesses of the latter. Although O’Shaughnessy argues contra one’s having intrinsic occurrent conceptual inner awareness of one’s experiences, he maintains that every experience is its own “extensional object” (which is distinct from its being its own intentional object, as an intrinsic theory of inner awareness would imply). This non-conceptual reflexive relation of an experience to itself — “one’s experiential awareness of one’s experiences” — is claimed by O’Shaughnessy to be a case of awareness in exactly the same sense that any basic perceptual experience is awareness of its extensional object. The present article and the next one in the present series comprise an attempt to explicate O’Shaughnessy’s conception of inner awareness, in particular, aspects of the conception that may contribute to the positive case for intrinsic theory.
Requests for reprints should be sent to Thomas Natsoulas, Ph.D., Department of Psychology, University of California, Davis, One Shields Avenue, Davis, California, 95616-8686. Email: firstname.lastname@example.org
A review of over thirty neuroimaging studies on children diagnosed with Attention Deficit/Hyperactivity Disorder (ADD, ADHD) by Giedd, Blumenthal, Molloy, and Castellanos (2001) is organized around tables listing the main findings of studies using different types of neuroimaging. Like most researchers in this field, Giedd et al. conclude that the evidence supports the involvement of right frontal–striatal circuitry with cerebellar modulation in ADHD. However, Giedd et al. do not report on a confounding variable of crucial interest in this field of research — whether subjects had been previously treated with stimulants or other psychotropic drugs. In the present paper, we have redone five of the tables from the Giedd et al. review, adding information on the subjects’ prior medication exposure, as reported in the individual studies included in the review. We found that most subjects diagnosed with ADD or ADHD had prior medication use, often for several months or years. This substantial confound invalidates any suggestion of ADHD-specific neuropathology. Moreover, the few recent studies using unmedicated ADHD subjects have inexplicably avoided making straightforward comparisons of these subjects with controls.
Request for reprints should be sent to Jonathan Leo, Ph.D., Department of Anatomy, Western University of Health Sciences, 309 East Second Street, Pomona, California 91767. Email: email@example.com; Email: David.Cohen@fiu.edu
Spiders’ nests, birds’ wings, airplanes, and scientific theories are all instances of adaptations. Instructionist theories (analogous to Lamarckism) implies that adaptive novelties are imposed directly on an entity by the environment (from without) while selectionist theories (analogous to Darwinism) explains adaptive novelties to be the product of mechanisms including trial and error (from within). This article argues that adaptive novelties are the result of selectionist mechanisms while instructionist production of adaptive novelties is impossible due to the second law of thermodynamics. Even long-term preservation of adaptive information is dependent on selectionist mechanisms. These findings have important implications for both human and societal development because of the prevalence of instructionist theories.
Requests for reprints should be sent to Halvor Naess, M.D., Institute of Neurology, Haukeland University Hospital, 5021 Bergen, Norway. Email: firstname.lastname@example.org
Attempts to explain behavior genetically face two major problems: the application of the concept of genetic coding and the theoretical possibility of decomposing behavior. This paper argues that using the notion of genetic coding is appropriate in explanations of protein synthesis but inadequate and even misleading in the context of explanations of behavior. Genes should be regarded as disparate components of mechanisms that account for behavior rather than as codes for behavioral phenotypes. Such mechanistic explanations, however, presuppose the possibility of decomposing behavioral phenotypes, which is strongly disputed by researchers holding an interactionist view of behavior. It is argued that these researchers fail to distinguish etiological from constitutive decomposition, and that their objections apply to the former but not to the latter kind. Constitutive decomposition might identify genes as disparate components and open up the possibility of explaining behavior mechanistically by isolating causal paths from genes to behavior. Finally, research on the single gene disorder phenylketonuria is introduced to illustrate and test these views. With respect to this disorder it is demonstrated that applying the concept of genetic coding would be inappropriate and misguiding, while nonetheless the phenotype is decomposable and can be explained mechanistically by singling out a genetic causal path.t is demonstrated that applying the concept of genetic coding would be inappropriate and misguiding, while nonetheless the phenotype is decomposable and can be explained mechanistically by singling out a genetic causal path.
Requests for reprints should be sent to Marko Barendregt, Department of Theoretical Psychology, Vrije Universiteit Amsterdam, Van der Boechorststraat 1, 1081 BT Amsterdam. Email: email@example.com
The Journal of Mind and Behavior, Winter 2003, Volume 24, Number 1, Pages 91–118, ISSN 0271–0137 This paper focuses on a logical systems flow-down of a set of consciousness requirements, which together with biological quantification of human brain anatomy sets limits on the neurological network in the cerebrum in order to produce the mind. It employs data (where available) to validate inferences, or when data do not exist, proposes methods for acquiring valid evidence. Many of these systems requirements will be imposed after some fundamental assumptions are made. These assumptions are not new to theories on consciousness. However, their application as fundamentals may actually represent a new approach. Concurrent with these fundamentals, explicit periods of awareness while conscious are employed. Justification for their use is found in a theoretical process described as cerebral fusion. Additionally, storage of memory elements is postulated within local glia sites, proximal to synaptic nodes, and conductive transport through the astrocytes responsible for recall of data. The model permits variations in neural–glial interface physics and allows forecasts of mind/brain dysfunctions to be inferred. One key result from the model is hypothesized and expanded upon, and may have impact in certain types of dementia, such as Alzheimer’s disease.
Requests for reprints should be sent to Martin L. Lonky, Ph.D., The Trylon Corporation, 970 W. 190th Street, Suite 850, Torrance, California 90502–1037.
Handbook of Self-Determination Research
The Journal of Mind and Behavior, Winter 2003, Volume 24, Number 1, Pages 119–124 ISSN 0271–0137
[Note: First paragraph, no abstract available.] The Handbook of Self-Determination Research is the outcome of various research projects in self-determination theory (SDT), which began with a conference in 1999 devoted exclusively to SDT. The book, comprising 19 chapters, begins with an introductory section and overview of SDT. The second section (chapters 2–7) explores theoretical issues, the third section (chapters 8–13) examines SDT applications in life settings, the fourth section (chapters 14–18) incorporates other theoretical perspectives, and the fifth section (chapter 19) presents conclusory comments.
Requests for reprints should be sent to Daryl S. Paulson, Ph.D., BioScience Laboratories, Inc., 300 North Willson, Suite 1, Bozeman, Montana 59715. Email: firstname.lastname@example.org