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Human Evolution: A Discussion of Antecedent Factors in Bipedal Movement and Brain Expansion

April 21st, 2012 by Robert DePaolo | Posted in Psychology | No Comments » | 268 views | Print this Article


This article discusses causation regarding two core aspects of human evolution: bipedal movement and brain expansion. Rather than focusing on their retroactive adaptive benefits, the discussion revolves around typical causes of mutation, particularly metabolic changes fomented by climate shifts over the course of time.

The causal origins of two distinctly human traits; bipedal movement and brain expansion are unclear. With respect to upright walking, a number of theories have been put forth over time. So- called “savanna theory” (generically) is based on the premise that nature selected bipedal locomotion because it facilitated food carrying (Hewes, 1961) and provided heat resistance in the African flatlands (Wheeler 1991) and facilitate a throwing capacity for hunting and self defense. (Calvin 1990).

Another is the“generalist/fisherman” theory (my term) (Niemitz 2010) which holds that an upright posture evolved because it is readily supported by water and that early hominids spent considerable time by water’s edge in search of a plentiful, convenient aquatic food supply. Still another, free-hands theory, suggests that an upright posture allowed the first hominids to make tools (Darwin 1861) and/or throw objects to hunt or defend themselves (Young, 2003) (Kirschmann, 1999).

Meanwhile, aquatic ape theory provides a scenario in which homo sapiens became adapted to water environments. It is based on the fact that our species has tear ducts and other features seen in aquatic creatures. (Morgan 1997)

Each of these theories has merit but each has been subject to criticism. With respect to Aquatic Ape theory, Preuschoft has argued humans are biomechanically suited to life in the water, that too many of us are afraid of water and/or poor swimmers for this to be a species indigenous trait (1991). It begs the question of how competitive would we be in an aquatic milieu; for example vis a vis crocodiles and boas? Could we submerge without air for long periods of time as they do? Could we employ stealth in fleeing from predators? Even the most adept Olympic swimmers splash too much to rely on stealth in the water.

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Intelligence & ADD/ADHD: Breaking The Myths

April 16th, 2012 by Maximilian M. Bolejko | Posted in Disorders and Pathologies | No Comments » | 719 views | Print this Article

There are a lot of ideas flying around where most of the typical layman’s knowledge of ADD/ADHD usually asserts that the condition is not in fact a real mental health issue, or that it is the cause of poor schooling or poor parenting. The opinion that children with ADHD are of poor intelligence due to a perceived inability to focus on a given task is quite a commonality. It is not then difficult to imagine that parents who have been told their son or daughter was very bright, but was doing poorly in school due to inconsistencies or poor focus, have great difficulty acknowledging the fact that their child might have an attention deficit disorder. In fact, many parents have been told that such problems do not occur amongst individuals with higher levels of intellectual ability. Yet studies have shown that individuals with ADD/ADHD demonstrate the same cognitive problems in all ranges of IQ, even well above the 120 range.[1]

ADHD stands for Attention Deficit Hyperactivity Disorder and is a real mental health condition with strong scientific evidence pointing towards an inherited genetic basis with significant neurological abnormalities in the brain. Hence, in order to fully diagnose an individual for ADHD a neurological exam is required. Medication treatment studies were first to show persuasive evidence of ADHD impairment being the cause of two primary neurotransmitters not functioning properly. These are norepinephrine and dopamine. Several genes determining low dopamine levels (named DRD4, DAT1, etc.) have also been found to be associated with ADHD.[2] Another important factor in the condition was recently discovered in a study by the renomed ADHD specialist Prof. Russell Barkley and colleagues at the Medical University of South Carolina. The finding had to do with the decreased levels of GABA (gamma amino butyric acid) found in ADHD children. These low levels of which is yet another neurotransmitter, were found to explain the deficient impulse control and constant interchanging thoughts associated with the condition.[3] In other words, in order for the brain to stop an action, in this case a thought, it has to use the brains inhibitory neurons, this in order to prevent the ongoing surge of excitatory neurons from firing and generating new thoughts. Blocking excitatory neurons is precisely the task of GABA. This is a process that requires much more effort for the brain, equivalent to the increased effort for individuals with ADHD to get themselves to actually relax. A factor intertwined with dysfunctional dopamine circuits in ADHD is “proneness to boredom” which is a major fact in the condition and other hyperactivity/impulsivity-related conditions. It is often not comprehensible of just how painful the experience of boredom can be to people who do not have their brains wired in this way. Reduced GABA and dopamine levels might also explain the phenomenon of instable sleep patterns in individuals with ADHD, often times, as understood from individual reports, these individuals find themselves having to completely wear themselves out before a relaxed state becomes a possible. Of course we could just as well apply the finding of decreased GABA levels and their effects on more general terms as Prof. Daniela Cavetti states in a publication of the Journal of Cerebral Blood Flow & Metabolism.[4]

Maybe this explains why it is so tiring to relax and think about nothing.[5] Daniela Cavetti.

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Phase Sequences, Language and Psychological Adaptation

April 5th, 2012 by Robert DePaolo | Posted in Psychology | No Comments » | 497 views | Print this Article

By Robert DePaolo


This article discusses a model of psychological adaptation by applying components of Donald Hebb’s phasic model of cognition/ brain function to the clinical concept of experiential congruity as seen in the psychoanalytic, client-centered and cognitive-behavioral methods. The possible use of a-training (psycho-innoculation) method analogous to that of Seligman is discussed and self directive language is described as a mechanism of implementation.

Theory and Research…

Donald Hebb’ proposed a neurophysiological model of learning and memory, partly in response to his frustration over the impasse during his time between the behaviorists and introspectionists. He was interested in the meditational process in the brain, specifically what happens in the period between presentation of a stimulus and subsequent response that finally consolidates learning and memory. His solution was something he called the cell assembly. He suggested that the brain is organized into cellular configurations which become hypersensitized to specific inputs with repetition of those inputs (1949). In a sense this notion not only built a bridge between introspectionism and learning theory but also between respondent and classical learning theories since they were seen as theories devoid of a meditational, cognitive component..

Hebb postulated that with repeated inputs specific cell assemblies are activated in the form of loops or circuits. These loops could be more or less exclusive, depending on the habit strength incurred through repetition. However Hebb also felt brain activity consisted of multiple assemblies, trended toward formation of hierarchical loops, and that there was some probability that one cell assembly could merge with and be influence by another to form a higher order, mega-circuit. Hebb referred to the interactions among cell assemblies and the hierarchical influence they purveyed as phase sequences.

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