anti-Causality


anti-Causality

Knowledge is a tree, not a conclusion, and it has been a tree for all of time. Sometime, however, it verboten in the Bible with a didactic “tale” apparently by oligarchs telling the average religious person to view the tree of knowledge and its information as verboten. This is the beginning of the limits and control of information necessary for oligarchic dominance, as opposed to capital-type control which is more commodity-based --though information is now a commodity as “intellectual property.” (With “intellectual” being a strong word for the slurry capital pumps into the population.)

The most important extension of this type of information control currently exists as academia with its early revival of control as the dialectic and didactic by academy founders Socrates and Plato in ancient Athens, and recently by Hegel to fit current capital. Important is that these instructors specifically used sexual abuse to control, which survived to our time as, for instance, the Aboriginal residence schools openly, and covertly elsewhere.

Causality is a rational reduction of the complexity of life saying that “if something happens in relation to something else, that something else caused the first thing.” As a rational reduction, it is a “dumbing-down” of all the highly sophisticade life-system that affect us. Knowledge is naturally structured both in society and in our minds in tree structures, also called “complex data structures” Personally, I have never been “causal” (I believe) because I have been influenced by aboriginal knowledge organization, and also abstract art and music early on as a child with access to all of New York’s museums and libraries (access has since been restricted to children.)

If I something is unavoidably causal, I say “simple math” --this causes that, w/o making a bid deal about it.

Empiricism is the scientific method (and system) built from causality and is considered the only (measurement) science, even by scientist who should know better. It suffers from being highly-fractured, as it is built from independent causal conclusions that also tend to be ego-vehicles from empiricist scientists. Another widely-misused term is “objective” as a synomym for “cruel” such that normal human thinking, such as the recollection of experiences, is excluded from empiricist conclusions; only empiricist numbers are used, often as an output of highly-purposed statistical systems. Dependance on statistics is such that statistics now often produce hypothesis and theory, that is validated by the same statistical systems. Information from other sources such as experience and observation, no matter how detailed, cannot test well against conclusive information produced specifically to test well by statistical systems. This statistical reality is most true for current control of the mind (both human and animal) in cognitive-behavioral strategies of CBT. Interestingly, in CBT, the dialectic method as the socratic method is also key for (as they say) “thought control.”

Objectivism, such as Ayn Rand’s and (current-capital’s) Adam Smith’s objectivism simply “objectify’s” people to make then inanimate numbers rather than feeling people to allow for capital exploitation. As it happens, capital-supporting empiricism, as info-oligarchic, also leverages this, and fills its capital-supportive role by defining and maintaining it as its own from of exploitation, originally sexual abuse.

Tuesday, January 18, 2011

Schizophrenia's genetic signalling protein and receptors

A search for genetic information about schizophrenia shows that a genetically expressed protein, NRG1, and two of its receptors, ErbB3 and ErbB4, are central to schizophrenia. Recent studies implicating NRG1 in schizophrenia often implicate it in bipolar disorder with the same evidence. But different studies focus on two different areas, myelin and neurotransmitters, and hence seem contradictory. Myelin implies neural speed, and neurotransmitters bring to mind, as an example, dopamine as a component of stress.

A myelin, or ErbB3, study (McIntosh, 2009), shows that NRG1/ErbB3 signaling failures cause oligodendrocyte activity to be impaired so that less "white matter" is produced resulting in a diminished "anterior internal capsule in subjects with both disorders" (p. 2). This effect is assumed to be developmental, and myelin formation in "frontal lobes, continues into late adolescence and beyond" (p. 3), giving optimism that new drugs based on NRG1 could reinforce myelination (p. 4).

Genetic loading for psychosis and the internal capsule (McIntosh, 2009)

Neurotransmitter, or ErbB4, studies have a brain-wide view with a focus on neuron development and transmitter activities such glutamatergic hypofunction (Li, 2007), failures in the formation of inhibitory synapses (Fazzari, 2010), and the "wiring" of GABA-mediated circuits (Fazzari, 2010), all in the context of schizophrenia. While bipolar disorder can be linked to schizophrenia in the context of ErbB4 (Chong, 2007), the more detailed material on neural activity focuses on schizophrenia.

As dopamine hyperactivity is part of the schizophrenia pharmacological model (Stone, 2007), and methamphetamine is used to simulate it experimentally (Homayoun, 2008), studies concentrating on stimulants may give clues about the neural activity of schizophrenia and bipolar disorder in relation to behavior.

The "white matter" study is optimistic that new drugs may reinforce myelination, and so raises an idea about myelination and plasticity with respect to maturity: could such drugs help the elderly retain plasticity?



References

Chong, V., Thompson, M., Beltaifa, S., Webster, M., Law A., and Weickertad, S. (2007). Elevated Neuregulin-1 and ErbB4 protein in the prefrontal cortex of schizophrenic patients: Schizophr Res. 2008 March ; 100(1-3): 270–280. doi:10.1016/j.schres.2007.12.474.

Fazzari, P., Paternain, A., Valiente, M., Pla, R., Luján, R., Lloyd, K., et al. (2010). Control of cortical GABA circuitry development by Nrg1 and ErbB4 signalling. Nature, 464(7293), 1376-1380. doi:10.1038/nature08928.

Homayoun, H., & Moghaddam, B. (2008). Orbitofrontal cortex neurons as a common target for classic and glutamatergic antipsychotic drugs. Proceedings of the National Academy of Sciences of the United States of America, 105(46), 18041-18046. doi:10.1073/pnas0806669105.

Li, B., Woo, R., Mei L., Malinow, R., (2007, May 24). The neuregulin-1 receptor ErbB4 controls glutamatergic synapse maturation and plasticity. Neuron, 54(4), 583-597.

McIntosh, A., Hall, J., Lymer, G., Sussmann, J., and Lawrie, S. (2009). Genetic risk for white matter abnormalities in bipolar disorder. International Review of Psychiatry, 21(4), 387-393. doi:10.1080/09540260902962180.

McIntosh, A., Hall, J., Lymer, G., Sussmann, J., and Lawrie, S. (2009).
Genetic loading for psychosis and the internal capsule disorder. International Review of Psychiatry, 21(4), 387-393. doi:10.1080/09540260902962180.

S
tone, J., Morrison, P., and Pilowski, L. (2007, January 26). Review: Glutamate and dopamine dysregulation in schizophrenia — a synthesis and selective review. Journal of Psychopharmacology June 2007 vol. 21 no. 4 440-452

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