UNIVERSAL SOCIALIZATION FACTOR

O-C): “UNIVERSAL SOCIALIZATION FACTOR.” This paper presents the possibility that there is a process in every brain which either gives or denies “permission” for the individual to participate in or to block out the socializing functions of the brain – especially speech. The phenomenon of blocking socialization is seen as a consequence of normal societal structure but capable of causing symptoms of mental illness in some situations.

O-C1) The various disorders which seem to have significant inhibition of socialization include:
O-C1.a) Autism, Pervasive Developmental Disorder, Asperger’s
syndrome, Childhood Degenerative Disorder and related conditions.
O-C1.b) Negative symptoms of Schizophrenia

O-C2) Conditions that seem to be strongly tied with socialization
inhibition are:
O-C2.a) Social Phobia
O-C2.b) Catatonia
O-C2.c) Speech blocking as seen in stuttering and brain injury
O-C2.d) Selective Mutism
O-C3) Conditions which may be more adequately understood when their
relationship to the socialization factor is considered—such as
O-C3.a) Bipolar mania
O-C3.b) Any disability such as a speech, hearing, physical or mental dysfunction which might interfere with the ability to fit into normal social order.
O-C3.c) Global Amnesia (loss of connection of memory to
consciousness.)
O-C3.d) Dissociative reactions (though inhibition of the socialization function may be a dissociation.)

O-C4 A LIST OF THE VARIOUS PRINCIPLES INVOLVED IN THE UNDERSTANDING OF THE SOCIALIZATION PRINCIPLE

[1] That there can be normal socialization drives functioning in individuals with symptoms of serious mental illness, but they may not be able to be expressed to the outside world. 1-A1.b
[2]- That medications vary in their ability to enhance socialization. 1-A3.c
[3]- That it is possible for medications to encourage inappropriate, disinhibited socialization . 1-A3.c
[4]- That mania may represent a loosening of the natural regulation of socialization impulses. 1-A3.c
[5]- That there exists a drive for socialization in individuals while they are demonstrating autistic behavior. 1-B3.b
[6]- That this socialization drive can suddenly be turned on allowing expression. 1-B3.b
[7]- That low doses of medication can effect socialization changes. 1-B3.b
[8]- That various symptoms can result from having inhibited socialization. 1-C5
[9]- That atypical antipsychotics can increase the capacity for socialization for individuals who are not schizophrenic. 1-C5
[10]- That drugs with pro-socialization effects may cause an unacceptable over- stimulation of socialization drive. 1-C5
[11] That a significant percentage of chronic schizophrenics respond to glycine agents with increased socializing activities. 2-B6.a
[12] That all of the glycine agents can improve negative symptoms when added in patients receiving typical antipsychotics. 2-B6.a
[13] That most of the time the glycine agents provided improved benefits in treating negative symptoms when added to atypical antipsychotics. 2-B6.a
[14] That D-cycloserine, a partial glycine agonist, apparently reverses some of the benefit of the atypical antipsychotic clozapine/ Clozaril – suggesting that clozapine has some effect on the glycine/MNDA receptor complex. 2-B6.a
[15] That improvement in socialization which occurred during treatment of negative symptoms of schizophrenia with glycine agents sometimes persisted AFTER THE MEDICATION WAS STOPPED. 2-B6.a
[16] Glycine agonist agents produce improved socialization in autistic individuals beyond the effect of atypical antipsychotics. 2-C1.c
[17]- There is sometimes an increase in impulsive undesirable behavior occurring at the same time as there is increased socialization activity. 2-C2.b
[18] That the glycine-serine receptor mechanism has effects in non-schizophrenic and non-autistic individuals, and those effects increase tolerance to outside stimulation. This is similar to a prosocialization effect. 2-D.a
[19] That individuals with severe autistic symptoms can develop normal socialization. 3-B2.a
[20] That behavioral techniques based on extensively sharing time with the individual in his or her autistic world and introducing contact with the outside
world seem most likely to produce normalizing results. 3-B2.a
[21] That the improvement may be gradual, or may be sudden. 3-B2.a
[22] That individuals can revert back from socialization to autistic isolation. 3-B2.a
[ 23] That a short-acting medication can have prolonged results. 3-C1.a
[ 24] That the capacity for increased socialization can suddenly be turned on –implying that it was already present but not available for voluntary use. 3-C1.a
[25] That there may be problems in one area of the body that indirectly affect brain socialization function. (A number of responders to Secretin had severe gut dysfunction; Secretin is a hormone which regulates gut function.) 3-C1.a)
[26] That there is no one “cause” of autism that will respond to one cure, but many modes of therapy can improve socialization. 3-C1.a
[27] That intense behavioral programs claim the highest rate of cure. 3-C1.a
[28]. That treatments other than intense behavior programs, cure very few, provide some improvement for others, and do nothing for a significant number. 3-C1.a
[29] That our society has not made a meaningful attempt at communication or integration of the skills of the three major treatment concepts – standard medicine techniques, diet and supplement treatments, and behavioral methods. 3-C1.a
[30] That the new “pro-socialization medications would seem to be indicated for early use, as soon as the socialization block is noted – not started as a last resort when all else has failed. 5-B1.2i
[32] That a large percentage of the DD population have dissociatively repressed behavior patterns. 5-B1.2i
[33] That the communication barrier in autism is at least in part from a psychological (dissociative) block and is not exclusively caused by a neurological deficit. 5-B1.2i
[34] That unexpectedly, It seems that the communication blocks found in autistic individuals are similar to those in non-autistic DD individuals. 5-B1.2i
[35] That there is a enough of a similarity between (1) Margaret Mahler’s autistic and symbiotic stages of infant development, (2) the symptoms of the major psychotic breaks, and (3) the symptoms of psychotic isolation and manic disinhibition released as side effects of prosocialization medications to support the idea that all three must have some type or relationship in primitive brain function. 6-D
[36] That the socialization factor, which seems to be “released” by prosocialization medications, is seemingly a different, more mature dissociative process from these two primitive, psychotic personality states which are seemingly held in check in the subconscious by dissociative processes. 6-D
[37] In individuals who are responders to prosocialization medications, the ability to use the socialization response had been inhibited by a variety of factors including hereditary, social environment, physical health, abnormalities of the central nervous system, and experiences involving failure in attempts to socialize. 6-D