BY, FOR, AND OF PSYKOPATHS

Upon reflecting on J's posting, I am of the opinion that he is cointelpro simply because he includes people like Seymour Hersh, Phil Donahue, and Greg Palast in his list of psychopathic personalities, without giving little, if any, documentation for doing so.
As well, he excludes GW in spite of the horrific chain of events he helped to set in motion. Figure that one out!
J throws lots of stuff about psycopathology at the reader, but don't most-or at least a lot of us- have a better than average understanding of psychopathy?
And I'll bet you he knows that!
So throw in some lies with a lot of truth and we assume-at least I did initially- that what he says about the aforementioned folks is also true.
If my memory serves me correctly, I (at least subconsciously) had some alarms go off about Rense about eight months ago, and I don't remember why, but when Laura brought it up on the podcasts, I didn't exactly fall off my chair in amazement. And as for Alex Jones, I used to read his news reports, but subscribe and/or pay money for information that's available on umpteen zillion alternative sites for free? Well, I'm just too cheap, so tough luck Alex. Go find another chump to yell at.
 
Whoops, I forgot to mention that J also included Lewis Lapham, the editor of Harper's. Maybe J's definition of a psychopath differs from mine. And maybe we can only live and and function within the parameters of our present knowledge.
And I can't remember if he included Steve Harper, the PM of Canada, in his list of psychopaths, which in my opinion, he certainly should have.
 
redrock said:
Upon reflecting on J's posting, I am of the opinion that he is cointelpro simply because he includes people like Seymour Hersh, Phil Donahue, and Greg Palast in his list of psychopathic personalities, without giving little, if any, documentation for doing so.
As well, he excludes GW in spite of the horrific chain of events he helped to set in motion. Figure that one out!
J throws lots of stuff about psycopathology at the reader, but don't most-or at least a lot of us- have a better than average understanding of psychopathy?
I admit that Phil Donahue surprised me ... but then, I do know that the really good ones cannot be discerned unless one is close to them for a long time.

Same with Hersh.

But I didn't notice that he called Hersh or Palast psychopaths - he just referred to them as "sleeper agents" and talked about people who worked with the psychopaths. Correct me if I'm wrong as I don't have the whole text right in front of me - just parts of it.

He did point out:
I consider Michael Moore to be one of the "too-ugly-to-be-psychopaths" corrupt normies who serve the mutant psychopath CIA. Psychopaths, themselves, can always turn on the charm and attractiveness.
About Palast he only said:

Finally, you come to the 95%+ true disinformationists, such as Fletcher Prouty and Greg Palast. Obviously, you can learn a lot from the 95%+ truth spooks. If you can discover their lies, what it is that they are protecting, essentially you have the entire picture.
So he wasn't calling them psychopaths, but "95%+ true disinformationists." I don't think this guy meant what he was saying as a put down. I think he was trying to emphasize the point of how tight a grip they have on information. He doesn't discuss whether they are conscious of being disinformationists of not. That's always a useful question to ask. Any of us can be disinformationists if we pass on information that is not true or is only partly true, such as the way you yourself wrote your post. We may think we have done our homework, we may work very hard to try to learn, to think and analyze, but we always miss the mark. So if Palast is doing 95% +truth, that's pretty darn good.
 
You're right Laura. I based my own perception of Donahue on a video of him debating Bill O'Reilly regarding his support for Cindy Sheehan in an upcoming anti-war demonstration in NYC, and three or four of his shows. But I still find it hard to believe he's a psychopath.
Presently I'm reading Martha Stout's book and, although I've been around the block more than a few times in my sixty years, I'm just incredulous at how my naivete and matrix conditioning has blinded me to the paths manipulations and cruelty.
I thought by now, what with my extensive reading and life experiences, that I had a pretty good handle on people. Was I mistaken or what!
 
Wanted to add this: I think that listing Phil Donohue as a psychopath was a big mistake.

Have a look at this video.

http://www.brasscheck.com/videos/tv4us/tv4us2.html

Phil Donohue takes on Bill O'Reilly and shuts him UP!

It's a GREAT clip.

Bill O'Reilly is a CLASSIC example of a psychopath spewing paramoralistic jargon, doublespeak, and conversive thinking.

Sheesh! And Phil actually HANDLES him!

We should all be so capable...
 
Laura said:
Several times he refers to DNA and then he names a gene as being the "psychopathy" marker. I'm not too sure about that, either. Need to do some research. My initial impression was that the gene was the opposite thing... but if ya'll can dig up anything about it, it might help.

I also don't think he presented the thing about women very well. But then, he doesn't have the C's and he isn't a woman.

All in all, I was quite favorably impressed with the analysis and description of our real planetary problem as being psychopaths and his attempt to put it into terms that a lot of people could understand.

Also, Fifth Way, his reference to "by, of and for psychopaths" was, I think, a play on words. You know, "government of the people, by the people, and for the people."

I think I'm going to include an edited version of it in the new edition of 911.
Interesting. Just recently found this thread and I kept thinking as I read that the gene sounds familiar. I spent the past year working with the DRD2 gene. The DRD4 7R is the dopamine receptor type 4 gene with 7 repeats of 48 base pairs. It is what one would call the long form of the D4 gene. The version of the DRD2 I worked on was also the long form of the D2 receptor gene which is implicated in schizophrenia. It was originally thought that the long form of the D4 was the schizophrenia gene. The D4 receptor is part of the D2 receptor family which also includes the D3 receptor. These 3 receptors are similar in that they play an inhibitory role in neurotransmission unlike the stimulatory role of the D1 receptor family (D1 and D5 receptors). Most antipsychotic drugs target D2-D4 receptors to decrease their activity but the primary target is usually D2. What is more interesting is the long form of the D2 receptors in the striatum causes too much dopamine in this area but low functioning of D1 receptors in the pre-frontal cortex. Enough dopamine is not being metabolized in the cortical areas which results in some of the cognitive deficits seen in schizophrenia.

Anyway, the long form of the D4 receptor is also associated with various psychiatric disorders including OCD and ADHD. D4 receptors are found mostly in the limbic system (emotional) and in schizophrenia a lot of these D4s are in the striatum but again it's the frontal cortex D1 that is affected. The best schizophrenia drug actually target D4 receptors while traditional drugs targeted D2. Go figure. I think it's both receptors. Im not sure D4 alone would be a psychopathic gene which is what this J is pushing. The DRD4 2R which is another form of the D4 gene is implicated in mood disorders like depression, bi polar etc. There is heated debate about this particular mutation (DRD4 R7 ) and ADHD There are loads of studies I don't have time to go into but I included a PubMed link below that links to many other papers.

Personally I think combined mutations in dopamine and serotonin receptor genes may have something to do with psychopathy. Depression is a sign that one can empathize with the others and studies indicate that slightly depressed people are better at gauging the reality of the situation. Depression is usually low dopamine and serotonin. There are also loads of excitatory neurotransmittors in food (aspartate, glutamate) which will also screw up the dopaminergic and serotonergic system. The brain works in a homeostatic manner. If you throw off one chemical the others get screwed up. I swear, if you're not born a psychopath, everything from social programming to the food you eat is such that your brain chemistry and behaviors get as close to psychopathy as possible. If not the depression gets so bad you can't do anything.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=gene&cmd=retrieve&dopt=default&list_uids=1815
 
What I've been wondering about lately is: if it is so that the "soul" marries with the genetic construct if present, is there some way to determine those individuals who have higher soul potential via DNA codons? And if so, could it be possible that this is one of the reasons for the great effort to "decode the human genome"? Are they looking for ways to target souled individuals with "ethnic specific weapons"? Is the research in "ethnic specific weapons" just a cover for something else?

For example: if they found a way to target everyone EXCEPT psychopaths, that would be no good because then everyone would die except the psychopaths and they would have no one to be their servants, so it seems unlikely that this would be the approach. So, instead, they might think of targeting just those with higher soul potential, leaving psychopaths AND the remainder of the population that could not achieve the higher potentials... and that way, they would have a servant population that would never be capable of doing anything other than being imprisoned in physical bodies with no hope for developing higher organs of perception and/or doing.

The reason I started thinking this way was because I read all the papers I could find on the so-called ethnic specific weapons issue, where, supposedly, they were developing weapons that would target Arabs but not Jews. But that isn't possible (it seems) since Jews and Arabs (excluding Ashkenazi, for the most part) are so close in genetic terms that anything which would kill Arabs would also kill Jews (excluding Ashkenazi, for the most part.) So, either they are going after all Jews excluding Ashkenazi (and they can't be certain there because there IS some intermixing), or they are doing something entirely different and this is just a cover. Because, of course, to exclude Ashkenazi means to also exclude a lot of the European genetic lines and that wouldn't really serve their alleged purposes. Or would it?

It's all so sick I can hardly wrap my mind around it.
 
I think you could be right Laura, if you see souled people as an "antidote" to the effect of psychopaths, then their number one goal would be to neutralise them. If there is anything unique about the genetics of such people, then this is their weakness.

I think the psychopaths are losing... or, they are getting desperate. They know that they are hanging by a thread. If they don't do something about it, they are the ones who are going to be neutralised, simply by not having any vunerabilities to exploit. It seems we are reaching a point where psychopaths are going to have to fight for their survival - the first time they have been backed into a corner.

The power of the psychopaths is the people they control, if those people "wake up" then the psychos lose their power. They are outnumbered and so rely on being hidden. Thus the exposure work that souled people initiate through not being able to bear the sight of people being "duped" and used, giving people fair chance - the option of seeing the other side of the coin, is the only thing they fear and the only thing we have to defend ourselves against them.
 
What I'm struggling to understand is where does the 4d sts candidates fit into all this. Psychopaths haven't got souls so could it be that some of the 'secondary' psychopaths, those that choose to copy psychopathic behaviour but some have a soul, are likely to be 4d sts candidates? Those that have grown a black magnetic centre and their emotional centre has become similar to a shrivelled prune.

If that's so, could they be targeted with being wiped out with ethnic specific weapons as well and be just as unaware of it as anyone else?
 
Laura said:
What I've been wondering about lately is: if it is so that the "soul" marries with the genetic construct if present, is there some way to determine those individuals who have higher soul potential via DNA codons? And if so, could it be possible that this is one of the reasons for the great effort to "decode the human genome"? Are they looking for ways to target souled individuals with "ethnic specific weapons"? Is the research in "ethnic specific weapons" just a cover for something else?
Dunno. I think it includes the ethnic specific weapons as well as a cover for something else (creating monsters) because the way I see thigs going it is a mad rush to get to every single gene and find out what they do. I say creating monsters tongue in cheek but I wouldn't be suprised if that's the case. In the neurobiology and behavior lab I was in just about all the fulltime researchers except the primary investigator are microbiologists. It's a huge huge lab. There are collaborations with other labs and that's when they bring in the psychiartrists and behaviorists because they play around with genes, create transgenics and knockout mice that are supposed to mimic known disorders. The problem is these animals display unexpected and unexplainable behavios even when the neurobio says it shouldn't. It is then that they really have to figure out what the gene is really doing but they are often not well versed in behavior. If anything maybe they are practicing for just in case there are unexpected behaviors lurking in souled beings.


laura said:
For example: if they found a way to target everyone EXCEPT psychopaths, that would be no good because then everyone would die except the psychopaths and they would have no one to be their servants, so it seems unlikely that this would be the approach. So, instead, they might think of targeting just those with higher soul potential, leaving psychopaths AND the remainder of the population that could not achieve the higher potentials... and that way, they would have a servant population that would never be capable of doing anything other than being imprisoned in physical bodies with no hope for developing higher organs of perception and/or doing.
I was thinking this way based on some things the Cs said. They say STS 'feeding' on certain types is like a gourmet meal. In the case of psychopaths, having a souled person under their control is similar..
I also wonder if it can't be both what you wrote and also ethnic specific weapons to enhance their genes too. There there may be variations in being souled. There are variations in everything else right? So maybe ethnic specific weapons are for some souled that also have certain genes or some unsouled with certain genes that can get vamped up and the genetic work serves both. Maybe the ones they are really worried about are those with unpredictible behavior patterns under certain circumstances or certain manipulations whether souled or unsouled.


I was also thinking in terms of the Cs when they say the earth is going to transform anyway, and they wish to control you in 4D. Maybe they need souled or those with certain genes because only certain types can get to places or states of being. Maybe the souled gets eveyone else to 4D by pulling along those without the 'gene stuff' to hold the frequency like you proposed in other writings, then armed with the knowledge from the genome, the ones with souled gene stuff they use as souled robots.

I keep thinking of what is done in research and when certain type of animals are needed in the wild. You will have the same species but with a subset that behaves in one way while another subset behaves exactly opposite in the same situation. Special traps are made that takes advantages of these stereotyped, species specific behavior patterns depending on what is wanted playing one off the other. Maybe what the psychopaths want to get to is not just the genes but the conditions that acts as regulators for certain genes being on or off using those with certain genes as the bait maybe they want to turn on or off some of their genes. Epigenetics and the idea of methylation and palmitolation and transposons are things to consider. It all amounts to the same thing you propose anyway- a sad state of affairs for those not inclined to psychopathy.
 
If there are 'souled' STS, I don't think they'd much appreciate a 'soul-specific' weapon. Plus, I think it's possible 4D STS involves 'souled' 3D STS in their plans. They do have an interest in 'harvesting' a 4D STS stock, if they can, according to Ra.

Perhaps the 'non-psychopath-specific' weapons are for use specifically in the Middle East. They are intent on killing ANYONE that may have Semitic genes. "Let God sort them out" as the saying goes. Whatever assets they have in the Middle East that will be killed are collateral damage to them, osit.
 
Couple of articles in Journal of Child Psychology and Psychiatry (only abstracts are available without subscription)

R.J.R. Blair, K.S. Peschardt, S. Budhani, D.G.V. Mitchell, D.S. Pine
The development of psychopathy
Journal of Child Psychology and Psychiatry 47 (3-4), 262–276.
The current review focuses on the construct of psychopathy, conceptualized as a clinical entity that is fundamentally distinct from a heterogeneous collection of syndromes encompassed by the term 'conduct disorder'. We will provide an account of the development of psychopathy at multiple levels: ultimate causal (the genetic or social primary cause), molecular, neural, cognitive and behavioral. The following main claims will be made: (1) that there is a stronger genetic as opposed to social ultimate cause to this disorder. The types of social causes proposed (e.g., childhood sexual/physical abuse) should elevate emotional responsiveness, not lead to the specific form of reduced responsiveness seen in psychopathy; (2) The genetic influence leads to the emotional dysfunction that is the core of psychopathy; (3) The genetic influence at the molecular level remains unknown. However, it appears to impact the functional integrity of the amygdala and orbital/ventrolateral frontal cortex (and possibly additional systems); (4) Disruption within these two neural systems leads to impairment in the ability to form stimulus–reinforcement associations and to alter stimulus–response associations as a function of contingency change. These impairments disrupt the impact of standard socialization techniques and increase the risk for frustration-induced reactive aggression respectively.

Journal of Child Psychology and Psychiatry 46 (6), 592–597
Essi Viding, R. James R. Blair, Terrie E. Moffitt, Robert Plomin (2005)
Evidence for substantial genetic risk for psychopathy in 7-year-olds

1Social Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, London, UK; 2Mood and Anxiety Disorders Program NIMH, Bethesda, MD, USA
Background: Individuals with early warning signs of life-long psychopathy, callous-unemotional traits (CU) and high levels of antisocial behaviour (AB) can be identified in childhood. We report here the first twin study of high levels of psychopathic tendencies in young children.
Methods: At the end of the first school year, teachers provided ratings of CU and AB for 3687 twin pairs from the Twins Early Development Study (TEDS). For the analyses of extreme CU, we selected same-sex twin pairs where at least one twin scored 1.3 or more standard deviations above the mean on the CU scale (612 probands, 459 twin pairs). For the analysis of extreme AB, we selected same-sex twin pairs where at least one twin scored 1.3 or more standard deviations above the mean on AB scale (444 probands, 364 twin pairs). Furthermore, the extreme AB sample was divided into those who were also extreme on CU (children with psychopathic tendencies; 234 probands, 187 twin pairs) and those who did not score in the extreme for CU (children without psychopathic tendencies; 210 probands, 177 twin pairs).
Results: DeFries–Fulker extremes analysis indicated that exhibiting high levels of CU is under strong genetic influence. Furthermore, separating children with AB into those with high and low levels of CU showed striking results: AB in children with high levels of CU is under extremely strong genetic influence and no influence of shared environment, whereas AB in children with low levels of CU shows moderate genetic and shared environmental influence.
Conclusions: The remarkably high heritability for CU, and for AB children with CU, suggests that molecular genetic research on antisocial behaviour should focus on the CU core of psychopathy. Our findings also raise questions for public policy on interventions for antisocial behaviour.

and this:
http://www.york.cuny.edu/~seitz/Autism.html
SOCIAL DEFICITS IN AUTISTIC CHILDREN:
THE ROLE OF EMOTION AND EMPATHY
Research Plan
Jay A. Seitz, Ph.D.
Department of Political Science and Psychology
York College/CUNY

A. Specific Aims
Recent neurobiological and neuropsychological evidence suggests that the profound social deficits observed in early infantile autism may be more effectively viewed as the abnormal development of a distinct functional system or area of the brain that subserves social interaction and imaginative activities. Current theories of emotional "intelligence" indicate that understanding of one’s own self and one’s relation to others consist of two essential "core" abilities. Intrapersonal abilities include (a) one's affective range and intensity, (b) the ability to discriminate among the emotions, (c) the ability to label them appropriately, and (d) the ability to use them to guide one's behavior. Interpersonal abilities include (a) the ability to decode feelings, intentions, and motivations in others, (b) recognize characteristics among people (e.g., age, gender, ethnicity) and (c) influence others to behave in desired ways. Autistic children's social impairment appears to involve deficits in both intrapersonal and interpersonal abilities. If this is so, then past attempts to characterize autism as arising from central cognitive deficits (e.g., memory, cross-modal processing, visual-spatial skills, development of object permanence or lacking a "theory of mind") are theoretically inadequate to account for the social deficits in behavior found in autistic children.
Objective. The objective of the proposed research is to examine these "core" intrapersonal and interpersonal abilities in autistic children and the nature of the developmental and maturational changes in these social impairments over the early childhood (2-5 years) and middle childhood (6-9 years) years.
Its relevance to birth defects and reproductive health. Autism, a rare but devastating disorder of early childhood, results in profound social impairment, wide-ranging deficits in verbal and nonverbal communication, and extensive behavioral stereotypies in infants and young children that collectively interfere with social and emotional development. All major neuropathological theories of autism place its genesis in abnormalities during the prenatal and/or perinatal periods, that is, a congenital birth defect that frequently goes undiagnosed until the early childhood years.
The hypotheses to be tested. Our working hypotheses are that autism is the result of either deficits in emotional recognition or empathic awareness or both. The study thus addresses the following two hypotheses: The central pathology in autism is (a) a defect in the ability to discriminate and symbolically elaborate upon the emotions and/or (b) a defect in the ability to attribute and decode feelings in others, that is, impaired empathic understanding.
B. Background and Significance
Autism, a rare but devastating disorder of childhood, was originally defined as a constitutional inability to make emotional contact with people (Kanner, 1943). More than a decade later, it was widely agreed that the two central deficits in autism were social impairment and insistence by the child on sameness in behavioral routines (Eisenberg and Kanner, 1956). Currently, the received view designates a triad of symptoms as central to the autistic syndrome: Social impairment, deficits in verbal and nonverbal communication, and behavioral stereotypies (American Psychiatric Association, 1994). The nature of the social deficits has increasingly taken front stage in studies of autism (e.g., Fein, Pennington, Mackowitz, Braverman, & Waterhouse, 1986). Moreover, newer theories of intellective processes indicate that social "intelligence" consists of two essential components (Gardner, 1983). Intrapersonal abilities include (a) one's affective range and intensity, (b) the ability to discriminate among the emotions, (c) the ability to label them appropriately, and (d) the ability to use them to guide one's behavior. Interpersonal abilities include (a) the ability to decode feelings, intentions, and motivations in others, (b) recognize characteristics among people (e.g., age, gender, and ethnicity) and (c) influence others to behave in desired ways. Autistic children's social impairment appears to involve deficits in both intrapersonal and interpersonal abilities.
Social abilities are profoundly important for autistic children's adjustment and success in the classroom, in forming social relationships with peers, and for understanding and interacting with the social world around them. Long-term social adaptation of autistic children indicates that their social and emotional handicaps continue well into adolescence and adulthood (DesLauriers, 1978; Kanner, 1971; Kanner, Rodriquez, & Ashenden, 1972). Even with improvements on standard IQ tests the core handicaps continue throughout life. Moreover, changes in self-concept, an important aspect of intrapersonal abilities, affects social adaptation in the later adolescent years (Kanner, 1971). Autistic adolescents tend to become more aware of their social oddities and may begin to make conscious effort to work on their social problems. Nonetheless, the social impairments still remain. Unfortunately, there has been little, if any, research to date on the emotional underpinnings of social impairment in autism. The objective of the proposed research, therefore, is to study the underlying deficits in both intrapersonal and interpersonal abilities.
Despite the profound emotional impairment found in autistic children, some researchers (Baron-Cohen, in press; Baron-Cohen, Leslie, & Frith, 1985; Leslie & Frith, 1988; Perner, Frith, Leslie, & Leekam, 1989) have claimed that there is instead a central cognitive deficit in social understanding (e.g., imputing beliefs to others). However, these theoretical claims fail to account for the emotional nature of the social deficits. Specifically, they have ignored autistic children's failure to use emotions as a source of knowledge. Their claims fail to take account of numerous reports and frequent observations (e.g., Seitz, 1988) that there are profound deficits in the decoding, range, expression, and symbolic labeling of the emotions as well as their interpersonal elaboration (e.g., empathic understanding). Regarding intrapersonal abilities, autistic children show a preference for pairing facial expressions with nonaffective stimuli and using the lower half of the face in recognition of peers unlike normal children who use the upper half of the face. They are also poor at matching various graphic representations of emotions with facial expressions. However, many of these latter tasks involved intermodal recognition of emotion that may have confounded the results. As a consequence, little conclusive evidence can be drawn from these studies. With regard to interpersonal abilities, autistic children are poor in understanding humor, in detecting social deception in picture stories, in differentiating the social categories of age and gender, and in role-taking tasks that require empathic understanding. However, the empathy tasks administered to autistic children are marred by floor effects and argue for the development of better instruments for the assessment of empathy.
The social deficits, moreover, appear to affect the class of symbolic skills that autistic children acquire. That is, autistic children's social deficits appear to interfere with the acquisition of symbolic skills dependent on social processes (e.g., communicative language, symbolic play, and empathy). For example, the word 'apple' serves as a label (a symbol) for the actual physical object. In like manner, a child may use a broomstick to represent a horse in play, and may offer to another child a toy as symbolic of his feelings toward the child. The literature on language development, development of symbolic play, and growth of empathic awareness in early childhood, indicates that these symbolic skills arise largely as a result of social interaction with others. However, other symbolic skills acquired in the early childhood years are largely independent of social processes (e.g., visual-spatial skills, attainment of object permanence, number skills, cross-modal processing of stimuli) and appear not be compromised to the same extent in autistic children. The development of these skills does not require extensive emotional processing by areas of the brain that subserve social interaction. As a result, it can be argued that cognitive and social abilities are dissociable in autism. Autistic children demonstrate enhanced performance on some cognitive tasks in contrast to poorer performance on many social tasks. Nevertheless, practically nothing is known about the emotional deficits and their intrapersonal and interpersonal expression in autistic children. Tasks of emotional recognition have been limited in scope and often the results have been confounded with other factors. Tasks of interpersonal abilities, specifically empathy, have been poor measures of the construct they have purportedly been designed to assess. There is a pressing need to understand social processes in autistic children, and this research will address this need while addressing autistic children's strengths in cognitive areas, essential to rehabilitative efforts.
The objective of the research described in this proposal is to examine intrapersonal and interpersonal abilities in autistic children. In addition, autistic children will be assessed on standard measures of intellective skills to establish a baseline index of cognitive abilities. One series of tasks will investigate intrapersonal abilities using measures of emotional recognition to assess the decoding of affect with and without symbolic mediation (labeling an emotion, recognizing faces, respectively). Another series of tasks will examine interpersonal abilities. Tasks will assess the ability to empathize with others using measures that require little symbolic mediation (attributing feelings to inanimate objects) to those that require extensive symbolic elaboration (e.g., identification of affect in a story character). As a result, it will be possible to separate the effect of symbolic mediation from the deficits in the decoding of intrapersonal and interpersonal affect. Our working hypothesis is that autism is a result of either deficits in emotional recognition or empathic awareness or both. The study thus addresses the following two hypotheses:
The central pathology in autism is (1) a defect in the ability to discriminate and symbolically elaborate upon the emotions and/or (2) a defect in the ability to attribute and decode feelings in others, that is, impaired empathic understanding.
The research should pinpoint more clearly the central problems of autism and thus suggest more fruitful therapeutic interventions. It should thus enable educators, and others involved with behavioral intervention in the classroom, to more effectively address the cognitive strengths of autistic children while at the same time remedying their social impairments. It should also add immeasurably to our understanding of how the emotions function in human development as well as how they interact with social processes.


Somebody wonders what compulsory vaccination program of our kids (= thimerosal = autism) is all about? everything in me wants to vomit
 
If anybody has membership or access, it would be good to have the complete articles.
 
I could get the pdf file for the second article, "Evidence for substantial genetic risk for psychopathy in 7-year-olds " but the copyright states that its not to be distributed on a list group, but personal email is okay. I can send it to whoever would like a copy.

Edit: correction the copy can be posted to a user groups but needs written permission - I'll send an email to see.
 
I went to the publishing company website and found that the article below was free (which is probably why the research database I have a subscription to had it) - I sent an email asking for permission but since its free I'll just post it.

http://www.blackwell-synergy.com/doi/full/10.1111/j.1469-7610.2004.00393.x?prevSearch=allfield%3A%28Evidence+for+substantial+genetic+risk++for+psychopathy+in+7-year+olds%29


Evidence for substantial genetic risk for psychopathy in 7-year-olds

* Essi Viding11Social Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, London, UK,
* R. James R. Blair22Mood and Anxiety Disorders Program NIMH, Bethesda, MD, USA,
* Terrie E. Moffitt11Social Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, London, UK, and
* Robert Plomin11Social Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, London, UK

*
1Social Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, London, UK; 2Mood and Anxiety Disorders Program NIMH, Bethesda, MD, USA

Essi Viding, Social Genetic and Developmental Psychiatry Centre, Box Number P080, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK;
Email: spjgemc@iop.kcl.ac.uk
Abstract

Background: Individuals with early warning signs of life-long psychopathy, callous-unemotional traits (CU) and high levels of antisocial behaviour (AB) can be identified in childhood. We report here the first twin study of high levels of psychopathic tendencies in young children.

Methods: At the end of the first school year, teachers provided ratings of CU and AB for 3687 twin pairs from the Twins Early Development Study (TEDS). For the analyses of extreme CU, we selected same-sex twin pairs where at least one twin scored 1.3 or more standard deviations above the mean on the CU scale (612 probands, 459 twin pairs). For the analysis of extreme AB, we selected same-sex twin pairs where at least one twin scored 1.3 or more standard deviations above the mean on AB scale (444 probands, 364 twin pairs). Furthermore, the extreme AB sample was divided into those who were also extreme on CU (children with psychopathic tendencies; 234 probands, 187 twin pairs) and those who did not score in the extreme for CU (children without psychopathic tendencies; 210 probands, 177 twin pairs).

Results: DeFries–Fulker extremes analysis indicated that exhibiting high levels of CU is under strong genetic influence. Furthermore, separating children with AB into those with high and low levels of CU showed striking results: AB in children with high levels of CU is under extremely strong genetic influence and no influence of shared environment, whereas AB in children with low levels of CU shows moderate genetic and shared environmental influence.

Conclusions: The remarkably high heritability for CU, and for AB children with CU, suggests that molecular genetic research on antisocial behaviour should focus on the CU core of psychopathy. Our findings also raise questions for public policy on interventions for antisocial behaviour.

'Mark does not feel guilty if he has done something wrong, he does not show feelings or emotions, and he is rarely helpful if someone is hurt.' This description of one of the 7-year-old children (name changed) in our twin study captures the core emotional impairment of individuals with psychopathy. Psychopathy in both childhood (psychopathic tendencies) and adulthood involves both affective-interpersonal impairment (callous-unemotional traits; e.g., lack of empathy, lack of guilt, shallow emotions) and overt antisocial behaviour (Blair, 2001). As such, individuals with psychopathy represent a subset of those who would meet diagnostic criteria for Conduct Disorder (CD) in childhood or Antisocial Personality Disorder (APD) in adulthood (Blair, 2001). Diagnostic criteria for these childhood and adulthood manifestations of antisocial behaviour include overt antisocial acts (such as violence towards other people or stealing), but do not distinguish subgroups of antisocial individuals on the basis of their callous-unemotional profile (DSM-IV, APA, 1994; Hart & Hare, 1997). Most adults diagnosed with APD do not fulfil the diagnostic criteria for psychopathy, as they lack the concomitant callous-unemotional features (Hart & Hare, 1997). Equally, not all children who have CD also display callous-unemotional traits (CU).

Children who show antisocial behaviour from early childhood are at great risk for showing antisocial and criminal behaviour in adulthood, a pattern known as life-course persistent antisocial behaviour (Moffitt, 2003). Such individuals can be 10 times more costly to the society than the average citizen (Scott, Knapp, Henderson, & Maughan, 2001). It is important to learn about risk factors that predict persistent antisocial behaviour early in life. Callous-unemotional traits may be one such risk factor that makes children vulnerable for life-course persistent antisocial behaviour of a particularly serious nature (Frick & Hare, 2001; Frick, 1998). Indeed, antisocial individuals who present with the affective core of callous-unemotional traits (individuals with psychopathy) start offending at a young age and continue across the lifespan with acts that are often predatory in nature (Hart & Hare, 1997). The predatory nature of their crimes reflects the lack of empathy (CU personality core) of psychopaths. A recent study found that psychopathic murderers were highly likely to have committed premeditated murder, whereas this was not the case for non-psychopathic murderers, whose offence was often a result of a heated dispute or a 'crime of passion' (Woodworth & Porter, 2002). Even when residing in a correctional institution, individuals with psychopathy are six times as likely to offend as their convicted peers (Wong, 1985).

Mirroring the findings on adults, children with psychopathic tendencies have a greater number and variety of conduct problems and are also more likely to come into contact with the police than children with conduct problems who do not have elevated CU scores (Christian, Frick, Hill, Taylor, & Frazer, 1997). Children with psychopathic tendencies are also less distressed about their behavioural problems than other children with extreme externalising pathology, suggesting that psychopathic personality traits moderate the level of distress experienced by the perpetrator (Barry et al., 2000), presumably facilitating persistent antisocial conduct seen in these individuals.

Given the early emergence of antisocial behaviour in individuals with psychopathy and its long-term impact – even as compared with other antisocial individuals – it is important to understand the heritable and environmental origins of the callous-unemotional traits, and their function as a risk factor for early emerging antisocial behaviour (itself a risk marker for life-course persistent antisocial behaviour). Broadening this understanding will inform future research, as well as design of prevention and treatment programmes.

Genetically sensitive study designs, such as twin studies, can provide a much-needed perspective on the developmental origins of callous-unemotional traits and on heterogeneity within individuals with antisocial behaviour. Genetic research on antisocial behaviour has generally found that both early-onset and persistent antisocial behaviour show moderate to substantial genetic influence, as well as moderate shared and non-shared environmental influences (Moffitt, 2003). However, none of the studies to date have investigated whether the aetiology of extreme antisocial behaviour differs between those individuals with CU (or individuals with psychopathy/psychopathic tendencies) and those without CU (individuals lacking psychopathy/psychopathic tendencies). It is particularly important to investigate this question in children because preventative efforts early in life are likely to be most successful in combating life-course persistent antisocial behaviour.

The Twins Early Development Study, a birth-record-based representative sample of twins born in the UK 1994–96 (Trouton, Spinath, & Plomin, 2002), includes teacher assessments of CU as well as AB for 3487 pairs of twins at 7 years of age. We used the twin method to investigate the extent to which extreme callous-unemotional traits are heritable at this early age and to consider the extent to which callous-unemotional traits distinguish aetiologically different groups of children with antisocial behaviour (i.e., antisocial children with and without psychopathic tendencies).
Method

Participants

The sampling frame for the present study was 7374 twins from the 1994 and 1995 birth cohorts of the Twins Early Development Study (TEDS). The average age of the participants at the time of assessment was 7.1 years (SD = .23 years). The sample and its history are described in detail elsewhere (Trouton, Spinath, & Plomin, 2002).

For the analyses of extreme CU, we selected same-sex twin pairs where at least one twin scored 1.31 or more standard deviations above the mean on CU scale (612 probands, 459 twin pairs). For the analysis of extreme AB we selected same-sex twin pairs where at least one twin scored 1.28 or more standard deviations above the mean on AB scale (444 probands, 364 twin pairs). This cut-off score was closest to the cut-off score on the CU scale. This selection procedure guaranteed that the probands would score beyond the 'average range' (i.e., not within one SD), yet yielded enough probands to perform the twin analyses. Furthermore, the selection conferred approximately the top 10% of the sample for both CU and AB. This is the percentage band which is designated as 'abnormal' for AB according to the Strengths and Difficulties Questionnaire (SDQ; Goodman, 1997).

The extreme AB sample was further divided into those who were also extreme on CU (children with psychopathic tendencies; 234probands, 187 twin pairs) and those who did not score in the extreme for CU (children without psychopathic tendencies; 210 probands, 177 twin pairs). Maternal educational level was not significantly different for the two groups of children with extreme antisocial behaviour.
Testing procedures

Informed, written consent was obtained from all of the families who agreed to take part in the study. Teachers were approached only if there was family consent to teacher involvement.
Measures

Teachers provided ratings of CU and AB. The response rate of teachers was high: 88% of the approached teachers responded by filling in the TEDS assessment. Teachers are familiar with a broad range of children and have expertise regarding normative child development. Teacher ratings have been found to show higher internal consistency and stability than parent ratings (Gomez, Harvey, Quick, Scharer, & Harris, 1999), and twin analyses indicate that teacher ratings are free of rater bias typically found in parent ratings (Nadder, Silberg, Rutter, Maes, & Eaves, 2001). In line with this, we found that while teacher ratings for CU and AB showed good internal consistency (see below), indicating reliable detection of the latent constructs of interest, parent ratings of CU and AB showed much poorer levels of internal consistency (α = .45 and α = .58 for the CU and AB scales respectively). In addition, parent ratings correlated even less than usual with teacher ratings (r = .20 and .27 for the CU and AB scales, respectively). Finally, the means and variances for the CU scale were lower for parents than teachers, indicating that parents did not discriminate children high in CU. These problems with the parent rating scales led us to focus on the teacher ratings.

Although CU was not assessed directly in TEDS, we were able to create a novel CU scale by using 7 items available in TEDS: three Antisocial Process Screening Device (Frick & Hare, 2001) items, as well as four items from the SDQ. These items were either original CU items ('Does not show feelings or emotions', 'Feels bad or guilty if he/she does something wrong' [reverse scored], 'Is concerned about how well he/she does at school' [reverse scored]) or were selected to reflect CU (e.g., Considerate of other people's feelings [reverse scored]). None of the items overlapped with any of the AB items (see Table 1 for the complete list of items on both scales).

Teacher ratings on the CU scale showed good internal consistency (α = .74). Our AB scale was the SDQ 5-item scale used to assess conduct problems (e.g., 'Often fights with other children or bullies them', 'Often has temper tantrums or hot tempers'). The SDQ scales have both good reliability and validity (Goodman, 1997), and the teacher ratings on the AB scale showed good internal consistency in the TEDS sample (α = .71). The scale scores on CU and AB were converted to z-scores to facilitate comparison between the two scales. The two scale scores correlated .51, indicating that, although there was overlapping variance, the scales were not measuring an identical construct.
Analyses

For same-sex twin pairs, the estimates of group heritability and group shared environment were calculated using the DF extremes analysis regression model (DeFries & Fulker, 1988), which is illustrated in Figure 1. The basic DF model is represented as the regression, C = B1P + B2R + A, in which the co-twin's score (C) is predicted from the proband's score (P) and the coefficient of relatedness (R), which is 1.0 for MZ and .5 for DZ pairs. Proband means for both MZ and DZ probands are transformed to 1.0 and the population mean is transformed to 0. The regression weight B2 estimates group differences heritability; it compares the MZ and DZ co-twin means taking into account genetic relatedness (R). Group heritability (h2g) can be interpreted as the extent to which the average difference between the probands and the population on the quantitative trait measure can be ascribed to genetic influences. Group shared environmental influence (c2g), twin resemblance not explained by genetic factors, is estimated by subtracting group differences heritability from MZ group differences familiality (the transformed MZ co-twin mean). Group non-shared environmental influence (e2g) is estimated by subtracting h2g and c2g from 1. Analyses were conducted using a double-entered dataset such that both members of a twin pair could be selected as probands. Standard errors were corrected in order to take into account the artificial inflation of sample size (Stevenson, Pennington, Gilger, DeFries, & Gillis, 1993).
Results


Table 2 shows the mean z-scores for CU and AB scales for probands with extreme CU and probands with extreme AB (divided into two groups, those with and without concomitant extreme CU scores). We first conducted DF analyses selecting same-sex twins assessed by their teachers as extreme on callous-unemotional traits. As indicated by the co-twin means in Table 2a, co-twins of MZ extreme CU probands were 73% similar to the probands, whereas co-twins of DZ probands were only 39% similar. Doubling the difference in these co-twin means, which can be considered as twin 'group' correlations, yields an estimate of .68 for group heritability. This estimate of group heritability (.68) is nearly as great as the MZ twin group correlation (.73), suggesting that group shared environment is minimal (.73–.68 = .05). DF extremes analysis confirms these findings, yielding minimal estimates of group shared environmental influence (c = .06) and high group heritability (h = .67). In other words, two-thirds of the difference between the extreme callous-unemotional children and the population can be explained genetically.

We then examined whether the aetiology of extreme AB, a concomitant feature of psychopathic syndrome, is different for children with and without psychopathic tendencies as indexed by extreme CU. As shown in Table 2b, for the psychopathic tendencies antisocial group (AB/CU+), DF regression analysis yielded a group heritability estimate of .81 and no shared environmental influence for extreme AB. Shown in Table 2c, for antisocial children without psychopathic tendencies (AB/CU−), we found modest group heritability (h = .30) and moderate shared environmental (C = .34) influence. Although the difference in heritabilities for the (AB/CU+) (.81) and (AB/CU−) (.30) groups was large, their overlapping confidence intervals indicate that the difference is not statistically significant. The results replicated when twin pairs were rated by the same teachers(2/3 of the sample) and by different teachers (1/3 sample) were analysed separately. This was done to ascertain that having a common rater does not introduce bias to heritability and environmental estimates. The result, also replicated at 5% and 15% severity cut-offs (results available from EV).

Because probands in the AB/CU+ (psychopathic tendencies) group had a higher mean AB score than probands in the AB/CU− (without psychopathic tendencies) group (see Table 2b and 2c), it is possible that this difference is responsible for the difference in group heritability between the two groups. For this reason, we assessed the heritability of AB at different severity cut-offs without regard to psychopathy status. The heritability estimates for AB did not vary as a function of severity of AB (results available from EV). This indicates that the high heritability of AB seen in the AB/CU+ group is not mediated by mean levels of AB and is thus more likely to be mediated by the CU traits.
Discussion


Our results indicate that exhibiting high levels of callous-unemotional traits (CU) at 7 years, as assessed by teachers at the end of the first year of school, is under strong genetic influence. Minimal shared environmental influences on callous-unemotional traits were detected, suggesting that at the age of 7, environmental factors common to both members of the twin pair (such as socio-economic status, school and neighbourhood) do not account for extreme CU. Moreover, antisocial behaviour (AB) for children who are high on CU (i.e., children with psychopathic tendencies) is highly heritable. In contrast, the extreme AB of those without psychopathic traits was under strong environmental influence – shared as well as non-shared.

Before discussing the implications of our findings, some general limitations of the study should be mentioned. First of all, the twin data may not be generalisable to singletons. We are currently collecting CU and AB information on the younger siblings of our twins and will be able to repeat our analysis with that sample in the future. Another possible limitation is that our CU scale was not a standard instrument. However, it is worth noting that teacher ratings on this scale showed good internal consistency and distinguished an aetiologically distinct group of children with early-onset antisocial behaviour. Relying on a single source of measurement could also be considered to be a limitation of our study. Given that CU was used as a moderator for dividing our group of children with extreme levels of antisocial behaviour, we were concerned that the CU measure should show good internal consistency, indicating reliable measurement of a latent construct. As the parent ratings of CU did not show good internal consistency, it seemed dubious to use parent ratings of this trait to divide children into subgroups for the purposes of our analyses. Finally, it could be argued that collection of data at a single age and using questionnaire measurement only is a limitation. We are currently following up the twins at nine years of age and will thus be able to add a longitudinal aspect in the future. Furthermore, we are collecting cognitive data at nine, to add endophenotype measurement to the questionnaire information. Regardless of these possible limitations, we think that our present findings have important implications as discussed below.

Although it should be emphasised that not all children with the combination of callous-unemotional traits and antisocial behaviour will become psychopathic criminals as adults, our findings have clear implications for research, treatment, and public policy. With regard to research, it will be important to document how developmental trajectories differ for antisocial children with and without CU. In contrast, children who commence their antisocial behaviour prior to puberty are currently often treated as a single group, without differentiating them on the basis of those traits. Whether presence or absence of CU has long-term implications for crime is a matter for empirical enquiry – although current retrospective data suggests that it does (Hart & Hare, 1997). In addition, the remarkably high heritability for CU and for AB in children with CU suggests that molecular genetic research on antisocial behaviour should focus on the callous-unemotional core of psychopathy. Finally, combining neuroscience and genetic methodologies should be at the forefront of future research on psychopathy (Viding, in press). Current research implicates emotion-related dysfunction in the amygdala and orbitofrontal cortex (both important for emotion processing) as possible brain correlates of adult psychopathy (Abbott, 2001; Blair, 2001, 2003). Preliminary neuropsychological evidence suggests that similar brain dysfunction is also found in children with psychopathic tendencies (Blair, 2001; Viding, in press). This dysfunction might be related to genetic vulnerability. When genes are found that are associated with psychopathy/psychopathic tendencies or with brain circuits, brain scans of groups selected on the basis of genotype will shed light on 'genes–brain–behaviour' pathways in psychopathy.

This approach is also likely to inform treatment options. Better understanding of how genetic vulnerability translates into brain function will contribute to both pharmacological and environmental interventions. This gives hope that psychopathy can be treated as successfully as are other emotional disorders, such as Generalised Anxiety Disorder or Depression. A more immediate clinical implication of the present results is the confirmation of the importance of focusing on CU as well as AB in diagnosis and prevention/treatment efforts (Frick & Hare, 2001).

Finally, with regard to public policy, these results confirm the notion that prevention efforts need to begin in the preschool years. As the large genetic component to psychopathic antisocial behaviour is likely to reflect not only the direct effects of genes, but also gene–environment interaction (Moffitt, 2003), preventative efforts for psychopathy will benefit from developmental investigations of this interaction using measured genes and environments. Finding a large shared and non-shared environmental influence on the AB of children without psychopathic tendencies suggests that this subgroup of children with early onset AB is probably amenable to traditional interventions aimed at improving family, school and neighbourhood conditions. Consideration of the aetiological differences between children with early onset AB will thus assist in evaluation of true effectiveness of prevention and treatment programmes, as well as give pointers to the steps needed for devising more effective and targeted future prevention and treatment efforts.
Acknowledgements


The authors are indebted to the parents of the twins in the Twins Early Development Study (TEDS) for making the study possible. TEDS is supported by a programme grant (G9424799) from the UK Medical Research Council. TEDS psychopathic tendencies research also receives support from the Department of Health and Home Office National Forensic Mental Health R & D Programme (MRD12/37).
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