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Old 07-15-2003, 07:54 AM   #11
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Originally posted by echidna
Patrick, has the APA at all revised its statement from 1995, “Report of a Task Force established by the Board of Scientific Affairs of the American Psychological Association” ?
As far as I know, the APA has not said anything officially on the subject since 1995. Critics of the APA's position on group differences would contend that they never reviewed the empirical support in the first place, and so their conclusion in the 1995 APA report is not particularly relevant.

I've seen subsequent statements from some of the members of the APA task force to the effect that there may or may not be a genetic component to between-group differences, that the evidence that exists is equivocal for various reasons, and that little or no purpose would be served by doing additional research to answer those types of questions. I agree to an extent in that I do not see any use in determining the nature of between-group differences in cognitive abilities, especially when the range of individual ability within any group is so large, and when data on a genetic component if any is all too likely to be misused or misinterpreted. But to answer your question, no, I don't think the APA has issued any further statements on the matter.

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Old 07-15-2003, 08:04 AM   #12
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Originally posted by karthik
So doesnt this make programs like affirmative action all the more worthwhile? If it is indeed true that some genes determine wiring of the brain and hence the likelyhood of success in the future, people with this gene deficiency should be given some assistance in leveling the playing field for all.
Indeed, that is precisely the position some have taken. Consider the following scenarios.

Two men apply for a technical job. One has an IQ of 160, and can easily understand complex engineering problems, while the other an IQ of 80 and has difficulty putting oil in his car. The higher IQ applicant is hired.

Two men apply for a job as a bouncer at a bar. One is 6'3'' and 280 pounds of lean muscle, the other is 5'10'' and 160 flabby pounds. The bigger guy is hired.

Two men apply for a job as a police officer. One is brave, quick-thinking, and eager to help others out of dangerous situations. The other is extremely shy, faints at the slightest hint of danger, and avoids contact with other as much as possible. The brave person is hired.

Two older men apply for an executive job. Both are tested for genes associated with degenerative diseases that strike later in life. One has many such 'disease' genes, and the other has none. The disease-gene-less person is hired.

Now, which one of these scenarios is based on genetic discrimination? The answer is all four, though most people would assume that only the employer in the fourth scenario is engaging in genetic discrimination.

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Old 07-15-2003, 03:14 PM   #13
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Patrick, sorry to nitpick, but several of those examples are not necessarily solely genetic.

Maybe height & weight are best understood in their genetic & environmental factors, in terms of height Europeans are roughly 4 or more inches taller (top of my head number) today than 500 years ago, purely through improved diet. This is also reflected that second generation immigrants to Australia & the US from developing countries are taller than their parents. IQ’s genetic component is still somewhat contentious & shyness is definitely most likely environmental at this stage (I’m unaware of any genetic studies).

To clarify, the four decisions represent a mixture of environmental and genetic discrimination.
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Old 07-16-2003, 05:35 AM   #14
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Originally posted by echidna
Patrick, sorry to nitpick, but several of those examples are not necessarily solely genetic.
Never apologize for nitpicking.

However, I did not imply an any way that any of those phenotypes were 'solely' genetic, and have pointed out ad nauseum that no phenotype in any animal is ever 'solely' genetic, so in this instance your nitpick is misplaced. My point requires only that for each of those phenotypes, there is substantial genetic vartiance, a proposition which is very well supported.

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Echidna:
IQ’s genetic component is still somewhat contentious & shyness is definitely most likely environmental at this stage
Oh, I disagree on both counts, as would the majority of researchers in the APA report you cited. There is no disagreement in the professional literature that both IQ and the so-called Big Five personality factors, including the so-called neuroticism factor, are substantially genetically influenced. Far from being contentious, this is mainstream science. The debate now is only about how substantial those genetic variance components are. For a review of some of this literature, I recommend Bouchard and McGue, 2003. Genetic And Environmental Influences On Human Psychological Differences. Journal of Neurobiology 54, pp. 4-45.

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Echidna:
(I’m unaware of any genetic studies).
You may be unaware of studies analyzing genetic influences on personality, but they certainly exist. For instance:

Champoux, M, Bennett, A., Shannon, C., Higley, J.D., Lesch, K.P., and Suomi, S.J., 2002. Serotonin transporter gene polymorphism, differential early rearing, and behavior in rhesus monkey neonates. Molecular Psychiatry 7, pp. 1058-1063.

Cherny, S. S., Fulker, D. W., Corley, R. P., Plomin, R., & DeFries, J. C., 1994. Continuity and change in infant shyness from 14 to 20 months. Behavior Genetics 24, pp. 365-379.

DiLalla, L. F., Kagan, J., & Reznick, J. S., 1994. Genetic etiology of behavioral inhibition among two-year-old children. Infant Behavior and Development 17, pp. 401-408.

Eaves, L., Heath, A., Martin, N., Maes, H., Neale, M., Kendler, K., Kirk, K., and Corey, L., 1999. Comparing the biological and cultural inheritance of personality and social attitudes in the Virginia 30,000 study of twins and their relatives. Twin Research 2, pp. 62-80.

Enoch et al., 2003. Genetic origins of anxiety in women: a role for a functional catechol-O-methyltransferase polymorphism. Psychiatric Genetics 13, pp. 33-41.

Finkel, D., McGue, M., 1997. Sex differences and nonadditivity in heritability of the Multidimensional Personality Questionnaire Scales. Journal Personality and Social Psychology 72, pp. 929-938.

Flint, J., 2002. Genetic effects on an animal model of anxiety. FEBS Letters 529, pp. 131-134.

Fullerton et al., 2003. Linkage Analysis of Extremely Discordant and Concordant Sibling Pairs Identifies Quantitative-Trait Loci That Influence Variation in the Human Personality Trait Neuroticism. American Journal of Human Genetics 72.

Kagan, J., Reznick, J.S., & Snidman, N., 1988. Biological bases of childhood shyness. Science 240, pp. 167-171.

Lake, R.I., Eaves, L.J., Maes, H.H., Heath, A.C., Martin, N.G., 2000. Further evidence against the environmental transmission of individual differences in neuroticism from a collaborative study of 45,850 twins and relatives on two continents. Behavior Genetics 30, pp. 223-233.

Loehlin, J. C., McCrae, R. R., Costa, P. T., Jr., and John, O. P.,1998. Heritabilities of common and measure-specific components of the Big Five personality factors. Journal of Research in Personality 32, pp. 431-453.

Plomin, R., & Daniels, D., 1986. Developmental behavioral genetics and shyness. In W. H. Jones, J. M. Cheek, & S. R. Briggs (Eds.), Shyness: Perspectives on research and treatment (pp. 63-80).

Riemann, R., Angleitner, A. & Strelau, J., 1997. Genetic and environmental influences on personality: A study of twins using the self- and peer report NEO-FFI scales. Journal of Personality 65, pp. 449-475.

Robinson, J. L., Kagan, J., Reznick, J. S., & Corley, R., 1992. The heritability of inhibited behavior: A twin study. Developmental Psychology 28, pp. 1030-1037.

Sen et al., 2003. A BDNF Coding Variant is Associated with the NEO Personality Inventory Domain Neuroticism, a Risk Factor for Depression. Neuropsychopharmacology 28, pp. 397-401.

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Old 07-17-2003, 01:11 AM   #15
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Originally posted by ps418
However, I did not imply an any way that any of those phenotypes were 'solely' genetic, and have pointed out ad nauseum that no phenotype in any animal is ever 'solely' genetic, so in this instance your nitpick is misplaced. My point requires only that for each of those phenotypes, there is substantial genetic vartiance, a proposition which is very well supported.
Quote:
Now, which one of these scenarios is based on genetic discrimination?
Patrick, my quibble was mainly that I would have preferred the wording : “Now, which one of these scenarios is based in part on genetic discrimination?”, or as I phrased, “To clarify, the four decisions represent a mixture of environmental and genetic discrimination”. Semantics only I believe.
Quote:
Originally posted by ps418
Oh, I disagree on both counts, as would the majority of researchers in the APA report you cited. There is no disagreement in the professional literature that both IQ and the so-called Big Five personality factors, including the so-called neuroticism factor, are substantially genetically influenced. Far from being contentious, this is mainstream science. The debate now is only about how substantial those genetic variance components are. For a review of some of this literature, I recommend Bouchard and McGue, 2003. Genetic And Environmental Influences On Human Psychological Differences. Journal of Neurobiology 54, pp. 4-45.
Bear in mind that when I referred to "contentious" it is a reference to what that value is, not whether or not there is a component. When you say “substantially”, do you mean “mostly” on both counts ? IQ possibly, but what are the general error bars around the nominal values ? However to what extent is shyness considered genetic ? With even the simple quality of IQ so difficult to objectivise, how does one even begin to determine accurately enough psychometric methods to measure with the same confidence level the far more abstract concept of shyness ?
Quote:
Originally posted by ps418
You may be unaware of studies analyzing genetic influences on personality, but they certainly exist. For instance:
lol. I should have known better than to challenge you to a list of references, even a list not written by Bouchard. So what is the *agreed* genetic component for shyness ? I still believe there is no such creature.

For another example of behavioural psychometrics into Large Twin Studies of Emotional Stability/Neuroticism,

http://www.faseb.org/genetics/ashg/policy/pol-28t1.htm

Certainly at face value, the heritability value seems to include a function of the test method itself to say nothing of the actual results themselves. Yet I find more discussion over heritability values than scientific comparison of the psychometric measures used to determine them. If one is to deduce that from this test the heritability of neuroticism is .27-.61 (as the researcher does), then this would seem to me to be assuming that these tests employed fully and accurately define the full window of neuroticism. But with such an apparently wide discrepancy between test methods (assuming some degree of population uniformity - which I realise is not a strictly legitimate assumption), much doubt seems present as to how to measure the characteristic, and likely the "true" psychometric method is much broader than even these tests employed here.

Forgive me, I realise this is my example, not yours. But in my layman's reading of behavioural genetics I observe this commonly. With regards the intelligence debate psychometrics worked for many many years refining and testing methods before agreeing that g is generally acceptable. But I see no such psychometric history for other behavioural characteristics.
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Old 07-17-2003, 07:25 AM   #16
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Originally posted by echidna
When you say “substantially”, do you mean “mostly” on both counts ? IQ possibly, but what are the general error bars around the nominal values ?
No dimension of personality is as heritable as cognitive ability. As my references show, the heritability of most personality dimensions, including neuroticism, is between 0.3-0.6. So, no I do not mean that individual differences in neuroticism are "mostly" due to genetic differences. On the contrary, it appears at this point that environmental influences account for signficantly more than genetic influences.


Quote:
Echidna:
With even the simple quality of IQ so difficult to objectivise, how does one even begin to determine accurately enough psychometric methods to measure with the same confidence level the far more abstract concept of shyness ?
Though there is always messiness in trying to measure any variable, the papers I cited answer that very question in detail. For instance, you can measure shyness in terms of physiological responsiveness to novel situations or to startle. In children, for isntance, you might measure 'shyness' by things like physiological (e.g. heart rate, pupillary, vocal cord tension, etc.) response to novel situations and people in a controlled setting. 'Shyness' here means the tendency to respond to these types of tests with a fear/avoidance response and exaggerated physiological activation. In adults this type of information would be collected probably through a questionairre or some type of personality assessment instrument.

Kagan and others have shown that these differences are present in the first months of life and persist into adulthood, so purely environmental explanations of individual differences in these traits will need to take that into accont. There was an interesting paper, btw, in Science last month, following up on a subset of a famous group of children that Kagan and colleagues have been following since birth. Before getting to their results, I'll paste their introduction for background.

Quote:
Two of the most extensively studied temperamental constructs are related to the behavioral dimension of approach and withdrawal (2), which refers to the child’s typical response to unfamiliar people, objects, and situations. The extremes of this dimension define two categories of children called behaviorally inhibited and uninhibited (1, 3, 4). Children with an inhibited temperament tend to be timid with people, objects, and situations
that are novel or unfamiliar, whereas uninhibited children spontaneously approach novel persons, objects, and situations. These behavioral differences in young children were accompanied by distinctive physiological differences, including differences in heart rate and heart rate variability, pupillary dilation during cognitive tasks, vocal cord tension when speaking under moderate stress, and salivary cortisol levels (5, 6).

The footprint of these early individual temperamental differences is discernible in later childhood (7–11) and early adolescence (12–14). Furthermore, the two temperamental types are at risk for developing different symptom profiles. An uninhibited temperament in early childhood is associated, given particular rearing environments, with externalizing behavior at adolescence (13), which ranges from display of a hot temper and stubbornness, to impulsive, aggressive, and antisocial behavior. In contrast, an inhibited temperament in early childhood is a risk factor for the development of one of the anxiety disorders in both children (15, 16) and adolescents (14), especially generalized social phobia (alternatively termed social anxiety disorder) (14, 17). The demonstration that these temperamental categories were heritable fueled interest in the basic brain properties that might mediate the temperamental biases observed in infancy (18, 19). It has been suggested that the complex behavioral and physiological profiles of these two temperamental categories might be the result of differing responses to novelty in the amygdala (5, 6).
Schwartz et al (2003) tested their hypothesis by examining amygdalar response to novel faces using fMRI. These are adults who were tested for "shyness" as young children and catagorized as inhibited or uninhibited. Consistent with their hypothesis, those who had been classified as inhibited as young children showed a significantly greater amygdalar response to novel faces than to familiar faces (even in the experimental situation where there clearly is no objective threat of any kind).

Quote:
These findings support the hypothesis (5,6) that inhibited and uninhibited infants are characterized by different amygdalar responses to novelty and suggest that some brain properties relating to temperament are preserved from infancy into early adulthood.
. . .
An inhibited temperament is a risk factor for the development of generalized social phobia (14, 17), a psychiatric disorder characterized by persistent and pervasive fear of interaction with unfamiliar people and avoidance of situations where such interactions are anticipated.
You can read a short summary of their research at: Shyness linked to brain differences


Quote:
Echidna:
If one is to deduce that from this test the heritability of neuroticism is .27-.61 (as the researcher does), then this would seem to me to be assuming that these tests employed fully and accurately define the full window of neuroticism.
Not so. In tests like this, neuroticism (for example) is defined by the tests themselves, i.e. a highly neurotic person is a person that scores high on the neuroticism scale questionairre. It is not at all necessary to assume that you are capturing everything that everyone means by the word.

Quote:
Echidna:
But with such an apparently wide discrepancy between test methods (assuming some degree of population uniformity - which I realise is not a strictly legitimate assumption), much doubt seems present . . .
No, again I disagree. If you look at quantitative genetic studies of things like milk yield in cows, beak size in birds, height in humans and all sorts of other phenotypes that no critic disagrees are substantially heritable, you'll still find a range of results there as well, sometimes a wide range. This does not in any way indicate that the true heritability of these phenotypes is 0, or that the methods are flawed. Further, it is the case that heritability can change with age, with the particular population sampled, with different outcome measures, and so on, so it is not even expected a priori that every study will produce an identical result. Also, no measurement of any real world variable can ever be perfect, so there is always variability due to measurement error, but that does not in any way indicate that all such measurements are uninformative. For instance, there is overwhelming evidence that bipolar disorder and schizophrenia are substantially heritable, and a concensus that genetic factors contribute to risk of developing these disorders, yet the range of reported heritabilities is fairly broad from study to study.

Quote:
Echidna:
So what is the *agreed* genetic component for shyness ? I still believe there is no such creature.
You are entitled to your beliefs. As far as the 'agreed' upon genetic component, I'd say that in adults most researchers would agree that it is greater than 0.2 and less than 0.6. The most data exist on the so-caled neuroticism factor, which is more encompassing than simple shyness. The quote below from an older post outlines some of the results from recent major studies on the neuroticism factor:

Quote:
Several recent twin studies investigated environmental and genetic influences for each of the Big Five personality factors. For each study, all five factors showed signficant heritability, even greater unique environmental influences, but insignficant shared environment influences. The "Negative Emotionality" factor (roughly, the tendency to experience negative emotions), also referred to as the Neuroticism factor, has a broad heritability of ~0.4-0.6, essentially identical to the broad heritability of the MPQ well-being scale. Jang et al. (1996) calculated a broad heritability of 0.41 for a Canadian twin sample (MZ=123 pairs, DZ=127 pairs); Riemann et al. (1997) calculated a broad heritability of 0.53 for a German twin sample (MZ=660 pairs, DZ=304 pairs); Loehlin et al. (1998) calculated a broad heritability of 0.56 for an American twin sample (MZ=490 pairs, DZ=317 pairs), which is very close to an estimate of 0.58 calculated by Waller et al. (1999) for a smaller American sample (MZ=313 pairs, DZs=91 pairs). Lake et al. (2000) report a sex-difference in the heritability of Neuroticism (M=0.423, F=0.504), based on a combined sample of 45,850 members of extended twin kinships from Australia and the United States.
Recently the case has been strengthened considerably by the discovery of chromosomal loci and actual genes associated with these personality measures (e.g. Enoch et al, 2003; Fullerton et al., 2003; Sen et al, 2003). Obviously any such finding needs to be replicated, but as it stands there are some good reasons to believe that there exists a signficant genetic component to individual differences in these personality domains. Interestingly, at least one gene, an allele or version of the serotonin transporter gene (SLC6A4), has been associated with differential amagdylar response to "fearful" faces, as assessed by fMRI (Hariri et al, 2002). Champoux and colleagues (2002) have shown that the same gene (a serotonin transporter gene) influences variation in inhibition/disinhibition in rhesus monkies. They also showed that in these rhesus monkies, differences in early rearing also had a significant influence on inhibition/disinhibition.

Quote:
Echidna:
With regards the intelligence debate psychometrics worked for many many years refining and testing methods before agreeing that g is generally acceptable. But I see no such psychometric history for other behavioural characteristics.
Interesting. Did you look at Child Development, Depression and Anxiety, Journal of Personality, Personality and Social Psychology Review, Journal of Personality Assessment, Personality and Individual Differences, Social Behavior and Personality, and Personality and Social Psychology? There has in fact been a large amount of work over many decades determining the reliability and validity of widely-used personality measures such as the TPQ, MPQ, MMPI, MMPI-2, NEO, and so on. One can always wish for more and better instruments, but the ones that exist are not all that bad.

Refs

Champoux et al, 2002. Serotonin transporter gene polymorphism, differential early rearing, and behavior in rhesus monkey neonates. Molecular Psychiatry 7, pp. 1058-1063.

Enoch et al., 2003. Genetic origins of anxiety in women: a role for a functional catechol-O-methyltransferase polymorphism. Psychiatric Genetics 13, pp. 33-41.

Fullerton et al., 2003. Linkage Analysis of Extremely Discordant and Concordant Sibling Pairs Identifies Quantitative-Trait Loci That Influence Variation in the Human Personality Trait Neuroticism. American Journal of Human Genetics 72.

Hariri et al, 2002. Serotonin Transporter Genetic Variation and the Response of the Human Amygdala. Science 297, pp. 400-403.

Lake, R.I., Eaves, L.J., Maes, H.H., Heath, A.C., Martin, N.G., 2000. Further evidence against the environmental transmission of individual differences in neuroticism from a collaborative study of 45,850 twins and relatives on two continents. Behavior Genetics 30, pp. 223-233.

Riemann, R., Angleitner, A. & Strelau, J., 1997. Genetic and environmental influences on personality: A study of twins using the self- and peer report NEO-FFI scales. Journal of Personality 65, pp. 449-475.

Schartz et al, 2003. Inhibited and Uninhibited Infants “Grown Up”: Adult Amygdalar Response to Novelty. Science 300, 1952-1953.

Sen et al., 2003. A BDNF Coding Variant is Associated with the NEO Personality Inventory Domain Neuroticism, a Risk Factor for Depression. Neuropsychopharmacology 28, pp. 397-401.

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Old 07-17-2003, 04:58 PM   #17
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Old 07-18-2003, 07:25 AM   #18
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Originally posted by ps418
Interestingly, at least one gene, an allele or version of the serotonin transporter gene (SLC6A4), has been associated with differential amagdylar response to "fearful" faces, as assessed by fMRI (Hariri et al, 2002). Champoux and colleagues (2002) have shown that the same gene (a serotonin transporter gene) influences variation in inhibition/disinhibition in rhesus monkies.
Speak of the devil. . . In today's issue of Science, Caspi et al report that this same polymorphism is a significant risk factor for depression, based on results from a large birth cohort. I was wrong to say that this was a variation in the transporter gene itself. BTW, the poymorphism (SLC6A4) is actually in the promotor region not the gene, and affects the transcription level of the gene rather than the structure of the gene itself. From the commentary by Holden:

Quote:
A team headed by Avshalom Caspi at the U.K. Medical Research Council's psychiatry research center at King's College, London, has nailed down the association through an unusual longitudinal study of New Zealanders. The ongoing project is designed to uncover genes activated by environmental circumstances--in this case, adverse life events.

It's "absolutely spectacular" work, says psychiatrist Daniel Weinberger of the National Institute of Mental Health in Bethesda, Maryland, who says this is the biggest genetic fish yet netted for psychiatry. The study, he says, provides hard data for a principle clinicians and epidemiologists have known for a long time: Many genes related to psychiatric ills don't "make you sick in a vacuum [but help determine] how one deals with the environment."

The gene in question is for a chemical transporter called 5-HTT that fine-tunes transmission of serotonin, the neurotransmitter affected by the antidepressant Prozac and others of its ilk. The gene comes in two common versions: the long (l) allele and the short (s) allele. Animal studies have shown that in stressful conditions, those with two l's cope better. Mice with one or two copies of the s allele show more fearful reactions to stresses such as loud sounds. And monkeys with the s allele that are raised in stressful conditions have impaired serotonin transmission.

The new study, reported on page 386, is based on a cohort of 847 members of the Dunedin Multidisciplinary Health and Development Study, who have undergone a variety of assessments over more than 2 decades, starting at the age of 3. The researchers counted stressful life events, such as romantic disasters, bereavements, illnesses, and job crises, occurring between the ages of 21 and 26. Subjects were also assessed for whether, at age 26, they had been depressed in the past year. The researchers double-checked mood ratings by asking close friends about the subjects' depression symptoms.

Overall, 17% of the study participants reported a major depressive episode in the prior year and 3% reported having felt suicidal. Among people who had not reported any major stresses, the probability of depression was the same regardless of their 5-HTT alleles. But the negative effects of adverse experiences were stronger among people with one s allele and stronger still for those with two s alleles. For people with two s alleles (17% of the group), the probability of a major depressive episode rose to 43% among those who had been through four or more stressful experiences. That was more than double the risk for the subjects with two l's (who made up 31% of the group) who had been similarly buffeted by life's vicissitudes. The average score on a depression symptom inventory was likewise more than twice as high for stressed people with two s alleles as for those with two l versions.
Caspi et al, 2003. Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene. Science 301, pp. 386-389.

Holden, 2003. Getting the Short End of the Allele. Science 301, pp. 291-293.

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