Ethical Issues Surrounding Newborn Medical and Genetic Screening: Project Update

It has been some time since I have written here concerning the UROP project with Professor Tabery. Since I am presenting today at the capital, I thought I'd share this with everyone as well.

Currently, there are over 1,200 tests available to determine the genetic component of various medical disorders, predispositions, and traits. The state of Utah currently mandates that 46 screening tests be performed on all newborns to identify and treat certain disorders. The number of genetic tests will increase in the future, requiring policymakers to make decisions concerning what tests to require, allow, or prohibit. Guidelines for making such decisions require standardized, objective criteria; however, critical analysis of the criteria to justify these decisions is lacking in scientific and public policy literature.

In 1968, Wilson and Jungner were the first to develop criteria for making such decisions. In 2004, the American College of Medical Genetics developed more sophisticated criteria for newborn screening tests. Our analysis found that these criteria either consist of ambiguous language or are insufficient when applied to some current newborn screening tests and some tests for disorders currently being debated for possible mandate. Our research also found that significant variation exists between states related to newborn screening ranging from 17 to 53 mandated tests. Our goal is to provide policymakers with usable guidelines to make informed, ethical decisions for requiring, allowing, or prohibiting newborn screening tests. Our guidelines include two philosophical concepts necessary to make an informed, ethical decision concerning permissibility:

1. Understanding of the causal relationship between genes and disorders. The genetic component must be high in order for the state to consider a newborn screening test mandatory. In addition, the causal relationship between genes and disorders must be morally positive or neutral and free from scientific controversy. All tests within the impermissible category have a significant environmental component or are morally controversial related to causation and/or treatment.
2. Treatability. In order for a test to be mandatory, the treatment must be readily available, of reasonable cost to the parents, and benefit the least advantaged. A test may still be mandated by the state if it does not meet these criteria if and only if it is of significant public health concern and is currently under debate for possible public assistance related to treatment. We name the first category as mandatory-treatable (MT) and the latter as mandatory-informational (MI).
   

The following provides a brief outline of key concepts and arguments that we have developed to support this legislative formula.

The causal relationship between genes and phenotypic traits or disorders is important in the permissibility debate on newborn screening because it relates to a level of confidence medical professionals and patients may place in test results. In the traditional equation for phenotypic expression, P = G + E + (G x E), G must be high and E negligible for any test to be considered mandatory. This means that scientific consensus must conclude that a test have an insignificant environmental (E) component in order to justify mandatory testing and have a high correlation between specific genetic markers and expression of disorder near or at 100%. If there is a high genetic component but expression is not at or near 100%, then it may still be considered MI or permissible. In regards to justifying permissible or impermissible newborn tests, we argue that that the causal understanding of the genetic component may be high or low but are excluded from the mandatory category due treatability factors discussed below. The paradigmatic disorders for both ends of this spectrum include phenylketonuria (PKU) on the mandatory side and anti-social personality disorder (ASPD) on the impermissible side.

Newborn testing of PKU utilizes high-performance liquid chromatography (HPLC) as part of a tandem mass spectrometry (TMS) panel in most states. This tests for the genetic markers associated with the absence of an enzyme necessary to break down phenylalanine. Without this enzyme, the brain builds up toxic levels of phenylalanine resulting in mental retardation, brain damage, and eventually death. Early detection and a carefully controlled diet free of phenylalanine prevent morbidity and mortality in those individuals with this genetic disorder. The genetic component in this case is 100% with no environmental component in the expression of the disorder. The expression correlation of this disorder is also 100%. If a child is born with the defective gene, he or she will develop the disorder. PKU was the first newborn screening test used in the United States and is part of the mandatory testing program in each of the 50 states.

ASPD is a psychiatric condition symptomatic of behaviors associated with the term "evil" or "predator". The terms "sociopath" and "psychopath" are also sometimes used to describe a person with ASPD. Characteristics of the disorder include deception, violence, criminal acts, lack of empathy, and disregard for social norms. Many with ASPD simply do not seem able to emotionally differentiate or "morally" restrain their actions. Poverty, alcoholism, and drug abuse also are related to ASPD. It is estimated that in the U.S. general population as many as 5.8% of males and 1.2% of females meet the criteria for ASPD while the incidence in U.S. prison populations is anywhere from 50-80%. A genetic test for ASPD has been proposed that determines the markers associated with low levels of monoamine oxidase A (MAOA), correlated with ASPD in conjunction with severe childhood maltreatment. The association of ASPD with low levels of MAOA functions off an interactive predisposition model developed and is significantly impacted by the environmental component in expression of the disorder. No states currently require newborn testing of MAOA although its requirement was proposed by former British Prime Minister Tony Blair before the House of Commons in 2005. We argue that screening for this disorder should be impermissible because the high environmental component associated with its expression and the controversy surrounding genes and behavior. The causal component must be understood in consensus with the scientific community to have a genetic component of near 100% and be free from association related to behavior or other moral considerations that are still currently under debate. We believe that testing for ASPD in newborns represents a clear case of a test that should be made impermissible by the state.

Treatability is also important in any decision factoring for mandatory, permissible, or impermissible newborn testing. The American College of Medical Genetics (ACMG) developed criteria in 2004 that includes scores for availability, cost of treatment, efficacy, and benefits to both the individual and society. We argue that although this is a significant improvement from the ambiguous language used in the Wilson and Jungner criteria, it is still missing an important component related to inequality and social justice. This component derives from philosopher John Rawls’ Difference Principle from his work A Theory of Justice. The Difference Principle states that any system of justice must address the need and indeed benefit the least advantaged within the system. He also argues that even though the system will allow for inequality, it should be minimized at birth so everyone starts with an equal opportunity. This is important to any legislative decision regarding newborn screening because the state should not perpetuate or increase differences between classes of people. In other words, any test that is possible for mandate in the future must be treatable by means of availability, benefit, and cost across all classes of people including the least advantaged. Any newborn test for which treatment perpetuates or increases inequality between classes should be judged impermissible by legislators. Any test that is deemed permissible may involve treatment that is morally neutral or does not promote any type of inequality.

The role of the legislature as it relates to newborn screening must address the needs of public health and rights of the individual. Our formula includes the components of causal understanding of the underlying genetic mechanisms and a universal notion of treatability that follows a theory of justice. This will give legislators the tools to evaluate both current newborn screening tests for possible revision and more importantly, future tests that may not be as paradigmatic as PKU or ASPD. Our formula will also help standardize the number and type of newborn screening tests performed between states so that all American newborns may have a healthy start on life. We believe the newborn screening issue and our proposed solution is both conceptually important and practically necessary in the field of medical ethics.

Wachbroit's “Normality and the Significance of Difference”

Wachbroit, Robert (2006). “Normality and the Significance of Difference” in Parens, Eric, Chapman, Audrey R, and Press, Nancy (eds.) Wrestling with Behavioral Genetics. Baltimore: Johns Hopkins University Press, 235-53.

Wachbroit argues that current investigations into human genetics do not seem capable of identifying the essential properties of being human. Genetic discoveries will affect our conception, which is directly related to how we understand “normal”. The more we learn about the genetic causal factors of various conditions the more explanatory language will be in genetic terms. What constitutes normality of health will be reassessed medically and socially. Discoveries in the fields of medicine and psychology in relation to genetics will alter out understanding of normality and how we conceptualize others and ourselves. Normality may be defined as:

1. A mathematical concept.
2. An evaluative concept.
3. A biological concept.

Mathematical normality is understood to refer to the mean, median, or mode of a distribution. The Bell Curve, Gaussian distribution, and Normal Curve are roughly equivalent and examples of normality in mathematics. Evaluative normality refers to conventional, cultural, institutional, and ethical norms. Less precise and more subjective than mathematical normality, evaluative norms are often context specific, as one type of behavior in one cultural setting may not be considered normal in another. Biological normality refers to the language that biologists, physicians, or psychologist use to refer to a biological unit such as an organ, a physical reaction, or an environment a person experiences. For example, "You have a normal heart", "Her vital signs were normal", or "He had a normal childhood" all refer to a biological concept of normality.

The biological concept of normality is problematic because it refers to the subjective meaning of 'healthy' and may not point to the average, majority, or ideal. When a physician says that a patient has a normal heart she is not referring to the average heart because that is epistemologically impossible. Secondly, when a psychologist determines that someone had a normal childhood, it does not point to a specific home environment but rather a healthy one, which may or may not realistically reflect the majority of home environments. Lastly, when an optometrist says that a person has normal vision she is not appealing to ideal vision, which may be closer to that of a fighter pilot. Behavioral concepts of normality also suffer from subjective meaning and are contextually problematic related to definitions of average, majority, or ideal. Lastly, not always do statistical, social, and biological understandings coincide although advances in science can shorten the gap in some cases. They are three categories of meaning, not three different meanings.

Why different parts of an organism evolve the way it does (Wright) or whether function is to be understood in terms of the organism’s overall ability to survive and reproduce (Boorse) will affect one’s conception of biological normality. When applied to behavior, we may actual redefine the type of behavior under examination, which may affect the social meaning of the term normal. Like Press, Wachbroit refers to medicalization of behavior as problematic within the context of normality because of the conflation of social and biological meanings. He points to education of the public of the distinction so that conflation is minimized. He shows that Fukuyama’s defintion of human nature conflates the distinction. His definition of human nature allows for change over time in case of disease or medical advances but Wachbroit rejects a changing view of what it means to be human. He concludes by asking the question, which is relevant to our research, whether something is human nature if there is 51% or more of a genetic component versus something that is 49% genetic in nature? Does the environmental factors of causation have anything to do with human nature?

Duster's "Behavioral Genetics and Crime, Violence, and Race"

Duster, Troy (2006). “Behavioral Genetics and Explanations of the Link between Crime, Violence, and Race” in Parens, Eric, Chapman, Audrey R, and Press, Nancy (eds.) Wrestling with Behavioral Genetics. Baltimore: Johns Hopkins University Press, 150-75.

Duster argues that scrutiny and skepticism should be employed in behavioral genetic research because of the trend to more between population differentials and the socially constructed bias of the criminal justice system. Lewontin commented on statistical problems related to comparing within group variance and between group variance related to the IQ controversy of the 1970s. The problem here lies within the idea that humans share 99.9% of identical DNA and research that tries to correlate genetic ancestry with behaviors such as violence, criminality, and impulsivity. Like Press, he appeals to the notion of social constructionism as it relates to behavior. Many researchers also argue that physical variations in the human species have no meaning except the social ones we create, which have no constancy. “Race” can have a substantial effect on how people behave but that does entail a link to genetic causation. If, however, researchers initiate research based on certain trends such as the disproportionate number of African Americans incarcerated compared to the general population, then run the risk of making invalid conclusions similar to the “science” of phrenology in the late 19th century. He does argue that we should eliminate racial and ethnic classifications in the routine collection and analysis of data but rather that we need to recognize, engage, and clarify the complexity of interaction between taxonomies of race and genetic outcomes.

I agree with his idea of the Zeitgeist or spirit of the time in conducting research because we must accept that, in many ways, we are products of our environment and societies as much as we are products of our genome. Duster provides a slew of evidence to back up his claim that we may want to revisit. He also speaks to the circular nature of labeling theory in hat he terms a “looping effect”. This will be especially important related to ASPD and the MAOA connection. Then again, in the context of drug treatment, is genetic “profiling” to eliminate disability really a bad thing? He sites cystic fibrosis and beta-thallosemia as examples of ethnic or group specific diseases that may warrant research. The important difference is that of a physical disorder and that of behavior but this does not address the question of whether physicalism or genetics gives rise to behavior. He also speaks of the difference between genetic markers and explanatory causation of crime that we will have to keep in mind.

Kaebnick's “Behavioral Genetics and Moral Responsibility”

Kaebnick, Gregory E. (2006). “Behavioral Genetics and Moral Responsibility” in Parens, Eric, Chapman, Audrey R, and Press, Nancy (eds.) Wrestling with Behavioral Genetics. Baltimore: Johns Hopkins University Press, 199-219.

Kaebnick explores three philosophical positions related to behavioral genetics, free will, and determinism:
1. Strong defenses of free will rejecting determinism.
2. Hard determinism, which rejects free will
3. Compatibilism, which accepts both.

The idea of agency is relevant to the discussion of behavioral genetics because of claims to genetic causation and questions of exculpation. It seems that few argue that genes made anybody do anything but the argument from predisposition begs a threshold question of how much is too much impulse. He raises an interesting question concerning the conviction of two individuals for violent crimes. One has a genetic marker for what is claimed to be criminality or violence and the other does not. If we are a product of genes and environment, then it is possible that they are exculpable as well. Is it right to say that neither have free will? I think not, again from cases of similar genotype or environment that so not commit crime or violence. He argues that behavioral genetics increases the sophistication of language used in the free will or determinist debate but not the framework. In other words, the timeless question is not in danger of being resolved anytime soon. Could this be, as Brock and Buchanan posit, because both rest on metaphysical claims that no empirical investigation can overturn? Ask Jim to expand on the compatibilist account because I do not see how human behavior can be fully determined by natural forces (genes) but still allow for free will except in relationship to certain types of behavior. How would we know if the social constructionist position has value? I agree with the idea of strong impulse versus overwhelming impulse as it relates to strengthening the free will position. If it is overwhelming, does this not point to lack of control or insanity as Edgar spoke to? He appealed to Kant and Wittgenstein as an alternative perspective that relied on the power of language and perspective to relay a different idea of free will. Kant believed that we must assume ourselves to be free for practical purposes even if did not fit with our scientific understanding of the world. We may not be able to ever to resolve the debate because of the metaphysical uncertainty of what genetics can reveal but as Wittgenstein claims, the language we use in this age will have to change to make for meaningful dialogue between nature and nurture, genes and environment, and responsibility and blame.

Edgar's "Impulsivity, Responsibility, and the Criminal Law"

Edgar, Harold (2006). “Impulsivity, Responsibility, and the Criminal Law” in Parens, Eric, Chapman, Audrey R, and Press, Nancy (eds.) Wrestling with Behavioral Genetics. Baltimore: Johns Hopkins University Press, 176-98.

Edgar argues that behavioral genetic research will not have a significant impact on the criminal justice system because the idea that most people are responsible for their actions most of the time is central to law and will not change anytime soon. He makes the distinction between the purpose of the law and the process of deciding what criteria is justified for the relatively few people who are not responsible for their actions. He claims that the current work in genetics of impulsivity is unlikely to have an impact on the responsibility doctrine of because society’s impulse to collective self-protection may be stronger than that of collective compassion. He does add that if treatment of disorders that are argued to have a strong genetic causal component, then the system already has judiciary discretion built into the system. The point here is that the science would have to be strongly conclusive that treatment would work, i.e., criminal behavior will not be repeated. The difference between violent and nonviolent behavior is socially relevant and may not change regardless of what science discovers related to causation.

He then discuses the issue of free will as it relates to the justice system. Does a social moray disappear once it is known that a label, punishment, or stigma is morally undeserved? Psychology, genetics may yield as yet unknown understanding of the why but the criminal justice system will not abandon threats and disapproval associated with certain actions. He then discusses the case of Kansas v. Hendricks to point out that predisposition alone is not enough to convict but rather specific behaviors in the past. This will be important if we stick with ASPD and the MAOA link. It recognizes that past behavior may indicate future recidivism but it provided cautionary language in the definition of “mental abnormality”. The most interesting point he makes is that once a person is proved to have done some criminal act, that person is another category outside of those who do not commit criminal acts. He concludes this section with an appeal for public discourse on the subject, which will be complicated and difficult.

The strongest point Edgar makes concerning the stability of the criminal law doctrine is that some people who do not commit crimes have the same genetic endowment (or lack thereof) and similar environments as those who do point to choice rather than determinism. He also mentions that the law should actually be tougher on those who have a stronger impulse to violate, not the other way around. In order to have significant effect on legal doctrine, science would have to provide stronger evidence of exculpability than the literature currently provides. Most states only recognize a “mental” condition as insanity. His last point is that legal doctrine only changes with majority findings, which may be difficult to show in cases of ASPD, impulsivity, and chronic recidivism. I believe teasing apart the environmental component may be even more difficult here making the case for genetic determinism as a legal defense even more difficult.

Brock's “Behavioral Genetics and Equality”

Brock, Dan W. (2006). “Behavioral Genetics and Equality” in Parens, Eric, Chapman, Audrey R, and Press, Nancy (eds.) Wrestling with Behavioral Genetics. Baltimore: Johns Hopkins University Press, 220-34.

Brock argues that the there is not a moral objection to enhancement technologies but to selective access to them in ways that would exacerbate social, moral, and economic inequalities. The future holds the possibility that many natural differences in life and well being may become more into our control but not without the risk that moral, social, and economic inequality would increase. How much of class structure is based on heredity and wouldn’t any new medical or genetic treatment related to enhancement necessarily be outside the purview of anyone but the rich? Many may think that significant enhancement technology is science fiction but the notion of increasing inequality is not a far stretch. He discusses social justice and distinguishes between formal and fair equality appealing to Rawls to claim that fair equality of opportunity requires equal opportunities of those similarly endowed and motivated. Rawls may argue for physical enhancement behind the veil of ignorance but not for enhancement available to a select group of individuals in the society giving them unfair advantage over the rest. Ask Jim why he claims that diversity and idiosyncrasy would diminish in such a state when he argues for the potentiality of an increased gap. I thought he made a rather poignant analogy to the dismal quality of public education in the U.S and opportunity for individuals in that lower income group. He comments on the difference between brute luck and option luck to claim that our current system accepts bad brute luck but not bad option luck. The point is that bad brute luck may only be available to a few further inequitizing society thereby being an issue of injustice.

Brock argues that the value of traits change over time due to the social, political, economic, and I argue technological framework of society. How do we decide what traits will be of value in an unknowable future? Take height. There seems to be cultural value to being thin and tall but that could change. History shows us that women with more curves were more sought after than thin women. The idea of equalizing is not feasible because that means that we would have to de-enhance those with extraordinary ability but enhancing based on cultural values that may change is not in the long run equalizing natural assets. It may be fine motor skills that are of value today ad brute strength tomorrow. I find it interesting that he withholds speculation on the potential for inequality simply within the context of preventing genetic disease. He agrees that limiting the use of genetic technology will be difficult because of the complexity of positional and intrinsic value to cases of benefit to the individual and society. What if we could make firefighters stronger with more stamina? It still comes down to where do we draw the line. He concludes with a discussion of human nature, dignity, and evolution arguing that it would be problematic to sustain a moral community or democratic institution that respected the human rights of all. He speaks of a natural aristocracy that might develop. Would we not look at this as an instance if speciation, which still begs the question of what is it that makes us human.

Press' "Social Constructionism and Medicalization"

Press, Nancy (2006). “Social Construction and Medicalization” in Parens, Eric, Chapman, Audrey R, and Press, Nancy (eds.) Wrestling with Behavioral Genetics. Baltimore: Johns Hopkins University Press, 131-49.

Press argues that behavioral genetics depends on traits, concepts, and phenotypes that may not be the product of nature but socially constructed and therefore inconstant phenomena. This does not allow for the construct validity needed for natural inquiry and could lead the field astray with negative social consequences. Social constructionism is the idea that the traits under question have a social or environmental basis. Medicalization helps construct and reify the behaviors under which behavior geneticists engage. It can also refer to the increasing number of aspects of life that are being brought under the purview of medicine thereby making medicine more of a social force in social constructionism. Geneticization describes the extension of medicalization to the genetic realm. She attempts to get to the heart if universal versus localized traits and it’s link to genetic research. Do traits have to be universal to have a valid genetic component or is this more of the “gloomy prospect” applied to group? Her claim that it is possible to undertake a biographical investigation of a social construct speaks to the Husserlean idea of presuppositionlessness but that is also problematic. Can behavior ever be reduced away from the micro or macrocosm of the environment? My thoughts are that it might be possible in some cases. She may be onto something concerning universals but what about reexamining a “universal” within a cultural context? That would address her concern that culture dictates what we research but it does raise the issues of “What is believed to be true about behavior affects the very behavior which it purports to explain”. (Eisenberg, 1988, 145)

Press speaks to the way science should work against a holistic view that local interactions lend support. Ask Jim about the trend to be interdisciplinary with academic research. Would this not speak to a more holistic view of causation? The problem is that we cannot extract ourselves from within the social construct we are living and this is a difficulty with the scientific method we employ, the conclusions we make, and the very questions, as Press points out, we ask about human behavior. We have to remember to take a look at the possible difficulties with the DSM-IV and its susceptibility to social constructionism. It seems that Press thinks that psychiatry is more grounded in physicalism than psychology but the distinction and difficulties will be important when we start drawing the line based on APA criteria. We will also have to reference the idea of health as a status symbol in addition to normative language. I agree that medicalization and social constructionism surrounding traits in question may lead researchers astray but the question is how much is this a factor or does it depend on the trait in question as we seems to be heading for our project. I more strongly agree that the conclusions of genetic study have a impact on perception of behavior in society and that we are working along a continuum where we draw the line viz. “no bright line” is drawn”.

The last part of the essay speak to research with low rates of probability of success because of the aforementioned difficulties but what if the genetics drove the cultural norm in the first place. The debate for the evolutionary basis of altruism continues and it is here that we may or may not be able to tease apart nature versus nurture. She references Turkheimer and her slightly more positive take on the gloomy hypothesis. Last thought: she makes the distinction between smoking behavior and lung cancer as a focus for research as an example of medicalization but didn’t the research on the disease of lung cancer lead to a social construct that smoking is harmful and undesirable thereby pointing a reciprocal relationship between physical inquiry and social constructs? Hasn’t that been a good thing that we socially frown on smoking than we did 20 years ago or is that just my own perspective on the matter due to my own relationship to and within my society?

Ethical Issues Concerning Genetic Screening for Complex Behavioral Traits

In addition to Wrestling with Behavioral Genetics (Parens, 2006), the following books are next on the list to read and work through fro my UROP project with Jim. After we rough up an idea for a thesis today, I need to spend some time in the library researching the most current journal articles n the subject. Are we pointing in the direction of causation and behavior or will we more or less accept the tenants of genetic links to behavior and argue for drawing a line somewhere between treatment and enhancement? Will we focus on ASPD that probably has the most social relevance and potential for arguments in the realm of policy or more in the medical arena for traits such as depression that may have more medical implications?

Enhancing Evolution – Harris argues that we are morally obligated to enhance but how does factor into intervention on the behalf of others, i.e., children. He appeals to political and moral philosophers such as Bentham, Rousseau, Locke, and Russell. He seems to argue against the model for health and disease proposed by Boorse and Daniels. He speaks to arguments of sufficient seriousness, sufficient probability, and proximity to justify human freedom.

Choosing Children – Glover argues that in order to make the claim that enhancement will minimize or eliminate disability, we must first understand and define disability. Also, how are we to ethically argue for the elimination of certain disabilities such as deafness? This is especially relevant when many in the deaf community do not view deafness as a disability. I think the disability component will be good to explore since the question of normality and possible dichotomous relationship between disability and enhancement. It also appears that he tries to distinguish between the rights of parents and the right of children in addition to arguing that there should be constraints on parental choice. He seems to tackle the idea of a modern eugenics with an emphasis on what enhancement means to notions of justice and genetic competitiveness. Based on the introduction and skimming, he seems to argue for intervention and the redrawing of the line to push the envelope of “normal” while arguing against enhancement that leads to societal inequities.

From Chance to Choice: Genetics and Justice – Buchanan et al. offer a systematic analysis of issues surrounding genetic technology, ethics, and social policy. Published in 2000, it may start to date itself except for the arguments on more timeless philosophical issues of justice and human nature. While the history of eugenics leading up to Nazi Germany is important, it seems that there was a case to be made for the existence of a form of modern eugenics before completion of the human genome project so if we move in a positive direction, maybe we should not shy away from the past but embrace a redefinition that incorporates ethics, social theory, and learning from the past. Just an idea … not quite sure if it’s a good one. It seems that the Buchanan essays are more relevant to our research but we should selectively read arguments by the other authors including those concerning:
1. Distributive justice
2. Human nature and bases of inequality
3. Normality
4. Tailoring environments
5. Moral boundaries
6. Treatment versus enhancement
7. Egalitarianism
8. Normal function model
9. The idea of “best”
10. The right to an open future
11. Reproductive freedom

Schaffner's "Behavior: Its Nature and Nurture Pt. 1"

Schaffner, Kenneth F (2006). “Behavior: Its Nature and Nurture, Part 1” in Parens, Eric, Chapman, Audrey R, and Press, Nancy (eds.) Wrestling with Behavioral Genetics. Baltimore: Johns Hopkins University Press, 3-39.

Schaffner attempts to provide an overview of various concepts of behavioral causation with an emphasis on explaining the genetic component. The following are thoughts and questions that may help piece together the puzzle to ultimately form a thesis concerning ethical issues of genetic screening for complex behavioral traits. This is more like free association but its purpose is to get thoughts out. How does moral relativism play into our discussion? Schaffner speaks to genetic and environmental causation but how do psychological factors play into the equation? What about behavior as a phenomenological factor rather than a trait? By calling behavior a trait, are we not presupposing a form of reductionism to genetics? In more touchy-feely language, am I not more than what my genetics, environment, and a G x E interaction dictate? We need to check out Rawls? He is used as an argument for genetic enhancement and intervention. Hat is the effect of environment on evolution? What about environmental heritability? How will w divide up quantitative versus molecular approaches to behavioral genetics? Schizophrenia too genetic to study? Depression too environmental? We may want to stick with ASPD due to the link to criminality. We may also want to explore thresholds of risk to help draw the line if we are not going to reject any intervention or enhancement?

In the first dialogue, Schaffner appeals to Lewontin on red blood cell phosphatase activity to explain environmental and genetic variation. He mentions on pp. 13 a study in which all phenotypic variation is due to environmental factors. What about Stotz’s claim that the gene also acts as an environment, i.e., what is the effect of the rest of the genome on the trait? Have Jim show you the math concerning the heritability of having a brain being zero (pp. 16). We need to explore problems with the equal environment assumption if we are to argue against the benefit of genetic testing o n ASPD. What is the best argument for behavior being genetically linked (broad)? The problem with the fearful mice experiment is that what if a mouse ate some bad cheese and had diarrhea? Would it be classified as fearful? How to distinguish?

Rowe and Jacobson (1999) developed criteria for factors deemed shared environmental effect
1. Near universals in culture do not count.
2. Environmental exposure must be common to all siblings.
3. The environmental exposure must have directional effect on the trait in question.
4. The environmental exposure must change the trait in a constant direction in order for it to be shared.

Problem with (1) if environment does have an effect on gene frequency. Problem with (2) is that how do you define common experience? Problem with (3, 4) is how do you tease out other effects (both genetic and environmental)? Even Schaffner realizes this difficulty since he places this idea as a “term of art”. He seems to agree with the “gloomy prospect” of possibly never being able to tease out environmental effects in the narrow, non-shared sense. Has anyone looked at DNA from 100 years ago compared to now? If there is a significant difference (problems with qualifying significance) would that not point to environmental inheritance or would it be argued as genetic? Problems with models. What the simplest and most complex model for behavioral genetics?