First, do no harm
While teaching a course on law and ethics to students in a counseling psychology graduate program, I came across the March Monitor article on Burger's replication of the infamous Milgram study. I presented the replicated research, asking my students to critique the study based on ethical principles and standards. Not surprisingly, they quickly identified a number of ethical issues, concluding: "First and foremost, we are to do no harm."
In the replicated study, efforts to alter the original Milgram design in order to prevent harm do not begin to offset potentially damaging effects, even though the researcher attempted to screen out vulnerable participants.
The replicated study lowered the threshold for termination of the "electrical shock" administered by participants, arguing that this protected participants from psychological harm.
However, administering any level of "shock" that induces perceived life-threatening pain in the recipient is potentially damaging to the participant. In fact, the "confederate" in the replicated study was instructed to "grunt" more loudly with each increased "shock," and to finally yell (at the 150-volt shock level): "Ugh. That's all. Get me out of here. I told you I had heart trouble. My heart's starting to bother me. I refuse to go on. Let me out." (Burger, 2009, p. 7.)
There are good reasons to use Milgram's research as a case study of what not to do in research ethics. Replicating it does not send a constructive message to the next generation of psychologists.
Joan S. Kimball, PhD
Pay more attention to asexuals
I found the article on so-called "female sexuality disorder" in the April Monitor lacking. Equating medical and therapeutic "cures" for low libido with the drug Viagra confuses several issues: physical sexual responses, sexual desire and relationship issues. In addition, the article doesn't mention the burgeoning community of people identifying as asexual. In this community, both men and women with low libido recognize that it is not a disorder to be fixed, but merely a way of being. They creatively build romantic relationships that are not based on sexual activity or sexual desire. I believe that psychologists should pay more attention to asexuals because they could teach us a lot about relationships. What is most troubling about the article is that it assumes that low libido is so distressful (for women) that it becomes a DSM disorder; asexuals are an example of how the expression of (a)sexuality by a minority is not a disorder if it is not distressful for the individual and does not impair their lives. Only 30 or so years ago, homosexuals were painting a similar picture; this article fails to see the connection.
A reductionist term?
I have never felt comfortable with the term "science of behavior" to describe psychology. Those of us who work daily to understand, predict and control very real phenomena such as cognition, emotion, motivation, internal conflict, self-esteem and the like can be pardoned, I think, for feeling a bit excluded when that term is used. So it was particularly frustrating to read of Dr. Katherine Nordal's use of that term in her testimony about the need for a holistic, "mind-body" orientation (and therefore the inclusion of psychologists) when thinking about health-care reform (May Monitor). As Dr. Nordal suggested elsewhere in her remarks, psychologists have demonstrated convincingly that phenomena like hope, expectation, anxiety, etc., can be intimately related to health status and health-care outcomes. It strikes me that use of a term suggesting that psychology is involved primarily with behavior is reductionistic and inaccurate and will only serve to restrict, rather than expand, the public's and the policy-makers' perceptions of our legitimate scope of practice.
William P. Reich, PhD
A lesson in genetics
It is good that Francis Collins will be presenting at APA this year since, if one is to judge by the two errors regarding genetics in May's issue, psychologists are sorely in need of proper education on this topic. First, the "In Brief" section reported that "childhood abuse or neglect alters DNA in the brain." Absolutely wrong. This study reported that childhood abuse altered stress responses through epigenetic changes which do not alter the DNA sequence, but can alter gene expression through various chemical modifications. Altering DNA sequences and epigenetic modification are two radically different mechanisms that cannot be conflated or confused.
Second, although the article on "The Genetic Revolution" correctly reported that 3 billion base pairs had been sequenced in 2003, this sequencing represented only half the human genome (23 chromosomes). It was not until 2007 that the full genome (46 chromosomes, 6 billion based pairs) of a single individual were sequenced.
Robert Eme, PhD
Response from the researcher on the previous letter's first point:
Epigenetic modifications come in two principal forms: modifications to chromatin structure, the proteins associated with the DNA that alter its accessibility to regulatory proteins such as transcription factors, and biochemical modifications to the structure of the DNA itself through DNA methylation. The covalent modification of a cytosine residue by methylation is one of the most stable chemical bonds known. It is precisely this kind of alteration in DNA that our data suggest is modified in the brain as a function of childhood abuse or neglect. Thus, as the methyl groups are part of the DNA itself, the APA Monitor was correct in stating that "childhood abuse or neglect alters DNA in the brain."
We acknowledge that our conclusions are based on samples that differ along a wide range of experiential and potentially genetic dimensions. Our data certainly do not exclude alternative mechanisms of vulnerability. Indeed, the challenge for the future is to understand how epigenetic variation overlaying that occurring in nucleotide sequence might explain the developmental origins of vulnerability for chronic illness. Our data are merely consistent with observations from animal studies investigating epigenetic regulation of the Nr3c1 gene and with the hypothesis that early life events can alter the epigenetic state of relevant genomic regions, the expression of which may contribute to individual differences in the risk for psychopathology.
Patrick McGowan, PhD
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