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Lock - Eclipse

Lock - Eclipse

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Eclipse of the Gene and the Return of DivinationAuthor(s): Margaret LockSource:
Current Anthropology,
Vol. 46, No. S5 (December 2005), pp. S47-S70Published by:
on behalf of
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S
47
Current Anthropology
Volume
46
, Supplement, December
2005
2005
by The Wenner-Gren Foundation for Anthropological Research. All rights reserved
0011-3204/2005/4605S5-0003$10.00
Eclipse of the Geneand the Return ofDivination
1
by Margaret Lock
Research in the field of epigenetics challenges the assumption onwhich the molecular genetics of the past
50
years has beenbased, namely, genetic determinism. This paper reviews the so-cial science literature that considers the social effects of the ap-plication of molecular genetics and genetic testing in connectionwith Mendelian conditions. It is argued that anthropologistsmust now go farther and respond to the challenge posed by cur-rent moves toward the implementation of genetic profiling andtesting for susceptibility genes. Following a discussion of onto-logical problems associated with molecular genetics raised byphilosophers and biologists who subscribe to epigenetics, currentknowledge about molecular and population genetics of late-onsetAlzheimer’s disease and cross-cultural findings about the epide-miology of this disease are introduced. These findings illustratethe provisional nature of these bodies of knowledge and the com-plexity associated with susceptibility genes, which makes esti-mations of probabilities of individual risk unrealistic. A con-trolled clinical trial is discussed in which first-degree relatives ofAlzheimer’s disease patients are genotyped for risk for late-onsetAlzheimer’s disease. In conclusion, the social implications oftesting for susceptibility genes are discussed, with commentsabout the role that anthropologists might play in future research.
margaret lock
is Marjorie Bronfman Professor of SocialStudies in Medicine at McGill University (
3647
Peel St., Mon-treal, Quebec, Canada H
3
A
1
X
1
[margaret.lock@mcgill.ca]). Bornin
1936
, she was educated at the University of California, Berke-ley (Ph.D.,
1976
). Her research interests include medical anthro-pology, the anthropology of biomedical technologies, and the an-thropology of genomics. Her publications include
Encounterswith Aging: Mythologies of Menopause in Japan and NorthAmerica
(Berkeley: University of California Press,
1993
),
TwiceDead: Organ Transplants and the Reinvention of Death
(Berke-ley: University of California Press,
2002
), and (edited with SarahFranklin)
Remaking Life and Death: Towards an Anthropology of the Biosciences
(Santa Fe: School of American Research,
2003
).The present paper was submitted
6 x 04
and accepted
2 ii 05
.
1.
Funding for this research was provided by the Social Sciencesand Humanities Research Council of Canada (SSHRC) grant #
205806
.
When mapping the human genome, the scientists in-volved set aside approximately
98
% of the DNA theyhad isolated, labeling it as “junk” because it did not con-form to their idea of how the blueprint for life worked.In the short time since the announcement in early
2001
that the Human Genome Project was more or less com-plete, things have changed dramatically, and “junkDNA, thrust summarily to one side in order to focus onthe task of mapping only those genes that code directlyfor proteins, can no longer be ignored. A
2003
article in
Scientific American
notes that “new evidence. . . con-tradicts conventional notions that genes. . . are the solemainspring of heredity and the complete blueprint forall life. Much as dark matter influences the fate of gal-axies, dark parts of the genome exert control over thedevelopment and the distinctive traits of all organisms,from bacteria to humans” (Gibbs
2003
:
48
). The articlecontinues: “Some scientists now suspect that much ofwhat makes one person, and one species, different fromthe next are variations in the gems hidden within our’junk’ DNA.” This junk produces largelyRNA
2
thatdoesnot code for protein production but, even so, is deeplyimplicatedingeneexpressionandregulationandsomustnow be sifted through (Eddy
2001
; Mattick
2003
,
2004
).The result is that we have entered an era, almost over-night, in which the “dark” parts of the genome are start-ing to fluoresce.The activities of noncoding RNA are believed to com-prise the most comprehensive regulatorysystemincom-plex organisms, a system that functions to create the“architecture” of organisms without which chaos wouldreign (Mattick
2003
). To this end, noncoding RNA hasbeen shown to have a profound effect on the timing ofprocessesthatoccurduringdevelopment,includingstemcell maintenance, cell proliferation, apoptosis (pro-grammed cell death), and the occurrence of cancer andother complex ailments (Petronius
2001
). Consequently,the research interests of molecular biology are no longerconfined largely to mapping structurebuthaveexpandedto unraveling the mechanisms of cell and organ functionthrough time. Central to this endeavor is to understandgene regulation—above all how and under what circum-stances genes are switched on and off.
3
In the rapidlydeveloping science known as epigenetics, organizedcomplexity is recognized and activities of the cell,ratherthan simply those of genes, are the primary target ofinvestigation, although the effects of evolutionary, his-torical, and environmental variables on cellular activity,developmental processes, health, and disease are freelyacknowledged.
2.
During the latter part of the twentieth century, molecular ge-netics was primarily concerned with the interrelationshipbetweenthe macromolecules of DNA (deoxyribonucleic acid) and RNA (ri-bonucleic acid) and how these molecules synthesize polypeptides,the basic components of all proteins. Only in the past few yearshas attention been turned to the numerous critical activities ofRNA that are not directly involved with protein production.
3.
The importance of gene regulation was first noted by Jacob andMonod (
1961
), but the mapping of DNA structure was givenpriority.
 
S
48
F
current anthropology
Volume
46 
, Supplement, December
2005
This emerging knowledge has exploded the centraldogma on which molecular genetics was founded. Themetaphors associated with the mapping of the humangenome—the Book of Life, the Code of Codes, the HolyGrail, and so on—are entirely outmoded. The result isthat gene fetishism, never embraced wholeheartedly byall the scientists involved (see Berg
1991
and Davis
1990
,to name just two), is now clearly on the wane amongmany (perhaps the majority of) experts, and this declineis hastened by the undeniable fact that genomic “deliv-erables” are as yet few and far between. Only one newdrug the development of which was based on informa-tionobtainedfromgenomicswasmarketedin
2003
(Dut-ton
2003
; see also Angell
2004
).In this paper I want first to consider very briefly therise and fall of the genotype/phenotype dogma—a posi-tion that increasingly appears as an aberration in thehistory of genetics (Fox Keller
2000
, Rheinberger
2000
a
).Thiswillbefollowedbyabriefoverviewofsocialsciencecommentaryonperceivedindividual,familial,andsocialeffects of the application of the molecularized geneticsassociated with the dogma. The epigeneticapproachthatrejectsthedogmawillthenbediscussed.Itwillbearguedthat, despite a shift of attention on the part of numerousresearchers away from genes to cells and organisms,manybasicscientists,eventhoughtheyareemphaticallyopposed to genetic determinism, nevertheless embracea form of neoreductionism in which virtuallyeverythingexternal to the material body remains black-boxed.In the second half of the paper, a movement towardthe routinization of genetic testing for susceptibilitygenes associated with complex diseases will be exam-ined, using late-onset Alzheimer’s disease as an illustra-tive example. This section will highlight an apparentcontradictioninconnectionwiththistesting.Ontheonehand, given the current state of scientific knowledge,predictions about being at increased risk for complex,adult-onset neurological disease based on the presenceof a specific susceptibility gene
4
in one’s genotype areno more accurate than fortune-telling. Such calculationsare what Ulrich Beck describes as “risks that cannot beknown” (quoted in Yates
2003
:
96
). In other words, forindividuals to be told that they have one or more genesthat
may 
put them at an increased risk for a disease suchas Alzheimer’s under circumstances that are very poorlyunderstood can hardly be counted as prescient knowl-
4.
Many genes are polymorphic and have a number of variationsthat are widespread in the human population. Those allelic varia-tions that have been associatedwithan increasedriskofdevelopingnamed disorders are known as “susceptibility genes.” Such genevariants are neither necessary nor sufficient to cause specific dis-eases. However, compared with the population at large, an indi-vidual who carries one and especially two copies of such alleles isbelieved to have an increased risk of contracting the relevant dis-ease. Even so, people with two copies of a susceptibility gene maynot get the disease, indicating that other, as yet unidentifiedfactorsare involved. The gene that causes Huntington’s disease, an adult-onset neurological disease, is not a susceptibility gene but an au-tosomal dominant, Mendelian-type gene in which accurate predic-tions can be made about disease susceptibility based on genetictesting.
edge upon which people should act. On the other hand,if scientific knowledge about human molecular gen-omics, proteomics, and epigenetics is to make headway,particularly in connection with preventive medicineandpharmacogenetics, then researchers must procure DNAsamples from thousands of volunteer subjects. This isalready taking place in clinics around the world whenpatientsagree, with “informedconsent,”todonatebloodthat is then anonymized for use in basic-science re-search. Any right to be given test results is relinquishedin such a situation, and individuals are told that theirbloodsampleswillnotproduceknowledgethatwillhaveany direct effect on their own clinical care.However,thelong-term goal of such research is inevitably to createfindings that will eventually be of relevance for theclinic. Although most researchers believe that we havenot yet reached a point where such profiling should becarried out routinely, it is likely that in the not-too-dis-tant future patients will be made aware of their genomicprofiles as part of basic clinical care (Brice
2004
). Fur-thermore, some researchers argue that, among patientswith, for example, Alzheimer’s disease, responses tomedication will increasingly be shown to be dependentupon genotype, adding further incentive to genotype pa-tients, their families, and eventually the public at large.How might this tension be resolved as genomic pro-filing becomes increasingly routinized? Should such ge-netictestingbelimitedtotheworldofresearch,inwhichcase individuals would not be made aware of their ge-notype until such time as they actually became sick,when, possibly, such knowledge might be of relevancefor their care? Or should patients routinely be tested andreceive information about susceptibility genes as part ofbasic medical care prior to the onset of sickness, in thesame way as we are already informed about cholesterollevels, blood pressure, and the results of prostate-spe-cific-antigens (PSA) tests?
5
Even though informationabout susceptibility genes is inevitably subject to mis-understanding (some would insist that this is “disinfor-mation”), it is often argued that people have a “right toknow” about their genomes and that if they are madeaware that their genetic profiles place them at risk theymay be better motivated to practice prevention. How-ever, accumulating evidence in molecular genetics sug-gests that we may never be able to calculate risk esti-mates in connection with susceptibility genes that aremeaningful predictors of future probabilities (Moss
2003
).Recognition of discontinuities and ruptures acrossknowledge domains is crucial in coming to grips withthis predicament. Genes may no longer be conceptual-ized as deterministic by the majority of researchers, butsweeping claims continue to be made—by evolutionarypsychologists and evolutionary psychiatrists, for exam-ple—about causal relationships between genes and be-havior. We would do well to understand the extent towhich basic scientists, clinicians, patients, families, ad-vocacy groups, and the public are captivated by genetic
5.
The PSA test is used to detect early signs of prostate cancer.

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