Born That Way

by William Wright

  He moved quickly to the main complaint: more similar upbringings for identicals than for fraternals. The first study utilized the difficulty, in some cases, in determining zygosity—whether a twin is identical or fraternal. Because this is sometimes outwardly deceptive, a number of twins have, over the years, grown up misdiagnosed. By finding a group of such “false identicals” and comparing them with “real identicals,” researchers could determine whether or not being treated as identicals had any effect on the fraternals. Similarly, by measuring identicals who were mistakenly raised as fraternals—that is, “false fraternals”—researchers were able to determine if the results were consistent with the type of twin they were perceived to be or with the type they actually were. Either way, the twins invariably tested as the kind of twin they actually were, not as the kind they were thought to be.

  Said in another way, if identical twins through some misperception were brought up as fraternals, as adults they tested in I.Q., temperament, personality inventories, and other areas with the same high rate of concordance as identicals, not as fraternals. The opposite was an even more telling refutation of the point. Occasionally, fraternal twins looked as much alike as identicals and were brought up as such. In spite of this misapprehension that existed throughout their childhoods, and receiving the upbringings identical twins receive, as adults they tested as the fraternals they were, with far lower concordances than bona fide identicals.

  Another set of tests cited by Kendler found a number of identical twins who had been brought up to be as similar as possible, whose parents took every opportunity to emphasize their sameness—matching outfits, haircuts, toys—then compared these twins to identicals whose parents made every effort to minimize their sameness. The testers found plenty of both. The opposite upbringing styles had no noticeable effect on the twins’ similarities when measured later in life. Again, the possibility of distorting effects had been sought but not found.

  The different upbringing proposition was tested in still another way. Kendler cited a body of research that examined the possibility that twins highly similar in appearance might elicit different treatment from their environment. This could have an effect on their development and therefore skew efforts to sort out genetic from environmental influence. Here again, test results of high look-alikes were compared with the results of low look-alikes, and there was no appreciable difference between the test scores. An appearance of sameness apparently had no effect on the overall degree of sameness.

  All in all, Kendler cited nine studies that tested for possible bias in identical-fraternal comparisons. All found no validity to the supposed weaknesses in the study design. Also, to avoid any accusations of lax self-policing on the part of the behavioral geneticists—rather like the Justice Department investigating itself to stave off a special prosecutor—Kendler, like any good scientist, laid out the basic data of the earlier studies in great detail and cited the relevant papers.

  In his summary of these heroic efforts on the part of the behavioral geneticists to meet this frequent objection of the environmentalists, Kendler made no mention of the complete substantiation these studies have received from the Minnesota and Swedish reared-apart twin studies, which lack the potential pitfall of different MZ-DZ upbringings in the same home. He laboriously showed that the one complaint has no basis in fact. It would seem to put to rest once and for all this one complaint and force the critics to find different ones.

  This was not to be the case. For more than ten years after Kendler’s paper, opponents continued to cite the possibility of different upbringings given identicals as opposed to fraternals as invalidating twin studies. As late as 1994, the objection was raised in the pages of Scientific American. Sometimes the criticism is not alluded to directly. When other critics referred darkly to the “seriously flawed” nature of twin studies that compared monozygotic with dizygotic twins, more often than not the unnamed flaw turned out to be the one Kendler and others had refuted a decade earlier. And there is no possibility the critics who keep resurrecting this charge are unaware of the refutation. Each time the flaw is cited in print, a weary behavioral geneticist will write a letter to the editor pointing out the research that obviates the complaint, but the critics continue to make it year after year.

  As an outsider, I came into this field believing scientists were simply truth seekers, men and women dedicated to discovering the functioning of the world around them, to understanding the givens. I saw them as driven by profound curiosity. It was, therefore, disheartening for me to learn that many scientists with broad reputations do not place truth at the top of their agendas and react in sadly unscientific ways when confronted with evidence they feel threatens their ideological positions. Aware of the scientific rules, they first attempt to discredit with counterarguments, but when these are shown empirically to be invalid, they simply pretend that the evidence they were unable to shoot down doesn’t exist. Such selective memory permeates the behavioral genetics debate. In the nonscientific world we have a word for such behavior: dishonesty.

  1In 1996 Pope John Paul II softened this position by stating evolution was “more than just a theory.”

  TEN

  THE OTHER END—SEARCHING THE DNA

  IN A SUNNY GROUND-FLOOR LABORATORY in the Clinical Research Building at the University of Pennsylvania, Dani Reed, a young woman who looks a little like Pia Zadora and not much like a postdoctoral research fellow in molecular biology, spends her day extracting DNA from human blood cells, replicating it about a million fold through a process known as the polymerase chain reaction, then “running gels.” This means she separates the nucleic bases that make up the segment of molecule, segregating them by an ingenious process known as electrophoresis. Using the electrical charge in all DNA—as if things weren’t complicated enough—the bases are slowly drawn through a gelled substance (British geneticist Steve Jones has made do with strawberry Jell-O). Because the varying size of the bases causes them to travel at different speeds, the gene fragment is eventually separated and readable.

  I was visiting the laboratory to learn as much as possible about the DNA scanning process, and Dani patiently explained the operation while she worked. At a conference at Cold Spring Harbor some months later, the sponsors hoped to educate the group and allowed us to run gels. The journalist with whom I was paired had done the operation before and grew impatient with the tedious process. His fidgetiness made me think of Dani and the hundreds of others of highly educated people around the globe quietly spending their working days repeating this same operation. For genetic research you clearly need knowledge and the brains to assimilate it, but you also need patience. Lurking within the gel plates with their amplified strands of DNA are nothing less than most of life’s mysteries, perhaps all of them. To many knowledgeable people, these chemicals en gelée are the day’s most important scientific frontier.

  As I was being carried away by the epic significance of it all, Dani showed me a fingertip glob of translucent substance that she said was a few million molecules of the DNA she was examining.

  “That’s what DNA looks like?” I asked.

  “That’s it,” she said happily. “Looks slimy, doesn’t it?”

  The DNA on which Dani and her colleagues were working came from a group of people who were the subjects of a study on obesity. The DNA was being scanned in the hope of finding an irregularity common to the obese, one not found in the DNA of nonobese people. Such a discovery might indicate a gene that causes, or at least contributes to, human obesity. The search required endless DNA scans. Such is the drudgery of gene mapping. Similar work—all of it in search of genes related to behavioral problems like addiction, depression, and violent aggression—is proceeding in at least a hundred laboratories around the world.

  For all the monotony of the work, gene mapping is now the glamour end of the business. When Bouchard, Plomin, Kendler, and all the others devote enormous energy and money to their observational studies, they are basically looking for nu
mbers, for heritability figures. Years of such effort have produced a series of two-digit figures that indicate the mean heritability of a trait. Although these numbers have been powerful enough to turn the field of psychology upside down, they are general mean figures for a population and lack the scientific precision of locating a subinfinitesimal bit of nucleic acid that might condemn an individual to a lifetime of depression, retardation, or obesity.

  A number of considerations go into selecting a trait for a DNA search. Obesity is on the border between physical affliction and behavior, a border that is rapidly disappearing or being made irrelevant by behavioral genetics research such as this. Many might not consider being fat a matter of great medical urgency, certainly not as dire as being afflicted with cystic fibrosis or Huntington’s disease. It is, however, an excellent trait for genetic research in that the condition is easily recognized and diagnosed, unlike traits like depression and alcoholism, which occur in many forms. Obese people, often hating their condition and eager to find a cure, are easily recruited. The ultimate goal is not a cure for obesity, although that would be greatly welcomed, but rather unraveling the mysteries of gene function. The N.I.H.’s Dean Hamer, referring to his 1993 study linking genes and homosexuality, said, “It is likely that finding a ‘gay gene’ will be remembered as a breakthrough not so much for what it explained about sexuality as for opening another door to understanding genetic links to many equally complicated human behaviors and conditions.” Hamer’s point is true of all quests for behavioral genes.

  The director of the University of Pennsylvania obesity study is molecular geneticist Arlen Price, a slender, bearded man in his forties with a soft voice and an academic air. He was the Minnesota Study kibitzer who goaded his graduate school friend Nancy Segal to speed up publishing the twin data. Price has spent ten years researching obesity, four of them mapping DNA, and is optimistic that a recent discovery has brought his goal nearer. “It is not a major breakthrough,” he told me when I visited his office, “but it’s the kind of development that keeps us coming to work every day.”

  In November 1994, Price and his group feared they were scooped when a group at New York’s Rockefeller Institute, also engaged in obesity research, announced that they had found a gene in mice that was directly tied to obesity. The gene underlies a signaling mechanism that tells the mouse’s brain when enough food has been eaten. After a mouse consumes enough food, the gene, when working properly, initiates a biochemical chain of events that culminates in the brain’s telling the mouse he is no longer hungry, to stop eating. In certain mice this gene does not function, and the result is obesity. The Rockefeller group had reason to believe that in humans the same gene might malfunction in the same way. (It was later found that the human version of the gene did not commonly have mutations similar to those in mice, dashing hopes for an obesity cure and leaving the field open to Price and his team. The animal-human parlay sometimes pays off, sometimes not.)

  In their work with human DNA, Price and his team had already been zeroing in on the same genetic region as the Rockefeller people. In a model of scientific cooperation, the two groups immediately began trading information, vastly speeding up the progress of both. By December 1994, the University of Pennsylvania team was ready to announce that it had reached an intermediate finish line: They had linked the gene but could not demonstrate its role in creating human obesity.

  Price is an example of the new breed of crossover behavioral scientist. Since his student days, he has shuttled between psychology and molecular biology, before those disciplines drew as close as they are now. He began his academic career in the sixties as a biochemist, then switched to psychology and obtained his Ph.D. at the University of Colorado. When the Jensen controversy erupted in 1969, Price was troubled by science’s failure to answer definitively such fundamental questions as whether or not I.Q. was genetically based. He wondered if there might be a way to establish, with this or any trait, a genetic component that would be beyond argument, a DNA proof of some sort. He saw the unfairness of the attacks on twin and adoption studies and watched in dismay as these painstaking efforts were shot down by armchair critics, environmentalists like Leon Kamin who comb the data in search of potential flaws with which to discredit the findings or at least spread debilitating doubt.

  Seeing how easy it was for the opponents of behavioral genetics to wound the most cautious studies, not by counterresearch, but by ad hoc sniping, Price despaired of the observational studies’ ever satisfying the critics’ objections, yet he remained convinced of a genes-behavior link. He decided he did not want to devote his life to devising ever more ingenious ways to plug possible holes, to knock himself out anticipating every conceivable vulnerability. He knew that even if such airtight studies could be created, the opponents would still claim to have found holes. After working in the field for a time, he sadly acknowledged that with behavioral genetics, as much energy had to be spent defending data as producing it. Convinced the observational studies would never be free from attacks, he made the switch to molecular biology, first by doing postdoctoral research at Stanford with eminent population geneticist Luca Cavalli-Sforza, by working on DNA-behavioral research with Kenneth Kidd at Yale, and then by starting a molecular laboratory at the University of Pennsylvania.

  “I saw the whole thing continually collapsing into unresolvable arguments, so I grew envious of the molecular biologists down the hall, the people who worked with concrete experiments cloning genes, not as hypothetical elements, but as sequences of bases. I liked that their work was not controversial.”

  The wistfulness Price felt about hard science is not uncommon among those toiling in the soft terrain of psychology and sociology. There is even a term for the condition, “physics envy,” which describes the feelings of all those who wish their observations could be codified into the numbers and formulae physicists use to record their discoveries. In fact, psychologists, in particular behavioral geneticists, have taken to their own brand of formula—rather like fortifying their conclusions with the chain mail of hard science. These highly complex constructions of letters and numbers that occasionally erupt in psychological papers can be daunting even to those with long experience in the field. But not everyone takes them seriously. An eminent psychologist, an elderly German, was asked how he dealt with these intricate environment-genetics formulae when he encountered them in a text. His face lit up and he said, “I hum them.”

  But instead of aping the hard-science vernacular in presenting their observation data, more and more behavioral geneticists were, like Price, jumping onto the hard-science bandwagon made available by the advances in molecular genetics. They are examining the DNA itself in an effort to isolate anomalies that can be positively identified as at least a contributing cause of specific human traits and idiosyncrasies. Neurobiologist Simon LeVay’s image for the two approaches to behavioral genes has it that traditional approaches with twins and adoptees are looking at behavior “from the top down,” while molecular biologists are tracking it from “the bottom up.”

  To many in the field, pinpointing the specific DNA for a behavior is the Holy Grail of behavioral genetics and a reason why more and more psychologists are lured to the molecular end of the quest. Finding a specific gene for a specific behavior would mean that after twenty years of circumstantial evidence from the observational studies—not to mention the two thousand years of casual observation of family traits and animal-breeding techniques—hard proof of a genes-behavior link would finally be on the table.

  Finding and implicating specific genes would not, however, signal the ultimate untangling of the human-behavior enigma. As Thomas Bouchard said, “We know that genes make proteins, but that is many biochemical steps away from behavior. What lies in between is pretty much a mystery.” Since Bouchard made the remark in 1992, significant advances have been made in understanding what lies “in between,” but there is still much that is not yet understood. A lot of research under way is aimed at understanding the
biological mechanisms that translate chemicals into behavior. With the combined efforts of biochemists, molecular biologists, and behavioral geneticists, advances are rapid. Together they are prying open the secrets of what they reverentially refer to as “the black box.”

  Although much still has to be learned, there is no doubt that pinpointing specific genes for specific behaviors is an important next step in unraveling the gene-behavior mystery. In addition to representing a giant leap forward in scientific understanding, the incontrovertible locating of specific behavioral genes—whose functions have been established, the experiments replicated, and the DNA sequenced—would force the consideration of genetic elements in all behaviors. With luck, it would go far toward silencing the obstructive heckling from the environmentalists. Because this is a totally different method of exploring the gene-behavior connection, the genephobic environmentalists will have to come up with an entirely new battery of “flaws.”

  BEFORE DELVING INTO the methods for locating behavioral genes, it is helpful to have some understanding of human DNA, the decade’s scientific superstar. Books on genetics aimed at the general reader invariably have a brief course on DNA, including such fundamentals as the arrangement of genes along a chromosome, the way in which cells divide, and the way DNA replicates itself. When I began seriously investigating the field, I became somewhat of a connoisseur of these primers and came to appreciate the authors’ valiant efforts to make the process appear, if not simple, at least straightforward and accessible. The sad truth is that it is of a complexity to daunt the most intrepid intellect and at the same time strike a reverential awe for nature into the most blasé and thrill-weary.

  To have a comprehensive understanding of the present state of the science, one would need a solid grasp of molecular biology and biochemistry. A good grounding in physics would come in handy as well. As the miracle of it all unfolds, it might be a good idea to have some theology at the ready, if for no other reason than to stave off the inevitable question of how any process so magnificently intricate could come into existence. Actually, for this you only need a solid understanding of Darwin’s principles, followed up by a reading of Stephen Jay Gould and Richard Dawkins, two reigning evolutionary theorists, who disagree on some points, but who are both masterful at clarifying the knotty ramifications of Darwin’s simple but profound insight. Dawkins is particularly good at making plausible such complex evolutionary products as a bat’s night-flying ability, and he does so without postulating a deity who fancied having a creature around who could fly in the dark without bumping into things.