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← In the Realm of Hungry Ghosts Close Encounters with Addiction

In the Realm of Hungry Ghosts Close Encounters with Addiction Chapter 19. It’s Not in the Genes

Author: Gabor Mate Publisher: Berkeley, CA: North Atlantic Books. Publish Date: 2010-1-5 Review Date: Status:📚

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Why, then, are narrow genetic assumptions so widely accepted and, in particular, so enthusiastically embraced by the media? The neglect of developmental science is one factor. Our preference for a simple and quickly understood explanation is another, as is our tendency to look for one-to-one causations for almost everything. Life in its wondrous complexity does not conform to such easy reductions.
There is a psychological fact that, I believe, provides a powerful incentive for people to cling to genetic theories. We human beings don’t like feeling responsible: as individuals for our own actions; as parents for our children’s hurts; or as a society for our many failings. Genetics—that neutral, impassive, impersonal handmaiden of Nature—would absolve us of responsibility and of its ominous shadow, guilt. If genetics ruled our fate, we would not need to blame ourselves or anyone else. Genetic explanations get us off the hook. The possibility does not occur to us that we can accept or assign responsibility without taking on the useless baggage of guilt or blame.
More daunting for those who hope for scientific and social progress, the genetic argument is easily used to justify all kinds of inequalities and injustices that are otherwise hard to defend. It serves a deeply conservative function: if a phenomenon like addiction is determined mostly by biological heredity, we are spared from having to look at how our social environment supports, or does not support, the parents of young children and at how social attitudes, prejudices, and policies burden, stress, and exclude certain segments of the population and thereby increase their propensity for addiction. The writer Louis Menand said it well in a New Yorker article:

“It’s all in the genes”: an explanation for the way things are that does not threaten the way things are. Why should someone feel unhappy or engage in antisocial behavior when that person is living in the freest and most prosperous nation on earth? It can’t be the system! There must be a flaw in the wiring somewhere.24
Succumbing to the common human urge to absolve ourselves of responsibility, our culture has too avidly embraced genetic fundamentalism. That leaves us far less empowered to deal either actively or proactively with the tragedy of addiction. We ignore the good news that nothing is irrevocably dictated by our genes and that, therefore, there is much we can do.

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In 1990, newspapers and broadcast outlets across North America reported that researchers at the University of Texas had identified the gene for alcoholism. This news was greeted with tremendous interest, and the major media waxed enthusiastic with pronouncements about the imminent end of alcoholism. Time magazine was among the foremost cheerleaders:

The benefits from this line of research may be huge. In five years, scientists should have perfected a blood test for the gene, to help spot children at risk. And within a decade, doctors may have in hand a drug that either blocks the gene’s action or controls some forms of alcoholism by altering the absorption of dopamine. Eventually, with genetic engineering, experts may find a way to eliminate altogether the suspect gene from affected individuals.1

The researchers in question had never made the claim that they had discovered the “alcoholism gene,” but they came close to making it. Some of their public statements fed that mistaken impression. Six years later the lead scientist, pharmacologist Kenneth Blum, published a much more subdued assessment:

Unfortunately it was erroneously reported that [we] had found the “alcoholism gene,” implying that there was a one-to-one relation between a gene and a specific behavior. Such misinterpretations are common—readers may recall accounts of an “obesity gene,” or a “personality gene.” Needless to say, there is no such thing as a specific gene for alcoholism, obesity, or a particular type of personality.… Rather the issue at hand is to understand how certain genes and behavioral traits

  1. Kenneth Blum et al., “Reward Deficiency Syndrome,” American Scientist, March 1, 1996, 132–46. Italics are mine.

  2. Time, April 30, 1990; http://www.time.com/time/magazine/article/0,9171,969965,_00.html.

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What the Texas group had located was a variation of the dopamine receptor gene (DRD2) that appears more commonly among alcoholics than nonalcoholics and “confers susceptibility to at least one form of alcoholism”—or so they thought after examining the brains of a few dozen corpses.3 Even this more modest hypothesis, however, failed to stand up to future investigation. Subsequent studies were unable to confirm any association between the gene variant and alcoholism.4 “The most important finding of research into a genetic role for alcoholism is that there is no such thing as a gene for alcoholism,” writes the addiction specialist Lance Dodes. “Nor can you directly inherit alcoholism.”5

  1. Kenneth Blum, “Allelic Association of Human Dopamine D2 Receptor Gene in Alcoholism,” Journal of the American Medical Association 263(15) (April 18, 1990): 2055–60.

  2. J. Gelernter and H. Kranzler, “D2 Dopamine Receptor Gene (DRD2) Allele and Haplotype Frequencies and Control Subjects: No Association with Phenotype or Severity of Phenotype,” Neurospsychopharmacology 20(6) (1999): 642–49.

  3. Lance Dodes, The Heart of Addiction (New York: HarperCollins, 2002), 81.

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Whatever problem we are hoping to resolve or prevent—be it war, terrorism, economic inequality, a marriage in trouble, climate change, or addiction—the way we see its origins will largely determine our course of action. I present the case that the early environment plays a major role in a person’s vulnerability to addiction not to exclude genetics but to counter what I see as an imbalance. Genes certainly appear to influence, among other features, such traits as temperament and sensitivity. These, in turn, have a huge impact on how we experience our environment. In the real world there is no nature versus nurture argument, only an infinitely complex and moment-by-moment interaction between genetic and environmental effects. For this reason, as two psychiatrists at the University of Pittsburgh School of Medicine have pointed out, “the liability trait for alcoholism is not static.” Owing to developmental and environmental factors, “the risk of alcoholism fluctuates over time.”6 Even if, against all available evidence, it were demonstrated conclusively that 70 percent of addiction is programmed by our DNA, I would still be more interested in the remaining 30 percent. After all, we cannot change our genetic makeup, and at this point, ideas of gene therapies to change human behaviors are fantasies at best. It makes sense to focus on what we can immediately affect: how children are raised, what social support parenting receives, how we handle adolescent drug users, and how we treat addicted adults.

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The current consensus—among those who accept a high degree of hereditary causation for alcoholism—is that predisposition to the disorder is about 50 percent genetically determined.7 Equally extravagant estimates are applied to other addictions. Heavy marijuana use is said to be 60 to 80 percent heritable,8 while the inherited liability to long-term heavy nicotine use has been calculated to be an astonishing 70 percent.9 Cocaine abuse and dependence are also reported to be “substantially influenced by genetic factors.”10 Some researchers have even suggested that alcoholism and divorce may share the same genetic propensity. Such high figures are beyond possibility. The logic behind them rests on mistaken assumptions that owe less to science than to an exaggerated belief in the power of genes to determine our lives. In genetic theories of mental disorders, “unscientific beliefs play a major role,” write the authors of a research review.11

  1. M. A. Enoch and D. Goldman, “The Genetics of Alcoholism and Alcohol Abuse,” Current Psychiatry Reports 3 (2002): 144–51.

  2. K. S. Kendler and C. A. Prescott, “Cannabis Use, Abuse, and Dependence in a Population-Based Sample of Female Twins,” American Journal of Psychiatry 155 (1998): 1016–22.

  3. S. W. Lin and R. M. Anthenelli, “Genetic Factors in the Risk for Substance Use Disorders,” chap. 4 in Substance Abuse: A Comprehensive Textbook, by Joyce H. Lowinson et al. (Philadelphia: Lippincott, Williams, & Wilkins, 2005), 39.

  4. K. S. Kendler and C. A. Prescott, “Cocaine Use, Abuse, and Dependence in a Population Sample of Female Twins,” British Journal of Psychiatry 173 (1998): 345–50.

  5. J. S. Alper and J. Beckwith, “Genetic Fatalism and Social Policy: The Implications of Behavior Genetics Research,” Yale Journal of Biology and Medicine 66(6) (November–December 1993): 511–24.

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It’s not that genes do not matter—they certainly do. It’s only that they do not and cannot determine even simple behaviors, let alone complex ones like addiction. Not only is there no addiction gene, there couldn’t be one. Until recently it was thought that there were one hundred thousand genes in the human genome. Even that number would have been inadequate to account for the unbelievable synaptic complexity and variability of the human brain.12 However, it has now been discovered that there are only about thirty thousand gene sequences in our DNA—even less than in some lowly worms. “Our DNA is simply too paltry to spell out the wiring diagram for the human brain,” writes UCLA research psychiatrist Jeffrey Schwartz.13 Far from being the autonomous dictators of our destinies, genes are controlled by their environment, and without environmental signals they could not function. In effect, they are turned on and off by the environment; human life could not exist if it weren’t so. Every cell in every organ in our bodies has exactly the same complement of genes, yet a brain cell does not look or act like a bone cell, and a liver cell does not resemble or function like a muscle cell. It is the environment within and outside the body that determines which genes are switched on, or activated, in which cell. “The cell’s operations are primarily molded by its interaction with the environment, not by its genetic code,” the cell biologist Bruce Lipton has written.14

  1. “The number of synaptic contacts in the human cerebral cortex is staggeringly high,” writes Peter Huttenlocher, a neuroscientist at the University of Chicago. “It is clear that this large number cannot be determined by a genetic program, in which each synapse has an exact assigned location. More likely, only the general outlines of basic connectivity are genetically determined.” In Kurt W. Dawson and Geraldine Fischer, eds., Human Behavior and the Developing Brain (New York: Guildford Press, 1994), 138.

  2. Jeffrey M. Schwartz and Sharon Begley, The Mind and the Brain: Neuroplasticity and the Power of Mental Force (New York: ReganBooks, 2002), 112.

  3. Bruce Lipton, The Biology of Belief (Santa Rosa, CA: Elite Books, 2005), 86.

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There is a new and rapidly growing science that focuses on how life experiences influence the function of genes. It’s called epigenetics. As a result of life events, chemicals attach themselves to DNA and direct gene activities. The licking of a rat pup by the mother in the early hours of life turns on a gene in the brain that helps protect the animal from being overwhelmed by stress even as an adult. In rats deprived of such grooming, the same gene remains dormant. Epigenetic effects are most powerful during early development and have now been shown to be transmittable from one generation to the next, without any change in the genes themselves.15 Environmentally induced epigenetic influences powerfully modulate genetic ones. How a gene acts is called gene expression. It is now clear that “the early environment, consisting of both the prenatal and postnatal periods, has a profound effect on gene expression and adult patterns of behavior,” to quote a recent article from the Journal of Neuroscience.16 One example is related to alcohol consumption. A certain variation of a particular gene, found in some monkeys, reduces alcohol’s sedative effects and also its disorganizing and unpleasant influence on balance and coordination. In other words, monkeys with this gene are less likely to feel semicomatose from drinking and less likely to lurch about like drunken sailors. They have the capacity to imbibe greater amounts of alcohol without side effects and are more likely to drink until they’re drunk. However, it was found that in mother-reared monkeys the gene was not expressed—that is, it had no impact on drinking behavior. It did so only in monkeys who had been stressed in early life by being deprived of maternal contact and reared among peers.17

  1. M. J. Meaney, “Maternal Care, Gene Expression, and the Transmission of Individual Differences in Stress Reactivity across Generations,” Annual Review of Neuroscience 24 (2001): 1161–92.

  2. C. S. Barr, “Serotonin Transporter Gene Variation Is Associated with Alcohol Sensitivity in Rhesus Macaques Exposed to Early-Life Stress,” Alcoholism: Clinical and Experimental Research 27(5) (May 2003): 812–17.

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Numerous studies in both animals and humans have found that maternal stress or anxiety during pregnancy can lead to a broad range of problems in the offspring, from infantile colic to later learning difficulties19 and the establishment of behavioral and emotional patterns that increase a person’s predilection for addiction. Stress on the mother would result in higher levels of cortisol reaching the baby; and, as already mentioned, chronically elevated cortisol is harmful to important brain structures especially during periods of rapid brain development. A recent British study, for example, found that children whose mothers were stressed during pregnancy are vulnerable to mental and behavioral problems like attention deficit/hyperactivity disorder (ADHD) or to being anxious or fearful. (ADHD and anxiety are powerful risk factors for addiction.) “Professor Yvette Glover of Imperial College London found stress caused by rows with or violence by a partner was particularly damaging,” noted a BBC report. “Experts blame high levels of the stress hormone cortisol crossing the placenta. Professor Glover found high cortisol in the amniotic fluid bathing the baby in the womb tallied with the damage.”20 The study’s results are consistent with previous evidence that stress on the mother during pregnancy affects the brain of the infant, with long-term and perhaps permanent effects.21 This is where the father comes in, because the quality of the relationship with her partner is often a woman’s best protection from stress or, on the other hand, the greatest source of it.

  1. P. Zelkowitz and A. Papageorgiou, “Maternal Anxiety: An Emerging Prognostic Factor in Neonatology,” Acta Paediatr 94(12) (December 2005): 1771–76; C. Sondergaard et al., “Psychosocial Distress during Pregnancy and the Risk of Infantile Colic: A Follow-Up Study,” Acta Paediatr 92(7) (July 2003): 811–16. These are only two examples. The list of animal and human studies on this topic easily extends into the hundreds.

  2. http://news.bbc.co.uk/2/hi/health/6298909.stm.

  3. J. R. Seckl, “Prenatal Glucocorticoids and Long-Term Programming,” European Journal of Endocrinology 151(Suppl 3) (2004): U49–U62, quoted in R. Yehuda et al., “Transgenerational Effects of Post-traumatic Stress Disorder in Babies of Mothers Exposed to the World Trade Center Attacks during Pregnancy,” Journal of Clinical Endocrinology and Metabolism 90(7): 4115–18.

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So the fact that the stage of pregnancy a woman was at when the tragedy occurred was correlated with the degree of cortisol abnormality suggests that we are looking at an in utero effect.22 It turns out that during gestation, just as after birth, brain systems undergo sensitive periods of development.

  1. R. Yehuda et al., “Transgenerational Effects of Post-traumatic Stress Disorder in Babies of Mothers Exposed to the World Trade Center Attacks during Pregnancy,” Journal of Clinical Endocrinology and Metabolism 90(7): 4115–18.

  2. K. H. DeTurck and L. A. Pohorecky, “Ethanol Sensitivity in Rats: Effect of Prenatal Stress,” Physiological Behavior 40 (1987): 407–10; L. A. Pohorecky, “Interaction of Ethanol and Stress: Research with Experimental Animals; An Update,” Alcohol and Alcoholism 25(2/3) (1990): 263–76.

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It has been demonstrated that both animals and humans who experienced the stress of their mothers during pregnancy are more likely to have disturbed stress-control mechanisms long after birth, which creates a risk factor for addiction. Maternal stress during pregnancy can, for example, increase the offspring’s sensitivity to alcohol.23 As mentioned, a relative scarcity of dopamine receptors also elevates the addiction risk. “We’ve done work, and a lot of other people have done work, showing that essentially the number and density of dopamine receptors in these receptive areas is determined in utero,” psychiatric researcher Dr. Bruce Perry told me in an interview.

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For these reasons, adoption studies cannot decide questions of generic inheritance. Any woman who has to give up her baby for adoption is, by definition, a stressed woman. She is stressed not just because she knows she’ll be separated from her baby but primarily because if she wasn’t stressed in the first place, she would never have had to consider giving up her child: the pregnancy was unwanted or the mother was poor, single, or in a bad relationship; or she was an immature teenager who conceived involuntarily or was a drug user or was raped or confronted by some other adversity. Any of these situations would be enough to impose tremendous stress on any person, and so for many months the developing fetus would be exposed to high cortisol levels through the placenta. A proclivity for addiction is one possible consequence.

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It is commonly assumed, with no scientific basis, that if a condition “runs in a family,” appearing in successive generations, it must be genetic. Yet as we have seen, for example with my Downtown Eastside patients, pre- and postnatal environments can be recreated from one generation to the next in a way that would impair a child’s healthy development without any genetic contribution. Parenting styles are often inherited epigenetically—that is, passed on biologically, but not through DNA transmission from parent to child.

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