Sapolsky (2005) presents us with research which demonstrates the importance of the environment in gene expression. Genes, stretches of DNA, do not code for behaviors, hallucinations or delusions. They code for proteins and some of these proteins certainly are related to how we think, feel and act. Neurotransmitters, neurohormones, receptors, enzymes, intracellular messengers, etc., are all made of proteins. However, it is rare that such molecules cause a particular behavior. Rather, they produce tendencies to react to particular environments in particular ways. Sapolsky uses the subject of anxiety to illustrate this: neurotransmitters and genes do not make you anxious-they make you more sensitive to anxiety-provoking situations and may make it more difficult to detect safety signals within those environments. Genetic status, in many of the psychiatric disorders, is not all that predictive in and of itself. The biological factors coded for by genes do not typically determine behavior, rather they influence responsiveness to environmental influences. In our field we are often dealing with genetic vulnerabilities and biases, not genetic inevitabilities.

It is important to note that there are long stretches of DNA, perhaps 95% of our DNA, which do not get transcribed. Some of this noncoding DNA-regulatory elements, promoters, repressors, responsive elements- is used as an instructional manual for how and when to activate genes. Often, it is the environment which regulates this genetic activity. On another level of complexity, the environments which we generate as individuals and as a cultural group, can change the pattern of gene activity in oneself and within other individuals. Genes can be viewed as convenient tools which are used by environmental factors to influence behaviors. In addition, there is a significant degree of variability in DNA sequences among individuals and it is the noncoding regions of DNA which contain the greater share of this variability. Therefore, evolution can productively be viewed as a process of natural selection for different genetic sensitivities and reactions to environmental influences.

A research study by Crabbe et al (1999-“Genetics of mouse behavior: Interactions with laboratory environments.” Science 284:1670), using genetically similar mice raised in virtually identical environments across multiple labs, demonstrated that the environment, even a subtle change in one, can contribute more to certain behaviors than genes. Francis et al (2003 -“Epigenetic sources of behavioral differences in mice” Nature Neuroscience 6:445) examined two strains of mice, relaxed and timid. Relaxed strain mice raised by timid mothers grew up to be relaxed. However, the researchers implanted fertilized relaxed-strain eggs into timid-strain females as well as relaxed-strain females who carried them to term. After birth, some of the relaxed-strain pups were raised by timid-strain mothers as well as some others were raised by relaxed-strain mothers. The relaxed-strain pups carried to term and raised by timid-strain mothers, became just as timid as any other timid-strain ones. Prenatal environments were deemed of importance. Relaxed-strain mice are relaxed not only because of their genes, but also because of their fetal and postnatal environments. Rampon et al (2000- “Enrichment induces structural changes and recovery from nonspatial memory deficits in CA1 NMDAR 1-knockout mice,” Nature Neuroscience 3:238) generated a ‘knockout’ mouse that lacked a key gene relevant to a neurotransmitter system which coded for a receptor for that neurotransmitter system in a key area of the brain critical to learning and memory. As a result, these mice had various learning problems. The researchers placed these learning impaired mice, as adults, in an enriched environment. The result was that this environment corrected for some of the genetically based learning deficits. Sapolsky (2005), in commenting on this research, noted: “This was a massive genetic defect, the complete obliteration of a critical gene in a part of the brain vital to learning and memory. And the right sort of stimulating environment could correct it” (p.54).

Caspi et al (2003- “Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene,” Science 301: 386) followed more than a thousand New Zealand children into adulthood in order to assess rates of clinical depression. They examined the serotonin transporter gene-5-HTT- and its two variants. One variant of the 5-HTT gene only in a particular environment can increase the rates of clinical depression: an environment characterized by major stress, trauma, loss, separations, etc. Another research team (this one in Warburg, Germany) demonstrated that stress hormones regulate the activity of the gene for 5-HTT (Glatz et al “Glucocorticoid-regulated human serotonin transporter (5-HTT) expression is modulated by the 5-HTT gene-promoter-linked polymorphic region,” Journal of Neurochemistry, 86 (2003):1,072).

Sapolsky (2005), in considering the lessons from the above research studies, concluded:

“Obviously, beware of simple explanations; it is rare that nature is parsimonious.... Sometimes genetics is about inevitability-if you have the gene for Huntington’s disease...there’s a 100 percent chance you’re going to have this awful neurological disease by middle age. But in far more realms than people usually expect, genes are about vulnerabilities and potentials, rather than about destiny.

And out of that comes a social imperative-genes do indeed seem to play a role in some of our less desirable behaviors. But what knowledge about those genes keeps teaching us is that we have that much more of a responsibility to create environments that interact benignly with those genes” (p.56).

Brian Koehler PhD
New York University
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brian_koehler@psychoanalysis.net