AUTHOR: Jonah Lehrer
SOURCE: Seed Magazine
COMMENTARY: Allen MacNeill (following the excerpt)
It has been received dogma for about a century that our cognitive potential (i.e. our "intelligence") is essentially fixed at birth or shortly thereafter, and that whatever debate has swirled around this topic has had primarily to do with how much influence very early environmental conditions have on our "innate" intelligence. What Gould's work shows is that the primate brain is continuously remodeled throughout life, in response to shifting environment pressures:
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Eight years after Gould defied the entrenched dogma of her science and proved that the primate brain is always creating new neurons, she has gone on to demonstrate an even more startling fact: The structure of our brain, from the details of our dendrites to the density of our hippocampus, is incredibly influenced by our surroundings. Put a primate under stressful conditions, and its brain begins to starve. It stops creating new cells. The cells it already has retreat inwards. The mind is disfigured.
The social implications of this research are staggering. If boring environments, stressful noises, and the primate’s particular slot in the dominance hierarchy all shape the architecture of the brain—and Gould’s team has shown that they do—then the playing field isn’t level. Poverty and stress aren’t just an idea: they are an anatomy. Some brains never even have a chance.
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But it isn't all bad news; the process can go the other way, as well, making new pathways and connections:
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Chronic stress, predictably enough, decreases neurogenesis. As Christian Mirescu, one of Gould’s post-docs, put it, “When a brain is worried, it’s just thinking about survival. It isn’t interested in investing in new cells for the future.”
On the other hand, enriched animal environments—enclosures that simulate the complexity of a natural habitat—lead to dramatic increases in both neurogenesis and the density of neuronal dendrites, the branches that connect one neuron to another. Complex surroundings create a complex brain.
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To understand how revolutionary this finding is, consider the following statements about this process from the pre-eminent researcher in this field twenty years ago:
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“All neurons of the rhesus monkey brain are generated during pre-natal and early post-natal life,” Rakic wrote in his 1985 paper, “Limits of Neurogenesis in Primates.” “Not a single” new neuron “was observed in the brain of any adult animal.” While Rakic admitted that his proof was limited, he persuasively defended the dogma. He even went so far as to construct a plausible evolutionary theory as to why neurons can’t divide: Rakic imagined that at some point in our distant past, primates had traded the ability to give birth to new neurons for the ability to retain plasticity in our old neurons. According to Rakic, the “social and cognitive” behavior of primates required the absence of neurogenesis. His paper, with its thorough demonstration of what everyone already believed, seemed like the final word on the matter. No one bothered to verify his findings.
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And Gould's findings have political and economic implications:
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Gould’s research inevitably conjures up comparisons to societal problems. And while Gould, like all rigorous bench scientists, prefers to focus on the strictly scientific aspects of her data—she is wary of having it twisted for political purposes—she is also acutely aware of the potential implications of her research.
“Poverty is stress,” she says, with more than a little passion in her voice. “One thing that always strikes me is that when you ask Americans why the poor are poor, they always say it’s because they don’t work hard enough, or don’t want to do better. They act like poverty is a character issue.”
Gould’s work implies that the symptoms of poverty are not simply states of mind; they actually warp the mind. Because neurons are designed to reflect their circumstances, not to rise above them, the monotonous stress of living in a slum literally limits the brain.
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That the architecture of the brain actually changes over time should not come as a complete surprise. Neuroscientists have known for a while that synapses can change, for example as the result of antidepressant drugs:
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For the last 40 years, medical science has operated on the understanding that depression is caused by a lack of serotonin, a neurotransmitter that plays a role in just about everything the mind does, thinks or feels. The theory is appealingly simple: sadness is simply a shortage of chemical happiness. The typical antidepressant—like Prozac or Zoloft—works by increasing the brain’s access to serotonin. If depression is a hunger for neurotransmitter, then these little pills fill us up.
Unfortunately, the serotonergic hypothesis is mostly wrong. After all, within hours of swallowing an antidepressant, the brain is flushed with excess serotonin. Yet nothing happens; the patient is no less depressed. Weeks pass drearily by. Finally, after a month or two of this agony, the torpor begins to lift.
But why the delay? If depression is simply a lack of serotonin, shouldn’t the effect of antidepressants be immediate?
The paradox of the Prozac lag has been the guiding question of Dr. Ronald Duman’s career....When Duman began studying the molecular basis of antidepressants back in the early 90s, the first thing he realized was that the serotonin hypothesis made no sense. A competing theory, which was supposed to explain the Prozaz lag, was that antidepressants increase the number of serotonin receptors. However, that theory was also disproved. “It quickly became clear that serotonin wasn’t the whole story,” Duman says. “Our working hypothesis at the time just wasn’t right.”
But if missing serotonin isn’t the underlying cause of depression, then how do antidepressants work? As millions will attest, Prozac does do something. Duman’s insight, which he began to test gradually, was that a range of antidepressants trigger a molecular pathway that has little, if anything, to do with serotonin. Instead, this chemical cascade leads to an increase in the production of a class of proteins known as trophic factors. Trophic factors make neurons grow. What water and sun do for trees, trophic factors do for brain cells. Depression was like an extended drought: It deprived neurons of the sustenance they need.
Duman’s discovery of a link between trophic factors and antidepressant treatments still left the essential question unanswered: What was causing depressed brains to stop producing trophins? Why was the brain hurting itself? It was at this point that Duman’s research intersected the work of Robert Sapolsky and Bruce McEwen (Gould’s advisor at Rockefeller), who were both studying the effects of stress on the mammalian brain. In an influential set of studies, Sapolsky and McEwen had shown that prolonged bouts of stress were devastating to neurons, especially in the hippocampus. In one particularly poignant experiment, male vervet monkeys bullied by their more dominant peers suffered serious and structural brain damage. Furthermore, this neural wound seemed to be caused by a decrease in the same trophic factors that Duman had been studying. From the perspective of the brain, stress and depression produced eerily similar symptoms. They shared a destructive anatomy.
Just as Duman was beginning to see the biochemical connections between trophins, stress, and depression, Gould was starting to document neurogenesis in the hippocampus of the primate brain. Reading Altman’s and Kaplan’s papers, Gould had realized that her neuron-counting wasn’t erroneous: She was just witnessing an ignored fact. The anomaly had been suppressed. But the final piece of the puzzle came when Gould heard about the work of Fernando Nottebohm, who was, coincidentally, also at Rockefeller. Nottebohm, in a series of beautiful studies on birds, had showed that neurogenesis was essential to birdsong. To sing their complex melodies, male birds needed new brain cells. In fact, up to 1% of the neurons in the bird’s song center were created anew, every day.
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Perhaps the time lag of antidepressants was simply the time it took for new cells to be created....In December 2000, Duman’s lab published a paper in the Journal of Neuroscience demonstrating that antidepressants increased neurogenesis in the adult rat brain. In fact, the two most effective treatments they looked at—electroconvulsive therapy and fluoxetine, the chemical name for Prozac—increased neurogenesis in the hippocampus by 75% and 50%, respectively. Subsequent studies did this by increasing the exact same molecules, especially trophic factors, that are suppressed by stress.
Duman was surprised by his own data. Fluoxetine, after all, had been invented by accident. (It was originally studied as an antihistamine.) “The idea that Prozac triggers all these different trophic factors that ultimately lead to increased neurogenesis is just totally serendipitous,” Duman says. “Pure luck.”
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Several major drug companies and a host of startups are now frantically trying to invent the next generation of antidepressants (a $12-billion-a-year business). Many expect these future drugs to selectively target the neurogenesis pathway. If these pills are successful, they will be definitive proof that antidepressants work by increasing neurogenesis. Depression is not simply the antagonist of happiness. Instead, despair might be caused by the loss of the brain’s essential plasticity. A person’s inability to change herself is what drags her down.
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COMMENTARY:
It would be difficult to overemphasize how revolutionary Gould's findings are to the fields of evolutionary psychology and psychology in general. That we had a limited ability to do this has been increasingly recognized over the past two decades, as neuroscientists discovered that new synapses could be formed, not just by altering the quantities of neurotransmitters released by existing synapses, but also by building new receptors or eliminating existing ones. However, until this new work by Gould and her colleagues, it was assumed that the underlying neural architecture of the brain was essentially predetermined by genetics, and that all the environment could do was to downgrade that architecture as a result of malnutrition, under-stimulation, and other environmental injuries and insults.
Now, however, it looks like the brain can be remodeled throughout life, with whole new neurons being added along with multiple synapses, thereby fundamentally altering the cognitive potential of individuals throughout life. In other words, the nervous system is much more plastic than heretofore suspected, and can therefore respond much more robustly to environmental changes, in both positive and negative directions.
This discovery has political ramifications, as well as scientific ones. Programs like Head Start and other early educational "interventions" have all been premised on the idea that such remediation only works if instituted very early in development, and even then probably have little effect. However, if the architecture of our brains is modifiable throughout life, it may be possible to successfully intervene at nearly any stage of cognitive development. Therefore, withholding such intervention as the result of economic or political exigencies becomes even more egregious than it is at present.
As far as evolutionary psychology is concerned, it would seem on reflection that discoveries like these make perfect evolutionary sense. Primates are known for our behavioral plasticity; it's our most obvious (and most valuable) adaptive trait. Finding out that this plasticity goes all the way down to the neural architecture itself shouldn't be that surprising. However, it does cast even more doubt on the "hard inheritance" stance of people like Herrnstein, Murray, et al, and even the "hard hereditarian" position of E. O. Wilson and other "genetic sociobiologists." If Gould's findings hold up, and even moreso if they are expanded, it seems as though the environmental plays an even more important role in altering primate behavior and "intelligence" than formerly thought.
And so the pendulum swings again...
--Allen
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ORIGINAL PUBLICATION REFERENCE:
Location Online: Seed Magazine
URL: http://www.seedmagazine.com/news/2006/02/the_reinvention_of_the_self.php
Original posting/publication date timestamp:
February 23, 2006 12:37 AM