Determined, page 25
Thus, a variety of studies shows that when it comes to theists versus nontheists being kind to someone, it really depends on who that someone is. And the majority of experimental studies examining these issues have involved subjects thinking about in-group members. Just imagine—a professor who studies the subject recruits a bunch of Psych 101 students to participate in a study of how generous and trustworthy they are. As part of it, they play an online economic game, supposedly against someone in the next room. Who do you imagine the students implicitly assume is in that next room—a fellow classmate or a yak herder from Bhutan? Experimental designs like these implicitly prompt subjects to think of other participants, hypothetical or otherwise, as in-group members, thus disproportionately priming for more prosociality from theists than from atheists.
How would the issue of who is being helped play out in comparing free-will believers with skeptics? I would imagine that free-will believers will feel more of a moral imperative (versus an instrumental strategy) to help someone who is making an extra effort at something, while free-will skeptics will feel more of an imperative to understand the actions of someone very different from them.
We return to the broad question in this section: Does disbelief that one’s actions are judged by an omnipotent force degrade morality? Seemingly so. That is, as long as you are asking people to say how moral they are rather than to demonstrate it, or you prime them with religious cues rather than secular ones of equivalent symbolic power. And as long as “good acts” are individualistic rather than collective, and are directed at people who look like them. Skepticism about the existence of a moralizing god(s) doesn’t particularly generate immoral behavior; this is the case for underlying reasons that help explain why being skeptical about free will doesn’t either.
Now to the most important point about the menace of skeptics running amok. Asking about differences between free-will believers and skeptics is the wrong question.
Into the Valley of the Indifferent
Consider this U-shaped curve:
On the left (A) are people who firmly believe that there is no free will, period; in the trough (B) are those whose belief in free will is a bit malleable, while on the right (C) are those whose belief in free will is unshakable.
Back to the Temptation of Crick. The collection of volunteer subjects in the studies reviewed was almost certainly comprised of people in category B or C, given the rarity with which free will is completely rejected. What, collectively, do those studies show?
—First, when free-will believers read about how there is no free will, on the average, there is a small decrease in belief in free will, and with a lot of variability, reflecting the fact that some of the people are unmoved by arguments against free will. As such, subjects whose belief shifts can be thought of as category B, those who are unshakable, category C.
—The more a subject’s faith in free will is shifted, the more likely they are to act unethically in the experiment.
In other words, when it comes to beliefs about the nature of human agency and responsibility, it’s category B people who run amok, not those in category C. This entire literature bypasses the thing we’re really interested in, which is whether categories A and C differ in their moral uprightness.
To my knowledge, only one study has examined this explicit question, carried out by psychologist Damien Crone, then at the University of Melbourne in Australia, and philosopher Neil Levy, whose ideas have already been discussed. Subjects stoutly believed in free will, or were those who identified their free-will skepticism as long-standing. The really excellent study even examined the reasons why particular subjects rejected free will, contrasting scientific determinists (endorsing statements like “Your genes determine your future”[*]), with fatalistic determinists (“The future has already been determined by fate”). In other words, these were free-will skeptics who had arrived at their stances through different emotional and cognitive routes. The commonality was that they had rejected belief in free will long ago.[35]
The results? Free-will skeptics (of whatever stripe) and free-will believers were identical in their ethical behavior. And as a finding that ultimately tells the whole story, people who most defined themselves by their moral identity were the most honest and generous, regardless of their stance about free will.[36]
The identical pattern holds when considering religious belief and morality. Category A are atheists whose paths to that view are scarred with craters—“Losing my religion was the loneliest moment of my life” or “It would have been so easy to continue after all those years, but that’s when I left my seminary.” Category C? People for whom their belief is daily bread rather than cake on Sunday,[*] informing their every action, who know who they are and what God expects them to do.[*] And then there is category B, covering the range from apatheists, for whom saying that they don’t believe in God is like saying that they don’t ski,[*] as well as those whose religiosity is out of habit, convention, nostalgia, an example for the kids—of the 90 percent of Americans who are theists, probably half fall into this category, given that approximately half don’t go to religious services regularly. As the immensely important point, when it comes to ethical behavior, daily-bread theists and daily-bread atheists resemble each other more than they resemble those in category B.[37]
For example, highly religious and highly secular people score the same on tests of conscientiousness, coming out higher than those in the third group. In experimental studies of obedience (usually variants on the classic research of Stanley Milgram examining how willing subjects are to obey an order to shock someone), the greatest rates of compliance came from religious “moderates,” whereas “extreme believers” and “extreme nonbelievers” were equally resistant. In another study, doctors who had chosen to care for the underserved at the cost of personal income were disproportionately highly religious or highly irreligious. Moreover, classic studies of the people who risked their lives to save Jews during the Holocaust documented that these people who could not look the other way were disproportionately likely to be either highly religious or highly irreligious.[38]
Here is our vitally important reason for optimism, about how the sky won’t necessarily fall if people come to stop believing in free will. There are people who have thought long and hard about, say, what early-life privilege or adversity does to the development of the frontal cortex, and have concluded, “There’s no free will and here’s why.” They are a mirror of the people who have thought long and hard about the same and concluded, “There’s still free will and here’s why.” The similarities between the two are ultimately greater than the differences, and the real contrast is between them and those whose reaction to questions about the roots of our moral decency is “Whatever.”
12
The Ancient Gears within Us: How Does Change Happen?
This book has a goal—to get people to think differently about moral responsibility, blame and praise, and the notion of our being free agents. And to feel differently about those issues as well. And most of all, to change fundamental aspects of how we behave.
This is the goal of many of the things we are exposed to: to change our behavior. That’s certainly what is going on with most speeches, lectures, books—e.g., to change whom you vote for, what you believe the first seven days of the universe were like, or your commitment to the workers of the world uniting and losing their chains. The same for lots of our interpersonal interactions—to persuade, convince, recruit, compel, repel, induce, seduce. And of course, there are the efforts to get you to change your behavior in a way that will make every remaining moment of your life so much happier if only you buy the object being advertised.
All these ways to make you and everyone else change their behavior.
Which raises a gigantic question. Last chapter’s question was “If people stopped believing in free will, would there be amoral chaos?” This chapter’s question is “If there is no free will, how does anything ever change?” How do you decide shortly after this sentence to change your behavior and grab a brownie? If the world is deterministic on the level that matters, isn’t everything thus already determined?
The answer is that we don’t change our minds. Our minds, which are the end products of all the biological moments that came before, are changed by circumstances around us. Which seems like a thoroughly unsatisfying response that is incompatible with your intuitions about how you function.
As such, the goal of this chapter is to reconcile an absence of free will with the fact that change occurs. To do so, we’re going to look at how behavior changes in organisms far simpler than humans, down on the level of molecules and genes. This will segue to considering behavioral change in us. Hopefully, this will make clear an immensely important point: When our behavior changes, it doesn’t involve biology with some themes and motifs similar to ones seen in these simpler organisms. It involves the same molecules, genes, and mechanisms of neuronal function. When you begin to be biased against some alien group of people because their customs differ from your own, the biology underlying your change in behavior is the same as when a sea slug learns to avoid a shock administered by a researcher. And that sea slug sure isn’t displaying free will when that change occurs. Remarkably and probably most important, the antiquity and ubiquity of these biological gears explaining behavioral change wind up being grounds for optimism.
Protecting Your Gill
We start with a sea slug, specifically Aplysia californica, the California sea hare, a gigantic slug that can be more than two feet long. Neuroscientists love this species, write operas about it, all because one of the most important, beautiful, inspiring pieces of neuroscience research in the twentieth century was done with it.
On the surface of an Aplysia is its gill, which is majorly important to an Aplysia surviving. If you lightly touch the area surrounding the gill, called the siphon, the Aplysia protectively retracts its gill inward for a while:
The circuitry underlying this is straightforward: throughout the siphon are sensory neurons (SNs), which have action potentials if anything touches the siphon. Once activated, the SNs activate motor neurons (MNs), which retract the gill:
The gill is essential for survival, and Aplysia have evolved a backup pathway in case the SN-MN connection fails. It turns out that the SN also sends a projection to a little local excitatory node (Exc). Now, when the siphon is touched, the SN activates both the MNs and this Exc node; the latter sends a projection on to the MN, activating it. Thus, if the SN-MN connection fails, there’s still the SN-Exc-MN route available:[*]
The gill can’t remain retracted forever, as it needs to be on the surface to function. Thus, after a bit of time, retraction has to be halted; an off switch has evolved to do this. When the SN is activated, not only does it activate MN and Exc but, after a delay, it also activates a small inhibitory node (Inh). This node then inhibits the Exc branch (which, remember, is the delayed route from SN to MN, so it’s the one to target with this delayed inhibition). Result: the MN is no longer being activated, so the gill defaults back to the surface:
This SN/MN/Exc/Inh circuitry is not a world unto itself; the way it works can be altered by what’s happening throughout the rest of the Aplysia. At the tail end of an Aplysia is its, well, tail. If you shock the tail, it basically sends an alarm signal to the siphon; as a result, if the siphon is touched soon after that, the gill is withdrawn for twice as long as usual. Worrisome news at the tail makes the siphon more responsive to its own worrisome news.
How are we going to wire things up so that events in the tail make gill withdrawal more sensitive? Pretty straightforward. There has to be a tail sensory neuron (TSN) that is responsive to shock, and it has to have the means to then talk to the SN/MN/Exc/Inh circuit. When the TSN is activated, it makes both the SN and the Exc more excitable:
Note that a tail shock doesn’t cause the gill to be retracted—the excitation from TSN isn’t strong enough to activate MN on its own. Instead, the TSN input is enhancing the strength of SN-MN signaling in response to the siphon being touched. In other words, a tail shock sensitizes the gill withdrawal reflex.
Perfect. The Aplysia can retract the gill in response to the siphon being perturbed, has a backup system for that just in case, has a means to reverse the process back to where things started, and can make the circuit more jumpy and vigilant if bad things are happening to other parts of the Aplysia.
Why do we know so much about the inner life of an Aplysia? Because of the work of one of the gods of neuroscience, Eric Kandel of Columbia University. Here is a figure from his 2000 Nobel Prize lecture:[1]
Some minor details: 5HT is the chemical abbreviation for the neurotransmitter (serotonin) used by the TSN. SCP and L29 fine-tune the system; we’ve ignored them, for simplicity. There are 24 SNs in a siphon, converging on to 6 MNs.
This is cool beyond description, just the clarity of this wiring system that this slug evolved. Unfortunately, though, it is also irrelevant to our interests; it has more in common with how your microwave works than with what’s going on in us when we erroneously believe that we are acting out of free will. For that, we need to look at something much more interesting that happens in an Aplysia—this circuit will change in response to experience. It can be trained. It learns.
The Learned Aplysia
As we’ve seen, here are two basic rules. First, if an Aplysia’s siphon is touched, the gill retracts for a bit; second, if the siphon is touched within a minute of the tail being shocked, the gill is retracted for twice as long. But there’s more. How about if the tail has been shocked four times? If the siphon is touched within four hours of that happening, the gill is retracted three times longer than usual. Shock the tail a cluster of times, and if the siphon is then touched within the next few weeks, the gill is retracted ten times longer than usual. As the world becomes a more menacing place, an Aplysia becomes more protective of its gill.
How does that work?
We know from our basic neuro how the SN-MN connection works—as a result of the siphon being touched, the SN releases neurotransmitter (which then triggers the MN into retracting the gill):
Now we need to see what happens inside the SN when the tail is getting shocked. The SM and MN are drawn very differently now, with little packets of neurotransmitter lined up at the bottom of the SN (the little circles), and with the MN and its neurotransmitter receptors (little horizontal lines) on the lower side of the synapse. The tail sensory neuron has been activated by one shock, causing it to release its neurotransmitter, which binds to a receptor on the SN. As a result of a single shock, some sort of “TSN activity–dependent stuff” (which we’ll call Stuff) is released inside the SN:
That Stuff within the SN glides to the bottom, where it beefs up the amount of neurotransmitter stored there (step #1). As a result, if the siphon is touched, enough additional neurotransmitter is released by the SN to cause the gill to retract for twice as long as usual. Within a minute or so of the single shock, the extra neurotransmitter stored in the SN is degraded, and things go back to normal:
What if the tail is shocked four times in rapid succession? As a result, a whole lot more Stuff is liberated inside the SN than with one shock. Not only does this trigger the events of step #1, obviously, but also the surplus Stuff is enough to trigger step #2—that additional Stuff activates a gene on the DNA that produces a protein that stabilizes the neurotransmitter so that it is resistant to degradation. As a result, the neurotransmitter sticks around longer, and if the siphon is touched, enough additional neurotransmitter is released by the SN to cause the gill to retract for three times as long as usual. By four hours after that quartet of shocks, the degradation-inhibiting protein is itself degraded; as a result, the extra neurotransmitter is degraded, and things go back to normal (see the top figure on the next page).
Now, what if the tail is shocked with an intense, sustained cluster of shocks on a few successive days? Humongous amounts of Stuff are released, enough to activate not only steps #1 and #2 but #3 as well. For that final step, Stuff activates a whole string of genes[*] whose resulting proteins, collectively, lead to the construction of an additional synapse. Now, if the siphon is touched, enough additional neurotransmitter is released by the SN to cause the gill to retract for ten times as long as usual. Weeks to months later, the new synapse is deconstructed, and things go back to normal:[*]
