Will Power and Its Limits

How to strengthen your self-control.

Reason in man obscured, or not obeyed,
Immediately inordinate desires,
And upstart passions, catch the government
From reason; and to servitude reduce
Man, till then free.
—John Milton, Paradise Lost

What is will power? Is it the same as delayed gratification? Why is will power “far from bulletproof,” as researchers put it in a recent article for Neuron? Why is willpower “less successful during ‘hot’ emotional states”? And why do people “ration their access to ‘vices’ like cigarettes and junk foods by purchasing them in smaller quantities,” despite the fact that it’s cheaper to buy in bulk?

 Everyone, from children to grandparents, can be lured by the pull of immediate gratification, at the expense of large—but delayed—rewards. By means of a process known as temporal discounting, the subjective value of a reward declines as the delay to its receipt increases. Rational Man, Economic Man, shouldn’t behave in a manner clearly contrary to his or her own best interest. However, as Crockett et. al. point out in a recent paper in Neuron “struggles with self-control pervade daily life and characterize an array of dysfunctional behaviors, including addiction, overeating, overspending, and procrastination.”

Previous research has focused primarily on “the effortful inhibition of impulses” known as will power. Crockett and coworkers wanted to investigate another means by which people resist temptations. This alternative self-control strategy is called precommitment, “in which people anticipate self-control failures and prospectively restrict their access to temptations.” Good examples of this approach include avoiding the purchase of unhealthy foods so that they don’t constitute a short-term temptation at home, and putting money in financial accounts featuring steep penalties for early withdrawal. These strategies are commonplace, and that’s because people generally understand that will power is far from foolproof against short-term temptation. People adopt strategies, like precommitment, precisely because they are anticipating the possibility of a failure of self-control. We talk a good game about will power and self-control in addiction treatment, but the truth is, nobody really trusts it—and for good reason.  The person who still trusts will power has not been sufficiently tempted.

The researchers were looking for the neural mechanisms that underlie precommitment, so that they could compare them with brain scans of people exercising simple self-control in the face of short-term temptation.

After behavioral and fMRI testing, the investigators used preselected erotic imagery rated by subjects as either less desirable ( smaller-sooner reward, or SS), or more highly desirable ( larger-later reward, or LL). The protocol is complicated, and the analysis of brain scans is inherently controversial. But previous studies have shown heightened activity in three brain areas when subjects are engaged in “effortful inhibition of impulses.” These are the dorsolateral prefrontal cortex (DLPFC), the inferior frontal gyrus (IFG), and the posterior parietal cortex (PPC). But when presented with opportunities to precommit by making a binding choice that eliminated short-term temptation, activity increased in a brain region known as the lateral frontopolar cortex (LFPC).  Study participants who scored high on impulsivity tests were inclined to precommit to the binding choice.

In that sense, impulsivity can be defined as the abrupt breakdown of will power. Activity in the LFPC has been associated with value-based decision-making and counterfactual thinking. LFPC activity barely rose above zero when subjects actively resisted a short-term temptation using will power.  Subjects who chose the option to precommit, who were sensitive to the opportunity to make binding choices about the picture they most wanted to see, showed significant activity in the LFPC. “Participants were less likely to receive large delayed reward when they had to actively resist smaller-sooner reward, compared to when they could precommit to choosing the larger reward before being exposed to temptation.”

Here is how it looks to Molly Crockett and her fellow authors of the Neuron article:

Precommitment is adaptive when willpower failures are expected…. One computationally plausible neural mechanism is a hierarchical model of self-control in which an anatomically distinct network monitors the integrity of will-power processes and implements precommitment decisions by controlling activity in those same regions. The lateral frontopolar cortex (LFPC) is a strong candidate for serving this role.

None of the three brain regions implicated in the act of will power were active when opportunities to precommit were presented.  Precommitment, the authors conclude, “may involve recognizing, based on past experience, that future self-control failures are likely if temptations are present. Previous studies of the LFPC suggest that this region specifically plays a role in comparing alternative courses of action with potentially different expected values.” Precommitment, then, may arise as an alternative strategy; a byproduct of learning and memory related to experiences “about one’s own self-control abilities.”

There are plenty of caveats for this study: A small number of participants, the use of pictorial temptations, and the short time span for precommitment decisions, compared to real-world scenarios where delays to greater rewards can take weeks or months. But clearly something in us often knows that, in the immortal words of Carrie Fisher, “instant gratification takes too long.” For this unlucky subset, precommitment may be a vitally important cognitive strategy. “Humans may be woefully vulnerable to self-control failures,” the authors conclude, “but thankfully, we are sometimes sufficiently far-sighted to circumvent our inevitable shortcomings.” We learn—some of us—not to put ourselves in the path of temptation so readily.

Crockett M., Braams B., Clark L., Tobler P., Robbins T. & Kalenscher T. (2013). Restricting Temptations: Neural Mechanisms of Precommitment, Neuron, 79 (2) 391-401. DOI: 10.1016/j.neuron.2013.05.028

Photo Credit: http://tommyboland.com/2011/05/27/white-knuckle-living/

How Junk Food Works

Ex-FDA chief offers clues to food addiction.

It is a perplexingly common experience: You open a bag of cookies, intending to have one or two. An hour later, the bag is empty, and your self-loathing is at its peak.

But compulsive overeating is not a character flaw, according to David Kessler, former head of the Food and Drug Administration. It is, rather, a “biological challenge.”

Readers may remember Kessler from his anti-cigarette and food product labeling crusades during the Clinton administration. In his forthcoming book, The End of Overeating: Taking Control of the Insatiable American Appetite, Kessler notes that while food took over his brain, the foods in question were not carrots, apples and green leafy vegetables. “Conditioned overeating,” as Kessler dubs it, is driven by a biological drive to eat high-fat, high-sugar foods even when we are not hungry. Moreover, such foods are cheaper than more healthy alternatives.

What Kessler describes in his book is a system of reward-driven eating abetted by a food industry fully aware of the biological attraction exerted by salt, fat, and sugar. Kessler himself is no stranger to this attraction. “I have suits in every size,” Kessler writes, according to a report by Lauren Neergaard for AP. “Once you know what’s driving your behavior, you can put steps in place.”

Kessler has also served as dean of the medical schools at Yale and the University of California at San Francisco. On the book’s Amazon site, Michael Pollan, author of In Defense of Food, calls Kessler’s book “a fascinating account of the science of human appetite, as well as its exploitation by the food industry.”

It is becoming increasingly clear that fat and sugar in combination are capable of producing a dopamine-driven surge of intense pleasure in people with a propensity for addictive behavior. Mice that have been genetic altered so that they lack the ability to taste sweet foods still prefer sugar water to regular water. (See my post on Dopamine and Obesity.) Kessler provides additional evidence that certain forms of overeating qualify as legitimate drug addictions. Just as it is with, say, cocaine addicts, the supersaturated reward pathways of the brain do not have effective mechanisms for signaling: “That’s enough. Stop eating.”

It may seem obvious in retrospect that the same mechanisms that make it so difficult for many drug addicts to “just say no” would also function in the case of addicted overeaters. What happens is similar to the flooding of reward circuitry that occurs in cases of what we might call “compulsive overdrugging,” otherwise known as addiction. The food industry, according to Kessler, has figured out what works, has packaged fat-and-sugar foods in products that scarcely even have to be chewed, and it has priced these products to move.

Yale university conducted studies in which “hypereaters” were given the odor of chocolate during an MRI scan. Normal eaters get used to the odor and habituate rapidly. Hypereaters find that the odor of chocolate becomes more demanding and overpowering with time. And even drinking a complete chocolate milkshake did not quell the craving.

According to Publisher’s Weekly, Kessler’s book, set to be released on April 28, “provides a simple food rehab program to fight back against the [food] industry’s relentless quest for profits while an entire country of people gain weight and get sick.”

Photo Credit: Neurological Correlates

Dopamine and Obesity

Overeating, drug abuse, and the D2 receptor.

A genetic variation in the dopamine D2 receptor predisposes women toward obesity, according to a small but potentially significant study published in the October 17 issue of Science.

While numerous twins studies demonstrate the likelihood of biological factors in obesity, there are few rigorous studies that back up the contention. Now researchers from Yale University and the University of Texas have used brain scans to show that a dopamine-rich structure called the dorsal striatum exhibits “reduced D2 receptor density and compromised signaling” in obese individuals.

Why would this matter? The dorsal striatum releases dopamine in response to the consumption of tasty food. Going right to the sugary heart of the tasty food cornucopia, the researchers used chocolate milkshakes. Women volunteers underwent MRI scans while researchers administered either squirts of milkshake or squirts of a tasteless liquid. The lower the dopamine response to the milkshake in the dorsal striatum, the more likely the woman was to gain weight over the following year. Reduced dopamine receptor density in the dorsal striatum “may prompt them to overeat in an effort to compensate for this reward deficit,” the study authors concluded. The all-female study lends more evidence to the notion that dopamine D2 variations “are associated with both obesity and substance abuse....”

Dr. Nora Volkow, director of the National Institute on Drug Abuse (NIDA), told Associated Press: “It takes the gene associated with greater vulnerability for obesity and asks the question why. What is it doing to the way the brain is functioning that would make a person more vulnerable to compulsively eat food and become obese?”

Historically, however, the D2 allele has been a controversial locus of research in addiction medicine. In 1990, a research team reported in the Journal of the American Medical Association that the A-1 allele controlling production of the dopamine D2 receptor was three times as common in the brains of deceased alcoholics. The aberrant form of the gene was found in 77 per cent of the alcoholics, compared with only 28 per cent of the non-alcoholics. But attempts to replicate the research did not meet with much success. (See Bower, Bruce. “Gene in the Bottle.” Science News, September 21, 1991. p.19). In addition, the findings from the nationwide Collaborative Study on the Genetics of Alcoholism were not supportive of the D2 hypothesis. (“We believe it doesn’t increase the risk for anything,” one researcher said bluntly.) Well-known researcher Robert Cloninger weighed in with a paper demonstrating that when you broadened the samples and took another look, the D2 connection faded away, suggesting that the D2 allele in question may play a second-order role of some sort. (See Holden, Constance. “A Cautionary Genetic Tale: The Sobering Story of D2.” Science. June 17, 1994. 264 p.1696 ).

The current Science study concludes that “individuals who show blunted striatal activation during food intake are at risk for obesity.... behavioral or pharmacologic interventions that remedy striatal hypofunctioning may assist in the prevent and treatment of this pernicioujs health problem.” NIDA’s Volkow, quoted in the Washington Post, said: “Dieting is a complex process and people don’t like it. Physical activity, which also activates the dopamine pathway, may be a mechanism for reducing the compulsive activity of overeating.”

Dr. Eric Stice of the Oregon Research Institute, the lead scientist on the study, told AP that the findings might have implications for parents. Since most parents don’t know if they possess the suspect variation, Stice suggested than parents could start attending more to the diets of children, “and not get their brains used to having crappy food.”


Photo Credit: Cell Science

dopamine