The same dangerous recklessness can be seen in the methodology used for the Fukushima nuclear reactor, built to the worst past outcome and not imagining and extrapolating to much worse. Well, nature, unlike risk engineers, prepares for what has not happened before, assuming worse harm is possible.
So if humans fight the last war, nature fights the next war. Of course, there is a biological limit to our overcompensation.
This form of redundancy remains vastly more extrapolative than our minds, which are intrapolative.
The great Benoit Mandelbrot, now gone for two years, saw the same fractal self-similarity in nature and in probabilities of historical and economic events. It is thrilling to see how the two domains unite under the notion of fractal-based redundancy.
P.S.: The word “fitness” in the common scientific discourse does not appear to be precise enough. I am unable to figure out if what is called “Darwinian fitness” is merely intrapolative adaptation to the current environment or if it contains an element of statistical extrapolation. In other words, there is a significant difference between robustness (is not harmed by stressors) and what I’ve called antifragility (i.e., gains from stressors).
THE BEAUTIFUL LAW OF UNINTENDED CONSEQUENCES
ROBERT KURZBAN
Associate professor of evolutionary psychology, University of Pennsylvania; director, Pennsylvania Laboratory for Experimental Evolutionary Psychology (PLEEP); author, Why Everyone (Else) is a Hypocrite
According to the guide on my walking tour of The Rocks neighborhood in Sydney, Australia, when the plague hit the city around 1900 a bounty was placed on rats to encourage people to kill them, since it was known that rats bore the fleas that communicated the disease to humans. The intent of the bounty was plain enough: reducing the number of rats to reduce the spread of the plague. An unintended consequence, however, was that residents, tempted by the rat bounty, began breeding rats.
The law of unintended consequences is often associated with the American sociologist Robert Merton, though its general spirit appears in various forms, not least in Adam Smith’s notion of the Invisible Hand, and is somehow delightful in its chaos, as if Nature were continually thumbing her nose at our attempts to control her.
The idea is that when people intervene in systems with a lot of moving parts—especially ecologies and economies—the intervention, because of the complex interrelationships among the system’s parts, will have effects beyond those intended, including many that were unforeseen or unforeseeable.
Examples abound. Returning to Australia, one of the best known examples of an unintended consequence is the case of rabbits, brought by the First Fleet as food, released into the wild for hunting, with the unintended consequence that rabbit populations grew to staggering proportions, causing untold ecological devastation. This in turn led to the development of measures to control the rabbits, including an exceptionally long fence, which had the unintended consequence of guiding three young girls home in the 1930s—which in turn had the unintended consequence of inspiring an award-winning motion picture (Rabbit-Proof Fence, 2002).
These chains of consequences occur because making changes to one part of a system with many interacting parts leads to changes in other parts of the system. Because many of the systems we try to influence are complex but incompletely understood—bodies, habitats, markets—there are bound to be consequences that are difficult to predict.
This is not to say that the consequences will always be undesirable. Recently, certain municipalities changed the laws governing the use of marijuana, making it easier to obtain for medical purposes. The law might or might not have reduced the suffering of glaucoma victims, but data from traffic accidents suggest that the change in the legislation did reduce fatalities on the road by about 9 percent. (People substituted marijuana for alcohol and apparently drive better stoned than drunk.) Saving drivers’ lives was not the intent of the law, but that was the effect. Another example, smaller in scale though closer to my heart, was the recent abrupt increase of parking rates by a third in University City, Philadelphia, where I work. The intent of the law was to raise revenue to help fund the city’s schools. An unintended consequence—because students seem disinclined to pay the higher price—is that I can rely on getting a parking spot when I have to drive to school.
Intervention in any sufficiently complicated system is bound to produce unintended effects. We treat patients with antibiotics, and we select for resistant strains of pathogens. We artificially select for wrinkly-faced bulldogs, and less pleasant traits, such as respiratory problems, come along for the ride. We treat morning sickness with thalidomide, and babies with birth defects follow.
In the economic sphere, most policies have various sorts of knock-on effects, with prohibitions and bans providing some of the most profound examples—including, of course, Prohibition, which itself spun off various consequences, among them, arguably, the rise of organized crime. Because governments typically ban only those things for which people have a taste, when bans do arise people find ways to satisfy those tastes, either through substitutes or black markets, both of which lead to varied consequences. Ban sodas, boost sports-drink sales. Ban the sale of kidneys, spawn an international black market for organs and underground surgeries. Ban the hunting of mountain lions, endanger local joggers.
There is something oddly beautiful about the tendrils of causality in complex systems, holding the same appeal we find in the deliberate inelegance of Rube Goldberg machines. And none of this is to say that the inevitable chances of being surprised by our interventions means that we must give in to pessimism. Rather, it reminds us to exercise caution and humility. As we gradually increase our understanding of large, complicated systems, we will develop new ways to glimpse the unintended consequences of our actions. We already have some guiderails: People will find substitutes for banned or taxed products; removing one species in an ecology typically penalizes populations that prey on them and aids species that compete with them; and so on. So whereas there will probably always be unintended consequences, they needn’t be completely unanticipated.
WE ARE WHAT WE DO
TIMOTHY D. WILSON
Sherrell J. Aston Professor of Psychology, University of Virginia; author, Redirect: The Surprising New Science of Psychological Change
People become what they do. This explanation of how people acquire attitudes and traits dates back to the late British philosopher Gilbert Ryle but was formalized by the social psychologist Daryl Bem in his self-perception theory. People draw inferences about who they are, Bem suggests, by observing their own behavior.
Self-perception theory turns common wisdom on its head. People act the way they do because of their personality traits and attitudes, right? They return a lost wallet because they’re honest, recycle their trash because they care about the environment, and pay $5 for a caramel brulée latte because they like expensive coffee drinks. It’s evident that behavior emanates from our inner dispositions, but Bem’s insight was to suggest that the reverse also holds. If we return a lost wallet, there’s an upward tick on our honesty meter. After we drag the recycling bin to the curb, we infer that we really care about the environment. And after purchasing the latte, we assume that we are coffee connoisseurs.
Hundreds of experiments have confirmed the theory and shown when this self-inference process is most likely to operate (for example, when people believe they freely chose to behave as they did and when they weren’t sure at the outset how they felt).
Self-perception theory is elegant in its simplicity. But it is also deep, with important implications for the nature of the human mind. Two other powerful ideas follow from it. The first is that we are strangers to ourselves. After all, if we knew our own minds, why would we need to guess what our preferences are from our behavior? If our minds were an open book, we would know exactly how honest we are and how much we like lattes. Instead, we often need to look to our behavior to figure out who we are. Self-perception theory thus anticipated
the revolution in psychology in the study of human consciousness, a revolution that revealed the limits of introspection.
But it turns out that we don’t just use our behavior to reveal our dispositions—we infer dispositions that weren’t there before. Often our behavior is shaped by subtle pressures around us, but we fail to recognize those pressures. Thus, we mistakenly believe that our behavior emanated from some inner disposition. Perhaps we aren’t particularly trustworthy and instead returned the wallet in order to impress the people around us. But, failing to realize that, we infer that we’re squeaky-clean honest. Maybe we recycle because the city has made it easy to do so (by giving us a bin and picking up every Tuesday) and our spouse and neighbors would disapprove if we didn’t. Instead of recognizing those reasons, though, we assume that we should be nominated for the Green Neighbor of the Month Award. Countless studies have shown that people are highly susceptible to social influence but rarely recognize the full extent of that susceptibility, thereby misattributing their compliance to their true desires.
Like all good psychological explanations, self-perception theory has practical uses. It is implicit in several versions of psychotherapy, in which clients are encouraged to change their behavior first, on the assumption that changes in their inner dispositions will follow. It has been used to prevent teenage pregnancies, by getting teens to do community service. The volunteer work triggers a change in their self-image, making them feel more a part of their community and less inclined to engage in risky behaviors. In short, we should all heed Kurt Vonnegut’s advice: “We are what we pretend to be, so we must be careful about what we pretend to be.”
PERSONALITY DIFFERENCES: THE IMPORTANCE OF CHANCE
SAMUEL BARONDES
Jeanne and Sanford Robertson Professor of Neurobiology and Psychiatry, University of California–San Francisco; author, Making Sense of People
In the golden age of Greek philosophy, Theophrastus, Aristotle’s successor, posed a question for which he is still remembered: “Why has it come about that, albeit the whole of Greece lies in the same clime, and all Greeks have a like upbringing, we have not the same constitution of character [personality]?” The question is especially noteworthy because it bears on our sense of who each of us is, and we now know enough to offer an answer: Each personality reflects the activities of brain circuits that gradually develop under the combined direction of the person’s unique set of genes and experiences. What makes the implications of this answer so profound is that they lead to the inescapable conclusion that personality differences are greatly influenced by chance events.
Two types of chance events influence the genetic contribution to personality. The first, and most obvious, is the events that brought together the person’s mom and dad. Each of them has a particular collection of gene variants—a personal sample of the variants that have accumulated in the collective human genome—and the two parental genetic repertoires set limits on the possible variants that can be transmitted to their offspring. The second chance event is the hit-or-miss union of the particular egg and sperm that make the offspring, each of which contains a random selection of half of the gene variants of each parent. It is the interactions of the resultant unique mixture of maternal and paternal gene variants that play a major part in the twenty-five-year-long developmental process that builds the person’s brain and personality. So two accidents of birth—the parents who conceive us, and the egg/sperm combinations that make us—have decisive influences on the kinds of people we become.
But genes don’t act alone. Although there are innate programs of gene expression that continue to unfold through early adulthood to direct the construction of rough drafts of brain circuits, these programs are specifically designed to incorporate information from the person’s physical and social world. Some of this adaptation to the person’s particular circumstances must come at specific developmental periods, called critical periods. For example, the brain circuits that control the characteristic intonations of a person’s native language are open for environmental input only during a limited window of development.
And just as chance influences the particular set of genes we are born with, so does it influence the particular environment we are born into. Just as our genes incline us to be more or less friendly, or confident, or reliable, the worlds we grow up in incline us to adopt particular goals, opportunities, and rules of conduct. The most obvious aspects of these worlds are cultural, religious, social, and economic, each transmitted by critical agents: parents, siblings, teachers, and peers. And the specific content of these important influences—the specific era, place, culture, etc., that we happen to have been born into—is as much a toss of the dice as the specific content of the egg and sperm that formed us.
Of course, chance is not fate. Recognizing that chance events contribute to individual personality differences doesn’t mean that each life is predetermined or that there is no free will. The personality arising through biological and sociocultural accidents of birth can be deliberately modified in many ways, even in maturity. Nevertheless, the chance events that direct brain development in our first few decades leave enduring residues.
When thinking about a particular personality, it is therefore helpful to be aware of the powerful role chance played in its construction. Recognizing the importance of chance in our individual differences doesn’t just remove some of their mystery—it can also have moral consequences by promoting understanding and compassion for the wide range of people with whom we share our lives.
METABOLIC SYNDROME: CELL ENERGY ADAPTATIONS IN A TOXIC WORLD?
BEATRICE GOLOMB
Professor of medicine, University of California–San Diego
Metabolic syndrome (MetSyn) has been called the epidemic of the 21st century. MetSyn is an accretion of symptoms, including high body-mass index, high blood sugar, high blood pressure, high blood triglycerides, high waist circumference, and/or reduced HDL cholesterol, the so-called good cholesterol. Epidemics of obesity and diabetes are intertwined with and accompany the meteoric rise in MetSyn.
The prevalent view is that MetSyn is due to a glut of food calories (“energy”) consumed and a dearth of exercise energy expended, spurring weight gain—an “energy surfeit”—with the other features arising in consequence. After all, we have more access to calories, and are more often sedentary, than in times gone by. MetSyn factors are each linked, in otherwise healthy young populations, to higher mortality.
But this view leaves many questions unanswered: Why do elements of MetSyn correlate? Why are overweight people today more likely to have diabetes than hitherto? Why are elements of MetSyn now emerging in infancy? Why is MetSyn materializing in poor and third-world nations?
The customary explanation also creates paradoxes. If MetSyn stems from energy surfeit, why do the following factors, which reduce energy supply or increase demand, promote MetSyn—far from protecting against it?
• Sleep apnea (It’s a stronger MetSyn risk factor than being overweight; moreover, sleep-apnea treatment benefits each MetSyn element)
• Ultra low-calorie or low-fat diets
• Fasting, skipped meals
• Hypoglycemia-promoting diets (high-carbohydrate/low-fat/low-protein diets lead to unopposed insulin surge)
• Deficient sleep (more energy-expending wake time)
• Illness/injury/surgery (high energy demand)
• Cold weather (mandating energy expenditure for thermogenesis)
• Nutrient and antioxidant deficiencies (adequacy required for energy production)
• Oxidative stressor exposure (impairs function of mitochondria, the energy-producing elements of cells)
• Mitochondrial pathology
Why do factors that protect from energy-deficit (antioxidant cocoa and cinnamon, mitochondria-supportive coenzyme Q10) reduce MetSyn factors?
Why does exercise, which expends energy but boosts energy production via antioxidant effects, mitochondrial biogenesis, enhanced circulation, a
nd cardiopulmonary function (improving oxygen intake, delivery, and conversion to energy) reduce MetSyn factors?
Why does MetSyn cease to elevate mortality (indeed, sometimes boost survival) when the group studied is of advanced age or suffers from heart failure or severe kidney disease—all conditions that impair cell energy?
Suppose the correct explanation were the complete opposite of the accepted one. Could the features of MetSyn be the adaptive response to inadequate energy? After all, fat depots, glucose, and triglycerides are each accessory energy sources (oxygen is primary); blood pressure is needed to deliver these to tissues, especially when underperfused. Cell energy, central to cell and organism survival, is needed continuously; we live only minutes without oxygen. The stretch is not so great: Populations in which prior generations were energy-starved now have increased obesity/MetSyn, and low energy supply in utero is understood to foster MetSyn in adulthood.
This explains, as the energy-surfeit view does not, why MetSyn exists at all: why elevated glucose, triglycerides, blood pressure (carrying oxygen, glucose, nutrients), and abdominal fat deposition cohere statistically. It explains why other energy-supportive adaptations, like free fatty acids and (metabolically active) ectopic fat (fatty-liver, fatty-pancreas, fatty-kidney, even fatty-streaks in the blood vessels) accompany those Met Syn factors; why MetSyn is linked to fatigue and increased sleep duration (which conserves energy). Indeed, increased caloric intake and reduced exercise—the usual MetSyn explanation—arise, too, as fellow energetic adaptations. Thus, this view is arguably not antithetical to the canonical one but in one sense subsumes it. It explains, as the energy-surfeit view does not, the populations at risk for MetSyn, such as the elderly (mitochondrial function declines exponentially with age) and those afflicted with sleep apnea or any cause for recurrent impairment of energy production. And it explains why, in studies focused on persons with conditions that blight energy, those with MetSyn features paradoxically don’t do worse, or even fare better.
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