sábado, 21 de octubre de 2017

Esclavo del Ruido

The case against sugar


A potent toxin that alters hormones and metabolism, sugar sets the stage for epidemic levels of obesity and diabetestes

Virtually zero.’ That’s a reasonable estimate of the probability that public health authorities in the foreseeable future will successfully curb the worldwide epidemics of obesity and diabetes, at least according to Margaret Chan, the director general of the World Health Organization (WHO) – a person who should know. Virtually zero is the likelihood, Chan said at the National Academy of Medicine’s annual meeting in October, that she and her many colleagues worldwide will successfully prevent ‘a bad situation’ from ‘getting much worse’. That Chan also described these epidemics as a ‘slow-motion disaster’ suggests the critical nature of the problem: ‘population-wide’ explosions in the prevalence of obesity along with increases in the occurrence of diabetes that frankly strain the imagination: a disease that leads to blindness, kidney failure, amputation, heart disease and premature death, and that was virtually non-existent in hospital inpatient records from the mid-19th century, now afflicts one in 11 Americans; in some populations, as many as one in two adults are diabetic.
In the midst of such a public health crisis, the obvious question to ask is why. Many reasons can be imagined for any public health failure, but we have no precedents for a failure of this magnitude. As such, the simplest explanation is that we’re not targeting the right agent of disease; that our understanding of the aetiology of both obesity and diabetes is somehow flawed, perhaps tragically so.

Researchers in harder sciences have a name for such situations: ‘pathological science’, defined by the Nobel Laureate chemist Irving Langmuir in 1953 as ‘the science of things that aren’t so’. Where experimental investigation is prohibitively expensive or impossible to do, mistaken assumptions, misconceived paradigms and pathological science can survive indefinitely. Whether this is the case with the current epidemics is an all-too-regrettable possibility: perhaps we’ve simply misconceived the reality of the link between diet, lifestyle and the related disorders of obesity and diabetes? As the Oxford scholar Robert Burton suggested in The Anatomy of Melancholy (1621), in cases in which the cures are ‘imperfect, lame, and to no purpose’ it’s quite possible that the causes are misunderstood.

The history of obesity and nutrition research suggests that this is indeed what has happened. In the decades leading up to the Second World War, German and Austrian clinical investigators had concluded that common obesity was clearly caused by a hormonal disturbance; starting in the 1960s, other research would link that disturbance to the sugar in our diets. But the German and Austrian thinking evaporated with the war, and the possibility that sugar was to blame never took hold, dismissed by a nutrition community who, by the 1970s, became fixated on dietary fat as the trigger of our chronic diseases. Now, with an explosion of the epidemic and compelling new research, it’s time to reconsider both our causal thinking on obesity and diabetes, and the possibility that sugar is playing the critical role.

When researchers and public health authorities today discuss their failure to curb the rising tide of obesity and diabetes, they offer the explanation that these disorders are ‘multifactorial and complex’, implying that failure is somehow understandable. But this obscures the reality that prescriptions to prevent and treat the two depend almost entirely on two simple causal concepts, neither one of which is necessarily correct.

The first assumption equates obesity and Type 2 diabetes (the common form of the disease, formerly known as ‘adult-onset’ until it began appearing in children as well). Because obesity and Type 2 diabetes are so closely associated in both individuals and populations, the assumption is that it’s the obesity – or at least the accumulation of excess fat – that causes the diabetes. By this logic, whatever causes obesity is ultimately the cause of the diabetes as well.

The second assumption then strives to explain ‘the fundamental cause’ of the obesity itself: an energy imbalance between calories consumed on one hand, and calories expended on the other hand.

This thinking, espoused by the WHO and virtually every other medical authority, is a paradigm in the true Kuhnian sense of the word. Researchers and public health authorities describe obesity as a disorder of ‘energy balance’. This conception underlies virtually all aspects of obesity research from prevention through treatment, and, by association, diabetes. As such, it has also shaped how we think about the role of what is now, finally, considered a prime suspect – refined or ‘added’ sugars, and specifically, sucrose (table sugar) and high-fructose corn syrup.



The WHO and other health organisations have recently taken to arguing that sugar and particularly sugary beverages should be taxed heavily or regulated. But they do so not because they say sugar causes disease – using the same definition of causality that we use when we say cigarettes cause lung cancer – but, rather, because, from their perspective, sugar represents ‘empty calories’ that we eat in excess. By this thinking, we still get fatter because we eat too much or exercise too little. The solution is to eat in moderation, and consume sugar in moderation or balance it with more physical activity.

The energy balance paradigm implies that the only way in which foods influence our body fat is through their energy content, or calories – that is, through the energy that we absorb without excreting, and so make available to be oxidised or stored. This is the only variable that matters. It’s the implication of the phrase ‘a calorie is a calorie’, which, by the 1960s, had become a mantra of nutrition and obesity researchers, evoked invariably to support the dogma that only calories count when it comes to understanding and treating human obesity.

This logic has been the lifeblood of the sugar industry. If sugar was uniquely toxic, in that it possessed some special property that made us respond to it by accumulating fat or becoming diabetic, then government health agencies would have to regulate it. If all sugar does is add calories to the diet, just as any other food does, then it is, in effect, benign. When the sugar industry embarked in 1956 on a nationwide advertising offensive to knock down reports that sugar is ‘fattening’, it did so on the seemingly sound scientific basis that ‘[s]ugar is neither a “reducing food” nor a “fattening food”’, as the industry advertisementsexplained. ‘There are no such things. All foods supply calories and there is no difference between the calories that come from sugar or steak or grapefruit or ice cream.’

Thinking of obesity as an energy-balance disorder is as meaningless as calling poverty a money-balance problem 

Even 60 years later, in 2015, when The New York Times reported that academic researchers were doing the bidding of Coca-Cola by taking its money to fund a Global Energy Balance Network and ‘shift blame for obesity away from bad diets’, this was still the logic invoked in sugar’s defence: if you believe that obesity is caused by a mere caloric surplus, then the solution to the epidemic is not necessarily to avoid Coca-Cola, but to either consume it (and everything else) in moderation or to burn off the excess calories with physical activity. For the sugar industry and the purveyors, such as Coca-Cola, of sugar-rich foods and beverages, this remarkably resilient, century-old conception of why some of us get fat (or are born fat) and others don’t (or aren’t) has been the gift that keeps on giving.

So here’s another way to frame what is now the imperative question: is the energy-balance hypothesis of obesity correct? Is it the right paradigm to understand the disorder? The competing hypothesis has existed for over a century: in this paradigm, obesity is not an energy-balance disorder but a disorder of excess fat accumulation and so, clearly, a hormonal and metabolic disorder – the result of an ‘endocrine disturbance’, as it was phrased in the 1930s by Eugene Du Bois, then the leading American authority on metabolism. By this logic, the foods we eat influence fat accumulation not because of their caloric content but because of their macronutrient content, the proteins, fats and carbohydrates they contain. This paradigm attends to how organisms (humans, of course, in particular) orchestrate the careful ‘partitioning’ of the macronutrient fuels they consume, determining whether they will be burned for energy or stored or used to rebuild tissues and organs. It proposes that dysregulation of this exquisitely-evolved, finely-tuned homeostatic system (a system that is biologically balanced) is the necessary component to explain both the excessive storage of calories of fat – obesity – and the diabetes that accompanies it. 

This alternate hypothesis implies that sugar has unique effects in the human body leading directly to both diabetes and obesity, independent of the calories consumed. By this way of thinking, refined sugars are indeed toxic, albeit over the course of years or decades. We get fat and diabetic not because we eat too much of them – although that is implied tautologically merely by the terms ‘overconsumption’ and ‘overeating’ – but because they have unique physiological, metabolic and hormonal effects that directly trigger these disorders. If all this is right, then thinking of obesity as an energy-balance disorder is as meaningless as calling poverty a money-balance problem (caused, of course, by earning too little or spending too much, or both). By conceiving of obesity as a problem caused by the behaviours of excessive consumption and physical inactivity, researchers not only took a physiological defect – the excess accumulation of fat, often to a massive extent – and turned it into a behavioural problem. But they made a critical error, one that has grown over the course of decades into an idea that seems too big to fail.

Understanding how this happened requires we attend to history. The modern era of nutrition science dates to the late 1860s, when German researchers pioneered the use of room-sized devices called calorimeters. These allowed them to measure the energy expended by human or animal subjects under different conditions of diet and activity. For the next half a century, effectively all nutrition research was directed toward studying energy balance (the energy content of foods and the energy expended or excreted by those who ate it) and the protein, vitamins, minerals and fibre necessary for health and wellbeing. This was a function of the research tools available at the time, and it has remained the foundation of nutrition wisdom ever since.

Today, when nutritionists say that sugar consists of ‘empty calories’, they’re defining it in the terms of this century-old research and the tools available to researchers of that era. When obesity researchers blame obesity on the imbalance of energy consumed to expended, they’re doing the same. Both are assuming that the science that came after, including the emergence of entire disciplines of medicine, is irrelevant.

The idea of obesity as an energy-balance disorder emerged directly from what was considered one of the great triumphs in nutrition in the late 19th-century: the confirmation that the laws of thermodynamics – conservation of energy, specifically – applied not just to inanimate matter but to living organisms and humans. In line with this research, nutritionists embraced calories and energy as the currency of their discipline, and physicians, speculating as to the cause of obesity, naturally did the same. By the early 1900s, the German diabetes specialist Carl von Noorden was proposing that ‘the ingestion of a quantity of food greater than that required by the body, leads to an accumulation of fat, and to obesity, should the disproportion be continued over a considerable period’.

In the 1920s, Von Noorden’s ideas were taken up in the United States by Louis Newburgh, a physician at the University of Michigan, who espoused what he considered an indisputable truth: ‘All obese persons are alike in one fundamental respect – they literally overeat.’ By assuming that this overeating must be the cause of obesity, Newburgh proceeded to blame the disorder on some combination of a ‘perverted appetite’ (excessive energy consumption) and a ‘lessened outflow of energy’ (insufficient expenditure). To explain why obese individuals failed to respond to this imbalance by either eating less or exercising more – both, after all, should be under conscious control – Newburgh also suggested that the overeating and/or under-expending were often compounded by ‘various human weaknesses such as overindulgence and ignorance’, thus blaming the victim and beginning the process that would turn obesity research in the 1960s into a subdiscipline of psychology and behavioural science. 

This logic is still with us today. By 1939, Newburgh’s biography at the University of Michigan was already crediting him with the discovery that ‘the whole problem of weight lies in regulation of the inflow and outflow of calories’ and for having ‘undermined conclusively the generally held theory that obesity is the result of some fundamental fault’.

The existence of a fundamental fault, however, could not be dismissed so lightly, as German and Austrian investigators were still arguing at the time. They had concluded that obesity could be explained only by such a fault, a hormonal or regulatory defect. Worth noting is that the German and Austrian research communities had pioneered all the fields of science relevant to understanding obesity – including nutrition, metabolism, endocrinology and genetics. They dominated medical science, just as they did physics and chemistry through the Second World War. This was an era during which the lingua francaof science – medical or otherwise – was German, and when individuals serious about pursuing science travelled to Germany and Austria to learn from, if not mentor with, these authorities.

Coincident with von Noorden’s suggestion that obesity was an energy-balance disorder, his contemporary, Gustav von Bergmann, who would become the leading German authority on internal medicine, argued that it was clearly not. Von Bergmann pointed out that the overconsumption of energy that von Noorden was blaming as the cause of obesity – more energy in than out – was merely a description of what happened when the mass of any system increased, not an explanation at all.

The purpose of a hypothesis in science, quite simply, is to offer an explanation for what we observe, either in nature or the laboratory. How many of these observations can the hypothesis explain or predict in a simple and straightforward way? Yet the energy-balance conception fails to explain anything: it cannot explain why calories of fat are trapped in fat tissue rather than oxidised for fuel, nor such simple observations as the genetic basis of obesity (identical twins, after all, are identical not just in their facial features, height and colouring, but in body type too) or why fat accumulates differently in men and women.

With obesity, ‘a sort of anarchy exists, the adipose tissue does not fit into the precisely regulated management of the whole organism’

By von Bergmann’s logic, obesity was clearly not a problem of energy balance, but of fat trapping (just as global warming is not an energy-balance problem, but an energy-trapping one). The question that had to be answered is why this trapping occurs. Any viable hypothesis of obesity had to explain why the fat tissue of the obese is so avid in hoarding calories as fat, rather than allowing that fat to be metabolised and provide energy for the body.

By 1930, Julius Bauer of the University of Vienna – the ‘noted Vienna authority on internal diseases’, as The New York Times called him – had taken up von Bergmann’s ideas, arguing that obesity had to result from a dysregulation of the biological factors that normally work to keep fat accumulation under check. Bauer argued that fat cells are clearly being driven by these factors to hoard excessive calories as fat, and this in turn would deprive the rest of the body of the energy it needed to thrive. In this hormonal/regulatory conception, excessive fat-accumulation causes hunger and physical inactivity, not the other way around.

Bauer likened the fat tissue of an obese person to that of ‘a malignant tumour or … the foetus, the uterus or the breasts of a pregnant woman’, all with independent agendas, causing them to take up calories of fuel from the circulation and hoard them or put them to localised use, regardless of how much the person might be eating or exercising. With obesity, wrote Bauer, ‘a sort of anarchy exists, the adipose tissue lives for itself and does not fit into the precisely regulated management of the whole organism’.

By 1938, Russell Wilder, head of the department of medicine at the Mayo Clinic, was writing that this German/Austrian hypothesis ‘deserves attentive consideration’, and that ‘the effect after meals of withdrawing from the circulation even a little more fat than usual might well account both for the delayed sense of satiety and for the frequently abnormal taste for carbohydrate encountered in obese persons … A slight tendency in this direction would have a profound effect in the course of time.’

In 1940, when Hugo Rony, an endocrinologist at Northwestern University in Chicago, published the first academic treatise written on obesity in the US, he asserted that the hormonal/regulatory hypothesis was ‘more or less fully accepted’ by the European authorities.

And then it vanished. The German and Austrian medical-research community evaporated with the rise of Hitler, and the nexus of medical science shifted from Germany and Austria to the US, a nation not devastated by the war; the lingua franca of medical science shifted as well from German to English. With those shifts, arguably the best thinking of the era in medical science would no longer be read, nor would it be referenced. The conception of obesity as a hormonal regulatory disorder faded out of fashion.

In the post-war era of nutrition and obesity research, Newburgh’s energy balance conception was fixed as the obesity paradigm, not because it answered any meaningful questions about obesity and how, why and when we accumulate excess fat, but because it was a US conception at a time when young American physicians, many with little scientific training, came to dominate the field.

Embrace of the energy-balance paradigm and, with it, the death of the hormonal/regulatory hypothesis, can be seen clearly in the citation records. In 1941, Bauer published what would be his second and last English-language article on obesity: a 27-page review in Archives of Internal Medicine entitled ‘Obesity: Its Pathogenesis, Etiology and Treatment’. (By then, he had fled to the US and was living unaffiliated in Los Angeles). He spent the first third of the article critiquing, point by point, Newburgh’s ‘energy theory of obesity’, and the remainder discussing the ‘biologic theory’, and the evidence for why obesity had to be a hormonal/regulatory disorder. In 1942, Newburgh countered with a 64-page review in the same journal, refuting the biologic hypothesis and insisting that obesity is ‘invariably the result of a disproportion between the inflow and the outflow of energy’. In 1944, Newburgh published a second review, this one in Physiological Reviews, again insisting that von Bergmann and Bauer’s ideas had been refuted.

By 1959, Bauer’s article had been referenced only 10 times and would not be cited again in the indexed medical literature for another half a century. Meanwhile, Newburgh’s two articles on obesity as an energy-balance disorder would continue to be cited through to the end of the 1970s – accumulating 69 and 64 citations by that time respectively, enormous numbers for that era.

Despite its almost-universal acceptance, the energy theory remained at loggerheads with much of the science. For instance, animal models of obesity – the first of which was discussed in the literature in the late 1930s – consistently refuted Newburgh’s arguments and supported Bauer’s. Obese animals would frequently manifest what Newburgh might have described as a perverted appetite (technically, hyperphagia): as they grew fatter they would be exceedingly hungry and consume great amounts of food. But they would invariably get obese, or at least significantly fatter, even when they didn’t eat any more, or weren’t allowed to eat any more than control animals, often littermates, that remained lean. Some of these animals would remain excessively fat even as they were being starved.

Insulin partitions how we use the fuels we consume: it directs fat cells to store fat

Whatever the defect or fundamental fault that caused these animals to accumulate excessive fat, a perverted appetite (ie, overeating) could be ruled out. The defect had to be working either to cause the fat cells to hoard calories as fat, or to suppress the animals’ ability to burn fatty acids for fuel. Or both.

Not until the 1960s, though, would researchers elucidate the basic mechanisms of fat accumulation. To do so required invention of a technology that allowed researchers to accurately measure the level of hormones circulating in the bloodstream. This was the work of Rosalyn Yalow, a medical physicist, and Solomon Berson, a physician. When Yalow was awarded the Nobel Prize for the work in 1977 (by then, Berson was not alive to share it), the Nobel Foundation described it aptly as bringing about ‘a revolution in biological and medical research’. Those interested in obesity could now finally answer the questions on which the pre-war European clinicians could only speculate: what hormones regulate the storage of fat in fat cells and its use for fuel by the rest of the body?

Answers began coming with the very first publications out of Yalow and Berson’s laboratory and were swiftly confirmed. As it turns out, virtually all hormones work to mobilise fatty acids from fat cells so that they can then be used for fuel. The one dominant exception to this fuel-mobilisation signalling is insulin, which partitions how we use the fuels we consume: in particular, it directs fat cells to store fat, while facilitating the uptake and oxidation of glucose (blood sugar) by muscle and organ cells. In other words, when insulin is secreted – primarily in response to the carbohydrates in our diet – it directs our cells to burn carbohydrate as fuel and store fat. And so, the one biological factor necessary to mobilise fat from storage and have it used for fuel, as Yalow and Berson suggested in 1965, is ‘the negative stimulus of insulin deficiency’. Put simply, when insulin levels in circulation are elevated, we store fat and use glucose for fuel; as insulin levels drop, fat is mobilized and we burn it instead.

Yalow and Berson themselves described insulin as a ‘lipogenic’, or fat-forming hormone. This lipogenic signal must be turned off, or at least muted significantly, for the fat cells to release their stored fat and for the body to metabolise it for energy. While obesity researchers like to say that the sine qua non of a weight reduction diet is calorie-restriction, this alternative, biologically-based hypothesis would say that the sine qua non is lowering insulin. The more we consume carbohydrates, though, and particularly sugar, the higher i our insulin levels will be.

The potential role of insulin in obesity was illuminated further by a second revelation from Yalow and Berson’s early research: both Type 2 diabetics and the obese tend to have elevated levels of blood sugar and abnormally high levels of circulating insulin. This implies that the cells of their muscles and organs are resistant to the insulin circulating in their blood, an observation that was also quickly and widely confirmed. By the mid-1960s, both physicians and researchers were realising that Type 2 diabetes was not a disease of insulin deficiency – as Type 1 diabetes is – at least not at first, but one of insulin resistance. But if insulin is a fat-forming hormone and Type 2 diabetes is a disorder of insulin resistance, it then follows that high circulating levels of insulin in the blood, rather than insulin deficiency, could be the cause of the disease and obesity as well.

Perhaps the obese get that way not because they eat too much or exercise too little, but because they have elevated levels of insulin or their fat tissue is excessively sensitive to the insulin they secrete. Perhaps the relationship between obesity and Type 2 diabetes is not one of cause and effect, as doctors have said for years.

Berson and Yalow saw it another way: ‘We generally accept that obesity predisposes to diabetes; but does not mild diabetes predispose to obesity?’ the team wrote in 1965. ‘Since insulin is a most potent lipogenic agent, chronic [elevated insulin] would favour the accumulation of body fat.’

If Yalow and Berson’s speculation were to be true, and it certainly made sense from a biological perspective, then obesity could clearly be a hormonal/regulatory defect and Bauer and von Bergmann would have been right. Embracing this conclusion, though, depended on explaining why we become insulin-resistant. By rejecting a hormonal hypothesis of obesity two decades earlier, obesity researchers had predetermined how they would answer the question: by assuming that insulin resistance was caused by obesity, and insisting that obesity itself was caused merely by taking in more calories than expended. And that’s what they did.

The problem, as ever, appears to have been cognitive dissonance: Yalow and Berson’s revelations led both directly and indirectly to the notion that diets restricted in carbohydrates – and restricted in sugar most of all – would be uniquely effective in slimming the obese. By the mid-1960s, these carbohydrate-restricted diets, typically high in fat, were becoming fashionable, promoted by working physicians often in the form of hugely successful diet books.

Academic nutritionists led by Fred Stare and Jean Mayer of Harvard denounced these diets as dangerous fads because of their high fat content and perhaps, in Stare’s case, because of funding from the sugar and grain industries. They suggested that the physician-authors were trying to con the obese with the fraudulent argument that they could become lean without doing the hard work of curbing their perverted appetites.

This battle played out through the mid-1970s, with the academic nutritionists and obesity researchers on one side, and the physicians-turned-diet-book-authors on the other. The obesity researchers began the 1960s believing that obesity was indeed an eating disorder – Newburgh’s perverted appetite. The ongoing revolution in endocrinology, spurred by Yalow and Berson’s groundbreaking invention, failed to convince them otherwise.

The cognitive dissonance created by the biological revelations of the role of insulin in fat storage can still be seen in textbooks today. These books – for instance, the LehningerPrinciples of Biochemistry, now in its sixth edition – have discussions of the regulation of fat accumulation in fat cells, in which the process is said to be driven by ‘high blood glucose elicit[ing] the release of insulin’, which favours fat storage ‘while inhibiting fatty acid mobilisation in adipose tissue’. And yet they also have sections on human obesity that state dogmatically that it is ‘the result of taking in more calories in the diet than are expended by the body’s energy-consuming activities’. Both exist side by side in the same books. Both cannot be true. The unjustifiable implication is that the mechanism determining whether or not our fat cells accumulate excessive fat are somehow different from those determining whether we become fat ourselves, despite our excess fat accumulation being merely a summation of all the excess fat stored in those cells.

Focusing on the problems of eating too much and exercising too little, health authorities have failed to target the correct causes

A far more parsimonious hypothesis is that the same thing that makes our fat cells fat makes us fat: ‘high blood glucose’ and concomitant elevated levels of insulin and the insulin resistance itself, both caused by the carbohydrate content of our diets. Insulin is secreted in response to rising blood sugar, and rising blood sugar is a response to a carbohydrate-rich meal. Sugar is implicated, in particular, because its chemical structure includes a large proportion of the carbohydrate fructose, and fructose is preferentially metabolised in the liver. As such, it is a prime suspect for the fat accumulation in liver cells that is hypothesised to be the trigger of insulin resistance itself.

If we accept von Bergmann and Bauer’s thinking that obesity is a hormonal/regulatory disorder and combine it with the revelations of the 1960s about the hormonal regulation of fat accumulation and the insulin resistance that is associated with obesity and diabetes, then the result is a very simple hypothesis that explains not just obesity but also the current epidemics and our failures to curb them. The sugars and refined grains that make up such a high proportion of the foods we consume in modern Westernised diets trigger the dysregulation of a homeostatic system that has evolved to depend on insulin to regulate both fat accumulation and blood sugar. Hence, the same dietary factors – sugars and refined grains – trigger both obesity and diabetes. By focusing on the problems of eating too much and exercising too little, public health authorities have simply failed to target the correct causes.

Scientific understanding is always driven by the tools available to do the research. These tools dictate the questions that can be asked, and the answers that can be obtained – and that, in turn, tends to shape causal hypotheses and paradigms. Ideally, when new technology comes along and new questions can be asked, then new answers can be obtained, and paradigms can shift. But this requires that the research community be open to new evidence and new ways of thinking. In nutrition and obesity research, particularly at critical times in the evolution of the science, this was simply not the case. With the epidemics of obesity and diabetes having long ago passed into crisis level, isn’t it time we finally considered seriously the possibility that our prescriptions and approaches to prevention and treatment of these diseases are simply wrong, based on incorrect paradigms and a century of misguided science?

Adapted from ‘The Case Against Sugar’ by Gary Taubes. Copyright © 2016 by Penguin Random House. Adapted by permission of Alfred A Knopf, a division of Penguin Random House LLC. All rights reserved. No part of this piece may be reproduced or reprinted without permission in writing from the publisher.

viernes, 13 de octubre de 2017

Please, Not Another Bias! The Problem with Behavioral Economics An evolutionary take on behavioral economics


By Jason Collin

Below is a transcript of my planned presentation at today’s Marketing Science Ideas Xchange. The important images from the slide pack are below, but the full set of slides is available here.
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Please, not another bias! An evolutionary take on behavioural economics
Thank you for the invitation to speak today.
I accepted the invite because natural selection has shaped the human mind to take actions that have, in our past, tended increase reproductive success.
That statement isn’t as creepy as it sounds. I did not calculate the direct reproductive opportunity of this speaking engagement. Rather, our evolutionary past means that we are inclined to pursue proximate objectives that lead to the ultimate goal.
For example, we seek status – and what could be more status-enhancing than speaking here. And we engage in the costly signalling of our traits – such as intelligence – to the opposite sex, allies or rivals.
Another place where I signal is my blog, Evolving Economics. A copy of these slides and the text of what I plan to speak about today – which should approximate what I actually will speak about – will be posted onto Evolving Economics before the end of today’s talk. That text includes links to the studies I will refer to.
To explain why I engage in this costly signalling – conference speaking, blogging and the like – I will first take a step back and explain how the evolutionary approach to decision making relates to other approaches, starting with behavioural economics.
And I should say that I am going to refer to “behavioural economics” today, even though what I am going to talk about is more rightfully called “behavioural science”.
I once had an online discussion about this point with last year’s MSiX headlining speaker Rory Sutherland. I was in the behavioural science camp, but he said that the term behavioural economics was fantastic marketing and is effective in getting the attention of economists. Even though calling it behavioural economics is a slight to the psychological foundations of this work, we should live with it.
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Now that I work in this space and I have used the terms behavioural science and behavioural economics with a range of clients and colleagues, I am convinced that Rory was right. I receive blank looks when I use the term behavioural science. I attract immediate interest when I use the term behavioural economics.
So, to content. And I am going to start with a complaint. In some ways I am following the traditional format of a behavioural economics talk, which sets up the rational homo economicus straw man, and beats it to death with a series of examples of how irrational we really are. But for a change, I am going to start by beating up on behavioural economics.
And I should say that, despite this bit of bashing, I have a soft spot for behavioural economics. It’s my day job for a start – helping clients in the private and public sectors better understand how their customers, employees and citizens make decisions, and how they can help them to make better ones. It’s just that behavioural economics could be so much more.
There are not 165 human biases
Wikipedia
So, I want to take you to a Wikipedia page that I first saw when someone tweeted that they had found “the best page on the internet”. The “List of cognitive biases” was up to 165 entries on the day I took this snapshot, and it contains most of your behavioural science favourites … the availability heuristic, confirmation bias, the decoy effect – a favourite of marketers, the endowment effect and so on ….
But this page, to me, points to what I see as a fundamental problem with behavioural economics.
Let me draw an analogy with the history of astronomy. In 1500, the dominant model of the universe involved the sun, planets and stars orbiting around the earth.
Since that wasn’t what was actually happening, there was a huge list of deviations from this model. We have the Venus effect, where Venus appears in the evening and morning and never crosses the night sky. We have the Jupiter bias, where it moves across the night sky, but then suddenly starts going the other way.
CassiniPutting all the biases in the orbits of the planets and sun together, we end up with a picture of the orbits that looks something like this picture – epicycles on epicycles.
But instead of this model of biases, deviations and epicycles, what about an alternative model?
The earth and the planets orbit the sun.
CopernicusOf course, it’s not quite as simple as this picture – the orbits of the planets around the sun are elliptical, not circular. But, essentially, by adopting this new model of how the solar system worked, a large collection of “biases” was able to become a coherent theory.
Behavioural economics has some similarities to the state of astronomy in 1500 – it is still at the collection of deviation stage. There aren’t 165 human biases. There are 165 deviations from the wrong model.
So what is this unifying theory? I suggest the first place to look is evolutionary biology. Human minds are the product of evolution, shaped by millions of years of natural selection.
A hierarchy of decision making
To help you understand what an evolutionary lens adds to our understanding of human decision making, I am going to place evolutionary biology in a hierarchy of possible ways to consider the mind.
The first four reflect a hierarchy presented by Gerd Gigerenzer in his book Rationality for Mortals (if you haven’t read any Gigerenzer, do).
First, we have the perfectly rational decision maker, homo economicus, who exhibits unbounded rationality. If you have been to enough behavioural economics presentations, you have already seen this model beaten to death.
The next is a model provided by economists in response to some of the behavioural critiques – a model of decision making under constraints. If you add costs to information search – there is your role for advertising and marketing – and possibly some limits to computational power, we get different decisions. It is a nice idea, but an even less realistic version of how people actually think. If you have done any late secondary or early tertiary mathematics, you will know it’s typically harder to make calculations with constraints than it is to be the unbounded rationaliser.
The third model is the heuristics and biases program of behavioural economics. Gigerenzer calls this work the search for “cognitive illusions.” I have already complained about that.
Next comes what Gigerenzer calls ecological rationality. I want to spend a moment or two talking about this as it is very similar to an evolutionary approach, minus one important feature.
Ecological rationality
The ecological rationality approach involves asking what decision making tools the user possesses. You then look at the environment in which those tools are used, and then you can assess how those tools perform in that environment. The decision making tools and environment in which they are used are two blades of the same scissors (Herbert Simon used this description) – and you need to examine both the tool and the environment to understand the nature of the decision that has been made.
Through this approach you might see what are called “biases” emerge, but an ecological rationality approach allows you to understand the basis of the bias. Instead of just noting someone has made a poor decision, you might note why they were wrong and in what alternative environments those decision rules might be more effective.
Let me give you an example – the gaze heuristic (a heuristic is a mental shortcut). The gaze heuristic is a tool that people – and dogs – use to catch balls. The heuristic is simply this – maintain the ball at a constant angle of gaze. If you move to keep this angle constant, you will end up where the ball lands. Obviously, this is easier than calculating where you should be from the velocity of the ball, angle of flight, the effect of wind resistance and so on.
But it results in a strange pattern of movement. Suppose you are close to the point where the ball is first hit into the air. As it rises you will tend to back away from the ball. As it then starts to fall, you will move back in. If it is hit up to the side of you, you will move to the ball in a curve. Now, if you had a behavioural economist look at the path you took to catch the ball, they might call it the curve bias or something like that – but it is actually the result of a very effective decision making tool.
There are also some circumstances where it works better, and some where it fails. It tends to work best when the ball is already high in the air. If you catch sight of a ball hit straight up before it has risen far, using the heuristic for its entire flight could require an impossible feat of first running away from the ball and then toward it. When we see fielders messing up a catch when the ball is hit straight up, it can be the backfire of this heuristic.
Understanding this is a much richer understanding than saying that the fielder is biased because he did not run straight to where the ball was going to land. It also points to the power of heuristics. Try to train someone to run straight to where a ball will land and watch them fail. Don’t see these decision making shortcuts as poor cousins of the “more rational” approaches.
Let me give another more marketing orientated example – the recognition heuristic. The heuristic runs along the line of “If I recognise one of two objects and not the other, then infer that the object I recognise has higher value.”
Obviously, people might use the recognition heuristic when shopping for a product. If I recognise one brand but not the other, I might assume the brand I know is superior.
The recognition heuristic will work when recognition is correlated with the quality of the product. I am sure you know plenty of products where brand strength is a good indicator of quality. And of course, one of the jobs of marketers is to make sure the recognition heuristic delivers success for their client – you are trying to achieve brand recognition. Then again, there are other products where brand strength probably leads people to make some poor decisions. My personal view is that the recognition heuristic works particularly poorly when it comes to beer.
Evolutionary rationality
Now, I consider Gigerenzer’s approach to be superior to the biases and heuristics or “cognitive illusions” approach. But it still leaves open the question of where these heuristics and other decision making tools come from. And this is where we get to the fifth level – what I will call evolutionary rationality. The toolbox that we use today has been honed by millennia of natural selection.
Anticipating two common responses to this point, I am not going to spend today trying to convince the doubters in the audience that the human mind is a product of evolution – although I am happy to do that over a drink later.
And I will highlight that humans are cultural and well as biological creatures. That we have a range of universal instincts and preferences shaped by natural selection does not say that culture is not important. What we see is a combination of evolved preferences, social norms, technologies and the like, each interacting with and shaping the others. Yes environment matters, but if you ignore the biology, you will do a poor job of understanding why consumers act the way they do.
So what does an evolutionary approach tell us about the human mind?
For a start, it tells us something about our objectives. Those who are in the audience today – all of your ancestors, without fail, have managed to do two things: survive to reproductive age, and reproduce. As little as you might like to think about it, your parents, grandparents and so on all the way back until the evolution of sex have always successfully attracted a partner to reproduce with.
This does not mean that we literally walk around assessing every action by whether it aids survival or reproduction. Instead, evolution shapes proximate mechanisms that lead to that ultimate goal. And consumer preferences are manifestations of our innate needs and preferences.
For example, on survival – we are obsessed with food – and in particular, crave sweet and fatty foods – which in historical times increased survival. Most of the successful global fast-food restaurants target those evolved tastes (in fact, you could say that the market has evolved to match those propensities).
We have an innate sense of danger – for example, we (and other animals) are quicker at detecting snakes than other stimuli, even when we have never seen them before.
On reproduction, we enjoy sex – which has obvious reproductive benefits, at least before the spread of effective contraception. We accumulate resources far beyond those required for survival. And so on.
Before going on, however, I should say that the shaping of proximate rather than ultimate mechanisms for survival and reproduction has some interesting consequences. Our evolved traits and preferences were shaped in times vastly different to today. Our taste for food was shaped at a time when calories were generally scarce and provided in the form of meat, tubers, nuts, vegetables and Glyptodons. The gorging that would occur after the occasional slaughter of a large prey is very different to the eating that occurs in today’s age of grain and calorie abundance. Today, we are effectively calorie unconstrained.
And the joy of sex that once led us to have children clearly isn’t working as efficiently as it once did. Fertility across the developed world has plunged – although I’d be happy argue later over a drink that evolutionary forces will tend to drive fertility back up.
This backfiring of our evolved traits and preferences is known as mismatch. Our evolved traits do not always match the new modern environment – and this is something that makes Gigerenzer’s model of looking at the interaction of the decision making tools with the environment such a useful tool for analysis. Sometimes the tool works. Sometimes it doesn’t.
So what does evolutionary biology tell us about human decision making, behavioural economics and marketing?
Sex
FerrariSo, let’s do a quick quiz. Tell me two things about the driver of this Ferrari (I have stolen this example from University of New South Wales evolutionary biologist Rob Brooks).
First, the driver was male. Yes, men and women are different – we will touch on the reasons for this in a moment – although I expect most marketers already knew this.
Second, the driver is likely young (in this case, 25).
So why is this the case?
Females – and in biology, this is in part how females are defined – produce a large immobile egg. Males produce a smaller gamete – sperm. The egg is the scarce resource. Women are born with a million or so eggs, but they release only one or so a month. Men produce 1,500 sperm a second. Each man in this room will produce enough sperm during this talk to fertilise every egg the women in this room will ever produce.
Then there is what happens when a sperm and an egg are joined. The woman spends nine months carrying the baby – and is unable to reproduce during that time. She then provides the majority of infant care. Men are less constrained by any such barriers.
Then throw in that women are certain of maternity, whereas men may not be certain of paternity, and you have vastly different patterns of reproduction between the sexes.
More men than women have zero children – the worst possible evolutionary outcome. A man who applies no standards to a mate choice may still go without. A woman would never have that problem.
Then, for a few men, the rewards are vast.
As one example, approximately 16 million men in central Asia carry the same Y chromosome – the Y chromosome is passed from down the male lineage from father to son. This chromosome originated in Mongolia around 1000 AD with around 8 per cent of the men in the region carrying it (0.5% of the world’s male population) – they all trace their male lineage back to the same man.
One possibility is that this chromosome was so successful as it was carried by Genghis Khan and his close relatives. Genghis had multiple wives and a harem. He may have fathered thousands of children. His grandson Kublai Khan was famous for the size of his harem – I have seen some estimates that it contained 7,000 women (although haven’t been able to reliably source those estimates). Whether that number is accurate or not, it is feasible that Kublai Khan could have been having hundreds of children a year.
No woman could ever have that level of success – but for men, the evolutionary rewards to success can be vast.
This brings us back to our Ferrari driver. As a male, the risk-reward calculation in evolutionary terms is quite different from women. Men face a higher probability of evolutionary oblivion, and small chance of an evolutionary extravaganza. It makes sense to take risks that may lead to inordinate evolutionary success – or at least to avoid evolutionary oblivion.
One of my favourite examples of this comes from research by Richard Ronay and Bill von Hippel. They got some young male skateboarders to perform tricks, including a difficult trick that they could complete only half the time. Halfway through filming, a woman rated as highly attractive (corroborated by “many informal comments and phone number requests from the skateboarders”) walked onto the scene. Once she appeared, they took more risks and were less likely to bail a trick half-way through, instead riding all the way through to the crash landing (a story on ABC’s Catalyst demonstrates this effect).
First, this risk taking should be seen in the context of what they are trying to achieve – attracting the female. So much of economics – and behavioural economics – is looking at the wrong objective.
Second, this change in risk preference in the presence of a women points to one of the most important findings in evolutionary psychology – our decision-making changes with the immediate context. We might be considered to be different personalities. Evolution has not shaped an all-knowing computer, but rather a modular computer for making different decisions based on different contexts.
As an example of this, show one group of people the movie The Shining, the other half a romantic movie starring Ethan Hawke. Then manipulate the ads they see during the movies to either accentuate the uniqueness of the product, or its popularity.
Those watching The Shining are more likely to prefer popular products – safety in numbers as their danger avoidance personality is triggered. For those watching the romantic movie, they wanted unique products so that they would stand out from the crowd. Their mating motives have been triggered. You effectively get a change in preferences based on which movie they are watching and which self is answering the questions about the products. The effectiveness of social proof varied with context.
Present bias
Let’s look at a traditional behavioural economics problem – present bias, which is the strong preference for present rewards over those in the future. The largest discount for the initial delay.
If I ask you the following question, some of you will choose A, and some B.
Choose between:
  1. One apple today
  2. Two apples tomorrow
But if I ask you the following question, almost no-one will choose A:
Choose between:
  1. One apple in one year
  2. Two apples in one year and one day
This change in preference shouldn’t be seen if we discount the future consistently. And if I asked you to revise your choice in the second question at the one year mark, I am effectively asking you the first question and some of you might change your mind.
On the one hand this seems irrational. But what if the immediate objective isn’t maximising lifetime consumption of apples?
In an experiment by Margo Wilson and Martin Daly – two of the pioneers of evolutionary psychology, and I recommend you read their book Homicide if you haven’t – they exposed men and women to either pictures of attractive faces or pictures of cars before undergoing tests of their degree of present bias.
The men who had seen the attractive faces became more severe discounters than those who had seen the cars. They became focused on the present – the mating opportunity.  The women did not become increasingly severe discounters in this experiment – although there may be a smaller effect that the experiment did not have the power to detect.
So here, what might be called a very strong present bias has a degree of rationality to it in that the objective of the participants is mating. Obviously, they didn’t have a chance to mate with these pictures – so there we have the issue of mismatch – but you can see the evolutionary foundation of their decision. If they did manage to capitalise on that moment and manage to mate, their evolutionary future is set.
MantisAn extreme example of this is seen in other species. A male black widow or preying mantis would allow themselves to be eaten at the moment of mating – this picture is of a male preying mantis getting lucky but losing his head as a consequence – massive present bias in terms of the typical measures an economist might use, highly rational from an evolutionary perspective.
Costly signalling
Now I want to move to what I believe is the most important idea I will communicate today.
Shortly after publishing The Origin of Species, Charles Darwin wrote “The sight of a feather in a peacock’s tail, whenever I gaze at it, makes me sick!”. He wrote this because, to him, the tail simply did not make any sense. It harmed the peacocks chance of survival. Why would a female mate with a long-tailed male and subject her long-tailed son to the same dilemma.
But in the mid-1970’s an evolutionary biologist, Amotz Zahavi, proposed that signals such as peacock tails can be a trusted as they handicap the bearer. Only a high quality peacock can bear the cost. If a sickly peacock tried to carry such a large tail, they’d be toast. In evolutionary lingo, the peacock’s tail is an excellent fitness indicator.
Biologists argued about whether signals could be honest because they create a handicap for fifteen or so years after Zahavi espoused this theory. But in the early 1990s it was agreed that the maths checked out, and the idea is now broadly accepted by biologists.
This handicap principle also applies to human signalling. When humans are seeking a mate, you want to know as much as you can about them. You want to know their intelligence, their health, the level of conscientiousness, their kindness, the resources at their disposal and so on. You can’t just see this straight away – so people seek to signal these traits. And the products they buy are a major part of that signal.
Conspicuous consumption
The most obvious example of this type of signalling is conspicuous consumption. Conspicuous consumption is a signal of resources and the traits required to acquire those resources.
One of the most expensive watches in the world is the Patek Philippe Calibre 89. I first heard of this watch when I read Robert Franks Luxury Fever. Only four were made, with the first selling for $2.5 million and the last auction price I can find was over $5 million.  The watch has 1728 components, gives you the date of Easter each year, and unlike most mechanical watches, will not record the years 2100, 2200 and 2300 as leap years, while still recording 2400 as one (as per the order of Pope Gregory XIII in 1582). It has 28 hands and there are 2800 stars on the star chart.
Since it is mechanical, it includes a tourbillon, a mechanism to improve accuracy by accounting for the earth’s rotation. But the funny thing is that my cheap quartz watch does not require such a mechanism, as gravity does not affect the vibrations of the crystal. The Calibre 89 also weights over a kilo and is the size of a hockey puck. For several million dollars less, I have scored a more accurate watch that I can wear.
But it is the waste inherent in the Calibre 89 that makes it a reliable signal of resources – and the qualities required to accumulate those resources. All that extra expenditure is effectively waste that a man with low resources cannot bear. Think of all the most expensive consumer goods – super yachts, high quality sports cars, gold Apple watches. In terms of transport or timekeeping there are much cheaper and in fact much more reliable methods, but the waste inherent in these goods makes them an excellent signal of resources.
So, does this conspicuous consumption actually work as a signal?
There’s a decent size literature on this topic, so let’s look at two typical experiments – one on the desire of men to conspicuously consume, a second on the effect of that consumption on women.
Take a group of men and show them pictures of attractive women and then ask them what they will do with their money. The mating prime makes men more likely to engage in conspicuous consumption or conspicuous charitable donation, but has no effect on inconspicuous consumption.
Women can also be affected by mating primes, although in that particular experiment their change in behaviour in response to pictures of attractive men was an desired increase in volunteering in a public way (but no increase in private benevolence).
The difference reflects the different traits each are communicating – men are communicating resources and the traits required to accumulate them, women their conscientiousness.
Dunn et alOn the effect of the signal, in one studymen and women were shown pictures of members of the opposite sex in either a red Ford Fiesta or a silver Bentley. Unfortunately the photos in the paper are provided in black and white – as shown in this slide – but these indicate the types of images the experimental subjects were shown.
The result – the expensive car made the male more attractive to the females, whereas there was no effect on male perception of the female drivers. The increase in male’s attractiveness was equivalent to around 1 point on a scale of 1 to 10.
Signalling other traits
Of course, signalling involves far more than conspicuous consumption. We don’t only signal resources, but want to signal intelligence, conscientiousness, agreeableness or other features.
We buy a Cassini 1100 mm reflecting telescope to signal our intelligence. We subject ourselves to year’s of post-secondary education to signal intelligence and conscientiousness. We buy hybrid cars to signal our agreeableness. And we don’t only signal to potential mates. We also signal to friends, relatives and rivals.
Importantly, good signals are difficult to fake. It is difficult to exploit many products if you don’t have the right personality traits – faking education below certain levels of intelligence or conscientious is too difficult, faking wealth will run a poor person dry, faking appreciation of jazz if you have low openness will drive you nuts – the handicap is what makes the signal reliable.
Ultimately, this approach indicates that there is an important question to be asked when marketing a product. How does your product or brand allow the consumer to signal their traits to potential mates, their spouse, allies or rivals?
Unfortunately, it’s not as simple as communicating this point directly to a potential consumer in your advertisements. A sports car ad for young males does not directly inform them that it will attract more females.
That is, unless you are Lynx, or Axe as it seems to be called in most countries. Lynx states the strategy overtly – “Lynx gives guys the edge in the mating game”.
But is this actually the strategy for most products? It is just a question of how many times removed the product is from mating outcomes. The product will increase your status, giving you an edge in the mating game. This product will intimidate rivals, giving you an edge in the mating game. This product will indicate your wealth, giving you an edge in the mating game. This product will allow you to get a high paying job to buy a sports car to indicate your wealth to give you an edge in the mating game.
So when a man sees a billboard with an attractive woman on a billboard, it gets attention. And from an evolutionary perspective, this is exactly the sort of thing that would draw attention. In our evolutionary past, an attractive woman would have been right there – you might think you are in with a shot.
But there is another more important, subtle message. This product will help you in the mating game. The girl on the car gets attention, but the more important implicit message is that this car can get you the girl. I understand there is the saying “sex sells”, and then the rebuttal, “sex sells, but only if you are selling sex”. Well, far more of you are selling sex than you realise.
Personally, I’d like to see more research in this area. Survey the buyers of different cars for number of sexual encounters too see if there is a difference. Of course, we have selection bias issues with those who buy the cars – so maybe we need some random allocation of sports cars to get some reliable results.
A reading list
Now, I have only scratched the surface over the last half hour or so, but if you are interested in this area, here are a few books to get you started – and I should say that these books heavily influenced what I have talked about today.
MSiX reading
The Red Queen: Sex and the Evolution of Human Nature by Matt Ridley was the first book that made me realise that evolutionary biology was at the core of understanding human behaviour. The first half gives a great synopsis of the origins of sex – that is, why we have sex as opposed to budding off clones – and the second asks what this means for human interactions.
In Spent: Sex, Evolution and Consumer Behavior, Geoffrey Miller asks whether the signalling we engage in in a mass-consumerist society does a good job of signalling the traits of interest. A consumer culture has a degree of self-deception – that above average products can compensate for below average traits. We get to know each other in minutes and are quite good at judging other people’s qualities from our interactions – that is, our intelligence, conscientiousness and so on. We can see through the product haze, and most products do a crap job of signalling the traits we think we are.
Next, Gad Saad is the pioneer of examining consumption through an evolutionary lens.The Evolutionary Bases of Consumption is a more technical book, while The Consuming Instinct: What Juicy Burgers, Ferraris, Pornography, and Gift Giving Reveal About Human Nature is an easier read. By the end of those two books the idea that evolutionary theory is important for understanding consumption decisions will have been well and truly hammered into you.
I spoke a lot about signalling, and Amotz Zahavi was the person in the mid-1970’s who first saw how important this is in biology. The Handicap Principle: A Missing Piece of Darwin’s Puzzle is his popular book on the topic. Robert Frank’s Luxury Fever extends the examination of signalling to conspicuous consumption.
Gerd Gigerenzer’s Rationality for Mortals: How People Cope with Uncertaintyis from where I stole the first four stages of human decision making. If you do start reading Gigerenzer’s books, I suggest you don’t stop there.
The Rational Animal: How Evolution Made Us Smarter Than We Think by Douglas Kendrick and Vlad Griskevicus in some ways does what I did in the early part of the presentation – they show that many apparently irrational actions are actually quite rational from an evolutionary perspective. They are behind a lot of the studies I have referred to.
And then there are some related articles that I also recommend reading – particularly by Owen Jones who writes a lot about the need to interface behavioural economics and evolutionary biology.
I have a longer reading list on my blog, where I have reviews of many of these books and links to interesting papers.
Three thoughts to chew on
So, having said all this, here are three ideas for you to walk away from this presentation with.
Obviously, to understand humans you need to understand our evolutionary past. An evolutionary lens provides a guide as to what people are looking for in a product. As Gad Saad points out in The Consuming Instinct, try selling Harlequin-type romance novels to men and see where that takes you – some strategies will be doomed to failure because they do not align with our evolved preferences.
Second, a large part of our evolved behaviour involves our desire to signal important traits and qualities to potential mates, allies and rivals. When buying a product, what traits does the consumer believe they will be signalling?
And third, our evolved minds are sometimes out-of-sync with our modern environments. Use Gigerenzer’s framework (or Herbert Simon’s scissors) – what are the decision making tools we have evolved to use, what is the environment we intend to use them in, and what is the resulting decision? Biases, purchases and a large range of human behaviour will make much more sense when looked at from this lens.
2016 September 25