49 pages • 1 hour read
Chris van TullekenUltra-Processed People: The Science Behind Food That Isn't Food
Nonfiction | Book | Adult | Published in 2023A modern alternative to SparkNotes and CliffsNotes, SuperSummary offers high-quality Study Guides with detailed chapter summaries and analysis of major themes, characters, and more.
Part 2Chapter Summaries & Analyses
Part 2, Chapter 5 Summary: “The Three Ages of Eating”
In this chapter, van Tulleken attempts to better understand UPF and its effects on our bodies by looking at what he calls the three “ages of eating” (79). He looks at the means, in these different ages, by which life extracts energy from its environment to grow and procreate. In the first age, bacteria “ate” inorganic materials like iron to make energy. In the second age of eating, an evolutionary shortcut emerged where some animals got their energy from eating other life that had already processed energy. As animals became more complex in this second age, so did their eating requirements. Eating was needed to provide both energy to live and “the elements and molecules that we need to make our bodies” (84).
The evolutionary competition of the second age drove complex systems, like the gut microbiome, to extract the necessary energy and materials from food and to neutralize toxins produced by plants to protect themselves. As a development of this age, processing and cooking gave humans a large evolutionary edge over other predators. It allowed them to kill parasites and extract more energy from food. In 1879, with the invention of saccharin, humans entered the third age of eating. This involved the eating of molecules not found in nature but artificially created by industrial processes.
Part 2, Chapter 6 Summary: “How Our Bodies Really Manage Calories”
Van Tulleken argues that due to the evolutionary arms race in the second age of eating, human beings have developed an internal regulatory mechanism governing caloric and nutrient intake and the way we store calories as fat. This complex system, rooted in our microbiomes, organs, and fat tissue, also regulates the hormones governing when, what, and how much to eat. The process includes the regulation of feelings of satiation and fullness. Van Tulleken suggests that there is something about UPF, beyond it being more appetizing, that disrupts or bypasses those mechanisms governing appetite and weight gain. Further, van Tulleken argues that it is this disruption that is responsible for growing rates of obesity.
Part 2, Chapter 7 Summary: “‘Why It Isn’t About Sugar…”
In 2002, the US nutritionist Gary Taubes challenged what had been, up to that point, the orthodox view that fat was responsible for people being overweight. This was partly a response to the fact that low-fat diets had been recommended since the 1970s but obesity levels had risen in the same period. In a 2002 paper, Taubes argued that carbohydrates are to blame. This is because, he says, carbohydrates raise insulin by spiking blood sugar, which turns sugars into fat while also reducing blood sugar, leading to more hunger.
Van Tulleken argues that there are serious flaws with Taubes’s hypothesis. While dietary advice has suggested since the 1970s that people should eat less fat, “they had not been eating less fat” but had “been eating more” (112). As such, it is still not clear that fat is not a cause of obesity. A 2012 Nutrition Science Initiative experiment run by Kevin Hall found that there was no difference in weight gain in a two-week period between those put on a high- or low-carbohydrate diet.
Part 2, Chapter 8 Summary: “…Or About Exercise”
Van Tulleken discusses one of the other most cited causes of rising obesity levels—lack of exercise. According to this view, lack of physical activity in the Western world in the 20th century, and especially since the 1970s, has led to growing obesity because, as a culture, we are burning fewer calories. However, van Tulleken argues that studies, including one by Herman Pontzer at Duke University, have undermined this view. Pontzer measured levels of oxygen inhaled and carbon dioxide, as a measurement of calories burned, and found that the number of calories burned by the Hadza, a contemporary hunter-gatherer community, was “very similar to that of American and European populations” (130). Likewise, captive chimpanzees have been shown to burn the same number of calories as wild chimpanzees.
These apparently counterintuitive findings are possible, suggests van Tulleken, because when we do more physical activity, our bodies scale back on the energy expended on nonessential physical and bodily processes. As such, when we exercise, less energy is expended on the immune, endocrine, reproductive, and stress systems. This is to maintain a relatively constant level of caloric expenditure regardless of the physical activity done. Consequently, exercise does not cause weight loss and is not responsible for the obesity crisis.
Part 2, Chapter 9 Summary: “…Or About Willpower”
Another popular idea, linked to the exercise thesis, is that obesity is connected to a failure of willpower. According to this view, while some people are obese due to their genes, others are obese because of an inability to exercise restraint in their eating. Van Tulleken argues against this. He says that while genes influence our eating behavior, their activation is caused by the environment and whether it is conducive or obstructive to proper eating. “Food environments” include the “physical, economic, political, social and cultural contexts” that affect what we buy and eat (143). It is beyond our control if we find ourselves in a bad food environment and whether genes for overeating are activated. Therefore, obesity has nothing to do with willpower or its lack.
Part 2, Chapter 10 Summary: “How UPF Hacks Our Brains”
As part of his four-week experiment with a UPF diet, van Tulleken went to have an MRI scan. This was to test the effect UPF might be having on his brain, alongside the physical effects of weight gain, constipation, and “totally deranged” appetite hormones (160). The scans found increased connectivity between brain areas involving hormonal control of food intake and those involved in desire and reward. Van Tulleken says that these changes in brain states reflect a growing addiction to UPF. He explains that this coincides with his conscious feeling that it was increasingly difficult to resist UPF or control his intake of it.
Part 2 Analysis
Despite the commonly cited causes of obesity being in some sense varied, they are unified around the “abundance hypothesis.” This states that obesity is caused by life for contemporary humans becoming too easy, both in terms of access to food and the need to exercise. This model stresses that in our evolutionary past, “food had generally been hard to get hold of” (102). Acquiring food involved hunting and gathering seasonal fruits and vegetables, both of which were temperamental and uncertain. As such, “we have evolved to find food rewarding” and are “driven to consume as much as we can” while we can (102). In our evolutionary past, we could not be certain of when the next meal would arrive.
In the contemporary world, the supply of food, and especially the high-calorie food people have evolved to enjoy, is plentiful and consistent. Inevitably, people eat more than they need. This leads to weight gain. At the same time, “we’re doing a lot less than we used to throughout the industrialized world” (123). In humans’ evolutionary past and until the late 20th century, most people “were doing jobs that demanded physical labour, such as agriculture or manufacturing” (123). In contrast, automation and the rise of the service economy mean that 75% of UK and US workers now work in offices. The resulting lack of physical activity at work, along with automation in the household and increasing car use, means that they will burn fewer calories. According to the abundance hypothesis, the increased consumption of appetizing, high-calorie food combined with a “sedentary lifestyle” caused the obesity epidemic.
This theory has a variety of shortcomings. As van Tulleken highlights, the theory does not explain why, in the UK, “being born into a lower-income household can double the risk of obesity” (145). If the abundance hypothesis were correct, poverty would be correlated with less obesity since individuals would have less money to spend on food. Lower-income groups are also more likely to still be doing manual jobs and not have cars relative to those with more money. Yet both in the US and UK, income is inversely correlated with obesity, the opposite of what the abundance hypothesis would predict. This problem is replicated on a global scale. Obesity rates have grown fastest among some of the poorest groups in South and Central America, for example. In the book, Van Tulleken highlights The Correlation Between UPF, Poverty, and Inequality. Individuals in poor communities eat more UPF-laden food, he argues, leading to rises in obesity.
The policy prescriptions derived from the abundance hypothesis have failed. Despite governments since the 1970s promoting “healthier lifestyles” involving lower-calorie foods and more exercise, obesity rates have not fallen. On the contrary, rates have continued to grow, with childhood obesity in the US, for example, trebling in the past 30 years. As such, van Tulleken builds on the study by Herman Pontzer, which shows that the calories burned by hunter gatherers are the same as contemporary, less active Americans and Europeans. He suggests that something else is at play. Just as the body has a complex regulatory system for determining calories burned, he argues, there is “an internal system that precisely regulates food intake” (100). This highly evolved system, based on “a dialogue between organs” and other signals in the body, closely regulates not just what to eat but “when to eat it, and when to stop” (105). This has several consequences for the way we understand obesity and its causes.
Human beings are not necessarily hardwired to consume to excess, or to consume calorie-dense foods, when there is abundance. The body’s regulatory mechanisms and their influence on appetite also limit excess eating when they are functioning normally. The “deliciousness” of normal food is regulated in accordance with the needs and context of the body at any moment. If correct, this idea suggests the mechanism by which UPF might be responsible for obesity. If the novel chemicals and form of UPF are “affecting our ability to self-regulate” (107), interfering with the complex feedback loops of hunger and satiation, then they may lead us to eat in excessive and unhealthy ways. This coincides with what van Tulleken describes as “the sensation of many of us as being unable to stop eating even though we want to” (107).
By seeing UPF in this way, van Tulleken argues, we can shift the paradigm of obesity from one of individual responsibility to that of seeing people as victims of “an addictive edible substance” (165). This helps reduce the blame and stigma around obesity. It also opens a new way of understanding diet, UPF, and the industrial-commercial machine integral to UPF production and consumption.
