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Ending the Hunger Games

New pharmaceuticals appear to offer a genuine solution to the problem of excess appetite, that uncontrollable urge to eat more than we need to that keeps so many of us fat.

· 25 min read
Ending the Hunger Games


Although it remains unclear whether obesity has now become a bigger killer worldwide than hunger, there can be no doubt that it is one of the greatest problems facing humanity today. More than a quarter of all adults are estimated to be clinically obese in a slew of countries as culturally and geographically diverse as Samoa, Egypt, Argentina, Costa Rica, Israel, Saudi Arabia, the Czech Republic, and the United States. Some models predict that this will cost the global economy $4 trillion (2.9 percent of global GDP) by 2035.

According to a January 2023 briefing presented to the UK House of Commons, almost one in three British adults are obese, up from one in ten in 1970. This is an estimated 37.7 million people. The results of a 2022 study in the British Medical Journal suggest that this is costing the UK’s National Health Service (NHS) £1.6 billion and the wider British economy as much as £27 billion (mostly in lost earnings) per year.

The British experience is not unusual. Here in Australia, for example, according to the Australian Bureau of Health and Statistics, around 31 percent of the population was obese in 2017–18 (the most recent year for which figures are available). Obesity, which is the second largest source of medical costs after smoking, accounts for 8.4 percent of Australian healthcare spending, according to a 2021 report published in Nature.

Given the myriad false promises the diet industry has offered in the past and the number of failed attempts many of us have made to lose weight, it’s unsurprising that so many commentators are reluctant to accept the idea that an effective, scalable solution to the problem of obesity may be finally in view. After all, in the years 1964–2009, more than 20 weight-loss pharmaceuticals were first approved and then withdrawn from circulation (most notoriously, the so-called “fen-phen”), as the evidence of their severe side effects and/or addictive potential accumulated.

Yet, new pharmaceuticals do appear to offer a genuine solution to the problem of excess appetite, a real way of dampening that clamorous, deep-seated, and uncontrollable daily urge to eat more than we need to that keeps so many of us fat. If they prove safe and effective, these novel medications will help many (though not all) of the overweight and obese lose weight more easily and effectively. And we badly need a radically new approach to obesity. Governmental measures have failed; societal measures have failed; individual efforts have largely failed. Most of us are now fatter than our parents and grandparents were, fatter than we ever intended to become, fatter than we would like to be—and are growing fatter still.


The drugs are currently available in several forms and dosages, including Ozempic and Wegovy (weekly subcutaneous injectables) and Rybelsus (daily oral tablets). Ozempic was approved in 2017 by the US Food and Drug Administration (FDA) for the treatment of type 2 diabetes. After many patients reported weight loss as a side effect, the Danish drug company Novo Nordisk developed a higher-dose version, Wegovy, and began marketing it specifically for the treatment of obesity.

The active ingredient in most of these drugs is semaglutide (variously pronounced ‘sema-gloo-tide’ and ‘se-mag-loo-tide’): a glucagon-like peptide-1 (GLP-1) receptor agonist. GLP-1 is an incretin, which is a metabolic hormone that helps the body produce insulin, reduce the amount of glucose manufactured by the liver, and regulate the movement of food through the gastrointestinal system. It is released after eating and has a half-life of only two minutes. Semaglutide has an amino acid sequence that differs by only 6 percent from naturally occurring GLP-1 and mimics the action of that molecule, but it is broken down by the body far more slowly. The mechanism involved is not fully understood, but semaglutide appears to work by affecting receptors in both the gut and the brain to keep GLP-1 levels artificially elevated for far longer than normal, with the result that users will generally become hungry more slowly and reach satiation more quickly when they do eat.

Eli Lilly has recently developed Mounjaro, an even more effective treatment that contains the active ingredient tirzepatide, a molecule that simulates both GLP-1 and another incretin, glucose-dependent insulinotropic polypeptide (GIP). Another, yet more potentially effective treatment, involving the molecule retatrutide, is currently undergoing clinical trials (as of September 2023). Further variants of these pharmaceuticals are already in the testing stages. A full discussion of the biochemistry involved is beyond the scope of this article.

For simplicity, from here on, I’ll use “semaglutide” as shorthand for “medications containing the active ingredient semaglutide and/or similar GLP-1 agonists.”

These drugs are extremely effective. In randomised, double-blind clinical trials, obese participants receiving semaglutide have lost significantly more weight than those in the control groups. As science writer Stuart Ritchie has pointed out, the dramatic graphs speak for themselves:

The drugs seem to have few downsides, at least over the short term. Rapid weight loss of any type can, of course, lead to lean muscle depletion, especially if it is not accompanied by resistance training and adequate protein intake. There seems to be little evidence, however, that the use of GLP-1 agonists results in greater muscle loss than comparably fast weight loss of the conventional kind.

Semaglutide also has a good safety record. While it is too early to make a judgement about its long-term effects, Ozempic has been in routine use for the treatment of type 2 diabetes since the subcutaneous form was approved by the FDA in 2017. It was endorsed as a treatment for diabetes by the European Medicines Agency, Health Canada, and Japan’s Ministry of Health, Labour, and Welfare in 2018 and by the Australian Pharmaceutical Benefits Scheme in 2020. The UK’s National Institute for Health and Care Excellence (NICE) considers its safety to be “well established.” A significant proportion of patients, however, have reported unpleasant side effects, especially nausea and vomiting, on first taking the drug or increasing the dosage, but most users have classified these side effects as mild to moderate, and the effects usually abate over time. (We’ll return to the impact of these side effects later.)

Some initial studies and anecdotal reports from doctors suggest that semaglutide may have beneficial side effects, too, such as decreasing cravings for nicotine, cocaine, alcohol, amphetamines, and other addictive substances and behaviours—perhaps because of an effect on dopaminergic signalling pathways in the brain.

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On 8 August 2023, Novo Nordisk announced the results of a clinical trial involving 18,000 participants, which showed that GLP-1 agonists can reduce the risk of cardiovascular problems such as heart disease and stroke by 20 percent. These results have not yet been peer-reviewed, but they are consistent with those of a 2018 phase 2 trial, which found significant improvements in blood pressure and other cardiovascular indicators such as lipids and high-sensitivity C-reactive protein measurements in some patient groups taking semaglutide compared with those taking a placebo.


The media usually respond enthusiastically to news of medical advances of this kind. Take, for example, the breathless coverage of donanemab, a possible new Alzheimer’s treatment, which has severe and dangerous side effects. Sky News called it “the beginning of the end” for Alzheimer’s; the Express called it “a wonder drug”; the Mirror described it as “a breakthrough”; and the Guardian declared it a “turning point.”

The response to GLP-1 agonists from the media has been more than merely sceptical, however; many have greeted the news with alarm and disdain. According to John Semley in the Guardian, semaglutide works “by triggering a chemical repugnance to food itself.… It’s the chemical realization of a behavioural psychologist’s wildest dream; A Clockwork Orange for junk food, an eating disorder in an injection.” (This is certainly not how it works.) The Guardian also published an article by former food critic Leila Latif, who lost all interest in eating while on a medication with appetite-suppressant side effects. But despite the misleading title (“Yes, England’s new weight-loss drug kills your appetite—but, as I know, that comes at a cost”), an erratum notice states that, in fact, Latif has never taken semaglutide.

As UK science communicator Stuart Ritchie has pointed out, many journalists are cherry-picking the data in order to focus on rare side effects in a way that the same media outlets would surely consider irresponsible if we were talking about, say, the Covid vaccines. This CNN report, for example, cites three women who have experienced severe reactions but, even as it describes their symptoms in graphic detail, admits that “cases like these are believed to be rare.”

The New York Times graphics cards advertising their Ozempic articles highlight the fact that “People taking Ozempic and Wegovy may experience nausea, dehydration, fatigue, and malaise. The drugs … carry serious risks, such as facial aging and kidney failure, and going off the drugs can also take a toll.” Their coverage includes a piece on “The Rise of Ozempic Face,” a term coined by dermatologist Dr Paul Jarrod Frank to describe the gaunt appearance that can be caused by losing buccal fat. However, while thinner cheeks can make you look older, there is no evidence that this is in any way specific to weight loss achieved through semaglutide.

Some of the studies showing the benefits of semaglutide have been funded and promoted by the drug companies themselves, a fact that journalists have noted. But, as obesity specialist Dr Yoni Freedhoff has pointed out, bringing any new drug to market entails a “multistakeholder process that at some point involves industry—drugs being expensive things to develop,” and the press is highly selective in deciding when this should cast suspicion on findings and when it need not. While it’s clear that Novo Nordisk, Eli Lilly, and other pharmaceutical manufacturers in the future are likely to make enormous profits from the sale of GLP-1 agonists like semaglutide, there are also many people who benefit financially from the restriction of these medications, including the authors of diet books and providers of alternative weight loss solutions.

Freedhoff rightly notes that “new obesity therapies and the people who make them happen are judged far more critically than in other chronic diseases.” Perhaps this is because obesity is usually caused by overeating, and overeating often results from excess appetite and hunger—subjective experiences that are very difficult to convey to those who don’t feel those impulses as strongly. As blogger Scott Alexander has written, this is a particularly striking example of the general principle that “it’s always really hard to generate the hypothesis ‘people’s different experiences aren’t an illusion; people are genuinely really different.’” The results of overeating are, on the other hand, often visible at a glance. We can see someone’s fat rolls, while we can’t see their bank balance or the state of their liver. The link between overeating and morality stems back to at least Old Testament times. Gluttony is a deadly sin.


Some of the widespread hostility towards appetite suppressants may be due to people’s natural suspicion of what Diana Fleischmann, in a different context, has called “counterfeit fitness.” Being slender is generally a signal of either genetic privilege or an ability to exercise iron willpower. If we can level the genetic playing field, so that obese people can experience the levels of hunger and appetite felt by those who are “naturally” thin, it will remove an important indicator that people are clearly using as a proxy for both moral virtue and evolutionary fitness. One commentator succinctly encapsulates this attitude when he asks, “Are you saying that being dependent on drugs for life is indistinguishable from putting in the work required to actually be healthy? Are there no moral considerations?”

At the opposite end of the spectrum are people who are suspicious of pharmaceutical solutions because they let “the real culprits”—government and industry—off the hook. They believe that we need to fix society rather than the individual. This desire for society-wide over individual solutions fits comfortably with a worldview in which the individual is seen as a powerless object impacted by irresistible large-scale forces like patriarchy and white supremacy.

Such commentators believe that reliance on semaglutide may stop governments from pursuing large-scale policy solutions to obesity. The British think tank Institute for Government, for example, has stated that we should focus instead on how to “tackle root problems within the food industry.” But, as they themselves wryly note, the UK has pursued at least 14 different anti-obesity strategies over the past 30 years. “It’s startling that the UK has never had a successful national obesity campaign,” comments Royal College of Paediatrics and Child Health president Camilla Kingdon. To “get a handle on obesity,” she nevertheless recommends more of the same: “government legislation, industry level regulation, and economic assistance.” Some academics in the discipline of public health view British obesity as the result of “a failure of leadership” and advocate “subsidising fruits, vegetables, and basic cooking ingredients, and putting taxes on junk food as has been done with sugary drinks.” In March 2023, the World Health Organization issued new guidelines on restricting the marketing of junk food to children, notes the Guardian’s former health editor, Sarah Boseley, approvingly. What we need, Boseley argues, are more such measures: “Britain should be taxing unhealthy food and clamping down on marketing,” instead of jumping on “the injection bandwagon.” However, such suggestions seem, at best, like searching for our car keys under the streetlamp, without having any idea where we actually dropped them.

Most of these paternalistic measures are probably ineffective. A 2016 metastudy found that adding calorie counts to menus in US restaurants, for example, rarely leads to reduced consumption, especially after the initial shock wears off. Repositioning foods in cafeterias and supermarkets to more prominently display healthy options has been proven to work only in the very short term—perhaps for only as long as people take to get used to the new layouts. Imposing taxes or size limits on sugar-sweetened beverages—as in California’s now-abandoned proposal to outlaw “Big Gulp” (around 900 ml) sodas—is unlikely to help people slim down, either. As behavioural economists Mario J. Rizzo and Glen Whitman have shown in their 2019 book, Escaping Paternalism: Rationality, Behavioral Economics and Public Policy, substituting artificially sweetened drinks for sugary ones does not necessarily lead to weight loss. It may even contribute to weight gain, since some people may compensate by eating more calories in food instead.

The UK instituted a soft drinks industry levy (SDIL), a “sugar tax,” in April 2018. Under the legislation, soft drink manufacturers have to pay a tax of 18p per litre on drinks containing 5–8g of sugar per 100ml and 24p per litre on those containing more than 8g. The measure was part of the government’s strategy to tackle childhood obesity. Like many such policies, its efficacy was assumed, rather than rigorously tested. As Stuart Ritchie has shown, there is little to no evidence that it has had any tangible effect on childhood obesity rates at all.

After a stint in intensive care after contracting Covid, Boris Johnson acknowledged that he had been at greater risk of serious consequences—even death—from the disease because of his weight. Among other measures to help his fellow Britons lose weight, he pledged to end BOGOF (buy-one-get-one-free) offers on confectionery, crisps, and other high-calorie junk foods. He later backpedalled on this promise—and, in fact, that may have been a blessing in disguise. As the work of Farasat Bokhari et al. on alcohol purchasing patterns suggests, banning volume discounts can encourage greater consumption. Although shoppers may buy less on each individual trip (or online order), they may shop more frequently to replenish their stores and end up consuming more overall. There are many such unintentional effects to be feared from governmental measures.

In any case, it seems that hunger and appetite are simply not as susceptible to policy nudges as we might wish. The idea of many nudges—such as enforced cooling-off periods—is, as Rizzo and Whitman explain, to help “people [who] make choices when they are in a biologically ‘hot’ state (such as anger, fear, excitement, or sexual arousal) that they would not make if they were in a ‘cool state’ (calm, reflective, and sober).” Hunger is clearly a “hot state”—but it makes little sense to encourage people to ignore hunger cues altogether or to eat when not hungry. And we do not have the option of complete abstention, as we do with other addictive behaviours. You can decide never to call your ex when drunk; you can’t decide never to eat food again. You can try to make all choices about what and how much to eat while in a “cool state” by, for example, doing your grocery shopping while satiated, but the ubiquity of rapid grocery and meal delivery services means that, in many places, you can order food 24/7. It’s impossible to regulate away every opportunity to overindulge. It is far more effective to enable people to strengthen their inner motivation to eat less—which semaglutide does directly by reducing appetite—rather than trying to indirectly nudge them towards doing so.


Some commentators have argued that what people need is more information on how to eat healthily. For example, Dr Jason Halford, president of the European Association for the Study of Obesity, has lamented the fact that people may be able to obtain semaglutide without having to enrol in a wider program of support, which should include “advice on nutrition and eating behaviour.”

The problem, however, is not lack of advice. There is a great deal of advice out there—most of it spurious. The diet industry is plagued by, to borrow Bruce Yandle’s terminology, coalitions of Baptists and bootleggers: true believers evangelising about the regimens that have helped them personally and a wide variety of scientists, doctors, dieticians, personal trainers, and celebrities peddling diet books, meal replacements, supplements, and exercise plans. The writing on this topic is generally presented in condescendingly simplistic terms and accompanied by a Gish gallop of scientific studies referenced in small print in the endnotes. It’s impossible for a layperson to evaluate which of these studies—if any—were well designed or have been replicated.

Even among registered dieticians, there is little consensus as to the optimal eating plan. Experts cannot even agree on whether the main culprit in weight gain is saturated fat or carbohydrates. In addition, the way individuals respond to specific foods may differ widely, as this study of post-prandial blood sugar levels has suggested. To make matters worse, official recommendations are often heavily influenced by vested interests. According to the Harvard School of Public Health, the composition of the United States Department of Agriculture’s healthy eating diagram MyPyramid (replaced by MyPlate in 2011) was largely the result of “[i]ntense lobbying efforts from a variety of food industries.”

We not only do not know what people should eat; we don’t have an accurate sense of what they do eat. Most nutritional studies rely on food frequency questionnaires; subjects are asked, for example, how many almonds they consumed last week, month, or year. The researchers are thus obliged to assume that participants have impeccable memories and are always truthful. Long-term studies in which subjects are randomly assigned to different eating patterns are no more reliable. There is no way to guarantee compliance or honesty.

Nutrition scientists have to rely on this kind of error-prone anecdotal evidence because of the thus-far insuperable practical and ethical difficulties of conducting a long-term, double-blind trial of any food, nutrient, dietary regimen, or macronutrient balance. To accurately track which eating patterns are most effective for weight loss, we would need to monitor large numbers of ordinary people under laboratory conditions for significant lengths of time. This is clearly impossible.

No wonder there is so much contradictory advice out there.


Even if we had precise, individually tailored data on which eating patterns would produce weight loss, I don’t think knowing what to do would be enough. Most people who are trying to lose weight have a clear idea of the basics of what they need to do—or, at least, what they need to avoid. The problem is that they are battling powerful, deep-seated urges to do otherwise.

Differences between individuals in their susceptibility to weight gain are strongly influenced by heredity. Overfeeding experiments suggest that individual propensities towards obesity vary enormously. Twin studies by Claude Bouchard et al. and Albert Stunkard et al., both published in 1990, confirm this hypothesis. In 1986, Stunkard led a study of 540 adult Danish adoptees that found

that there was a clear relation between the body-mass index of biologic parents and the weight class of adoptees, suggesting that genetic influences are important determinants of body fatness; and that there was no relation between the body-mass index of adoptive parents and the weight class of adoptees, suggesting that childhood family environment alone has little or no effect.

These differences, however, do not explain why the number of obese people has risen so dramatically over the past generation. In the US, for example, the proportion of obese adults has more than doubled, going from 15 percent of adults in 1976–80 to 34 percent in 2007–08 (the most recent period for which figures are available), according to the Centers for Disease Control and Prevention. According to the World Health Organization, there has been a similarly dramatic increase worldwide. Environmental factors must play a role in this.

At the most basic level, we know the causes of this steep uptick in the number of obese people: we are consuming more food. What we don’t know is why. Some have attributed the overconsumption to misguided governmental recommendations that led people to reduce their fat intake in favour of more carbohydrates, especially in the US, but the figures we have do not support this hypothesis. Over the past 20 years, as sugar and refined carbs have come to be seen as the biggest danger to waistlines, people have switched back to a higher-fat, lower-carb model, but obesity rates have continued to rise. Studies have failed to show significantly greater weight loss or long-term compliance on keto diets than on traditional calorie-controlled regimens.

While keto clearly works well for some, so far, the evidence that carbohydrates are responsible for the rise in obesity or that the widespread adoption of a keto diet would solve the problem is mixed, at best. Dr Atkins’ Diet Revolution was first published in 1972, and an updated version, Dr Atkins’ New Diet Revolution, was released in 1997. The book has sold 12 million copies and, at the height of its popularity, in the early 2000s, the diet may have had as many as 30 million adherents in the US alone. Yet the results speak for themselves: throughout this period, Americans have become steadily fatter. And so have the rest of us.

In his book The Hungry Brain, Stephan Guyenet argues that the problem is the abundance of hyperpalatable foods that overstimulate our appetites. This is intuitively convincing, but, unfortunately, it is just a guess. Much of the evidence Guyenet relies on to support his thesis is drawn from a few experiments in the 1960s that were extremely low-powered and had serious design flaws.

Whatever the causes of our increasing fatness, governmental measures have largely proved ineffective against the phenomenon. But could increasing the social stigma associated with overeating or excess weight help motivate people? Could we shame people into ignoring their hunger or cravings more often? I’m sceptical both as to whether we could and whether we even should. Hunger is an insistent, hard-to-ignore urge. When hungry, it can be difficult for a person to focus on work or family or on anything other than the urge to eat. The choices of whether, what, and how much to eat are not necessarily just about conflicts between a person’s lower-order desire for self-indulgence and their higher-order desire to get slimmer. Being thinner and healthier is not the only contribution an individual can make to society, nor is it the only factor in individual happiness and fulfilment. In any case, I would not wish to live in a society in which people routinely shamed each other for their appearance or food choices. This would have severe knock-on effects on mutual trust and goodwill.


In any case, it seems likely that most people who are overweight or obese would already prefer to be slimmer. The extreme perennial popularity of weight loss products and services—on which consumers spent an estimated US$255 billion in 2021—is sufficient evidence of this, and the semaglutide clinical trials confirm it. In one 2017 trial, for example, many of the participants (up to 82 percent in some groups) reported gastrointestinal distress, especially nausea, but less than 10 percent of them stopped taking the drug. Many people are clearly so motivated to slim down that they are willing to endure some pretty unpleasant (temporary) side effects in order to do so.

The challenges of maintaining significant weight loss are also concrete and daunting. This is particularly true if weight loss has been fast and extreme. Many of the former contestants on the American reality TV show The Biggest Loser have regained their weight, and all of those who participated in a 2016 study were found to have experienced severe metabolic slowdown. As obesity specialist Dr David Ludwig has commented,

There are no doubt exceptional individuals who can ignore primal biological signals and maintain weight loss for the long term by restricting calories … for most people, the combination of incessant hunger and slowing metabolism is a recipe for weight regain.

Dr Jeffrey Friedman puts it in even starker terms. Following weight loss,

[t]he feeling of hunger is intense and, if not as potent as the drive to breathe, is probably no less powerful than the drive to drink when one is thirsty. This is the feeling the obese must resist after they have lost a significant amount of weight.

Hunger has both physiological and psychological impacts. In Ancel Keys’s famous 1944 Minnesota Starvation Experiment, a group of healthy male volunteers were restricted to a diet of 1,570 calories per day. As the study continued, the subjects began obsessively talking, thinking, fantasising, and even dreaming about food: a phenomenon Keys dubbed “semistarvation neurosis.” Similar results were found in a study conducted by Dr Jules Hirsch in the 1980s. Hirsch found considerable metabolic slowdown among volunteers on an 800-calories-a-day regimen, as well as compulsive food fantasies. These findings were forgotten in the recent flurry of popularity around Dr Michael Mosley’s “Fast 800” diet, which was widely promoted by the UK media and sold over 5 million copies worldwide, at least 1 million of them in Australia and New Zealand alone.


Given how difficult it is to lose weight, coming to terms with one’s obesity can seem like the only feasible option; if you can’t beat it, celebrate it. Fat activism began in the 1960s in the US. In 1969, the National Association to Advance Fat Acceptance (NAAFA) was founded, and in the early 1970s, there was the Fat Underground movement. This form of activism came back into fashion in the late 1990s and early 2000s, with what Bradley Campbell and Jason Manning have dubbed “the rise of victimhood culture,” in which people are encouraged to see personal disadvantages or adverse experiences as identities that provide meaning and social status. A movement that promoted the idea that people can be healthy at any weight coalesced around 2003 when the Association for Size Diversity and Health trademarked the phrase “Health at Every Size.” This idea was further promulgated by psychotherapist Linda (now Lindo) Bacon’s 2008 book Health at Every Size: The Surprising Truth About Your Weight. In 2012, the movement gained its own academic journal: Fat Studies.

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Fat activists reject the medical consensus that obesity is implicated in a wide range of health problems. Instead, they see negative attitudes towards obesity as “fatphobia.” Some argue, somewhat incoherently, that this is a manifestation of misogyny or racism (some of their spokespeople make the unlikely claim that revulsion towards obesity stems from a disdain for full-figured black women). The central problem with this form of identity politics is that obesity is not an immutable feature—like race or sexuality—but usually the result of a behaviour: overeating. This doesn’t mean that we should blame individuals for their obesity. The drive to overeat has complex and deep-rooted causes. But it does make it difficult to see this as a civil rights cause. In addition, like many causes defined by shared victimhood, the body positivity movement has been plagued by bitter infighting, as this report by Kiana Docherty demonstrates.

Helen Pluckrose and James Lindsay have described Fat Studies as a prime example of “support-group scholarship” and warn that it is unlikely to “help anyone do anything other than temporarily feel special.” That feeling can be sustained only through uncomfortable cognitive dissonance—especially when it is dependent on how other people view us. While I agree that we shouldn’t discriminate against fat people in situations in which body size is irrelevant, most fat activists go beyond this, often demanding that people change what they find visually appealing or sexually attractive. These preferences may be influenced by societal trends, but they are not under any individual’s conscious control. Such activists often sound uncomfortably like Hugh Laurie as Louella della Twee, author of the fictitious book I Think I'm Great: Why Don't You?

As Pluckrose and Lindsay warn, “If fat activism succeeds in attaining the status currently assigned to feminist and antiracist activism, doctors, scientists, and researchers could feel [too] intimidated to provide factual information to the obese.” It’s extremely important for doctors to be able to talk frankly about serious health risks and not encourage their obese patients in any delusions they may have that all is well. As science writer Tom Chivers puts it, “It's not ‘society’ that says being slim is usually healthy, it’s your cardiovascular system.”


There are two diametrically opposed but equally wrongheaded models here. One considers weight loss to be entirely a matter of personal responsibility; the other considers it to be a result of the obesogenic environment and calls for government action. The likely solution is halfway between these approaches: weight loss is a matter for individuals, but they need assistance in achieving that difficult goal. Neither social engineering, nudges, nor willpower alone are likely to succeed.

Some of the society-wide measures proposed to curb obesity feel like win-wins, such as more cycle and walking paths and a greater availability of inexpensive fresh fruit and vegetables. These measures would probably improve people’s health and quality of life, but they might not have an impact on weight. If you’re hungry, vegetables alone will not usually cut it. The problem is not one of supply but of demand.

The new medications could revolutionise society by reducing the demand for hyperpalatable, indulgent, calorie-dense foods. If people taking semaglutide experience less hunger and, in particular, diminished cravings for junk food, this will in itself make that industry less profitable. The obesogenic environment does not have the same power over people when their appetites are lower. The doughnut shop simply does not leap out at you as strongly or exert the same pull when you are on semaglutide. Semaglutide levels the genetic playing field, allowing people to reach and sustain a healthy weight without having to white-knuckle it through daily hunger or try to silence an insistent inner monologue of constant cravings. This could make many of us happier and healthier. The superforecasters at the Swift Centre predict that widespread use of semaglutide could increase British lifespans by a whole year. I suspect it would increase average healthspans—the number of healthy, fully mobile years—by even more.

There will be a few obstacles to overcome first. Obesity is a chronic condition, and, like most medications that treat ongoing health issues, semaglutide isn’t a reset button. To be able to control their weight long term, many people would have to stay on the drug for life, just as many of those who struggle with excess weight currently have to remain vigilant about their food intake for life. (It might be possible to cycle on and off the drug as needed, however, especially given its long half-life in the body.) It’s too early to tell what the very long-term effects will be—though, once they are known, we will have to weigh them up against the many known health impacts of remaining obese for decades.

Administering the drug is also likely to be expensive. In the US, in particular, the costs could be prohibitive. The drugs currently cost around US$1,000 per month, and some insurance companies are refusing to cover them for non-diabetics. In Europe, the treatments are far more affordable; the list price for a 30-day supply of Ozempic is around a tenth of the US price in Germany, Denmark, and Sweden. In the UK, the drugs are available from private health clinics for around £200 (US$250) per month, a price that is higher than the NHS can afford to subsidise. The UK’s National Institute for Health and Care Excellence (NICE) has approved treatment for patients with a BMI of at least 35 (or at least 30 for some ethnic groups) and at least one weight-related comorbidity such as diabetes, hypertension, or sleep apnoea—but only for a maximum of two years. Under these rules, an estimated 35,000 people would be eligible. The guidance committee acknowledged that “treating a chronic condition for only two years was ‘not ideal,’ especially without the option for retreatment,” but they have to work within budgetary constraints. Costs may go down over the coming years, however, if competition between pharmaceutical companies leads to the availability of cheaper generics, which would allow governments more choice and, therefore, bargaining power. In addition, if semaglutide and its successors fulfil their promise to improve cardiovascular health and ameliorate alcoholism and drug addiction, governments and insurers may be more willing to finance them. Novo Nordisk has already announced its intention to request that regulators approve the drugs for treatment of conditions other than obesity and diabetes.

Some commentators have expressed concerns about the widespread availability of semaglutide, including online (where it can be obtained by the underweight without an in-person check-up). While anorexia is far less common than obesity, it is a life-threatening condition that is difficult to treat. We should not underestimate the dangers of making semaglutide freely available, especially to teenage girls, among whom it may facilitate a toxic cycle of competitive weight loss and undereating.

Then there are the side effects. While only a small minority of people seem unable to tolerate semaglutide at all, more than half of all users report deeply unpleasant side effects, chiefly nausea and vomiting, when they first take the drug—side effects that generally persist for weeks and sometimes for months. It may be difficult to avoid this. Semaglutide is a GLP-1 analogue, and naturally occurring GLP-1 is secreted by the gut in response to the ingestion of toxins. The nausea it induces is an important signal. For most sufferers, these effects will subside over time. However, if companies are able to reformulate the drug to prevent such side effects, demand is likely to skyrocket.


I have struggled all my adult life with intense hunger. No dietary regimen has ever been able to tame it, and I have tried everything: keto, carnivore, macrobiotic, vegan, intermittent fasting. No matter how I time my meals; no matter what their macronutrient composition; no matter what exercise routines I follow, if I am eating only enough calories to sustain a healthy weight, I am also struggling against an almost constant gnawing hunger, often accompanied by mild headaches and nausea. Or at least I was, until now. Semaglutide has dampened that hunger down to a manageable level and allowed me to feel well-nourished on an amount of food that does not cause weight gain. I still get hungry—but not hangry.

I haven’t lost a dramatic amount of weight, but my mental world has radically changed. I still enjoy food, but I’m not fantasising about it obsessively. I can focus on my conversation with someone, even if there is a large plate of chocolate-chip cookies on the table between us and it has been a few hours since lunch. When I am meeting friends for dinner, I am excited to see them and anticipating all the things we will talk about—rather than running through menus and selecting options in my head. When I am out walking, I’m fully absorbed in my surroundings, not trying to distract myself from a growling tummy. This has been a liberating, transformative experience. I feel happier, more comfortable, and, not least, more attractive in my slenderer body—an important consideration for a divorced woman in her mid-50s who would like to find another life partner. I feel as though I had been going through my life shackled to a snarling demon and someone has just sawn through the chain.

Each stage of human development has made new advances possible and created new problems to be solved in their turn. Our ancestors had to spend most of their time securing enough nourishment to survive. As we shifted from hunter–gatherer subsistence lifestyles to settled farming communities, and then, as we learned how to secure food ever more efficiently, new possibilities for human life and human flourishing arose. Abundance has brought problems in its turn. We live amid plenty in bodies and minds designed for famine. This has left many trapped in a miserable cycle that begins with food restriction, progresses through a predictable sequence of increasing hunger and cravings, inevitable backsliding, weight regain, self-loathing, and poor health and then returns to food restriction—with a slightly higher starting weight each time around. Semaglutide might help us to break that cycle. It wouldn’t be the first time human ingenuity has solved a seemingly intractable problem. It might just be the breakthrough we need.

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