Today, medical labels like obese and overweight are defined by how a person’s weight compares with their height, but this framework is a relatively new invention. Not so long ago, people could gauge height but almost never knew their weight, so descriptors such as slender, plump, stout, or corpulent were matters of judgment alone. The shift began with the arrival of the penny scale in the late 1800s, a name earned from the penny you paid to learn your weight. In just a few decades, affordable scales for home use appeared, and ordinary people could readily determine their weight. The natural question that followed was: what should that weight be?
The first figure to probe this question was Adolphe Quetelet (1796–1874), a Belgian polymath. Quetelet did not focus on obesity; his aim was to describe a “normal man” by employing spring scales and emerging statistical techniques. Since taller individuals weigh more than shorter ones, he asked what weight would be typical for a given height. From European male data, he concluded that body weight (in kilograms) tends to grow in proportion to the square of height (in meters). Consequently, two people sharing the same weight-to-height-squared ratio essentially have the same weight for their height. This ratio was initially called Quetelet’s index.
That kind of miscategorization highlights BMI’s most disturbing shortcomings: it is reductive, potentially misleading diagnostically, and stigmatizing.
Quetelet did not intend for his index to measure obesity, but once mass-produced scales spread, insurers realized that Quetelet’s index could boost profits. If you were selling life insurance, you could profit by charging more or denying coverage to people carrying extra body fat who might be more likely to die early. The first standardized weight tables emerged from the Connecticut Mutual Life Insurance Company, which initially deemed anyone whose Quetelet’s index landed in the top 20 percent of a sample of seven hundred thousand policyholders too risky to insure. For the following half-century, insurance companies, rather than physicians, were the principal arbiters of corpulence.
Then, in 1972, the influential American physiologist Ancel Keys considered how well Quetelet’s index predicts a person’s body fat percentage. Using a sample of roughly 7,500 American men (less than 2 percent Black and 14 percent Asian), Keys and colleagues demonstrated that Quetelet’s index—renamed the “body mass index” (BMI)—correlates strongly with body fat levels.11 Despite Keys’s warning that the “characterization of persons in terms of desirable weight percentage has resulted in attributing to ‘overweight’ some tendencies to ill health and death that are actually only related to age,” BMI eventually became the global standard for classifying people’s body fat. Today, the World Health Organization (WHO) has codified six categories into which most health professionals and researchers classify individuals based on BMI:
Underweight: <18.5 kg/m2 Normal: 18.5–24.9 kg/m2 Overweight: 25.0–29.9 kg/m2 Obese (Class I): 30–34.9 kg/m2 Obese (Class II): 35–39.9 kg/m2 Obese (Class III): >40 kg/m2
It’s often claimed that precise measurement yields reliable guidance, but that maxim is not always true. Even when a metric is accurate (or precise), it does not guarantee that its meaning is clear. Despite decades of widespread use, BMI categories carry substantial limitations. A principal flaw is that BMI does not reveal what portion of a person’s mass is fat versus muscle, bone, or other tissues. Highly muscular individuals can be mislabeled as overweight.
Furthermore, the proportion of fat and other tissues varies among individuals with respect to age, sex, and racial or ethnic background. A study of nearly twelve thousand Americans found that, for the same level of body fat, Black Americans tend to have BMI values about 1.3 kg/m2 higher than whites, while Asians have BMI values about 1.9 to 3.2 kg/m2 lower. In other words, BMI tends to overestimate fat for Black individuals and underestimate it for Asians. By fat percentage, a Black person with a BMI of 26 is more likely to be deemed overweight than normal.
If you ask (as I have) hunter-gatherers what they prefer to eat, more often than not the answer is meat, especially fatty meat.
That kind of miscategorization highlights BMI’s most disturbing shortcomings: it is reductive, potentially misleading diagnostically, and stigmatizing. Research shows that labeling individuals as obese or overweight based on this single ratio can provoke feelings of judgment, marginalization, and devaluation. Even if a person’s BMI accurately reflects their body fat percentage, BMI remains an incomplete measure of health.
At a minimum, health assessments should also consider blood pressure, resting heart rate, cholesterol, blood sugar, liver function, inflammation, and fitness. Moreover, reducing fat to a simple matter of too much or too little is overly simplistic. Fat is a vital class of molecules used by every cell; our bodies store fat in specialized cells—adipocytes—that perform many functions. And fat has played a special role in human evolution. To better understand obesity, we must learn more about fat itself.
If you ask (as I have) hunter-gatherers what they prefer to eat, more often than not the answer is meat, especially fatty meat. Most wild animals are exceptionally lean, so hunter-gatherers crave the fat-rich parts of the body, including marrow and liver. Like most people, they find fat delicious. They also recognize that enough fat is necessary for health, reproduction, and well-being.
Keep in mind that animals—humans included—store most of their energy as fat. Each fat molecule contains three fatty acid chains that extend from a small glycerol backbone, much like prongs on a fork. When fat is burned in cells, energy is released from the bonds among the numerous carbon atoms in the fatty acids, yielding about 9 calories per gram. Because fat is denser than carbohydrates, it can store more than twice as many calories per gram, making it our principal energy reservoir.
Fat is essential to life, but it has one key limitation: it does not dissolve in water. Consequently, we cannot accumulate fat inside tissues as we do carbohydrates. Instead, the bulk of our fat stores is housed in adipocytes—cells that are not merely passive fat containers but dynamic units with a nucleus, DNA, and organelles. Among their many roles, fat cells synthesize and release hormones and other signaling molecules that inform the body about how much fat they hold, whether they are shrinking or damaged, and much more.
At birth, humans possess roughly one billion fat cells, and by adulthood the number ranges from about ten to thirty billion. There is, of course, variation: women tend to have more fat cells than men, and those who are overweight or obese typically have more fat cells than those of normal weight, particularly if obesity developed during childhood or adolescence. Although about ten percent of fat cells are renewed each year, the overall count remains relatively stable with age. Like balloons, fat cells enlarge or shrink as we gain or lose weight.
The relatively steady number of adipocytes, coupled with their capacity to change size and function, has implications for an evolutionarily unusual condition: obesity. Although we cannot see or feel it directly, when fat cells accumulate too much fat they can become damaged—like an overstuffed suitcase that has bursts at the seams—and they may be deprived of adequate oxygen. Damaged fat cells then produce and release adipokines, signaling molecules that trigger an immune response and inflammation. This low-grade inflammation is a persistent, body-wide process rather than a sharp, obvious swelling, and since it occurs within fat tissue, you might not notice it.
Moreover, fat cells are dispersed throughout the body, and that inflammation can spread to nearly every nook and cranny. Scientists did not pay much attention to this simmering, systemic inflammation until modern technologies allowed measurement. The capacity to quantify this type of inflammation has been transformative, because when it endures for years, it can be harmful—gradually impairing cellular function across the body.
One common pattern of inflammatory damage is the obstruction of insulin signaling in fat and muscle cells. As we will learn, insulin is necessary to move sugars and fats from the bloodstream into cells. Inflammation prompted by obesity disrupts these processes, allowing blood sugar and cholesterol to rise quietly, incrementally, and dangerously. The consequences include type 2 diabetes and atherosclerosis. Elsewhere, chronic inflammation can impair other receptors and tissues, damage brain neurons, raise the risk of Alzheimer’s disease and other dementias, and increase the likelihood of cancers, osteoarthritis, asthma, inflammatory bowel disease, and other conditions. And this inflammatory state is often subtle, creeping into the body without obvious notice.
Whether we are normal weight or obese, shrinking fat cells induce powerful sensations of hunger and lethargy, countering efforts to lose weight.
To add insult to injury, the inflammation caused by excess fat sets in motion a self-perpetuating loop that can promote additional weight gain. Adipocytes produce hormones and other signaling molecules in response to how much fat they contain. The most important of these is leptin, which conveys information about the body’s energy reserves to the brain. When fat stores are ample, leptin levels rise and the brain suppresses appetite. When fat cells shrink as fat is burned, leptin falls, triggering hunger.
Normally, this system helps keep our weight relatively stable, but low-grade inflammation can damage the brain’s leptin receptors. When this occurs, the regulatory feedback system malfunctions like a broken thermostat. Even if fat cells release enough leptin to curb appetite, the brain fails to receive the signal, producing persistent hunger. Hunger, in turn, undermines weight loss and can even promote further gain.
And if that weren’t bad enough, fat cells cause trouble not only when they swell but also when they contract. As people shed fat and their cells shrink, leptin plummets, signaling to the brain that energy reserves are dwindling. This response, adaptive for our ancestors to prevent undernourishment, can be disastrous for modern dieters, whether we are normal weight or overweight.
The logic of evolution suggests we are built to store enough fat, but not too much. The philosopher Ralph Waldo Emerson (1803–1882) once quipped that “a foolish consistency is the hobgoblin of little minds.” While he aimed his remark at rigid dogmas in politics and religion, the line could just as well apply to how we medicalize obesity. For example, a person who stands 5 feet 10 inches tall and weighs 208.5 pounds has a BMI of 29.9 and is labeled overweight; if they gain merely half a pound, their BMI becomes 30.0 and they are deemed obese. By the American Medical Association’s standard, that shift classifies them as having a disease. In addition to being arbitrary, reductionist, and biased, relying on a single number to judge a person neglects the many complexities of body fat.
We are evidently best adapted to store enough but not too much.
“A rose is a rose is a rose,” Gertrude Stein once proclaimed, but the same cannot be said for body fat. There are several distinct fat compartments, and they do not behave identically. The most consequential distinction is between fat stored just under the skin (subcutaneous fat) and fat around organs such as the liver (abdominal fat, also called visceral or ectopic fat). We evolved to accumulate mainly subcutaneous fat and to harbor only modest abdominal fat. Abdominal fat, in addition, is more responsive to hormones and more richly supplied with blood vessels. In effect, abdominal fat represents a readily accessible, short-term energy reserve that the brain can mobilize, especially under stress, famine, or periods of heightened physical demand, when cortisol levels rise and promote greater abdominal fat deposition. This adaptation helps deal with short-term food shortages or periods of intense activity.
Yet an excess of abdominal fat is a health concern. When abdominal fat cells overextend, they provoke more chronic inflammation than subcutaneous fat does. Hundreds of studies have linked higher abdominal fat with increased risks of inflammation-related conditions, particularly type 2 diabetes and cardiovascular disease.
The disparity between abdominal and subcutaneous fat underscores a key concern with obesity—and a major limitation of BMI. Since BMI relies solely on weight and height, it cannot differentiate among these fat types. That matters because subcutaneous fat deposits in the hips and buttocks tend to trigger less inflammation than fat stored around muscles or internal organs. Consequently, BMI should not be the sole tool for assessing fatness; other metrics that estimate fat distribution are warranted. Some hospitals employ advanced scanners for this purpose, but a straightforward approach is to measure the waist relative to the hips or to height. A waist-to-hip ratio or a waist-to-height ratio can serve as practical proxies for abdominal fat.
Taken together, let us approach fat assessment with greater caution and nuance when evaluating health or any other trait. While stigmatizing or judging people by weight is wrong, high levels of body fat—especially in the abdominal region—do elevate the risk of many diseases. Even though BMI may be imperfect for individuals, it remains a useful indicator for studying how fat levels relate to health outcomes across populations. Figure 14 illustrates the association between BMI and the risk of death from any cause in more than 3.5 million men and women in the United Kingdom.
Note that this analysis encompasses people of all racial backgrounds; it assesses longevity rather than overall health; it does not distinguish between abdominal and subcutaneous fat; and it does not adjust for exercise, access to healthcare, or other influences. Despite these caveats, the data reveal the familiar J-shaped curve: those with BMIs below 18 and above 30 face greater risks of death, and there is a suggestion that a modest amount of fat becomes beneficial as people age. In short, we seem to be best suited to store enough, but not too much.
That, in turn, raises a difficult question: If excess fat is harmful, why are humans so prone to accumulating excess fat?
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From Fed Up by Daniel E Lieberman. Copyright © 2026 by Daniel Lieberman Published by arrangement with Alfred A Knopf, an imprint of The Knopf Doubleday Group, a division of Penguin Random House LLC
