Why We Get Fat

Why We Get Fat Plot Summary

Introduction

For decades, the prevailing wisdom about weight management has centered on a seemingly intuitive concept: calories in, calories out. We gain weight when we consume more calories than we expend, and we lose weight when we do the opposite. This concept has dominated medical advice, public health campaigns, and personal weight-loss strategies. Yet despite widespread adherence to this principle, obesity rates continue to climb globally, and most diets ultimately fail. At the heart of this paradox lies a fundamental misunderstanding about how our bodies regulate fat. The traditional view treats the human body as a simple mathematical equation, ignoring the complex hormonal and metabolic processes that actually determine fat storage and energy utilization. Through meticulous analysis of scientific evidence and challenging long-held assumptions, we see that obesity is not a moral failing or lack of willpower, but rather a hormonal disorder primarily triggered by the types of foods we eat—specifically, carbohydrates. This paradigm shift in understanding has profound implications not just for weight management but for treating numerous chronic diseases associated with modern diets.

Chapter 1: The Failure of Calories-In/Calories-Out as an Explanation for Obesity

The conventional wisdom that obesity results from consuming more calories than we burn seems intuitively obvious. If we take in more energy than we expend, the surplus must be stored somewhere, typically as fat. Yet this simplistic model fails to explain numerous observations about weight gain and loss. Consider the poor populations worldwide with high obesity rates. In the early 1900s, medical observers noted significant obesity among certain impoverished populations who certainly weren't consuming excess calories. Historical records show Native American tribes, West Indian communities, and populations in Africa and South America where obesity and malnutrition coexisted—sometimes even within the same families. How could mothers be obese while their children showed signs of undernourishment if obesity were simply about caloric excess? The calories-in/calories-out model also fails to explain why some people remain effortlessly lean despite consuming large quantities of food, while others struggle with weight despite careful monitoring of intake. The model suggests that to maintain a stable weight over decades requires balancing energy intake and expenditure with extraordinary precision—within 20 calories per day, less than a single bite of food—an implausible feat of biological engineering if accomplished consciously. When people attempt to lose weight by eating less, the results are typically disappointing. Studies consistently show that calorie-restricted diets produce modest initial weight loss followed by regain. Even the Women's Health Initiative, which tracked nearly 50,000 women over eight years, found that those who reduced their daily caloric intake by about 360 calories lost an average of only two pounds—far less than the mathematical model would predict. Moreover, our bodies don't respond passively to reduced caloric intake. When we eat less, our metabolic rate decreases, hunger increases, and energy expenditure drops. The body fights to maintain its fat stores rather than surrendering them easily. This compensatory response explains why semi-starvation diets rarely produce lasting results. The calorie model fundamentally misidentifies cause and effect. Children don't grow taller because they eat more; they eat more because they're growing. Similarly, obesity isn't caused by overeating—overeating is driven by the underlying biological processes that promote fat storage.

Chapter 2: The Biological Regulation of Fat Storage Through Insulin

Fat tissue is not merely a passive storage depot for excess calories; it is an active endocrine organ tightly regulated by hormones—most importantly, insulin. This hormone serves as the primary regulator of fat metabolism, determining whether energy is stored as fat or made available for use by the body's cells. When insulin levels are elevated, several critical processes occur simultaneously. First, insulin activates an enzyme called lipoprotein lipase (LPL) on fat cells, which pulls fat from the bloodstream into these cells for storage. Second, insulin suppresses hormone-sensitive lipase (HSL), the enzyme responsible for breaking down stored fat so it can be released and burned for energy. Third, insulin directs the liver to convert excess carbohydrates into fat, and signals muscle cells to prioritize burning glucose rather than fat. The combined effect is that elevated insulin levels lock fat into fat cells while simultaneously reducing the body's ability to access this stored energy. This regulatory system explains many observations that the calories model cannot. For instance, when researchers remove the ovaries from female rats, the animals become obese whether they eat more or not. If forced to eat the same amount of food as before, they become sedentary and still get fat. The surgery alters hormonal signals governing fat metabolism, causing more energy to be diverted into fat storage regardless of caloric intake. Human fat distribution follows predictable patterns based on sex hormones and insulin sensitivity. Women tend to store fat below the waist, while men accumulate it primarily around the abdomen. After menopause, women's fat distribution becomes more like men's. These patterns reflect the variable influence of insulin and sex hormones on fat cells in different parts of the body, not differences in eating behavior or exercise habits. The regulation of fat storage also explains why we gain weight with age. As we grow older, our muscle cells typically become more insulin resistant, meaning they respond less effectively to insulin's signal. The pancreas compensates by secreting more insulin, which drives greater fat storage. The problem isn't that older adults necessarily eat more; it's that their hormonal environment increasingly favors fat accumulation. Understanding insulin's central role shifts our focus from how much we eat to what we eat. The foods that stimulate the greatest insulin secretion will promote the most fat storage, regardless of their caloric content.

Chapter 3: Carbohydrates, Not Calories: The True Dietary Culprit

The traditional advice to simply "eat less and move more" overlooks a crucial reality: different foods have dramatically different effects on the hormones that regulate fat metabolism. Carbohydrates—particularly refined grains, starches, and sugars—are uniquely effective at stimulating insulin secretion, making them the primary dietary drivers of fat accumulation. When we consume carbohydrates, they are quickly broken down into glucose, which enters the bloodstream and triggers insulin release. The more rapidly digestible the carbohydrate, the more dramatic the insulin response. Refined flour products (bread, pasta, cereals), sugars, and starchy vegetables like potatoes cause particularly sharp spikes in blood sugar and insulin. These insulin surges promote fat storage and inhibit fat burning, creating a hormonal environment that favors weight gain regardless of total calorie content. Fructose, which makes up half of table sugar and 55% of high-fructose corn syrup, presents special problems. Unlike glucose, fructose is metabolized almost exclusively in the liver, where it can be rapidly converted to fat. It doesn't immediately raise blood sugar or insulin, but chronic fructose consumption promotes insulin resistance over time. This helps explain why sugar-sweetened beverages are strongly associated with obesity and metabolic disease—they deliver a double whammy of glucose (which drives immediate insulin secretion) and fructose (which promotes long-term insulin resistance). Protein and fat, by contrast, have minimal effects on insulin. Protein stimulates some insulin release, but far less than carbohydrates do, and primarily to help build or maintain muscle tissue. Dietary fat has virtually no direct effect on insulin. A meal of meat, eggs, and green vegetables will produce a much smaller insulin response than a calorically equivalent meal of bread, pasta, or rice, even if the total energy content is identical. The different hormonal effects of macronutrients explain why carbohydrate-restricted diets often produce greater weight loss than low-fat diets, despite similar or even higher caloric intake. When insulin levels fall due to carbohydrate restriction, fat cells release their stored energy, satisfying the body's needs without requiring additional food intake. Hunger naturally decreases, and metabolic rate remains stable or even increases as the body accesses abundant stored energy. This hormonal perspective also explains why many traditional societies consuming high-fat, animal-based diets remained lean, while modern populations eating low-fat, high-carbohydrate diets struggle with obesity. The critical factor isn't the caloric content or even the fat content of these diets, but their effects on insulin and fat metabolism.

Chapter 4: The Historical Evidence for Carbohydrate-Restricted Diets

The idea that carbohydrates, not calories or fat, are the primary dietary cause of obesity is not new. In fact, it was the dominant medical perspective for nearly 150 years before being supplanted by the calories-in/calories-out paradigm in the late 20th century. In 1825, the French physician Jean Anthelme Brillat-Savarin published "The Physiology of Taste," which identified "starches and flours" as the root cause of obesity. He observed that carnivorous animals remained lean while herbivores often grew fat, and noted that humans who avoided starches and ate primarily meat rarely developed obesity. Brillat-Savarin concluded that "a more or less rigid abstinence from everything that is starchy or floury will lead to the lessening of weight." By the mid-1800s, this understanding was widespread in European medical circles. The British undertaker William Banting published his famous "Letter on Corpulence" in 1863, describing how he lost 50 pounds by eliminating bread, sugar, beer, and potatoes from his diet while eating meat, fish, and green vegetables to satisfaction. Banting's letter became a bestseller, and his name entered the English language as a verb meaning "to diet" by restricting carbohydrates. Throughout the early 20th century, leading medical textbooks and physicians continued to prescribe carbohydrate restriction for obesity. The 1951 edition of "The Practice of Endocrinology," a standard British medical reference, instructed overweight patients to avoid "bread and everything else made with flour," "cereals, including breakfast cereals," "potatoes and all other white root vegetables," and "foods containing much sugar." Similar advice appeared in the U.S. military's guide for soldiers and in Dr. Spock's influential child-rearing manual. Clinical studies from the 1950s through the 1970s consistently demonstrated the effectiveness of carbohydrate-restricted diets. Alfred Pennington's research at DuPont showed that overweight employees lost significant weight on a low-carbohydrate diet without calorie counting. Michigan State University's Margaret Ohlson reported that students on carbohydrate-restricted diets lost three pounds weekly without hunger, while those on low-calorie diets lost little weight and felt constantly hungry. This historical consensus began to shift in the 1960s with the rise of concern about dietary fat and heart disease. Despite limited evidence, authorities began recommending low-fat, high-carbohydrate diets for heart health, making carbohydrate restriction seem dangerous regardless of its effectiveness for weight loss. The traditional understanding of obesity as a disorder of carbohydrate metabolism was gradually replaced by the simplistic calories-in/calories-out model. The historical record demonstrates that our current dietary predicament—increasing obesity amid increasingly desperate calorie-cutting efforts—is not inevitable. Earlier generations understood that what we eat, specifically the carbohydrate content of our diet, matters far more for weight regulation than how much we eat.

Chapter 5: Why Exercise Alone Cannot Solve the Obesity Problem

The belief that increased physical activity can prevent or reverse obesity is deeply ingrained in public health recommendations and personal weight-loss strategies. However, both scientific evidence and logical analysis suggest that exercise, while beneficial for many aspects of health, is remarkably ineffective for weight management. The first clue comes from epidemiological observations. Obesity rates have risen dramatically in recent decades despite unprecedented increases in leisure-time physical activity. The "exercise explosion" that began in the 1970s has coincided with, rather than prevented, the obesity epidemic. Health club memberships, marathon participation, and recreational sports have all surged while waistlines have expanded. Another telling observation is the association between obesity and socioeconomic status. In developed nations, obesity is more common among the poor than the wealthy. Yet the poor are more likely to work in physically demanding occupations—construction, agriculture, manufacturing—than their wealthier counterparts. If exercise prevented obesity, we would expect the opposite pattern. The scientific literature consistently shows that exercise interventions produce minimal weight loss. A review by Finnish exercise physiologists found that in controlled trials, exercise either slightly decreased the rate of weight gain or actually increased it. Even dedicated runners tend to gain weight over time unless they continuously increase their mileage year after year—an unsustainable solution for most people. Several physiological mechanisms explain why exercise is ineffective for weight loss. First, exercise accounts for a surprisingly small portion of daily energy expenditure for most people. A 250-pound person burns only three extra calories climbing one flight of stairs. Second, exercise stimulates appetite—it "works up an appetite," as the saying goes—leading to compensatory increases in food intake. Third, the body tends to reduce non-exercise activity following workouts, partially offsetting the calories burned during intentional exercise. The relationship between exercise and appetite was well understood by obesity researchers in the early 20th century. As Northwestern University's Hugo Rony noted in 1940, "Vigorous muscle exercise usually results in immediate demand for a large meal." This explains why lumberjacks consume more than twice the calories of tailors. However, this insight was largely forgotten after Jean Mayer popularized the notion that exercise could aid weight loss without increasing hunger, despite limited evidence for this claim. None of this diminishes the many health benefits of physical activity. Exercise improves cardiovascular fitness, builds strength, enhances mood, and may help prevent numerous diseases. But these benefits are largely independent of its effects on weight. In fact, the expectation that exercise should produce weight loss creates frustration when the pounds don't drop as predicted, potentially discouraging continued activity. A more accurate perspective is that obesity often causes sedentary behavior, rather than the reverse. When hormonal factors drive excess fat accumulation, this diverts energy away from muscles and other tissues, leaving less available for physical activity. Addressing the underlying metabolic and hormonal issues may naturally increase energy and the desire for movement without requiring conscious effort or willpower.

Chapter 6: Metabolic Health: Beyond Weight Loss to Disease Prevention

The carbohydrate-insulin model of obesity has profound implications not just for weight management but for understanding and preventing a wide range of chronic diseases. What we now call "metabolic syndrome"—a cluster of conditions including abdominal obesity, high blood pressure, elevated blood sugar, high triglycerides, and low HDL cholesterol—emerges as a unified disorder driven by insulin resistance and carbohydrate consumption. Insulin resistance develops when cells, particularly in muscle and liver, become less responsive to insulin's signal. The pancreas compensates by secreting more insulin, creating chronically elevated insulin levels in the bloodstream. This hyperinsulinemia drives fat accumulation around the abdomen, raises blood pressure by causing sodium retention in the kidneys, and creates the characteristic blood lipid pattern of high triglycerides and low HDL. The relationship between obesity and various diseases becomes clearer through this lens. Type 2 diabetes develops when insulin resistance reaches the point where even elevated insulin levels can no longer maintain normal blood sugar. Heart disease risk increases as small, dense LDL particles (promoted by carbohydrate consumption) penetrate arterial walls more easily than the large, fluffy LDL particles associated with low-carbohydrate diets. Cancer risk rises as insulin and related growth factors stimulate cell proliferation. Even Alzheimer's disease has been linked to insulin resistance in the brain, leading some researchers to call it "type 3 diabetes." Clinical trials comparing low-carbohydrate to low-fat diets reveal striking differences in metabolic health markers. Beyond greater weight loss, carbohydrate-restricted diets typically produce larger increases in HDL cholesterol, greater reductions in triglycerides, and more significant improvements in blood pressure and blood sugar control. In the Stanford A TO Z Weight Loss Study, subjects following the Atkins diet (which restricts carbohydrates) showed more favorable changes in all these parameters than those following the low-fat Ornish diet, the Zone diet, or the standard LEARN diet. The benefits extend to patients with existing disease. For diabetics, carbohydrate restriction often reduces or eliminates the need for medication while improving blood sugar control. For those with heart disease risk factors, the hormonal changes from carbohydrate restriction—even with increased saturated fat consumption—typically improve the overall risk profile. The "ketogenic" diet (very low in carbohydrates) has been used successfully since the 1920s to treat epilepsy and is now being investigated for other neurological conditions. This metabolic perspective explains why obesity, diabetes, heart disease, and other "diseases of civilization" appear almost simultaneously when traditional populations adopt Western diets. These conditions share a common environmental trigger—the consumption of refined carbohydrates and sugars—acting on genetically susceptible individuals. While some people remain lean despite high carbohydrate consumption due to robust insulin sensitivity, others develop insulin resistance and the cascade of metabolic disturbances that follow. The implications for public health are substantial. Rather than focusing narrowly on calorie reduction or fat avoidance, prevention efforts would more effectively target the foods that disrupt metabolic health—primarily refined grains, starches, and sugars. For individuals already experiencing metabolic disturbances, carbohydrate restriction offers a powerful intervention that addresses the underlying hormonal and metabolic dysfunction rather than merely treating symptoms.

Chapter 7: Challenging the Low-Fat Paradigm and Saturated Fat Myths

For decades, dietary recommendations have centered on reducing fat, particularly saturated fat, to prevent heart disease and obesity. This paradigm has been so dominant that even questioning it was considered dangerous or irresponsible. However, a critical examination of the scientific evidence reveals that the case against dietary fat rests on surprisingly weak foundations. The original hypothesis that saturated fat causes heart disease emerged in the 1950s based primarily on epidemiological associations and animal studies with numerous limitations. When researchers actually tested this hypothesis in controlled human trials, the results were consistently disappointing. The largest such trial, the Women's Health Initiative, enrolled nearly 50,000 women who were randomly assigned to either continue their normal diet or adopt a low-fat approach. After eight years, the low-fat group showed no reduction in heart disease, stroke, or cancer rates despite significant reductions in fat consumption. The Cochrane Collaboration, widely regarded as the most rigorous source for evaluating medical evidence, reviewed all available trials on fat reduction and concluded there was "only limited and inconclusive evidence" that reducing dietary fat or saturated fat affects cardiovascular disease. Meta-analyses published in recent years have similarly failed to find convincing evidence that saturated fat consumption increases heart disease risk. The weakness of the evidence against saturated fat contrasts sharply with the strong evidence linking refined carbohydrates and sugars to metabolic dysfunction. When people replace saturated fat with carbohydrates, their triglycerides typically increase and their HDL cholesterol decreases—both changes associated with increased heart disease risk. The ratio of total cholesterol to HDL, a stronger predictor of heart disease than LDL alone, often improves when saturated fat replaces carbohydrates in the diet. Modern research has also revealed that LDL cholesterol, long considered the primary mechanism by which saturated fat supposedly causes heart disease, is far more complex than originally thought. Some LDL particles are large and buoyant, while others are small and dense. The small, dense particles are strongly associated with heart disease risk, while the large, buoyant ones appear relatively benign. Carbohydrate consumption, not saturated fat, promotes the formation of small, dense LDL particles. Animal fats, long demonized for their saturated fat content, actually contain substantial amounts of monounsaturated and polyunsaturated fats. Lard, for example, is 47% monounsaturated fat (the same type found in olive oil), and much of its saturated fat is stearic acid, which has neutral effects on blood cholesterol. The nutritional complexity of natural foods cannot be reduced to single components like "saturated fat." The low-fat paradigm created a paradoxical situation where the diet that most effectively reduces body fat (carbohydrate restriction) was considered dangerous because it typically includes more saturated fat. This contradiction should have prompted reconsideration of the underlying assumptions, but instead, authorities doubled down on their recommendations, even as obesity and diabetes rates soared. Perhaps most telling is the dramatic mismatch between dietary trends and health outcomes over the past 40 years. Americans have significantly reduced their consumption of saturated fat and eggs while increasing their intake of "heart-healthy" carbohydrates, yet heart disease remains the leading cause of death. Meanwhile, populations that consume considerable saturated fat from animal sources, such as the Maasai in Africa or traditional Inuit, show remarkably low rates of heart disease and other chronic conditions. The evidence suggests we have been fighting the wrong dietary enemy. Natural fats, including saturated fats, appear to be healthful components of human diets when consumed in the context of low carbohydrate intake. The real dietary villains are the refined carbohydrates and sugars that disrupt metabolic health and drive chronic disease.

Summary

The conventional wisdom about obesity—that it results from consuming more calories than we expend—has dominated medical thinking and public health policy for decades. Yet this model fails to explain numerous observations about weight regulation and has led to increasingly desperate but ineffective interventions focused on eating less and exercising more. By shifting our perspective to understand obesity as a hormonal disorder driven by the consumption of carbohydrates, particularly refined grains, starches, and sugars, we gain powerful insights into why we get fat and what we can do about it. This carbohydrate-insulin model provides a comprehensive framework that explains diverse observations: why some populations remain lean despite high caloric intake while others become obese despite poverty, why exercise rarely produces significant weight loss, why certain foods are particularly fattening regardless of their caloric content, and why so many chronic diseases cluster together in modern societies. It also offers a path forward that doesn't rely on unsustainable hunger or constant willpower battles. By understanding the hormonal effects of different foods, we can make dietary choices that work with our biology rather than against it, addressing not just obesity but the entire spectrum of metabolic diseases that threaten public health. The solution isn't to eat less of everything, but to avoid the specific foods that disrupt our metabolic health—a message that has been periodically rediscovered and forgotten throughout medical history.

About Author

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Gary Taubes

Gary Taubes is an American science writer. He is the author of Nobel Dreams (1987), Bad Science: The Short Life and Weird Times of Cold Fusion (1993), and Good Calories, Bad Calories (2007), titled The Diet Delusion (2008) in the UK and Australia. His book Why We Get Fat: And What to Do About It was released in December 2010. In December 2010 Taubes launched a blog at GaryTaubes.com to promote the book's release and to respond to critics. His main hypothesis is based on: Carbohydrates generate insulin, which causes the body to store fat.Taubes studied applied physics at Harvard University (BS, 1977) and aerospace engineering at Stanford University (MS, 1978). After receiving a master's degree in journalism at Columbia University in 1981, Taubes joined Discover magazine as a staff reporter in 1982. Since then he has written numerous articles for Discover, Science and other magazines. Originally focusing on physics issues, his interests have more recently turned to medicine and nutrition.Taubes's books have all dealt with scientific controversies. Nobel Dreams takes a critical look at the politics and experimental techniques behind the Nobel Prize-winning work of physicist Carlo Rubbia. Bad Science is a chronicle of the short-lived media frenzy surrounding the Pons-Fleischmann cold fusion experiments of 1989. [wikipedia]

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