What is *Why We Get Fat* by Gary Taubes about?

*Why We Get Fat* challenges conventional weight-loss wisdom by arguing that refined carbohydrates—not calories or lack of exercise—drive obesity. Gary Taubes explains how insulin regulates fat storage, debunks the “calories-in/calories-out” model, and advocates for a low-carb, high-fat diet as the solution to weight management and metabolic health.

Who should read *Why We Get Fat*?

This book is ideal for individuals struggling with weight loss, low-carb diet enthusiasts, and anyone skeptical of mainstream nutrition advice. It’s also valuable for readers interested in the science behind obesity and how hormonal imbalances contribute to fat accumulation.

Is *Why We Get Fat* worth reading?

Yes, for its compelling critique of dietary myths and evidence-backed case against carbohydrates. However, readers should be aware of controversies, as some experts criticize Taubes for oversimplifying metabolic science and dismissing calorie moderation.

What are the main ideas in *Why We Get Fat*?

Key concepts include: - Carbohydrates, especially sugars and grains, spike insulin, promoting fat storage. - Obesity is a hormonal imbalance, not a result of overeating or laziness. - Traditional low-fat diets exacerbate weight gain, while low-carb diets stabilize metabolism.

How does *Why We Get Fat* differ from other diet books?

Unlike generic weight-loss guides, Taubes focuses on the *biology* of fat regulation, using decades of scientific research to argue that cutting carbohydrates—not counting calories—is the key to lasting health.

What diet does Gary Taubes recommend in *Why We Get Fat*?

Taubes advocates eliminating sugars, grains, and starchy vegetables while prioritizing proteins, healthy fats, and non-starchy vegetables. This approach aims to reduce insulin levels, allowing the body to burn stored fat.

What criticisms exist about *Why We Get Fat*?

Critics argue Taubes cherry-picks studies, oversimplifies metabolic processes, and underestimates the role of calorie intake. For example, Harriet A. Hall disputes his dismissal of the calorie deficit model, calling it “simply wrong”.

How does exercise factor into Taubes’ argument?

Taubes claims exercise has minimal impact on weight loss, as overeating carbohydrates—not inactivity—causes fat accumulation. He warns that intense workouts may increase hunger, leading to higher carb consumption.

我们为什么会发胖

以及该如何应对

盖里·陶布斯

4.03(22413 Reviews)

《我们为什么会发胖》概述

加里·陶布斯（Gary Taubes）的这部备受争议的畅销书挑战了我们对体重增加的所有认知，他认为导致肥胖的不是热量，而是碳水化合物。这本书得到了健康专家的认可，并因拆解了“热量摄入与消耗”的迷思而广受赞誉，它揭示了为什么仅靠运动无法拯救你。

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第 1 章

The Carbohydrate Paradox: Why Everything You Know About Fat Is Wrong

In 2002, award-winning science journalist Gary Taubes published a groundbreaking article in The New York Times Magazine titled "What If It's All Been a Big Fat Lie?" The piece challenged decades of nutritional orthodoxy and sparked a firestorm of controversy. His subsequent book, "Why We Get Fat," became a #1 bestseller, influencing millions to rethink their relationship with food. The book has been translated into 29 languages and remains required reading in many medical schools. Even celebrities like LeBron James and Halle Berry have credited Taubes' work for transforming their understanding of nutrition. What makes this book so revolutionary? It presents a simple but radical idea: what if obesity isn't about how much we eat, but what we eat?

第 2 章

The Poverty-Obesity Connection: A Glaring Contradiction

The conventional wisdom about obesity contains a glaring contradiction that should immediately make us suspicious. If obesity results from overeating in prosperous societies with abundant food, why does it associate so strongly with poverty? Since the 1960s, studies have consistently shown that poorer people are more likely to be obese-women in poverty are six times more likely to be obese than wealthy women. This paradox deepens when we examine populations that experienced obesity without any modern "toxic environment" factors. The Pima Indians of Arizona offer a striking example. While often cited as victims of modern American food culture, they were already notably obese when anthropologists studied them between 1901-1905. Anthropologist Frank Russell photographed "Fat Louisa" and noted many older Pima exhibited "striking" obesity, while Ales Hrdlicka observed obesity "almost exclusively among Indians on reservations." What makes this remarkable is that the Pima had just transitioned from prosperity to poverty. Through the 1850s, they were successful hunters, farmers, and traders with "storehouses full" of food. After the California gold rush, settlers diverted their water and hunted local game to extinction, leading to the "years of famine" by the 1870s. When the anthropologists arrived, the tribe relied on government rations. The key factor wasn't prosperity or quantity of food, but quality. Trading posts had introduced "sugar, coffee, and canned goods" while government rations consisted largely of white flour and sugar-the very foods that distinguish Western diets from traditional ones. This pattern repeats throughout history: when traditional populations adopt Western foods-particularly refined flour and sugar-obesity and diabetes follow, regardless of overall calorie intake or physical activity levels.

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第 3 章

The Twenty-Calorie Paradox: Why Calorie Math Doesn't Add Up

Twenty calories. This tiny number exposes the fundamental flaw in the "energy balance" theory of obesity. If weight gain is truly about calories-in versus calories-out, then consuming just twenty extra calories daily-less than a single bite of hamburger, three potato chips, or two ounces of soda-would cause someone to gain fifty pounds over twenty-five years. This arithmetic reveals an impossible paradox: how does anyone stay lean when the margin for error is less than 1% of our daily caloric intake? To maintain weight for decades requires matching energy intake and expenditure with an accuracy of one-twentieth of 1%-"an exactness," as Cornell's Eugene Du Bois wrote in 1936, "which is equaled by few mechanical devices." The fact that many people remain lean for decades, and even obese individuals maintain stable weights rather than continuously gaining, suggests something more sophisticated than simple calorie counting is regulating our body weight. As Du Bois observed, "there is no stranger phenomena than the maintenance of a constant body weight under marked variation in bodily activity and food consumption." Think about it-animals maintain stable weights without counting calories or checking scales. Your dog doesn't get progressively fatter year after year despite eating roughly the same amount daily. Something more fundamental is happening, suggesting our understanding of weight regulation is fundamentally flawed. The body must have sophisticated mechanisms for maintaining appropriate weight-mechanisms that can be disrupted by specific dietary factors.

第 4 章

The Mysterious Geography of Fat: Why There, Not Here?

Fat distribution on our bodies is far more complex than simply having excess fat or not. Where we accumulate fat matters greatly-abdominal obesity increases heart disease risk while hip fat doesn't. Some people develop double chins, others fat ankles or love handles. These patterns can't be explained by calories alone. Pre-WWII physicians like Gustav von Bergmann and Julius Bauer recognized that fat distribution provides crucial insights about obesity's nature. Genetics plays a major role-body types run in families, and identical twins show remarkably similar fat patterns whether lean or obese. This genetic component is obvious in livestock breeding, where cattle like Aberdeen Angus are bred for marbling fat while Jersey dairy cows remain lean. These differences aren't about how much they eat but how their bodies partition energy. Gender differences further undermine the calories-in/calories-out model. Men typically store fat above the waist while women store it below. During puberty, girls develop fat in breasts, hips, and thighs while boys lose fat and gain muscle. Rare disorders like progressive lipodystrophy-where patients lose fat above the waist while gaining it below-and HIV-related lipodystrophy demonstrate that fat distribution has little to do with eating habits or exercise levels. If obesity were simply about energy balance, wouldn't excess fat distribute evenly throughout the body? The fact that it doesn't-that it follows predictable patterns influenced by genetics, sex hormones, and other factors-suggests that sophisticated regulatory mechanisms, not simple calorie math, determine where and how much fat we store.

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第 5 章

The Compensation Problem: Why Diet and Exercise Fail

The conventional wisdom about weight loss-eat less, exercise more-rests on a fundamental misconception about energy balance. The error lies in assuming that calories consumed and calories expended are independent variables that don't influence each other. In reality, these factors are intimately linked. When we restrict calories, our bodies compensate by reducing energy expenditure. We become lethargic, our body temperature drops, and we feel cold all the time. Similarly, increasing physical activity increases hunger-exercise works up an appetite and makes us tired, causing us to expend less energy afterward. As Harvard Medical School's Jeffrey Flier and Terry Maratos-Flier explained in Scientific American, an animal whose food is suddenly restricted reduces its energy expenditure both through decreased activity and slowed cellular metabolism, limiting weight loss. It also experiences increased hunger, so once restrictions end, it eats more until regaining its original weight. This same principle applies to humans, explaining why conventional diet advice fails. Semi-starvation might produce short-term weight loss, but our bodies inevitably compensate, making such approaches unsustainable beyond a few months or a year. Consider the Women's Health Initiative, a billion-dollar NIH study where nearly fifty thousand women participated. Twenty thousand were randomly selected to follow a low-fat diet rich in fruits, vegetables, and fiber, supported by regular motivational counseling. These women consumed on average 360 fewer calories daily than before starting the diet-a significant reduction that should have produced substantial weight loss according to conventional wisdom. Yet after eight years, they had lost an average of only two pounds. Even more telling, their waistlines had increased by about half an inch, suggesting they'd actually gained abdominal fat despite eating less. This compensation phenomenon explains why traditional dieting has a 95% failure rate over five years. Our bodies aren't passive calorie processors-they actively defend against weight loss through powerful hormonal and metabolic adaptations.

第 6 章

The Forgotten History: Carbohydrates and Obesity Through Time

The idea that carbohydrates cause obesity dates back centuries. Jean Anthelme Brillat-Savarin, in his 1825 book "The Physiology of Taste," concluded after observing countless "fat men" that obesity had two causes: a natural predisposition to fatten and consumption of "starches and flours which man uses as the base of his daily nourishment," especially when combined with sugar. His solution was straightforward: "a more or less rigid abstinence from everything that is starchy or floury." This wisdom persisted through the 1960s. In literature, we see examples like Tolstoy's Count Vronsky avoiding "starchy foods and desserts" to maintain his weight for horse racing, and Bellow's Herzog denying himself a candy bar to fit into new clothes. Physicians routinely advised patients accordingly. Until the early 20th century, obesity was considered an almost incurable disease. While physicians tried various treatments including exercise and eating less, most failed. The French physician Jean-Francois Dancel argued in 1844 that he could cure obesity "without a single exception" if patients lived "chiefly upon meat" with minimal other foods. He noted that carnivores were never fat while herbivores often were. William Harvey reinvented this approach after learning about diabetes and glucose from Claude Bernard. Harvey prescribed a meat-based, low-carbohydrate diet to William Banting in 1862, helping him lose 50 pounds. Banting's published account became so popular that "banting" entered the English language as a verb meaning "to diet." Medical literature through the 1960s consistently advised avoiding carbohydrates for weight loss. From William Osler in 1901 to the U.S. Navy's WWII guide to Dr. Spock's Baby and Child Care, the message was clear: starches and sugars cause weight gain. Clinical studies from the 1940s through 1970s consistently showed that low-carbohydrate diets produced significant weight loss without hunger, across multiple countries and populations. However, starting in the 1960s and concluding in the late 1970s, medical authorities began rejecting this approach, labeling low-carbohydrate diets as "bizarre concepts of nutrition" and potentially dangerous-comparable to using cigarettes or cocaine for weight loss. Ironically, this shift coincided with the beginning of our current obesity and diabetes epidemics.

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第 7 章

The Exercise Myth: Why Running Doesn't Make You Thin

Since the 1970s, America has experienced an "exercise explosion"-a dramatic shift from viewing strenuous exercise as "bad for you" to embracing it as essential. By 1980, The Washington Post reported that 100 million Americans had joined this "new fitness revolution," a "major sociological event" of the late twentieth century. Yet paradoxically, this fitness boom coincided precisely with the obesity epidemic. This contradiction challenges the fundamental belief that sedentary behavior causes fatness and physical activity prevents it. Until the 1960s, most obesity specialists dismissed exercise for weight loss as naive. Mayo Clinic's Russell Wilder noted in 1932 that his patients lost more weight with bed rest, while strenuous exercise "slows the rate of loss." The reasoning was twofold: moderate exercise burns surprisingly few calories (a 250-pound man burns just three calories climbing one flight of stairs), and increased activity stimulates hunger. As Northwestern University's Hugo Rony observed in 1940, vigorous exercise "results in immediate demand for a large meal"-lumberjacks naturally eat 5,000 calories daily while tailors eat 2,500. The body naturally compensates for energy expenditure with increased appetite. The research consistently undermines the exercise-weight loss connection. Finnish physiologists reviewing the best experimental trials found everyone regained weight regardless of exercise, which at best slightly decreased the rate of regain. A 2006 study of 13,000 runners showed even those running 40+ miles weekly gained weight annually, leading researchers to suggest runners needed to add miles each year just to maintain weight-an absurd progression requiring middle-aged runners to log half-marathons five days weekly. The American Heart Association and American College of Sports Medicine reluctantly acknowledged in 2007 that evidence supporting exercise for weight control is "not particularly compelling." Other authorities recommend even more exercise-up to 90 minutes daily-not to lose weight but merely to avoid gaining more. The fundamental flaw is assuming we can increase energy expenditure without triggering increased energy intake. The body naturally compensates-we "work up an appetite" when physically active, a concept once obvious but now strangely forgotten.

第 8 章

The Hormonal Theory: Insulin as the Master Regulator

The science shows that obesity is fundamentally a hormonal imbalance, not a caloric one. Research since the early 1960s has established two critical factors: first, when insulin levels are elevated, we accumulate fat; when they fall, we burn fat for fuel. Second, insulin levels are primarily determined by the carbohydrates we eat-especially easily digestible, sweet carbohydrates. As Harvard's George Cahill put it: "Carbohydrate is driving insulin is driving fat." Fat exists in our bodies in two forms serving different purposes. Fatty acids are small enough to flow through cell membranes and can be burned for fuel. Triglycerides, composed of three fatty acids bound to glycerol, are too large to exit fat cells and represent stored fat. Anything promoting fatty acid flow into fat cells (where they become triglycerides) makes us fatter; anything breaking down triglycerides into fatty acids that can escape makes us leaner. While dozens of hormones and enzymes influence these processes, insulin dominates. As the "principal regulator of fat metabolism," insulin orchestrates fat storage and use. It works primarily through enzymes like lipoprotein lipase (LPL), which pulls fat from the bloodstream into cells. The distribution of LPL explains why men and women fatten differently-men have higher LPL activity in gut fat tissue, while women have higher activity below the waist. Insulin activates LPL on fat cells while suppressing it on muscle cells, directing fat storage rather than burning. It also suppresses hormone-sensitive lipase (HSL), the enzyme that breaks down stored fat, effectively trapping fat in cells. Even slightly elevated insulin prevents fat burning while promoting fat storage and creation of new fat cells. This explains why diabetics often gain weight on insulin therapy-it's the direct lipogenic effect of insulin, independent of food intake. When insulin levels rise, we store fat; when they fall, we burn it. This cycle normally balances over a 24-hour period, but even a tiny imbalance-just twenty calories a day-can lead to obesity over decades. Elevated insulin extends fat-storing periods while shortening fat-burning ones.

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第 9 章

The Three Laws of Adiposity: A New Framework for Understanding Obesity

To understand why we get fat, we must look beyond the simplistic calories-in/calories-out model to how our fat tissue is actually regulated. This reveals three fundamental laws of adiposity that explain obesity far better than thermodynamics. The first law: Body fat is carefully regulated, not just a passive storage depot. Evidence for this includes sex-specific fat patterns, genetic influences on fat distribution, and the way wild animals maintain optimal fat levels regardless of food availability. Like everything else in our bodies, fat storage is precisely controlled through hormones and enzymes. The second law: Obesity can result from a regulatory defect so small it's virtually undetectable. Just as twenty extra calories daily can transform someone from lean to obese over decades, a tiny error that diverts just 1% of calories into fat storage instead of energy use guarantees obesity. The third law: Whatever makes us fatter will also make us overeat. This counterintuitive principle explains why overeating is the effect, not the cause, of getting fat. Just as growing children don't grow tall because they overeat but overeat because they're growing, our fat tissue accumulates fat because of hormonal regulation, which then drives increased appetite to satisfy the energy demands. If a regulatory defect drives fat accumulation, it will inevitably increase appetite and/or decrease energy expenditure. Children provide the perfect metaphor-they don't grow because they overeat; they overeat because they're growing. Growth hormones drive their development, which creates energy demands that increase appetite. The same applies to fat tissue. As German internist Gustav von Bergmann noted eighty years ago, we would never consider height growth the result of overeating, so why assume fat accumulation works differently? "That which the body needs to grow it always finds," he wrote, "and that which it needs to become fat, even if it's ten times as much, the body will save for itself from the annual balance."

第 10 章

The Heart Disease Myth: Why Fat Isn't the Enemy

The Cochrane Collaboration's 2001 assessment found only 27 clinical trials reliable enough to judge whether reducing fat intake prevents heart attacks. Despite decades of research, they concluded evidence was "limited and inconclusive." The Women's Health Initiative-the largest diet trial ever conducted-followed 49,000 women, with 20,000 randomly assigned to eat low-fat, low-saturated-fat diets with more vegetables, fruits and whole grains. After six years, despite lowering their fat consumption by a quarter and slightly reducing their cholesterol levels, these women saw no beneficial effects on heart disease, stroke, cancer rates, or weight loss. This contradicts the "leap-of-faith" logic health authorities embraced in 1984. The belief that saturated fat causes heart disease persists not because evidence supports it, but because it aligns with the cholesterol-lowering effects of statin drugs. However, this logic is flawed: drugs and diets work differently, and just because statins prevent heart disease while lowering LDL doesn't mean they prevent heart disease because they lower LDL-just as aspirin prevents heart disease but not because it cures headaches. Triglycerides are a significant heart disease risk factor, and they're elevated by carbohydrates, not fat. When you replace saturated fat with carbohydrates, your LDL might decrease, but your triglycerides will rise. Similarly, low HDL cholesterol strongly predicts heart attack risk-especially for women-and carbohydrate-rich diets lower HDL levels. Replacing fat with carbohydrates lowers your "good" cholesterol, increasing heart attack risk. Conversely, replacing carbohydrates with fat raises HDL and reduces risk. Recent clinical trials comparing low-carbohydrate, high-fat diets (like Atkins) with low-fat, calorie-restricted diets show remarkably consistent results. The Stanford University A TO Z Weight Loss Study compared four diets: Atkins (very low carb), traditional low-fat (LEARN), Ornish (ultra-low fat), and Zone (moderate carb). Despite eating unlimited meat and fat, Atkins dieters lost more weight and showed better improvements in triglycerides, HDL cholesterol, and blood pressure than those on other diets.

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第 11 章

Beyond Weight: Carbohydrates and Modern Disease

Metabolic syndrome represents the intermediate step between carbohydrate consumption and heart disease. When we become insulin-resistant, we develop a cluster of related conditions: expanding waistlines, high blood pressure, elevated triglycerides, low HDL, small dense LDL, glucose intolerance, and potentially type 2 diabetes. Over a quarter of American adults now suffer from this syndrome. Stanford physician Gerald Reaven identified excessive insulin secretion and insulin resistance as the root causes of these metabolic disturbances in the 1980s, but his research was initially resisted because it implicated carbohydrates, not fat, as the dietary culprits. Today, metabolic syndrome science represents the greatest advance in understanding heart disease and its connection to hypertension, obesity, and diabetes. Low-carbohydrate, high-fat diets improve every marker of metabolic syndrome, confirming that the same carbohydrates making us fat are causing these dangerous conditions. Metabolic syndrome extends beyond heart disease to Alzheimer's and most cancers. Researchers have begun calling Alzheimer's "type 3 diabetes" as they discover how insulin and high blood sugar deteriorate the brain. Cancer's link to metabolic syndrome is so well-established that the World Cancer Research Fund recommends being "as lean as possible" to prevent cancer. The simplest explanation for all these associations is that what makes us fat-the quality and quantity of carbohydrates we consume-also makes us sick. This isn't just about weight anymore; it's about understanding the fundamental dietary causes of modern chronic diseases.

第 12 章

Practical Solutions: How to Eat in an Insulin-Dominated World

Since carbohydrates make us fat, the logical conclusion is that avoiding carbohydrate-rich foods is the best way to prevent or reverse fat accumulation. Not all carbohydrates are equally fattening. The most problematic are those that rapidly digest and spike blood sugar: refined flour products (bread, cereals, pasta), liquid carbohydrates (beer, fruit juices, sodas), and starches (potatoes, rice, corn). The worst foods are sugars-sucrose (table sugar) and high-fructose corn syrup. Since HFCS replaced sugar in most American soft drinks by the mid-1980s, per capita sugar consumption jumped from 120 to 150 pounds yearly. Both are effectively identical: sucrose is half fructose and half glucose, while HFCS-55 is 55% fructose, 42% glucose, and 3% other carbohydrates. The fructose component makes these sweeteners particularly harmful. Unlike glucose from starches that enters general circulation, fructose is metabolized almost exclusively by the liver, which never evolved to handle modern fructose loads. While a cup of blueberries contains thirty calories of fructose, a twelve-ounce soda has eighty calories worth. The liver responds by converting much fructose to fat and shipping it to fat tissue. Meanwhile, the accompanying glucose raises blood sugar and stimulates insulin, putting fat cells in storage mode. Physicians promoting carbohydrate restriction typically take one of three approaches. The first establishes an ideal carbohydrate amount-like Wolfgang Lutz's 72 grams (300 calories) daily-which minimizes transition side effects while allowing small amounts of sugar, occasional desserts, and carbohydrates from vegetables and fruit. This works for some but not all. The second approach aims for minimal carbohydrates immediately, reasoning they're unnecessary and any adjustment side effects can be managed. The third approach, pioneered by Robert Atkins forty years ago, is a compromise recognizing that weight loss is the primary goal and gustatory desires should be temporarily suspended until that goal is achieved. Atkins' approach begins with an "induction phase" allowing virtually no carbohydrates (under 20 grams daily) except small portions of leafy greens. This accelerates initial weight loss and provides motivation. Once fat-burning is established, minimal carbohydrates can be reintroduced. If weight loss stops, that indicates your body can't tolerate those carbohydrates and they should be eliminated. Unlike traditional diets that fail because they require semi-starvation (leading to metabolic adaptation, chronic hunger, and depression), carbohydrate restriction works differently. When you restrict only fattening carbohydrates, you don't need to consciously limit protein and fat intake-you can eat until satisfied.

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《我们为什么会发胖》核心主题

insulin signaling
carbohydrate-insulin model
nutritional orthodoxy
refined sugar impact
metabolic regulation

《我们为什么会发胖》经典语录

What if obesity isn't about how much we eat, but what we eat?
Poorer people are more likely to be obese.
The key factor wasn't prosperity or quantity of food, but quality.
Fat distribution provides crucial insights about obesity's nature.
Semi-starvation might produce short-term weight loss, but our bodies inevitably compensate.

《我们为什么会发胖》主要人物

Gary TaubesAuthor and science journalist
Fat LouisaPima Indian woman photographed by anthropologists
Frank RussellAnthropologist who studied the Pima Indians
Eugene Du BoisCornell researcher who studied weight regulation
Gustav von BergmannPre-WWII physician who studied fat distribution

关于作者

加里·陶布斯（Gary Taubes）是一位屡获殊荣的科学记者，也是《我们为什么会发胖》（Why We Get Fat and What to Do About It）一书的作者。他是挑战传统营养学和肥胖观点的领军人物。

作为一名受教于哈佛大学和哥伦比亚大学的调查员，陶布斯将严谨的研究与通俗易懂的叙述相结合，认为导致体重增加的是过量的碳水化合物——而非热量——因为它们破坏了胰岛素调节。他在《好卡路里，坏卡路里》（Good Calories, Bad Calories，2007年）和《反糖案例》（The Case Against Sugar，2016年）中的著作进一步批评了存在缺陷的饮食指南，巩固了他作为代谢健康领域逆向思维者的声誉。

作为非营利组织“营养科学倡议”（Nutrition Science Initiative）的联合创始人，陶布斯因其开创性的报道三次获得美国科学作家协会奖。他2020年的著作《生酮案例》（The Case for Keto）扩展了低碳水化合物解决方案，提供了与其胰岛素核心模型相一致的实用策略。

陶布斯的著作已被翻译成20多种语言，引发了全球范围内的辩论，其中《我们为什么会发胖》仍然是碳水化合物限制饮食倡导者的基石之作。

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由哥伦比亚大学校友在旧金山创建

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1,000,000+ curious minds.

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1M+ learners

"Instead of endless scrolling, I just hit play on BeFreed. It saves me so much time."

@Moemenn

"I never knew where to start with nonfiction—BeFreed’s book lists turned into podcasts gave me a clear path."

@Chloe, Solo founder, LA

117

"Perfect balance between learning and entertainment. Finished ‘Thinking, Fast and Slow’ on my commute this week."

@Raaaaaachelw

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@Matt, YC alum

108

"Reading used to feel like a chore. Now it’s just part of my lifestyle."

@Erin, Investment Banking Associate , NYC

254

"Feels effortless compared to reading. I’ve finished 6 books this month already."

@djmikemoore

"BeFreed turned my guilty doomscrolling into something that feels productive and inspiring."

@Pitiful

4.5K

"BeFreed turned my commute into learning time. 20-min podcasts are perfect for finishing books I never had time for."

@SofiaP

"BeFreed replaced my podcast queue. Imagine Spotify for books — that’s it. 🙌"

@Jaded_Falcon

201

"It is great for me to learn something from the book without reading it."

@OojasSalunke

"The themed book list podcasts help me connect ideas across authors—like a guided audio journey."

@Leo, Law Student, UPenn

483

"Makes me feel smarter every time before going to work"

@Cashflowbubu

"Instead of endless scrolling, I just hit play on BeFreed. It saves me so much time."

@Moemenn

"I never knew where to start with nonfiction—BeFreed’s book lists turned into podcasts gave me a clear path."

@Chloe, Solo founder, LA

117

"Perfect balance between learning and entertainment. Finished ‘Thinking, Fast and Slow’ on my commute this week."

@Raaaaaachelw

"Crazy how much I learned while walking the dog. BeFreed = small habits → big gains."

@Matt, YC alum

108

"Reading used to feel like a chore. Now it’s just part of my lifestyle."

@Erin, Investment Banking Associate , NYC

254

"Feels effortless compared to reading. I’ve finished 6 books this month already."

@djmikemoore

"BeFreed turned my guilty doomscrolling into something that feels productive and inspiring."

@Pitiful

4.5K

"BeFreed turned my commute into learning time. 20-min podcasts are perfect for finishing books I never had time for."

@SofiaP

"BeFreed replaced my podcast queue. Imagine Spotify for books — that’s it. 🙌"

@Jaded_Falcon

201

"It is great for me to learn something from the book without reading it."

@OojasSalunke

"The themed book list podcasts help me connect ideas across authors—like a guided audio journey."

@Leo, Law Student, UPenn

483

"Makes me feel smarter every time before going to work"

@Cashflowbubu

"Instead of endless scrolling, I just hit play on BeFreed. It saves me so much time."

@Moemenn

"I never knew where to start with nonfiction—BeFreed’s book lists turned into podcasts gave me a clear path."

@Chloe, Solo founder, LA

117

"Perfect balance between learning and entertainment. Finished ‘Thinking, Fast and Slow’ on my commute this week."

@Raaaaaachelw

"Crazy how much I learned while walking the dog. BeFreed = small habits → big gains."

@Matt, YC alum

108

"Reading used to feel like a chore. Now it’s just part of my lifestyle."

@Erin, Investment Banking Associate , NYC

254

"Feels effortless compared to reading. I’ve finished 6 books this month already."

@djmikemoore

"BeFreed turned my guilty doomscrolling into something that feels productive and inspiring."

@Pitiful

4.5K

"BeFreed turned my commute into learning time. 20-min podcasts are perfect for finishing books I never had time for."

@SofiaP

"BeFreed replaced my podcast queue. Imagine Spotify for books — that’s it. 🙌"

@Jaded_Falcon

201

"It is great for me to learn something from the book without reading it."

@OojasSalunke

"The themed book list podcasts help me connect ideas across authors—like a guided audio journey."

@Leo, Law Student, UPenn

483

"Makes me feel smarter every time before going to work"

@Cashflowbubu

查看更多网络上关于 BeFreed 的讨论

开启你的学习之旅，就是现在

第 12 章

我们为什么会发胖

概述《我们为什么会发胖》概述

一本书，多种聆听方式。

The Carbohydrate Paradox: Why Everything You Know About Fat Is Wrong

The Poverty-Obesity Connection: A Glaring Contradiction

边听边看，每个词都清晰呈现

The Twenty-Calorie Paradox: Why Calorie Math Doesn't Add Up

The Mysterious Geography of Fat: Why There, Not Here?

从 《我们为什么会发胖》中收获更多

The Compensation Problem: Why Diet and Exercise Fail

The Forgotten History: Carbohydrates and Obesity Through Time

边听边看，每个词都清晰呈现

The Exercise Myth: Why Running Doesn't Make You Thin

The Hormonal Theory: Insulin as the Master Regulator

从 《我们为什么会发胖》中收获更多

The Three Laws of Adiposity: A New Framework for Understanding Obesity

The Heart Disease Myth: Why Fat Isn't the Enemy

边听边看，每个词都清晰呈现

Beyond Weight: Carbohydrates and Modern Disease

Practical Solutions: How to Eat in an Insulin-Dominated World

你已读完 《我们为什么会发胖》

《我们为什么会发胖》核心主题

《我们为什么会发胖》经典语录

《我们为什么会发胖》主要人物

关于作者

下载《我们为什么会发胖》摘要

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关于本书的常见问题

What is Why We Get Fat by Gary Taubes about?

Who should read Why We Get Fat?

Is Why We Get Fat worth reading?

What are the main ideas in Why We Get Fat?

发现更多

1,000,000+ curious minds.

1,000,000+ curious minds.

一本书，多种聆听方式。

The Carbohydrate Paradox: Why Everything You Know About Fat Is Wrong

The Poverty-Obesity Connection: A Glaring Contradiction

边听边看，每个词都清晰呈现

The Twenty-Calorie Paradox: Why Calorie Math Doesn't Add Up

The Mysterious Geography of Fat: Why There, Not Here?

从 《我们为什么会发胖》中收获更多

The Compensation Problem: Why Diet and Exercise Fail

The Forgotten History: Carbohydrates and Obesity Through Time

边听边看，每个词都清晰呈现

The Exercise Myth: Why Running Doesn't Make You Thin

The Hormonal Theory: Insulin as the Master Regulator

从 《我们为什么会发胖》中收获更多

The Three Laws of Adiposity: A New Framework for Understanding Obesity

The Heart Disease Myth: Why Fat Isn't the Enemy

边听边看，每个词都清晰呈现

Beyond Weight: Carbohydrates and Modern Disease

Practical Solutions: How to Eat in an Insulin-Dominated World

你已读完 《我们为什么会发胖》

用户还喜欢

发现更多

《我们为什么会发胖》概述

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从《我们为什么会发胖》中收获更多

你已读完《我们为什么会发胖》

从《我们为什么会发胖》中收获更多

从《我们为什么会发胖》中收获更多

你已读完《我们为什么会发胖》