What is *Why We Eat (Too Much)* by Andrew Jenkinson about?

*Why We Eat (Too Much)* explores the science behind appetite, metabolism, and weight regulation, challenging outdated diet myths. Surgeon Andrew Jenkinson introduces the **weight set-point theory**, explaining how hormonal and genetic factors control body weight, and critiques modern processed foods for disrupting natural metabolic processes. The book combines clinical insights with evolutionary biology to reframe obesity as a biological adaptation, not a failure of willpower.

Who should read *Why We Eat (Too Much*)?

This book is ideal for individuals frustrated by yo-yo dieting, healthcare professionals seeking evidence-based obesity insights, or anyone interested in metabolism and nutrition science. It’s particularly valuable for readers seeking to understand *why* diets fail long-term, rather than quick fixes. Jenkinson’s accessible approach makes complex hormonal concepts (like leptin and insulin resistance) digestible for non-experts.

Is *Why We Eat (Too Much)* worth reading?

Yes, for its groundbreaking perspective on weight regulation and critique of diet culture. While some readers note occasional tonal issues or desire more practical meal plans, the book’s science-backed explanations of appetite control and metabolic adaptation are widely praised. Jenkinson’s 20+ years as a bariatric surgeon lend unique credibility to his analysis of obesity’s root causes.

What is the weight set-point theory in *Why We Eat (Too Much*)?

The weight set-point theory posits that the brain regulates body fat stores through hormonal signals (like leptin), maintaining a genetically influenced “set point.” Diets often fail because calorie restriction triggers metabolic slowdown and hunger surges to defend this set point. Jenkinson argues modern processed foods disrupt this system, causing upward drift in set points over generations.

How does *Why We Eat (Too Much)* explain processed foods’ impact?

Processed foods—high in refined sugars, seed oils, and artificial additives—overstimulate reward pathways while lacking nutrients. This dysregulates appetite hormones, causing overeating and metabolic dysfunction. Jenkinson compares these foods to “drug-like” substances that hijack the brain’s evolutionary drive for energy-dense foods, leading to insulin resistance and inflammation.

What are the main criticisms of *Why We Eat (Too Much*)?

Critics highlight: - Occasional oversimplification of cultural/food-access factors in obesity. - Limited actionable advice for meal planning or portion control. - A tone some describe as dismissive toward non-scientific weight-loss approaches. However, most agree the core scientific framework is robust and enlightening.

How does *Why We Eat (Too Much)* compare to Jenkinson’s follow-up *How to Eat (and Still Lose Weight*)?

While *Why We Eat* focuses on the *science* of appetite, *How to Eat* offers practical strategies: avoiding processed foods, prioritizing protein/fiber, and resetting metabolic health. The latter expands on habit formation and reward systems, providing clearer steps to lower one’s weight set point sustainably.

What is the role of hormones in *Why We Eat (Too Much*)?

Key hormones include: - **Leptin**: Signals satiety and regulates energy expenditure. - **Insulin**: Manages blood sugar and fat storage. - **Ghrelin**: Stimulates hunger. Jenkinson explains how processed foods cause leptin resistance (blunting satiety signals) and chronic insulin spikes, trapping individuals in a cycle of hunger and fat storage.

¿Por qué comemos?

La nueva ciencia del apetito

Andrew Jenkinson

4.22(3318 Reviews)

Resumen de ¿Por qué comemos?

Descubre por qué las dietas fallan y por qué la fuerza de voluntad no es suficiente en esta innovadora exploración de la ciencia del apetito. Con una calificación de 4.1/5 en Goodreads, la controvertida visión de Jenkinson desafía a la industria de las dietas al revelar cómo hormonas como la leptina —y no la falta de disciplina— controlan nuestro peso.

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Capítulo 1

The Modern Obesity Paradox: Why We're Hungrier Than Ever

Why is it that despite an abundance of diet books, fitness trackers, and nutritional information, we're heavier than ever before? Dr. Andrew Jenkinson's groundbreaking book tackles this question with remarkable clarity, challenging conventional wisdom about weight management. As a bariatric surgeon who has helped thousands of patients, Jenkinson brings a unique perspective that combines medical expertise with compassionate understanding. The book has resonated with celebrities like Adele, who reportedly incorporated its principles during her weight loss journey. Its cultural impact extends beyond celebrity endorsements-it fundamentally challenges the "calories in, calories out" model that has dominated weight loss discourse for decades. With obesity rates tripling globally since the 1980s and affecting over 650 million people worldwide, Jenkinson's revolutionary approach to understanding our bodies' weight regulation systems couldn't be more timely.

Capítulo 2

The Body's Hidden Weight Control System

Imagine your body operating with the same energy as a standard light bulb-about 100 watts. Despite this modest energy requirement, humans have developed complex systems to regulate weight with remarkable precision. During medical training, Dr. Jenkinson noticed a critical gap in education: while doctors studied every organ system in detail, they discarded fat tissue during dissections, unaware they were throwing away "an important part of the body" that controls metabolism and appetite. Fat cells are marvels of biological engineering-lightweight, insulating, and capable of storing enormous energy. Each can expand to six times its original size before the body creates more cells, potentially increasing from 40 billion to over 100 billion. This explains why liposuction proves ineffective long-term; the body simply produces more fat cells to maintain its predetermined fat storage. Our bodies follow two fundamental metabolic rules. First, the energy equation: Energy Stored = Energy In - Energy Out. Surprisingly, 70% of our energy expenditure comes from unconscious processes like breathing and heartbeat, with only 2-3% from intentional exercise for sedentary people. The second rule involves negative feedback systems-like thermostats that maintain homeostasis through sensors and switches. This explains a startling inconsistency: Americans consuming 500 extra calories daily (182,500 yearly) should theoretically gain 26kg annually according to simple calorie math. Yet they gain merely 0.5kg yearly-regulating their energy balance to within 0.4% accuracy despite massive overconsumption. This precision suggests a powerful biological mechanism preventing runaway weight gain by somehow disposing of excess energy. The Vermont Prison experiment demonstrated this phenomenon dramatically. When prisoners voluntarily overate to gain weight, their bodies fought back by increasing metabolic rates-some requiring a staggering 8,000-10,000 calories daily just to continue gaining weight. Similarly, the Minnesota Starvation Experiment showed the opposite effect: when subjects reduced calories, their metabolic rates plummeted by 50%-twice what could be explained by reduced body size alone. These experiments reveal that our bodies possess a sophisticated weight regulation system centered in the hypothalamus-a small but mighty area at the brain's base. This system uses leptin, a hormone produced by fat cells, as a "fuel gauge" signaling the brain about energy reserves. When fat increases, leptin levels rise, decreasing appetite and boosting metabolism. When fat decreases, leptin levels fall, increasing hunger and slowing metabolism. This "weight set-point" functions like a thermostat maintaining your body at a specific weight through powerful biological mechanisms. Unfortunately, this set-point isn't always calibrated to a healthy weight-explaining why traditional dieting (eating less, moving more) ultimately fails as the body fights to restore its predetermined set-point.

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Capítulo 3

Why Some People Gain Weight While Others Don't

Walking through the Dubai Mall food court reveals a striking pattern: local Emiratis appear significantly more affected by obesity than Indian, Filipino, Caucasian and African residents despite equal exposure to Western fast food. This observation highlights a fundamental truth: genetic factors dramatically influence how individuals respond to modern food environments. The analogy of three cattle pens helps explain this phenomenon. In Pen 1, grass-fed cows remain lean with natural variation in size. In Pen 2, corn-fed cows grow significantly larger due to diet-induced elevation of their weight set-points, though individual variation remains. In Pen 3, selectively bred corn-fed cows appear enormous compared to Pen 1 and noticeably larger than average Pen 2 cows. This three-group model explains human obesity patterns. Those eating natural foods maintain normal weight (like Pen 1 cows), those consuming processed foods grow larger (like Pen 2), and those genetically predisposed to weight gain who eat processed foods become the largest group (like Pen 3). Jane Wardle's landmark study of identical twins separated at birth found approximately 75% consistency in adult BMI despite lifelong separation, with only 10% attributable to home environment. This conclusively demonstrates that obesity risk is predominantly genetic, not a matter of willpower or parenting. Some populations show extraordinary vulnerability to obesity when exposed to Western foods. Pacific Islanders top obesity charts (94% overweight in Nauru) due to their unique settlement history. As one of Earth's last inhabited regions, colonizing these remote islands required perilous sea voyages spanning thousands of miles. Only those with sufficient fat reserves or efficient metabolisms survived these journeys-creating a powerful selection bias that now manifests as extreme obesity when exposed to modern processed foods. Similarly, the transatlantic slave trade created another powerful genetic selection event. With 20% mortality during the two-month middle passage, only those with metabolically efficient genes and adequate fat stores survived the starvation and diseases. This genetic legacy now manifests in disproportionate obesity rates among African Americans (48% overall, with black women at 57%) compared to white Americans (33%). Beyond genetics, epigenetics plays a crucial role. During the 1944-45 Dutch famine, pregnant women survived on just 500 calories daily. Thirty years later, researchers found their children-though born smaller than siblings-had developed significantly more obesity in adulthood. This occurred because fetal development had been epigenetically "programmed" for food scarcity, creating efficient metabolisms and robust appetites-adaptive traits for continued famine but disastrous in post-war abundance.

Capítulo 4

The Metabolic Battlefield: Why Diets Fail

Reality TV shows like The Biggest Loser promote the idea that obesity can be overcome through sheer willpower and extreme dieting, but fail to show the long-term consequences. Dr. Kevin Hall's famous study followed fourteen Biggest Loser contestants six years after the show. Despite initially losing an average of 58kg each, they regained 41kg. More alarmingly, their metabolic rates dropped by 610kcal during the competition and remained 700kcal lower six years later-confirming that the subconscious brain ultimately wins the battle against conscious weight-loss efforts. This metabolic adaptation explains why standard weight-loss approaches often fail. Among ten people of identical size, metabolic rates can vary by as much as 715kcal/day-equivalent to one person needing a 10km daily run to match the natural energy expenditure of another. This variation is governed by whether current weight is above, below, or at one's weight set-point-with metabolism speeding up when above set-point and slowing when below it. Our metabolic rates function like a dimmer switch that can be set anywhere between glowing dimly and shining brightly. This variability explains why identical calorie intake produces dramatically different weight outcomes in different individuals. The autonomic nervous system plays a key role in this metabolic adaptation. Overeating appears to activate the sympathetic nervous system (SNS), creating recognizable symptoms: elevated pulse and blood pressure, increased sweating, higher blood glucose, muscle strength, mental clarity, and improved mood from endorphin release. Conversely, dieting activates the parasympathetic nervous system (PNS), reducing energy expenditure through lower heart rate and blood pressure, causing muscle fatigue, mental fog, confusion, irritability, and depression. Our appetite and satiety are also powerfully controlled by hormones-ghrelin from the stomach drives hunger while peptide-YY from the intestines signals fullness. After dieting, these hormonal signals become disrupted. Studies show that ghrelin (hunger hormone) levels remain elevated while peptide-YY (satiety hormone) levels stay lower than pre-diet levels, even a year after dieting ends. This explains why dieters constantly feel hungry and struggle with reduced feelings of fullness. These persistent hormonal disruptions make weight maintenance nearly impossible, as the body fights to return to its original set-point. The evidence confirms that diets don't just fail-they actually become counter-productive by stimulating longer-term weight gain.

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Capítulo 5

The Leptin Resistance Crisis

Leptin normally works as the master regulator of our weight, communicating directly between fat cells and the brain through a sophisticated feedback system. Like a car's fuel gauge, leptin signals our current nutritional status-high when carrying excess fat, low when slim. When functioning properly, leptin controls both appetite and metabolic rate through multiple mechanisms, including regulation of hunger hormones, energy expenditure, and fat burning, allowing effortless weight maintenance without conscious calorie control. However, in obesity, despite having up to four times normal leptin levels, this system somehow fails to function properly-a condition called leptin resistance. In this state, the brain falsely perceives starvation, triggering increased hunger through elevated ghrelin production and reduced metabolism via decreased thermogenesis, creating a vicious cycle of weight gain. This explains why simple calorie restriction often fails - the body actively fights against weight loss when leptin resistant. Two primary factors cause leptin resistance: chronically high insulin levels and systemic inflammation. Insulin interferes with leptin signaling because both hormones use overlapping cellular pathways in the hypothalamus-when insulin is consistently elevated, leptin's message goes unread, creating a false perception of low fat stores. This is particularly problematic with modern diets high in refined carbohydrates that trigger frequent insulin spikes. Meanwhile, obesity causes fat cells to swell and become dysfunctional, triggering an inflammatory response via TNF-alpha and other inflammatory proteins. This inflammation directly affects the hypothalamus, further promoting leptin resistance and disrupting appetite regulation. This creates a devastating cycle where the body constantly signals for more food despite already having excess fat. Like a faulty fuel gauge showing empty when the tank is full, the brain perceives starvation despite abundant fat stores, driving voracious hunger despite obesity. The body actively defends its elevated weight through multiple mechanisms, including increased appetite, reduced metabolic rate, and preferential fat storage. Fortunately, animal studies demonstrate that leptin resistance is reversible through dietary and lifestyle interventions. Rats fed Western-style diets high in sugar and refined oils develop insulin resistance leading to leptin resistance and weight gain. When returned to normal whole-food diets low in refined carbohydrates, their leptin sensitivity and insulin levels normalize within weeks, and weight returns to healthy levels. Similar improvements have been observed in human studies focusing on reducing inflammation and insulin levels through diet modification, suggesting practical strategies for addressing this metabolic dysfunction. The key to reversing leptin resistance appears to be addressing both insulin levels and inflammation simultaneously through diet quality improvement, stress reduction, and adequate sleep. This helps restore proper hormone signaling and allows the body's natural weight regulation systems to function properly again.

Capítulo 6

How Our Food Environment Changed Everything

Humans are uniquely fascinated by food preparation and cooking-as evidenced by the popularity of cooking shows and culinary media. This obsession with food reveals a fundamental aspect of human evolution and explains our current obesogenic environment. The development of the human brain, which requires enormous energy, presented an evolutionary challenge within our fixed energy budget. Evolutionary scientists debated this question until Wheeler and Aiello proposed the "Expensive-Tissue Hypothesis," explaining that humans sacrificed gut size to develop larger brains. This metabolic trade-off was only possible because we learned to cook food one million years ago. Cooking essentially pre-digests food, requiring less intestinal processing power. The energy saved from having a smaller digestive system could then be redirected to fuel our growing brains, making cooking the most important factor in our evolution as humans. A study of over 500 raw foodists in Germany confirmed this dependency-despite having modern advantages like supermarket variety and blenders, 50% of women stopped menstruating due to malnutrition, demonstrating that without cooking, humans struggle nutritionally. By 150,000 BCE, humans had evolved into anatomically modern form with shorter guts and larger brains, completely dependent on cooking for survival. A Cro-Magnon man from that era would appear indistinguishable from us externally but would have pristine arteries, athletic blood pressure, and absence of modern inflammatory diseases, diabetes or obesity. Our evolutionary weakness for sweetness traces back to ancient survival mechanisms. Humans developed taste buds to distinguish safe from dangerous foods-bitter and sour signaled caution, while salty, fatty and protein flavors were acceptable. But sweetness triggered intense pleasure, hardwired directly to the brain's reward center. This sweet craving drove our ancestors to seek out rare seasonal fruits. The Industrial Revolution transformed our relationship with food, enabling transport of products across continents but requiring preservation methods that stripped away nutritious elements and replaced them with preservatives, sugar, salt and fat combinations. Food became a business rather than sustenance. In the 1950s, heart disease rates spiked in America, bringing dietary factors-particularly fat and sugar-under scrutiny. While British scientist Dr. John Yudkin identified sugar as the culprit (publishing "Pure, White and Deadly"), the sugar industry secretly funded Harvard scientists who shifted blame to fat. Ancel Keys' influential "Seven Countries Study" showed a correlation between fat consumption and heart disease, but deliberately excluded countries that contradicted his hypothesis. Following the 1977 McGovern Report that made the unproven diet-heart hypothesis official policy, the food industry flooded supermarket shelves with "low cholesterol" and "low fat" products that tasted suspiciously sweet. Sugar consumption rose from 80 pounds per person annually to 100 pounds over the next twenty-five years. Food companies replaced saturated fats with "healthy" polyunsaturated vegetable oils like canola and soya oil-which ironically required hydrogenation that created dangerous trans-fats actually increasing heart disease risk. This dramatic dietary shift in the 1980s directly correlates with the sudden explosion of obesity rates in Western populations, creating the obesogenic environment we now inhabit.

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Capítulo 7

The Omega Imbalance: A Modern Nutritional Deficiency

Could obesity be a deficiency disease like beriberi or scurvy? The dramatic dietary changes preceding the obesity epidemic included a 63% increase in total fat consumption from 1970-2005, despite declining saturated fat intake. This was primarily due to increased vegetable oils, shortenings, and margarine. Fats serve vital roles beyond energy storage: our brains are 50% cholesterol; fats form hormones that drive behavior; fat-derived messengers coordinate inflammation and tissue repair; and fats constitute every cell wall on Earth, forming the crucial barrier between our DNA and the outside world. Omega-3 and omega-6 are special polyunsaturated fatty acids that, unlike saturated and monounsaturated fats, cannot be produced by our bodies. Like vitamins, they are essential fatty acids that must come from our diet. Omega-3 has a curlier, more flexible carbon tail that moves faster than omega-6, making tissues containing it more flexible, adaptable, and quick-responding. Throughout human history, our bodies maintained an omega-3 to omega-6 ratio between 1:1 and 1:4. But Western diets, with processed foods stripped of omega-3 and loaded with omega-6, have skewed this ratio to a staggering 1:50 in some urbanized populations. The opposing functions of omega fatty acids span three critical areas: defense (inflammation), cell wall permeability (insulin sensitivity), and messaging (mood and appetite). Omega-6 increases inflammatory response and blood clotting, while omega-3 reduces inflammation and decreases blood coagulability. An excess of omega-6 creates hypersensitive immune systems, potentially leading to autoimmune diseases, increased cancer risk, and heart disease. Critically, this low-grade inflammation increases TNF-alpha, which blocks leptin action, causing leptin resistance and promoting obesity. High omega-6 proportions create stiffer, less permeable cell walls with decreased metabolic adaptability and reduced hormone sensitivity. This crucially decreases insulin sensitivity in muscles and leptin sensitivity in the brain, raising insulin levels and creating leptin resistance-both factors that elevate the weight set-point and increase obesity risk. Omega-6 fatty acids also act as precursors to endocannabinoids that stimulate the same brain receptors triggered by cannabis. This stimulation creates elevated mood and potential euphoria, followed by sudden appetite increases, food-seeking behavior, enhanced pleasure from eating, and intensified sweet taste perception. High dietary omega-6 levels prevent the body from converting plant-based omega-3 into its more active form found in fish and animals. This means that even eating plenty of green vegetables won't help if your diet is already omega-6 heavy. Our weight set-point responds to environmental signals, with omega fatty acids acting as messengers about our future environment. In nature, omega-3 predominates in spring shoots while omega-6 increases in autumn seeds and nuts. These seasonal changes trigger behavioral adaptations in animals preparing for winter. As food energy decreases and heat requirements increase, animals increase their weight set-point, developing voracious appetites to store fat for hibernation. Our modern obesity epidemic represents this same protective response, but to an extreme, unnatural, and permanent shift in our food environment.

Capítulo 8

The Blueprint for Sustainable Weight Loss

The secret to sustainable weight loss lies in understanding how our bodies regulate our weight set-point. Various environmental, historical and genetic factors determine whether our individual set-point is set as slim, obese, or somewhere between. By changing environmental signals rather than restricting calories, we can naturally decrease appetite and increase metabolism, driving weight downward through hormonal and metabolic adjustments. Step 1 focuses on decreasing daily insulin levels while eating well. Since insulin drives weight set-point up or down, and is controlled by food choices, the plan eliminates the biggest insulin-spiking culprits-sugar, wheat and corn-replacing them with natural, nutritious foods. This approach provides essential vitamins for optimal metabolism while calming cortisol levels, without shocking the body through calorie restriction. Step 2 focuses on improving sleep quality by changing evening habits and creating better sleep conditions. Sleep deprivation increases ghrelin (the appetite hormone), causing people to consume about 300 more calories daily and raising blood sugar levels toward pre-diabetes. Achieving eight hours of sleep will naturally lower your set-point and help you lose weight. Step 3 focuses on rebalancing the body's omega-3 to omega-6 ratio by replacing vegetable oils with butter and olive oil for cooking and baking, avoiding foods cooked using vegetable oils (including fast foods, fried snacks, health bars, ready-made cooking sauces, and margarines), avoiding foods containing very high omega-6 content (certain meats, nuts and seeds), choosing meats and fish with higher omega-3 levels, and eating as many fresh vegetables and dairy products as desired. Step 4 involves regular exercise-not for calorie burning but for lowering your weight set-point through decreasing cortisol (stress hormone) and improving insulin sensitivity. Choose an enjoyable, practical activity you'll look forward to, exercise 2-3 times weekly for at least 20 minutes (enough to sweat), and focus on maintaining muscle mass, which is crucial for thermogenesis (burning excess calories as heat). Step 5 involves further reducing carbohydrate intake to lower insulin requirements. The glycaemic load (GL) measures the total glucose effect from a food portion. Start by targeting 150g of carbohydrates per day, gradually reducing to 100g over weeks, potentially reaching 80g depending on your body's response. Unlike quick-fix diets, this approach builds momentum gradually while improving overall health and happiness alongside weight loss. The changes this program creates can take weeks or months to fully manifest, but persistence will eventually ingrain them into your body. Your weight set-point will permanently lower, enabling easy, seamless weight regulation and long-term metabolic health improvement.

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Capítulo 9

Beyond Calories: A New Understanding of Weight

Our weight regulation involves sophisticated metabolic processes controlled by our subconscious brain, not our conscious mind. This complex system includes hormones like leptin and ghrelin, neural pathways in the hypothalamus, and intricate feedback mechanisms that maintain energy homeostasis. While we can temporarily override our subconscious through dieting, powerful negative feedback processes eventually return weight to our personal set-point, often with additional pounds as a protective mechanism. The traditional explanation for obesity's rise since the 1980s blames increased consumption combined with reduced physical activity-essentially, we've become too greedy and lazy. But this simplistic view ignores the powerful biological systems that regulate our weight with remarkable precision. Research shows that identical twins raised apart maintain nearly identical weights, while adopted children's weights correlate with their biological, not adoptive, parents. These findings strongly suggest genetic and biological factors play a more significant role than willpower or conscious choice. France has largely avoided both the heart disease epidemic and obesity crisis despite consuming more saturated fat and wine than neighboring countries-a phenomenon nutritionists call "the French Paradox" because it contradicts conventional wisdom. The French maintain lower weight set-points through their proud food culture: they eat fresh, unprocessed ingredients; cook traditional meals with natural fats; avoid snacking; and maintain better work-life balance. Their meals are social events, eaten slowly and mindfully, typically lasting 2-3 times longer than American meals. They also have stricter food quality regulations and smaller portion sizes. Many patients describe specific life events that triggered their weight gain after previously effortless weight regulation-leaving home, attending college, marriage, night shifts, new jobs, or relocating to different countries. These transitions often disrupt established eating patterns, sleep cycles, and stress levels, leading to hormonal changes that can permanently alter the body's weight set-point. When they attempt to address the weight gain through dieting, their set-point rises further, eventually leading to uncontrollable obesity. This pattern is particularly common among shift workers, whose disrupted circadian rhythms affect metabolic regulation. The key insight from Dr. Jenkinson's work is that sustained weight loss can only be achieved through lifelong eating and lifestyle adjustments that lower your weight set-point. This requires addressing multiple factors: meal timing, food quality, stress management, sleep patterns, and environmental influences. By understanding and working with your body's natural weight regulation systems rather than fighting against them, you can achieve lasting health improvements without the misery of constant hunger and metabolic adaptation that doom traditional diets to failure. Success stories often involve patients who made gradual, sustainable changes to their lifestyle rather than pursuing aggressive short-term weight loss goals.

★★★★★

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Temas clave en ¿Por qué comemos?

weight set-point
metabolic homeostasis
leptin resistance
biological weight regulation
evolutionary obesity genetics

Citas de ¿Por qué comemos?

Fat cells are marvels of biological engineering.
Obesity risk is predominantly genetic, not a matter of willpower.

Personajes en ¿Por qué comemos?

Andrew JenkinsonAuthor and bariatric surgeon
Jane WardleResearcher who studied BMI in identical twins

Sobre el Autor

Andrew Jenkinson, autor de los éxitos de ventas Why We Eat (Too Much): The New Science of Appetite, es un destacado cirujano bariátrico y una autoridad internacional en la regulación del peso y la salud metabólica. Cirujano consultor gastrointestinal superior en el University College London Hospital, Jenkinson combina más de dos décadas de práctica clínica con investigaciones innovadoras sobre los mecanismos del apetito y la obesidad. Su trabajo sobre la teoría del "punto de ajuste de peso" (weight set-point), arraigado tanto en el rigor científico como en la atención centrada en el paciente, constituye el núcleo de esta popular exploración científica de la cultura dietética moderna y los impulsores biológicos del comer en exceso.

Jenkinson amplía aún más su enfoque transformador en How to Eat (and Still Lose Weight), que examina la adicción a la comida, la formación de hábitos y el control de peso sostenible. Su investigación, respaldada por el NHS, ha producido más de 100 publicaciones revisadas por pares sobre la motilidad gastrointestinal y la innovación quirúrgica.

Why We Eat (Too Much) dominó las listas de los más vendidos, alcanzando el puesto número 2 en las listas de no ficción de Amazon y permaneciendo en el top 20 durante 18 meses. Elogiado por traducir la bioquímica compleja en conocimientos accesibles, el libro se ha convertido en un recurso fundamental en la ciencia de la nutrición y el discurso de la salud pública.

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Creado por exalumnos de la Universidad de Columbia en San Francisco

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1,000,000+ curious minds.

4.7

avg rating

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

"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."

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

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"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

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Capítulo 6

¿Por qué comemos?

ResumenResumen de ¿Por qué comemos?

Un libro. Muchas formas de escucharlo.

The Modern Obesity Paradox: Why We're Hungrier Than Ever

The Body's Hidden Weight Control System

Ve cada palabra mientras la escuchas

Why Some People Gain Weight While Others Don't

The Metabolic Battlefield: Why Diets Fail

Saca más partido a ¿Por qué comemos?

The Leptin Resistance Crisis

How Our Food Environment Changed Everything

Ve cada palabra mientras la escuchas

The Omega Imbalance: A Modern Nutritional Deficiency

The Blueprint for Sustainable Weight Loss

Saca más partido a ¿Por qué comemos?

Beyond Calories: A New Understanding of Weight

Has llegado al final de ¿Por qué comemos?

Temas clave en ¿Por qué comemos?

Citas de ¿Por qué comemos?

Personajes en ¿Por qué comemos?

Sobre el Autor

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What is Why We Eat (Too Much) by Andrew Jenkinson about?

Who should read Why We Eat (Too Much)?

Is Why We Eat (Too Much) worth reading?

What is the weight set-point theory in Why We Eat (Too Much)?

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1,000,000+ curious minds.

1,000,000+ curious minds.

Un libro. Muchas formas de escucharlo.

The Modern Obesity Paradox: Why We're Hungrier Than Ever

The Body's Hidden Weight Control System

Ve cada palabra mientras la escuchas

Why Some People Gain Weight While Others Don't

The Metabolic Battlefield: Why Diets Fail

Saca más partido a ¿Por qué comemos?

The Leptin Resistance Crisis

How Our Food Environment Changed Everything

Ve cada palabra mientras la escuchas

The Omega Imbalance: A Modern Nutritional Deficiency

The Blueprint for Sustainable Weight Loss

Saca más partido a ¿Por qué comemos?

Beyond Calories: A New Understanding of Weight

Has llegado al final de ¿Por qué comemos?

A los usuarios también les gustó

Descubre más

Resumen de ¿Por qué comemos?