The Obesity Code

Introduction

Overview

The introduction presents Dr. Jason Fung's primary motivation for writing the book: a fundamental dissatisfaction with the medical establishment's failed approach to treating obesity and type 2 diabetes. He argues that the prevailing calorie-centric model is not only ineffective but has directly contributed to a worsening global epidemic. The chapter establishes his credibility by outlining his clinical experience as a nephrologist, where he repeatedly witnessed the limitations of treating symptoms rather than root causes, and sets the stage for the hormonal theory of obesity that the book will explore.

The Failure of Conventional Wisdom

Dr. Fung opens with a stark critique of mainstream obesity treatment, comparing the decades-long prescription of low-fat, calorie-reduced diets to historical medical missteps like bloodletting with leeches. Despite universal adoption, this approach has coincided with skyrocketing obesity rates, proving it to be "completely and utterly ineffective." He notes the professional dissonance he faced when prescribing insulin for diabetes—a treatment known to cause weight gain—while simultaneously advising patients to lose weight, highlighting a critical flaw in the conventional understanding.

A Physician's Awakening

The narrative shifts to Dr. Fung's personal journey. As a kidney specialist, he observed that type 2 diabetes was the most common cause of kidney failure, yet treatment focused on end-stage symptoms rather than prevention. This led to an uncomfortable realization that medicine was ignoring the root cause—obesity itself. He admits that, like most doctors, his nutritional knowledge was minimal, and the field was ceded to commercial diet programs. The medical profession's focus on prescribing pills for the consequences of obesity (diabetes, hypertension) while ignoring the central problem struck him as illogical, especially when he saw that significant weight loss could reverse type 2 diabetes.

Navigating a Sea of Contradictions

Determined to understand obesity's true cause, Dr. Fung found the existing nutritional landscape hopelessly contradictory. He lists the common, conflicting advice on fat, carbs, meal frequency, and calories, noting that most arguments are based on authority (e.g., "Dr. X says...") rather than solid evidence. He identifies two core problems in obesity research: the lack of a coherent theoretical framework (often reducing a complex disease to a single factor like "excess calories") and a reliance on short-term studies that cannot capture a condition developing over decades.

Principles for a New Understanding

The author then outlines the evidence-based principles that will guide the book's exploration. He commits to relying on human studies only, famously illustrated by the "Parable of the Cow," which warns against applying animal research directly to humans. He prioritizes high-quality, peer-reviewed human studies and seeks causal factors over mere associations, acknowledging the limitations of nutritional science while striving for a more robust analytical framework.

A Roadmap to The Obesity Code

Finally, the introduction provides a clear guide to the book’s structure, mapping the journey ahead. It will:

1. Examine the timeline and familial patterns of the epidemic.
2. Deconstruct the prevailing but flawed calorie deception.
3. Introduce a new hormonal model of obesity, with insulin as the key regulator.
4. Use this model to explain obesity as a social phenomenon linked to poverty and childhood.
5. Analyze what’s specifically wrong with the modern diet, including fructose and artificial sweeteners.
6. Conclude with practical solutions focused on lowering insulin through dietary changes and intermittent fasting.

Key Takeaways

• The standard "eat less, move more" calorie model for treating obesity has failed completely, despite being the medical orthodoxy for over 50 years.
• Medicine often treats the diseases caused by obesity (like type 2 diabetes) while neglecting the root cause itself, creating a therapeutic contradiction.
• Understanding obesity requires moving beyond simplistic, single-cause theories and short-term studies to develop a multifactorial framework based on long-term human evidence.
• Dr. Fung proposes that obesity is primarily a hormonal disorder, with the hormone insulin playing the central role in driving fat storage and weight gain.
• The book promises to deconstruct old myths and provide a new, actionable model focused on the hormonal causes of weight gain rather than calorie counting.

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The Obesity Code

Chapter 1: How Obesity Became an Epidemic

Overview

The chapter begins with a powerful critique of modern medicine's approach to type 2 diabetes, arguing it treats the symptom—high blood sugar—while worsening the root disease. The real issue is insulin resistance driven by chronically high levels of insulin itself, making the standard treatment of prescribing more insulin fundamentally illogical. The biological solution lies in reducing dietary carbohydrates, the primary driver of insulin. This revelation leads directly to a historical mystery: if this understanding was once clear, how did we lose our way?

For over a century, common sense held that refined carbohydrates like sugar and starch were the primary drivers of weight gain. This changed in the mid-20th century when dietary fat was mistakenly cast as the villain behind heart disease. Official policy, exemplified by the 1977 U.S. Dietary Goals, mandated a shift to low-fat diets, which necessitated replacing fat calories with carbohydrates. To resolve the cognitive dissonance between carbs being both "fattening" and now "healthy," the foundational model of obesity was rewritten. The old "fattening carbohydrates" model was replaced by the Calories-In/Calories-Out model, reducing a complex biological process to a simple equation of personal responsibility.

This shift represents a critical philosophical error: confusing the proximate cause (calorie surplus) with the ultimate cause (why the surplus occurs). By framing obesity as a failure of willpower, medicine ignored the hormonal drivers of fat storage, particularly insulin. The "Eat Less, Move More" mantra became entrenched policy, leading to a massive, unintended public health experiment. As the population consciously ate less fat, food manufacturers flooded the market with low-fat, high-sugar products. The result was not better health, but the precise ignition of the twin epidemics of obesity and diabetes. The timeline is damning; the steep, sustained rise in obesity began almost exactly in 1977, charting a parallel course with the adoption of low-fat, high-carbohydrate eating. This stark correlation challenges us to reconsider everything we thought we knew about why we get fat.

The Flawed Logic of Diabetes Treatment

The chapter opens by challenging the conventional understanding of type 2 diabetes. It presents Dr. Fung's core argument that the standard medical approach is fundamentally backward. Type 2 diabetes is not primarily a disease of high blood sugar; it is a disease of insulin resistance and excessive insulin. Therefore, treating it by injecting more insulin—the very hormone that is already too high—is illogical and counterproductive, akin to treating alcoholism with more alcohol.

Modern medicine, he argues, mistakenly focuses on lowering the symptom (high blood glucose) instead of addressing the root cause (insulin resistance). The biological solution to insulin resistance is to reduce the dietary driver of insulin: carbohydrates. This revelation suggests the disease could be reversible, a possibility negated by current treatment protocols that allow continued high carbohydrate intake.

Dr. Fung's journey to this conclusion began with his discovery of research on low-carbohydrate, high-fat diets. Contrary to his medical training, which warned that such diets were dangerous, the evidence showed they produced superior metabolic outcomes, especially for those with insulin resistance and obesity.

A Historical Shift in Dietary Dogma

To understand how we arrived at the current ineffective strategy for obesity, the narrative looks back. For most of history, obesity was rare, and the link between refined carbohydrates (sugars and starches) and weight gain was widely recognized. Figures like Jean Anthelme Brillat-Savarin in the 1820s and William Banting in the 1860s identified starchy and sugary foods as the primary drivers of corpulence. This "fattening carbohydrates" model was common sense for over a century.

The shift began in the mid-20th century amidst fears of a heart disease "epidemic"—largely a perception fueled by people living longer and dying less from infectious diseases. Dietary fat, and its supposed link to cholesterol, was cast as the new villain. This created a nutritional dilemma: if you cut fat from the diet, you must replace those calories with something else, which inevitably meant more carbohydrates, typically refined ones.

A cognitive dissonance emerged: how could carbohydrates be both "fattening" (the old model) and "healthy" (as low-fat alternatives)? The solution, enforced not by robust science but by governmental decree like the 1977 U.S. Senate Dietary Goals, was to simply redefine the rules. Calories, not specific foods, were declared fattening. The "Calories-In/Calories-Out" model officially displaced the "fattening carbohydrates" model.

The Calorie-Counting Fallacy and the Real Cause

This leads to the core philosophical error in our understanding of obesity: confusing the proximate cause with the ultimate cause. The proximate cause of weight gain is indeed an excess of calories consumed over calories expended. But this is as useful as saying the cause of a sinking ship is "gravity exceeding buoyancy" or the cause of alcoholism is "drinking too much." It describes the mechanism, not the origin.

By focusing solely on the calorie balance, we implicitly assign the ultimate cause of obesity to personal failure—gluttony and sloth. This transforms a complex biological disease into a moral failing. Yet this explanation crumbles under scrutiny. It cannot explain why women naturally carry more fat than men after puberty, or why pregnancy causes weight gain. Hormones, not just personal choice, are clearly powerful ultimate causes.

Despite this flawed logic, the "Eat Less, Move More" mantra became entrenched as official policy from all major health institutions. The result of this grand dietary experiment was a nation consciously eating less fat and red meat, but more carbohydrates and sugar. Food manufacturers happily complied, creating low-fat, sugar-loaded products. The outcome was not improved health, but the dawn of the obesity and diabetes epidemics. The chapter sets the stage by revealing that our foundational understanding of why we get fat is wrong, and that the official dietary advice of the last 40 years is likely the engine of the crisis.

The American Heart Association's dismissal of low-carbohydrate diets as dangerous fads persisted until at least the year 2000, a stance that overlooked their documented use since 1863. This policy did not yield the expected decline in heart disease, but it inadvertently coincided with another dramatic shift in public health. Rates of obesity, defined by a BMI greater than 30, began a steep and sustained increase starting almost exactly in 1977.

This timing is visually stark in Figure 1.2, which charts the rapid ascent in the percentage of obese U.S. adults from that point forward. The curve upward aligns precisely with the national pivot toward officially recommended low-fat, high-carbohydrate dietary patterns. The correlation is so pronounced it begs a deeper inquiry: was this parallel occurrence simply accidental, or did the nutritional guidance itself plant the seeds of the epidemic? The text leaves us weighing this against the alternative explanation of genetic factors, setting the stage for a critical examination of cause and effect in the chapters to follow.

Key Takeaways

• The abrupt rise in obesity beginning in 1977 directly coincided with the official promotion of low-fat, high-carbohydrate diets.
• The longstanding institutional resistance to low-carbohydrate diets, despite their historical use, may have had significant unintended consequences for population health.
• The lack of improvement in heart disease rates alongside exploding obesity figures suggests a fundamental flaw in the nutritional axioms of the late 20th century.

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The Obesity Code

Chapter 2: Inheriting Obesity

Overview

The chapter confronts the undeniable fact that obesity runs in families, launching an investigation into whether this is due to shared genetics or a shared environment. It systematically dismantles the simplistic "calories in, calories out" environmental argument by examining powerful evidence from adoption and twin studies. These studies reveal that genetics, not the household environment, is the dominant factor in determining an individual's susceptibility to obesity. The chapter then critiques the once-popular "thrifty-gene" hypothesis, ultimately setting the stage for a new hormonal model of obesity that can reconcile strong genetic inheritance with a rapid population-wide epidemic.

The Shocking Power of Inheritance

Research on adoptive families provides a clear natural experiment. When scientists compared adult adoptees to both their biological and adoptive parents, they found no correlation between the adoptee's weight and that of their adoptive parents. The home environment—diet, lifestyle, attitudes—provided by the adoptive family showed no significant influence. In stark contrast, a strong correlation existed between the adoptees and their biological parents, whom they had never lived with. This suggests the tendency toward obesity is carried in our biology, not learned at the dinner table.

This genetic influence is quantified even more precisely by studies of twins. Research comparing identical twins (who share 100% of their genes) and fraternal twins (who share about 50%) raised together and apart led to a stunning conclusion: approximately 70 percent of an individual's susceptibility to obesity is determined by genetic factors. This inheritance is not about a single "fat gene," but a complex predisposition.

The Flawed "Thrifty-Gene" Explanation

Faced with the evidence for genetic inheritance, the chapter examines and rejects the thrifty-gene hypothesis, which proposed that humans evolved to store fat efficiently to survive famines. This idea fails on several fronts. First, in nature, excessive fat is a liability, making animals slower and more vulnerable. Second, humans have strong hormonal signals to stop eating (satiety), contradicting the idea of a genetic drive to endlessly overeat. Third, many traditional societies with abundant food did not experience obesity until their diets modernized. Finally, in animal populations, abundance leads to more offspring, not more obese individuals. The thrifty-gene hypothesis cannot explain why obesity, a state of detrimental fatness, has become a modern epidemic.

Bridging Genetics and the Epidemic

The chapter acknowledges the apparent contradiction: if 70% of obesity risk is genetic, how could obesity rates have skyrocketed in a single generation where our genes haven't changed? The answer previewed here is that genes set the susceptibility, but the modern environment provides the trigger. The explanation lies not in a simple caloric calculus, but in a hormonal imbalance, with elevated insulin playing a central role. This hormonal model can explain the genetic data, as a baby's hormonal environment in the womb can be influenced by the mother's condition, creating an inherited tendency for high insulin and weight gain. While 70% of the risk is not under our direct control, the chapter concludes by pointing toward the 30% we can influence, questioning whether conventional diet and exercise advice is the right tool for the job.

Key Takeaways

• Obesity is strongly inherited: Adoption and twin studies demonstrate that approximately 70% of an individual's risk for obesity is linked to genetic factors, far outweighing the influence of the shared family environment.
• The environment triggers, but genetics loads the gun: The rapid rise in obesity since the 1970s cannot be due to genetic change, indicating that modern environmental factors are activating a widespread genetic susceptibility.
• The "thrifty-gene" hypothesis is inadequate: The evolutionary idea that humans are genetically programmed to overeat and store fat fails to align with observed biology, animal behavior, or historical human patterns.
• A new model is needed: The chapter argues that the root cause must be a hormonal imbalance (highlighting insulin) that effectively explains both the strong genetic predisposition and the modern epidemic, moving beyond the simplistic focus on voluntary calorie intake and exercise.

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Chapter 4: The Exercise Myth

Overview

Let's get one thing straight: the most common advice for weight loss is built on a broken model. The entire idea of "calories in, calories out" rests on a series of false assumptions. It mistakenly treats our calorie intake and expenditure as independent variables, when in reality they’re deeply connected. It wrongly assumes our metabolism is stable, ignores the powerful hormonal control we have over hunger and fat storage, and commits the critical error of believing all calories are created equal. A calorie of sugar and a calorie of broccoli do wildly different things inside your body.

When you try to outsmart this system by simply eating less, your body fights back with a sophisticated survival strategy. Historic experiments, like the Minnesota Starvation Experiment, proved that slashing calories doesn’t lead to efficient fat loss. Instead, it triggers a drastic slowdown in metabolism and an overwhelming surge in hunger—a hormonal storm designed to make you regain the weight. This explains the inevitable plateau and rebound that frustrate every dieter, proving the failure is biological, not a lack of willpower.

This biological reality was confirmed on a massive scale. Definitive studies like the Women’s Health Initiative showed that even when people successfully ate less and moved more for years, they didn’t achieve lasting weight loss. The body’s compensatory mechanisms—slowing metabolism and ramping up hunger—create a vicious cycle that ends in fatigue, food obsession, and ultimate regain.

So what about the “move more” part of the equation? While critical for health, exercise is a surprisingly poor tool for fat loss. Data shows no correlation between a nation’s exercise levels and its obesity rates. This is because the body compensates for workouts in two key ways: by making you hungrier and encouraging you to eat more, and by reducing energy expenditure elsewhere, like through less fidgeting or a lower resting metabolic rate. The vast majority of the calories we burn each day are for basic bodily functions, not exercise. In the battle of the bulge, diet is Batman, and exercise is Robin.

Society has largely missed this point, directing enormous resources toward fighting obesity with gym memberships and school sports programs while underplaying the role of diet. It’s like studying hard for the wrong subject on a final exam. The path to lasting change, as illustrated by personal journeys from doctors and researchers, requires a fundamental shift in focus: away from counting calories and toward understanding how the hormonal regulation of fat storage actually works, starting with the food we choose to eat every day.

The Flawed Foundation of "Calories In, Calories Out"

The chapter begins by dismantling the foundational equation of traditional weight-loss thinking: Calories In – Calories Out = Body Fat. This model, while simple and intuitive, is built upon a series of critical false assumptions.

Assumption 1: Caloric Intake and Expenditure Are Independent This is a crucial error. In reality, these are deeply dependent variables. Reducing "Calories In" does not lead to a stable "Calories Out." Instead, the body responds by lowering its total energy expenditure. A 30% reduction in caloric intake can lead to a nearly 30% reduction in calories burned, resulting in minimal weight loss.

Assumption 2: Basal Metabolic Rate is Stable We tend to fixate on measuring caloric intake while assuming energy output (except for exercise) is constant. This is completely false. Total energy expenditure—comprising basal metabolic rate, the thermic effect of food, non-exercise activity, and more—is dynamic and can fluctuate by up to 50% based on caloric intake and other factors.

Assumption 3: We Exert Conscious Control Over "Calories In" While eating is a deliberate act, the decision to start and stop is powerfully driven by hormones, not just willpower. Hunger and satiety are hormonally mediated signals. The body's fat-regulation system operates under automatic, homeostatic control, much like breathing or heartbeat, making obesity a hormonal disorder, not simply a behavioral one.

Assumption 4: Fat Storage is Unregulated Every system in the body is hormonally regulated, and fat storage is no exception. The idea that excess calories are passively "dumped" into fat cells like objects in a sack is incorrect. Hormones like leptin, adiponectin, and others actively regulate fat growth, again pointing to a hormonal root for obesity.

Assumption 5: A Calorie is a Calorie This is the most dangerous assumption. While a calorie is a unit of energy, different calorie sources provoke vastly different metabolic and hormonal responses. A calorie of sugar triggers a sharp insulin spike, while a calorie of olive oil does not. Therefore, not all calories are equally likely to cause fat gain; the type of calorie matters profoundly.

The Body's Smart Response to Caloric Restriction

The chapter then explores what happens when the "eat less" doctrine is put into practice, drawing from historic experiments. The body does not passively surrender fat stores when calories are reduced. Instead, it implements a coordinated survival response.

• The Minnesota Starvation Experiment: This landmark study placed volunteers on a semi-starvation diet. Their bodies responded not with efficient fat loss, but with an across-the-board 40% reduction in resting metabolic rate. Participants suffered constant cold, slowed heart rates, low blood pressure, physical weakness, hair loss, and intense psychological obsession with food.
• The Mechanism: The body smartly balances its energy budget. When "Calories In" drop, it immediately reduces "Calories Out" by dialing down all non-essential functions—heat production, heart function, brain cognition, physical activity—to match the new, lower intake. This prevents rapid depletion of reserves and ensures survival.
• The Long-Term Adaptation: This metabolic slowdown is not temporary. Studies show that reduced energy expenditure persists indefinitely, for at least a year and likely longer. This explains the classic dieting plateau and the rapid weight regain that occurs when normal eating resumes, as the body is now burning far fewer calories at its new weight.

The failing, therefore, is not a lack of willpower but a flawed model. The portion-control, caloric-reduction diet is biologically destined to make you tired, hungry, and ultimately heavier, as the body fights to preserve its energy balance through hormonal regulation.

The Colossal Failure of "Eat Less, Move More"

The narrative turns to the early 2000s, where the definitive test of the "Eat Less, Move More" doctrine was conducted: the Women’s Health Initiative Dietary Modification Trial. This massive, 7.5-year study placed post-menopausal women on a precisely monitored low-fat, high-carbohydrate diet and encouraged increased exercise. The intervention group successfully reduced their daily calories by over 300 and increased physical activity. Yet, the results were a damning indictment of the theory. After an initial modest weight loss, the weight was steadily regained. By the study's end, there was no meaningful difference in weight between the dieting group and the control group, and body-fat measurements indicated the dieters had actually become fatter. This wasn't an anomaly but a confirmation of a consistent, decades-long failure of calorie-restriction diets.

The Hormonal Storm of Weight Loss

When calorie intake is reduced, the body fights back with powerful hormonal adaptations designed for survival. Two key changes occur:

1. Metabolism Slows: Total energy expenditure drops dramatically to conserve energy.
2. Hunger Skyrockets: Levels of the hunger hormone ghrelin increase, while satiety hormones (like peptide YY and cholecystokinin) decrease. This creates a persistent state of increased hunger and decreased fullness.

This hormonal shift is not a lack of willpower but a normal, biologically programmed response. Brain imaging shows that after weight loss, the brain's reward centers become more activated by food, while areas responsible for restraint become less active. The body is evolutionarily compelled to regain lost weight, making sustained calorie restriction a battle against our own physiology.

The Vicious Cycle and the Cruel Hoax

This leads to a predictable and discouraging cycle: a person eats less and loses some weight. In response, their metabolism slows and hunger intensifies. Weight regain begins, prompting them to eat even less, which only perpetuates the cycle of slowing metabolism and rising hunger. Eventually, the effort becomes intolerable—characterized by constant cold, fatigue, and food obsession—and the person resumes their previous eating habits. With a now-slowed metabolism, they often regain all the weight plus more.

The chapter argues that promoting this failed strategy is a "cruel hoax." When it inevitably fails, the blame is placed on the individual's character—being labeled a glutton or sloth—rather than on the flawed paradigm itself. Even pharmaceutical attempts to enforce caloric reduction, like the fat-blocker orlistat (Alli), resulted in minimal weight loss and significant, unpleasant side effects, further underscoring the strategy's futility.

Re-examining the Role of Exercise

The discussion then pivots to the second half of the "Move More" equation. While exercise is undeniably beneficial for overall health, its role in weight loss has been vastly overstated. Data reveals a stark reality: as exercise rates increased in populations like the U.S. and U.K., obesity rates continued to climb in parallel. International comparisons show no correlation between a nation's exercise frequency and its obesity levels.

Research challenges the assumption that modern sedentary lifestyles are the cause of obesity. Studies of hunter-gatherer societies like the Hadza, who are extremely active, show they burn the same number of daily calories as sedentary Western office workers. Furthermore, analysis indicates physical activity has not decreased since the 1980s, while obesity has soared. This strongly suggests that a lack of exercise did not cause the obesity epidemic.

Why Exercise Fails for Weight Loss

The ineffectiveness of exercise for significant weight loss stems from two compensation mechanisms:

1. Increased Caloric Intake: People tend to eat more after exercise, often unconsciously, negating the calories burned.
2. Metabolic Adaptation: The body can compensate by reducing energy expenditure elsewhere, such as lowering basal metabolic rate (the calories burned at rest for basic bodily functions) or reducing non-exercise activity (e.g., fidgeting).

Basal metabolic rate constitutes the vast majority (roughly 95%) of our total daily energy expenditure. Exercise, while important, is a minor component. Long-term studies consistently show that exercise produces only a fraction of the expected weight loss, and often none at all, especially in women. The chapter concludes that in the battle against obesity, diet is "Batman" and exercise is "Robin." Exercise is critical for health but is a poor tool for fat loss. The focus, it argues, must shift entirely to what we eat.

Compensation and Societal Misdirection

The text introduces two key biological mechanisms that explain why increased exercise fails to produce expected weight loss. First, it triggers a proportional increase in caloric intake—a homeostatic response where the body strives to maintain energy balance. The cited study of children found that for every extra hour of exercise, they consumed an extra 292 calories. This illustrates the fundamental principle: increasing Calories Out drives an increase in Calories In.

Second, compensation occurs through a reduction in non-exercise activity thermogenesis (NEAT). When structured exercise increases, spontaneous daily movement tends to decrease. This is demonstrated by the behavior of the physically active Hadza, who rest when possible, and by the study of schoolchildren where those with mandated phys ed became less active at home, resulting in no net gain in total weekly activity compared to their less-structured peers.

The chapter then argues that the benefits of exercise have a natural upper limit and can even become detrimental in excess, as it is a stressor on the body. The core conclusion is stated plainly: Exercise is simply not all that effective in the treatment of obesity.

This leads to a critique of societal strategy. Enormous resources—from school programs to public health initiatives—are devoted to promoting exercise based on the flawed idea that it is a primary weapon against obesity. The chapter uses the powerful analogy of a final exam: if obesity is caused 95% by diet and 5% by exercise, but we devote 50% of our effort to studying exercise, our failing grade is inevitable. The call is to redirect focus and resources toward the actual cause: diet.

The Postscript provides a tangible resolution to the chapter's argument. Dr. Peter Attia's personal journey mirrors the scientific conclusion. Only by ignoring conventional advice and focusing his investigation squarely on dietary overhaul was he able to achieve lasting fat loss, an experience that redirected his entire career toward obesity research.

Key Takeaways

• The body compensates for increased exercise by boosting calorie intake and reducing non-exercise movement, nullifying the expected energy deficit.
• Exercise has diminishing returns and is a relatively ineffective primary tool for weight loss compared to dietary modification.
• Society's overwhelming focus on exercise to combat obesity misallocates resources and attention away from the primary driver of the disease: diet.
• Lasting success requires a fundamental shift in focus from "Calories Out" to the quality and nature of "Calories In."

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