Why We Eat (Too Much)

Why do some people regain weight so easily while others maintain a steady physique for decades? In Why We Eat (Too Much), bariatric surgeon Andrew Jenkinson argues that the answer lies in a newly framed science he calls metabology—the study of how appetite, metabolism and environment interact to defend a biologically programmed weight set-point. This is not a moral or willpower problem; it’s an evolved survival system governed by your brain’s regulation of energy intake, hormone signaling and fat storage.

The Two Biological Rules

Jenkinson begins with two core rules. The first is the familiar energy balance equation: energy stored equals energy in minus energy out. But most of what you expend—roughly 70%—is your basal metabolic rate (BMR), not voluntary exercise. The second rule, less intuitively, is the principle of negative feedback regulation. Your brain continually adjusts hunger and metabolic rate to maintain stability—like a thermostat maintaining room temperature. If weight drops below the set-point, appetite hormones surge and energy burn decreases; if it rises, the opposite occurs.

Controlled studies prove this. In the Vermont Prison overfeeding study, men forced to eat massive surpluses struggled to gain much because metabolism rose to meet intake. Conversely, in the Minnesota Starvation Experiment, BMR crashed and hunger spiked, leading participants to quickly regain and even overshoot their original weight. This explains why dieting alone so often fails: it triggers physiology to fight back.

The Brain and Hormonal Control

Your hypothalamus is the central command center. It constantly monitors chemical messages from fat (leptin), the stomach (ghrelin), and the intestine (PYY and GLP‑1). These hormones determine hunger, satiety and metabolism on different time scales. Ghrelin rises before meals to encourage eating and surges when you diet. PYY and GLP‑1 signal fullness, but dieting depresses them. This biochemical conversation between gut and brain—what scientists call the gut–brain axis—explains why hunger after restraint feels overwhelming.

Leptin Resistance and the Vicious Cycle

Leptin normally tells the brain you have stored energy. Yet in obesity, despite high leptin levels, the brain behaves as if you are starving—a dysfunction termed leptin resistance. Jenkinson attributes this resistance to chronic inflammation and high insulin from modern diets rich in sugar and seed oils. These factors interfere with the hypothalamus’s interpretation of leptin, raising the weight set-point even higher. The result is a physiological “vicious cycle”: inflammation → leptin resistance → hunger → weight gain → more inflammation.

Genes, Epigenetics and Environment

Not everyone’s set-point reacts equally because genetics and epigenetics shape how sensitive this system is. Studies by Jane Wardle show BMI heritability at 70–75%, but early-life conditions also program vulnerability. During the Dutch Hunger Winter, children born to underfed mothers developed higher obesity and diabetes risk as adults—proof that famine cues can set a higher defensive weight later in life. Similarly, maternal obesity or gestational diabetes primes offspring for lifelong metabolic dysregulation.

A Dynamic, Not Fixed, Set‑Point

Your set-point isn’t fixed at birth. It adjusts to your diet, stress, sleep, and environment. Rapid dieting convinces your brain that food scarcity is common, nudging the set-point upward “just in case.” That’s why yo‑yo dieting often ends with increased weight. Conversely, calming metabolic alarm signals—through stable sleep patterns, reduced inflammation, and balanced nutrition—can persuade your brain to lower the defended weight without internal resistance.

Key Takeaway

Your body isn’t broken or weak; it’s exquisitely well designed for survival. The challenge is not to fight the set-point, but to reprogram it by changing the biological inputs your brain uses to calculate that target weight.

Jenkinson’s metabology reframes obesity as the predictable outcome of hormonal miscommunication between evolved physiology and an industrialized food environment. His core argument—echoing thinkers like Robert Lustig and Stephan Guyenet—is that the road to sustainable weight loss lies not in discipline but in recalibrating biology itself. The remainder of the book explores how to do exactly that through food, hormones, culture and everyday habits.

At the center of modern weight dysregulation lies one biochemical master switch: insulin. Jenkinson calls it the hormone that turns fat storage on and off. Chronic insulin elevation—driven by constant intake of fast carbohydrates—locks energy inside fat cells and distorts the brain’s ability to measure abundance.

The Sugar Roller Coaster

Each time you eat refined food—a breakfast cereal and orange juice combination, for instance—blood glucose spikes. Insulin surges to restore normal sugar levels, glucose plummets, and you experience sudden hunger or fatigue. You snack again and repeat the loop, driving an all-day insulin rhythm that promotes fat storage and hunger. Over months and years, this roller‑coaster teaches your hypothalamus to defend a higher weight as a buffer against perceived energy volatility.

Insulin and Set‑Point Shifts

Clinical evidence makes insulin’s power visible. In one San Diego study, diabetics who increased insulin doses gained about 8 kilograms even while eating 300 fewer calories per day. When physicians lowered insulin through octreotide therapy, patients lost weight effortlessly. The same effect appears in surgical cases and in bodybuilders who misuse insulin for muscle gains—proof that insulin itself determines energy partitioning, not just calories.

How to Lower Insulin Naturally

Jenkinson’s advice echoes nutritional endocrinologists like Jason Fung: avoid sugary drinks, fruit juices, and frequent snacking that elevate baseline insulin. Replace grain-based breakfasts with protein and healthy fat, and focus on whole foods with low glycaemic load rather than chasing low-fat labels. Stabilizing blood sugar reduces spikes, making the brain more responsive to leptin and helping the weight set-point decline without slimming-world austerity.

Practical Message

Every time you flatten your glucose curve, you lower insulin exposure—and give your body permission to burn stored fat again.

Through insulin, the book connects biochemistry to daily habit: what seems like a snack craving or energy crash is your physiology trying to defend stability after sugar-induced turbulence. End the roller-coaster, and the system begins to trust that famine is over.

Modern diets didn’t just add sugar—they also rewired your body’s cellular messaging by distorting the ratio of omega‑3 to omega‑6 fatty acids. According to Jenkinson, this shift explains much of today’s chronic inflammation, leptin resistance and heightened appetite.

The Omega Imbalance

Omega‑3 fats (from algae, fish and grass-fed meat) make your cell membranes flexible and anti-inflammatory. Omega‑6 fats (from industrial seed oils) make them stiff and pro‑inflammatory. When omega‑6 dominates—as it does in diets heavy in soybean, sunflower and corn oils—your immune cells stay on alert and your hypothalamus receives distorted satiety signals. The book cites Stephan Guyenet’s tissue analyses showing US linoleic acid levels rising from 8% to over 20% since the 1960s, mirroring the rise in processed seed-oil consumption.

How Inflammation Raises the Set‑Point

Inflammation sabotages leptin’s ability to reach the brain. Fat tissue and liver cells secrete inflammatory messengers like TNF‑alpha that blunt leptin reception, convincing the hypothalamus that your body is starving—even amid abundance. Meanwhile, omega‑6 derivatives activate the endocannabinoid system, the same neural pathway triggered by cannabis munchies, amplifying food pleasure and cravings. Together, these effects embed overeating at a biochemical level.

Rebalancing the Ratio

To reverse the damage, Jenkinson recommends rejecting processed frying oils and margarines. Cook with butter, ghee or olive oil, eat fatty fish twice weekly, and choose grass‑fed meats. Though nuts like walnuts claim omega‑3 content, they still contain overwhelming omega‑6 loads, so moderation matters. Small consistent swaps—like replacing store-bought dressings or takeaways—transform cell membrane composition within months.

Remember

Your fat intake rewires your body’s software. Fixing inflammation and restoring omega balance lets leptin speak clearly again, naturally reducing appetite and weight defense.

This argument reframes fat quality—not calories—as the true metabolic determinant. It turns the industrial seed-oil revolution into the 21st-century counterpart of scurvy or beriberi: a silent deficiency in essential signals that regulate human metabolism.

Repeated caloric restriction, Jenkinson warns, is biologically self-defeating. Dieting may melt pounds temporarily, but it simultaneously triggers hormonal alarms that program your body to prevent future 'famines'—raising the weight set‑point each time.

The Evidence from Starvation and Reality TV

The Minnesota Starvation Experiment proved that weight loss through restriction slows metabolism, destroys mood and induces food obsession. Kevin Hall’s research on The Biggest Loser contestants revealed that even six years later, their resting metabolism remained hundreds of calories below normal—and most had regained weight. The adaptation wasn’t psychological, it was physiological defense.

Weight Cycling Reinforces Famine Memory

Animal studies in Norway and Arizona confirm this pattern. Mice oscillating between dieting and normal feeding end up heavier than mice continuously fed excess—to the same caloric average. The brain logs each famine event as a lesson to store more next time. This phenomenon explains why serial dieters often grow heavier despite tremendous effort.

Jenkins's Warning

Every unsuccessful crash diet teaches your brain to defend a higher weight next time. The answer is not stricter self-control, but persuading biology that famine is over.

This insight connects with the author’s clinical experience of bariatric patients: sustainable change appears only when hormones and set-point signals are reset—through surgery, hormonal normalization, or long‑term diet pattern changes. Hunger is not a weakness but a defense mechanism honed by evolution.

Obesity unfolds differently across populations not only because of behavior but because genes and prenatal cues prime metabolism. Jenkinson’s discussion of heritability and epigenetic memory reveals weight control as an intergenerational story.

Inherited Predispositions

Twin and adoption studies (Jane Wardle) show that 70–75% of BMI variance arises from genetics, meaning siblings separated at birth resemble each other’s weight despite different upbringings. Populations historically exposed to famine or long voyages—like Pima Americans or Pacific Islanders—carry thrifty genes that once aided survival but now hinder it in a calorie‑dense world. Their metabolisms still hoard energy defensively.

Epigenetic Programming

Prenatal nutrition switches gene expression through chemical markings like methylation. Studies of the Dutch Hunger Winter show that babies conceived in famine later develop obesity, heart disease, and diabetes at higher rates. Jenkinson adds John Kral’s findings: women who underwent bariatric surgery before pregnancy bore children with dramatically lower obesity risk. These results prove that environment and physiology communicate across generations.

By viewing obesity through a genetic–epigenetic lens, Jenkinson reframes “personal responsibility.” Most vulnerability is inherited, but awareness allows prevention. Public health, not individual guilt, is the rational response.

After exploring biology, Jenkinson turns to history and policy. He argues that governmental dietary guidelines and industrial incentives have created a global environment that constantly manipulates our hunger circuits.

From Fire to Factory

Cooking once made us human. By pre‑digesting food, it allowed bigger brains and smaller guts—a transformation described by Aiello and Wheeler’s expensive-tissue hypothesis. But industrial processing reversed its benefits. The late 20th century’s low-fat revolution (sparked by the 1977 McGovern Report) demonized natural fats and celebrated grains and seed oils. Food industries complied by replacing saturated animal fats with cheap vegetable oils and sugars, increasing both glycaemic stress and omega‑6 exposure.

The Policy Backfire

By 2009, Americans consumed four times more vegetable oil than in 1970 and 30% more refined flour. The food supply became calorie‑dense but nutrient‑poor. Studies like the BMJ 2013 re‑analysis even suggest that substituting seed oils for saturated fat increased heart deaths—the opposite of the intended outcome. Meanwhile, the sugar industry secretly funded research shifting blame from sugar to fat, as later revealed in archival investigations.

An Obesogenic World

Supermarkets and fast‑food chains now flood the landscape with cheap, hyper‑palatable combinations of sugar, starch, and omega‑6 fats. These foods exploit your innate preference for energy-dense tastes formed on the savanna. When combined with sedentary life, sleep deprivation, and stress, the environment keeps your set‑point elevated. The implication: lasting weight control demands systemic reform as much as personal strategy.

Lesson

Policy, not personality, built this obesogenic landscape. Reversing it requires both cultural and structural redesign—starting in the kitchen, not just the clinic.

Understanding this history prepares you to make smarter choices: distrust low-fat processed promises, value real ingredients, and invest time in cooking as an act of metabolic integrity.

The final section translates science into action. Jenkinson’s five-step Blueprint is not another diet but a plan to persuade your hypothalamus to lower its defended weight voluntarily. The strategy interlocks food quality, hormonal modulation, sleep and behavioral change.

1. Eat More—but Differently

Eat nourishing, whole foods generously while removing sugar, refined wheat, and seed oils. Fix breakfast with fat and protein—eggs, salmon or bacon—so insulin stays low all morning. Pack real lunches rather than grazing. This restores glucose stability and leptin responsiveness.

2. Prioritize Sleep and Rhythm

Sleep deprivation amplifies hunger hormones and suppresses leptin. Dim lights two hours before bed and avoid screens. Night-shift studies reveal that one sleepless week can mimic diabetic metabolism. Darkness is your simplest hormonal therapy.

3. Change Your Fats

Swap industrial oils for butter and olive oil, eat oily fish twice weekly, and skip deep-fried or processed items. Within months, this rebalances your omega ratio, reduces inflammation, and improves membrane health—literally changing how your cells hear your hormones.

4. Move Enjoyably

Exercise becomes a signaling tool, not punishment. Weight-bearing, HIIT or dancing twice a week maintains sympathetic activity and thermogenesis without the rebound appetite of chronic cardio. Muscle acts as a metabolic spare battery storing glucose and producing heat.

5. Reduce Glycaemic Load

Lower total carbohydrate towards 150 g per day initially and possibly 80–100 g later, avoiding extreme keto swings. Apps like MyFitnessPal can guide you. By easing insulin exposure, you coax the brain to trust a new lower set‑point.

Behavioral Insight

Use mindfulness to ride cravings rather than suppress them—a three‑minute breathing pause or savor‑three‑bites technique rewires reward circuits faster than punishment ever can.

Jenkinson ends optimistically: you can win against obesity not by fighting hunger but by teaching your body that it’s safe to be lighter. Fix the environment, feed intelligently, sleep deeply, and trust biology to finish the work.