📖 Table of Contents
Why Start Here
What Is Obesity
Genetics
Epigenetics
Hormones
Environment
Trauma
Medical Conditions
Insulin Resistance
Medications
Food
Why “Eat Less, Move More” Fails
Eat Less
Move More
Set Point Theory
Dieting and Insulin Resistance
When Exercise Backfires
The Food Noise Revelation
The Myth of Noble Suffering
Say It With Me: “It’s Not My Fault”
Why Start Here
Before we can talk about scripts, strategies, or how to stand up to stigma, we need to begin with one truth: It’s not your fault.
This is the ground everything else in this book stands on:
If you carry shame, you will shrink when you should speak.
If you believe you’re to blame, you’ll hesitate to demand respect.
And if you think compassion is something you haven’t earned, you won’t believe you deserve it from anyone else.
Respect from others starts with respect for yourself. Compassion from others starts with compassion for yourself.
What Is Obesity
Obesity is a chronic, relapsing disease. It’s not caused by one thing, and it can’t be fixed by one thing.
“Obesity represents a chronic, complex, and multifactorial metabolic disease shaped by a convergence of genetic, biological, environmental, behavioral, sociocultural, and economic determinants. Obesity requires lifelong intervention. It poses numerous health-related risks.”
In other words, medical organizations around the world recognize it as a life-long medical condition that has many different overlapping causes that work together to damage your health.
Some of the factors that can contribute to obesity include:
Genetics
Your DNA is not just a backdrop; it is the stage. Genes influence appetite, metabolism, fat storage, and even how your brain responds to food.
Obesity tends to run in families
Genes explain about 40–70% risk of having obesity
In severe or early-onset cases of obesity, genes can account for 80-85% risk
Over 40 specific genes are linked to obesity and how fat is distributed in the body
FTO, can add 4-6 pounds of body weight
MC4R, is linked to bigger appetites and early-onset obesity in kids
Heritability tells us how important genes are in general
In a well-known study, identical twins were about twice as likely as fraternal twins to both have obesity, showing that genetics has a powerful influence on body weight.
Epigenetics
Epigenetics is the process that controls how your genes are switched on or off, without altering the DNA itself.
Think of your DNA as the instruction book, and epigenetics as the bookmarks, highlights, or sticky notes that tell your body which pages to read and which to skip.
It starts in the womb. A mother’s diet during pregnancy can leave marks on a baby’s genes, raising obesity risk later
It can pass to kids and grandkids. Some epigenetic changes can be inherited.
“Epigenetic scores” can measure and predict obesity risk, and they reflect both genes and environment
Epigenetic score can explain about 32% or one-third of why people’s body weights differ, these scores do a better job at predicting weight than DNA-only scores
Some people are predisposed to insulin resistance or slower metabolisms long before they take their first bite of food.
Hormones
Hormones are like the “control panel” for hunger and energy use. When these systems are dysregulated, the brain sends stronger “eat” signals and weaker “stop” signals.
Leptin: the fullness hormone
Signals the brain that you’re full and should stop eating
Helps your body burn energy
In obesity, leptin levels are high but the brain stops responding, this is called leptin resistance.
Ghrelin: the hunger hormone
Tells your brain when it’s time to eat
Levels go up before meals (that “I’m starving” feeling) and drop after eating
In obesity, fasting ghrelin levels are usually lower than in lean people
After eating, with obesity, ghrelin doesn’t drop as much as it should, so the brain doesn’t get a strong ‘I’m full’ signal.
Insulin: the blood sugar control hormone
Moves sugar from the blood into your cells for energy or storage
Obesity causes insulin resistance, so the body pumps out more insulin
Higher insulin levels predict more future weight gain
Insulin is like a key, and your cells are like locked doors. In a healthy body, the key (insulin) easily opens the door so sugar can move inside for energy.
With insulin resistance, the locks get rusty, the key still fits, but it doesn’t open the door all the way, so your body makes more and more keys (insulin) to force the doors open.
GLP-1: the satiety hormone
Sends signals to your brain that you’ve had enough to eat
Tells your pancreas to release insulin so sugar from food moves into your cells for energy
Keeps your liver from making too much sugar
Slows down how fast your stomach empties, so you feel fuller for longer
GLP-1 medications don’t make you feel artificially full, they mimic and extend your body’s natural GLP-1 hormone, helping your gut send clearer signals to your brain so it knows when you’ve eaten enough.
Cortisol: the stress hormone
Fuels cravings for quick, high-calorie foods
Chronic stress (stress that doesn’t go away) raises cortisol
Normally, cortisol peaks in the morning (to wake you up) and drops at night (so you can fall asleep). But with long-term stress, cortisol stays elevated into the evening, making it harder to fall asleep, stay asleep, or get deep, restful sleep.
Poor sleep then raises hunger hormones like ghrelin, lowers satiety hormones like leptin, and makes cravings even worse, creating a cycle that fuels weight gain.
Environment
The world around us shapes the bodies we live in.
Obesogens are chemicals that make you store fat.
Endocrine-disrupting chemicals (EDC)
Bisphenols (BPA, BPS, BPF): found in plastics, can linings, receipts
Phthalates: used in plastics, cosmetics, food packaging
Organotins (Tributyltin, TBT): once used in paints and industrial products
Perfluoroalkyl substances (PFAS): “forever chemicals” in non-stick pans, waterproof coatings, food wrappers
Polychlorinated biphenyls (PCBs): industrial chemicals, now banned but still persistent in the environment
Dioxins: byproducts of industrial processes and waste burning
Pesticides & fungicides
DDT/DDE: banned in many countries but still lingering in the environment.
Atrazine: a widely used herbicide in agriculture
Organophosphates and carbamates: pesticide groups with links to metabolic disruption
Other suspected obesogens
Polycyclic aromatic hydrocarbons (PAHs): from air pollution, smoke, and charred foods
Heavy metals: like arsenic and cadmium, which can disrupt metabolism
Parabens: preservatives in cosmetics and personal care products
Even at low levels, they can change how fat cells grow and store energy, shifting the body “set point” to hold more weight and interfering with appetite and blood sugar regulation.
Trauma & Depression
Depression and trauma can drive obesity, creating a cycle where pain fuels overeating, weight gain worsens mood, and both feed each other.
Trauma
Trauma doesn’t just live in memories. It lives in the body.
Early trauma (like abuse, neglect, or growing up in chaos): changes how the brain and hormones develop
Stress hormone overload: Chronic stress raises cortisol, which makes you crave comfort foods and pushes your body to store fat
Constant fight-or-flight: Living in survival mode keeps your system on high alert, draining energy and messing with appetite signals
Studies show that adults who experienced trauma as children have significantly higher rates of obesity. Trauma alters the stress-response system, rewiring metabolism and appetite.
This isn’t psychological weakness, it’s biological adaptation.
Depression
The relationship with depression goes both ways: obesity can contribute to depression through stigma, stress, and health effects, while depression can lead to weight gain through changes in appetite, activity, and hormones.
About 1 in 10 people have depression and 2 in 3 are overweight, so they often overlap.
Women with obesity are more likely to have depression
Depression can make obesity worse because it drains energy and motivation.
Exercising or cooking healthy meals can feel impossible, when it’s hard to even get out of bed or brush your teeth.
Medical Conditions
Some medical conditions can both cause obesity and also be caused by obesity, creating a vicious cycle that’s almost impossible to escape without medical help.
Hypothyroidism: Slows metabolism, making it easier to gain weight and harder to lose it.
Hypothalamic injury or disease: Damage from tumors, trauma, surgery, or radiation can disrupt appetite regulation and lead to severe weight gain.
Prader-Willi syndrome: A rare genetic disorder that causes constant hunger due to abnormal brain signaling, making obesity almost inevitable without strict intervention.
Other rare genetic syndromes (e.g., Bardet-Biedl, Alström): These inherited conditions include obesity as a core feature, often beginning in childhood.
Cushing’s syndrome: Causes chronically high cortisol, which promotes fat storage, especially around the belly.
Polycystic ovary syndrome (PCOS): Creates a hormonal imbalance and insulin resistance that both increase weight gain risk.
Hypogonadism / Low testosterone (in men): Lowers muscle mass and raises fat accumulation, shifting body composition.
Growth hormone deficiency: Reduces lean muscle while increasing fat mass, leading to slower metabolism and weight changes.
PCOS, low testosterone, and insulin resistance can all make weight gain easier, but once obesity develops, it worsens those same problems.
The result is a feedback loop: the condition fuels obesity, and obesity fuels the condition.
This cycle traps people in a state where their biology is actively working against weight loss, no matter how hard they try with diet and exercise.
Insulin Resistance
Insulin resistance happens when your cells stop responding properly to insulin.
To keep blood sugar stable, your pancreas produces more insulin, but those high insulin levels push your body to store more fat and make it harder to burn the fat you already have.
This creates a vicious cycle: obesity raises insulin resistance, and insulin resistance in turn drives more weight gain.
About 1 in 3 Americans has insulin resistance.
In the U.S., around 40% of younger adults (ages 18–44) have it.
More than 7 in 10 people with obesity also develop insulin resistance.
Type 2 Diabetes Link
Insulin resistance is the root problem behind prediabetes and type 2 diabetes.
At first, the pancreas produces extra insulin to keep blood sugar in check, but eventually it can’t keep up. That’s when prediabetes turns into full type 2 diabetes.
About 1 in 3 U.S. adults (96 million people) has prediabetes, and most don’t know it.
90–95% of all diabetes cases in the U.S. are type 2, which develops from insulin resistance.
Up to 70% of people with prediabetes will eventually develop type 2 diabetes without treatment (ADA).
People with obesity have about a 7 times higher risk of developing type 2 diabetes than those at a healthy weight (Harvard).
GLP-1 Connection
GLP-1s can reverse insulin resistance and put type 2 diabetes into remission.
They improve insulin sensitivity even before weight loss starts, lower inflammation in fat tissue, reduce appetite, and drive significant weight loss, tackling the root causes of type 2 diabetes.
Cut insulin resistance by about 30–45% in trials.
In the STEP trials, about 80% with prediabetes went back to normal blood sugar (vs 37% on placebo).
Many people with type 2 diabetes on semaglutide were able to reduce or stop other diabetes meds.
Improved insulin sensitivity by up to 65% — almost double what GLP-1s alone do.
Drove greater weight loss (20–22% of body weight vs ~15% with semaglutide).
More effective than semaglutide at improving insulin sensitivity and blood sugar control in type 2 diabetes.
This makes GLP-1s especially important for people with conditions like PCOS, low testosterone, or insulin resistance, who get trapped in the cycle where the disease drives obesity and obesity makes the disease worse.
GLP-1s offer a way to break the cycle when nothing else can, because they can improve insulin sensitivity even before weight loss.
Medications
Many common medications can cause weight gain by changing the way the body handles appetite, hormones, or energy use.
Steroids and some diabetes drugs raise insulin or cortisol levels, pushing the body to store more fat. Antidepressants and antipsychotics act on brain chemicals that increase hunger, cravings, or fatigue, making it easier to eat more and harder to move.
Even drugs not directly tied to metabolism, like antihistamines or beta-blockers, can slow energy burn or raise appetite.
Medications that cause weight gain:
Glucocorticoids (steroids)
Insulin & some diabetes meds (sulfonylureas, thiazolidinediones)
Antidepressants (SSRIs, tricyclics, MAOIs)
Antipsychotics (especially atypicals like olanzapine, clozapine)
Mood stabilizers (lithium, valproate)
Antihistamines & beta-blockers (in some cases)
Ironically, many of the very medications used to treat conditions tied to obesity, like diabetes, depression, or chronic pain, can actually cause weight gain themselves, creating a frustrating cycle.
Insulin and certain older diabetes drugs promote fat storage, while antidepressants and antipsychotics drive appetite.
For many, the weight gain isn’t about lifestyle at all, but about the chemical side effects of the drugs they need to stay alive.
People are often “medicated into obesity.”
Food
The link between food and obesity is undeniable.
The modern diet is dominated by ultra-processed products, oversized portions, and sugar-laden drinks and snacks, all reinforced by an environment where unhealthy options are cheaper, easier, and more aggressively marketed than healthier ones.
Together, these factors don’t just add calories, they create a system that makes weight gain likely and weight loss difficult.
Ultra-Processed Foods
In the U.S., 57–60% of daily calories now come from ultra-processed foods.
These foods are calorie-dense, low in fiber, and engineered to trigger overeating.
Controlled NIH trial: People eating an ultra-processed diet consumed ~500 extra calories/day and gained weight in just 2 weeks compared to when the same people ate minimally processed foods..
Portion Sizes & Calories
Portion sizes of packaged and restaurant food have doubled or tripled since the 1970s, adding 200–300 calories per meal.
Restaurant meals average 1,200 calories per plate, nearly twice what’s recommended for a meal.
Sugary Drinks & Snacks
Just one sugary drink a day increases obesity risk by 26%.
Snacking now makes up 1 in 4 calories Americans eat, compared to minimal snacking 40 years ago.
Americans consume ~17 teaspoons of added sugar daily, over twice the WHO’s limit.
Food Environment
People living in “food swamps” (fast food and convenience store dense areas) face 5–20% higher obesity risk, even after adjusting for income.
More than 18 million Americans live in food deserts where access to fresh, affordable produce is limited.
On average, U.S. adults get 11% of daily calories from fast food.
Marketing & Cost
Calorie-for-calorie, junk food is 1.5–2x cheaper than fruits and vegetables, pushing low-income families toward processed foods.
Global Evidence
Countries adopting Western diets (fast food, sugary drinks, ultra-processed snacks) see obesity rates double within one generation.
Since 1975, global obesity rates have tripled, with obesity now killing more people worldwide than undernutrition.
While food is a contributing factor to obesity, it is never the sole cause of obesity.
As you can see from the factors listed in this chapter, it’s the combination of multiple issues all working together to create a cycle that makes obesity inevitable for some and incredibly difficult to escape.
With that said, food is more than fuel. It’s culture, celebration, and connection. It’s how we gather, how we show love, and how we express creativity. Food is woven into memory and meaning, into holidays, family tables, and daily rituals. That’s why this conversation is so complicated: food is both the nutrients we put into our bodies and the way we experience the world.
Why “Eat Less, Move More” Fails
If you live with obesity, you’ve heard it: “Just eat less and move more.”
Yes, food and exercise matter for health. But they are not a cure for obesity. For most people, dieting and exercise alone don’t just fail, they backfire.
Research shows almost anyone can lose weight short-term. But about 80% of people regain most or all of it within 2–5 years if they rely on diet and exercise alone.
Eat Less
When you cut calories, your body fights back.
Your brain doesn’t think, “Great, we’re getting healthy.”
It thinks, “We’re starving.”
And it pushes you, with cravings, low energy, and slowed metabolism, back toward your starting weight.
After dieting, calorie burn per day can drop by 200–500 calories
People who lose 10% of body weight often experience about a 15% drop in metabolism, making maintenance much harder
Hormone Changes After Dieting:
Hunger hormones rise 20%
Fullness hormones drop 30%
Your metabolism slows down to save energy
These changes last for at least 1 year
Brain scans show stronger reward response to food cues, especially energy-dense foods, after weight loss.
Dieting & Insulin Resistance
When you slash calories, your body doesn’t cheer you on.
It panics.
Hunger hormones like ghrelin rise, fullness hormones like leptin plummet, and metabolism slows down to conserve energy.
At first, you may see weight loss. But eventually, the hunger wins.
Rebound eating floods your body with insulin (the hormone that helps store sugar from food)
Over time, those repeated insulin surges make your cells stop responding as well (insulin resistance)
Once insulin resistance develops, your body pumps out more and more insulin to manage food
High insulin doesn’t just sit quietly in the background, it actively promotes fat storage
This is why research shows about 80% of regain most or all the weight they lose within 2–5 years of dieting.
Insulin resistance can improve with weight loss especially early on or in prediabetes.
But with long‑standing obesity, type 2 diabetes, or repeated weight cycling, sensitivity may not fully “reset,” though meaningful improvements are still possible.
Move More
Exercise is vital for health, but the way society pushes it as a “fix” for obesity often causes more harm than good.
Exercise alone: Only contributes to about 4–6 lbs average weight loss
Yes, a long run burns calories in the moment. But if you aren’t protecting your muscle with strength training and enough fuel, your body burns muscle along with fat.
Cardio without strength training = muscle loss → lower metabolism → increased hunger
25–30% of weight loss can come from lean muscle instead of fat (without strength training).
For every pound of muscle lost, your body burns 30–50 fewer calories per day while at rest.
Endurance exercise often increases appetite (especially in women).
Cardio example:
You’re body burns 2,000 calories a day at rest (your resting metabolic rate).
After repeated restrictive diets and muscle loss, maybe that number drops to 1,500 calories a day.
You go for a run and burn 500 calories.
Instead of creating a meaningful deficit, you’ve just punished a system that now burns far less all day, every day.
It’s like downsizing the engine in your car, it uses less fuel no matter how far you drive.
On top of that, exercise increases hunger. Your body’s natural response to burning energy is to demand more energy.
If you’re restricting calories at the same time, the hunger can become overwhelming, and when the rebound happens, insulin resistance deepens.
Strength training = higher metabolism → increased hunger
Gaining 10 pounds of muscle can increase your resting calorie burn by about 130 calories per day.
More lean muscle also boosts appetite because it takes more energy for your body to maintain.
If you stop working out as intensely or cut back your routine, you lose muscle and burn fewer calories, but your appetite often stays the same.
This is one reason many retired athletes gain weight once they’re no longer training at the same level.
Strength training example:
You’re body burns 2,000 calories a day at rest (your resting metabolic rate).
After strength training daily, you build muscle and now burn an additional 1,000 calories per day from a higher resting burn plus your workouts.
You increase your daily calorie intake to feed the new muscle.
You stop training at the same level and now burn only 500 calories per day instead of 1,000.
Your hunger does not drop right away. You keep eating as if you were still training.
You end up about 500 calories over maintenance each day.
Weight lifting is powerful for health and body composition, but it is not a standalone cure for obesity.
The single best thing you can do is choose a way of moving that you are willing to keep doing for years, not weeks. If the routine changes, the results will change too, so pick activities you actually enjoy.
Consistency beats perfection.
There are about a hundred different weight lifting scenarios that we could go over but for the sake of staying on track I’m only sharing this very common one.Cardio is good for overall health, but strength training is essential for protecting muscle, keeping your metabolism higher, and making weight loss sustainable.
Set Point Theory
Set point theory suggests every person has a defended weight range. When you lose weight, the body treats it as a threat and pulls you back by increasing hunger and lowering energy expenditure.
Your weight is like a thermostat. Drop below the range and biology heats the system back up.
In episode 8 of the GLP-1 Collective Podcast, Dr. Lindsay Ogle, MD an Obesity Specialist with her own private practice, Missouri Metabolic Health, describes set point theory as the reason why “eat less, move more” fails.
“When we’re trying to lose weight now, our body is trying to protect us. It thinks It’s starving. It’s in a dangerous state when we’re cutting back on calories. And so to protect us, it slows our metabolism, it increases our hunger hormones. And those are measured, those are real changes that happen in the body. And it is really impossible to overcome that long term. And so that is why, even if you are successful on a diet, it is very unlikely that it’s going to be maintained long term, that weight loss is going to be maintained long term.”
The Food Noise Revelation
GLP-1 medications like semaglutide and tirzepatide don’t just help people lose weight, they quiet the food noise.
Food noise is that constant chatter in your head about food:
What’s in the fridge?
What will I eat next?
How much should I have?
It’s relentless.
When GLP-1s work, the noise goes quiet.
In episode 3 of the GLP-1 Collective Podcast, described this as the moment her life changed.
“I don’t know how to explain it. I feel like anybody that’s listening that’s had food noise turns off understands that moment, that moment where you go, oh my god, it wasn’t my fault, like that moment. And then all you do is want everybody else to know, because it’s earth shattering. and life-changing. And I just couldn’t shut up about it then.”
— Kim Carlos
Oprah herself has described the same experience, saying GLP-1s silenced the food noise she had battled her entire life.
“One of the things that I realized the very first time I took a GLP-1 was that all these years I thought that thin people, those people just had more willpower...And then I realized the very first time I took the GLP-1 that, oh, they’re not even thinking about it. They’re only eating when they’re hungry. They’re stopping when they’re full.”
— Opra Winfrey
This silence is why so many patients fight desperately for access.
Once you’ve experienced it, you understand: this disease was never about weakness. It was about biology.
Willpower alone cannot overcome biology. And if you’ve regained weight, it isn’t because you were weak. It’s because your body is designed to fight back.
The failure of “eat less, move more” has been used as evidence of weakness, rather than evidence that the method itself doesn’t work for most people
The Myth of Noble Suffering
Our culture worships grit. “Push harder. Restrict more. Sweat more.”
But is it noble to try and fail again and again while your biology pulls you further away from success?
Or is it wiser, and braver, to recognize that suffering for the sake of suffering doesn’t heal you? That using medical tools science has given us is actually safer for your health and your future?
The truth is this: you cannot shame, starve, or sweat your way out of obesity.
Say It With Me: “It’s Not My Fault”
Before we move forward, I want you to pause.
Take a deep breath.
Put a hand on your chest if you need to.
And repeat these words:
“It’s not my fault.”
Good.
Now say it again and again until you believe it and forgive yourself for being so hard on yourself.
Obesity is a complex disease, not a moral failing:
You don’t owe anyone an explanation for your weight.
You don’t need to apologize for your body.
You don’t need to carry around the shame.
You take your power back with this one simple truth:
It’s not your fault.
You didn’t cause this, and you don’t deserve to feel ashamed for your biology.
Before you can advocate in the doctor’s office, with your partner, at work, or anywhere else, you have to start here: with yourself.
Because when you know it’s not your fault, you finally begin to stand S-T-R-O-N-G.
This is where your advocacy begins. With yourself.