The Obesity Code

What are the big ideas?

1. The caloric theory of obesity is inadequate: This book challenges the widely accepted belief that obesity is solely caused by consuming more calories than burned. Instead, it introduces a hormonal theory that explains how insulin resistance and persistent high insulin levels are driving factors behind weight gain and obesity.
2. Insulin resistance compartmentalizes in different tissues: The book breaks down the concept of insulin resistance by explaining how it develops differently in various tissues, such as the brain, liver, and muscle. This nuanced understanding is not typically addressed in other obesity literature.
3. Persistent high insulin levels lead to a vicious cycle: The book explains that high insulin levels do not directly cause insulin resistance, but rather, the persistence of these levels over time leads to the development of resistance and a vicious cycle where higher insulin levels result in even more resistance.
4. Reducing sugar intake is key to combating obesity: The book advocates for reducing added sugars as an effective way to combat childhood obesity, which goes against the common advice of caloric restriction and increased exercise. It also highlights the role of insulin in driving weight gain, even in infants.
5. Intermittent fasting is a hormonal approach to weight loss: The book presents intermittent fasting as a hormonal solution for obesity, focusing on addressing the root cause of insulin imbalance rather than just caloric reduction. It provides practical meal plans and guidelines for implementing this approach into one's lifestyle.

Summary

Introduction

Takeaways

• The art of medicine includes outdated and ineffective treatments, such as obesity treatment through caloric reduction.
• Obesity, defined by body mass index (BMI), has tripled worldwide since 1985, despite the recommendation of low-fat, calorie-reduced diets.
• Doctors have limited knowledge on obesity and its treatment, often relying on large corporations or charlatans for guidance.
• Current theories explaining obesity are overly simplistic and do not consider the multifactorial nature of chronic diseases.
• The focus on short-term studies in understanding long-term conditions like obesity may not be informative.
• Evidence-based medicine should rely on human studies, focusing on causal factors rather than association studies when possible.
• Part 1: The timeline of the obesity epidemic and family history contribute to understanding its underlying causes.
• Part 2: The caloric theory is inadequate for explaining obesity and its shortcomings are highlighted.
• Part 3: Introduces hormonal theory, explaining insulin's role in regulating body weight and the importance of insulin resistance.
• Part 4: Discusses how hormonal obesity theory explains certain associations with obesity, such as poverty and childhood obesity.
• Part 5: Explores the role of macronutrients (fat, protein, carbohydrates) and fructose in weight gain and the effects of artificial sweeteners.
• Part 6: Guidelines for treating obesity by addressing hormonal imbalance through dietary changes, intermittent fasting, stress management, and sleep improvement.

Quotes

“The Parable of the Cow”: Two cows were discussing the latest nutritional research, which had been done on lions. One cow says to the other, “Did you hear that we’ve been wrong these last 200 years? The latest research shows that eating grass is bad for you and eating meat is good.” So the two cows began eating meat. Shortly afterward, they got sick and they died. One year later, two lions were discussing the latest nutritional research, which was done on cows. One lion said to the other that the latest research showed that eating meat kills you and eating grass is good. So, the two lions started eating grass, and they died. What’s the moral of the story? We are not mice. We are not rats. We are not chimpanzees or spider monkeys. We are human beings, and therefore we should consider only human studies.”

Part One: The Epidemic

Takeaways

• Obesity runs in families: obese children often have obese siblings, become obese adults, and go on to have obese children.
• Families share genetic characteristics that may contribute to obesity but obesity has become rampant only since the 1970s.
• The classic method for determining the relative impact of genetic versus environmental factors is to study adoptive families, but Danish adoption studies showed a strong correlation between the weights of biological parents and their adopted children.
• Identical twins raised apart also showed a strong correlation in weight, suggesting that approximately 70% of the variance in obesity is familial.
• The thrifty-gene hypothesis assumes all humans are genetically predisposed to gain weight as a survival mechanism but it has been largely discredited due to numerous flaws and inconsistencies.
• Inherited factors account for about 70% of the tendency to obesity, but the other 30% can be influenced by diet and exercise. However, caloric imbalance theories cannot explain the genetic component of obesity.

Quotes

“What’s the difference between proximate and ultimate? The proximate cause is immediately responsible, whereas the ultimate cause is what started the chain of events.”

“Throughout most of human history, obesity has been rare. Individuals in traditional societies eating traditional diets seldom became obese, even in times of abundant food. As”

“So, if one were to restrict dietary fats, then one must increase dietary carbohydrates and vice versa. In the developed world, these carbohydrates all tend to be highly refined. Low Fat = High Carbohydrate This dilemma created significant cognitive dissonance. Refined carbohydrates could not simultaneously be both good (because they are low in fat) and bad (because they are fattening). The solution adopted by most nutrition experts was to suggest that carbohydrates were no longer fattening. Instead, calories were fattening. Without evidence or historical precedent, it was arbitrarily decided that excess calories caused weight gain, not specific foods. Fat, as the dietary villain, was now deemed fattening—a previously unknown concept. The Calories-In/Calories-Out model began to displace the prevailing “fattening carbohydrates” model.”

Part Two: The Calorie Deception

Takeaways

• The body has a "set point" for weight and fatness, which it defends against changes, both up and down. This is known as homeostasis.
• If weight drops below body set weight, the body responds by increasing appetite (ghrelin) and decreasing satiety hormones (amylin, peptide YY, and cholecystokinin), while also reducing total energy expenditure to try to regain the lost weight.
• If weight goes above body set weight, the body responds by decreasing appetite and increasing metabolism to lose the excess weight.
• Obese people have a higher body set weight, which makes it difficult for them to maintain weight loss through caloric restriction alone.
• Leptin is a hormone produced by fat cells that regulates energy balance by reducing appetite and increasing metabolism. However, in obesity, leptin resistance develops, making exogenous leptin ineffective at promoting weight loss.
• The cause of leptin resistance is still not fully understood but may involve inflammation and insulin resistance.
• Lowering the body set weight through lifestyle interventions and medications is a more effective approach to treating obesity than focusing solely on caloric restriction.

Quotes

“There are an almost infinite number of ways that the body can dissipate excess energy instead of storing it as body fat.”

“What would happen if the body continued to expend 3000 calories daily while taking in only 1500? Soon fat stores would be burned, then protein stores would be burned, and then you would die. Nice. The smart course of action for the body is to immediately reduce caloric expenditure to 1500 calories per day to restore balance. Caloric”

“Instead, we believe that the fault lies in ourselves. We feel we have failed. Some silently criticize us for not adhering to the diet. Others silently think we have no willpower and offer us meaningless platitudes. Sound familiar? The failing isn’t ours. The portion-control caloric-reduction diet is virtually guaranteed to fail. Eating less does not result in lasting weight loss.”

“Various hormonal levels, including ghrelin—a hormone that, essentially, makes us hungry—were analyzed. Weight loss significantly increased ghrelin levels in the study’s subjects, even after more than one year, compared to the subjects’ usual baseline. What does that mean? It means that the subjects felt hungrier and continued to feel so, right up to end of the study. The study also measured several satiety hormones, including peptide YY, amylin and cholecystokinin, all of which are released in response to proteins and fats in our diet and serve to make us feel full. This response, in turn, produces the desired effect of keeping us from overeating. More than a year after initial weight loss, the levels of all three satiety hormones were significantly lower than before. What does that mean? It means that the subjects felt less full. With increased hunger and decreased satiety, the desire to eat rises. Moreover, these hormonal changes occur almost immediately and persist almost indefinitely. People on a diet tend to feel hungrier, and that effect isn’t some kind of psychological voodoo, nor is it a loss of willpower. Increased hunger is a normal and expected hormonal response to weight loss.”

“Dr. Keys’s Minnesota Starvation Experiment first documented the effect of “semi-starvation neurosis.” People who lose weight dream about food. They obsess about food. All they can think about is food. Interest in all else diminishes. This behavior is not some strange affliction of the obese. In fact, it’s entirely hormonally driven and normal. The body, through hunger and satiety signaling, is compelling us to get more food. Losing weight triggers two important responses. First, total energy expenditure is immediately and indefinitely reduced in order to conserve the available energy. Second, hormonal hunger signaling is immediately and indefinitely amplified in an effort to acquire more food. Weight loss results in increased hunger and decreased metabolism. This evolutionary survival strategy has a single purpose: to make us regain the lost weight.”

“Functional magnetic resonance imaging studies show that areas of the brain controlling emotion and cognition light up in response to food stimuli. Areas of the prefrontal cortex involved with restraint show decreased activity. In other words, it is harder for people who have lost weight to resist food. 15 This has nothing whatsoever to do with a lack of willpower or any kind of moral failure. It’s a normal hormonal fact of life. We feel hungry, cold, tired and depressed. These are all real, measurable physical effects of calorie restriction.”

“But diet and exercise are not fifty-fifty partners like macaroni and cheese. Diet is Batman and exercise is Robin. Diet does 95 per cent of the work and deserves all the attention; so, logically, it would be sensible to focus on diet. Exercise is still healthy and important—just not equally important. It has many benefits, but weight loss is not among them. Exercise is like brushing your teeth. It is good for you and should be done every day. Just don’t expect to lose weight.”

“In a modern twist to the classic overeating experiments, Feltham decided that he would eat 5794 calories per day and document his weight gain. But the diet he chose was not a random 5794 calories. He followed a low-carbohydrate, high-fat diet of natural foods for twenty-one days. Feltham believed, based on clinical experience, that refined carbohydrates, not total calories, caused weight gain. The macronutrient breakdown of his diet was 10 percent carbohydrate, 53 percent fat and 37 percent protein. Standard calorie calculations predicted a weight gain of about 16 pounds (7.3 kilograms). Actual weight gain, however, was only about 2.8 pounds (1.3 kilograms). Even more interesting, he dropped more than 1 inch (2.5 centimeters) from his waist measurement. He gained weight, but it was lean mass.”

Part Three: A New Model of Obesity

Takeaways

• Obesity is time-dependent and driven by high insulin levels, which in turn cause insulin resistance.
• Insulin resistance is compartmentalized—it develops differently in various tissues (brain, liver, muscle).
• High insulin levels alone do not cause insulin resistance; the persistence of high levels is necessary for resistance to develop.
• Persistent exposure to insulin leads to a vicious cycle: higher insulin levels lead to more resistance, which in turn leads to even higher insulin levels.
• The number of meals per day has increased since the 1970s from three to six or more, and the balance between feeding and fasting has been destroyed.
• Myths perpetuate the notion that snacking is beneficial:
  • Snacking will increase metabolic rate
  • Snacking controls hunger
  • Snacking keeps blood glucose stable.
• Evidence supports none of those myths, and society norms encourage constant eating, leading to a drastic imbalance between insulin-dominant and insulin-deficient states per day.
• The increase in eating opportunities has led to persistence of high levels of insulin, which in turn causes development of insulin resistance.

Quotes

“OBESITY IS NOT caused by an excess of calories, but instead by a body set weight that is too high because of a hormonal imbalance in the body.”

“Sulfonylureas and metformin Several pills are available for the drug treatment of type 2 diabetes. The sulfonylurea class work by stimulating the pancreas to produce more insulin to lower blood sugars. All drugs in this class are well known to cause weight gain.”

“-2 inhibitors The newest class of medication for type 2 diabetes is the SGLT-2 (sodium-glucose linked transporter) inhibitors. These drugs block the reabsorption of glucose by the kidney, so that it spills out in the urine. This lowers blood sugars, resulting in less insulin production. SGLT-2 inhibitors can lower glucose and insulin levels after a meal by as much as 35 per cent and 43 per cent respectively.21 But what effect do SGLT-2 inhibitors have on weight? Studies consistently show a sustained and significant weight loss in patients taking these drugs.22 Unlike virtually all dietary studies that show an initial weight loss followed by weight regain, this study found that the weight loss experienced by patients on SGLT-2 inhibitors continued for one year and longer.”

“Furthermore, their weight loss was predominantly loss of fat rather than lean muscle, although it was generally modest: around 2.5 per cent of body weight. (We lowered insulin. Patients lost weight.)”

“Type 1 diabetes is an autoimmune disease that destroys the insulin-producing beta cells of the pancreas. Insulin falls to extremely low levels. Blood sugar increases, but the hallmark of this condition is severe weight loss. Type 1 diabetes has been described since ancient times. Aretaeus of Cappadocia, a renowned ancient Greek physician, wrote the classic description: ‘Diabetes is... a melting down of flesh and limbs into urine.’ No matter how many calories the patient ingests, he or she cannot gain any weight. Until the discovery of insulin, this disease was almost universally fatal. Insulin levels go waaayyy down. Patients lose a lot of weight.”

“THE RESULTS ARE very consistent. Drugs that raise insulin levels cause weight gain. Drugs that have no effect on insulin levels are weight neutral. Drugs that lower insulin levels cause weight loss. The effect on weight is independent of the effect on blood sugar. A recent study suggests that 75 per cent of the weight-loss response in obesity is predicted by insulin levels.29 Not willpower. Not caloric intake. Not peer support or peer pressure. Not exercise. Just insulin.”

“As insulin goes up, the body set weight goes up. The hypothalamus sends out hormonal signals to the body to gain weight. We become hungry and eat. If we deliberately restrict caloric intake, then our total energy expenditure will decrease. The result is still the same—weight gain.”

“As the insightful Gary Taubes wrote in his book Why We Get Fat: And What to Do about It, ‘We do not get fat because we overeat. We overeat because we get fat.’ And why do we get fat? We get fat because our body set weight thermostat is set too high. Why? Because our insulin levels are too high. Hormones are central to understanding obesity. Everything about human metabolism, including the body set weight, is hormonally regulated. A critical physiological variable such as body fatness is not left up to the vagaries of daily caloric intake and exercise. Instead, hormones precisely and tightly regulate body fat. We don’t consciously control our body weight any more than we control our heart rates, our basal metabolic rates, our body temperatures or our breathing. These are all automatically regulated, and so is our weight. Hormones tell us we are hungry (ghrelin). Hormones tell us we are full (peptide YY, cholecystokinin). Hormones increase energy expenditure (adrenalin). Hormones shut down energy expenditure (thyroid hormone). Obesity is a hormonal dysregulation of fat accumulation. Calories are nothing more than the proximate cause of obesity. Obesity is a hormonal, not a caloric imbalance.”

“Once we understand that obesity is a hormonal imbalance, we can begin to treat it. If we believe that excess calories cause obesity, then the treatment is to reduce calories. But this method has been a complete failure. However, if too much insulin causes obesity, then it becomes clear we need to lower insulin levels.”

“Cortisol raises blood sugar, while insulin lowers it. Insulin resistance (discussed in depth in chapter 10) is crucial to the development of obesity. Insulin resistance leads directly to higher insulin levels, and increased insulin levels are a major driver of obesity. Multiple studies confirm that increasing cortisol increases insulin resistance.9,10,11”

“Therefore, the hormonal theory of obesity takes shape: chronically high cortisol raises insulin levels, which in turn leads to obesity.”

“Refined carbohydrates are easy to become addicted to and overeat precisely because there are no natural satiety hormones for refined carbs. The reason, of course, is that refined carbohydrates are not natural foods but are highly processed. Their toxicity lies in that processing. p101”

“Unfortunately, we spend obsessive amounts of time and energy trying to understand what we should be eating and devote virtually no time to when we should be eating. We are only seeing half the picture.”

“In 1960, we ate three meals a day. There wasn’t much obesity. In 2014, we eat six meals a day. There is an obesity epidemic. So, do you really think we should eat six meals day? While”

Part Four: The Social Phenomenon

Takeaways

• Newborn obesity is a growing problem, affecting 14 percent of babies born in the United States and more than 20 percent in some other countries.
• The causes of newborn obesity are not the same as those for adults. Newborns cannot eat too much or exercise too little.
• Insulin is the primary driver of weight gain, including in infants. High levels of insulin during pregnancy can lead to large babies and insulin resistance, which increases the risk of childhood and adult obesity.
• Previous attempts to prevent childhood obesity through caloric restriction and increased exercise have failed.
• Successful programs focus on reducing intake of sugar-sweetened beverages and snacks, as well as encouraging water and milk consumption.
• Reducing added sugars is an effective way to combat childhood obesity, as evidenced by a recent decrease in obesity rates for children aged two to five years.
• Dr. Benjamin Spock recommended reducing sugars and starchy foods for overweight children more than seventy years ago, but his advice was largely ignored in favor of caloric reduction and increased exercise.

Quotes

“BREAKFAST: THE MOST IMPORTANT MEAL TO SKIP?”

“So why are we unable to acknowledge the truth? Dr. Fung’s answer is simple: we doctors lie to ourselves. If type 2 diabetes is a curable disease but all our patients are getting worse on the treatments we prescribe, then we must be bad doctors. And since we did not study for so long at such great cost to become bad doctors, this failure cannot be our fault. Instead, we must believe we are doing the best for our patients, who must unfortunately be suffering from a chronically progressive and incurable disease. It is not a deliberate lie, Dr. Fung concludes, but one of cognitive dissonance—the inability to accept a blatant truth because accepting it would be too emotionally devastating.”

“The government is subsidizing, with our own tax dollars, the very foods that are making us obese. Obesity is effectively the result of government policy.”

Part Five: What's Wrong with Our Diet?

Takeaways

• The diet-heart hypothesis originated from observational studies that showed correlation between high cholesterol levels and heart disease, but failed to establish causation or identify the specific cause of elevated cholesterol.
• The Framingham Diet Study (1948-1970) found no association between dietary saturated fat intake and risk of heart disease. The study also found no relationship between percent of calories from fat and serum cholesterol levels, or ratio of plant to animal fat intake and serum cholesterol levels.
• Trans fats were introduced as a replacement for saturated fats in order to increase stability and shelf life. They have been linked to increased risk of heart disease and stroke.
• Recent research has shown that high dietary fat intake, especially saturated and monounsaturated fats, is not associated with obesity or weight gain. In fact, dietary fat may protect against obesity by decreasing glucose and insulin spikes when consumed with other foods.
• The low-fat paradigm has been a distraction in efforts to control obesity and improve overall health. The Women's Health Initiative Dietary Modification Trial (2001) failed to show any benefits of a low-fat, calorie-restricted diet in terms of weight loss, heart protection, cancer incidence, or stroke incidence.
• Key takeaways: 1. The diet-heart hypothesis originated from observational studies that showed correlation between high cholesterol levels and heart disease, but failed to establish causation or identify the specific cause of elevated cholesterol. 2. The Framingham Diet Study (1948-1970) found no association between dietary saturated fat intake and risk of heart disease. The study also found no relationship between percent of calories from fat and serum cholesterol levels, or ratio of plant to animal fat intake and serum cholesterol levels. 3. Trans fats were introduced as a replacement for saturated fats in order to increase stability and shelf life, but have been linked to increased risk of heart disease and stroke. 4. High dietary fat intake, especially saturated and monounsaturated fats, is not associated with obesity or weight gain. In fact, dietary fat may protect against obesity by decreasing glucose and insulin spikes when consumed with other foods. 5. The low-fat paradigm has been a distraction in efforts to control obesity and improve overall health. The Women's Health Initiative Dietary Modification Trial (2001) failed to show any benefits of a low-fat, calorie-restricted diet in terms of weight loss, heart protection, cancer incidence, or stroke incidence.
• Takeaways: 1. The diet-heart hypothesis originated from observational studies that showed correlation between high cholesterol levels and heart disease, but failed to establish causation or identify the specific cause of elevated cholesterol. 2. The Framingham Diet Study (1948-1970) found no association between dietary saturated fat intake and risk of heart disease. The study also found no relationship between percent of calories from fat and serum cholesterol levels, or ratio of plant to animal fat intake and serum cholesterol levels. 3. Trans fats were introduced as a replacement for saturated fats in order to increase stability and shelf life, but have been linked to increased risk of heart disease and stroke. 4. High dietary fat intake, especially saturated and monounsaturated fats, is not associated with obesity or weight gain. In fact, dietary fat may protect against obesity by decreasing glucose and insulin spikes when consumed with other foods. 5. The low-fat paradigm has been a distraction in efforts to control obesity and improve overall health. The Women's Health Initiative Dietary Modification Trial (2001) failed to show any benefits of a low-fat, calorie-restricted diet in terms of weight loss, heart protection, cancer incidence, or stroke incidence.

Quotes

“IF YOU WANT to avoid weight gain, remove all added sugars from your diet. On”

“that drinking diet soda was associated with a 43 percent increase in risk of vascular events (strokes and heart attacks). The 2008 Atherosclerosis Risk in Communities Study (ARIC)10 found a 34 percent increased incidence of metabolic syndrome in diet soda users, which is consistent with data from the 2007 Framingham Heart Study,11 which showed a 50 percent higher incidence of metabolic syndrome. In 2014, Dr. Ankur Vyas from the University of Iowa Hospitals and Clinics 12 presented a study following 59,614 women over 8.7 years in the Women’s Health Initiative Observational Study. The study found a 30 percent increase risk of cardiovascular events (heart attacks and”

“Type 2 diabetics drinking two tablespoons of apple cider vinegar diluted in water at bedtime reduced their fasting morning blood sugars.32 Higher doses of vinegar also seem to increase satiety, resulting in slightly lower caloric intake through the rest of the day (approximately 200 to 275 calories less). This effect was also noted for peanut products. Interestingly, peanuts also resulted in a reduction of glycemic response by 55 per cent.”

“Simplistic arguments that “Carbs make you fat!” or “Calories make you fat!” or “Red meat makes you fat!” or “Sugar makes you fat!” do not fully capture the complexity of human obesity. The”

“Even the National Cholesterol Education Program admits, “The percentage of total fat in the diet, independent of caloric intake, has not been documented to be related to body weight.”

Part Six: The Solution

Takeaways

• Obesity is a hormonal imbalance, specifically an insulin imbalance.
• Insulin resistance leads to weight gain and metabolic syndrome.
• Caloric reduction alone does not address the root cause of obesity.
• Fasting increases insulin sensitivity and reduces insulin resistance.
• Fasting can be done safely and effectively for weight loss.
• Intermittent fasting is effective when combined with caloric reduction.
• Fasting saves time, money, and simplifies food choices.
• Regular fasting has been practiced throughout history and across cultures.
• Incorporating intermittent fasting into your lifestyle is achievable and beneficial.

Quotes

“THERE ARE TWO prominent findings from all the dietary studies done over the years. First: all diets work. Second: all diets fail.”

“Too often, our current model of obesity assumes that there is only one single true cause, and that all others are pretenders to the throne. Endless debates ensue. Too many calories cause obesity. No, too many carbohydrates. No, too much saturated fat. No, too much red meat. No, too much processed foods. No, too much high fat dairy. No, too much wheat. No, too much sugar. No, too much highly palatable foods. No, too much eating out. It goes on and on. They are all partially correct.”

“Let’s face the truth. Low-calorie diets have been tried again and again and again. They fail every single time.”

“Obesity is a hormonal disorder of fat regulation. Insulin is the major hormone that drives weight gain, so the rational therapy is to lower insulin levels.”

“STEP 1: REDUCE YOUR CONSUMPTION OF ADDED SUGARS”

“The healthy snack is one of the greatest weight-loss deceptions. The myth that ‘grazing is healthy’ has attained legendary status. If we were meant to ‘graze,’ we would be cows. Grazing is the direct opposite of virtually all food traditions. Even as recently as the 1960s, most people still ate just three meals per day. Constant stimulation of insulin eventually leads to insulin resistance. (For”

“There’s a simple answer to the question of what to eat at snack time. Nothing. Don’t eat snacks. Period. Simplify your life.”

“Coffee, even the decaffeinated version, appears to protect against type 2 diabetes. In a 2009 review, each additional daily cup of coffee lowered the risk of diabetes by 7 percent, even up to six cups per day.23”

“STEP 2: REDUCE YOUR CONSUMPTION OF REFINED GRAINS”

“If you reduce your consumption of flour and refined grains, you will substantially improve your weight-loss potential. White”

“the toxicity in much Western food lies in the processing, rather than in the food itself. The carbohydrates in Western diets are heavily skewed toward refined grains, and are thus highly obesogenic. Eggplant, kale, spinach, carrots, broccoli, peas, Brussels sprouts, tomatoes, asparagus, bell peppers, zucchini, cauliflower, avocados, lettuce, beets, cucumbers, watercress, cabbage, among others, are all extremely healthy carbohydrate-containing foods.”

“STEP 3: MODERATE YOUR PROTEIN CONSUMPTION”

“THE LAST PIECE OF THE PUZZLE THERE ARE FIVE basic steps in weight loss: Reduce your consumption of added sugars. Reduced your consumption of refined grains. Moderate your protein intake. Increase your consumption of natural fats. Increase your consumption of fiber and vinegar.”

“Paracelsus (1493–1541), the founder of toxicology and one of the three fathers of modern Western medicine (along with Hippocrates and Galen), wrote, ‘Fasting is the greatest remedy—the physician within.’ Benjamin Franklin (1706–90), one of America’s founding fathers and renowned for wide knowledge, once wrote of fasting, ‘The best of all medicines is resting and fasting.”

“GLUCOSE AND FAT are the body’s main sources of energy. When glucose is not available, then the body adjusts by using fat, without any health detriment.”

“The transition from the fed state to the fasted state occurs in several stages:3 1.Feeding: During meals, insulin levels are raised. This allows glucose uptake by tissues such as the muscle or brain for direct use as energy. Excess glucose is stored as glycogen in the liver. 2.The post-absorptive phase (six to twenty-four hours after fasting starts): Insulin levels begin to fall. The breakdown of glycogen releases glucose for energy. Glycogen stores last for roughly twenty-four hours. 3.Gluconeogenesis (twenty-four hours to two days): The liver manufactures new glucose from amino acids and glycerol. In non-diabetic persons, glucose levels fall but stay within the normal range. 4.Ketosis (one to three days after fasting starts): The storage form of fat, triglycerides, is broken into the glycerol backbone and three fatty acid chains. Glycerol is used for gluconeogenesis. Fatty acids may be used directly for energy by many tissues in the body, but not the brain. Ketone bodies, capable of crossing the blood-brain barrier, are produced from fatty acids for use by the brain. Ketones can supply up to 75 percent of the energy used by the brain.4 The two major types of ketones produced are beta hydroxybutyrate and acetoacetate, which can increase more than seventy-fold during fasting.5 5.Protein conservation phase (after five days): High levels of growth hormone maintain muscle mass and lean tissues. The energy for maintenance of basal metabolism is almost entirely met by the use of free fatty acids and ketones. Increased norepinephrine (adrenalin) levels prevent the decrease in metabolic rate.”

“Regular fasting, by routinely lowering insulin levels, has been shown to significantly improve insulin sensitivity.8 This finding is the missing piece in the weight-loss puzzle.”

“There are, in fact, no species of animal, humans included, that have evolved to require three meals a day, everyday.”

“This is the ancient secret. This is the cycle of life. Fasting follows feasting. Feasting follows fasting. Diets must be intermittent, not steady. Food is a celebration of life. Every single culture in the world celebrates with large feasts. That’s normal, and it’s good. However, religion has always reminded us that we must balance our feasting with periods of fasting—“atonement,” “repentance” or “cleansing.” These ideas are ancient and time-tested. Should you eat lots of food on your birthday? Absolutely. Should you eat lots of food at a wedding? Absolutely. These are times to celebrate and indulge. But there is also a time to fast. We cannot change this cycle of life. We cannot feast all the time. We cannot fast all the time. It won’t work. It doesn’t work.”

“Fasting carries significant health benefits. Metabolism increases, energy increases and blood sugars decrease. The only remaining question is this: Can you do it? I hear this one all the time. Absolutely, 100 percent yes. In fact, fasting has been a part of human culture since the dawn of our species.”

Appendix A: Meal Plans

Takeaways

• Follow a 7-day meal plan for either 24-hour or 36-hour fasting protocols.
• Refrain from snacking completely during the fasting periods.

Monday:

• FAST DAY: Drink water and coffee, have a Western omelet or All-Bran Buds with milk for breakfast. Consume vegetable broth and green tea for lunch. Have herbed chicken and green beans or ginger chicken lettuce cups and stir-fried vegetables for dinner.
• Non-FAST DAY: Eat normally.

Tuesday:

• FAST DAY: Drink water and coffee, have a green apple or mixed berries for breakfast. Consume vegetable broth and green tea for lunch. Have ginger chicken lettuce cups and stir-fried vegetables or grilled chicken salad for dinner.
• Non-FAST DAY: Eat normally.

Wednesday:

• FAST DAY: Drink water and coffee, have a fast day with only water and coffee for all meals.
• Non-FAST DAY: Eat normally.

Thursday:

• FAST DAY: Drink water and coffee, have two eggs, bacon, or steel-cut oatmeal for breakfast. Consume chicken broth and green tea for lunch. Have mixed green vegetables sautéed in olive oil and grilled salmon with horseradish sauce for dinner.
• Non-FAST DAY: Eat normally.

Friday:

• FAST DAY: Drink water and coffee, have a Western omelet or All-Bran Buds with milk for breakfast. Consume chicken broth and green tea for lunch. Have Indian chicken curry and cauliflower or peppered steak and baby bok choy stir-fry for dinner.
• Non-FAST DAY: Eat normally.

Saturday:

• FAST DAY: Drink water and coffee, have a green apple or none for breakfast. Consume vegetable broth and green tea for lunch. Have asparagus or seasonal fruits for dinner.
• Non-FAST DAY: Eat normally.

Sunday:

• FAST DAY: Drink water and coffee, have a fast day with only water and coffee for all meals.
• Non-FAST DAY: Eat normally.

Appendix B: Fasting: A Practical Guide

Takeaways

• Intermittent fasting involves alternating periods of eating and fasting.
• It can help improve metabolic health, aid weight loss, and enhance cognitive function.
• Fasting is safe for most people, but those with certain medical conditions should consult their healthcare provider before trying it.
• During a fast, drink plenty of water, stay busy, and avoid binge eating on non-fasting days.
• Adjust your fasting schedule to fit your lifestyle.
• Weight loss varies from person to person, and plateaus may occur, but changing the fasting protocol can help break through them.
• Bone broth is a good source of nutrients during a fast and can be made by simmering vegetables and bones in water for several hours.

Appendix C: Meditation and Sleep Hygiene to Reduce Cortisol

Takeaways

• Reduce stress and cortisol levels for weight loss through active methods like meditation, regular exercise, social connectivity, and stress management techniques.
• Meditation practices, such as mindfulness meditation, help become more aware of thoughts and alleviate stress by practicing being present.
• Body awareness during meditation involves finding a quiet location, sitting comfortably, focusing on breath, and gently bringing focus back to the body and breath when thoughts wander.
• Good sleep hygiene practices include sleeping in complete darkness, wearing loose fitting clothes, keeping regular sleeping hours, aiming for 7-9 hours of sleep per night, seeing natural light first thing in the morning, keeping bedroom cool, and avoiding TV in the bedroom.

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