The Obesity Code : Unlocking The Secret Of Weight Loss - Jason Fung

The Obesity Code : Unlocking The Secret Of Weight Loss

Why we need a new framework for the understanding and treatment of obesity

The art of medicine is quite peculiar. Once in a while, medical treatments become established, that doesn’t really work. Through sheer inertia, these treatments get handed down from one generation of doctors to the next and survive for a surprisingly long time, despite their lack of effectiveness. Consider the medicinal use of leeches (bleeding) or, say, routine tonsillectomy.

Unfortunately, the treatment of obesity is also one such example. Obesity is defined in terms of a person’s body mass index, calculated as a person’s weight in kilograms divided by the square of their height in meters. A body mass index greater than 30 is defined as obese. For more than thirty years, doctors have recommended a low – fat, calorie – reduced diet as the treatment of choice for obesity. Yet the obesity epidemic accelerates. From 1985 to 2011, the prevalence of obesity in Canada tripled, from 6 % to 18 %.

This phenomenon is not unique to North America but involves most of the nations of the world. Virtually every person who has used caloric reduction for weight loss has failed. And, really, who hasn’t tried it? By every objective measure, this treatment is completely and utterly ineffective. Yet it remains the treatment of choice, defended vigorously by nutritional authorities.

The need to treat obesity prompted the author to establish the Intensive Dietary Management Clinic in Toronto, Canada. The conventional view of obesity as a caloric imbalance did not make sense. Caloric reduction had been prescribed for the last fifty years with startling ineffectiveness.

Reading books on nutrition was of no help. That was mostly a game of “he said, she said,” with many quoting “authoritative” doctors. For example, Dr. Dean Ornish says that dietary fat is bad, and carbohydrates are good. He is a respected doctor, so we should listen to him. But Dr. Robert Atkins said dietary fat is good and carbohydrates are bad. He was also a respected doctor, so we should listen to him. Who is right? Who is wrong?

To discover the answers, we need to turn to evidence-based medicine rather than vague opinion. Literally, thousands of books are devoted to dieting and weight loss, usually written by doctors, nutritionists, personal trainers, and other “health experts.” However, with a few exceptions, rarely is more than a cursory thought spared for the actual causes of obesity. What makes us gain weight? Why do we get fat?

The major problem is the complete lack of a theoretical framework for understanding obesity. Current theories are ridiculously simplistic, often taking only one factor into account:
• Excess calories cause obesity.
• Excess carbohydrates cause obesity.
• Excess meat consumption causes obesity.
• Excess dietary fat causes obesity.
• Too little exercise causes obesity.

But all chronic diseases are multifactorial, and these factors are not mutually exclusive. They may all contribute to varying degrees. For example, heart disease has numerous contributing factors—family history, gender, smoking, diabetes, high cholesterol, high blood pressure, and a lack of physical activity, to name only a few—and that fact is well accepted. But such is not the case in obesity research.

The process of challenging current nutritional dogma is, at times, unsettling, but the health consequences are too important to ignore. What actually causes weight gain, and what can we do about it? This question is the overall theme of this book. A fresh framework for the understanding and treatment of obesity represents a new hope for a healthier future.

Our entire understanding of obesity is fundamentally flawed

Why are there doctors who are fat? Accepted as authorities in human physiology, doctors should be true experts on the causes and treatments of obesity. Most doctors are also very hardworking and self-disciplined. Since nobody wants to be fat, doctors, in particular, should have both the knowledge and dedication to stay thin and healthy.

So why are there fat doctors?

The standard prescription for weight loss is “Eat Less, Move More.” It sounds perfectly reasonable. But why doesn’t it work? Perhaps people wanting to lose weight are not following this advice. The mind is willing, but the flesh is weak.

Yet consider the self-discipline and dedication needed to complete an undergraduate degree, medical school, internship, residency, and fellowship. It is hardly conceivable that overweight doctors simply lack the willpower to follow their own advice.

This leaves the possibility that the conventional advice is simply wrong. And if it is, then our entire understanding of obesity is fundamentally flawed.

We must start with the most critical question regarding obesity or any disease: “What causes it?” We spend no time considering this crucial question because we think we already know the answer. It seems so obvious: it’s a matter of Calories In versus Calories Out.

A calorie is a unit of food energy used by the body for various functions such as breathing, building new muscle and bone, pumping blood, and other metabolic tasks. Some food energy is stored as fat. Calories in is the food energy that we eat. Calories Out is the energy expended for all of these various metabolic functions.

When the number of calories we take in exceeds the number of calories we burn, weight gain results, we say. Eating too much and exercising too little causes weight gain, we say. Eating too many calories causes weight gain, we say. These “truths” seem so self-evident that we do not question whether they are actually true. But are they?

We weren’t always so obsessed with calories. 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 civilizations developed, obesity followed. Speculating on the cause, many identified the refined carbohydrates of sugar and starches.

Jean Anthelme Brillat-Savarin (1755-1826) wrote an influential textbook, “The Physiology of Taste”, in 1825. There he wrote: “The second of the chief causes of obesity is the floury and starchy substances which man makes the prime ingredients of his daily nourishment.”

By the 1950s, diets low in refined carbohydrates were accepted as the standard treatment for obesity.

If you were to ask your grandparents what caused obesity, they would not talk about calories. Instead, they would tell you to stop eating sugary and starchy foods. Common sense and empirical observation served to confirm the truth. Nutritional “experts” and government opinions were not needed.

Calorie counting had begun in the early 1900s with the book “Eat Your Way to Health”, written by Dr. Robert Hugh Rose as a “scientific system of weight control.” That book was followed up in 1918 with the bestseller Diet and Health, with Key to the Calories, written by Dr. Lulu Hunt Peters, an American doctor and newspaper columnist.

Herbert Hoover, then the head of the U.S. Food Administration, converted to calorie counting. Dr. Peters advised patients to start with a fast, one to two days abstaining from all foods, and then stick strictly to 1200 calories per day. While the advice to fast was quickly forgotten, modern calorie-counting schedules are not very different.

The Calorie Reduction Error

Traditionally, obesity has been seen as a result of how people process calories, that is, that a person’s weight could be predicted by a simple equation:

Calories In – Calories Out = Body Fat

This key equation perpetuates what the author calls the calorie deception. It is dangerous precisely because it appears so simple and intuitive. But what you need to understand is that many false assumptions are built in.

Assumption 1: Calories in and calories out are independent of each other

This assumption is a crucial mistake. Experiments and experience have proven this assumption false. Caloric intake and expenditure are intimately dependent variables. Decreasing Calories In triggers a decrease in Calories Out. A 30 % reduction in caloric intake results in a 30 % decrease in caloric expenditure. The end result is minimal weight loss.

Assumption 2: Basal metabolic rate is stable

We obsess about caloric intake with barely a thought for caloric expenditure, except for exercise. Measuring caloric intake is simple, but measuring the body’s total energy expenditure is complicated. Therefore, the simple but completely erroneous assumption is made that energy expenditure remains constant except for exercise.

Total energy expenditure is the sum of basal metabolic rate, the thermogenic effect of food, nonexercise activity thermogenesis, excess post-exercise oxygen consumption, and exercise. The total energy expenditure can go up or down by as much as 50 %, depending upon the caloric intake as well as other factors.

Assumption 3: Fat stores are essentially unregulated

Every single system in the body is regulated. Growth in height is regulated by growth hormone. Blood sugars are regulated by the hormones insulin and glucagon, among others. Sexual maturation is regulated by testosterone and estrogen. Body temperature is regulated by a thyroid-stimulating hormone and free thyroxine. The list is endless.

We are asked to believe, however, that the growth of fat cells is essentially unregulated. The simple act of eating, without any interference from any hormones, will result in fat growth. Extra calories are dumped into fat cells like doorknobs into a sack.

This assumption is false.

Assumption 4: A calorie is a calorie

This assumption is the most dangerous of all. “A calorie is a calorie” implies that the only important variable in weight gain is the total caloric intake, and thus, all foods can be reduced to their caloric energy. But does a calorie of olive oil cause the same metabolic response as a calorie of sugar? The answer is, obviously, no. These two foods have many easily measurable differences. Sugar will increase the blood glucose level and provoke an insulin response from the pancreas. Olive oil will not. When olive oil is absorbed by the small intestine and transported to the liver, there is no significant increase in blood glucose or insulin. The two different foods evoke vastly different metabolic and hormonal responses.

Insulin Can Make You Fat

You can become fat. How? By prescribing insulin. It won’t matter if you have willpower, or that you exercise. It won’t matter what you choose to eat. You will get fat. It’s simply a matter of enough insulin and enough time.

High insulin secretion has long been associated with obesity: obese people secrete much higher levels of insulin than do those of normal weight. Also, in lean subjects, insulin levels quickly return to baseline after a meal, but in the obese, these levels remain elevated.

Insulin levels are almost 20% higher in obese subjects, and these elevated levels are strongly correlated to important indices such as waist circumference and waist/hip ratio. The close association between insulin levels and obesity certainly suggests — but does not prove — the causal nature of this relationship.

Insulin levels can be difficult to measure since levels fluctuate widely throughout the day in response to food. It is possible to measure an “average” level, but doing so requires multiple measurements throughout the day.

Fasting insulin levels (measured after an overnight fast) are a simpler, one-step measurement. Sure enough, research reveals a close association between high fasting insulin levels and obesity, and this relationship becomes even stronger when we consider only a person’s fat mass rather than his or her total weight. In a San Antonio Heart Study, high fasting insulin was tightly correlated to weight gain over eight years of follow up.

A 2005 case study describes a 21-old woman diagnosed with insulinoma. She had gained 25 pounds over the year before her diagnosis. Increased caloric intake did not account for the weight gain. Reduced caloric intake did not account for the weight loss. The defining element was insulin: its rise and fall corresponded to the rise and fall in weight.

If insulin causes weight gain, does lowering its levels have the opposite effect? As insulin is reduced to very low levels, we should expect significant and severe weight loss. The SGLT-2 (sodium-glucose linked transporter) inhibitors, which lower glucose and insulin, are an example of the effect that lowering insulin may have on weight (albeit in their case, the effect is mild). Another more dramatic example is untreated type 1 diabetic patient.

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.

Insulin levels go waaayyy down. Patients lose a lot of weight. In the type 1 diabetic community, there is a disorder called “diabulimia.”

Today, type 1 diabetic patients are treated by daily injections of insulin. There are some patients who wish to lose weight for cosmetic reasons. Diabulimia is the deliberate under-dosing of insulin for the purpose of immediate and substantial weight loss. It is extremely dangerous and certainly not advisable.

However, the practice persists because it is an extremely effective form of weight loss. Insulin levels go down. Weight is lost.

Cortisol Can Make You Fat

How? If you get a prescription for prednisone, a synthetic version of the human hormone cortisol. Prednisone is used to treat many diseases, including asthma, rheumatoid arthritis, lupus, psoriasis, inflammatory bowel disease, cancer, glomerulonephritis, and myasthenia gravis.

And what is one of the most consistent effects of prednisone? Like insulin, it makes you fat. Not coincidentally, both insulin and cortisol play a key role in carbohydrate metabolism. Prolonged cortisol stimulation will raise glucose levels and, subsequently, insulin. This increase in insulin plays a substantial role in the resulting weight gain.

Cortisol is the so-called stress hormone, which mediates the flight-or-fight response, a set of physiological responses to perceived threats. Cortisol, part of a class of steroid hormones called glucocorticoids (glucose + cortex + steroid), is produced in the adrenal cortex. In Paleolithic times, the stress that led to a release of cortisol was often physical: for instance, being chased by a predator.

Cortisol is essential in preparing our bodies for action — to fight or flee. Once released, cortisol substantially enhances glucose availability, which provides energy for muscles — very necessary in helping us to run and avoid being eaten. All available energy is directed toward surviving the stressful event.

And that’s the point: the body is well adapted to a short-term increase in cortisol and glucose levels. Over the long term, however, a problem arises.

It is helpful to look at what happens to people with certain diseases, particularly Cushing’s disease or Cushing’s syndrome, which is characterized by long-term excessive cortisol production. In up to one-third of Cushing’s cases, high blood sugars and overt diabetes are also present. But the hallmark of Cushing’s syndrome, even in people with mild forms, is weight gain. In one case series, 97 % of patients show abdominal weight gain, and 94 % showed increased body weight.

Patients gain weight no matter how little they eat and no matter how much they exercise. Any disease that causes excess cortisol secretion results in weight gain. Cortisol causes weight gain. However, there’s evidence of the association between cortisol and weight gain, even in people who don’t have Cushing’s syndrome.

In a random sample from north Glasgow, Scotland, cortisol-excretion rates were strongly correlated to body mass index and waist measurements. Higher cortisol levels were seen in heavier people. Cortisol – related weight gain, particularly abdominal fat deposits, results in an increased waist-to-hip ratio. (This effect is significant because abdominal fat deposits are more dangerous to health than all-over weight gain.)

How do we develop insulin resistance?

The human body is characterized by the fundamental biological principle of homeostasis. If things change in one direction, the body reacts by changing in the opposite direction to return closer to its original state. For instance, if we become very cold, the body adapts by increasing body-heat generation. If we become very hot, the body sweats to try to cool itself. Adaptability is a prerequisite for survival and generally holds true for all biological systems. In other words, the body develops resistance. The body resists changes out of its comfort range by adapting to it.

What happens in the case of insulin resistance? A hormone acts on a cell as a key that fits into a lock. When insulin (the key) no longer fits into the receptor (the lock), the cell is called insulin resistant. Because the fit is poor, the door does not open fully. As a result, less glucose enters. The cell senses that there is too little glucose inside. Instead, glucose is piling up outside the door. Starved for glucose, the cell demands more. To compensate, the body produces extra keys (insulin). The fit is still poor, but more doors are opened, allowing a normal amount of glucose to enter.

Suppose that in the normal situation, we produce ten keys (insulin). Each key opens a locked door that lets two glucose molecules inside. With ten keys, twenty glucose molecules enter the cell. Under conditions of resistance, the key does not fully open the locked door. Only one glucose molecule is allowed in.

With ten keys, only ten glucose molecules are allowed in. To compensate, we now produce a total of twenty keys. Now, twenty glucose molecules are allowed in, but only because we have increased the number of keys. As we develop insulin resistance, our bodies increase our insulin levels to get the same result — glucose in the cell. However, we pay the price in constantly elevated insulin levels.

Why do we care? Because insulin resistance leads to high insulin levels, and as we’ve seen, high insulin levels cause obesity.

But what caused the insulin resistance in the first place? Does the problem lie with the key (insulin) or the lock (insulin receptor)? Insulin is the same hormone, whether found in an obese or a lean person. There is no difference in amino – acid sequence or any other measurable quality. Therefore, the problem of insulin resistance must lie with the receptor. The insulin receptor does not respond properly and locks the glucose out of the cell. But why?

To begin solving this puzzle, let us back up and look for clues from other biological systems.

Antibiotic resistance

When new antibiotics are introduced, they kill virtually all the bacteria they’re designed to kill. Over time, some bacteria develop the ability to survive high doses of these antibiotics. They’ve become drug-resistant “superbugs,” and infections from them are difficult to treat and can sometimes lead to death. Superbug infections are a large and growing problem in many urban hospitals worldwide. All antibiotics have begun to lose their effectiveness due to resistance.

Insulin causes insulin resistance

If insulin resistance is similar to this form of resistance, the first thing to look at is high, persistent levels of insulin itself. If we increase insulin levels, do we get insulin resistance? That’s an easy hypothesis to test — and luckily, studies have already been conducted on it.

A 1993 study measured this effect. Patients were started on intensive insulin treatment. In six months, they went from no insulin to 100 units a day on average. Their blood sugars were very, very well controlled. But the more insulin they took, the more insulin resistance they got — a direct causal relationship, as inseparable as a shadow is from a body.

Even as their sugars got better, their diabetes was getting worse! These patients also gained an average of approximately 19 pounds (8.7 kilograms), despite reducing their calorie intake by 300 calories per day. It didn’t matter. Not only does insulin cause insulin resistance, but it also causes weight gain.

Is breakfast the most important meal to skip?

The majority of Americans identify breakfast as the most important meal of the day. Eating a hearty breakfast is considered a cornerstone of a healthy diet.

Skipping it, we are told, will make us ravenously hungry and prone to overeat for the rest of the day. Although we think it’s a universal truth, it’s really only a North American custom. Many people in France (a famously skinny nation) drink coffee in the morning and skip breakfast. The French term for breakfast, petit déjeuner (little lunch), implicitly acknowledges that this meal should be kept small.

It is simply not necessary to eat the minute we wake up. We imagine the need to “fuel up” for the day ahead. However, our body has already done that automatically. Every morning, just before we wake up, a natural circadian rhythm jolts our bodies with a heady mix of growth hormone, cortisol, epinephrine, and norepinephrine (adrenaline). This cocktail stimulates the liver to make new glucose, essentially giving us a shot of the good stuff to wake us up.

This effect is called the dawn phenomenon, and it has been well described for decades. Many people are not hungry in the morning. The natural cortisol and adrenaline released to stimulate a mild flight-or-fight response, which activates the sympathetic nervous system. Our bodies are gearing up for action in the morning, not for eating. All these hormones release glucose into the blood for quick energy. We’re already gassed up and ready to go. There is simply no need to refuel with sugary cereals and bagels. Morning hunger is often a behavior learned over decades, starting in childhood.

The word breakfast literally means the meal that breaks our fast, which is the period when we are sleeping and, therefore, not eating. If we eat our first meal at 12 noon, then grilled salmon salad will be our “breakfast” meal — and there’s nothing wrong with that.

A large breakfast is thought to reduce food intake throughout the rest of the day. However, such does not always seem to be the case. Studies show that lunch and dinner portions tend to stay constant, regardless of the number of calories taken at breakfast. The more one eats at breakfast, the higher the total caloric intake over the entire day. Worse, taking breakfast increases the number of eating opportunities in a day. Breakfast eaters, therefore, tend to eat more and eat more often — a deadly combination.

Furthermore, many people confess that they are not hungry first thing in the morning and force themselves to eat only because they feel that doing so is the healthy choice. As ridiculous as it sounds, many people force themselves to eat more in an effort to lose weight. In 2014, a sixteen-week randomized controlled trial of breakfast eating found that “contrary to widely espoused views this had no discernible effect on weight loss.”

There are some common sense questions you can ask yourself about breakfast. Are you hungry at breakfast? If not, listen to your body and don’t eat. Does breakfast make you hungry? If you eat a slice of toast and drink a glass of orange juice in the morning — are you hungry an hour later? If so, then don’t eat breakfast. If you are hungry and want to eat breakfast, then do so. But avoid sugars and refined carbohydrates. Skipping breakfast does not give you the freedom to eat a Krispy Kreme donut as a mid-morning snack, either.

Obesity is no longer just for adults

During the years 1977 to 2000, the prevalence of childhood obesity has skyrocketed in every age category. Obesity in children aged six to eleven increased from 7% to 15.3%. For children aged twelve to nineteen, it more than tripled, from 5% to 15.5%. Obesity-related diseases such as type 2 diabetes and high blood pressure, previously rare in children, are becoming more common. Obesity has metastasized from being solely an adult concern to being a pediatric one too.

Childhood obesity also leads to adult obesity and future health problems, particularly cardiovascular issues. The Bogalusa Heart Study concluded, “childhood obesity tracked into young adulthood,” which is obvious to almost everybody. Childhood obesity is a predictor of increased mortality, but, most importantly, also a reversible risk factor. Overweight children who became normal weight as adults have the same mortality risk as those who have never been overweight.

Obesity has begun to afflict younger and younger children. In one study covering a twenty-two-year period ending in 2001, children of all ages show an increased prevalence of obesity, even in the zero-to six-month-old age range.

That finding is especially interesting. Conventional calorie – based theories of obesity are unable to explain this trend. Obesity is considered an energy-balance problem, one of eating too much or exercising too little. Since six-month-olds eat on demand and are often breastfed, it is impossible that they eat too much.

Since six-month-olds do not walk, it is impossible that they exercise too little. Similarly, birth weight has increased by as much as half a pound (200 grams) over the last twenty-five years. The newborn cannot eat too much or exercise too little.

What is going on here?

It’s insulin.

The answer is simpler once we understand the hormonal obesity theory. Insulin is the major hormonal driver of weight gain. Insulin causes adult obesity. Insulin causes newborn obesity. Insulin causes infant obesity. Insulin causes childhood obesity. Where would an infant get high insulin levels? From his or her mother.

Dr. David Ludwig recently examined the relationship between the weights of 513,501 women and their 1,164,750 offspring.9 Increased maternal weight gain is strongly associated with increased neonatal weight gain. Because both the mother and the fetus share the same blood supply, any hormonal imbalances, such as high insulin levels, are automatically and directly transmitted through the placenta from the mother to the growing fetus.

The logical consequence of too much insulin in the newborn is the development of insulin resistance, which leads to even higher levels of insulin in a classic vicious cycle. The high insulin levels produce obesity in the newborn as well as the six-month-old infant. The origins of both infant obesity and adult obesity are the same: insulin. These are not two separate diseases, but two sides of the same coin. Babies born to mothers with gestational diabetes mellitus have three times the risk of obesity and diabetes in later life, and one of the biggest risk factors for obesity in young adulthood is obesity in childhood.

Those who are obese in childhood have more than seventeen times the risk of obesity going into adulthood! Even large-for-gestational-age babies whose mothers do not have gestational diabetes are also at risk. They have double the risk of metabolic syndrome.

The sad but inescapable conclusion is that we are now passing on our obesity to our children. Why? Because we are now marinating our children in insulin starting in the womb, they develop more severe obesity sooner than ever before. Because obesity is time-dependent and gets worse, fat babies become fat children. Fat children become fat adults. And fat adults have fat babies in turn, passing obesity on to the next generation.

What to eat to lower insulin levels, the chief hormone that drives weight gain

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. There are multiple ways to achieve this, and we should take advantage of each one. The following is a step-by-step approach to accomplish this goal.

Step 1: Reduce your consumption of added sugars

Sugar stimulates insulin secretion, but it is far more sinister than that. Sugar is particularly fattening because it increases insulin both immediately and over the long term. Sugar is comprised of equal amounts of glucose and fructose, and fructose contributes directly to insulin resistance in the liver. Over time, insulin resistance leads to higher insulin levels.

Therefore, sucrose and high fructose corn syrup are exceptionally fattening, far in excess of other foods. Sugar is uniquely fattening because it directly produces insulin resistance. With no redeeming nutritional qualities, added sugars are usually one of the first foods to be eliminated in any diet.

Many natural, unprocessed whole foods contain sugar. For example, fruit contains fructose, and milk contains lactose. Naturally occurring and added sugars are distinct from one another. The two key differences between them are amount and concentration.

Obviously, first, you should remove your sugar bowl from your table. There is no reason to add sugar to any food or beverage. But sugars are often hidden in the preparation of food, which means that avoiding sugar is often difficult, and you can ingest a surprisingly large amount without knowing it. Sugars are often added to foods during processing or cooking, which presents dieters with several potential pitfalls. First, sugars may be added in unlimited amounts. Second, sugar may be present in processed food in much higher concentrations than in natural foods. Some processed foods are virtually 100 % sugar.

This condition almost does not exist in natural foods, with honey possibly being the exception. Candy is often little more than flavored sugar. Third, sugar may be ingested by itself, which may cause people to overeat sugary treats, as there is nothing else within the food to make you “full.” There is often no dietary fiber to help offset the harmful effects. For these reasons, we direct most of our efforts toward reducing added, rather than natural sugars in our diet.

Step 2: Reduce your consumption of refined grains

Refined grains such as white flour stimulate insulin to a greater degree than virtually any other food. If you reduce your consumption of flour and refined grains, you will substantially improve your weight loss potential. White flour, being nutritionally bankrupt, can be safely reduced or even eliminated from your diet. Enriched white flours have had all their nutrients stripped out during processing and later added back to retain a veneer of healthiness.

Avoid processed bakery foods that are mostly flour and other starches: bread, bagels, English muffins, roti, naan bread, dinner rolls, breadsticks, Melba toast, crackers, tea biscuits, scones, tortillas, wraps, muffins, cookies, cakes, cupcakes, and donuts. Pasta and noodles of all varieties are also concentrated sources of refined carbohydrates; reduce these to a minimum. The whole-grain pasta that is now widely available is a better choice, though far from ideal.

Carbohydrates should be enjoyed in their natural, whole, unprocessed form.

Step 3: Moderate your protein consumption

In contrast to refined grains, protein cannot and should not be eliminated from your diet. Instead, moderate the amount of protein in your diet to fall within 20% to 30% of your total calories.

Step 4: Increase your consumption of natural fats

Of the three major macronutrients (carbohydrates, proteins, and fats), dietary fat is the least likely to stimulate insulin. Thus, dietary fat is not inherently fattening, but potentially protective. In choosing fats, strive for a higher proportion of natural fats. Natural, unprocessed fats include olive oil, butter, coconut oil, beef tallow, and leaf lard. The highly processed vegetable oils, high in inflammatory omega 6 fatty acids, may have some detrimental health effects.

Step 5: Increase your consumption of protective factors

Fiber can reduce the insulin – stimulating effects of carbohydrates, making it one of the main protective factors against obesity, but the average North American diet falls far short of recommended daily intakes. Numerous studies and observations have confirmed the weight-lowering effects of dietary fiber. Natural whole foods contain plenty of fiber, which is often removed during processing. Fruits, berries, vegetables, whole grains, flax seeds, chia seeds, beans, popcorn, nuts, oatmeal, and pumpkin seeds provide ample fiber.

The last piece of the puzzle.

There are five basic steps in weight loss:
1. Reduce your consumption of added sugars.
2. Reduced your consumption of refined grains.
3. Moderate your protein intake.
4. Increase your consumption of natural fats.
5. Increase your consumption of fiber and vinegar.

When it comes to the question of what to eat, you pretty much already knew the answer. Most diets very conspicuously resemble each other. There is far more agreement than discord. Eliminate sugars and refined grains. Eat more fiber. Eat vegetables. Eat organic. Eat more home-cooked meals. Avoid fast food. Eat whole unprocessed foods. Avoid artificial colors and flavors. Avoid processed or microwavable foods.

How to induce your body into a temporary state of very low insulin levels

Long-term dieting is futile. After the initial weight loss, the dreaded plateau appears, followed by the even more dreaded weight regain. The body reacts to weight loss by trying to return to its original body set weight. We hope our body set weight will decrease over time, but that hoped-for reduction does not materialize. Even if we eat all the right things, our insulin levels stay elevated.

But we’ve been addressing only half of the problem. Long-term weight loss is really a two-step process. Two major factors maintain our insulin at a high level. The first is the foods that we eat — which are what we usually change when we go on a diet. But we fail to address the other factor: the long-term problem of insulin resistance. This problem is one of meal timing.

Insulin resistance keeps our insulin levels high. High insulin maintains our high body set weight. Inexorably, our high body set weight erodes our weight loss efforts. We start feeling hungrier. Our metabolism (that is, our total energy expenditure) relentlessly decreases until it falls below the level of our energy intake. Our weight plateaus and ruthlessly climbs back up to our original body set weight, even as we keep dieting. Clearly, changing what we eat is not always enough.

To succeed, we must break the insulin-resistance cycle. But how? The body’s knee-jerk reaction to insulin resistance is to increase insulin levels, which, in turn, creates even more resistance. To break the insulin-resistance cycle, we must have recurrent periods of very low insulin levels. (Remember that resistance depends on having both persistent and high levels.) But how can we induce our body into a temporary state of very low insulin levels?

The answer we are looking for is, in a word, fasting.

When we talk about fasting to break insulin resistance and lose weight, we are talking about intermittent fasts of 24 to 36 hours.

Instead of searching for some exotic, never-seen-before diet miracle to help us break insulin resistance, let’s instead focus on a tried-and-true ancient healing tradition. Fasting is one of the oldest remedies in human history and has been part of the practice of virtually every culture and religion on earth.

Whenever fasting is mentioned, there is always the same eye-rolling response: Starvation? That’s the answer? No. Fasting is completely different. Starvation is the involuntary absence of food. It is neither deliberate nor controlled. Starving people have no idea when and where their next meal will come from. Fasting, however, is the voluntary abstinence from food for spiritual, health, or other reasons. Fasting may be done for any period of time, from a few hours to a few months. In a sense, fasting is part of everyday life. The term “breakfast” is the meal that breaks the fast — which we do daily.

How your hormones adapt to fasting?

1. Insulin.

Fasting is the most efficient and consistent strategy to decrease insulin levels, a fact first noted decades ago and widely accepted as true. All foods raise insulin; therefore, the most effective method of reducing insulin is to avoid all foods.

Regular fasting, by routinely lowering insulin levels, has been shown to improve insulin sensitivity significantly. This finding is the missing piece in the weight loss puzzle. Most diets restrict the intake of foods that cause increased insulin secretion but don’t address insulin resistance. You lose weight initially, but insulin resistance keeps your insulin levels and body set weight high. By fasting, you can efficiently reduce your body’s insulin resistance since it requires both persistent and high levels.

2. Growth hormone.

The growth hormone is known to increase the availability and utility of fats for fuel. It also helps to preserve muscle mass and bone density. Growth hormone secretion is difficult to measure accurately because of its intermittent release, but it decreases steadily with age. One of the most potent stimuli to growth hormone secretion is fasting. Over a 5-day fasting period, growth hormone secretion more than doubled. The net physiologic effect is to maintain muscle and bone tissue mass during the fasting period.

3. Adrenaline

Fasting increases adrenaline levels, starting at around 24 hours. 48 hours of fasting produces a 3.6% increase in metabolic rate, not the dreaded metabolic shutdown so often seen in caloric-reduction strategies. In response to a four – day fast, resting energy expenditure increased by up to 14%. Rather than slowing metabolism, the body revs it up instead. Presumably, it does this, so we have the energy to go out and find more food.

4. Electrolytes

Many people worry that fasting may cause malnutrition, but this concern is misplaced. The body’s fat stores are, for most of us, quite ample for our bodies’ needs. Even studies of prolonged fasting have found no evidence of malnutrition or micronutrient deficiency. Potassium levels may decrease slightly, but even two months of continuous fasting did not decrease levels below normal, even without the use of supplements. Note that this duration of fasting is far longer than is generally recommended without medical supervision.

Magnesium, calcium, and phosphorus levels during fasting are stable — presumably, because of the large stores of these minerals in the bones. Ninetynine % of the body’s calcium and phosphorus is stored in the bones. A multivitamin supplement will provide the recommended daily allowance of micronutrients.

Conclusion

If excessive stress and the cortisol response are causing obesity, then the treatment is to reduce stress, but that’s easier said than done. Removing yourself from stressful situations is important, but not always possible. Work and family demands won’t go away by themselves. Luckily, there are some time-tested methods of stress relief that can help us cope.

It’s a popular misconception that stress relief involves sitting in front of the television and doing nothing. In fact, you can’t relieve stress by doing nothing. Stress relief is an active process. Meditation, tai chi, yoga, religious practice, and massage are all good choices. Regular exercise is an excellent way to relieve stress and lower cortisol levels.

The following are simple but effective ways to improve sleep hygiene:
• Sleep in complete darkness.
• Sleep in loose-fitting clothes.
• Keep regular sleeping hours.
• Try to get seven to nine hours of sleep each night.
• See the light first thing in the morning.
• Keep your bedroom slightly cool.
• Do not keep a TV in your bedroom.