I found Fung’s online materials and was interested enough to grab this book. Basic concepts:

• obesity isn’t as simple as calories in / calories out
• nutritional advice is pretty much shit
• when to eat is just as important as what to eat
• fasting is good

Chapter 1

• Excess calories as a proximate cause of weight gain, not ultimate cause.
  • Proximate cause = what is immediately responsible
  • Ultimate cause = what started the chain of events

…the solution to the proximate cause of the problem is neither lasting nor meaningful. By contrast, treatment of the ultimate cause is far more successful.

• Obesity in human history

Individuals in traditional societies eating traditional diets seldom became obese, even in times of abundant food. As civilizations developed, obesity followed.

Mid 1800s - mid 1900s: “diets low in refined carbohydrates were accepted as the standard treament for obesity.”

Early 1900s: introduction of calorie counting as “a scientific system of weight control.”

1950s: the heart disease epidemic which was actually the “natural consequence of a longer life expectancy” ⮕ the demonization of dietary fat.

• 3 macronutrients: fat, protein, carbohydrates.
• In order to eat low fat, have to up the intake of protein and/or carbs. Much protein is also high in fat. Dilemma! What to eat on a low fat diet? Solution: forget worrying about carbohydrates, and focus on calories.

Without evidence or historical precedent, it was arbitrarily decided that excess calories caused weight gain, not specific foods.

• Continued debate over whether the main culprit of obesity and heart disease was dietary fat or sugar.

1977: the gov’t decided it was dietary fat. The Dietary Guidelines for Americans - now updated every 5 years - spawned the food pyramid - etc. Promoted lots of carbs and sugary things that are low in fat (recently, too; see the 1995 excerpt).

• sugar consumption increased
• refined grain consumption increased
• average fat intake decreased and the results:
• the incidence of heart disease did NOT decrease
• and the rate of obesity dramatically increased

Chapter 2

• Genetics and obesity
• There are certainly genetic characteristics that may lead to obesity but

…obesity has become rampant only since the 1970s. Our genes count not have changed within such a short time.

• Genetic versus environmental factors
  • Study of Danish adult adoptees found that the “environment provided by the adoptive parents was largely irrelevant”
  • and a “strong, consistent correlation” between the weight of biological parents and adoptees.
  • Final findings (other studies involved) - App. 70% of your tendency to gain weight is inherited - determined by parentage.
• However, since most of ‘the obesity epidemic’ materialized quickly (within a single generation) genetics cannot be the only factor. Clearly.
• The other factor: HORMONES, baby.

The hormonal profile of a baby is influenced by the environment in the mother’s body before birth, setting up a tendency for high insulin levels and associated obeisty later in life.

Chapter 3

• Calories in / calories out seems like a simple and reasonable equation but “is dangerous precisely because it appears so simple and intuitive.”
• False assumptions that fuck things up:
  • assumption 1: calories in and calories out are independent of each other
  • assumption 2: basal metabolic rate is stable
  • assumption 3: we exert conscious control over calories in
  • assumption 4: fat stores are essentially unregulated
  • assumption 5: a calorie is a calorie
• Calories = energy

There are an almost infinite number of ways that the body can dissipate excess energy instead of storing it as body fat. … The problem of fat accumulation is really a problem of distribution of energy.

Hormones tightly regulate every single system in the body.

• The problem with calorie reduction as a way to lose weight:

Reducing Calories In works only if Calories Out remains stable. What we find instead is that a sudden reduction of Calories In causes a similar reduction in Calories Out, and no weight is lost as the body balances its energy budget.

• Study (1919) - volunteers on ‘semi-starvation diets’ experienced a 30% decrease in total energy expenditure (calories out). Another study (1944-45, Dr. Ancel Keys) showed a 40% decrease in resting metabolic rate.
• The body is smart. The body wants to live. The body does not want to starve. So when caloric intake is reduced, the body adjusts to reduce caloric expenditure as well.
• Starvation mode…and it tends to last.

In response to caloric reduction, metabolism decreases almost immediately, and that decrease persists more or less indefinitely.

• So if you diet (caloric intake reduced) ⮕ your TEE goes down ⮕ you don’t lose weight ⮕ you quit dieting and re-up your caloric intake ⮕ but your TEE doesn’t adjust with it as ‘that decrease persists more or less indefinitely’ ⮕ so you gain more weight eating the same amount you did before the diet.

  • fuck that, man.

• The eat less / move more approach to weight loss (in short) does NOT work.

• Homeostasis

The defining characteristic of the human body is homeostasis, or adaptation to change. Our body deals with an ever-changing environment. In response, the body makes adjustments to minimize the effects of such changes and return to its original condition.

• Two major adaptations to caloric reduction:
  • dramatic reduction in TEE
  • hormonal signals change to stimulate hunger and decrease satiety
    • ghrelin (the hormone that makes us hungry) increased after weight loss… even after a year.
    • satiety hormones on the other hand were significantly lower
• The vicious cycle of under-eating:
  • we eat less, we lose some weight
  • our metabolism slows
  • our hunger increases
  • we gain weight back
  • we try to eat less again
  • and once again TEE decreases and hunger increases
  • and we gain weight back
  • and we finally give up
  • go back to old way of eating
  • and gain even more weight back than originally

Chapter 4

• Exercise has great health benefits but weight loss isn’t one of them
• Lots of data shows that physical activity has zero effect on obesity prevalence
• TEE (total energy expenditure) is not the same as exercise.
• Most of TEE is not exercise but is the basal metabolic rate.
• Basal metabolic rate is complex. Lots of factors. It does not stay stable.
• Just as decreasing caloriest in can reduce basal metabolic rate, increasing calories in can increase BMR.
• Lots of studies showing that increased exercise has little to no effect on loss of body fat or even body-fat percentage.
• Look once again at homeostasis - eg compensation:
  • we tend to eat more when we exercise more
  • people who exercise tend to do less movement at other times … because the body wants to be stable.

Chapter 5

• All calories are not created equal
• Overfeeding experiments = eating a lot of calories a day resulted in total energy expenditure ALSO going up… by 50%
  • after the experiment ended, the participants quickly and easily returned to normal weight
• The body is always trying to return to ‘normal’ and normal is whatever it was before things started to change.
• The “set point” for body weight and fatness

Homeostatic mechanisms defend this body set weight against changes, both up and down. Compensatory mechanisms start almost immediately and persist almost indefinitely.

• Obesity = the set point is too high.
• You gotta CHANGE THE THERMOSTAT SETTING. Okay great, how?

…identify the body’s homeostatic mechanism and adjust it downward…

• Leptin = the secret magical satiety factor to signal out reduction in appetite, increase in metabolism etc

The vast majority of obese people are not deficient in leptin. Their leptin levels are high, not low. But these high levels did not produce the desired effect of lowering body fatness. Obesity is a state of leptin resistance.

• So what causes leptin resistance?

Chapter 6

Obesity is a hormonal dysregulation of fat mass.

• When the body set weight is too high = obesity results.
• The body will adjust (stimulating hunger, decreasing metabolism) to counteract any attempts to lose weight in order to keep the body at the programmed set weight.
• Lots of hormones involved in regulating fat, appetite, etc but none of these are the main hormone involved in setting the body weight
• INSULIN AND CORTISOL are the ones. Little boogers.
• Insulin
  • tells the cells to take glucose out of the blood to use for energy
  • Insulin ⮕ insulin receptor ⮕ opens cell and pulls in glucose
  • Rise in blood sugar stimulates insuline release
  • Some foods raise blood sugar more than others
  • Refined carbs raise blood sugar lots, thus insulin also
  • Protein raises insulin levels but doesn’t do much to blood sugar levels
  • Dietary fats = minimal increase of blood sugar and insulin levels
  • Insulin = key regulator of energy metabolism, fundamental hormone promoting fat accumulation and uptake. Facilitates glucose going into cells for energy.
• How it works
  • Ingested carb = more glucose available than needed ⮕
  • Insulin moves flood of glucose from bloodstream into storage ⮕
  • Stored glucose = glycogen in the liver, until there’s no more room for glycogen in the liver ⮕
  • Excess carbs (glucose) are turned into fat. Oh yay!
  • A few hours after eating, blood sugars + insulin levels drop. Less glucose available to use for energy ⮕ liver starts to turn glycogen back into glucose and release it for use.
• Short-term fast (eg a few hours) = body has enough glycogen available to function
• Prolonged fast = body calls on fat stores to make new glucose (converting fat to sugar, gluconeogenesis). Fat is burned to release energy for use.
• Insulin is a storage hormone.

When there is no intake of food, insulin levels fall, and burning of sugar and fat is turned on. If you continually refill your glycogen stores, you never need to use your fat stores for energy.

• High insulin levels = sugar and fat storage
• Low insulin levels = glycogen and fat burning
• Sustained levels of excessive insulin = increased fat storage
• Imbalance between feeding and fasting = increased insulin Could it be that “high insulin levels increase the body set weight”?
• Obese patients tend to have higher fasting insulin level

Chapter 7

Does insulin cause obesity?

• Obese people (tendencies)
  • secrete higher levels of insulin (20% higher)
  • insulin levels remain elevated
• Fasting insulin level = insulin level after an overnight fast
  • High fasting insulin levels associated with obesity
  • An insulin-resistant state leads to high fasting insulin
• Testing the “insulin causes obesity” hypothesis
• Experiment: if you take insulin, will you get fat? Short answer: Yes.

Numerous studies … demonstrated this fact. Insulin causes weight gain.

• Really, lots of studies. Lots.
• So many studies.
• Even when blood sugar doesn’t go up but insulin does, people gain weight.
• Really, quite a lot. Okay. You’ve convinced me.

A recent study suggests that 75 percent of the weight-loss response in obesity is predicted by insulin levels.

• As insulin goes up, the body set weight goes up. (And then the body does all the things it does to maintain homeostasis at that higher set weight.)
• Interplay between insulin and leptin…
  • Insulin promotes fat storage.
  • Leptin reduces fat storage.

Both fasting insulin and fasting leptin levels are higher in obese people, indicating a state of both insulin and leptin resistance.

Chapter 8

On to CORTISOL

• Cortisol also makes you fat
• Both insulin and cortisol are involved in carbohydrate metabolism.

Prolonged cortisol stimulation will raise glucose levels and, subsequently, insulin.

• Cortisol is the stress hormone - essential for preparing our bodies for action.
  • substantially enhances glucose availability
  • temporarily restricts growth, digestion, and other long-term metabolic activities
  • breaks down proteins for glucose
• Short-term high cortisol level = fine
• Long-term high cortisol level = not fine at all

With short-term physical stress, insulin and cortisol play opposite roles. Something quite different happens, though, when we’re under long-term psychological stress.

• Chronic stress ⮕ glucose levels remain high

• Chronically elevated cortisol levels ⮕ increased insulin levels

• More studies show that cortisol causes weight gain.

• Sleep deprivation is a major cause of chronic stress.

  • potent psychological stressor which stimulates cortisol
  • leading to high insulin levels and insulin resistance

A single night of sleep deprivation increases cortisol levels by more than 10 percent.

• Sleep restriction / ongoing deprivation leads to increase in insulin secretion (levels) and a decrease in insulin sensitivity

Chapter 9

Let’s take a look at Atkins

• Atkins diet
  • Works really well for weight loss
  • Good effect on metabolism
  • NOT great for sustainability
  • Incomplete thesis
• Also, consider the “paradox of the Asian rice eater”
  • diet based on white, polished rice - highly refined carb
  • but obesity quite rare in these populations (recently/comparatively)
  • Carb intake in Japan and China is high
  • Sugar intake is low
• Carbs aren’t the whole story - maybe sugar is.
• Studies of different people groups with high unrefined carb intake but low sugar intake show very low insulin levels

…it is not at all clear that high carbohydrate intake is always the primary cause of high insulin levels.

Chapter 10

Insulin resistance

• The time frame of weight gain matters
  • long-standing obesity is much more difficult to treat
  • why? because insulin resistance
• Insulin resistance = more insulin needed to do the same thing

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.

• The thing causes the thing resistance.
  • overuse of antibiotics ⮕ antibiotic resistance
  • use of drugs ⮕ tolerance (i.e. resistance)
  • Increasing the dosage of the thing to overcome the resistance to the thing leads to more resistance of the thing. “Raising the dose raises resistance.”
• Insulin resistane is caused by high, persistent levels of insulin

The higher the insulin levels, the greater the insulin resistance. …The longer the cycle continues, the worse it becomes—that’s why obesity is so time dependent.

• Over time, this vicious cycle can lead to high insulin levels independent of diet. High insulin = high body set weight.
• What starts the cycle? High insulin levels

Persistent high insulin levels lead gradually and eventually to insulin resistance. Insulin resistance in turn leads to higher insulin levels. But the crucial starting point … is high insulin levels.

• Insulin resistance is compartmentalized
  • brain, liver, and muscle
  • “Changing the resistance of one does not change resistance in the others.”
  • the brain never develops insulin resistance, so it responds to the high levels with the “full effect to raise body set weight.”

High levels alone do not lead to resistance. There are two requirements for resistance—high hormonal levels and constant stimulus.

• constant bombardment of insulin ⮕ insulin resistance
• two factors:
  • meal composition: the types of foods we eat influence insulin levels
  • meal timing: when we eat influences the constancy of insulin levels
• Snacking / eating lots of little meals = never giving the body a chance to fully reduce insulin levels

… in the development of obesity, the increase in meals is almost twice as important as the change in diet.

• Constant eating / snacking leads to most time = insulin-dominant state

Chapter 11

…nobody makes any money when you eat less.

• Breakfast is not important, like, at all.

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 norepinephrene (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.

Our bodies are gearing up for action in the morning, not for eating.

• eating more fruits and vegetables won’t help you lose weight
• Eat more fruits and vegetables to replace unhealthier foods, not just to eat more of them.

Chapter 12

Poverty and obesity…

• huge increase in obesity in the US in the last 30 years
• socioeconomic status is a big factor - states with the most poverty tend to have the most obesity
• cheap food = refined carbs
• And the US gov helps by subsidizing the worst kinds of foods, which is why they’re cheaper

Food additives receive almost thirty times more in subsidies…

Obesity is effectively the result of government policy.

The driving factor in obesity is insulin, and in many cases, the wide availability of refined carbohydrates.

Chapter 13

Childhood obesity:

• infants get high insulin levels from the mother

Because both 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.

• Logical consequence: insulin resistance very very early in life.
• …which leads to childhood obesity.
• Lots of studies show that the ‘counting calories’ approach does not combat childhood obesity.

They ate less and exercised more. They just didn’t lose any weight.

• Compare to a study which encouraged kids to
  • 1 Cut down on sugars and starches
  • 2 Stop snacking
  • Results: weight loss.

Chapter 14

Sugar is bad, yo.

• Sugar is fattening.
• And it’s all over the place.
• Worst offender = sugar-sweetened drinks (soft drinks, juices, sweet teas, sports drinks, lemonade, etc.)
• Glucose v fructose
  • glucose = six-sided ring molecule. Main energy source in the body. Delish. We love it. Circulates throughout the body. Preferred energy source of the brain. Muscles love it.
  • fructose = five-sided ring molecule. Found naturally in fruit. Metabolized only in the liver and does not circulate in the blood. Most tissues cannot use fructose directly for energy.
• Table sugar/sucrose = one glucose linked to one fructose
• Glycemic index
  • classification of foods according to their blood glucose effect. Measures blood glucose NOT blood insulin.
  • Glucose = value 100. Other foods measured against it.
  • Bread = glycemic index 73
  • Coca=cola = 63
  • Peanuts = 7

There is an unspoken assumption that most of the negative effects of carbohydrates are due to their effect on blood glucose, but this idea is not necessarily true.

• Fructose = has an extremely low glycemic index.
  • Natural fruit consumption doesn’t add that much fructose to our diet. Know what does?
  • HIGH FRUCTOSE CORN SYRUP
  • Which is in every fucking thing.
• The body has ways to handle excess glucose consumption, but not excess fructose consumption.
  • all fructose goes to the liver for processing
  • all fructose that goes in must be metabolized (there’s nowhere else for it to go)
  • Excess fructose is changed into fat in the liver
  • High levels of fructose ⮕ fatty liver

Fatty liver is absolutely crucial to the development of insulin resistance in the liver.

• Fructose (not glucose) causes the development of insulin resistance in humans
  • When the liver has too much glucose it will store the excess as fat, then as insulin levels fall, it will convert the glycogen and fat stores back into glucose and distribute for energy.
  • Like a balloon: “As energy comes in, it fills up. As energy is needed, it deflates.”
  • When the liver is already crammed full of fat from all that excess fructose—what happens?
    • Insulin tries to force more fat and sugar into the liver but it’s already full.
    • It takes higher and higher levels of insulin to move the same amount of food energy into a fatty liver. AIN’t no SPACE, bro.
    • The body is now resistant to the efforts of insulin. Normal levels will not be enough to push sugar into the liver.
    • The liver wants to push the extra sugar back into circulation, so the body has to keep insulin levels continuously high to prevent that.
• Sucrose: no good. 50/50 glucose and fructose
  • glucose = refined carb = directly stimulates insulin
  • fructose excess ⮕ fatty liver = insulin resistance

Sucrose stimulates insulin production both in the short term and in the long term. In this way, sucrose is twice as bad as glucose. The effect of glucose is obvious in the glycemic index, but the effect of fructose is completely hidden.

Chapter 15

Diet sweeteners are no good…

• artificial sweeteners also raise insulin levels

Chapter 16

Okay okay, so what carbs should we eat?

• Refined carbs cause the greatest increase in insulin levels.
• Sugar is basically the devil when it comes to weight gain.
• Avoid processed foods:

Carbohydrates are not inherently fattening. Their toxicity lies in the way they are processed.

• Fiber is good
  • makes blood glucose and insulin levels slower to rise
  • may reduce food intake
  • increases energy density of foods
  • increases satiety
  • reduces caloric absorption
  • keeps ya regular

Fiber’s effect… is not as a nutrient, but as an anti- nutrient… Fiber has the ability to reduce absorption and digestion. Fiber subtracts rather than adds. In the case of sugars and insulin, this is good. Soluble fiber reduces carbohydrate absorption, which in turn reduces glucose and insulin levels.

• Vinegar is also good
  • may help reduce insulin resistance
  • 2 t taken with a high-carb meal lowers blood sugar and insulin by as much as 34%
  • having vinegar alongside rice lowers its glycemic index by 40%
  • vinegar-dressed potatoes have a lower glycemic index than regular potatoes

Vinegar does not displace the carbohydrate, but actually seems to exert a protective effect on the serum insulin response.

Chapter 17

What about the proteins?

• All foods stimulate insulin, so, you know, keep that in mind.

  • Dairy esp milk has a pretty extreme insulin level raising effect.

• Dietary fat has the weakest insulin-stimulating effect.

• Pure fats (eg olive oil) do not stimulate insulin or glucose.

• Vegetable proteins raise insulin minimal amount

• Whey protein and meat including seafood cause significant insulin secreation

• PERO… the incretin hormones in animal hormones also increase satiety

• So, eat the meats and dairy, or not?

• Meats:

  • associated with weight gain
  • but comes with the protective effect of satiety

• Dairy

  • not associated with weight gain (EXCEPT for lowfat milk hahahahahahahahhaahhaah)
  • “Milk and cheese were essentially weight neutral.”

Chapter 18

Fat is… pretty good, actually.

• Total dietary fat is not correlated with heart disease.

• All fat is not created equal

  • Omega 6s are awful gross yuck
    • vegetable oils
  • Omega 3s are good, yay.
    • anti-inflammatory
    • flax seeds, walnuts, oil fish
  • Butter > margarine (DUH)
  • Trans fats ie partially hydrogenated vegetable oil = gross

• Saturated-fat intake can not be linked to heart disease.

• Saturated fats have some protective effects (stroke risk)

• also good: monounsaturated fats (olive oil)

• There is no association between dietary fat and obesity

• Whole fat foods (dairy) tend to be better than low-fat dairy

Eating fat does not make you fat, but may protect you against it. Eating fat together with other foods tends to decrease glucose and insulin spikes.

Chapter 19

What to eat

• Diets:
  • almost any diet in the short-term will produce weight loss
  • almost every diet in the long-term will fail (plateau then weight regain)
• Permanent weight loss = two-step process
  • Short-term: various diets can bring actual body weight down
  • Long-term: reducing the body set weight so we don’t regain the weight because “the body actively resists long-term weight loss.”
• Obesity is multifactorial, not simplistic

All these factors converge on several hormonal pathways that lead to weight gain, and insulin is the most important of these.

• Uniting theme = hormonal imbalnce of hyper-insulinemia
• Multiple factors / pathways to dealing with that hormonal imbalance
  • if sugar/refined carbs are the problem ⮕ low-carb diet
  • insulin resistance ⮕ intermittent fasting
  • cortisol levels ⮕ stress reduction and better sleep
• Consider the whole picture and compose a strategy that makes sense

…tailor the approach individually to address the cause of the high insulin levels.

Ways to lower insulin levels

• reduce consumption of added sugars
  • sugar is uniquely fattening because it directly produces insulin resistance
  • beware processed foods, they have so much added sugar
  • instead, have : berries with whipped cream (not sweetened), dark chocolate and the occasional celebratory sugar-laden dessert
• don’t snack
  • most snacks are processed unhealthy foods
  • snacks keeps insulin levels up (remember: all foods raise insulin)
• breakfast is optional
  • consider not eating breakfast at all
  • if you do eat breakfast, have something healthy — not refined carbs and sugars
• don’t drink sugar
  • unsweetened beverages are the way to go
  • red wine is good
    • does not raise insulin or impair insulin sensitivity
    • 2 glasses a day may improve insulin sensitivity
  • coffee is good
    • antioxidants and more!
    • protects against type 2 diabetes
    • reduces most major causes of death
    • may guard against diseases
  • tea is good
    • green tea is especially good for you
      • antioxidants!
      • may help with lower glucose levels!
      • may aid with fat burning!
      • increased fat oxidation and REE and lower risk of cancer!
      • drink up!
    • black tea also good!
      • antioxidants!
    • really any tea is good just don’t add sugar
  • bone broth is good
    • homemade!
    • long simmering time!
    • add vinegar!
• don’t eat many refined grains
  • white flour is nutritionally bankrupt and makes you fat
  • whole wheat / whole grains are slightly better than white flour but not by much
  • if you’re gonna have wehat, have stone-mill ground
• eat fiber
  • quinoa is good!
  • chia seeds are good!
  • beans are good!
• moderate protein eating
  • just be reasonable about it, honestly
• eat more natural fats
  • dietary fat is the least likely to stimulate insulin
  • natural fats are good:
    • olive oil, butter, coconut oil, beef tallow, leaf lard
    • get the good stuff
    • olives! nuts! full-fat dairy! avocados!
• eat more foods with protective factors
  • like FIBER:
    • get it in fruits, berries, vegetables, whole grains, flax, chia, beans, popcorn, nuts, oatmeal, pumpkin seeds
    • glucomannan (konjac tuber) - herbal remedy / konjac jelly? - VERY FIBER
  • vinegar!

Chapter 20

When to eat

• the way to solve the long-term problem of insulin resistance:
  • meal timing

To break the insulin-resistance cycle, we must have recurrent periods of very low insulin levels. If all foods raise insulin, then the only way for us to lower it is to completely abstain from food… fasting.

• intemittent fasts of 24 - 36 hours
• transition from fed to fasted state:
  • feeding - insulin levels are raised. glucose uptake. excess glucose stored as glycogen in the liver.
  • start fast
  • post-absorptive phase (6-24 hours in) - insulin levels fall. glycogen is broken down for glucose. Glycogen stores last for roughly 24 hours
  • gluconeogenesis (24-48 hours in) - the liver makes new glucose
  • ketosis - (1-3 days in) stored fat is broken down to make new glucose. ketone bodies start swimming around
  • protein conservation phase (5+ days in) - all your fatty acids and ketons are providing energy. increased adrenaline levels prevent decrease in metabolic rate.
• regular fasting routinely lower insulin levels and significantly improves insulin sensitivity
• fasting can efficiently reduce insulin resistance
• fasting
  • stimulates release of growth hormone
  • increases adrenalin levels (which increases metabolism)
• alternate daily fasting over 70 days:
  • decreased body weight by 6%
  • decreased fat mass by 11.4%
  • lean mass did not change
  • improved good stuff
• eating a single meal a day versus eating 3 meals at a day
  • same caloric intake
  • single meal = more fat loss
• fasting does not cause decreased metabolism

Decreasing food intake is matched by decreased energy expenditure. However, as food intakes goes to zero, the body switches energy input from food to stored food (fat). This strategy significantly increases the availability of “food,” which is matched by an increase in energy expenditure.

• fasting often increases TEE
• women: plasma glucose tends to fall faster and ketosis develops more quickly
• intermitten fasting works because it is intermittent — does not allow the body to adapt and find a new way to preserve homeostasis.
• feasting and fasting

This is the ancient secret. This is the cycle of life. Fasting follows feasting. Feasting follow fasting. Diets must be intermittent, not steady. Food is a celebration of life… we must balance our feasting with periods of fasting.

• Use fasting to balance insulin-dominant periods with insulin-deficient periods
• pay attention to other factors such as sleep deprivation, stress

Highlights: 📖 Fung - The Obesity Code