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BOOK - THE OBESITY CODE - Jason Fung

Preface by Timothy Noakes (doctor and emeritus professor at the University of Cape Town,
South Africa
Dr. Jason Fung, a nephrologist in Toronto, observed that type 2 diabetes is the only
a common cause among patients with acute kidney injury is that dialysis only treats the consequence and
not of the underlying disease cause. The current model of treatment for type 2 diabetes in
The world must be readdressed. Consider 2 big lies about type 2 diabetes:
1. It is a chronically progressive disease that worsens over time. JF says that
50% of your patients treated with a low CH diet + fasting succeed.
stop using insulin after a few months.
2. What is a disease of abnormal blood glucose levels, for which the only
treatment is to increase the doses of insulin.

Dr. JF is convinced that type 2 diabetes is a disease of insulin resistance, with secretion
excessive insulin (unlike T1D) and treating both the same way does not make sense.
the purpose is that to address insulin resistance, it is to limit carbohydrate intake.

Dr. JF reports that many doctors already knew that the low-fat diet and
calorie restriction is completely ineffective in the treatment of obesity

INTRODUCTION
Obesity is measured as: weight (kg)/ height (m)² > 30
Obesity has increased worldwide.
The caloric reduction method is ineffective. It has shown this for over 50 years.
● many doubts linger: is fat good or bad; are carbohydrates bad or good?; eating several
meals a day or fewer meals a day?; count calories or not count; the milk is
good or bad?; does meat do good or does it do harm?
There is a total absence of a theoretical framework for understanding obesity.

We must rely on evidence-based medicine and not on vague observation.

Current theories about obesity are simplistic:

excess calories cause obesity
Excessive sugar causes obesity.
excessive meat consumption causes obesity
excessive fat consumption causes obesity
not exercising much causes obesity

Obesity is a long-term disease.

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(PART 1) THE EPIDEMIC

HOW DID OBESITY BECOME AN EPIDEMIC?

The standard recipe is "eat less and exercise more," a relationship between "calorie consumption and
calorie burning. The definition of calorie: one calorie is a unit of energy
nutrient used by the body for various bodily functions. A part is stored
Like fat. Eating too much and spending too little causes obesity. Really?

Immediate causes and ultimate causes

Excess calories may be the immediate cause of weight gain, but it is not the cause.
last.
Ex:
alcoholism
drinking too much alcohol
b. ultimate cause: additive nature of alcohol, family history, stress, tendency
to addiction.
2. Why does a plane crash?
a. immediate cause: there was not enough elevation to overcome gravity
b. ultimate cause: human error, mechanical failure
3. Why do we gain weight?
a. immediate cause: consuming more calories than burning. The personal choice of
to eat french fries instead of broccoli and to choose to watch TV rather than
exercise. A character flaw
b. ultimate cause: ?? we must question.

We discriminate against the obese, feel pity, and also despise them.

The dietary guidelines from the U.S. Department of Agriculture, the CDC, and the Institutes
U.S. health officials strongly recommend: reducing calories and
move more. Why hasn't it worked?

Anatomy of an epidemic

For most of human history, obesity was a rare thing.

1825 the book "The Physiology of Taste" - CH causes obesity. 1863 published "open letter
about body mass" - Refined carbs cause obesity.
Until 1950, low CHI diets were recommended and accepted as the standard treatment.
for obesity.

In the early 1900s, calorie counting emerged with the book "Eat to be Healthy" (Dr.
Robert Hugh Rose
1918 - best seller "Diet and Health, with the Key to Calories" (dr Lulu Hunt Peters,
doctor and newspaper columnist.
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Herbert Hoover, head of the US Food Administration, began to adopt the counting of
calories
In the 1950s: with the treatment of previously lethal infections (tuberculosis,
pneumonia and dysentery), heart diseases became more evident, mistakenly
like an epidemic.
Increase in life expectancy between 1900 and 1950 reinforced the perception of an epidemic.
of coronary disease. with a longer life expectancy (1900/ 50 years; 1950/ 66
years; 1970/ 68 years), more heart attacks naturally occur.

Villain: fat as a cause of increased cholesterol, a fatty substance,

present in the blood. Doctors accepted it as a cause of heart attacks. However, if there are 3
macronutrients and one of them is fat, there has been an increase in the intake of carbohydrates, given that
meat and dairy products contained fats.

Reduction of fat consumption = increase in carbohydrate consumption

So there was a dilemma: the CH cannot be good at the same time (because they have low
fat) and bad (because they make you gain weight), so they created a solution: calories! What
I was gaining weight from the calories. It was arbitrarily decided that the excess calories
was causing weight gain, not the specific foods.

Most bought into this idea, however, the British nutritionist John Yudkin (1910-1995) did not.
It found a relationship between heart disease and fat intake, but rather sugars! In 1972
released the book: “Pure, white and deadly: how sugar is killing us.”

The dietary guidelines

In 1977, by government decree, George McGovern (chairman of the Senate Committee

from the USA on Nutrition and Human Needs) deliberated that fats were
causes of obesity and heart diseases. This statement has become dietary goals.
for all the USA.

There was a break with tradition. A government decree deciding on food.

in the country with great global influence: increase CH consumption to 55 to 65% of
calories and reduce fat intake from 40% to 30%, and of these, ⅓ would come only from
saturated fats.

1980 - the Dietary Guidelines published changed the nutritional landscape in the world and generated the
famous food pyramid, where the base was bread, pasta, and potatoes.

1995 - AHA (American Heart Association): we should eat 6 or more servings of bread,
cereals, pasta and starchy vegetables that have low fat and cholesterol levels.

When everything suggested eating less fat or foods with low cholesterol levels,
we take the eye off the sugar. Food manufacturers soon realized this and increased
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the level of sugar in processed foods to give better flavor. The consumption of
refined grains increased by 45%.

By distancing ourselves from natural fats (eggs, butter, meats), we embrace refined carbohydrates.
low in fat.

2000 - AHA declared that low-carb diets were dangerous, despite this
diets have been used continuously since 1863,

Result:
Heart diseases have not decreased as expected.
Obesity rates (BMI > 30) have increased significantly, starting in 1977.
from 15% to 40% of obese people in the US), precisely with the beginning of the low fat and high carb diet.

INHERITING OBESITY

An undeniable fact is that obesity develops within families. This is a trend.

genetic or environmental?
Obesity became rampant starting in the 1970s. Genes could not have
changed in such a short time.

Conventional theories blame the 'toxic' family environment that encourages eating and
discourages physical effort. Habits that changed after 1970:
low fat and high carb diet
increase the number of meals per day
more meals outside the home
more fast food restaurants
more time in cars and vehicles
increased popularity of video games
increase in the use of computers
greater use of sugar in diets
increase in portion sizes

These factors are indeed crucial in the development of obesity, but we must
consider genetics.

Nature vs culture

There was no relation between the weight of the adoptive parents and the adopted children. In case the
whether the parents were skinny or fat, it made no difference to the weight of the children
adopted. The environment provided by the adoptive parents was largely irrelevant.
There was an important correlation when comparing adopted children to their parents.
biological obesity, as there was a trend towards obesity.
Even when taking an obese child and placing them in a 'thin' household, they still remained.
obese.
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Conclusion: Approximately 70% of the variance in obesity is familial. Obesity is

overwhelmingly inherited! However, our genes have not changed within a single
generation. How to explain this contradiction?

The hypothesis of the economic gene

1970 - the first attempt to explain obesity based on genetics, where all the
humans are evolutionarily predisposed to gain weight as a mechanism of
survival. This way we increase the fat reserve in our body for eventual
moment of scarcity.

This theory stopped being taken seriously, but it remains in the media.

To survive in nature, we should have neither a lack nor an excess of weight (agility x
slowness). Just as in humans there are hormonal signs of hunger, there are also several
hormones that prevent us from eating when we are full.

(PART 2) THE CALORIES FRAUD

THE ERROR OF CALORIE REDUCTION

A simplistic equation: obesity = calorie intake - fat burning = fat

corporal. Considered a fraud of calories!

It is dangerous because it seems to have a certain logic, with false assumptions of reduction of
calories for weight loss:
1) The intake of calories and the burning of calories are independent of each other.
This assumption is a mistake, as they are closely dependent.
The basal metabolic rate is stable.
Measuring caloric intake is easy, but measuring the total energy expenditure of the body is
complicated because it is not just physical exercise that alters energy expenditure.
Total energy expenditure = basal metabolic rate + thermic effect of food +
thermogenesis of activities that are not physical exercises + oxygen consumption
post-exercise + physical exercise. Total energy expenditure can increase or decrease
up to 50% depending on caloric intake, as well as other factors.
We have a conscious control over calorie intake.
Numerous hormones influence this decision. The regulation of body fat,
just like breathing, is under automatic control. Once the
Hormones control the intake and burning of calories, obesity is a problem
hormonal and not caloric.
4) The fat reserves are deregulated.
The increase in fat cells is not deregulated. Leptin is the hormone.
better known for regulating fat growth. They also play a role
important in this process: adiponectin, hormone-sensitive lipase,
lipoprotein lipase and adipose triglyceride lipase.
A calorie is a calorie
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Are all calories equally likely to gain fat? The calorie from
Does olive oil cause the same metabolic response as sugar? No, of course.

How do we process food?

A calorie is a unit of energy.

Caloric reduction is not the primary factor in weight loss.

In the American and British experience, there was no association with weight gain by
increase in calorie consumption.
Reducing calorie intake would only work if calorie burning remained.
stable. What happens is that a sudden reduction in calorie intake causes a
similar reduction in calorie burning and no weight loss occurs when the body tries to balance
this 'budget' of energy. The burning of calories is highly dependent on intake of
calories.

A false assumption
We have heard for decades that 'caloric reduction is essential', 'eat less, move more'
but”. We have heard this so many times that we don’t even question it anymore.

What we know is that there is metabolic slowdown, with low calorie intake.
The lower the calorie intake, the lower the basal metabolic rate (burn). In response to
caloric reduction, the metabolism remains slowed down indefinitely.

Playing with hunger

There is a constant homeostasis in our body, which is an adaptation to changes to
maintain the initial balance.
There are 2 major adaptations to calorie reduction:
1. Reduction of energy expenditure (reduction of caloric burning)
2. Hormonal signals that stimulate hunger were stimulated:
a. ghrelin (hormone that stimulates hunger) remained elevated even
after 1 year of completing the calorie restriction.
b. satiety hormones: peptide YY, amylin, cholecystokinin were
reduced, even after 1 year of the caloric restriction ending.

A cruel farce
the low-fat and low-calorie diet doesn't work. this is the cruel hoax!

(4) THE MYTH OF EXERCISE

There is an increasing prevalence of obesity worldwide in countries where it is practiced more.

physical exercise. There is no association between physical activity and obesity.
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Burning calories
Total energy expenditure = basal metabolic rate + thermic effect of food +
thermogenesis of non-exercise activities + oxygen consumption in
excess after exercise + exercise.

Due to the complexity of measuring other elements, we take physical activity as what
but more influence on calorie burning. Weight loss through exercise is not a
effective practice.

Compensation: the hidden culprit

Calorie intake increases in response to physical exercise.

Conclusion: diet influences 95% and exercise 5% of weight loss.

THE PARADOX OF OVERFEEDING

An increase in caloric intake leads to an increase in metabolic rate consequently

increase in caloric burn.

Body mechanism for weight adjustment

Overeating becomes a behavior driven by hormones (and not by
a personal choice). It is a natural consequence of the hunger hormone (ghrelin) and
decrease in satiety hormones.
There is a threshold point for weight adjustment, where everything tends to return to each person's weight.
Like a thermostat.
How do we lower our thermostat?

Leptin: in search of a hormonal regulator

1890 - study of the neuro-hormonal basis of obesity (Dr. Alfred Frohlich/Vienna): the region
hypothalamic as a key regulator of energy balance.

Leptin, a protein produced by fat cells ('lepto' in Greek = thin).

Higher levels of adipose tissue lead to higher levels of leptin. Circulating
up to the brain, it inhibits hunger to prevent greater fat storage.
Obesity is a state of leptin resistance.

What causes leptin resistance? What causes obesity?

(PART 3) A NEW MODEL OF OBESITY

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A NEW HOPE

The hormonal theory of obesity

Obesity develops over decades. Obesity is a dysregulation of

fat mass. when the defined body weight is very high, it results in obesity. What
does it make the thermostat set at a higher threshold?

Hormones responsible for obesity:

Leptin, a regulator of body fat;
● Ghrelin, a hormone that regulates hunger;
Peptide YY and cholecystokinin, which regulate satiety

The mechanics of digestion

Hormones are molecules that provide messages to target cells. To deliver

this message has a lock-key mechanism with target cell receptors.

Insulin is a key regulator of energy metabolism. It is one of the main

hormones that promote the accumulation and storage of energy.

1923 - discovery of insulin (Frederick Banting and J.J.R. Macleod)

CH of foods > increase in available glucose

greater than necessary.
Insulin > glucose from the current to be.
stored (reserved for later use)

Glucose > stored in the liver (in the form of

glycogen) with glycogenesis. Glycogen is
concatenated glucose molecules.

Insulin is the main stimulus for glycogenesis.

We can convert glucose into glycogen and this

converts to glucose very easily.

The liver has a limited storage capacity for glycogen. Once saturated, the carbohydrates in
excess is converted into fats, called 'de novo lipogenesis' (that is, to create
new fat). This recently synthesized fat is stored:
no subcutaneous
in the liver
in the viscera
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‘
Hours after a meal (or in the early morning) occurs:
levels of sugar and insulin drop in the blood,
there is less glucose available to be used by the muscles, brain, and organs,
the liver >> breaks down glycogen into glucose,
glucose enters the circulation to generate energy

During prolonged fasting, the body can create new glucose from its reserves of
fat (gluconeogenesis). Fat is burned to release energy.

Insulin is a storage hormone. The large intake of food leads to the release.
of insulin, which stores energy in the form of sugar (glycogen) and fat. When not
after food intake, insulin levels drop and fat and sugar burning is
activated.

Glycogen is released easily, but its supply is limited. (e.g.: money in your
wallet)
Fat has unlimited space in our body. (e.g., money in the bank)

The explanation for the difficulty in losing weight is that we first access the wallet (reserve of
glycogen/glucose) than the bank (energy stored in the form of fat). In the event that
glycogen wallet is continuously replenished, there will be no reason to use the
bank reserve (fats).
Low levels of insulin activate the burning of glycogen and fat.

Insulin, body weight definition and obesity.

Obesity develops when the hypothalamus orders the body to increase mass.
fat to achieve.

Obesity is controlled by the CNS through the weight adjustment mechanism, where the threshold of this
Weight increases over time. Obesity is not controlled in the brain's periphery.
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Certainly, the response to insulin differs in lean and obese patients. Patients
obese individuals tend to have a higher level of fasting insulin, as well as a response
exaggerated insulin response to food.

The key to understanding obesity is to understand what regulates the bodily mechanism.
of weight adjustment, because the weight set by this mechanism is so high and how to redefine it
downward.

Insulin

I can make you gain weight

How? Prescribing insulin.

Fasting insulin levels are 20% higher in obese individuals and these levels are
strongly correlated to indices such as waist circumference and the ratio
waist-hip. Insulin resistance also leads to a high insulin rate in
fast

The close relationship between insulin levels suggests, but does not prove, a causal nature.
of this relationship.

Testing the hypothesis: does insulin cause obesity?

When using insulin or increasing the dose of insulin, several studies report weight gain.
reducing caloric intake becomes useless.