Eat Stop Eat Advanced Transcripts-1

The Eat Stop Eat Advanced
Audio Files
-The Transcripts-
Brad Pilon www.EatStopEat.com
Strength Works, Inc Eat Stop Eat Advanced Audio Transcripts Page 2 of 107
 
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Brad Pilon, Strength Works, Inc.
Copyright © 2008 by Strength Works, Inc Page 2 of 107

Table of Contents: 
Episode 1: Eat Stop Eat, Metabolism and ‘Starvation Mode’
Episode 2: Eat Stop Eat and the Metabolism of Fat Burning
Episode 3: Eat Stop Eat and Muscle Metabolism
Episode 4: Eat Stop Eat, Insulin and Blood Sugar Metabolism
Episode 5: Eat Stop Eat, Exercise and Your Body Composition
Episode 6: Eat Stop Eat, Health and Weight Loss
*The following pages are transcripts of the Eat Stop Eat Advanced Audio
Files, and are meant as an advanced discussion of the original Eat Stop Eat
philosophy of Flexible Intermittent Fasting. To learn more about Eat Stop
Eat please visit www.EatStopEat.com

Episode 1: Eat Stop Eat, Metabolism, and Starvation Mode 

Episode 1: Eat Stop Eat, Metabolism, and Starvation Mode  
Welcome to the Eat Stop Eat advanced audio files Transcripts. This is Part 1 of a six-part
series exploring the science behind the Eat Stop Eat lifestyle. In Part 1, we’ll explore the
science behind fasting, your metabolism, and the dreaded starvation mode.
All right, let’s get started. We know that the size and frequency of a meal is a
fundamental aspect of human nutrition, and it can have profound effects on many
markers of health and longevity in both human subjects and in laboratory animals.
We also know that in humans, chronic, excessive energy intake, (or overeating) is
associated with an increased incidence of cardiovascular disease, diabetes, certain
cancers, and is a major contributing factor to death, disability, and unnecessary suffering,
in almost all industrialized countries. So that being said, why not just eat less? That
seems logical. Even better, we could eat less and eat less often.
Well, there’s a common belief that there is a phenomena called “starvation mode,” and
that eating less or eating less often will cause us to go into starvation mode. Now you
might ask, “Well, what is starvation mode?” That is a good question. You see, it’s one
of my biggest pet peeves about the idea of starvation mode. It doesn’t have a clear-cut
definition.
From searching the net, I was able to come up with the idea that starvation mode is an
adaptive survival response to a decrease in calorie intake, where your metabolism slows
to a “crawl” (whatever that means), and despite the calorie intake, you start to actually
put on fat. Sounds pretty crazy to me, but let’s investigate.
To scientifically investigate starvation mode, we’re going to need something to measure,
and some theories we can test. So based on this loose definition, I came up with several
metabolic events that would absolutely have to happen for starvation mode to be true.
First, your energy expenditure, or the amount of calories you burn per day, is going to
have to be reduced as a result of dieting.
Secondly, you would have to actually burn less fat while you’re dieting.
We can use a measure called “RQ,” or respiratory quotient to measure the amount of fat
versus carbohydrate you are burning. RQ is a ratio of the amount of carbon dioxide
(CO2) you exhale and oxygen (O2) you are inhaling. If RQ is 1, you’re burning mostly
carbohydrate. If it’s 0.7, you’re burning mostly fat.
Lastly, we’re going to have to look at the changes in the enzymes responsible for
lipolysis, or fat being released from your fat stores. Luckily, we can look at adipose LPL
and adipose HSL enzymes and see what happens with them. Adipose tissue LPL is

responsible for moving free fatty acids from your blood into your fat stores; whereas
adipose tissue HSL is responsible for moving fatty acids out of your fat stores and back
into your blood.
I know that was all pretty complicated. Just remember, adipose tissue LPL means fat into
your fat stores. Adipose tissue HSL means fat out of your fat stores.
So for starvation mode to exist, the activity or amount of adipose tissue HSL would have
to decrease, while the amount or activity of adipose tissue LPL would have to increase.
If all these things happen - your energy expenditure is reduced, your RQ doesn’t change,
and the changes in adipose tissue LPL and HSL favor the preservation of fat mass, then
we will have a good indication that starvation mode definitely exists.
All right, so let’s start with energy expenditure.
Total energy expenditure = the amount of calories that you burn per day (or in a 24 hour
period).
We know that your lean body mass is a major determinant of this rate, so how many
calories you burn in a day is largely determined by your lean body mass. And remember
lean body mass includes much more than just muscle. In fact, the vast majority of the
effect of your lean body mass comes from the big three organs; your heart, your liver, and

your brain. So since we know that lean body mass is what’s responsible for the majority
of your metabolic rate, we have to look at where this idea of a lowered energy
metabolism comes from. It comes from the idea of adaptive thermogenesis (or a
lowering of your metabolism due to a decrease in calorie consumption), mostly as a result
or as a response to starvation.
And there are clinical studies on this phenomenon. These studies suggest that when
obese people diet for long periods of time and lose a considerable amount of weight, their
metabolism becomes lower than what a predictive estimate using mathematical
equations, suggest they should be.
How different? How much lower?
Typically, about the same number of calories that are in a large cup of coffee. That’s all.
These people were dieting for 19 weeks and managed to lose more than 10 percent of
their original body weight. We’re talking well over 20 pounds. And some of these
people’s metabolisms were 120 to 150 calories lower than a mathematical prediction
suggests that they should be.
Of course, these same mathematical equations also predicted that these people’s
metabolisms should be 190 calories lower at the very beginning of the study. But even if

these predictions were true, if it meant losing 22 pounds of body fat, I would give up one
cup of coffee per day worth of calories (but just one).
Now there are also some studies that show your body burns significantly less calories
during exercise while you are dieting. This reduction isn’t exactly big. It’s a whole
whopping 11 percent of your exercise induced calorie burning, or about 27 calories per
hour of exercise. We’re talking about less calories than an apple here.
So while studies showing a reduced metabolism during dieting do exist, their real-world
application is limited as they only show that over long periods of dieting, the metabolism
of an obese person is slightly lower than what a predictive mathematical equation says it
should be.
This really doesn’t answer the question of ‘what happens when you fast?’, and
specifically to the Eat Stop Eat lifestyle, ‘what happens when you fast in conjunction with
resistance training?’
Research conducted by a group led by Bryner suggests that even during prolonged caloric
restriction, metabolic rate will not be changed if lean body mass is maintained. And
what’s a better way to maintain lean body mass than by lifting weights?

In this study, healthy men and women ate 800 calories per day (with roughly 80 grams of
protein per day) for 12 weeks. You can’t get much lower than that. They also used
resistance training as a method to maintain their lean body mass. At the end of the 12
weeks, there were massive losses in weight with no significant change in metabolic rate.
So despite substantial reductions in total body mass, and 12 weeks of an 800-calorie per
day diet, Bryner had found that their metabolism, in fact, did not change. In fact, very
similar results were found by a group led by Bill Kreider, using a very similar study
design. Kreider’s research also showed that while eating very low calories, lean mass and
metabolic rate can be preserved by lifting weights.
These are examples of long periods of dieting and still don’t answer the question: “What
happens when you fast?” Specifically, of course, for Eat Stop Eat, “What happens when
you fast for 24 hours?” To answer this question, we can examine the research on fasting
that examined people who fasted between 12 and 72 hours. This research also agrees with
the theory that lean body mass is the main determinant of a person’s metabolic rate.
Even when a person does not eat for three days, the loss of lean body mass is found to be
minimal, as well as any changes in metabolic rate. In fact, measures of metabolic rate
either remain the same or actually increase during short periods of fasting. This suggests
that the unique metabolic adaptations that occur during a fast are able to counteract any
losses in metabolic expenditure. This has been found by a large group of papers,

including those by Carlson in 1994, Klein in 1993, Mansell in 1990, Webber in 1994, and
Zauner in 2000, and most recently Gjedsted in 2007.
Let’s take a closer look at the paper written by J. Webber and I.A. MacDonald,
specifically because it has a large number of subjects, and it included both men and
women.
In this trial, all the people were studied on three different occasions after a 12, 36, or 72
hour fast. The studies were conducted in random order, and there was a gap of at least
seven days of normal eating between each fast.
We can use this research to get an idea of what would happen during an Eat Stop Eat
style fast. Metabolic rate was calculated from a continuous recording of oxygen and
carbon dioxide consumption and production, using a ventilated canopy (indirect
calorimetry), which is a pretty standard measure of metabolic rate in research studies.
The results of this trial showed that there’s a significant increase in resting metabolic rate
between 12 and 36 hours of fasting.
We’re talking about roughly 100 calories, so nothing to get overly excited about, but if
we ignore the increase, the most important point is that there was definitely no decrease
in metabolic rate. A 100 calorie increase isn’t that important the same way that 100-
calorie decrease is also not that important in real life applications. It’s roughly a cup of

coffee worth of calories in any given day. Now this increase was found in both men and
women.
Interestingly, for both men and women their RQ, or the amount of carbohydrate versus
fat they burned, dropped progressively during the 72 hour period; starting at about 0.8,
which is average for most people, burning a little bit of fat and a little bit of
carbohydrates. RQ dropped down to 0.76 at 36 hours and 0.72 at 72 hours (remember
that the closer RQ gets to 0.7 the more fat you are burning, and the closer it gets to 1.0
the more carbohydrate you are burning), showing the longer they fasted, the more they
relied on a fat as a fuel source.
These results show that the theory that muscle is being burned for fuel during the first
stages of fasting is false. This theory has never made any sense to me, and now we know
that it is not supported by research.
So far our review of the research shows the starvation mode theory doesn’t seem to be
holding a lot of weight. We know that your metabolism does not slow down even during
a fast of up to three days.
We also know that as long as the fast keeps going, you burn more and more fat. (I don’t
recommend a three-day fast, I’m a fan of a 24-hour fast, it’s simple and it’s easy.) And
we know, from this body of research, that during this 24-hour fast, your metabolism will

not slow down and that you will burn more fat. So much for the idea that you have to eat
every 2-3 hours to prevent starvation mode.
The one last thing we need to look at is fat burning enzymes, and their activity while you
fast.
Luckily for us, there are some studies on both LPL and HSL activity during fasting. It’s
also very important to note that it’s widely recognized that by about 15 hours of fasting,
there’s an increase in the amount of free fatty acids that appear in your blood. This isn’t
up for debate - this is a well established physiological phenomenon that you can find in
any good physiology or nutrition textbook. And since you haven’t’ eaten in 15 hours,
these free fatty acids must be coming from somewhere.
We can look to a study by Ruge et al. that looked at the activity of adipose tissue LPL
during brief periods of fasting. In this trial they studied fat biopsies from subcutaneous
adipose tissue stores, in other words they literally cut out some fat from the belly area of
these people as well as from the muscle on the outside of the shin bone.
They found the LPL activity and mass decreased by approximately 50 percent in the fat
tissue, and increased more than 100 percent in skeletal muscle in response to 30 hours of
fasting.

This makes perfect sense. As the fat is released from your fat stores, it has to travel to
your muscle where it’s then burned for energy. So obviously, LPL would decrease in
your fat because you don’t want your fat storing more fat, but it would increase in your
muscles so that once the fat is released, it can be taken up by the muscle to be burned as
fuel. (Remember LPL moves fat into fat cells for storage or into muscle cells for
burning).
So that’s LPL, what about HSL? Well, there’s a study by Samra, et al., looking at 24
healthy adults, and these are, again, men and women, during the early stages of a fast, 14
to 20 hours. They found a noticeable and significant increase in the activity of HSL in fat
cells after 20 hours of fasting. This rise in HSL activity was also positively correlated
with the appearance of increasing free fatty acids in the blood.
So we can see from this research that as you fast the enzyme responsible for releasing fat
from your fat stores increase. And as you fast, the enzyme responsible for storing fat into
your fat stores decreases. And even better, as you fast, the enzyme responsible for
moving fat into your muscles to be burned as a fuel, also increases.
So there you have it. When you look at the science behind the popular notion of
‘starvation mode’, we see that is does not exist during short periods of fasting, and in fact
your metabolism stays the same.

What we did see is that during a short fast you start burning more fat as a fuel and direct
evidence that the enzymes responsible for moving fat out of your fat stores and into your
muscle (where they must be burned as energy) change in a way that’s favorable for
increased fat burning. So based on this evidence, we know that when you’re fasting, your
metabolic rate, and your rate of fat burning, and your fat burning enzymes are all shifted
towards increased fat burning.
So much for starvation mode during a 24-hour fast. This research proves that short
periods of fasting mixed with periods of normal food intake, combined with resistance
training, are going to result in a maintenance of energy expenditure with increased fat
burning.
So as a result of these results, we now know that we can use fasting as a way to decrease
body fat and use resistance training to maintain lean body mass without worrying about
your metabolic rate slowing down.

Episode 2: Eat Stop Eat and Fat Burning Metabolism  

Episode 2: Eat Stop Eat and Fat Burning Metabolism  
This is Part 2 of a six-part audio series exploring the science behind Eat Stop Eat
lifestyle. In Part 2, we’ll investigate the science supporting the fact that fasting burns fat.
For most of us, one of the major benefits of fasting is the fact that it burns fat, so it helps
us lose weight and make sure that weight is from our body fat. But really, what do I
mean by “burns”? Well, logically, if you don’t eat, the energy it takes for you to live has
to come from somewhere.
As the body’s largest energy reservoir, your adipose tissue ( aka fat stores) play a vital
role in the process of regulating energy balance. So during periods of caloric excess
(when you eat too much), your fat cells store energy as triglycerols, and during periods of
caloric restriction, like fasting, these reserves of fat are then mobilized for use as an
energy substrate. The fat in your body is a fuel source. It’s an energy reserve, like a gas
tank.
The mobilization of fatty acids from fat tissue to their ultimate site of oxidation, which is
inside the mitochondria in the muscle cell, involves numerous steps. When you’re
fasting, the release of free fatty acids from adipose tissue determines the plasma
concentration (plasma means blood concentration), which in turn is an important

determinate of the rate of oxidation. That’s pretty “sciencey.” What I’m telling you is
when you’re fasting the blood levels of free fatty acids go up. And since you haven’t
eaten food, those free fatty acids must have come from your fat stores. And since the
amount of free fatty acids in your plasma, or blood, determines how many free fatty acids
get burned as a fuel, the more free fatty acids released from your fat stores, the more will
be burned by your muscles.
This is an accepted scientific fact. I’m going to back it with references later, but right
now I want to point out that this really puts a ‘nail in the coffin’ of the idea that when you
fast, especially short-term fasting, that the energy comes from muscle.
This never made sense to me.
Why would we have fat stores, if when you’re fasting, your body uses muscle for energy.
Why not then, if you overeat, build lots and lots of muscle? This is completely illogical;
it never made sense and still doesn’t make sense. And I’m about to show you the research
behind why it is simply not true.
Short periods of fasting are known to cause a rapid depletion of glycogen stores.
Glycogen is a storage form of glucose, or sugar, in your liver and your muscles.

Depleting glycogen stores causes an essential adaptive increase in lipolysis (aka: the
release of free fatty acids from your fat stores). This increase in lipolysis also causes an
increase in fatty acid oxidation (aka: the burning of fat as a fuel), in order to maintain the
fuel needs of your body. Periods of 22 hours of fasting can result in substantial increases
in plasma free fatty acids. Again, since you haven’t eaten, this is coming from your fat
stores. And this has been proven by Mittendorfer in 2001.
Now if you remember from Part 1, during a fast, there is a constant and linear decrease in
your RQ (remember the lower the RQ the more fat you are burning). And this result has
been shown consistently in research by Mansell in 1990, Webber in 1994, and Zauner in
2000, Gjedsted in 2007. So we know that when you’re fasting, you start burning more fat
as a fuel. But how? Why? This process is thought to be regulated by actions of growth
hormone (aka: GH), which has been shown by Fowelin in 1991, Moller in 1991, and
Halberg in 2005, just to name a couple studies.
Let’s delve deeper into world of growth hormone and fat burning. The majority of the
metabolic effects that occur as a result of fasting can be seen within the first 24 hours of
fasting. This is part of the reason why with Eat Stop Eat you fast for 24 hour periods.
During this time, there are significant decreases in plasma insulin. There’s also
increasing concentrations of free fatty acids, glycerol, and growth hormone. The fact that
fasting causes GH to increase in your body has been consistently found throughout the

research. From Ho in 1988, to Hartman in 1882, Fesling in 1992, Riedel in 1995,
Maccario in 2005 and Bergendahl in 1999, we can see that it’s a well established that
fasting causes growth hormone to increase.
Between 18 and 24 hours of fasting, there’s a marked shift in substrate oxidation, where
fat oxidation increases by as much as 50 percent. And that was shown by Klein in 1992.
Not surprisingly, we see a rise in fat burning at the same time as a rise in growth
hormone. Let’s take a closer look and see how growth hormone is involved in fasting
induced fat burning.
Researchers Glick in 1963, and Sengupta in 1981, have explored the role of GH in fat
burning. They found that when fat cells were exposed to growth hormone, they release
free fatty acids. However, when they’re exposed to insulin, these same adipose tissues
lost this fat releasing response, to growth hormone (found by Fain in 1966). So when you
study human fat cells, you can see that GH can cause them to release fat. However,
insulin prevents GH from being able to do so.
These findings clearly illustrate the opposing roles that GH and insulin play on fat
metabolism. There are lots of theories on exactly how and why this happens, but it has
been proposed that the effect GH has on fat release when you’re fasting may be due to its
ability to increase the fat releasing response of fat cells to circulation catecholamine’s,
epinephrine, norepinephrine (aka: adrenaline). This was proposed by Marcus in 1994.

However, other researchers have suggested that the fat releasing effects of GH are due to
its direct effects on HSL and LPL. Now if you remember from Part 1, HSL and LPL are
the so called, “fat-burning enzymes,” as adipose tissue HSL is responsible for releasing
fat from your fat stores; and adipose tissue LPL is responsible for moving fat into your fat
stores.
So how do we test this theory? Well, we turn to some of my favorite research in the
world of growth hormone in a fasted state performed by Helene Norrelund in 2001.
Norrelund had a pretty clever idea. She thought, “Well, if we know that during fasting
free fatty acids increase, and we think that it’s GH that’s making them increase, we can
block the release of GH with something called somatostatin and see what happens.”
So they did a study blocking GH release in people who were fasting for 40 hours. They
found a significant decrease in free fatty acid appearance, even though these people were
fasting.
In the next step of her research, Norrelund thought, “Okay, we’ve proven that when you
take GH away, free fatty acid release decreases. What happens if we add GH back in, but
instead of people’s normal GH, we use a synthetic form of GH called “Norditropin”?
Sure enough, when Norditropin was injected, free fatty acid levels were equal to those of
fasting subjects with normal GH release, showing that GH is intimately connected to free
fatty acid release while you’re fasting.

So I wasn’t exaggerating when, in Eat Stop Eat, I told you that GH may be the master
metabolic controller when you’re fasting. From Norrelund’s research, it becomes evident
that you need the GH release that occurs during fasting to release free fatty acids so you
can burn fat. In fact, I’d go so far as to say that GH may have been misnamed. When
you look at all of its effects, it would probably be much better named ‘fasting hormone’
instead of ‘growth hormone’.
So by now, I hope you’re beginning to see the very intricate connection between GH and
insulin, and the fact that GH is responsible for releasing free fatty acids to be used as a
fuel source, when food sources of fuel aren’t available. And insulin, which is secreted
when food is available, is responsible for storing fat. Not only that, but insulin
diminishes the effect of GH and GH’s ability to increase fat release.
With any research, it’s important to make sure that your results are found in a number of
different subjects. The phenomena of an insulin-induced decrease in serum GH has been
seen in both young boys and girls, by Misra in 2007, and in adult men and women, by
Glick in 1963. After the ingestion of a glucose based drink, serum (serum also means
blood) GH levels were significantly reduced for a three-hour period. That was found by
Glick in 1963. So we see a very obvious connection between insulin and growth
hormone, and they’re really the master controllers of my ying and yang of fed and fasted.

Let’s move on, if you remember in Part 1, we talked about the fat-burning enzymes. You
know the enzymes that so many people tell you are diminished or decreased when you’re
fasting, and that’s why you store fat when you don’t eat every couple of hours? So let’s
take a closer look at GH and its effect on these enzymes, namely HSL and LPL.
The rate at which fat release can occur in fat cells, or how fast your fat can release free
fatty acids, is controlled by the enzyme hormone-sensitive lipase, that’s what HSL stands
for. In human trials, increased HSL activity has been noted to occur after an overnight
fast, (Samra 1996). This increase occurs in conjunction with an increased rate of free
fatty acid appearance. Also GH is able to produce a dose-dependant increase in your
release of free fatty acids from fat cells.
So the next thought I had; is GH having an effect on HSL. It was Dietz in 1991 who
showed that there is a GH-induced increase in the activity of hormone-sensitive lipase.
What Dietz found was an increase in HSL activity stimulated by epinephrine, and this
activity was potentiated by GH.
Now we don’t know for sure whether it’s a direct effective GH has on HSL activity, or if
it’s GH acting to increase the effect of catecholamines on HSL activity, but what we do
know is that fasting induced increases in GH increases the activity of HSL, which is the
enzyme responsible for releasing fat from your fat stores.

So if you consider GH as a fat-burning hormone, or a fat-releasing hormone, and HSL to
be a fat-releasing or fat-burning enzyme, what you get is an increase in both fat-burning
hormones and fat-burning enzymes while you are fasting.
So what about LPL or the enzyme responsible for making you store fat? Well, LPL is the
predominate enzyme responsible for the incorporation of free fatty acids into tissues. Not
just fat tissues, but also into your muscles and other organs. The effect that 30 hours of
fasting has on LPL activity was explored by studying biopsied fat and muscle, in other
words, fat and muscle that’s been withdrawn from the body. At the completion of the
fast, there was a decrease in LPL activity by approximately 50%. You might remember
this research from part 1 that was done by Ruge et al.
The interesting thing is that in investigations where obese, but otherwise healthy women
were treated with GH, there is a marked reduction in adipose tissue LPL, but not skeletal
muscle LPL, (Richelsen in 1998). So we see here in obese women, GH caused a
decreased activity in adipose tissue LPL, which is the enzyme responsible for moving fat
into your fat stores. But it didn’t decrease the LPL in the skeletal muscle, which is the
enzyme responsible for moving fat into your muscle so that it can be burned as a fuel.
This tells us that similar to its effects on HSL, the effects GH has on LPL may either be a
direct effect of GH, or may be due to GH’s ability to potentiate the effects of the
catecholamines.

Regardless of how the effect actually occurs, what we know from this research that
during fasting, GH has an effect on LPL in a manner that prevents fat from being stored.
So again, we look at starvation mode, or people who say that fasting will ruin your
metabolism or ruin your fat-burning ability, and we begin to see that this is simply not
supported by the available science.
Ok that’s enough of ripping on the starvation mode people. Let’s move on and look at
GH and fasting, and some cool science involving things like uncoupling proteins.
Remember I told you that fat moves from your fat stores to your muscle, where they’re
eventually burned as a fuel? Well, burning fat as a fuel is called “beta oxidation,” and
not only does it happen in the muscle, but actually occurs in the mitochondria of the
muscle.
Inside the mitochondria, or more correctly, on the walls of the mitochondria, there are
things called “uncoupling proteins”. These are part of a complex protein group that are
important for the production of energy and in thermogenesis (aka: heat production). The
net result of the activity of these uncoupling proteins is movement of protons in and out
of mitochondrial membranes, (it actually a very complicated system). Most importantly
we know uncoupling proteins are involved in our metabolic rate, the use of fuel sources
as energy and that they’re expressed at a very high level in human muscle.

So let’s look what happens to one of the uncoupling proteins when you fast. Research
done in 12 healthy adults, six men and six women found after 15 hours of fasting, plasma
free fatty acids were, of course, significantly elevated, and insulin and glucose were
significantly decreased, as compared to about three hours after eating a meal. What’s
really cool is they found that uncoupling protein 3 gene expression increased five-fold
after 15 hours of fasting, and by ten-fold after 40 hours of fasting. This is a very quick
and dramatic increase in uncoupling protein gene expression. As a result of a very short
period of fasting (Tunstall 2002).
Now what’s really cool is that some researchers looked at growth hormone deficient
people and treated them with GH for four months. They found the level of uncoupling
protein 3 messenger RNA increased threefold in skeletal muscle, and almost twofold in
fat cells (Pedersen in 1999). So these findings suggest that the rise in GH associated with
fasting is at least partly responsible for the fasting-induced increase in uncoupling protein
3 expression. So I hope by now you’re really beginning to see the intimate connection
between your growth hormone levels, your ability to burn fat, and fasting. And also
remember that insulin completely diminishes the effective that GH has on all these things
(fat release and fat burning).
Okay, so right about now, you might be thinking, “But Brad, what about all those other
fat-burning hormones that people always tell me about? Leptin, ghrelin, those types of
things?” What I am going to show you is that these hormones are involved in the

regulation of the way growth hormone affects fat loss. In the end, it all comes down to
higher levels of growth hormone and lower levels of insulin, which is what you get when
you fast.
Let’s start with ghrelin. Ghrelin is a hormone secreted by cells lining your stomach.
Ghrelin levels increase acutely during fasting, and if you inject ghrelin, it stimulates
growth hormone release in humans in a dose dependent manner (Wren, 2000). So the
more ghrelin you inject, the higher growth hormone goes.
The fact that you can find GH secreting cells in the stomach suggests that ghrelin
mediates some of the known effects of nutrient status and intake on pituitary GH release.
So what this means is ghrelin may be the way your body knows that you’re not getting
any food, and is a signal to increase GH release. (Wren 2000).
It is important to note that while there’s a correlation between GH and ghrelin, it’s not
absolute as circulating ghrelin levels are unchanged during acute exercise bouts. At the
same time, during acute exercise bouts, there’s a marked increase in GH (Dahl 2002). So
while they’re related, they’re not necessarily completely intertwined.
Leptin is generally referred to as the product of the obesity gene, and as your fat mass
goes up, so does the amount of leptin in your body. For this reason, leptin is often
thought of as an internal marker the size your body fat stores. Fasting for periods of two

to three days have been shown to decrease serum leptin levels (Bergendahl 1999). This
fasting-induced decline of serum leptin levels is out of proportion with the loss of fat
mass during fasting, suggesting that the role of leptin in metabolic control far exceeds the
typically held belief that leptin acts solely as an internal marker of body fat stores. This
research was conducted by Chan in 2003, Boden in 1996 and Weigle in 1997.
This tells us there may be other things that influence your leptin levels. In fact, a fasting
induced decrease in leptin is a most likely a result of plasma glucose levels, or insulin
levels decreasing. This is based on a study done by Boden in 1996; where normal
subjects who fasted for 72 hours, and had their plasma glucose levels kept constant, saw
no changes in either concentrations of insulin or leptin. These findings suggest that
similar to ghrelin, leptin acts as a secondary messenger, as opposed to a direct influencer
of fat metabolism.
Peptide YY is a polypeptide that is produced in the small intestine and colon, and is also
thought to reduce appetite as a response to feeding. Peptide YY is believed to be closely
related to the function of leptin because of its similar function in appetite control. Fasting
for periods of two to three days have been shown to produce a decrease in circulating
PYY levels (Peptide YY) by between 40 to 60 percent (Chan 2006). This reduction in
PYY has been shown to be transient, meaning that as soon as you start eating again, your
levels of PYY just go right back up. However, the relationship between PYY and

nutrient intake is independent of leptin levels, as it was found that if you administer leptin
by giving enough in an injection, there’s no effect on circulating PYY levels.
Another hormone that you may have heard about when reading about fat loss and fat
burning is adiponectin. Adiponectin is a protein hormone secreted almost exclusively
from your fat stores, and it plays a role in modulating or supporting a number of
metabolic processes, including glucose regulation and fatty acid metabolism. Levels of
this hormone are related to your body fat percentage, and adiponectin levels do decrease
as you lose weight, especially if that weight is from fat.
In both animal and human trials, neither short-term fasting nor refeeding after a fast
change adiponectin levels (Kmiec 2005). We also know that adiponectin appears to
affect primarily long-term changes in body weight with little evidence for any
dependence on short-term regulatory influences, like a 24-hour fast (Merl 2005).
While research has shown that short periods of fasting do not effect adiponectin levels,
other studies have found that acute changes in GH concentrations can affect serum
adiponectin levels. What this illustrates is that we don’t really know adiponectin’s role
yet, and we need more research to figure out adiponectin’s role in fat loss or obesity.
One last hormone I want to talk about is FGF-21, a newly discovered protein that is
produced in the liver and seems to be important during the intermediate time periods at

the beginning of a fast (Badman 2007). And while there’s a limited body of research
right now in FGF-21, what it does show is that it seems to be a mediator in fasting
metabolism, and it may be related to GH, leptin, and ghrelin.
In spite of the novelty of the recent discovered roles of leptin, ghrelin, Peptide YY,
adiponectin and even FGF-21, the role of these hormones seem to be that of identifiers of
energy status and as secondary messengers for the hormonal adaptations of fasting. The
overall body of research available to us today agrees with the suggestion that there’s a
complex interaction between nutrient intake, body composition status, and many
hormonal markers within the body, and that the majority of the metabolic alterations
associated with the fasting state is governed by the role of GH in the body.
So there you have it. While these hormones are interesting, I think they’re often played
up and hyped up in the media and by a lot of people writing about fitness and nutrition
(especially leptin). When it comes down to it, when you explore the research, you see
that growth hormone is the primary regulator of your ability to lose fat. And insulin
diminishes this effect, which is why I believe that fasting plays such a vital role in our
ability to maintain our weight, and lose fat when we want to. Fasting increases growth
hormone and decreases insulin, setting up the perfect hormonal environment for fat loss.
Remember in Part 1 how I told you that fasting does not decrease your metabolism even
though you’re not eating? And we do know that eating contributes at least a small

amount of energy expenditure to your metabolism? So if you’re not eating, but your
metabolism stayed the same, where does the extra calorie burning come from? Well,
when your body releases free fatty acids from your fat stores, if those free fatty acids
aren’t burned as a fuel, then they have to be reincorporated back into either your fat
stores or into your muscle cells. This cycling of free fatty acids actually costs energy,
and it’s this energy that may, in part, make up for the fact that you’re not eating.
What happens is as follows: there’s an up-regulation of many other pathways in your
body that cost energy, so in the end, it ends up being a win-win. You’re actually paying
for your fat to be burned. It’s costing you metabolic energy to burn fat. It sounds like a
great deal to me.
Okay, so let’s sum up this discussion. We know that during fasting there’s a GH-
dependant increase in serum free fatty acids, in other words, the amount of free fatty
acids that appear in your blood. We know that since you’re not eating, these free fatty
acids are obviously coming from your fat stores, and we know that free fatty acids are
primary metabolic fuel during fasting. We also know that while there may be many other
hormones involved in the process, it is growth hormone that is the key regulator, and
growth hormone is increased during fasting. And remember, insulin diminishes this
effect, so when you start eating, the growth hormone effect disappears, and you’re no
longer getting growth hormone related release of free fatty acids to be burned as a fuel.

So really, when you look at all the available evidence, I hope you are confident in saying,
“It is obvious that when you’re fasting, fat is burned as a fuel, your metabolism does not
slow down, growth hormone increases, and growth hormone (aka: GH) is a key regulator
in many of these processes.”

Episode 3: Eat Stop Eat and Muscle Metabolism  

Episode 3: Eat Stop Eat and Muscle Metabolism  
This is Part 3 of a six-part series exploring the science behind the Eat Stop Eat lifestyle.
In Part 3, we’ll explore the science behind fasting, protein metabolism, and what happens
to your muscles when you fast.
The two biggest questions about Eat Stop Eat are, “Will I go into starvation mode?” and
“Will I burn fat?” Easily the third most common question is, “Won’t I lose muscle if I
fast?” or “What happens to my muscle when I fast?”
We’re going to take an in-depth look at what happens to your muscles when you fast and
look at the effects of fasting on protein metabolism. The control of protein metabolism in
your body involves a complex regulation of the process of both building up proteins and
breaking down proteins, also referred to as protein synthesis and protein degradation.
Unlike fats or carbohydrates, your body doesn’t really have a true storage form of
proteins. In fact, the major protein reserve in your body is actually found in your skeletal
muscle. And since your muscles contribute a large part to your lean body mass, and your
lean body mass is a vital component to your energy expenditure (aka: your basal
metabolic rate), it’s very important that we understand how fasting affects protein
metabolism and specifically, your lean muscle mass.

We know that during prolonged periods of caloric restriction, the process of protein
breakdown may be up-regulated, resulting in amino acids being taken from your body
tissues, such as your skeletal muscle and your GI tract and serve as precursors for
gluconoegenesis in the liver and kidney. So your amino acids can be taken from your
muscle, your liver, your saliva, or any spot where there’s extra amino acids, and be used
to produce sugar, to be burned as energy, or to be used in other enzyme systems or other
bodily proteins, depending on where they’re needed the most.
We also know that people who do prolonged periods of caloric restriction combined with
resistance training, they maintain their lean body mass. We’ve seen this by Bryner, and
again in a paper by Krieder, and most recently in 2008, in a paper by Hunter.
In the most recent research paper (by Hunter), 94 women were asked to lose 25 pounds or
reduce their body mass index to 25 or below. For a majority of these women, this meant
losing up to 25 pounds, and it took them almost five months on an 800-calorie per day
diet. The coolest thing about this trial was that some of these women were asked to
perform resistance training along with this 800-calorie per day diet. These women
maintained their fat free mass for the entire time they were on this diet, which meant as
long as five months, eating as little of 800 calories. This also means that the 25 pounds
that they lost, if it didn’t come from their fat free mass, must have come from their fat
mass.

So by introducing resistance training, these women, once again, made sure that all the
weight they lost was from their body fat and maintained a lean body mass, which of
course, then, led to them maintaining their metabolism (energy expenditure). So this is
another trial showing that in long periods of extreme caloric restriction (far more extreme
than I would ever recommend), you can still maintain your lean body mass and, thus,
your metabolism, by weight-training. So we’ve seen enough trials to say that resistance
training combined with dieting can preserve lean body mass.
Let’s take a closer look at what happens when you’re fasting. What hormonal changes
happen, and how this might affect the way your muscles respond to fasting. Everybody
likes to pretend like they’ve got the biochemical principles of muscle growth all figured
out, but in reality, these principles are very poorly defined. It has long been recognized
that the increase in serum growth hormone found during fasting, acts to reduce muscle
loss during these periods of caloric restriction. This research is especially strong in trials
of acute, short-term periods of fasting, in other words, between 12 and 72 hours without
eating.
Now if you remember back to Part 2, we saw that during short periods of fasting, free
fatty acids are oxidized as a preferential fuel. That means they’re oxidized in preference
to amino acids, so increasing levels of free fatty acids in blood act to preserve the amino
acids from being used as a fuel source. So we know that GH is essential to this process;

however, GH is just as important to your muscle as it is to your fat. In experimental
models where GH secretion is suppressed during fasting, there’s a marked reduction in
circulating free fatty acids, and there’s also a 50% increase in skeletal muscle protein
loss. This effect is largely caused by the fact that without GH, there wasn’t an increase in
serum-free fatty acids or fat being released from fat stores. Without these free fatty acids
the body went looking for other sources of fuel and it found the skeletal muscle proteins.
So we know from this research, and again, this is by Helene Norrelund in 2001, that GH
and its ability to increase your fat release, also affects your ability to preserve your
muscle proteins. GH may also act on many of the hormones or messengers that affect
your muscle protein. For instance, in hypopituitary adults, that is adults with low release
of GH from their pituitary gland, it was found that the expression of MNRA from
myostatin was significantly inhibited by GH (Kojima 1999). What’s cool about this is
that myostatin is a growth factor that limits the growth of skeletal muscle, so this is an
example of GH having a direct effect on some of the protein signals and hormones
responsible for maintaining your muscle mass. So from looking at this research, we now
know that the combination of high GH, as well as high serum free fatty acids, acts to
preserve your muscle while you’re fasting.
Research shows that injecting growth hormone can increase protein synthesis in adult
patients with a growth hormone deficiency. Similar to these results, it has been noted
that when obese women underwent four weeks of a very low-calorie diet, in combination

with GH treatment or a placebo, there was a decrease in fat free mass in the placebo
group, but not in the GH group. So really what we’re seeing here is plenty of evidence
that GH is responsible for maintaining muscle mass, and we know that it’s generally
accepted that prolonged GH administration results in increased lean body mass and
decreased fat mass with minimal changes in bone mass. This has been shown in growth
hormone deficient adults by Salomon F in 1989 and Jorgensen in 1996. It’s also shown
in obese, pre-pubertal boys by Kamel in 2000. This has also been shown in prepubescent
girls by Richelsen in 1984. It’s been shown in obese women by Skaggs in 1991 and
obese men by Johannsson in 1997, as well as normal-weight adults by Crist in 1998.
So what you can see here is that it’s becoming fairly obvious that the GH release that
occurs when you’re fasting plays a very large role in maintaining your lean mass while
allowing you to lose fat mass. So hopefully by now, you’re becoming convinced that GH
is the primary regulator of the preservation of your lean body mass while you’re fasting.
Now let’s look a little bit closer and find out different ways this may be possible, or how
GH may be exerting this effect. We’re going to have to look at some rather complex cell-
culture type trials, where GH was found to acutely initiate protein synthesis via the
phosphorylation of something called “mTOR” and it’s downstream metabolites signaling
molecules for binding protein 1 in ribosomal protein S6. (Hayashi 2007).

So that probably didn’t mean a whole lot to you, but what I’m telling you is that this
mTOR pathway, is the same pathway that leucine uses to stimulate protein synthesis. If
you’re familiar with the body-building market at all, you know that there are quite a
number of products right now that are based on leucine because of leucine’s ability to
stimulate this pathway. Interestingly you can stimulate this pathway by simply not eating
anything, just by the effects of growth hormone and fasting.
While the exact mechanisms of the effect of GH on skeletal muscle remain controversial,
its role in fasted state metabolism has been theorized by several authors for a long time.
As early as 1963, Rabinowitz and Zierler proposed that a fasting induced rise in GH was
responsible for increased protein synthesis and that the cessation of the fast, (once you
introduce food back into your system), while still in a GH-dominant system, you could
increase insulin while there’s still high GH levels, which creates this heightened state
where you could begin building muscle.
So building on this theory by Zierler and Rabinowitz, research has shown an increase in
rates of both protein synthesis and catabolism during fasting. So yes, you do start
releasing some amino acids from your muscle, but you also start reincorporating amino
acids into your muscle. This is called “substrate cycling,” where the amino acids go out
and come back in, then go out, and then come back in. And this, again, plays a role in
increasing and maintaining your energy expenditure while you fast.

Now right about now, you may start to wonder about your workouts. I’ve told you that
when you’re fasting your lean muscle is not at risk of being lost. In fact, there’s an
increase in both protein synthesis and protein catabolism, and amino acid cycling is
responsible for maintaining energy expenditure while you fast.
So you’ve heard all that and you might be thinking, “Well, what about the whole idea of
working out and that common bodybuilder, fitness/nutrition type think that I need insulin
to build muscle?” Well, Dr. Michael Rennie, who is one of the premier authors and
researchers on the topic of amino acids and muscle-building, has said that while insulin
may stimulate muscle protein synthesis in young rodents and in human cells growing in
petri dishes, studies on humans have shown, convincingly, that insulin is not required for
protein synthesis in adult human beings. That was from an article in the New York
Times in 2008.
What we can see here is that if you discard some of this popular nutritionism mentality,
and bodybuilder mentality, the research starts to make sense. If you really don’t need
insulin to build or preserve your muscle mass, and we have lots of trials showing that as
long as 72 hours fasted, you’re going to maintain your muscle mass, largely due to the
fact that growth hormone is directing your body to use free fatty acids as a fuel.
And we have lots of evidence showing that even on prolonged 800-calorie per day diets,
you can maintain your muscle masses as long as you’re resistance training. You can start

to see that with the Eat Stop Eat lifestyle (which involves one to two fasts per week and
resistance training) there’s virtually no risk of you losing lean mass. Furthermore, if your
resistance training program or your exercise routine is set up properly, you can even build
muscle while following Eat Stop Eat.
The primary goal of dieting is the loss of body fat, which also acts to preserve your lean
muscle mass. In other words, the minute free fatty acids enter your bloodstream from
your fat stores, they become your body’s number one priority as a fuel source, it wants to
burn them as fuel first, and this preserves your lean body mass.
If you can think back to some of the common folklore you’ve heard about fasting, one of
the most annoying things you hear is that when you begin a fast, you mostly burn your
muscles for fuel. I hope I’ve shown you now, definitively, that the research on up to 72
hours of fasting shows that this does not happen. And these fasting trials didn’t include
resistance training as the Eat Stop Eat lifestyle does. You should now be confident that
you can follow the Eat Stop Eat lifestyle without losing muscle mass and that free fatty
acids and GH, or the combination of the two serve to protect against protein loss during
your fasts.
Finally, from exploring data on a acute feedings of amino acids at the end of a fast, we
know that whatever small amounts of protein may possibly have been lost during a fast,
will be built right back up when you start eating again, which brings me to my very last

point: post-workout nutrition. I’m hard at work writing my new book, “How Much
Protein?” on this very topic, but as a sneak preview for you, I want to briefly go over
what some researchers say about the idea that you need to eat right after your workout in
order to build muscle.
Again, quoting Dr. Mike Rennie, in that same New York Times Article, in 2008, he
stated that the idea of a possible golden period for getting amino acids into muscle
remains speculative, no matter how attractive the concept. This means that the whole
idea that you need to eat right after your workout in order to make your muscles grow is
not so concrete. In fact, what most scientific researchers will agree on is that no matter
what you’re doing or how you work out, what you need to do is make sure you eat
between training sessions.
With Eat Stop Eat, no matter how you set up your fasts, you still eat every single day. As
long as you’re following a fairly simple workout program that doesn’t involve working
out with weights two to three times per day, you should be able to get in a meal
somewhere between one training session and the next. Not only does this make sure you
preserve your lean muscle mass, this also allows you to actually build muscle while
following the Eat Stop Eat lifestyle.
You can see from this evidence that by following Eat Stop Eat and the Eat Stop Eat
lifestyle of intermittent fasting plus resistance training that you’re really at no risk of

losing muscle mass. In spite of all the stories you may have been told by fitness trainers
or other nutrition writers, (and they may talk about cortisol, or testosterone, or any other
hormone or enzyme pathway), we’ve seen from clear evidence, using true endpoints of
muscle mass, that prolonged periods of dieting, in combination with resistance training,
will prevent you from losing muscle mass while you’re dieting. We also know that this is
predominately moderated by the actions of GH.
So regardless of what happens to your cortisol (and by the way, most research says it
remains unchanged for 24 hours after a fast), or your testosterone, (again, unchanged
during your 24- hour fast) we still know that your muscle mass will not decrease.
All right, so there you have it. I think now we’ve really proven the case, that by
following the Eat Stop Eat lifestyle, you’re not at risk of losing muscle mass, and that you
can actually build muscle mass while fasting once or twice a week. From Episodes 1 and
2, we know that you’re not going to go into starvation mode and that you will be burning
fat.

Episode 4: Eat Stop Eat, Insulin and Blood Sugar 
Metabolism 

Episode 4: Eat Stop Eat, Insulin and Blood Sugar 
Metabolism 
This is Part 4 of a 6-part series exploring the science behind the Eat Stop Eat lifestyle. In
Part 4, we will explore the very controversial science behind fasting, glucose metabolism,
insulin, GH, FFAs, and the control of your body’s blood sugar.
I apologize ahead of time because this episode is going to be fairly science-intensive. To
really get down to the nuts and bolts of the control of your blood sugar, we’re going to
have to cover numerous scientific principles and terminologies.
So let’s get started right away with the term “glycemia”. Glycemia refers to the amount
of sugar that’s currently in your blood. Euglycemia means normal glycemia: refers to the
amount of sugar in your blood in a fasting state that is independent of eating meals. For
most people, this range is between 3.3 and 5.6 mmol/L. Now depending on which
medical reference you use, 3.3 tends to be a little low and is sometimes considered to be
“hypoglycemia,” which is a pathological state produced by lower than normal levels of
glucose (sugar in the blood). So hypoglycemia, depending on the reference, happens at
around 3.3 to 3.5 mmols/L of sugar in your blood.

And then you have “hyperglycemia.” Hyperglycemia is a condition defined by excessive
amounts of glucose circulating in your blood. A chronic hyperglycemia is mostly related
to diabetes mellitus. In fact, chronic hyperglycemia is a defining characteristic of
diabetes. A subject who consistently has a blood sugar of above 7 mmols/L, is generally
believed to have hyperglycemia, and is typically at risk of having diabetes.
We see that there is classifications of blood sugar levels:
1) Euglycemia - normal amount of sugar in your blood.
2) Hypoglycemia - low amount of sugar in your blood
3) Hyperglycemia - high amounts of sugar in your blood.
So what controls the amount of sugar in your blood and how does fasting play a role in
this. One of the major concerns people bring up about Eat Stop Eat is that they are
concerned about hypoglycemia and more correctly, hypoglycemia-like symptoms
occurring while they’re fasting.
Every paper that I reviewed involving people who were fasting between 12 and 72 hours,
showed that their blood sugar was maintained in the euglycemic or normal levels.
Sometimes it approached the lower end of these levels, and blood sugar continued to drop
very slowly as the fast progressed, nevertheless even during a fast, your body still
maintains blood sugar levels in normal ranges. After all, when you’re getting your blood
sugar tested by a doctor, they are always testing your fasting blood sugar. So you fast

overnight, you go into the doctor’s office, and they draw blood to see how much sugar is
in your blood knowing that you should come in at euglycemic values (normal values).
This test is done this way because your body has the ability to maintain your blood sugar
levels even while you’re not eating.
The idea that you need to eat every three hours to maintain your blood sugar is, in fact
false for 95% of the population. In fact, trials have actually looked into different people
and their claims that they are prone to periods of hypoglycemia or low blood sugar.
These people claim that they can feel nauseous and dizzy and kind of foggy in their head,
and they claim it is due to low blood sugar. Alkin, et al. in 2007 examined the effect of
fasting for 24 hours on young adults who have symptoms of hypoglycemia in the absence
of frequent meals. So they took two groups of people, one group who had said they don’t
really have a problem with hypoglycemia, and another group who said they were actually
very sensitive to hypoglycemia and get dizzy and shaky, etc.
What they found was blood sugar did not drop into hypoglycemic ranges in either group
during a 24-hour fast. Blood sugar did drop very slowly, but they maintained within the
normal glycemic area. This shows us that people who claimed to have hypoglycemic
episodes of feeling dizzy or nauseous, had similar blood sugar levels to those people who
reported no hypoglycemic symptoms.

This research has been replicated a number of times in papers examining the effect of
fasting on insulin or fasting on free fatty acids and never found blood sugar to fall below
normal levels.
Another interesting research paper looking at the Cori cycle sheds more light on this
subject, specifically how they designed the study and how they recruited their subjects.
Their subjects were brought in because they were characteristically having hypoglycemic
episodes, or periods of dizziness and shakiness due to hypoglycemia. The researchers
noted that during the study, their subjects never had a case of documented hypoglycemia,
in other words, these peoples’ blood sugar never dropped below normal, even when these
people were in the middle of an “attack”. So even when people were feeling dizzy,
nauseous, and foggy, their blood sugar was normal. This led the researchers to conclude
these hypoglycemic symptoms were related to the anxiety of not eating and not due to
hypoglycemia itself.
There is a large amount of evidence to show that in a 24-hour fast or an Eat Stop Eat
length fast, 95 percent of the population should never have an issues with hypoglycemia.
I want to explore the role that, believe it or not, again, growth hormone and free fatty
acids have in the maintenance of your blood sugar levels.

I’m about to say something very profound. I need you to promise me that you’re not
going freak out when I tell you this, and that you’re going to listen to the rest of this
episode to understand why this occurs and why it’s not something you should be
concerned about. Short periods of fasting have been shown in clinical trials to produce
acute, transient periods of insulin resistance.
I know we all know that insulin resistance is a bad thing, and it’s not what we’re looking
for from fasting. In fact, we’re looking for fasting to not only cause weight loss, but
improve insulin sensitivity. So I’m about to tell you there’s no way around it, that
anytime you’re burning fat, there will be an increase in insulin resistance, and I’m going
to show you the evidence behind this. I’m also going to show you why insulin resistance
is not necessarily a bad thing when you’re fasting, and I’m gonna prove to you that it is
transient and it goes away the minute you’re no longer fasting.
Lets get into this right now so that you understand the science behind it fully. We know
from reviewing clinical research, that short-term fasting, between 12 and 72 hours, is
associated with a marked decrease in serum insulin and a marked depletion of liver
glycogen stores. So your liver is able to store glucose in a form of glycogen and then
when you’re fasting, your liver releases this glucose as a way to maintain your blood
sugar.

Subsequently, there’s an increase in serum free fatty acids. (We’ve already talked about
this in detail in the last episodes). This increase in serum free fatty acids concentration is,
of course, accompanied by an increase in free fatty acid oxidation (fat burning). Within
48 to 72 hours of fasting, (longer than an Eat Stop Eat fast), the contribution to blood
glucose from hepatic glycogen (hepatic glycogen means: glycogen that is stored in your
liver), becomes essentially zero (Cahill 2006).
During the initial periods of fasting, liver glycogen is the main source of blood glucose.
Even in complete absence of caloric intake (fasting) skeletal muscle cannot share its
glycogen source with the rest of your body. The glycogen or glucose storage that’s in
your left bicep is only to be used by your left bicep, it can’t share it with any other part of
your body, can’t share it with your right bicep, you can’t share it with your leg, you can’t
share it with your brain. It’s just there for use of your bicep.
This occurs because skeletal muscle lacks the glucose-6 phosphates enzyme, which is the
enzyme that is needed to release glycogen-derived glucose into the blood stream.
(However there is one caveat to this: During intense exercise your muscle can contribute
some glucose to the blood due to the Cori cycle. We will discuss this in more detail later)
Firstly, I want to discuss the causes of this insulin resistance. It’s been well described in
the existing literature that after prolonged fasting, there’s a marked increase in many
measures of insulin resistance. Really, all that means is poor handling of your blood

glucose. This has been speculated to be resultant from the increased serum free fatty
acids or increased circulation GH. (recall from previous chapters we saw that during a
fast free fatty acids increase as does growth hormone).
Research by Helene Norrelund showed that by infusing people with the anti-lipolysis
agent, acipimax (a drug that prevents free fatty acid from being released while you’re
fasting) their free fatty acid levels were lowered and remained low even these people
were given extra GH. It is also important to note that these people had no change in
insulin-stimulated glucose metabolism. This shows us that it’s not the GH that’s causing
this insulin resistance that we’re talking about, instead it suggest that it may be the free
fatty acids.
Interestingly, Gormsen, et al., in 2007, found that you can recreate fasting-induced
insulin resistance by artificially elevating free fatty acids even in the fed state. So in
people who have just eaten, if you increase levels of free fatty acids, you get the same
insulin resistance. Now not only did Gormsen find this in 2007, but a group at the
University of Guelph found similar results in a very interesting paper published in 2008
looking at the effects of coffee before a meal. What they found was that coffee was able
to impair blood glucose homeostasis, or cause a certain degree of insulin resistance,
when fed prior to a large glucose load. This is interesting because we know that coffee
contains caffeine and that caffeine can increase the release of free fatty acids from your
fat stores. So very similar to the Gormsen data, we find that an increased level of free

fatty acids, caused by approx 2 cups of coffee, can impair glucose homeostasis or insulin
resistance.
This tells us that your body preferentially burns free fatty acids whenever they are
elevated, leaving the blood glucose in the blood. In other words, if you’re increasing the
amount of calories that are coming from fat, there has to be a decreased amount that are
coming from sugar. This means the concentration of free fatty acids in your blood dictate
how fast they will be oxidized.
This also means that anytime you burn fat, even is it’s during prolonged exercise where
there’s increased free fatty acids in your blood (increased free fatty acid oxidation), there
will always be an increase in insulin resistance.
Now in no way is being insulin resistant ideal. It’s just not something we want. It’s very
important to point out that it has been found that this fasting-induced insulin resistance is
transient. It can be reversed by refeeding, and a recent research paper shows this. In this
research trial fasting induced insulin resistance was completely reversed within 1 day
after a 48 hour fast simply be refeeding the subjects some carbohydrates. This effect is
also mirrored by changes in insulin receptors and many of the other cellular mechanisms
responsible for proper insulin functioning.

Once again this research by Norrelund in 2007 shows you that during fasting, blood
levels of free fatty acids go up, therefore blood sugar handling and blood sugar
metabolism goes down. Then once the 48-hour fast is complete and you begin to eat
again, your insulin levels go back up. This increase in insulin levels stimulate the removal
of free fatty acids from the blood, and causes your body’s insulin sensitivity to go right
back to normal, the way it was before you started fasting.
Here’s a very logical explanation for all this insulin resistance stuff. We talked about
hormone-sensitive lipase or HSL activity. In the first episode and the second episode, we
talked about how HSL is the main regulator of the release of free fatty acids into your
blood. It is this concentration of the free fatty acids in your blood that dictates how much
free fatty acids are going to be oxidized. Therefore HSL releases fat from fat stores, and
the amount of fat in your blood dictates how much fat will be used as fuel. The more fat
in your blood the more it gets burned as fuel.
Insulin is the main inhibitor of HSL activity. So while you’re fasting, HSL becomes
active. HSL causes an increase in free fatty acids. This causes an insulin resistance
because you don’t need your muscles to be taking up glucose to be used as a fuel if
you’re already using fats. But then, when you start eating again, you introduce food-
derived glucose in your blood, insulin levels increase, and these high insulin levels turn
off HSL activity. The free fatty acid levels in your blood drop and then insulin sensitivity
goes back to normal because now you need to use glucose as a fuel.

All the examples I just gave you were from research looking at one acute fast. And since
Eat Stop Eat is a 24-hour fast once or twice a week, you’re probably more interested in
what happens during chronic short-term fasting. So while observation of single acute
periods of short-term fasting have found fasting-induced insulin resistance, the good
news is research on forms of longer term alternate day fasting, have found no effect, or
even an improvement on insulin sensitivity. (Johnson 2007, Halberg 2005).
In another trial a form of every other day fasting was studied for its ability to reduce
oxidative stress. The subjects in this study alternated between eating either a single drink
consisting of 300 calories per day, or just eating normally for a period of eight weeks.
Glucose and insulin levels remained unaffected despite a significant 8.5% decrease in
body weight.
In another trial examining alternate day fasting in eight men and eight women for a
period of 22 days, it was found that fasting plasma insulin concentrations were similar
before and after the fasting period. But they also found a significant increase in insulin
action. What we learn from this is that when people fast for prolonged periods of time,
they lose body weight, which on its own will affect insulin sensitivity, but we actually
have research trials showing improved insulin action and decreased diabetes risk factors.

Therefore even though an acute fast may cause acute transient increases in insulin
resistance, this is only because fat burning has increased, and any time fat burning is
increased, so is insulin resistance. Over the long haul, as you decrease or get rid of body
fat, you actually see improvements in your insulin sensitivity and a decreasing risk for
diabetes.
Short periods of fasting induce changes in glucose metabolism in the body. This we
know. There’s no doubt about it. During the fasting period, insulin levels drop quickly
and growth hormone levels go up. Because insulin levels drop, so does the use of
glucose as fuel. And during the same time, free fatty acids increase in the blood, so fat
burning goes up.
While fasting for periods of 72 hours have been noted to cause varying degrees of insulin
resistance (remember this is 72 hours, not the 24 from Eat Stop Eat) trials of long-term
intermittent fasting have noted no change in scores of glucose metabolism.
It’s theorized that during acute periods of fasting, transient insulin resistance may be a
necessary metabolic reaction to the increased fatty acids and is a precursor step to
increase fat burning. This response has been shown to be transient and reversible after
the introduction of refeeding.

Longer term periods of intermittent fasting, even with no change in either insulin or
insulin sensitivity, will produce a reduction in the area under the curve for both serum
insulin and serum glucose over long periods. This is because both glucose and insulin
drop during the fasting periods. Without glucose being introduced into the bloodstream
via food, serum insulin levels will be lowered. Thus, the two key factors that are
negative outcomes associated with metabolic syndrome and diabetes (blood sugar and
insulin), are both lowered during chronic periods of intermittent short-term fasting. This
is one of the major health benefits fasting can have on glucose metabolism.
Hopefully, now you see the connection that in order for you to burn fat, you have to be in
a fasting state. It seems to be almost essential because the minute insulin is introduced
into your bloodstream, HSL activities decrease and there is a decrease in fat released
from your fat stores. Now fat burning itself may not decrease a lot because you’re still
oxidizing some of the fat that came in from your food, but the actual burning of body fat
seems to be a phenomenon unique to the fasting period.
Now I know you’re thinking right about now. “Brad, what about eating six or seven
meals a day? In fact, we know that you say that almost every diet works.” And that’s
true. When you eat six or seven very small meals a day, you decrease the glycemic load
of the amount of glucose your body has to handle, so you introduce short, little periods of
fasting in between each meal. Following this dietary protocol, will work and some
people do see fat loss as a result of this protocol, however it’s only because the meals are

so small, that there are small gaps in between meals where you have entered the fasting
state and free fatty acid released from your fat stores has increased. You must be in a
fasted state to burn body fat. There’s no way that your body will burn bodyfat in the
presence of dietary sugars (glucose).
You may be wondering, “Okay, Brad, what about exercise?” Exercise is very interesting
because exercise is actually a mimic of the fasted state. When you exercise, insulin
levels decrease, free fatty acid release increases, growth hormone tends to increase and
what you get is a mimic of the fasting state. You get an increase in free fatty acids and an
increase in fat burning. If you exercise at a high enough intensity for long enough, it will
mimic the fasted state and you will burn body fat even if you’ve just eaten. So exercise is
the one exception. Speaking of exercise, let’s talk about the Cori cycle and how exercise
can cause you to actually be able to use glucose from your muscle.
Now you may be familiar with lactic acid. People often think of it with the burn
associated with exercise and whether or not that’s true, I’m not sure, but the key is that
lactic acid is a byproduct of hard-working muscles. What many people don’t know is
that lactic acid can enter your blood stream, travel back to your liver, your liver can turn
lactic acid back into glycogen, and then re-release it into your blood as glucose.
This is part of the reason why resistance training is part of the Eat Stop Eat lifestyle.
During exercise you can actually use byproducts from muscle activity to maintain blood

sugar levels. So exercise is a very important part in learning to maintain your blood
sugar. The Cori cycle is very well known, but not often talked about. There is research
dating back as far as the ‘60s looking at the contribution of the Cori cycle to maintaining
blood sugar.
So this leads us to bonking and the whole idea of exercise-induced hypoglycemia. What
happen with bonking during either prolonged or excessively intense exercise, people will
experience symptoms that are very similar to the supposed hypoglycemic symptoms of
dizziness, fatigue, drowsiness and blurriness. Bonking is a result of you exerting yourself
beyond your capacity. And your body’s metabolic cycles, metabolic functions cannot
keep up with the demand you’re putting on them. Bonking can occur as an effective and
improper warm-up, trying to keep a pace that’s above your threshold or simply trying to
do too much work in too little time. It actually has very little to do with what you ate
before your workout, as it is more of a result of your body’s ability to maintain blood
sugar from its own sources, including things like the Cori cycle.
Think of bonking this way: You and the worlds current Iron Man triathlon champion
decide to go out for a bike ride today, he is at the end of a 24 hour fast and you have been
eating normally all day and you get to bring sport drinks and gels with you, but he
doesn’t. If the Iron Man champion sets the pace, chances are you’re gonna bonk before
he does even though he hasn’t eaten for 24 hours and you have. Bonking is a reflection of
an exertion above and beyond your current work capacity.

There’s lots of research showing that you can perform resistance training while fasted.
You can perform short periods of fairly intense exercise while fasted, but I do not
recommend you perform long endurance activities while fasted (if performance is your
goal). If you’re trying to improve your time (for example: running or cycling), then I do
not recommend doing these exercises fasted, as your goal is to actually improve
performance and not decrease body fat.
So getting back to the actual metabolism of blood sugar in your body, I hope you realize
now that just like protein metabolism, when you fast, insulin, which is a key regulator of
blood glucose decreases, and growth hormone increases. Accompanying this increase in
growth hormone is an increase in your fatty acid activity. Free fatty acid concentration in
your blood increases, therefore, fat burning increases. As a result of this, glucose burning
must decrease because your metabolism has stayed the same therefore you need the same
amount of fuel no matter what it just happens to be coming as a different ratio, and in this
case the majority is coming from fat as opposed to sugar. So therefore, you get a slight
insulin resistance because you do not need blood sugar being pushed into muscle cells
because you’re using fat as a fuel.
When you break your fast, it doesn’t matter if it’s a low glycemic or high glycemic meal
because it takes a very small amount of insulin to cause this effect. Insulin inactivates
HSL, (which is the hormone responsible for releasing free fatty acids from your body fat

into your blood). As a result of this, free fatty acid levels decrease; therefore, fat burning
decreases; and therefore, we need to increase our burning of sugar as a fuel. So insulin
insensitivity needs to return so that insulin can push sugar back into your muscles to be
used as a fuel to replenish glycogen stores. The sugar that is not being burned as fuel is
now being stored again for later use. So by decreasing your glycogen stores in your liver
and your muscle, you’re actually creating a reserve where the sugar you eat isn’t
immediately being used either as a fuel source or being stored as fat. It’s also being used
to replenish glycogen, which is a good thing because it’s not being reused to replenish
your fat stores.
So there you have it. This is a very simplified version of what happens to your blood
sugar when you’re fasting. But I hope it dispels some of the myths of hypoglycemia, or
that fasting causes you to become insulin resistant long-term. Again this also shows you
how important fasting is to the fat burning process and how fasting and its effect on HSL,
growth hormone, and free fatty acids, is what really dictates the metabolism of your
body.
Now I hope you can see this preferential use of fat as a fuel, not only preserves body
protein but also tends to preserve body glucose, helping to preserve your body’s glycogen
stores while you’re in the fasted state.

And lastly, we know from research by Weiss et al in 2006, that improvements in glucose
tolerance and insulin action are induced by either exercise increased energy expenditure,
or decrease in energy intake and a subsequent reduction in body weight and body fat. By
fasting, you reduce your body weight by means of reducing your body fat and long-term,
this actually improves insulin action and improves glucose tolerance. Therefore by
fasting, what you end up getting is reduced body weight, reduced body fat, better insulin
sensitivity and better handling of blood glucose.
Hopefully by now, you see the role that growth hormone and free fatty acids play in
fasting and glucose metabolism and how fasting predisposes your body to burning fat as a
fuel. Also that fat is a preferential fuel while you’re fasting, (so glucose metabolism is
lowered) and how in the end, as long as you’re fasting, (especially the Eat Stop East style
of fasting) that decreases in body weight and body fat, over long periods of time,
decrease both insulin and glucose levels, which are key markers in long-term health. In
the next Episode we’re going to talk about the rules of Eat Stop Eat and markers of health
and longevity.

Episode 5: Eat Stop Eat, Exercise and Your Body Composition.  

Episode 5: Eat Stop Eat, Exercise and Your Body Composition.  
I want to answer the number one question I get all the time about Eat Stop Eat and
exercise. And that is, “Why is there no exercise chapter in Eat Stop Eat?” And the
answer is there’s no workout program in Eat Stop Eat because your workout should be
designed to fit your specific needs. And since you are going to decide exactly what your
goals are and what will fit your lifestyle you should find a workout that fits for you.
Therefore the key to exercise with Eat Stop Eat is that it has to be tailored to fit your own,
unique personal needs.
Let me give you an example. You could either be a forty year old, stay at home mom or
a 22 year old, amateur bodybuilder. Now, if I gave the stay at home mom the amateur
bodybuilder’s workout routine, she would probably scream and go running for the hills.
Similarly, if I gave the bodybuilder the stay at home mom’s routine, he’d probably laugh
at me. You build up a certain tolerance to working out and the amount of work it takes
for a 250 pound man to maintain 250 pounds of whatever composition of lean mass to fat
mass he has, is much different than the amount of work it would take a 150 pound stay at

home mom to maintain her body. So, your workouts have to be tailored to yourself and
your own personal needs.
There are a variety of workouts available for you on the net and I guarantee you’re going
to be able to find one that fits your goals. If you are a stay at home mom, there’s Holly
Rigsby’s Fit Yummy Mummy. If you’re a stay at home dad or a busy dad there’s Chris
Lopez’s Fit and Busy Dad. If you want an all around fat loss conditioning workout,
check out Craig Ballantyne’s Turbulence Training. If you’re looking to build the ideal
male body try John Barban and Brad Howard’s Adonis Effect. If you want to build
muscle fast, there is Vince DelMontes programs. The list goes on, but these are the ones
I know are of high quality and produce results.
But the moral here is that I really don’t know your specific needs when it comes to
exercise. From a nutrition point of view, I can help you cut your calories in an easy and
effective way using Eat Stop Eat. But your workout is when the magic happens and a lot
of people who don’t see results or their body doesn’t change in the way they want it to
change, is because the workout wasn’t suited to them. So I don’t feel comfortable giving
a ‘one size fits all’ recommendation about how you should workout. This is why there is
not, and will not be, a workout included in Eat Stop Eat. I may put together examples of
workouts I like doing sometime in the future but there will never be the Eat Stop Eat
Workout as a chapter in the book. The best thing to do is research it online and find one

that works for your goals and lifestyle, I guarantee you’ll find a good one. A good start
would be to look up the workouts I mentioned previously in this chapter.
Okay. So that being said, you’re probably thinking to yourself “but Brad, you’re really,
really high on the need to workout while you’re doing Eat Stop Eat”. And, obviously by
now, you know it’s because I think the preservation of lean mass is what preserves your
metabolic rate, is a large component of your overall health, and is an essential part of Eat
Stop Eat lifestyle. You should be fasting and you should be working out.
I get a lot of questions about the workout like “Brad, does Eat Stop Eat or does fasting
affect my workouts?” And the answer is yes and no. It depends on what you mean by
affects. If by workout you mean, long endurance type activities – and by performance
you mean you’re actually racing for time – then I will say that based on the research
available that’s probably not the best combination. Now that doesn’t mean you can’t do
Eat Stop Eat and perform endurance activities like marathons. You just don’t want to do
them during the time you’re fasting.
We can look at an example by Neiman in 1987, it was nine experienced marathon
athletes. They ran about an average of 40 miles per week. They’ve been running for an
average of seven years, and had marathon times around 3 hours, these guys were pros.
They were all around 40 years old with a max VO2 of around 60. They did two tests.
They ran once, just three hours after eating, or they ran after a 27 hour fast, separated by

a 2 week interval between the tests. They were done on the same day of the week at the
same time of day so you didn’t get any of those confounding variables. When they were
fed, they easily ran for 160 minutes; when they were fasted, they barely made it past 90
minutes. Again, they worked out at a very high rate – a rate that I couldn’t run for more
than 20 minutes – and they still did it for 90 minutes. Even though this is impressive to
me, for an “I want to win a marathon” point of view, this is evidence that maybe you
shouldn’t try to run a marathon while fasted.
So why did these runners have a poor performance? At the end of the trial, the glycogen
levels were actually higher in the fasted runners, and glycogen levels were not depleted in
either group. So it wasn’t lack of glycogen that caused these people to stop. The free
fatty acids were almost double in the fasted runners, so obviously, while their
performance wasn’t so great, these guys probably burned a lot more fat. In fact, it took
90 minutes for the free fatty acid levels of the fed runners to approach the pre race level
of the fasted runners. This is a massive difference in free fatty acids in the blood, which,
as you remember, means a massive difference in the amount of free fatty acids being
burned as fuel. Only two subjects in the fasted group demonstrated any signs of
hypoglycemia. So it wasn’t low blood sugar that was causing people to stop. For the
most part, the blood glucose remained constant, whether they were in the fed or fasted
state.

The authors made this interesting statement; “The fatigue experienced in our study
appears not to be related to metabolic factors in either the fasted or non fasted state for
most of the subjects. Although often unmeasured and ignored, the psychological state of
the subject in each test may be an important factor in fatigue.” This is something I want
to point out to you about this trial: when people are told to fast, unless you’re really
sneaky and have some really good study design going on, it’s very hard to blind them to
the fact that they’re not eating. Duh! So, in the best research study design, subjects don’t
know what’s being tested on them, maybe you get the placebo, maybe you get the
treatment. But whatever it is, you don’t know if you’re the group getting the special mix
or the ingredient being looked at. Well, in a trial where people are fasting, especially
marathon runners, they know that they’re fasted. And in fact, it’s not even double
blinded, because the researchers know which runners are fasted as well. This presents the
possibility of a bias that could creep into the trial as psychologically an endurance athlete
would most likely expect to perform worse when fasted.
Note:
If I could repeat this study, I would feed the fed group a supplement. And what the allows
me to do is put a certain amount of proteins, fats and carbs into a drink and make it taste
like chocolate or fruit punch and control the amount of calories they’re getting. And then
give the exact same looking and tasting drink to the fasted group, but it would only have
aspartame and a zero calorie thickening agent. So neither group would really know if
they’re fed or fasted. They’ll probably still be able to have some degree of understanding

but at least they wouldn’t already be psyching themselves out before they even started
running.
Regardless of that one small problem with the study design, these results are found rather
consistently. Whether you’re looking at marathon runners or elite endurance cyclists, if
you are a performance or endurance athlete you can still do frequent fasts, however you
should perform your actual tests and races on a normal eating day. I would even argue,
that I would do much of my training in the fasted state and possibly then do my really
strenuous work in the fed state. I find that especially with the training I currently do,
whether it’s hockey or KravMaga fight training, this is actually beneficial. Again, that
last little blurb I just told you; completely anecdotal, not based on science, just something
I’ve noticed myself.
We can look to the effects of fasting in anaerobic high output performance. In a study
done by Carlile studied the effects of Ramadan fasting. Ramadan fasting is, fairly similar
in duration and length to Eat Stop Eat fasting as depending on the time of the year, these
fasts can be as long as nineteen hours. The difference is that during Ramadan they fast
every single day whereas Eat Stop Eat is once or twice a week. What Carlile found was
that despite the fact that these people were slightly dehydrated (because during Ramadan,
not only do you not eat but you don’t drink), there is no decrease in their anaerobic power
or lactic acid metabolism. What we’re learning here is that while fasting for performance
and endurance activity may not be the best idea, fasting during anaerobic activity lasting

around an hour should not hinder performance at all. And I can tell you from the
numerous people I’ve talked to about Eat Stop Eat who have been on the program for
well over a year now that this is indeed true. I know power lifters who can perform high
level lifts while fasted. I know hockey players and people I fight with who actually
prefer to train anaerobically while fasted. So if you are training for performance and
endurance, do that on a day when you’re not fasting but for general weight training it’s
ok to be in the fasted state.
Interesting note: Much of the nutrition research we have on performance and
supplemental protein and amino acids are all done on people who have been fasting. Here
is an example of what it would be like if you were a subject in an amino acid study
designed to test protein synthesis. You would show up the night before the experiment to
the laboratory around 8-9 pm, no more food for the night. The next day you get all your
blood work done in the morning around 9am and then you would proceed to do a very
intense weight training workout. They would make you do a workout consisting of
things like eight sets of eight reps at close to 70% of your one rep max on leg press while
fasted for sixteen-seventeen hours. This would be a brutally intense workout. Then you
would have to wait up to another two hours before getting 6-7 grams of amino acids in a
drink to test anabolic effects. I’m not going to get into amino acid metabolism here but
what I wanted to point out to you was that all the subjects in these trials, (and there’s a lot
of these trials), consistently perform these strenuous weight training workouts while

fasted. These research trials prove that you can do intense weight training exercises
while fasted and still build muscle.
Hopefully you’ve noticed that when I talk about exercise, I’m talking about the
importance of maintaining your muscle mass while you’re fasting. If you want to do
endurance activities because you’re an endurance athlete that is something different and
not what I am talking about with the exercise portion of Eat Stop Eat. As it applies to Eat
Stop Eat, the roll of exercise is to maintain lean mass. I don’t believe that adding in
hours and hours of aerobic activity will significantly add to your weight loss if you are on
a proper diet like Eat Stop Eat.
I can look back at research done by Donnelly in 1991 which put 69 obese women on 520
calories a day for 90 days divided into five meals. That means each meal was only 105
calories each! That’s it!
The weight loss for these girls was massive. They lost about 45 pounds or a half pound
per day. Note: To all those people who say it’s impossible to lose weight on a very low
calorie diet. This is evidence that you’re wrong.
Okay, so back to it. In Donnelly’s research, these women weight trained four times per
week, starting with two sets of eight and then slowly working up to three sets of eight as
the study progressed, making sure that as they got stronger the weights were increased.

Along with these women who did weights only there was two other groups that
performed cardio only or cardio as well as weights. So there was a control group who
just did the diet eating 520 calories per day, the second group did endurance training four
days a week for 60 minutes, and a third group working out with weights four days a week
or a group that did both weights and endurance training four times a week.
And what they found was that the weight training group definitely got stronger, and
interestingly, all the groups lost a little bit of lean body mass. (Remember I said LEAN
BODY MASS because we’re going to get back to this). All three of the exercise groups
lost about the same amount of weight and the same amount of fat as the group that was
only dieting. So even though the last group doing cardio and weights spent a
significantly greater amount of time training as the control group, they didn’t really reap
the benefits in terms of extra weight loss.
The author speculated that the lack of workout volume may have influenced this effect
noting that in similar trials by Baylor et al they used twice as many exercises and were
able to increase their lean body mass.
I think the Donnelly group sat back and thought about the conundrum they were in here
where A: the endurance training and all the extra supposed calories these women burned
didn’t really contribute largely to their weight loss, but also that the weight training group
didn’t see the preservation of muscle mass that we all believe to happen. And then they

realized something, and I think this is what happened. They realized that lean body mass,
and this is very important, is not just your muscle. But lean body mass is everything
that’s not fat, and depending on how you measured it, it includes your organs such as
your liver, small intestine, large intestine, stomach, your heart, your lungs, bones
everything in your body that isn’t fat.
An extremely obese woman may have a seriously overworked digestive system.
Dropping down to a 520 calorie per day diet may very well have caused the mass of the
digestive system of the women in this study to shrink. This could account for a large
decrease in lean mass from the digestive track which would hide any measureable
increased in muscle mass.
So the Donnelly group, being really smart published another study in 1993 where they
did a very similar study. This time the subjects (14 women) ate 800 calories per day for
90 days. And again, these women had a really impressive weight loss of 35 pounds over
the course of the 90 days. They did eight weight training exercises at each training
session; bench press, lat pull, knee extension, knee flexion, military press, bicep curl,
tricep extension – your typical sort of research study workout program. They did this
three times a week for 30 to 40 minutes. So again, similar to their last trial, these women
got stronger but still lost some lean mass.

However, in this trial, they actually biopsied muscle. A biopsy is when they take a little
piece of muscle out to measure it. They took biopsy samples before the beginning of the
trial and a little piece of muscle at the end of the trial. They used the biopsied muscle
samples to measured the cross sectional area of the muscle (the actual size of the muscle
fibers). And what they found was that muscle fibers, both fast twitch and slow twitch had
grown by over 20%. This is evidence for an increase in muscle size while on an 800
calorie per day diet in obese women training three times a week for 30 to 40 minutes.
Okay, so we move on to the paper that Bryner et al did in 1999. This was twelve weeks,
800 calories per day, 80 grams of protein per day, divided five times per day, basically
the same diet used by Donnelly et al in 1993. This was twenty subjects which included
men and women, again, all over 200 pounds. This group was all approaching over 40%
body fat. And they did workouts three days per week doing ten exercise, four lower
body, six upper body exercises. They gradually worked their way up in a progressive
training style so that they would end up doing four sets of eight to twelve reps with about
one minute rest. By the end of the trial, they’re doing a pretty impressive workout
program.
This group saw no change in lean body mass or metabolic rate despite dropping over 30
pounds. And they key point is that they got stronger during the study so we can theorize
that they did not lose any muscle mass.

We can follow that up with a study by Jensen done in 2002 on 38 woman. In Jansen’s
study they used an MRI which is a great machine that lets you measure skeletal muscle
directly and separate that from all the other lean body mass in the body, instead of just
measuring lean body mass and guessing how much is skeletal muscle.
The subjects in this study lost 22 pounds while doing three days per week of fairly
intensive weight training. The majority of the weight loss was fat as these people all lost
less than one pound of muscle. So on sixteen weeks of a very low calorie diet these
people loss less than 1 pound of muscle.
Hopefully you’re starting to see the trend. And that is that, while endurance training
doesn’t seem to improve weight loss all that much, resistance training is very important
in maintaining your muscle mass. And by maintaining your muscle mass you ensure that
the weight you’re losing is fat. So, in essence, weight training, is probably the best form
of fat burning exercise because it makes sure that what your body does burn is fat. And
that’s why I’m such an advocate of weight training with Eat Stop Eat lifestyle. In email
communications with Eat Stop Eaters I’ve gone so far as to say that if you’re just fasting
and not resistance training, you’re really not doing Eat Stop Eat properly. You need to
have some form of resistance training in there to preserve your lean body mass. In
addition I wouldn’t recommend wearing down your body with hours and hours on
treadmills and other ‘cardio’ machines if it doesn’t seem to add a significant benefit.

So that’s my basic take on exercise training, let’s do a quick review. We know that if
you’re training for performance and endurance activity that you should do it on your non-
fasting days but I must stress that you truly have to be training for performance. If your
goal is fat loss, then I wouldn’t worry about it because using our marathon runner as an
example, even though performance was compromised (the runners were only able to run
for 90 minutes) the amount of free fatty acids in their blood was, at times, more than
double what the fed group was, meaning they were burning more body fat as a fuel. The
fatty acids in the fed group were much lower than the group that was fasted and a portion
of those fatty acids could have come from the food they previously had eaten. This
means they weren’t burning body fat, they were burning food fat. So if your goal is fat
loss, I wouldn’t worry too much about it. Secondly, if your goal is fat loss, you should
make sure psychologically you’re prepared to say, “I’m not concerned about the fact that
I’m fasting.” I do believe the psychological effect of fasting on athletes who expect
fasting to decrease their performance, was a significant confounding variable in some of
these trials.
We know from research that anaerobic exercise can be done without any decrease in
performance. And from research on amino acids and protein feeding, where people were
fasted for overnight sometimes as long as seventeen-eighteen hours, that they were still
able to perform a very strenuous weight training workouts while fasted.

So what’ the answer to the question: “When should I work out when I’m fasting?” Well,
if you’re doing anaerobic activities or strength training then the answer is, whenever you
feel like it. If you’re following Eat Stop Eat, you can workout while you’re fasted, you
can workout while you’re fed, it’s not going to make a big difference. If you’re an
endurance athlete, who is training for performance and not fat loss, I recommend that
your very long, endurance type workouts or an actual event should always be done on a
regular eating day. The key here is for you to understand the importance of weight
training with fasting.
Let’s move on and look at the metabolic effects of exercise and how they are very similar
to metabolic effects of fasting. Other than fasting and sleep, exercise is the most potent
stimulator of growth hormone release. Exactly like fasting, exercise promotes GH
release, and this is why I sometimes joke that exercise is just really a fake fast, but there
are many metabolic similarities between fasting and exercise, let’s take a second to
explore these.
We know there’s a substantial amount of evidence that shows giving GH to people in
injections results in markedly increased resting energy expenditure by as much as ten to
twenty percent (Bak et al in 1991, Gravholt et al in 1999). We also know there is a large
increase in fat oxidation and this was found by Moore et al in 1990, Back et all in ’91, in
Gravholt et all in 1999. Therefore, similar to the GH effects caused by fasting, exercise
induced rises in GH tend to increase both your energy expenditure and your fat oxidation.

So this all looks really good, we know that GH it’s a principal regulator of fats and
metabolism. My theory is that GH is the reason that you burn fat while you’re fasting
and now we know that exercise also increases GH. So we see that exercise and fasting
have a lot in common. Through the use of increased levels of GH in the body, you see an
increased level of free fatty acids in the blood, which means an increased amount of fat is
being oxidized or burned as a fuel. You also see an increase in protein turnover, or
muscle being degraded and replaced which means an increase in protein cycling, which
hopefully means and increase in lean muscle mass. This further shows there’s a lot of
similarities between how fasting and exercise work.
So right about now, you might be thinking, “Well if fasting and exercise work the same,
why didn’t adding exercise to a very low calorie diet produce any more weight loss?”
And the answer to that is kind of tricky. You see, endurance training, especially the way
it’s done in these studies doesn’t actually cause a very large increase in calorie burning.
These are very overweight women who are trying very hard to workout but they only
exercise for one hour out of a 24 hour day. I’m imagining their intensity level was a high
as they could manage but may not have actually been that high as compared to what a
more athletic person could accomplish. So the extra calorie burning may not have been
too significant.

Let’s just say, hypothetically, they burned and extra 200 calories from their exercise
(remember the role of GH is to make sure that calories being burnt are from fat but not
that more calories are being burnt). So if they were already in a fasted state, considering
how little calories they were eating and the amount of time in between when they were
eating, adding more GH may not have meant more fat burning, I hope you’re following
me here.
So the exercise caused an extra, let’s say, 200 calories being burned over that day. So for
example on that day instead of burning 1800 calories they burned 2000. Even if the
percentage of body fat burned from that 200 extra calories was still very high, over all in
a nine week period it still wouldn’t add up to that much extra weight loss.
When we talk about the differences being “significant”, I am referring to “significance”
in a research point of view, which means statistically there’s a very low probability that
this finding happened simply by chance. What I’m trying to tell you is that if the groups
had a three or four pound difference in fat loss, in research talk we’d say that’s not
significant, but to you it may help explain why the people who were in fact dieting didn’t
see a ‘significant’ change. Therefore the change may have been a small, it may have only
been two or three pounds, and in research terms this doesn’t count as ‘significant’.
In other words, even though losing an extra 2-3 pounds of bodyweight might seem like
legitimate results to you, from a statistical research definition of ‘significance’ it didn’t

count as being any different. And in real life, for the amount of extra work these people
put in, I don’t think it’s significant in real life either. I don’t know about you but I
wouldn’t want to put in an extra four times endurance training and four times weight
training for an extra two or three pounds of weight loss over a 9 week period, that’s just
too much work for not enough payoff.
So hopefully you now see why I’m not a big fan of using exercise to burn extra fat. What
I am a fan of is using weight training to preserve muscle mass, thereby making sure what
you do burn is fat. And that’s really my entire point with Eat Stop Eat and exercise. I’m
trying to get across to you that research doesn’t really show any reason to workout at a
special time of day or whether or not you should workout fasted or not fasted, as your
results are typically going to be the same. From a quality of life and pure practicality
point of view that is backed by research, the Eat Stop Eat lifestyle involves fasting for
weight loss and the use of weight training to preserve muscle mass with the goal of using
them together in a synergistic way. If you’re going to be spending time in the gym, you
may as well make that time work for you and get the most out of it as possible. This is
why I believe that your number one priority should be weight training and it should be
weight training with the intent to preserve, or as we’ve seen, to increase the size of your
muscles. I wouldn’t worry too much about going into the gym trying to burn fat,
especially if you’re already fasting once or twice a week, because the fasting should be
taking care of your fat burning for you.

I’m sure that by now you’re confident in your understanding that you can work out
whenever you want while you’re following Eat Stop Eat. You’re always going to get the
same benefits if you have a properly planned workout program, that you don’t need to
spend hours in the gym doing cardio because the benefits are going to be small, and why
I consider weight training to be such an important part of the Eat Stop Eat lifestyle.

Episode 6: Eat Stop Eat, Health and Weight Loss.

Episode 6: Eat Stop Eat, Health and Weight Loss. 
This is part six of a six-part series exploring the science behind the Eat Stop Eat lifestyle.
In part six, we’re going to explore the science behind the Eat Stop Eat style of fasting,
and how it affects health and weight loss.
It is well known that nutritional habits, sleeping patterns, caloric intake and meal
frequency all have a pronounced effect on our health. In fact, you could say, that the
three major components of health are: how you eat, how you sleep, and how you
exercise. If you’re going to explore the health benefits of the Eat Stop Eat lifestyle, we
first have to define exactly what we consider health to be; and if you’ve ever actually
tried to define the word ‘health’ before you already know this is no easy task. A broad
definition of health, would be that health is a general condition of health and wellness.
Obviously, you can see the problem with this definition. You can’t describe health as a
condition of health. It just doesn’t make sense, and it doesn’t really give us anything to
measure. And since science is all about the measurement of outcomes, this definition is
actually useless for us from a scientific perspective.
For a slightly better definition, we can turn to the definition that was ratified during the
first world health assembly in 1948. This definition states that, health can be best defined
as a state of complete physical, mental and social wellbeing, and not merely the absence
of disease. After hearing this definition, it should become obvious that you really cannot
measure health. There is no true scientific measurement of improved health, because
health is actually a very holistic thing (which we will talk about a bit later).
Therefore, since we can’t actually measure health, what scientists do is measure what we
call surrogate endpoints, to define changes in health and research studies. A surrogate
endpoint is a physiological marker in your body, like cholesterol, or blood sugar, that
may indicate a change in desirable but un-measureable endpoint. In this case, total body
health. So, instead of measuring health, scientists measure markers of health to try and
guess if something is able to improve a person’s whole-body health. An example of one
of these markers would be longevity, or how long a person or animal can live for.
There is lots of research in animals to show that forms of caloric restriction, such as
fasting, can greatly improve an animal’s lifespan. The earliest paper I’ve ever found on
this topic was published in 1935, by McKay et al, showing that you can extend the
lifespan of an animal by feeding it less. Since 1935, the study of caloric restriction and
increasing lifespan has become very popular. And, here’s where it gets interesting. Just
like anyone who has tried dieting for an extended period of time, the people responsible
for studying caloric restriction have found that lowering your calories every single day
and maintaining them at this level, can be a daunting, boring and rather unfulfilling task.
So, they’ve started to study, you guessed it, intermittent fasting, as a way of reducing

your calories or a method of caloric restriction. And, they came up with some pretty
interesting information.
In animals, intermittent fasting can greatly decrease the risk of diabetes, cardiovascular
disease, and even cancer; decreasing both the development and growth of tumors. If
you’re a mouse, fasting works amazingly well. But, for people, the results aren’t so clear.
In people, this research is a little more difficult to conduct. I simply can’t take you and
thirty of your friends, and put you in cages, and feed and exercise you whenever I want.
For some reason, there are some laws against this! So, you can’t control a study with
people the same way you control a study with animals. Also, with people, we can’t
simply dissect them at the end a study, which is another reason why we have to measured
surrogate endpoints.
Using surrogate endpoints of health, we have been able to see that simply restricting daily
energy intake by 15-40%, can improve glucose tolerance and insulin action, reduce blood
pressure, increase HDL cholesterol, as well as improve many other endpoints of health.
Two of these major endpoints are: inflammation, and oxidative stress. Two endpoints
that I believe are excellent markers for the overall health of a person or animal. Every
second of your life there are thousands of chemical reactions happening in your body as a
result of your metabolism. These reactions generate reactive oxygen species, also known

as free radicals, or ROS. R.O.S. for Reactive Oxygen Species. These ROS can damage
the cellular structures of your body, including your DNA.
Your body has several defense systems to protect itself against these ROS, but these
systems are not perfect. And, over the years, ROS cause a small amount of damage on a
daily basis that simply cannot be repaired. This is why older people and older animals
have higher levels of DNA damage, and protein and lipid damage through oxidation, than
younger animals. We know that overeating causes an increase in oxidant stress, in other
words, an increase in ROS damage. We know that chronic overeating then causes
chronic damage, and that chronically increased blood glucose, using that as a marker of
overeating, leads to cellular alterations commonly seen in the elderly, including the
accumulation of things called advanced glycation end-products.
It has been found that diabetics tend to have tissues in their body that have the oxidant
damage similar to that of non diabetic people who are much older than they are. This
information supports the idea that it’s important to minimize oxidant damage. This is
also further proof that oxidant damage is involved in the aging of your body. This is not
to be confused with the aging of your body in the chronological sense, but rather it refers
to the age of your body in terms of the damage and health of your DNA and cellular
structure.

So, how does fasting affect oxidant damage? Well, when ten subjects, eight women and
two men, took part in an eight-week program of intermittent fasting, it was found that
they had a marked decrease in many markers of oxidant stress and lipid oxidation
(Johnson et al 2007). In other research exploring the metabolic effects of caloric
restriction, it was found that DNA damage was significantly reduced after six months of
calorie restriction (Heilbronn 2006). In another interesting paper it was found that calorie
restriction can actually increase the oxidant defense in your brain cells, helping to protect
your brain against age-related oxidant stress (Hayoun 2006).
What we can see here is that reducing calories, whether through traditional dieting or
intermittent fasting via the Eat Stop Eat lifestyle, is able to reduce the amount of oxidant
damage in your body, which I believe to be an excellent marker of whole-body health.
Other than oxidant damage, we also have to look at inflammation. Inflammation is one
of those things that, like oxidant stress, can be good and bad. In the absence of any
inflammation, wounds and infections would never heal. They would just get worse and
worse, and destroy tissue around them, and eventually compromise your life. However,
inflammation that completely runs unchecked can lead to a whole host of diseases.
Therefore, just like oxidant stress, inflammation has to be kept in a certain balance in
your body.
There are two types of inflammation. There’s acute inflammation, and chronic
inflammation. Acute inflammation is like a bump on your head or a temporary sore knee

after a long run. Chronic inflammation can occur due to constant overuse of a joint, or
constant environmental insult to a body system such as smoking to your lungs or high
stress on your arteries. Unchecked chronic inflammation can lead to things such as
rheumatoid arthritis. So, we want to maintain a lower level of chronic inflammation in
our lives.
I believe that we’re going to find that inflammation is more and more involved in issues
such as cancer, and cardiovascular disease (as research is already showing chronic
inflammation of coronary arteries plays an integral role in heart disease). Because of this,
it is very important for us to explore the role that our diet (including how much we eat
and how often we eat) plays in maintaining or regulating inflammation, and the
inflammation process.
Research shows that subjects following periods of brief, intermittent fasting were found
to have lower levels of the pro-inflammatory Cytokine-IL6 after fasting, than they had
before fasting. Not only this, but also these levels continued to be lower even twenty
days after their fasting period (Aksungar 2007). So, these people had their pro-
inflammatory Cytokine-IL6 measured, and then they went through a trial of intermittent
fasting, and found this pro-inflammatory Cytokine was lower after fasting. After
returning to eating normally, 20 days later their Cytokine was still lower, showing that
intermittent fasting in and of itself can seem to have the ability to help regulate the
inflammation response in your body; which is a very good thing.

We see from this research that the two major markers of health, inflammation and
oxidant stress are both benefitted through periods of caloric restriction, and especially
through the process of intermittent fasting.
Now I want to get back to the idea of the holistic approach to health. Holism is the idea
that the properties of a given system, like your body, and all its properties, including
biological, chemical, social, economic, mental – everything must be incorporated to
determine health. In fact, the health of a system or the health of your body is determined
by everything together and how they behave with each other.
I think the principle summarized by Aristotle in his metaphysics by saying the whole is
more than the sum of the parts. The holistic view of health is actually a big, large step
away from the typical reductionist view that science holds on health. But, I do think it’s
very fitting, in our discussions, because it’s the main reason why I think that we have a
hard time scientifically measuring health, and it’s also the main reason why I think the
Eat Stop Eat lifestyle is so effective at improving health.
I think being healthy, or improving your health lies in the way you approach life, the way
you think about what you eat, and how you exercise, and the decisions you make in life
and why you make them. ‘Healthy’, is finding a way of eating and of exercising that you
love, that causes you no stress (or as little stress as possible), and doesn’t leave you

injured or sick. It gives you a body that looks the way you want it to look, and it allows
you to do the things you want to do. So when it comes to being healthy, I think the key is
finding a balance between doing the things you love and the things you need to do. And
this is a perfect lead into our discussion on weight loss.
In scientific studies, there is definitely a benefit to reducing body weight. When
overweight people lose weight, many of the markers of health that we’re talking about
are improved. But, probably even more importantly, holistic health improves as well.
With weight loss there is an improvement in body image, and quality of life. So, if we’re
discussing the health benefits of the Eat Stop Eat lifestyle, we need to explore Eat Stop
Eat’s ability to help improve people’s life, help them lose weight, and maintain this
weight loss.
We know from reviewing clinical research that standard caloric restriction diets will
cause weight loss. We also know this research has shown the weight loss is typically
most impressive in the first two months of the diet, after which, weight loss tends to drop-
off. This has been found in studies like Gardner’s A-Z weight loss study, but not all
studies. In a study done by Heilbronn subjects lost weight over the course of six months.
Some subjects who were following a very low calorie diet, lost all the weight they needed
to lose in the first three months, and then kept that weight off for the rest of the six month
study.

We can see some contradictions in the research where some studies were able to help
people lose weight for a six month period, and some studies seem to find that they lose
the majority of their weight in the first two months, after which weight loss stalls or even
starts to go back up. We can explain this reduced weight loss as a function of what we
call compliance. I’m going to use low carbohydrate diets as an example.
When you first start a low carbohydrate diet, you would most likely limit yourself to
vegetables and meats that you’re familiar with. But, as you progress on this diet for any
length of time you start becoming a hunter-gatherer in the grocery store (a lack of food
variety always tends to push people to look for more foods to eat that fit into their diets).
You will quickly realize that cheese will fit in this diet, and then you soon figure out that
eggs will also fit in this diet. And not long after that you will discover ‘low carb’ protein
bars that will fit in this diet as well. You will keep adding food choices back into your
diet to the point where you’re eating the same amount of food you were before the low
carb diet because you’ve increased the variety back up to an acceptable level.
Issues like this fall into compliance as well as the simple unavoidable fact that people
will tired of diets that restrict their food choices. Therefore the main downfall of
traditional diets are boredom with food choices, and lack of variety, they are simply too
restrictive, and you start to miss the foods you like. This is what ultimately makes you
break your diet and just give-up on it. Now, with some studies, like the Heilbraun study
that are very well controlled, you find this does not happen. In trials where people are

taught how to eat, then left to go out on their own and live their normal lives, weight loss
is very impressive in the first couple months, and then tends to fall apart later on.
Eat Stop Eat is different, because you’re not dieting every day. You’re able to maintain
your diet long-term. In fact, fasting gets easier the longer you do it. It was mentioned by
Mark Mattson, (who is a famous researcher studying intermittent fasting), that if a person
could adhere to an intermittent fasting regimen for at least 10-14 days it becomes
relatively easy to continue on the diet. And, I find the same thing happens when I talk to
people who’ve been on Eat Stop Eat now for years.
At this point it should be clear that dieting can definitely improve or cause weight loss,
and that weight loss can improve many markers of health, both markers of scientific
health and the holistic whole-body approach to health which includes things like quality
of life and body image. But what I am sure you really want to know is “will Eat Stop Eat
cause me to lose weight?” To answer this let’s go over the research behind intermittent
fasting and weight loss.
The unique metabolism found during short-term fasting appears to be built around the
burning of body-fat as the predominant fuel source, and the preservation of lean mass.
The orchestration of these effects seem to be related to fasting-induced rises in growth
hormone which predispose you to burning fat while you’re fasting. I’ll be the first to
admit that I believe that the majority of the weight-loss benefits from the Eat Stop Eat

lifestyle are due to the caloric restriction. But, I am open to the idea that the unique
metabolism found during fasting is responsible for making sure that the majority of the
weight you lose comes from your body fat.
If we look to the scientific research, we can see that when 16 non-obese subjects, (eight
men and eight women) were fasted every other day for a period of only three weeks, the
subjects lost 2.5% of their body weight, and 4% of their fat-mass (Heilbronn 2005). In a
similar trial, ten subjects took part in an eight week period of alternating between a very
low calorie diet and normal eating, and by the end of this eight week period subjects lost
an average 8.5 kilograms, or closing in on 20 pounds of weight loss, in only eight weeks.
(Johnson 2007). If you add these two examples to the examples in your Eat Stop Eat e-
book, you realize that there is a fair amount of evidence showing that, at least for an eight
week to two month period, fasting is incredibly effective at causing weight loss.
What about long-term compliance. Well, the use of intermittent periods of short-term
fasting to lose weight, improves many markers of dietary compliance. There is research
to show that subjects in longer-term intermittent fasting weight loss trials would not need
to undergo the rigor of daily caloric restriction. This means they’re not going to get
bored and start hating dieting. In fact, it was Johnstone et al who found that subjects that
used fasting as a method for weight loss maintained most of their weight loss for up to a
year after starting the study. These people were involved in a research study, lost a lot of
weight, used fasting to maintain their weight loss, and at a follow-up meeting a year later

had maintained their weight loss. During routine follow-up questioning, the authors
noted that the subjects reported a trend of using fasting as a means to control their body
weight. So, the people who fasted tend to maintain weight loss, whereas the people who
weren’t fasting but trying to diet, tended to see their weight creep back up (Johnstone
2006).
The Eat Stop Eat lifestyle enables you to lose weight and then maintain that weight loss
for long periods of time because it is not restrictive and doesn’t intrude on your lifestyle.
Another key issue surrounding intermittent fasting, and one that a lot of people seem to
be concerned about, is the potential to over-eat once they start eating again. If you were
to fast for 24 hours, would you simply overeat the next day and never lose any weight.
While this is possible, if you force yourself to eat enough to cover the fasting period, you
probably won’t see any weight loss. It was noted in the research by Johnstone et al, that
after a 36-hour fast, people weren’t able to eat enough calories in the two-day period after
their fast to make up for the calorie deficit from the fast. The authors noted that while the
caloric intake during these two days after the fast was slightly increased relative to what
they were eating before the fast, the intake was not enough to counter the major calorie
deficit cause by the fasting.
This is evidence that caloric restriction obviously improves your health, and will
obviously cause you to lose weight. This is also evidence that intermittent fasting is an

excellent form of caloric restriction because it’s not as restricting and not as intrusive.
I’ve shown you evidence in the short-term, that fasting can actually cause very significant
losses in weight, and also that people who use fasting to maintain weight loss were able
to maintain that weight loss at a year follow-up. Based on this information it becomes
that very obvious that the Eat Stop Eat lifestyle not only should have benefits on many of
your markers of health, as well as your holistic health including your quality of life, it
will also help you lose weight and then maintain that weight loss.
Eat Stop Eat is an incredibly effective way to reduce body weight. It has unique effects
on protein metabolism, carbohydrate metabolism, fat metabolism, and your metabolic
rate. It also has unique benefits to health. And we’ve also seen that it is both an effective
way to lower your body weight, and maintain this weight loss. The difference between
lowering your body weight and maintaining your weight loss is really the frequency of
your fasts. If you started-off wanting to lose weight, perhaps you were fasting twice per
week. And then, once you’ve hit your ideal weight, perhaps you move your fast to being
once a week, or maybe once every five days. You can always use fasting, and adjust it
the way you see fit, to either get to your ideal weight or maintain your ideal weight.
I hope you enjoyed the Eat Stop Eat Advanced Audio files transcripts. If you have any
questions, about Eat Stop Eat, or my nutrition philosophies, please visit
www.BradPilon.com


REFERENCES CITED 

REFERENCES CITED 
Aksungar FB, Topkaya AE, Akyildiz M. Interleukin-6, C-reactive protein and

biochemical parameters during prolonged intermittent fasting. Ann Nutr Metab.
2007;51(1):88-95.
Astrup A, Thorbek G, Lind J, Isaksson B. Prediction of 24-h energy expenditure and its
components from physical characteristics and body composition in normal-weight
humans. Am J Clin Nutr. 1990 Nov;52(5):777-83.;
Bak JF, Moller N, Schmitz O. Effects of growth hormone on fuel utilization and muscle
glycogen synthase activity in normal humans. Am J Physiol 1991; 260( 5 pt 1): E736-
E742.
Bergendahl M, Evans WS, Pastor C, Patel A, Iranmanesh A, Veldhuis JD. Short-term

fasting suppresses leptin and (conversely) activates disorderly growth hormone secretion
in midluteal phase women--a clinical research center study. J Clin Endocrinol Metab.
1999 Mar;84(3):883-94.
Boden G, Chen X, Mozzoli M, Ryan I. Effect of fasting on serum leptin in normal human
subjects. J Clin Endocrinol Metab. 1996 Sep;81(9):3419-23.
Bryner RW, Ullrich IH, Sauers J, Donley D, Hornsby G, Kolar M, Yeater R. Effects of
resistance vs. aerobic training combined with an 800 calorie liquid diet on lean body
mass and resting metabolic rate. J Am Coll Nutr. 1999 Apr;18(2):115-21.
Buijs MM, Burggraaf J, Wijbrandts C, de Kam ML, Frölich M, Cohen AF, Romijn JA,
Sauerwein HP, Meinders AE, Pijl H. Blunted lipolytic response to fasting in abdominally
obese women: evidence for involvement of hyposomatotropism. Am J Clin Nutr. 2003
Mar;77(3):544-50.
Cahill GF Jr, Herrera MG, Morgan AP, Soeldner JS, Steinke J, Levy PL, Reichard GA Jr,
Kipnis DM.. Hormone-fuel interrelationships during fasting. J Clin Invest. 1966
Nov;45(11):1751-69.
Cahill GF Jr. Fuel metabolism in starvation. Annu Rev Nutr. 2006;26:1-22.

Carlson AJ, J Nutr 1:363-77, 1946];
Carlson MG, Snead WL, Campbell PJ. Fuel and energy metabolism in fasting humans.
Am J Clin Nutr. 1994 Jul;60(1):29-36.
Chan JL, Heist K, DePaoli AM, Veldhuis JD, Mantzoros CS. The role of falling leptin
levels in the neuroendocrine and metabolic adaptation to short-term starvation in healthy
men. J Clin Invest. 2003 May;111(9):1409-21.
Chan JL, Stoyneva V, Kelesidis T, Raciti P, Mantzoros CS. Peptide YY levels are
decreased by fasting and elevated following caloric intake but are not regulated by leptin.
Diabetologia. 2006 Jan;49(1):169-73. Epub 2005 Dec 9.
Considine RV, Sinha MK, Heiman ML, Kriauciunas A, Stephens TW, Nyce MR,
Ohannesian JP, Marco CC, McKee LJ, Bauer TL, et al. Serum immunoreactive-leptin
concentrations in normal-weight and obese humans. N Engl J Med. 1996 Feb
1;334(5):292-5.
Corvilain B, Abramowicz M, Féry F, Schoutens A, Verlinden M, Balasse E, Horowitz M.

Effect of short-term starvation on gastric emptying in humans: relationship to oral
glucose tolerance. Am J Physiol. 1995 Oct;269(4 Pt 1):G512-7.
Crist DM, Peake GT, Egan PA, Waters DL. Body composition response to exogenous
GH during training in highly conditioned adults. J Appl Physiol 1988; 65(2): 579-584
Dall R, Kanaley J, Hansen TK, Møller N, Christiansen JS, Hosoda H, Kangawa K,

Jørgensen JO. Plasma ghrelin levels during exercise in healthy subjects and in growth
hormone-deficient patients. Eur J Endocrinol. 2002 Jul;147(1):65-70.
Dehmelt H. Re-adaptation hypothesis: explaining health benefits of caloric restriction.

Med Hypotheses. 2004;62(4):620-624
Dietz J, Schwartz J. Growth hormone alters lipolysis and hormone-sensitive lipase

activity in 3T3-F442A adipocytes. Metabolism. 1991 Aug;40(8):800-6
Ebeling P, Koivisto VA. Non-esterified fatty acids regulate lipid and glucose oxidation
and glycogen synthesis in healthy man. Diabetologia. 1994 Feb;37(2):202-9.
Elliot DL, Goldberg L, Kuehl KS, Bennett WM. Sustained depression of the resting
metabolic rate after massive weight loss. Am J Clin Nutr. 1989 Jan;49(1):93-6.
Fain JN, Kovacev VP, Scow RO. Antilipolytic effect of insulin in isolated fat cells of the
rat. Endocrinology. 1966 Apr;78(4):773-8.

Felig P, Wahren J. Protein turnover and amino acid metabolism in the regulation of
gluconeogenesis. Fed Proc. 1974 Apr;33(4):1092-7.
Fesling NE, Brasel JA, Cooper DM. Effect of low and high intensity exercise on
circulating growth hormone in men. J Clin Endocrinol Metab 1992; 75: 157-162
Fowelin J, Attvall S, von Schenck H, Smith U, Lager I. Characterization of the insulin-

antagonistic effect of growth hormone in man. Diabetologia 1991; 34(7): 500-6
Fredrikson G, Tornqvist H, Belfrage P. Hormone sensitive lipase and monoacylglycerol

lipase are both required for complete degradation of adipocyte triacylglycerol. Biochem
Biophys Acta 1986; 876: 288-293
Fryburg DA, Barrett EJ. Growth hormone acutely stimulates skeletal muscle but not
whole-body protein synthesis in humans. Metabolism. 1993; 42(9): 1223-7.
Galton DJ, Fain JN. Effects of prolonged incubation of isolated fat cells on their response
to hormones stimulating lipolysis and glucose metabolism. Biochem J. 1966
Feb;98(2):557-61.
Gardner CD, Kiazand A, Alhassan S, Kim S, Stafford RS, Balise RR, Kraemer HC, King
AC Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and
related risk factors among overweight premenopausal women: the A TO Z Weight Loss
Study: a randomized trial JAMA. 2007 Mar 7;297(9):969-77.
Glick SM, Roth J, Yalow RS, Berson SA. Assay of human growth hormone in plasma.
Nature. 1963 Aug 24;199:784-7.
Goodrick CL, Ingram DK, Reynolds MA, Freeman JR, Cider NL. Effects of intermittent
feeding upon growth and life span in rats. Gerontology. 1982;28(4):233-41.
Gormsen LC, Jessen N, Gjedsted J, Gjedde S, Nørrelund H, Lund S, Christiansen JS,

Nielsen S, Schmitz O, Møller N. Dose-response effects of free fatty acids on glucose and
lipid metabolism during somatostatin blockade of growth hormone and insulin in
humans. J Clin Endocrinol Metab. 2007 May;92(5):1834-42.
Gormsen LC, Nielsen C, Gjedsted J, Gjedde S, Vestergaard ET, Christiansen JS,

Jørgensen JO, Møller N. Effects of free fatty acids, growth hormone and growth hormone
receptor blockade on serum ghrelin levels in humans. Clin Endocrinol (Oxf). 2007
May;66(5):641-5.

Gravholt CH, Schmitz O, Simonsen L, Bulow J, Christiansen JS, Moller N. Effects of a
physiological GH pulse on interstitial glycerol in abdominal and femoral adipose tissue.
Am J Physiol 1999, 277 (5 pt 1):E848-E854.
Halberg N, Henriksen M, Söderhamn N, Stallknecht B, Ploug T, Schjerling P, Dela F..

Effect of intermittent fasting and refeeding on insulin action in healthy men. J Appl
Phsiol 2005; 99: 2128-2136
Hansen M, Morthorst R, Larsson B, et al. Effects of 2 wk of GH administration on 24-h

indirect calorimtery in young, healthy, lean men. American Journal of Physiology and
Endocrinology in Metabolism. 2005; 289: E1030-1038
Hartman ML, Farello G, Pezzoli SS, Thorner MO. Oral administration of growth
hormone (GH)-releasing peptide stimulates GH secretion in normal men. J Clin
Endocrinol Metab. 1992 Jun;74(6):1378-84
Hartman ML, Pezzoli SS, Hellmann PJ, Suratt PM, Thorner MO. Pulsatile growth
hormone secretion in older persons is enhanced by fasting without relationship to sleep
stages. J Clin Endocrinol Metab. 1996 Jul;81(7):2694-701.
Hartman ML, Veldhuis JD, Johnson ML, Lee MM, Alberti KG, Samojlik E, Thorner
MO. Augmented growth hormone (GH) secretory burst frequency and amplitude mediate
enhanced GH secretion during a two-day fast in normal men. J Clin Endocrinol Metab
1992;74:757-765
Ho KY, Veldhuis JD, Johnson ML, Furlanetto R, Evans WS, Alberti KG, Thorner MO..
Fasting enhances growth hormone secretion and amplifies the complex rhythms of
growth hormone secretion in man. J Clin Invest 1988; 81: 968-975
Horowitz M, Edelbroek MA, Wishart JM, Straathof JW. Relationship between oral
glucose tolerance and gastric emptying in normal healthy subjects. Diabetologia. 1993
Sep;36(9):857-62.
Imbeault P, Alméras N, Richard D, Després JP, Tremblay A, Mauriège P. Effect of a

moderate weight loss on adipose tissue lipoprotein lipase activity and expression:
existence of sexual variation and regional differences. Int J Obes Relat Metab Disord.
1999 Sep;23(9):957-65.
Jensen MD, Ekberg K, Landau BR. Lipid metabolism during fasting. Am J Physiol
Endocrinol Metab. 2001 Oct;281(4):E789-93.
Johannsson G, Marin P, lnn L, Ottosson M, Stenlof K, Bjorntorp P, Sjostrom L, Begtsson

BA. Growth hormone treatment of abdominally obese men reduces abdominal fat mass

improves glucose and lipoprotein metabolism and reduces diastolic blood pressure. J Clin
Endocrinol Metab 1997; 82(3):727-734
Johnson NA, Stannard SR, Rowlands DS, Chapman PG, Thompson CH, O'Connor H,
Sachinwalla T, Thompson MW. Effect of short-term starvation versus high-fat diet on
intramyocellular triglyceride accumulation and insulin resistance in physically fit men.
Exp Physiol. 2006 Jul;91(4):693-703.
Johnstone AM, Faber P, Gibney ER, Elia M, Horgan G, Golden BE, Stubbs RJ. Effect of
an acute fast on energy compensation and feeding behaviour in lean men and women. Int
J Obes Relat Metab Disord. 2002 Dec;26(12):1623-8.
Johnstone AM. Fasting - the ultimate diet? Obes Rev. 2007 May;8(3):211-22.
Jorgensen JO, Vahl N, Hansen TB, Thuesen L, Hagen C, Christiansen JS. Growth
hormone vs placebo treatment for one year in growth hormone deficient adults: increase
in exercise capacity and normalization of body composition. Clin Endocrinol 1996;45(6):
681-688
Kamel A, Norgren S, Elimam A, Danielsson P, Marcus C. Effects of growth hormone

treatment in obese prepubertal boys. J Clin Endorcinol Metab 2000; 85(4):1412-1419
Kasa-Vubu JZ, Barkan A, Olton P, Meckmongkol T, Carlson NE, Foster CM. Incomplete
modified fast in obese early pubertal girls leads to an increase in 24-hour growth
hormone concentration and a lessening of the circadian pattern in leptin. J Clin
Endocrinol Metab. 2002 Apr;87(4):1885-93.
Klein S, Sakurai Y, Romijn JA, Carroll RM. Progressive alterations in lipid and glucose
metabolism during short-term fasting in young adult men. Am J Physiol. 1993 Nov;265(5
Pt 1):E801-6.
Kmiec Z, Pokrywka L, Kotlarz G, Kubasik J, Szutowicz A, Mysliwski A. Effects of

fasting and refeeding on serum leptin, adiponectin and free fatty acid concentrations in
young and old male rats. Gerontology. 2005 Nov-Dec;51(6):357-62.
KN Frayn, Metabolic Regulation. A Human Perspective, First Ed., Portland Press Ltd.,
London, 1996, pp.166-174.
Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-

hormone-releasing acylated peptide from stomach. Nature. 1999 Dec 9;402(6762):656-
60.

Kuczmarski RJ. Prevalence of overweight and weight gain in the United States. Am J
Clin Nutr. 1992 Feb;55(2 Suppl):495S-502S.
Larsen AE, Tunstall RJ, Carey KA, Nicholas G, Kambadur R, Crowe TC, Cameron-
Smith D. Actions of short-term fasting on human skeletal muscle myogenic and atrogenic
gene expression. Ann Nutr Metab. 2006;50(5):476-81. Epub 2006 Aug 24.
Larsen AE, Tunstall RJ, Carey KA, Nicholas G, Kambadur R, Crowe TC, Cameron-
Smith D. Fasting activates the gene expression of UCP3 independent of genes necessary
for lipid transport and oxidation in skeletal muscle. Biochemical and Biophysical
Research and Communications 2002;294:301-308
Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from

altered body weight. N Engl J Med. 1995 Mar 9;332(10):621-8.
Liu CD, Aloia T, Adrian TE, Newton TR, Bilchik AJ, Zinner MJ, Ashley SW, McFadden
DW. Peptide YY: a potential proabsorptive hormone for the treatment of malabsorptive
disorders. Am Surg. 1996 Mar;62(3):232-6.
Maccario M, Grottoli S, Procopio M, Oleandri SE, Rossetto R, Gauna C, Arvat E, Ghigo

E. The GH/IGF-I axis in obesity: influence of neuro-endocrine and metabolic factors Int J
Obes Relat Metab Disord. 2000 Jun;24 Suppl 2:S96-9.
Mansell PI, Macdonald IA. The effect of starvation on insulin-induced glucose disposal
and thermogenesis in humans. Metabolism. 1990 May;39(5):502-10.
Merl V, Peters A, Oltmanns KM, Kern W, Born J, Fehm HL, Schultes B. Serum
adiponectin concentrations during a 72-hour fast in over- and normal-weight humans. Int
J Obes (Lond). 2005 Aug;29(8):998-1001.
Misra M, Cord J, Prabhakaran R, Miller KK, Klibanski A. Growth Hormone Suppression

Following an Oral Glucose Load in Children. J Clin Endocrinol Metab. 2007;92:4623-
4629
Mittendorfer B, Horowitz JF, Klein S. Gender differences in lipid and glucose kinetics
during short-term fasting. Am J Physiol Endocrinol Metab. 2001 Dec;281(6):E1333-9.
Moller N, Jorgensen JO, Alberti KG, Fryberg A, Schmitz O. Short-term effects of growth
hormone on fuel oxidation and regional substrate metabolism in normal man J Clin
Endocrinol Metab. 1990 Apr;70(4):1179-86. J
Nørrelund H, Børglum J, Jørgensen JO, Richelsen B, Møller N, Nair KS, Christiansen JS.
Effects of growth hormone administration on protein dynamics and substrate metabolism

during 4 weeks of dietary restriction in obese women. Clin Endocrinol (Oxf). 2000
Mar;52(3):305-12.
Norrelund H, Nair SK, Jorgensen JOL. The protein-retaining effects of growth hormone
during fasting involve inhibition of muscle-protein breakdown. Diabetes 2001; 50: 96-
104
Nørrelund H, Nielsen S, Christiansen JS, Jørgensen JO, Møller N Modulation of basal

glucose metabolism and insulin sensitivity by growth hormone and free fatty acids during
short-term fasting Eur J Endocrinol. 2004 Jun;150(6):779-87.
Norrelund H, Riis AL, Moller N. Effects of GH on protein metabolism during dietary

restriction in man. Growth hormone & IFG Research 2002; 12: 196-207
Norton L, Parr T, Bardsley RG, Ye H, Tsintzas K. Characterization of GLUT4 and

calpain expression in healthy human skeletal muscle during fasting and refeeding. Acta
Physiol (Oxf). 2007 Mar;189(3):233-40.
Oscarsson J, Ottosson M, Johansson JO, Wiklund O, Mårin P, Björntorp P, Bengtsson

BA. Two weeks of daily injections and continuous infusion of recombinant human
growth hormone (GH) in GH-deficient adults. II. Effects on serum lipoproteins and
lipoprotein and hepatic lipase activity. Metabolism. 1996 Mar;45(3):370-7.
Parikh NI, Pencina MJ, Wang TJ, Lanier KJ, Fox CS, D'Agostino RB, Vasan RS..
Increasing trends in incidence of overweight and obesity over 5 decades Am J Med.
2007; 120(3): 242-50.
Pedersen SB, Kristensen K, Fisker S, Jørgensen JO, Christiansen JS, Richelsen B.

Regulation of uncoupling protein-2 and -3 by growth hormone in skeletal muscle and
adipose tissue in growth hormone-deficient adults. J Clin Endocrinol Metab. 1999
Nov;84(11):4073-8.
Rabinowitz D, Klassen GA, Zierler KL. Effect of human growth hormone on muscle and
adipose tissue metabolism in the forearm of man. J Clin Invest. 1965 Jan;44:51-61.
Ravussin E, Lillioja S, Anderson TE, Christin L, Bogardus C. Determinants of 24-hour

energy expenditure in man. Methods and results using a respiratory chamber. J Clin
Invest. 1986 Dec;78(6):1568-78.
Reitman ML. FGF21: A Missing Link in the Biology of Fasting. Cell Metab. 2007
Jun;5(6):405-7.

Richelsen B, Pedersen SB, Borglum JD, Moller-Pedersen T, Jorgensen J, Jogensen JO.
Growth hormone treatment of obese women for 5 wk effect on body composition and
adipose tissue LPL activity. Am J Physiol 1994;26 (2 pt 1): E211-E216
Richelsen B. Action of growth hormone in adipose tissue. Horm Res 1998: 48 Suppl 5:
105-110
Riedel M, Hoeft B, Blum WF, von zur Mühlen A, Brabant G. Pulsatile growth hormone
secretion in normal-weight and obese men: differential metabolic regulation during
energy restriction. Metabolism. 1995 May;44(5):605-10.
Ruge T, Svensson M, Eriksson JW, Olivecrona G. Tissue-specific regulation of

lipoprotein lipase in humans: effects of fasting. Eur J Clin Invest. 2005 Mar;35(3):194-
200.
Russell-Jones DL, Weissberger AJ, Bowes SB, Kelly JM, Thomason M, Umpleby AM,
Jones RH, Sönksen PH. The effects of growth hormone on protein metabolism in adult
growth hormone deficient patients. Clin Endocrinol Oxf 1993; 38: 427-431
Salomon F, Cumeo RC Hesp R, Sonksen PH, The effects of treatment with recombinant
human growth hormone on body composition and metabolism in adults with growth
hormone deficiency. N Engl J Med 1989; 321 (26):1797-1803
Samra JS, Clark ML, Humphreys SM, Macdonald IA, Frayn KN. Regulation of lipid
metabolism in adipose tissue during early starvation. Am J Physiol 1996;271:E541-
E546
Savastano S, Di Somma C, Belfiore A, Guida B, Orio F Jr, Rota F, Savanelli MC,

Cascella T, Mentone A, Angrisani L, Lombardi G, Colao A. Growth hormone status in
morbidly obese subjects and correlation with body composition. J Endocrinol Invest.
2006 Jun;29(6):536-43.
Sengupta K, Long KJ, Allen DO. Growth hormone stimulation of lipolysis and cyclic
AMP levels in perifused fat cells. J Pharmacol Exp Ther. 1981 Apr;217(1):15-9.
Skaggs SR, Crist DM. Exogenous human growth hormone reduces body fat in obese
women. Horm Res 1991; 35(1):19-24
Stote KS, Baer DJ, Spears K, Paul DR, Harris GK, Rumpler WV, Strycula P, Najjar SS,
Ferrucci L, Ingram DK, Longo DL, Mattson MP. A controlled trial of reduced meal
frequency without caloric restriction in healthy, normal-weight, middle-aged adults. Am J
Clin Nutr. 2007 Apr;85(4):981-8.

Tayek JA, Katz J. Glucose production, recycling, Cori cycle, and gluconeogenesis in
humans: relationship to serum cortisol. Am J Physiol. 1997 Mar;272(3 Pt 1):E476-84.
Toubro S, Sørensen TI, Rønn B, Christensen NJ, Astrup A. Twenty-four-hour energy

expenditure: the role of body composition, thyroid status, sympathetic activity, and
family membership. J Clin Endocrinol Metab. 1996 Jul;81(7):2670-4
Tschöp M, Wawarta R, Riepl RL, Friedrich S, Bidlingmaier M, Landgraf R, Folwaczny

C. Post-prandial decrease of circulating human ghrelin levels. J Endocrinol Invest. 2001
Jun;24(6):RC19-21.
Valcavi R, Zini M, Volta C, Ghizzoni L, Azzarito C, Bernasconi S, Portioli I. Effects of

oral glucose administration on spontaneous and growth hormone (GH)-releasing
hormone-stimulated GH release in children and adults. J Clin Endocrinol Metab. 1994
Oct;79(4):1152-7.
Veldhuis JD, Iranmanesh A, Ho KK, Waters MJ, Johnson ML, Lizarralde G. Dual
defects in pulsatile growth hormone secretion and clearance subserve the
hyposomatotropism of obesity in man. J Clin Endocrinol Metab 1991;72:51-69
Vu V, Riddell MC, Sweeney G. Circulating adiponectin and adiponectin receptor

expression in skeletal muscle: effects of exercise. Diabetes Metab Res Rev. 2007
Nov;23(8):600-11.
Webber J, Macdonald IA. The cardiovascular, metabolic and hormonal changes

accompanying acute starvation in men and women. Br J Nutr. 1994 Mar;71(3):437-47.
Weigle DS, Duell PB, Connor WE, Steiner RA, Soules MR, Kuijper JL. Effect of fasting,
refeeding, and dietary fat restriction on plasma leptin levels. J Clin Endocrinol Metab.
1997 Feb;82(2):561-5.
Wolfe RR, Peters EJ, Klein S, Holland OB, Rosenblatt J, Gary H Jr. Effect of short-term
fasting on lipolytic responsiveness in normal and obese human subjects. Am J Physiol.
1987 Feb;252(2 Pt 1):E189-96.
Wren AM, Small CJ, Ward HL, Murphy KG, Dakin CL, Taheri S, Kennedy AR, Roberts
GH, Morgan DG, Ghatei MA, Bloom SR The novel hypothalamic peptide ghrelin
stimulates food intake and growth hormone secretion. Endocrinology. 2000
Nov;141(11):4325-8.
Zauner C, Schneeweiss B, Kranz A, Madl C, Ratheiser K, Kramer L, Roth E, Schneider

B, Lenz K. Resting energy expenditure in short-term starvation is increased as a result of
an increase in serum norepinephrine. Am J Clin Nutr. 2000 Jun;71(6):1511-5.

Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM. Positional cloning

of the mouse obese gene and its human homologue. Nature. 1994 Dec 1;372(6505):425-
32.

  

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The Eat Stop Eat Advanced

All rights Reserved

No portion of this manual may be used, reproduced, or transmitted in any

The information in this book is for educational purposes only. The

The information within this book is meant for healthy adult

Brad Pilon, Strength Works, Inc.

Copyright © 2008 by Strength Works, Inc Page 2 of 107

Episode 1: Eat Stop Eat, Metabolism and ‘Starvation Mode’

Episode 2: Eat Stop Eat and the Metabolism of Fat Burning

Episode 3: Eat Stop Eat and Muscle Metabolism

Episode 4: Eat Stop Eat, Insulin and Blood Sugar Metabolism

Episode 5: Eat Stop Eat, Exercise and Your Body Composition

Episode 6: Eat Stop Eat, Health and Weight Loss

Copyright © 2008 by Strength Works, Inc Page 3 of 107

Copyright © 2008 by Strength Works, Inc Page 4 of 107

associated with an increased incidence of cardiovascular disease, diabetes, certain

put on fat. Sounds pretty crazy to me, but let’s investigate.

To scientifically investigate starvation mode, we’re going to need something to measure,

have to be reduced as a result of dieting.

carbohydrate. If it’s 0.7, you’re burning mostly fat.

Copyright © 2008 by Strength Works, Inc Page 6 of 107

into your blood.

we will have a good indication that starvation mode definitely exists.

All right, so let’s start with energy expenditure.

Copyright © 2008 by Strength Works, Inc Page 7 of 107

lowering of your metabolism due to a decrease in calorie consumption), mostly as a result

metabolism becomes lower than what a predictive estimate using mathematical

equations, suggest they should be.

How different? How much lower?

suggests that they should be.

Copyright © 2008 by Strength Works, Inc Page 8 of 107

cup of coffee per day worth of calories (but just one).

Copyright © 2008 by Strength Works, Inc Page 9 of 107

metabolic rate can be preserved by lifting weights.

Copyright © 2008 by Strength Works, Inc Page 10 of 107

Zauner in 2000, and most recently Gjedsted in 2007.

seven days of normal eating between each fast.

carbon dioxide consumption and production, using a ventilated canopy (indirect

calorimetry), which is a pretty standard measure of metabolic rate in research studies.

between 12 and 36 hours of fasting.

Copyright © 2008 by Strength Works, Inc Page 11 of 107

carbohydrates. RQ dropped down to 0.76 at 36 hours and 0.72 at 72 hours (remember

relied on a fat as a fuel source.

that it is not supported by research.

a fast of up to three days.

Copyright © 2008 by Strength Works, Inc Page 12 of 107

every 2-3 hours to prevent starvation mode.

these free fatty acids must be coming from somewhere.

Copyright © 2008 by Strength Works, Inc Page 13 of 107

with the appearance of increasing free fatty acids in the blood.

moving fat into your muscles to be burned as a fuel, also increases.

your metabolism stays the same.

Copyright © 2008 by Strength Works, Inc Page 14 of 107

towards increased fat burning.

your metabolic rate slowing down.

Copyright © 2008 by Strength Works, Inc Page 15 of 107

Copyright © 2008 by Strength Works, Inc Page 16 of 107

to come from somewhere.

concentration (plasma means blood concentration), which in turn is an important