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Copyright 2013, by Kiefer, Inc. All rights reserved.

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TABLE OF CONTENTS
Preface

04

Introduction

08

Chapter 01: Dont Just Burn Fat. Lose it.

14

Chapter 02: Metabolism and Fat Mobilisation 18


Chapter 03: Nicotine and Muscle Growth

25

Chapter 04: Controversial Aspects

31

Chapter 05: Unique Benefits of Nicotine

37

Chapter 06: The Protocols

40

Chapter 07: Ultimate Fat Burning Stack

49

Chapter 08: Frequently Asked Questions

56

References

61

PREFACE

PREFACE
For years, nicotine was little more to me then an object of scientific
curiosity. It was something to study. Id come across it from time
to time in fat loss and muscle building articles and studies, and I
certainly found some of the research thats been done intriguing, but
its never been an emotionally charged issue for me. Nothing scientific is, nor should it ever be, unless were talking about the euphoria
associated with a new discovery or a hypothesis thats just been
proven.
It wasnt until I tried to publish my own findings on nicotine in the
media, however, that it really piqued my interest and made me want
to do more. Nobody wanted to touch the subject, which is the sort
of truth avoidance that compels me to write longer books like Carb
Back-Loading and reports like this one: The idea that theres something out there that can help us get the bodies we want, that the
powers-that-be, for whatever reason, either dont want us to know
about or refuse to grant credibility to, despite what science is telling
us.

I regularly write for some of the biggest magazines in the fitness


industrywith Mens Health, Mens Fitness, Muscle & Fitness,
and Flex among these. I dont want to name names, but one major publica

tiontrust me, youve heard of itapproached me

to write a feature article on something unique and scientific that


works for the purposes of fat loss and muscle building. When I proposed a piece on the health and performance benefits of nicotine
supplementation, the editor-in-chief himself told me it couldnt, and
wouldnt ever, run in their family-oriented magazine.
Now, Ive heard all the rumors about nicotines hazards, but Im not
entirely sure what, if any, effects a naturally-occurring molecule can
have on our collective family values. Still, Ive found most magazine
editors to be nice, sensible people, so I didnt press the issue and
wrote about something else.
The more research I did on the subject, however, the more nicotines benefits nagged at meto the point where I decided to put
together this comprehensive report on its efficacy and use. Thats
the thing, though: Ive done my research, and Ive used nicotine
protocols both on myself and with my clients. With this release, Ive
done my absolute best to piece together a compendium of information that will guide you to make both intelligent decisions as to
whether you want to use nicotine or not, and to do it properly if you
decide to try it.

PREFACE

The other important thing to note here is that this information isnt
for everyone. This is high-performance stuff thats intended for the
use of serious people only. Nicotine isnt a magic bullet, so before
you consider taking it for the purposes were talking about, you need
to make sure everything elseyour diet, training, and all the other
supplementation youre doingis dialed in and on point.
Nicotine wont counteract the effects of doing any of these other
things wrong. Its not your diet and training savior. Instead, the idea
is to show you how to enhance the things youre doing rightbut
you need to be doing them right first for any of this to mean anything.
What youre about to read ventures far outside the box with regard
to whats typically recommended for health purposes. Ive written
this report to help you make sense of it all and decide for yourself.
When used under the correct conditions, nicotine can safely accelerate your progress without the side effects common to other fat
burnersbut again, when youre dealing with a substance thats
been stigmatized so viscerally for so long, theres a great deal to
discuss first.
Thats what I want to do with this report. The rest is up to you.
Kiefer

PREFACE

INTRODUCTION

Origin Story

INTRODUCTION
Origin Story
My professional background, aside from my work in physics and
software, involves working extensively with physique competitors
preparing for competition. I realize that many of you arent preparing for competition, but since fat loss and muscle gain mean literally
everything to competitorsafter all, theyve necessarily had to refine
the process to a far greater extent than anyone else in the world
Im using physique, and its methods, to explain how and why nicotine works.
What I found in the physique realm was that virtually all higher-level
competitorspeople who have to get down to insanely low levels of
body fat before getting on stageuse massive amounts of prescription medications like clenbuterol and albuterol, among other powerful fat burners. The less the coach understands about the human
body, the more fat burners they prescribe.

These drugs work essentially the way adrenaline and caffeine do,
by stimulating the sympathetic nervous systemthe flight-or-fight
response coordinatorthrough activation of the beta-adrenergic receptors. When you take these fat burners, youre piling them on top
of a stress load that already exists if youre attempting to lose body
fat with exercise and calorie restriction. This means youre eventually going to reach a point of diminishing returns where theyre no
longer effective.
The world of physique competition is saturated with these medications. Youll have a difficult time finding a conditioning coach for the
stage who doesnt recommend taking a lot of them.
The competitors coming to me didnt want to take these drugs
because they destroy the metabolism and can overtax the adrenal glands, leaving the body devastated after the competition.
Some of my clients experienced this themselves, and all of them
said theyd seen it happen with others in the aftermath of contest
preparation using fat burners. After youve taken them for a while,
you go through a rebound effect where you gain weight and fat,
and theres absolutely nothing you can do about itand its all as a
result of the drugs, which Ill explain as we go along.

INTRODUCTION

10

Although the right diet can get you very close to where you need
to be (unfortunately, most coaches dont use anything remotely
resembling the right diet), you can definitely give yourself an edge
if youre willing to take these prescription medications. After seeing their adverse effects, however, I wanted to give my competitors
a natural edgeand I wanted that edge to be even more effective
than the pharmaceutical one.
What These Drugs Actually Do To You
When prescription fat burners are working properlyIll explain
why they stop doing so, and what happens when they stop, later
onthey increase your metabolism and coax your fat cells to help
release fat into the system. This is especially important because
most, if not all, traditional diets stop this process. The diets that
most competitors use make it almost impossible to mobilize body
fatnote the use of the word mobilize, and not burnso you have
to add the drugs in order to make everything work.
From what Ive seen, the diets of the vast majority of competitors
are so bad that massive amounts of prescription drugs become
necessary to fix the damage these athletes nutritionists and coaches are inflicting on them.

INTRODUCTION

11

As usual, however, theres a nasty downside to all of this. Whats


happening here is that youre burning out your system. Your body
will try to decrease thyroid hormone because your energy expenditure has risen too high, so it will downregulate your metabolism.
When you take more drugs to bring your metabolism back up, your
thyroid shuts off.
When you stop taking the drugs, and start gaining weight back
normally, your metabolism will slow, and all the food you eat will be
channeled into restoring your body fat reserves. Your body does
this very well.
These drugs will also burn out your adrenal glands. These glands
are producing massive amounts of adrenaline and cortisol. As a result, theyre overstressed and overtaxed. At this point, they go into a
kind of survival mechanism where they dump cortisol, and continue
dumping it.
So here you are, with high cortisol levels and a very low metabolism. What do you think is going to happen when you start eating
carbohydrates? If youre thinking this is a recipe for disaster, youre
absolutely correct. The carbs plus the cortisol will lead you to massive and rapid fat regain, and most competitors end up getting far
fatter than they ever were before.

INTRODUCTION

12

Taboo, Yet Terribly Effective


When I was trying to figure everything outhow to help my clients
avoid this horrific rebound effectI saw some studies talking about
the benefits of nicotine as a fat mobilizer. This led me to think about
smokers. When people who smoke indulge their habit, theyre usually fairly lean. When they quit, however, they almost immediately
start gaining weight. More importantly, they gain this weight as
excess body fat.
Of course, the people were talking about here are profoundly unhealthy, but it struck me that, when all the peripheral carcinogens
from smoking are removed from the equation, this could conceivably
mean that nicotine is a viable and possibly safe fat burner. Insane?
Sure, but as it turns out, this may actually be the case.

INTRODUCTION

13

CHAPTER 01

Dont Just Burn Fat. Lose It.

CHAPTER 01
Dont Just Burn Fat. Lose It.
Exercise is supposed to get you lean, right? This is obviously the
common wisdom, because exercising burns more fat than activities
where youre not exercising. What you need to understand, however,
is that everything burns fat. Sitting at your computer all day burns
fat. Driving your car burns fat. Just about every activity you can possibly undertake will burn fat (even if at a very slow rate)1.
Trouble is, burning fat is a completely separate and independent
process from losing body fat, and thats the distinction most people
fail to understand or acknowledge. We know that fatty acids are
coming in, and we know they go into the oxidative pathway to get
burned for energy. Thats how fat is burned.
We know all this, but where does this fat come from? Well, its mostly from your dietand when your diet cant supply enough, it starts

15

to come from liver reserves, if possible. Weve also just learned that
the entire intestinal tract in the human body has specialized cells
that store fat, too2. In other words, youre getting a fat dump from
places that dont necessarily contain the body fat youre trying to
lose.
The solution? When youre trying to go into any kind of available
energy deficit (calorie deficit), or youre dieting down for the competitive stageor you simply want to stimulate fat cells to lose fatyou
have to create the right environment for this to happen.
For example, a very low-fat, high-carb diet for weight loss will actually force fat cells to refuse to release body fat3-5. This type of diet
will make them try very, very hard to hold onto body fat. Exercising
too much has the same effect, especially when were talking about
cardio. The misapplication of cardio actually forces fat cells to not
get rid of body fat6.
What this means is that even though youre burning fat in your muscles, youre not mobilizing your body fat reserves. This is why people who rely on cardio to get rid of body fat fail. Even though theyre
burning a lot of fat, its only the fat theyre eating and the fat stored
in muscle tissue7. Their fat cells arent releasing it to be burned.

CHAPTER 01

16

Were already in an environment where our bodies are burning fat.


This happens all the time. What we really need is to create an environment where our fat cells are dumping fat to be burned. Thats
the key distinction: Its easy to burn fat, but theres a huge difference
between fat burning and fat mobilisation.
Why Prescription Drugs Fail
Theres a simple explanation for what happens when you take the
conventional pharmaceutical fat burner regimen advocated by most
physique coaches. I coined the phrase adrenaline diabetes to describe why conventional fat burners fail.
When you get too much adrenaline, the beta-adrenergic receptors
on your cells downregulate8-12. Its almost as though theyve built
up a tolerance, and it takes more and more to stimulate them. This
eventually reaches a tipping point where its almost impossible to
stimulate them any furtherand when you eat carbohydrates after
finishing your drug regimen, youll have a rebound effect and get fat
in a hurry.
The simple solution to all of this: Properly dosed nicotine. Believe it
or not, nicotine even works for individuals in the throes of this adrenaline diabetes effect. In the following chapters, Ill explain how this
works.

CHAPTER 01

17

CHAPTER 02

Nicotine, Metabolism and Fat Mobilisation

CHAPTER 02

Nicotine, Metabolism and Fat Mobilisation


Fat Mobilisation
If youre using a sound nutritional system, nicotine will accelerate
body fat loss. In other words, if youre not already the proud owner
of a copy of Carb Back-Loading or The Carb Nite Solution, you
shouldnt be reading this report. Also, note again that Im referring
not to fat burning, but body fat loss. When used correctly, nicotine
is a natural and safe way to speed the results of any fat loss diet.
Remember that body fat loss requires fat cells to release stored fat.
Most energy deprivation dietsthose which require you to expend
more energy than you absorb, either through food restriction, exercise or bothcan eventually force fat cells to release some fat
through the beta-adrenergic pathway mentioned above. As the body
becomes stressed from energy restriction, it releases ever increasing amounts of cortisol and catecholamines (like adrenaline and noradrenaline) which will force fat cells to release fatty acids for energy.

19

These stress hormones work to release body fat by activating an


enzyme in fat cells called hormone-sensitive lipase (HSL). HSLs
main role is to release free fatty acids from fat cells for use as energy13, which decreases the size of adipose tissue. Because HSL
requires activation by these hormones, its no mystery why HSL is
labeled as hormone-sensitive. This is one way to cause fat cells to
mobilize body fat for energy.
Nicotine also stimulates the release of epinephrine, which contributes to nicotines utility as a fat-loss agent14-15. As mentioned above,
the problem with relying solely on this strategyincreasing stress
hormones and decreasing energy availabilityis that metabolism
slows to compensate for this energy deficit, and we develop adrenaline diabetes, resulting in less and less body fat lossalong with
other hormonal signals that make it nearly impossible to continue
losing body fat without total starvation.
Although nicotine can have profound effects on catecholamine release, fat cells contain specialized receptors to which nicotine binds.
Whats unusual about this is that these receptors are not the normal
pathway used by catecholamines, i.e. the beta-adrenergic receptors.
Instead, there exists a separate pathway we can activate that tells
fat cells to release fat16-17, which is apparently independent of HSL

CHAPTER 02

20

activity18. This is why, even if youre stuck in the adrenaline diabetes


discussed in the previous chapter, you can still take nicotine to tell
your fat cells to start dumping fat. This is essentially a back door into
fat mobilisation, and its the real power and magic of nicotine.
We can see this power of rapid fat release from adipose tissue in
human studies that show a massive rise in glycerinthe glue that
holds triglycerides together in fat cellsand free fatty acids in the
bloodstream after infusion of nicotine15. Since levels of catecholamines were elevated during this protocolan elevation that prevents muscle tissue from releasing triglyceridesits likely this surge
of fat came from the breakdown of tri- and diglycerides within adipose tissue.
Increased Metabolism and Resting Energy Expenditure
Nicotine needs no introduction as a stimulant. By activating the
sympathetic nervous system, both directly and by causing a release
of catecholamines as mentioned above, nicotine can increase resting energy expenditure14, 19-20. We know, unfortunately, how transient
this effect can be (if it even occurs at all), since you may already be
in a state of adrenaline diabetes.
The sympathetic nervous system is not the only path by which

CHAPTER 02

21

nicotine can increase resting energy expenditure. Nicotine can also


increase thermogenesis, making the body more inefficient. This is
how mammals regulate body temperature to stay warm, through the
oxidation of fatty acids.
Nicotine increases thermogenesis through upregulation of uncoupling protein 1 (UCP1)21-22. As levels of UCP1 increase, fatty acids
within the mitochondria no longer generate ATP. Instead, fatty acid
oxidation generates heat23-24. This happens primarily in adipose tissue (both brown and white).
By increasing the amount of uncoupling protein, we essentially
make the body into a heater, dissipating energy that we ingest and
release from fat cells in the form of heat. In studies with artificial uncoupling agents, this can increase resting energy expenditure by as
much as 30%. Although were unlikely to achieve that with nicotine
alone, well discuss later how this might be possible in conjunction
with nicotine use.
Of additional relevance is the fact that the bodys resting energy output decreases with any type of calorie deprivation, or (my preferred
term for this) energy deficit. Pay close attention to this if youre using
an intermittent fasting (IF) protocol, because its why starving yourself for fat loss decreases your energy output. Calorie deprivation

CHAPTER 02

22

downregulates UCP125-26. Nicotine re-stimulates it so you can keep


burning fat, even if your diet has you dropping calories, or going for
long periods without food, as happens with IF.
How This Works For Smokers
Smokers get and stay thin primarily because of nicotines power to
increase metabolism. As this power is turning on, however, its also
flipping a switch in the smokers fat cells that says, essentially, Hey,
dont store fat. No matter what you do, you cant store fat, and if
youve got any fat in storage, you have to get rid of it. Smoking puts
a limiting factor on how much fat your body can actually store, and
your body fights to not store body fat any longer.
The key to fat loss from smoking is this double whammy effect.
Smokers will increase their metabolism and burn more fat than
normal, while their fat cells have a very difficult time trying to store
fat. This is why they stay so thin. When they stop smoking, however,
this all comes to an abrupt halt. If you turn all these mechanisms off,
then flip the switch back the other way, youll then have a multitude
of empty fat cells saying, Oh, hell yeah! Now we can fill up! And
this is precisely what they do. Quickly.
Now, Im not advocating smoking as a protocol for losing body fat.

CHAPTER 02

23

Far from it, as Ill discuss later on. The purpose of this section is to
explain why chronic smokers are thin, and why they gain so much
weight back when they stop smoking. Smoking is a deadly habit
that devastates countless systems within the human body, and my
recommendation is to stay as far away from cigarettes as humanly
possible.

CHAPTER 02

24

CHAPTER 03

Nicotine and Muscle Growth

CHAPTER 03
Nicotine and Muscle Growth
Its fat loss properties notwithstanding, what really excited me about
nicotine originally was its potential as a muscle building agent.
Every cell in the human body has a pathway called the target of
rapamycin (TOR). TOR is essentially a regulatory chain for growth.
If its stimulated, your cells will tend to bring in nutrients, theyll grow,
and if theyre in the correct situation, theyll cause proliferation.
This, obviously, is the ideal situation for muscle cells, and its the
reason insulin and glucose help us growbecause theyre direct
stimulators of the TOR pathway. Leucine is also a regulator of the
TOR pathway, which is the reason youll always hear me recommend leucine supplementation with all my programs.
The problem with glucose and leucine, however, is that they can
both cause releases of insulin. This is not an ideal situation when
youre trying to get rid of body fat. In contrast, the amazing thing

26

about nicotine is that its one of the fewif onlynatural, nonnutritive substances that directly stimulates this TOR pathway of
growth27.
This has two advantageous effects. First, if youre trying to get rid of
as much body fat as possible, nicotine is helping to preserve your
muscle tissue. If youre getting a growth signal, your body wont
destroy this tissueor, at the very least, it will attempt to avoid
destroying it. Next, if youre in a hypertrophy phase where youre
trying to add mass, youll be giving a stronger growth signal to your
muscle tissue.
Nicotines Effect on TOR
If you want to increase growth in any cell in your body, you have to
activate the TOR pathway. If its turned off, its very hard for your
body to grow. Rapamycin is an anti-cancer drug that turns off the
TOR pathway, essentially negating any gains you get from resistance training. When this pathway is turned off, you can lift weights
all day, every day, without any benefit to your muscles.
When the TOR pathway shuts off, you cant grow. This is obviously
beneficial for cancer patients, because it means no cells can grow.
Cancer cells are typically highly rampant, and they grow rapidly, but

CHAPTER 03

27

rapamycin has the capability of shutting that growth down, including


skeletal muscle hypertrophy28-29.
When youre in available energy deprivation, or youre trying to lose
body fat, the TOR pathway can be turned off fairly easily. Nicotine
comes into play when youre trying to recomposition your body by
losing fat and gaining muscle at the same time. It allows this to happen much more effectively without the consequences of loading up
on sugar all the time.
Preventing Muscle Loss During Fat Loss
Moving back to our discussion about physique competitors, were
talking, in this case, about people who will often be in very intense
states of available energy deprivation. As this moves along, and
TOR gets shut off, it gives the entire body a signal that its okay
and necessaryfor it to catabolize lean tissue for energy. When you
keep the TOR pathway turned on, your body will try to preserve this
tissue, and it wont resort to catabolizing it for energy production.
Thats why nicotine has major advantages over the synthetic prescription drugs I outlined earlier. It gets your fat cells to release fat,
but it also potentially protects your muscle cells at the same time by
telling them to grow. Nicotine doesnt have enough nutrient resourc-

CHAPTER 03

28

es to actually grow muscle tissue, but its trying, so therefore your


body wont destroy it.
Theres one other thing thats worth noting in this section, especially
with regard to hypertrophy. Nicotine does two additional things here:
It can increase nitrous oxide (NO) production during training, and it
activates the AMP-activated protein kinase (AMPK) pathway30. Freeradical accumulation during training tends to ignite muscular growth,
but if this stays elevated for too long, its detrimental.
We cant ignore the role of free fatty acids on skeletal muscle preservation. Elevated free fatty acids can preserve muscle tissue, even
during periods of starvation or energy deprivation31-35. Its hard to
say the exact mechanisms responsible for this preservation, but
it could be related to ketone production. High levels of free fatty
acids is enough to spark ketogenesis36-37, which nicotine causes
through various pathways. Ketones have demonstrated the ability to
preserve muscle tissue, although the mechanisms for this are still
unknown38-39.
Nicotine also has a great advantage for glucose uptake, which can
be particularly useful with Carb Nite, Carb Back-Loading or other
cyclic ketogenic diets. AMPK activation can enhance glucose uptake
in skeletal muscle tissue and can also possibly increase mitochon-

CHAPTER 03

29

drial biogenesis40. Mitochondrial biogenesis relates to the maximum


size a muscle fiber can obtain through training, but this process is
beyond the scope of this book and will be covered in an upcoming
book thatll show you how to achieve metabolic flexibility for highintensity, strength-endurance sports.
Finally, recent animal studies have shown that nicotine may stimulate a pathway that downregulates myostatinthe protein that prevents muscles from getting big41.

CHAPTER 03

30

CHAPTER 04

Controversial Aspects

CHAPTER 04
Controversial Aspects
What, exactly, is nicotine?
Nicotine is just a naturally-occurring substance produced by a family
of plants called nightshades. This family includes tomatoes, potatoes, bell peppers, hot peppers, and the tobacco plant42, with which
its most commonly associated. Nicotine is really just a small natural
moleculelike caffeinethat happens to bind to some really cool
stuff in our system. And on its own, nicotine is nowhere near as evil
as youve been led to believe.
We regard nicotine as dangerous because our thinking has been guided, historically, by the effects we believe it has on smokers. What we
dont take into account, however, is that smokers ingest nicotine every
single day in dangerously high levels. For years, a typical smoker will
take in 60-80 mg on a daily basis. That kind of dosage for that length of
time is dangerous, and research has shown this time and time again.

32

We run into problems when we extrapolate our facts from this


data. When you get to the protocols section of this report, youll see
Im only recommending much smaller dosages of nicotine per day,
as opposed to smoker-level dosages. What weve extrapolated over
the years, though, is the notion that if megadoses of nicotine are
dangerous, then any amount of nicotine must necessarily be dangerous, too.
Research has shown this logic to be faulty, and that nicotine by itself
isnt necessarily carcinogenic43. This doesnt mean there arent any
downsides to it, but in order to recognize nicotines role in the hierarchy, you need to understand what a carcinogen actually is.
Carcinogens are substances that trigger the development of cancer.
When a carcinogen enters your body, it will disrupt cells and make
them start doing bad things, i.e., theyll become cancerous. Carcinogens are the genesis of cancer.
This, however, isnt the case with nicotine. It hasnt been shown to
be potently carcinogenic by itself. Problems occur when you already
have cancer, because nicotine will stimulate that growth pathway44-48.
This is why cancer patients cant take growth hormonebecause
GH will cause all the cells in the body to grow, including the cancerous ones. This, obviously, makes cancer worse.

CHAPTER 04

33

If youre young and healthy, theres very little risk of nicotine having
any deleterious effects with regard to cancer, but there are some
other negatives. Its been shown to age arterial tissueyour arteries
and veinsbut thats only when taken in very high dosages over a
long period of time.
We see this advanced aging of the circulatory system most frequently in smokers, who often experience a hardening of the arteries49.
The dosages of smokers, however, get up into the 60 mg per day
range on a daily basis, and this can happen for decades50. Again,
as youll see in the protocols section, Im recommending much lower
dosages, because you dont need anything near what smokers
ingest to experience the benefits of nicotine. These lower dosages
serve to attenuate the potential downside.
With smokers, nicotine adds yet another double whammy effect.
Everything else contained in cigarettesall the tar thats entering
your lungs, for examplewill create the cancer, and then with all
the nicotine smokers constantly take in, theyre essentially telling
the cancer to grow faster. This is why lung cancer is usually the first
form to develop in smokers, because the nicotine is having an effect
in the lungs very early and very quicklyinteracting with cancer
cells that are already growing rapidly.

CHAPTER 04

34

Why Its Safe


There are volumes of research available showing that it takes a long
time, with very high dosages, for nicotine to case anything negative
to happen, whether were talking about arterial hardening or cancer.
There are simply too many other factors in play to claim that nicotine
is the actual genesis of the damage.
Out in the real world, we see the real causes of cancer with people
who dont care about their health. Theyre sick, theyre malnourished, theyre vitamin deficient, and nicotine makes all of this worse
because its an extra stressor on the body.
When youre healthy, however, small dosages of nicotine can actually be beneficial for you because they can instigate tissue repair
and help mobilize body fatand weve found no evidence that small
doses, even taken over long periods of time, can have any negative
side effects at all.
One Final Consideration
The other major downside we see with most people is nicotines
ability to cause a dump of triglycerides, which in the presence of
glucose can actually exacerbate the development of diabetes27,51.

CHAPTER 04

35

This is especially dangerous when youre on a carbohydrate-based


diet.
The idea, then, is to avoid mixing nicotine with carb ingestion, because it can interfere with the absorption of glucose into your muscle cells. This is why people get sick, and research has shown that
smokers can develop diabetes without even being overweight51.

CHAPTER 04

36

CHAPTER 05

Unique Benefits of Nicotine

CHAPTER 05
Unique Benefits of Nicotine
Nootropic Effects
The ability to reason correctly and logically is a lost art in todays
world, and nowhere is this more evident than in the fitness, health
and medical industries. Logical thinking and the ability to make reasonable connections across large amounts of information depends
on whats called working memory52.
Both animal and human studies demonstrate that nicotine, through
novel receptors in neuronal tissue, can increase the efficiency of
working memory53-54. Nicotine can impart a clear benefit for test taking and technical tasks like figuring out your taxes or programming a
computer.
Appetite Suppression
The unfortunate downside of most fat burners is a potential increase

38

in appetite because of the increased energy demands placed on the


body by an accelerated metabolism. This, of course, is amplified by
the fact that most mainstream diets used for fat loss cause massive
hunger pangs and making sticking with a diet difficult. The rebound
effect after dieting is also worse because of the increased hunger.
Nicotine is a powerful appetite suppressant, probably more so than
any other naturally occurring substance55-57. People using the protocols outlined in this manual, particularly competitors, report extreme
hunger control to the point of losing the desire to eateven when
such a state would put them into an unfavorable energy deficit.
Regardless of performance or fat loss goals, or even the need to
endure long periods without adequate nutrition while maintaining
heightened cognition, short-term nicotine use can impart significant
benefits to anyone.

CHAPTER 05

39

CHAPTER 06

The Protocols

CHAPTER 06
The Protocols
To find the correct dosing necessary for the fat mobilizing and burning effects of nicotine, we first need to investigate nicotine metabolisation and blood concentrations necessary for these benefits. For
this section, Im going to discuss the use of nicotine gum, since
most of the data from human trials looks at peak nicotine levels and
clearance rate using gum. We can therefore make sure our dosing
achieves the blood concentrations needed for results.
Direct research on the increase in energy expenditure via nicotine
shows that a 1 or 2 mg piece significantly increased resting metabolism and demonstrated a dose-dependent response58. In other
words, the greater the dosage of nicotine in the gum, the greater
the effect. This study, unfortunately, didnt measure blood nicotine
levels.
In the above cited works17,19, the profound effects seen on fat mo-

41

bilisation and increased fat oxidations were achieved with intravenous infusion of nicotine until levels reached between 7 and 8 ng/ml
(nanograms per milliliter). This would require a piece of gum containing 4 mg of nicotine59.
So, if we want the maximum benefit of fat burning and fat mobilisation, well need to chew 4 mg pieces of nicotine gum. With this, peak
levels of nicotine will be achieved within 30 minutes of chewing and
maintained for roughly two hours or more59.
Researchers also demonstrated that even modest amounts of caffeine added to the nicotine gum significantly increased energy expenditure58,60. If you plan on taking caffeine to enhance the effects of
nicotine, I highly recommend drinking coffee, as it contains chemicalscholinomimetics61-62that may bind to the same receptors that
give nicotine its unique ability to empty fat cells63.
For most people using my programs, the basic beginner protocol
for nicotine entails taking 4 mg first thing in the morning. I advocate
morning ingestion for two primary reasons. First, as I discussed in
the previous chapter, its a good idea to keep your nicotine ingestion
away from your carbohydrate intake. This is why you want to make
sure its cleared from your system when youre loading up on carbs.

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42

Next, nicotine will elevate your body temperature, and its also a
stimulant. Both of these factors can and will affect the quality of
your sleep. So, at least until you figure out how your body reacts to
it, limit your nicotine intake to the first part of the day, so its at least
partially cleared out of your system before you go to sleep.
You should ramp up your dosage if youre not accustomed to nicotine. Start with half of a 2 mg piece for the first week of use and step
up the dosage by half of a 2 mg piece per week until you reach the
desired 4 mg level.
Nicotine For Carb Back-Loading
When youre on a typical Carb Back-Loading regimen, nicotine can
be one of the most powerful weapons in your arsenal. This is especially the case first thing in the morning, when youll either be skipping breakfast or eating pure fat in the form of heavy cream and/or
coconut or MCT oil. As weve discussed, nicotines primary advantage in this case is the mobilisation of body fat. This will trigger more
ketone production, and itll accelerate your body fat loss.
With Carb Back-Loading, I recommend training in the evening as
the best option, followed by training first thing in the morning as the
next best thing if evening workouts arent feasible. Since the ideal

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43

time to take nicotine is early in the morning, this is an especially effective protocol for people who train in the early AM hours.
Since nicotine is such an effective supplement for accelerating body
fat mobilisation from your body fat stores, itll ensure that your training does exactly what you want it to do. Again, training is going to
burn fat, but this isnt necessarily the fat thats actually on your body.
Nicotine helps you target body fat loss, making your workouts much
more effective60.
MORNING TRAINING PROTOCOL: 2 mg before training, then 2
mg immediately afterward.
When you train later in the evening, the key to using nicotine effectively is keeping it as far away from your carbohydrate loads as possible. In this case, the protocol remains the same, at least in terms
of restricting your nicotine ingestion to the morning hours.
EVENING TRAINING PROTOCOL: 4 mg upon waking.
For people using the Carb Back-Loading Density Bulking and
Strength Accumulation protocols, there are subtle differences between the way nicotine is used for each.

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44

DENSITY BULKING PROTOCOL: Take 4 mg upon waking, then


train in the evening. Do not take nicotine before or after training.
STRENGTH ACCUMULATION PROTOCOL: 2 mg upon waking, 4
mg roughly 2 hours before your evening workout.
Nicotine For The Carb Nite Solution
With Carb Nite, Im going to assume your workouts arent quite as
intense as they would be with Carb Back-Loading. Im also aware
that some people use Carb Nite without doing any heavy resistance
training at all (although you certainly can, and should). Here, the
best way to cycle nicotine would be to start off with 4 mg piece first
thing in the morning. If youre feeling adventurous, then roughly 6
hours later (around 3 PM) use another 2 mg.
The timing of your ingestion doesnt matter quite as much with Carb
Nite as it does with Carb Back-Loading, because you wont be eating carbs for the majority of the week, and you wont be touching
any nicotine on your actual carb niteor the day after. If you can tolerate taking nicotine at night without any adverse effect on the quality of your sleep, feel free to use it then. If youre resistance training
while on Carb Nite, cycle it around your workouts as outlined for
Carb Back-Loading.

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45

CARB NITE PROTOCOL (ON CARB NITE): Again, its crucial


that you avoid carbs when taking nicotine, so in order to make sure
youre staying highly sensitized, take two full days without ingesting
any nicotine: Your actual carb nite, and the following day.
Nicotine For Intermittent Fasting (IF)
With IF, nicotine offers a very interesting hack to an otherwise
misguided diet. When youre not eating for the first part of the day,
nicotine gives you a few advantages. As always, itll accelerate your
fat mobilisation, which is something that doesnt necessarily happen
when youre starving yourself. Next, nicotines potential as an appetite suppressant plays a helpful role when the object of the game is
to avoid eating.
Nicotines most important benefit with IF, however, pertains to the
TOR pathway of growth. After twelve hours or more with no food,
the TOR pathway starts to shut down. If your goal is performance,
and you want to put on some muscle mass in the process, youre
going to want something to boost that TOR pathway at some point
during the morning when youre not eating food. Nicotine is perfect
for this purpose, because its a direct stimulator of this pathway.

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46

INTERMITTENT FASTING (IF) PROTOCOL: Take 1 mg every 2


hours during your morning fast.
Stacking Nicotine With Caffeine
Taking nicotine and caffeine together will give you a nice little onetwo punch, especially before you train, but I wouldnt recommend
doing this if youre just coming off some form of contest prep, or if
youve just concluded a period of particularly intense training, i.e.,
CrossFit.
When youre at that point, its possibleand probablethat your
adrenal glands have been seriously taxed, and you could potentially
have the adrenaline diabetes I described earlier. Here, the caffeine
wont have much of an effect, and its a good idea to take a break
from this type of stacking for a while instead.
If youre rested and feeling good, however, stacking these two
supplements will help with fat release and burning, because caffeine
helps stimulate beta-adrenergic receptors to get fat moving. Couple
this with the independent receptors that nicotine hits, and youve got
two complementary supplements that can give your fat mobilisation
efforts a very nice boost.

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47

Cycling
Your goals for nicotine usage must necessarily be short-term in nature, as opposed to thinking youll be taking this for the purposes of
lifelong maintenance. Although the research says nicotine use in the
small doses Im recommending here is perfectly safeand highly
effectivefor fairly long periods of time, were still not completely
certain with regard to the absolute long-term safety of these protocols.
The idea, then, is to cycle your nicotine intake on and off. A good
rule of thumb is to try the protocols for four weeks, then take a break
of at least two weeks where youre not using any nicotine at all. This
cycling, as far as research can tell, should mitigate any of nicotines
downsides. When combined with the low doses youll be taking, this
wont have any adverse effects on your health.

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48

CHAPTER 07

Ultimate Fat Burning Stack

A
D
E
R
_
[

]
_
D
E
T
C

CHAPTER 08

Frequently Asked Questions

CHAPTER 08
Frequently Asked Questions
How do I take nicotine?
These protocols have you chewing nicotine gum in 1 mg segments.
Chew the gum for thirty seconds or so, then tuck it in your cheek.
Repeat this process until the nicotine in the gum is depleted.
How will this affect my training? Will I feel any difference?
Theoretically, nicotine should give you slightly more muscular endurance during your heavy training sessions, so you might be able to
squeeze out one more rep in some sets because nicotine adapts
your cells to fat oxidation more readily.
As far as feel is concerned, youll be warmer, youll sweat more,
and youll be slightly more intense because nicotine is a stimulant.
Remember, though, nicotines performance benefits are pretty

57

much theoretical. To be perfectly honest, you wont notice much of


a difference in your actual performance. Youll experience a greater
effect in that department simply by making the switch to Carb BackLoading or The Carb Nite Solution as your primary diet.
How does nicotine interact with the other supplements you
recommend for your programs?
I covered what happens with caffeine in the protocols chapter. Other
than that, I dont see any reason why youd have to change your
supplement regimen in any way to accommodate nicotine.
With that said, there are definitely some interesting dynamics between nicotine and creatine that could take place on the cellular
level. Since nicotine has such a profound effect on metabolism, you
theoretically may need more creatine than normal, or you may need
to start taking creatine if you dont already use it.
Is nicotine Paleo?
Technically, yes. Its an all-natural chemical that comes from plants,
so if we define being Paleo as staying all-natural, then yes, its Paleo.

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58

Can I use nicotine with cardio?


Nicotine will make short-burst cardio more effective, and it can also
mitigate some of the adverse effects of long-duration cardio, as well.
Too much long-duration cardio can prevent fat cells from releasing
fat as effectively as theyd normally be able to, and nicotine can help
attenuate that response.
You said earlier that nicotine is only dangerous if I already
have cancer. With this in mind, should I go have myself
checked for cancer before I start taking it?
Thats about as logical as getting yourself checked for cancer before eating a sandwichand Im not trying to be a wiseguy, either.
Glucose and insulin are both highly stimulating to the same pathway
that makes cancer cells grow. If youre worried about the effects of
nicotine on this pathway, you should stop eating carbs altogether
before you get checked for cancer. They have the same effect.
Are you really sure this is safe?
From the research thats out there, and from the experience Ive had
with clientswhich includes working with medical doctors and their
patientsweve seen no downside whatsoever to these protocols.
This isnt to say no downsides exist, because we dont have the

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59

long-term data to make definitive statements yet, but what Im trying to do here is give you cutting-edge information to increase your
performance and your fat loss results over the short-term. There are
always risks to being radical.

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60

REFERENCES

1.

Randle PJ, Garland PB, Hales CN, Newsholme EA. The glucose fatty-acid cycle. Its role
in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Lancet. 1963 Apr
13;1(7285):785-9.

2.

Lambert JE, Parks EJ. Postprandial metabolism of meal triglyceride in humans. Biochim
Biophys Acta. 2012 May;1821(5):721-6.

3.

Vaughan M, Berger JE, Steinberg D. Hormone-Sensitive Lipase and Monoglyceride


Lipase Activities in Adipose Tissue. J Biol Chem. 1964 Feb;239:401-9.

4.

Holm C, Osterlund T, Laurell H, Contreras JA. Molecular mechanisms regulating


hormone-sensitive lipase and lipolysis. Annu Rev Nutr. 2000;20:365-93. Review.

5.

Londos C, Brasaemle DL, Schultz CJ, Adler-Wailes DC, Levin DM, Kimmel AR,
Rondinone CM. On the control of lipolysis in adipocytes. Ann N Y Acad Sci. 1999 Nov
18;892:155-68. Review.

6.

De Glisezinski I, Crampes F, Harant I, Berlan M, Hejnova J, Langin D, Rivire D, Stich V.


Endurance training changes in lipolytic responsiveness of obese adipose tissue. Am J
Physiol. 1998 Dec;275(6 Pt 1):E951-6. (more sensitive to adrenaline)

7.

Alsted TJ, Nybo L, Schweiger M, Fledelius C, Jacobsen P, Zimmermann R, Zechner R,


Kiens B. Adipose triglyceride lipase in human skeletal muscle is upregulated by exercise
training. Am J Physiol Endocrinol Metab. 2009 Mar;296(3):E445-53.

8.

Hausdorff WP, Caron MG, Lefkowitz RJ. Turning off the signal: desensitization of betaadrenergic receptor function. FASEB J. 1990 Aug;4(11):2881-9. Review. Erratum in:
FASEB J 1990 Sep;4(12):3049.

9.

Lohse MJ, Engelhardt S, Danner S, Bhm M. Mechanisms of beta-adrenergic receptor


desensitization: from molecular biology to heart failure. Basic Res Cardiol. 1996;91 Suppl
2:29-34. Review.

10.

Bawa-Khalfe T, Altememi GF, Mandyam CD, Schwarz LA, Eikenburg DC, Standifer
KM. The presence of beta2-adrenoceptors sensitizes alpha2A-adrenoceptors to
desensitization after chronic epinephrine treatment. BMC Pharmacol. 2007 Dec 20;7:16.

11.

Sears MR. Adverse effects of beta-agonists. J Allergy Clin Immunol. 2002 Dec;110(6
Suppl):S322-8. Review.

12.

Lefkowitz RJ, Pitcher J, Krueger K, Daaka Y. Mechanisms of beta-adrenergic receptor


desensitization and resensitization. Adv Pharmacol. 1998;42:416-20.

13.

Kraemer FB, Shen WJ. Hormone-sensitive lipase: control of intracellular tri-(di-)


acylglycerol and cholesteryl ester hydrolysis. J Lipid Res. 2002 Oct;43(10):1585-94.
Review.

REFERENCES

62

14.

Cryer PE, Haymond MW, Santiago JV, Shah SD. Norepinephrine and epinephrine release
and adrenergic mediation of smoking-associated hemodynamic and metabolic events. N
Engl J Med. 1976 Sep 9;295(11):573-7.

15.

Andersson K, Eneroth P, Arner P. Changes in circulating lipid and carbohydrate metabolites


following systemic nicotine treatment in healthy men. Int J Obes Relat Metab Disord. 1993
Dec;17(12):675-80.

16.

Premont RT. Once and future signaling: G protein-coupled receptor kinase control of
neuronal sensitivity. Neuromolecular Med. 2005;7(1-2):129-47. Review.

17.

Andersson K, Arner P. Systemic nicotine stimulates human adipose tissue lipolysis through
local cholinergic and catecholaminergic receptors. Int J Obes Relat Metab Disord. 2001
Aug;25(8):1225-32.

18.

Sztalryd C, Hamilton J, Horwitz BA, Johnson P, Kraemer FB. Alterations of lipolysis and
lipoprotein lipase in chronically nicotine-treated rats. Am J Physiol Endocrinol Metab.
1996;270:E215E223.

19.

Narkiewicz K, van de Borne PJ, Hausberg M, Cooley RL, Winniford MD, Davison DE,
Somers VK. Cigarette smoking increases sympathetic outflow in humans. Circulation. 1998
Aug 11;98(6):528-34.

20.

Niedermaier ON, Smith ML, Beightol LA, Zukowska-Grojec Z, Goldstein DS, Eckberg
DL. Influence of cigarette smoking on human autonomic function. Circulation. 1993
Aug;88(2):562-71.

21.

Yoshida T, Sakane N, Umekawa T, Kogure A, Kondo M, Kumamoto K, Kawada T, Nagase I,


Saito M. Nicotine induces uncoupling protein 1 in white adipose tissue of obese mice. Int J
Obes Relat Metab Disord. 1999 Jun;23(6):570-5.

22.

Arai K, Kim K, Kaneko K, Iketani M, Otagiri A, Yamauchi N, Shibasaki T. Nicotine infusion


alters leptin and uncoupling protein 1 mRNA expression in adipose tissues of rats. Am J
Physiol Endocrinol Metab. 2001 Jun;280(6):E867-76.

23.

Klingenberg M. Uncoupling proteins--how do they work and how are they regulated. IUBMB
Life. 2001 Sep-Nov;52(3-5):175-9. Review.

24.

Gonzlez-Barroso MM, Fleury C, Bouillaud F, Nicholls DG, Rial E. The uncoupling protein
UCP1 does not increase the proton conductance of the inner mitochondrial membrane by
functioning as a fatty acid anion transporter. J Biol Chem. 1998 Jun 19;273(25):15528-32.

25.

Champigny O, Ricquier D. Effects of fasting and refeeding on the level of uncoupling protein
mRNA in rat brown adipose tissue: evidence for diet-induced and cold-induced responses. J
Nutr. 1990 Dec;120(12):1730-6.

REFERENCES

63

26.

Nedergaard J, Golozoubova V, Matthias A, Asadi A, Jacobsson A, Cannon B. UCP1: the only


protein able to mediate adaptive non-shivering thermogenesis and metabolic inefficiency.
Biochim Biophys Acta. 2001 Mar 1;1504(1):82-106. Review.

27.

Bergman BC, Perreault L, Hunerdosse D, Kerege A, Playdon M, Samek AM, Eckel RH. Novel
and Reversible Mechanisms of Smoking-Induced Insulin Resistance in Humans. Diabetes.
2012 Dec;61(12):3156-66.

28.

Umeki D, Ohnuki Y, Mototani Y, Shiozawa K, Fujita T, Nakamura Y, Saeki Y, Okumura S.


Effects of Chronic Akt/mTOR Inhibition by Rapamycin on Mechanical Overload-Induced
Hypertrophy and Myosin Heavy Chain Transition in Masseter Muscle. J Pharmacol Sci. 2013
Aug 20;122(4):278-88.

29.

Hourd C, Jagerschmidt C, Clment-Lacroix P, Vignaud A, Ammann P, Butler-Browne GS,


Ferry A. Androgen replacement therapy improves function in male rat muscles independently
of hypertrophy and activation of the Akt/mTOR pathway. Acta Physiol (Oxf). 2009
Apr;195(4):471-82.

30.

An Z, Wang H, Song P, Zhang M, Geng X, Zou MH. Nicotine-induced activation of AMPactivated protein kinase inhibits fatty acid synthase in 3T3L1 adipocytes: a role for oxidant
stress. J Biol Chem. 2007 Sep 14;282(37):26793-801.

31.

Norrelund H, Nair KS, Nielsen S, Frystyk J, Ivarsen P, Jorgensen JO, Christiansen JS, Moller
N. The decisive role of free fatty acids for protein conservation during fasting in humans with
and without growth hormone. J Clin Endocrinol Metab. 2003 Sep;88(9):4371-8. -1-1-

32.

Nielsen S, Jorgensen JO, Hartmund T, Norrelund H, Nair KS, Christiansen JS, Moller N.
Effects of lowering circulating free fatty acid levels on protein metabolism in adult growth
hormone deficient patients. Growth Horm IGF Res. 2002 Dec;12(6):425-33. -1-2-

33.

Pontiroli AE, Lanzi R, Monti LD, Sandoli E, Pozza G. Growth hormone (GH) autofeedback
on GH response to GH-releasing hormone. Role of free fatty acids and somatostatin. J Clin
Endocrinol Metab. 1991 Feb;72(2):492-5. -1-3-

34.

Norrelund H, Nair KS, Jorgensen JO, Christiansen JS, Moller N. The protein-retaining
effects of growth hormone during fasting involve inhibition of muscle-protein breakdown.
Diabetes. 2001 Jan;50(1):96-104. -16-1-

35.

Moller N, Norrelund H. The role of growth hormone in the regulation of protein metabolism
with particular reference to conditions of fasting. Horm Res. 2003;59 Suppl 1:62-8. Review.

36.

Fukao T, Lopaschuk GD, Mitchell GA. Pathways and control of ketone body metabolism:
on the fringe of lipid biochemistry. Prostaglandins Leukot Essent Fatty Acids. 2004
Mar;70(3):243-51.

37.

Beylot M. Regulation of in vivo ketogenesis: role of free fatty acids and control by

REFERENCES

64

epinephrine, thyroid hormones, insulin and glucagon. Diabetes Metab. 1996 Oct;22(5):299304. Review.
38.

Paoli A, Cenci L, Grimaldi KA. Effect of ketogenic Mediterranean diet with phytoextracts
and low carbohydrates/high-protein meals on weight, cardiovascular risk factors, body
composition and diet compliance in Italian council employees. Nutr J. 2011 Oct 12;10:112.

39.

Volek JS, Sharman MJ, Love DM, Avery NG, Gmez AL, Scheett TP, Kraemer WJ. Body
composition and hormonal responses to a carbohydrate-restricted diet. Metabolism. 2002
Jul;51(7):864-70.

40.

ONeill HM, Holloway GP, Steinberg GR. AMPK regulation of fatty acid metabolism
and mitochondrial biogenesis: implications for obesity. Mol Cell Endocrinol. 2013 Feb
25;366(2):135-51.

41.

Sadkowski T, Jank M, Zwierzchowski L, Siadkowska E, Oprzadek J, Motyl T. Gene


expression profiling in skeletal muscle of Holstein-Friesian bulls with single-nucleotide
polymorphism in the myostatin gene 5-flanking region. J Appl Genet. 2008;49(3):237-50.

42.

Siegmund B, Leitner E, Pfannhauser W. Determination of the nicotine content of various


edible nightshades (Solanaceae) and their products and estimation of the associated dietary
nicotine intake. J Agric Food Chem. 1999 Aug;47(8):3113-20.

43.

Tonini G, DOnofrio L, DellAquila E, Pezzuto A. New molecular insights in tobacco-induced


lung cancer. Future Oncol. 2013 May;9(5):649-55.

44.

Clark CA, McEachern MD, Shah SH, Rong Y, Rong X, Smelley CL, Caldito GC, Abreo
FW, Nathan CO. Curcumin inhibits carcinogen and nicotine-induced Mammalian target of
rapamycin pathway activation in head and neck squamous cell carcinoma. Cancer Prev Res
(Phila). 2010 Dec;3(12):1586-95.

45.

Sun X, Ritzenthaler JD, Zhong X, Zheng Y, Roman J, Han S. Nicotine stimulates PPARbeta/
delta expression in human lung carcinoma cells through activation of PI3K/mTOR and
suppression of AP-2alpha. Cancer Res. 2009 Aug 15;69(16):6445-53.

46.

Jin Q, Menter DG, Mao L, Hong WK, Lee HY. Survivin expression in normal human bronchial
epithelial cells: an early and critical step in tumorigenesis induced by tobacco exposure.
Carcinogenesis. 2008 Aug;29(8):1614-22.

47.

Zheng Y, Ritzenthaler JD, Roman J, Han S. Nicotine stimulates human lung cancer cell
growth by inducing fibronectin expression. Am J Respir Cell Mol Biol. 2007 Dec;37(6):681-90.

48.

Tsurutani J, Castillo SS, Brognard J, Granville CA, Zhang C, Gills JJ, Sayyah J, Dennis
PA. Tobacco components stimulate Akt-dependent proliferation and NFkappaB-dependent
survival in lung cancer cells. Carcinogenesis. 2005 Jul;26(7):1182-95.

REFERENCES

65

49.

Atkinson J, Poitevin P, Chillon JM, Lartaud I, Levy B. Vascular Ca overload produced


by vitamin D3 plus nicotine diminishes arterial distensibility in rats. Am J Physiol. 1994
Feb;266(2 Pt 2):H540-7.

50.

Nicita-Mauro V. Smoking, calcium, calcium antagonists, and aging. Exp Gerontol. 1990;25(34):393-9.

51.

Berlin I. Smoking-induced metabolic disorders: a review. Diabetes Metab. 2008 Sep;34(4 Pt


1):307-14.

52.

Kyllonen PC, Christal RE. Reasoning ability is (little more than) working-memory capacity?!
Intelligence. 1990 Oct-Dec;14(4):389-433.

53.

Levin ED. Nicotinic receptor subtypes and cognitive function. J Neurobiol. 2002
Dec;53(4):633-40. Review.

54.

Levin ED, Torry D. Acute and chronic nicotine effects on working memory in aged rats.
Psychopharmacology (Berl). 1996 Jan;123(1):88-97.

55.

Wager-Srdar SA, Levine AS, Morley JE, Hoidal JR, Niewoehner DE. Effects of cigarette
smoke and nicotine on feeding and energy. Physiol Behav. 1984 Mar;32(3):389-95.

56.

Grunberg NE, Bowen DJ, Winders SE. Effects of nicotine on body weight and food
consumption in female rats. Psychopharmacology (Berl). 1986;90(1):101-5.

57.

Fulkerson JA, French SA. Cigarette smoking for weight loss or control among adolescents:
gender and racial/ethnic differences. J Adolesc Health. 2003 Apr;32(4):306-13.

58.

Jessen AB, Toubro S, Astrup A. Effect of chewing gum containing nicotine and caffeine on
energy expenditure and substrate utilization in men. Am J Clin Nutr. 2003 Jun;77(6):1442-7.

59.

Benowitz NL, Porchet H, Sheiner L, Jacob P 3rd. Nicotine absorption and cardiovascular
effects with smokeless tobacco use: comparison with cigarettes and nicotine gum. Clin
Pharmacol Ther. 1988 Jul;44(1):23-8.

60.

Perkins KA, Sexton JE, Epstein LH, DiMarco A, Fonte C, Stiller RL, Scierka A, Jacob RG.
Acute thermogenic effects of nicotine combined with caffeine during light physical activity in
male and female smokers. Am J Clin Nutr. 1994 Sep;60(3):312-9.

61.

Tse SY. Coffee contains cholinomimetic compound distinct from caffeine. I: Purification and
chromatographic analysis. J Pharm Sci. 1991 Jul;80(7):665-9.

62.

Tse SY. Cholinomimetic compound distinct from caffeine contained in coffee. II: Muscarinic
actions. J Pharm Sci. 1992 May;81(5):449-52.

63.

Andersson K, Arner P. Cholinoceptor-mediated effects on glycerol output from human


adipose tissue using in situ microdialysis. Br J Pharmacol. 1995 Aug;115(7):1155-62.

REFERENCES

66

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