nicotine declassified

7/25/2019 Nicotine Declassified

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

printing in USA. No part of this publication may be repro-

duced or distributed in any way, nor electronically stored,

accessevd or shared, without the prior written approval of the

copyright holder, except as may otherwise be allowed by ap-

plicable law.

This book is not medical or any other form of professional ad-

vice that requires licensing in any jurisdiction. It is for scien-

tic and educational purposes only. Please consult a qualied

health care professional for medical advice. The author, any

contributors, publisher, and copyright holder(s) (and their suc-cessors) are not responsible for any adverse effects associ-

ated with any use of this book.

Where third party trademarks are used in this book reason-

able efforts were made to identify the trademark owner where

rst used, and in a customary manner. All such use is in an

editorial fashion with no intention of infringement. To be clear,

all third party trademarks are the property of their respective

owners.


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TABLE OF CONTENTS

Preface

Introduction

Chapter 01: Dont Just Burn Fat. Lose it.

Chapter 02: Metabolism and Fat Mobilisation

Chapter 03: Nicotine and Muscle Growth

Chapter 04: Controversial Aspects

Chapter 05: Unique Benets of Nicotine

Chapter 06: The Protocols

Chapter 07: Ultimate Fat Burning Stack

Chapter 08: Frequently Asked Questions

References

04

08

14

18

25

31

37

40

49

56

61

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PREFACE


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For years, nicotine was little more to me then an object of scientic

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 scien-

tic 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 ndings 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-Loadingand reports like this one: The idea that theres some-

thing 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.

PREFACE

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

industrywith Mens Health, Mens Fitness, Muscle & Fitness,

and Flexamong these. I dont want to name names, but one ma-

jor publica tiontrust me, youve heard of itapproached meto write a feature article on something unique and scientic that

works for the purposes of fat loss and muscle building. When I pro-

posed a piece on the health and performance benets 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 nico-

tines benets nagged at meto the point where I decided to put

together this comprehensive report on its efcacy 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 infor-mation 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.

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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 needto 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 rightbutyou need to be doing them right rst for any of this to mean any-

thing.

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 ac-

celerate 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 rst.

Thats what I want to do with this report. The rest is up to you.

Kiefer

7PREFACE


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INTRODUCTION

Origin Story


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INTRODUCTION

Origin Story

9

My professional background, aside from my work in physics and

software, involves working extensively with physique competitorspreparing for competition. I realize that many of you arent prepar-

ing for competition, but since fat loss and muscle gain mean literally

everything to competitorsafter all, theyve necessarily had to rene

the process to a far greater extent than anyone else in the world

Im using physique, and its methods, to explain how and why nico-

tine 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 prescrip-

tion medications like clenbuterol and albuterol, among other power-

ful fat burners. The less the coach understands about the humanbody, the more fat burners they prescribe.


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These drugs work essentially the way adrenaline and caffeine do,

by stimulating the sympathetic nervous systemthe ight-or-ght

response coordinatorthrough activation of the beta-adrenergic re-ceptors. 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 eventu-

ally going to reach a point of diminishing returns where theyre no

longer effective.

The world of physique competition is saturated with these medica-

tions. Youll have a difcult time nding 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 ad-renal 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 aresult of the drugs, which Ill explain as we go along.

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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 denitely give yourself an edge

if youre willing to take these prescription medications. After see-ing 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 bodyfatnote 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 x the damage these athletes nutritionists and coach-es are inicting on them.

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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 expen-

diture 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 doesthis very well.

These drugs will also burn out your adrenal glands. These glands

are producing massive amounts of adrenaline and cortisol. As a re-

sult, theyre overstressed and overtaxed. At this point, they go into a

kind of survival mechanism where they dump cortisol, and continuedumping it.

So here you are, with high cortisol levels and a very low metabo-

lism. 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 mas-sive and rapid fat regain, and most competitors end up getting far

fatter than they ever were before.

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Taboo, Yet Terribly Effective

When I was trying to gure everything outhow to help my clientsavoid this horric rebound effectI saw some studies talking about

the benets of nicotine as a fat mobilizer. This led me to think about

smokers. When people who smoke indulge their habit, theyre usu-

ally 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 un-

healthy, 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.

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CHAPTER01

Dont Just Burn Fat. Lose It.


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CHAPTER01

Dont Just Burn Fat. Lose It.

15

Exercise is supposed to get you lean, right? This is obviously the

common wisdom, because exercising burns more fat than activitieswhere 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 pos-

sibly undertake will burnfat (even if at a very slow rate)1.

Trouble is, burningfat is a completely separate and independentprocess 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 most-ly from your dietand when your diet cant supply enough, it starts


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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 tolose.

The solution? When youre trying to go into any kind of available

energy decit (calorie decit), or youre dieting down for the competi-

tive 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 actu-

ally 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 notget rid of body fat6.

What this means is that even though youre burning fat in your mus-

cles, youre not mobilizing your body fat reserves. This is why peo-

ple 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 storedin muscle tissue7. Their fat cells arent releasing it to be burned.

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

This happens all the time. What we really need is to create an en-

vironment where our fat cells are dumping fat to be burned. Thats

the key distinction: Its easy to burn fat, but theres a huge differencebetween fat burningand fat mobilisation.

Why Prescription Drugs Fail

Theres a simple explanation for what happens when you take the

conventional pharmaceutical fat burner regimen advocated by mostphysique coaches. I coined the phrase adrenaline diabetesto de-

scribe 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. Thiseventually reaches a tipping point where its almost impossible to

stimulate them any furtherand when you eat carbohydrates after

nishing 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 itor not, nicotine even works for individuals in the throes of this adren-

aline diabeteseffect. In the following chapters, Ill explain how this

works.

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CHAPTER02

Nicotine, Metabolism and Fat Mobilisation


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CHAPTER02

Nicotine, Metabolism and Fat Mobilisation

19

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-Loadingor 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, ex-

ercise 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 increas-

ing amounts of cortisol and catecholamines (like adrenaline and nor-

adrenaline) which will force fat cells to release fatty acids for energy.


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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 en-

ergy13

, which decreases the size of adipose tissue. Because HSLrequires 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 contrib-

utes 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 decit, and we develop adrena-

line 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 re-

lease, fat cells contain specialized receptors to which nicotine binds.

Whats unusual about this is that these receptors are notthe 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

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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 catechol-

amines were elevated during this protocolan elevation that pre-vents muscle tissue from releasing triglyceridesits likely this surge

of fat came from the breakdown of tri- and diglycerides within adi-

pose 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 rest-

ing 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

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nicotine can increase resting energy expenditure. Nicotine can also

increase thermogenesis, making the body more inefcient. This is

how mammals regulate body temperature to stay warm, through the

oxidation of fatty acids.

Nicotine increases thermogenesis through upregulation of uncou-

pling 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 tis-

sue (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 articial un-

coupling agents, this can increase resting energy expenditure by as

much as 30%. Although were unlikely to achieve that with nicotinealone, well discuss later how this might be possible in conjunction

with nicotine use.

Of additional relevance is the fact that the bodys resting energy out-

put decreases with any type of calorie deprivation, or (my preferred

term for this) energy decit. Pay close attention to this if youre usingan intermittent fasting (IF) protocol, because its why starving your-

self for fat loss decreases your energy output. Calorie deprivation

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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

ipping a switch in the smokers fat cells that says, essentially, Hey,

dont store fat. No matter what you do, you cant store fat, and ifyouve 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 ghts 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 thannormal, while their fat cells have a very difcult 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 ip the switch back the other way, youll then have a multitude

of empty fat cells saying, Oh, hell yeah! Now we can ll up! And

this is precisely what they do. Quickly.

Now, Im notadvocating smoking as a protocol for losing body fat.

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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 myrecommendation is to stay as far away from cigarettes as humanly

possible.

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CHAPTER03

Nicotine and Muscle Growth


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CHAPTER03

Nicotine and Muscle Growth

26

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 thereason 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 recom-

mend leucine supplementation with all my programs.

The problem with glucose and leucine, however, is that they canboth cause releases of insulin. This is notan ideal situation when

youre trying to get rid of body fat. In contrast, the amazing thing


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about nicotine is that its one of the fewif onlynatural, non-

nutritive 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 yourmuscle 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 yourbody to grow. Rapamycin is an anti-cancer drug that turns off the

TOR pathway, essentially negating any gains you get from resis-

tance training. When this pathway is turned off, you can lift weights

all day, every day, without any benet to your muscles.

When the TOR pathway shuts off, you cant grow. This is obviouslybenecial for cancer patients, because it means no cells can grow.

Cancer cells are typically highly rampant, and they grow rapidly, but

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rapamycin has the capability of shutting that growth down, including

skeletal muscle hypertrophy28-29.

When youre in available energy deprivation, or youre trying to losebody 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 hap-

pen 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 okayand 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 pre-

scription 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-

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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, especiallywith 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. Free-

radical 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 pres-

ervation. 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 causesthrough 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 othercyclic ketogenic diets. AMPK activation can enhance glucose uptake

in skeletal muscle tissue and can also possibly increase mitochon-

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drial biogenesis40. Mitochondrial biogenesis relates to the maximum

size a muscle ber 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 exibility for high-intensity, strength-endurance sports.

Finally, recent animal studies have shown that nicotine may stimu-

late a pathway that downregulates myostatinthe protein that pre-

vents muscles from getting big41.

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CHAPTER04

Controversial Aspects


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CHAPTER04

Controversial Aspects

32

What, exactly, is nicotine?

Nicotine is just a naturally-occurring substance produced by a family

of plants called nightshades. This family includes tomatoes, pota-

toes, 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 evilas youve been led to believe.

We regard nicotine as dangerous because our thinking has been guid-

ed, 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 willtake 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.


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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 overthe years, though, is the notion that if megadoses of nicotine are

dangerous, then any amount of nicotine must necessarily be dan-

gerous, too.

Research has shown this logic to be faulty, and that nicotine by itself

isnt necessarily carcinogenic43

. This doesnt mean there arent anydownsides to it, but in order to recognize nicotines role in the hierar-

chy, 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. Carcino-gens 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 hormonebecauseGH will cause all the cells in the body to grow, including the cancer-

ous ones. This, obviously, makes cancer worse.

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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 along period of time.

We see this advanced aging of the circulatory system most frequent-

ly 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 benets 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 rst

form to develop in smokers, because the nicotine is having an effect

in the lungs very early and very quicklyinteracting with cancercells that are already growing rapidly.

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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 negativeto 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 malnour-ished, theyre vitamin decient, and nicotine makes all of this worse

because its an extra stressor on the body.

When youre healthy, however, small dosages of nicotine can actu-

ally be benecial for you because they can instigate tissue repair

and help mobilize body fatand weve found no evidence that smalldoses, 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 nicotinesability to cause a dump of triglycerides, which in the presence of

glucose can actually exacerbate the development of diabetes27,51.

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This is especially dangerous when youre on a carbohydrate-based

diet.

The idea, then, is to avoid mixing nicotine with carb ingestion, be-cause it can interfere with the absorption of glucose into your mus-

cle cells. This is why people get sick, and research has shown that

smokers can develop diabetes without even being overweight51.

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CHAPTER05

Unique Benets of Nicotine


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CHAPTER05

Unique Benets of Nicotine

38

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 tness, health

and medical industries. Logical thinking and the ability to make rea-

sonable 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 efciency of

working memory53-54. Nicotine can impart a clear benet for test tak-

ing and technical tasks like guring out your taxes or programming a

computer.

Appetite Suppression

The unfortunate downside of most fat burners is a potential increase


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in appetite because of the increased energy demands placed on the

body by an accelerated metabolism. This, of course, is amplied by

the fact that most mainstream diets used for fat loss cause massive

hunger pangs and making sticking with a diet difcult. The reboundeffect 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 proto-

cols outlined in this manual, particularly competitors, report extreme

hunger control to the point of losing the desire to eateven whensuch a state would put them into an unfavorable energy decit.

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 signicant

benets to anyone.

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CHAPTER06

The Protocols


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CHAPTER06

The Protocols

41

To nd the correct dosing necessary for the fat mobilizing and burn-

ing effects of nicotine, we rst need to investigate nicotine metabo-lisation and blood concentrations necessary for these benets. 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 signicantly increased resting me-

tabolism 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-


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bilisation and increased fat oxidations were achieved with intrave-

nous infusion of nicotine until levels reached between 7 and 8 ng/ml

(nanograms per milliliter). This would require a piece of gum con-

taining 4 mg of nicotine59

.

So, if we want the maximum benet of fat burning and fat mobilisa-

tion, 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 caf-

feine added to the nicotine gum signicantly increased energy ex-

penditure58,60. If you plan on taking caffeine to enhance the effects of

nicotine, I highly recommend drinking coffee, as it contains chemi-

calscholinomimetics61-62that 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 rst 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 makesure its cleared from your system when youre loading up on carbs.

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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 gure out how your body reacts to

it, limit your nicotine intake to the rst part of the day, so its at leastpartially cleared out of your system before you go to sleep.

You should ramp up your dosage if youre not accustomed to nico-

tine. Start with half of a 2 mg piece for the rst 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 espe-

cially the case rst thing in the morning, when youll either be skip-ping breakfast or eating pure fat in the form of heavy cream and/or

coconut or MCT oil. As weve discussed, nicotines primary advan-

tage 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 asthe best option, followed by training rst thing in the morning as the

next best thing if evening workouts arent feasible. Since the ideal

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time to take nicotine is early in the morning, this is an especially ef-

fective protocol for people who train in the early AM hours.

Since nicotine is such an effective supplement for accelerating bodyfat mobilisation from your body fat stores, itll ensure that your train-

ing 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 effec-

tively is keeping it as far away from your carbohydrate loads as pos-

sible. In this case, the protocol remains the same, at least in termsof 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 be-tween the way nicotine is used for each.

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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, 4mg 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 awarethat 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 rst

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 eat-

ing 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 tol-

erate taking nicotine at night without any adverse effect on the qual-

ity of your sleep, feel free to use it then. If youre resistance trainingwhile on Carb Nite, cycle it around your workouts as outlined for

Carb Back-Loading.

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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 ingestingany 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 rst 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 appe-

tite suppressant plays a helpful role when the object of the game is

to avoid eating.

Nicotines most important benet 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 perfectfor this purpose, because its a direct stimulator of this pathway.

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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 one-

two 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 mobilisationefforts a very nice boost.

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Cycling

Your goals for nicotine usage must necessarily be short-term in na-

ture, as opposed to thinking youll be taking this for the purposes oflifelong 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 proto-

cols.

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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CHAPTER07

Ultimate Fat Burning Stack

[_REDACTED_]


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CHAPTER08

Frequently Asked Questions


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CHAPTER08

Frequently Asked Questions

57

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 endur-

ance 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 benets are pretty


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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 Back-

Loadingor The Carb Nite Solutionas 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 yoursupplement regimen in any way to accommodate nicotine.

With that said, there are denitely some interesting dynamics be-

tween 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 needto 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 dene being Paleo as staying all-natural, then yes, its Pa-leo.

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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 myselfchecked for cancer before I start taking it?

Thats about as logical as getting yourself checked for cancer be-

fore 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 ofnicotine 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 hadwith 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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long-term data to make denitive statements yet, but what Im try-

ing 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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REFERENCES


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62REFERENCES

1. Randle PJ, Garland PB, Hales CN, Newsholme EA. The glucose fatty-acid cycle. Its rolein 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. BiochimBiophys Acta. 2012 May;1821(5):721-6.

3. Vaughan M, Berger JE, Steinberg D. Hormone-Sensitive Lipase and MonoglycerideLipase Activities in Adipose Tissue. J Biol Chem. 1964 Feb;239:401-9.

4. Holm C, Osterlund T, Laurell H, Contreras JA. Molecular mechanisms regulatinghormone-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 Nov18;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 beta-

adrenergic 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 Suppl2:29-34. Review.

10. Bawa-Khalfe T, Altememi GF, Mandyam CD, Schwarz LA, Eikenburg DC, StandiferKM. 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.


57/60

14. Cryer PE, Haymond MW, Santiago JV, Shah SD. Norepinephrine and epinephrine releaseand 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 metabolitesfollowing systemic nicotine treatment in healthy men. Int J Obes Relat Metab Disord. 1993Dec;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. 2001Aug;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 outow in humans. Circulation. 1998

Aug 11;98(6):528-34.

20. Niedermaier ON, Smith ML, Beightol LA, Zukowska-Grojec Z, Goldstein DS, EckbergDL. Inuence of cigarette smoking on human autonomic function. Circulation. 1993Aug;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 JObes 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 infusionalters 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. IUBMBLife. 2001 Sep-Nov;52(3-5):175-9. Review.

24. Gonzlez-Barroso MM, Fleury C, Bouillaud F, Nicholls DG, Rial E. The uncoupling proteinUCP1 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 proteinmRNA in rat brown adipose tissue: evidence for diet-induced and cold-induced responses. JNutr. 1990 Dec;120(12):1730-6.

63REFERENCES


58/60

26. Nedergaard J, Golozoubova V, Matthias A, Asadi A, Jacobsson A, Cannon B. UCP1: the onlyprotein able to mediate adaptive non-shivering thermogenesis and metabolic inefciency.

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. Noveland 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-InducedHypertrophy and Myosin Heavy Chain Transition in Masseter Muscle. J Pharmacol Sci. 2013Aug 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 independentlyof hypertrophy and activation of the Akt/mTOR pathway. Acta Physiol (Oxf). 2009Apr;195(4):471-82.

30. An Z, Wang H, Song P, Zhang M, Geng X, Zou MH. Nicotine-induced activation of AMP-

activated protein kinase inhibits fatty acid synthase in 3T3L1 adipocytes: a role for oxidantstress. 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, MollerN. 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 growthhormone decient 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) autofeedbackon GH response to GH-releasing hormone. Role of free fatty acids and somatostatin. J ClinEndocrinol Metab. 1991 Feb;72(2):492-5. -1-3-

34. Norrelund H, Nair KS, Jorgensen JO, Christiansen JS, Moller N. The protein-retainingeffects 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 metabolismwith 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

64REFERENCES


59/60

epinephrine, thyroid hormones, insulin and glucagon. Diabetes Metab. 1996 Oct;22(5):299-304. 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, bodycomposition 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. Bodycomposition 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 Feb25;366(2):135-51.

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

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

42. Siegmund B, Leitner E, Pfannhauser W. Determination of the nicotine content of variousedible 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-inducedlung cancer. Future Oncol. 2013 May;9(5):649-55.

44. Clark CA, McEachern MD, Shah SH, Rong Y, Rong X, Smelley CL, Caldito GC, AbreoFW, 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 bronchialepithelial 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 bronectin 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, DennisPA. Tobacco components stimulate Akt-dependent proliferation and NFkappaB-dependentsurvival in lung cancer cells. Carcinogenesis. 2005 Jul;26(7):1182-95.

65REFERENCES


60/60

49. Atkinson J, Poitevin P, Chillon JM, Lartaud I, Levy B. Vascular Ca overload producedby 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(3-4):393-9.

51. Berlin I. Smoking-induced metabolic disorders: a review. Diabetes Metab. 2008 Sep;34(4 Pt1):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 cigarettesmoke 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 onenergy 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. ClinPharmacol 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: Purication andchromatographic analysis. J Pharm Sci. 1991 Jul;80(7):665-9.

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

nicotine declassified

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