Nicotine.. how to increase your Metabolic Rate by up to 10%!!!!

Recently "BajanBastard" posted a topic concerning Nicotine as a fat burner, .. He got a lot of mixed responses but most people didn't like the idea of using nicotine as a fat burning aid...
Well, that is what got me started initially, ..

General Information about Nicotine

Nicotine is an alkolid of the tabaco plant. In higher doses it can be toxic, but smaller doses are pleasantly stimulating. One cigarette contains approx 0,8 - 1,0 mg nicotine. Nicotine promotes the release of Adrenaline and Dopamine which leads to a rise in Blood pressure, blood-sugar-level and heart rate and a feeling of well beeing on the other hand.
The Dopamine release is the main cause for a possible addiction as u might expect.


Nicotine and Fat Loss

Any substance which promotes adrenaline release is very promising in regard to fat loss. The thermogenic effect of nicotine was tested in a randomized, double-blind, placebo-controlled, crossover study [ http://www.ajcn.org/cgi/content/full/77/6/1442#FN2 ] and it deliverd some very interesting findings. As i do not want to bother you with the exact study setup up and testing procedures (you can look that up under the link i posted above) i will get dircetly to the results:

Nicotine gum/caffeine--->Increase in MBR

1mg / 0mg -------> 3,7%
2mg / 0mg -------> 4,9%
2mg / 50mg -------> 6,3 %
1mg / 50mg -------> 7,9 %
1mg / 100mg ------> 8,5%
2mg / 100mg ------> 9,8 %

In conclusion we can clearly see, that 1mg of nicotine is able to boost your metabolisim up to almost 4% in a 2 hour period. 2 hours after consumption of the nicotine / caffeine gum, Metabolic Rate droped to normal values. Adding 100mg of caffeine can improve the thermogenic effect more than a 100%!!
Increasing the nicotine dose to 2 mg does not significantly increase the thermogenic effect but produces side effects in most subjects (strong nausea, etc..). So taking a dose higher than 1mg is not advised.

Moreover there is evidence that nicotine blunts the release of insulin (!) This may be of special interest as insulin inhibts lypolysis and promotes fat storage. In addition to that nicotine acts as a strong appetite supressant.

Another positive effect is nicotines ability to promote lipolysis (Chen H, Vlahos R, Bozinovski S, Jones J, Anderson GP, Morris MJ. Effect of short-term cigarette smoke exposure on body weight, appetite and brain neuropeptide Y in mice) and its possible ability to stimulate the uncoupling protein in fatty tissue (UCP1). This is the same effect which occurs when DNP is ingested but to a lot smaller extend.

Possible side effects

- rise in blood pressure
- nausea
- vomitting
- nicotine is not a tumor promoter, but it can delay cell-death(in Laymans terms: a possbile tumor cell may live longer than it should be)

and last but not least: Addiction. But when using nicotine chewing gums the chance of becoming addicted to nicotine is less than 1%.. so don't sweat it :lol:

Hope this one helps some guys. I will most certainly use nicotine gums in my upcoming cutting cycles.

RG

credits go to bulkolly, fronit (both androgen-steroids) and PartyBoy (muscletalk).

D@mn, good post

Nice post Alex, I even enjoyed your newly CREATED word "disadvocate".:lol:

Hooker recently employed Nicotine in his training of MJ, it's a good read...
http://www.*************/portal_incl...4-feature.html

M.

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Originally Posted by magic32

Nice post Alex, I even enjoyed your new word "disadvocate".:lol:
M.

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thanks an LMAO... edited above post.. :lol:

shameless :bbbump:

So I got to start smoking again?J/K

Not sure Alex, but doesn't an ECA stack boost MBR by about 9%? And how do you weigh the pros and cons of a conventional ECA stck vs. Nic/Caff?

ill stick to cardio....but good info anyways

Well what Attracts me to this disgusting drug is that it has great appetie Suppression effects that I would like in a complex cutting cycles.I know your a fan of DNP alex,but can you Believe they have things in common?

It`s crazy and like a Bizarre Fassbinder film;Nicotine appears to decrease lipolysis resulting in lower storage of adipose tissue,it acts a stimulus of uncopling protein1 which acts mitochnondria making the conversion of (APT) less efficent,resulting in heat rise.The mitochondria therfore need to work much harder to produce the same level of energy (APT),thus incresing metabolic rate,which burns fat.This is the same process is seen from DNP.I would guess DNP and Nicotine could have some synergy if used together.

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Originally Posted by goose4

Well what Attracts me to this disgusting drug is that it has great appetie Suppression effects that I would like in a complex cutting cycles.I know your a fan of DNP alex,but can you Believe they have things in common?

It`s crazy and like a Bizarre Fassbinder film;Nicotine appears to decrease lipolysis resulting in lower storage of adipose tissue,it acts a stimulus of uncopling protein1 which acts mitochnondria making the conversion of (APT) less efficent,resulting in heat rise.The mitochondria therfore need to work much harder to produce the same level of energy (APT),thus incresing metabolic rate,which burns fat.This is the same process is seen from DNP.I would guess DNP and Nicotine could have some synergy if used together.

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its not disgusting by any means goose :wg: granted i only tried it 2 times so far but i did not expierence any side effects like nausea, vomitting and so on.. it seems to be a real safe fat burning - and to an even greater degree apetite supressant - aid.

About DNP.. yes i think you are on the right track.. nicotine and DNP could work synergstic, but this could be potentinally dangerous as lower doses of DNP might be needed to be "lethal"... anyway i like your ideas - as usual :lol:

@shortie
yeah ECA is supposed to boost MBR by 9% also. that is another reason why i posted this thread as i personally feel that nicotine coffein is a much safer route to go - i for myself tolerate nic/caffein better than ECA.. I will have to wait a few weeks b4 i REALLY can comment on its fat burning effects, though.

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Originally Posted by AleX-69

its not disgusting by any means goose :wg: granted i only tried it 2 times so far but i did not expierence any side effects like nausea, vomitting and so on.. it seems to be a real safe fat burning - and to an even greater degree apetite supressant - aid.

About DNP.. yes i think you are on the right track.. nicotine and DNP could work synergstic, but this could be potentinally dangerous as lower doses of DNP might be needed to be "lethal"... anyway i like your ideas - as usual :lol:

@shortie
yeah ECA is supposed to boost MBR by 9% also. that is another reason why i posted this thread as i personally feel that nicotine coffein is a much safer route to go - i for myself tolerate nic/caffein better than ECA.. I will have to wait a few weeks b4 i REALLY can comment on its fat burning effects, though.

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I was joking about it being disgusting,it just gives me old memories when I was 16,LOL.What was your nicotine cycle? What results did you have? Was you on a Restricted diet? What type of nicotine did you use? Did you increase cardio while on your cycle?

Quote:

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Originally Posted by shortie

So I got to start smoking again?J/K

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wanted to come back on this:

most scientists believe addiction to nicotince has to do with its absorption speed. The faster the body absorbs the drug the greater the chance of addiction. Speaking of cigaretts - it only takes a few minutes to get the whole 1mg nicotine in your system, with chewing gums it takes about 20mins to release 70% of 1mg Nicotine.
That is the reason why it is less likely that you become addicted to nicotine if you choose chewing gums and the reason why it is a bad idea to somke...

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Originally Posted by goose4

I was joking about it being disgusting,it just gives me old memories when I was 16,LOL.What was your nicotine cycle? What results did you have? Was you on a Restricted diet? What type of nicotine did you use? Did you increase cardio while on your cycle?

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I am already IN a Propionate/winny/nicotine/caffein short cycle.. cardio 5-6 times a week...
But i really do know my body well so i can tell for sure if i lost a significant amount of fat due to the use of nicotine.. As i have only used it 2 times (2 days literally not cycles) give me two more weeks to really test its abilitys..

any yeah i am on an restricetd diet and used normal 2mg nicotine chewing gums..(2mg due to absorption rate..)

Nicotine also increases blood vessel growth in damaged tissue.

yeah? didn't know that.. NicE!

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Originally Posted by AleX-69

yeah? didn't know that.. NicE!

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no, i did not do you notice increased vascularity while on it? Ive never had nicotine before.

A female friend of mine posted some of the interviews I've done with the 'nation, where I mention Nicotine as a stimulant/Fat-Burner/Anti-Estrogen.

Check them out:

http://forums.steroid.com/anabolic-steroids-questions-answers/243151-anthony-roberts-full-interview.html
http://forums.steroid.com/anabolic-steroids-questions-answers/248695-stimulant-article-anthony-roberts-cy-wilson.html

That thread by Bajan was good, too...I saw it and sent him some comments when it was first posted.

damn.....who woulda ever known all the good reaped from something so bad!:rolleyes:

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Originally Posted by nalbano34

damn.....who woulda ever known all the good reaped from something so bad!:rolleyes:

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:lol:

Someone send me a batch and i'll let you know how it goes :lol:

Good thread

they are not that expensive nark.. 100 chewing gums (2mg) cost approx 30$.. You actually NEED 2mg chewing gums, as only 50-70% of the dose contained within a cheweing gum is absorbed.

Some interesting quotes from ARs articles:

"Nicotine, however, is a well known inhibitor of the aromatase enzyme, and that's one of the reasons women who smoke have lowered estrogen levels. Anyway, I went to the drugstore and got some nicotine gum and used that until I could get a proper aromatase inhibitor. My gyno pain and symptoms went away in about two days. It's not perfect, and was poor planning on my part, but it worked."

"But yeah, nicotine is a pretty potent cognitive enhancer. The Nicotinic systems in the hippocampus play important roles in memory function, and in fact, a reduced nicotinic receptor concentration is associated with severe cognitive impairment, like that seen with schizophrenia and Alzheimer's disease.

Nicotine and nicotinic agonists are strongly and positively correlated with improved memory function, and even have a strong anti-depressant effect."

Nice thread AleX.

thanks,... did you use nicotine recently? if so.. what have your results been like?

I haven't actually. I can get the gum but never got around to trying it. I better grab some tomorrow.

:thumbsup:

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Originally Posted by BajanBastard

I haven't actually. I can get the gum but never got around to trying it. I better grab some tomorrow.

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So I have just come back from my GYM,I had to Amplify this thread to a few guys,I was told that a drug called Cyclicone is around;it stimulates the same receptor as Nicotine, but isn’t addictive at all,it seems to be new,I will try and look into it.

... Great info guys ... :7up:

Sssc

very interesting

Cyclicone seems to be trademarked substance devolped by "legal gear" - a popular supplement company. Mh.. i don't know if i would trust them. Most hyped products nowadys are B*llSH*T (with some exceptions though)..
I'll stick to my nicotine gums.. and even if i get addicted - no problem - that way i'll never forget my daily doses at least :lol:

Quote:

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Originally Posted by AleX-69

Cyclicone seems to be trademarked substance devolped by "legal gear" - a popular supplement company. Mh.. i don't know if i would trust them. Most hyped products nowadys are B*llSH*T (with some exceptions though)..
I'll stick to my nictoine gums.. and even if i get addicted - no problem - that way i'll never forget my daily doses at least :lol:

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Cyclicone `legal gear` that is truly Disgusting:lol:

I going to give this a try,Alex ;what do you think about the potential of the Nicotine patches,as this is an effective method to enter the blood stream.When you take the gum, the substance is absorbed from the gut and goes into the bloodstream, and the body slowly gets rid of it over the following hours. This results in fairly high levels of the drug in the blood shortly after taking the gum, which drop down again until the next dose is taken. Patches, on the other hand, result in a much more constant amount of the substance being in the blood stream for the time the patch is attached.As far as nicotine is concerned and the fat loss qualities , this means that there is a constant but small amount in your bloodstream,do you think this would result in better results? I was thinking of Combing the two for Superior results,it would be a 24 hour Blazing on your fat cells,what a nice way to cut to 4%:wg:

here is a VERY informative article on nicotine and weight loss... it is rather long but a good read nevertheless:
_______________________

By: Andrew Novick

Background

Stemming from the frequent observation that cigarette smokers tend to maintain lower body weights than their non-smoking counterparts, it is an intriguing idea that by using a nicotine product (such as a patch or gum), one could experience beneficial body composition effects while avoiding the carcinogenic dangers of cigarette smoke. In this issue of "Chemically Correct," we take an in-depth look at the science behind one of the world's most popular drugs.

Chemistry

Despite having similar stimulant qualities, nicotine has a distinct chemical structure from the phenylethylamines such as amphetamine and ephedrine. As opposed to these substances, nicotine is comprised of a pyridine ring connected to a pyrrolidine ring. There are two stereoisomers, (-)-nicotine being the active isomer and having the most affinity for nicotinic acetylcholine receptors (nAChr). Because nicotine is a weak base, it requires an alkaline environment to cross cell membranes (1).



This explains the tobacco companies' use of the controversial "ammonia chemistry" to boost cigarette impact. What makes the chemical structure of nicotine particularly fascinating (or not particularly so, depending how you look at it) is its resemblance to the acetylcholine (ACh) molecule. Because of ACh's flexibility as a molecule, it can be configured to resemble nicotine. Both the pyridine nitrogen of nicotine and the keto oxygen of ACh are electron donors, while the positive charge of nicotine's pyrrolidine nitrogen is similar to that of ACh's nitrogen. Using computer graphics, the two molecules are even super-imposable (2).

Pharmacology

Although the pharmacological effects of nicotine span across multiple receptor systems, the primary mode of action is elicited through nicotinic acetylcholine receptors (nAChr's) (3). These receptors are divided into subunits: alpha2-alpha7 and beta2-beta4. It is known that nicotine binds with the highest affinity to the alpha4beta2 subunit, with an affinity approximately 13 times greater than ACh itself (4).

While the alpha4beta2 subunit appears to be responsible for most of nicotine's pharmacological effects-as determined by the use of genetically altered knockout mice-other subtypes may contribute as well. Particularly, alpha6 and beta3 impact sensitization and reinforcement of nicotine and alpha7 for nicotine's anti-anxiety effect (5,6). But the pharmacology does not end there, as it's not merely the nAChr subtype that does all the magic, but rather the cascade of events that occur once that particular subtype is triggered. This includes nicotine's effects on other neurotransmitter systems.

Dopamine

Dopamine neurons in the ventral tegmental area and the substantia nigra have nAChr's (particularly the alpha4beta2 and alpha3beta2 subunits) located on their nerve terminal membranes; when these receptors are stimulated, dopamine is secreted (7,8,9,10). Nicotine-evoked glutamate release can enhance such secretion due to the presence of NMDA receptors on the dopamine terminals (11, 12). However, despite such robust dopamine release, overflow of dopamine in areas of the brain like the nucleus accumbens is tightly controlled by the dopamine re-uptake system (13).

In order to overcome such an effect, a dopamine re-uptake inhibitor might prove very useful in potentiating nicotine's dopaminergic action. But even without a re-uptake inhibitor, chronic use of nicotine by itself can increase dopamine overflow (14), and it is the NMDA receptors that are at least somewhat responsible for this sensitization mechanism (15). Another sensitization mechanism could be induced via nicotine's upregulation of D1, D2, and D3 receptor mRNA (16,17).

A third mechanism by which dopamine release is sensitized by chronic nicotine treatment is through increased tyrosine hydoxylase expression. Nicotine increases tyrosine hydroxylase mRNA in the brain, as well as the actual tyrosine hydroxylase protein (18). Since tyrosine hydroxylase is the limiting factor in the conversion of L-tyrosine to dopamine, nicotine should result in increased synthesis of dopamine, assuming that L-tyrosine intake is adequate. And indeed, when L-tyrosine and nicotine are administered together in-vitro to human lymphocytes, synthesis of L-Dopa and norepinephrine commences. (19)

Monoamine Oxidase type B (MAO-B) is one of the enzymes responsible for degrading dopamine. It's been known for some time that cigarette smoke has the capability of irreversibly inhibiting MAO-B (20). And while nicotine metabolite concentration is inversely proportional to MAO-B levels, nicotine itself does not inhibit MAO-B (21). Inhibition of MAO-B compounded by nicotine's effects on dopamine release is probably one of the primary reasons why cigarettes are so rewarding and might add to their effect on body composition. In order to potentiate nicotine's dopaminergic action without smoking, one could take the MAO-B inhibitor l-deprenyl. Also, since l-deprenyl has dopamine re-uptake blocking activity (22), it would provide a double mechanism for making nicotine's effect on dopamine more pronounced.

Noradrenaline

As with dopamine, nicotine elicits noradrenaline secretion by binding to nAChr's on noradrenergic neurons (3). Chronic nicotine administration will cause sensitization to its effects on NA release through increased expression of tyrosine hydroxylase (23,18). An indirect mechanism by which nicotine releases NA is through secretion of GABA (24). But that doesn't make sense, you might assert, as GABA is an inhibitory neurotransmitter, right? Right; but by some unknown mechanism, activation of the GABA-A receptor stimulates NA release (25). Effects of nicotine on GABA will be discussed later.

Eventually, with chronic nicotine infusion, NA overflow is abolished, alluding to the possibility of receptor desensitization (3). Interestingly enough, this phenomenon might add to the reinforcing effects of nicotine use. Because NA release is a component of the response to stressful stimuli (26), halting NA overflow during a stressful situation would explain once more the calming effects of smoking (3, 27).

Serotonin

Nicotine increases the release of serotonin in various parts of the brain, though to a lesser extent than the catecholamines. Mixed evidence exists to whether serotonergic neurons express nAChr's (28,29). Instead, nicotine induced 5-HT release has been attributed to stimulation of nicotinic receptors located in the dorsal raphe nucleus, and such stimulation appears to be directly responsible for the anxiolytic effects of nicotine (28,30).

Serotonin release is controlled by several serotonergic-nicotinic interactions. One such example is that while stimulation of nicotinic receptors leads to 5-HT release (31), stimulation of 5-HT1A receptors will inhibit ACh release (33). Nicotine also increases serotonin transporter density-another inhibitory response to increased 5-HT release (34).

Since this is the case, one might wonder whether it would make sense to add an SSRI to a nicotine regimen? The answer is probably not; sensitization to nicotine's stimulatory effects has been shown to be blocked by increasing 5-HT levels with the SSRI citalopram, known more commonly as Celexa (35). Finally, in food-deprived rats, tryptophan hydroxylase and serotonin synthesis is upregulated by nicotine (36). This is probably a very important mechanism by which nicotine's exerts its appetite and weight-controlling effects.

GABA

Those who can remember their elementary school D.A.R.E seminar ("Drugs Are Really Expensive" was our favorite interpretation) might recall that nicotine fell under the category of "stimulants." Such a designation baffled many of us given that most people report they get a calming effect from smoking. So which is it: a stimulant, or a relaxant? So far we've mentioned two mechanisms by which nicotine might exert anxiolysis: desensitizing the noradrenergic response to stress and via the increase of serotonin release. The third mechanism by which this may occur is GABAergic in nature.

GABAergic neurons express nAChr's (37), and when stimulated by nicotine increase GABA release (38). Nicotine also decreases the expression of the GABA-B1 receptor, which serves as an inhibitory mechanism on GABA release and thereby minimizes negative feedback (39).

Leptin and Neuropeptide Y

While evidence of increased dopaminergic and serotonergic activity does much to explain nicotine's effects on body weight and food intake, such a discussion would not be complete without reference to the food intake regulators leptin and neuropeptide Y (NPY). A detailed discussion of these two peptides is beyond the scope of this article; I refer those interested in a comprehensive review of the physiology and function behind these hormones to Par Deus' "Leptin: The Next Big Thing" series.

It would be wonderful if we could conclude that nicotine raises leptin levels, lowers neuropeptide Y levels, and in turn decreases appetite and body weight. Unfortunately, as is so often the case, nicotine's effects on these hormones are unclear, and often conflictual. Several studies have demonstrated that smokers have lower leptin levels than non-smokers (40,41,42), while others have established that nicotine raises leptin concentrations (43). In obese rats, nicotine was able to lower bodyweight independent of its effects on leptin levels (44). Such contradictions are somewhat reconciled when we accept that nicotine doesn't modulate leptin levels per se, but rather increases leptin receptor expression and sensitivity (44,45).

Similar confusions arise with Nicotine's effects on NPY, as nicotine has been shown to both increase (45) and decrease (46) NPY expression in the hypothalamus. These contradictions are slightly easier to digest when we take into account the conditions in each study. NPY expression decreased under food deprivation and higher nicotine doses (12mg/kg in rats), while it increased with lower doses of nicotine (2-6mg/kg). Interestingly, despite the scenario in which NPY expression was increased, anorectic effects were still prevalent, which suggests that nicotine's effects on NPY might be the product of a desensitization phenomenon (47).

Steroidogenesis

From a hormonal perspective, nicotine is attractive to male athletes because it can lower estrogen levels by competitively inhibiting the aromatase enzyme (48-52). Also beneficial might be the observation that in dogs, nicotine inhibits 3 alpha-hydroxysteroid dehydrogenase, preventing metabolism of DHT to a less potent androgen (53). While theoretically, this would allow one to gain increased benefits from DHT, it might also potentiate DHT's negative effects on the prostate and hairline.

Unfortunately, beyond individual inhibition of enzymes, nicotine and its metabolite cotinine appear to have a largely negative effect on steroidogenesis. Both nicotine and cotinine have been implicated in decreasing testosterone synthesis in rodent leydig cells (54,55). This decrease might be due to nicotine's effect on increased ACTH release, leading to increased circulating coritcosteroids, which have been known to alter sex hormone synthesis. While the in vivo action of nicotine on sex steroids might be less pronounced (55), those using nicotine with the purpose of aromatase inhibition should be aware of its other effects on steroidogenesis.

nAChr Desensitization or Upregulation?

In most neurotransmitter systems, chronic administration of an agonist results in receptor desensitization; this is not surprising in view of the body's tendency towards homeostasis. At first glance, nicotinic receptors appear to be no exception in this regard, given that overnight exposure to nicotine does indeed cause desensitization (59).

However, with chronic nicotine exposure, it appears that nicotinic receptors, particularly the alpha4beta2 subtype, undergo what is termed "functional upregulation." It is proposed that with chronic exposure, the number of high affinity versus low affinity receptors for nicotine actually increases, causing enhanced synaptic transmission of neurotransmitters (60). This upregulation could help elucidate nicotine's sustained effect on body weight, as well as its addictive qualities.

Mechanisms of Nicotine Addiction

In developed countries, it is estimated that tobacco use is the leading single cause of premature death (63). The irony of this statistic is that in developed countries, we are constantly being badgered about the dangers of tobacco use. In the end, the rewarding characteristics that tobacco and nicotine exert upon our neurochemistry are enough to overpower any voice of reason. So what's going on here?

Enhancement of dopaminergic activity is considered the universal trademark shared by addictive drugs. When dopamine transmission is impaired, animals will no longer self-administer addictive drugs, including nicotine (64). As we've already discussed, nicotine not only causes dopamine release but also increases the concentration of various dopamine receptors and induces glutamate release, sensitizing the dopaminergic response overtime. Add functional upregulation to the mix, and not only is the dopaminergic response to nicotine robust, it only gets better with continued use.

Putting dopamine aside for a minute, often overlooked is the role of serotonin in drug addiction. Serotonin is intimately involved with our ability to feel satiated as well as control impulsive behavior. Depletion of serotonin levels causes an increase in impulsive behavior as well as a tendency to prefer small immediate rewards to larger delayed rewards (65). It is hypothesized that nicotine may cause a shift in the "balance of power" by increasing dopamine function while simultaneously decreasing serotonin function (66). This hypothesis is supported by the observation that in the frontocortio and limbic areas of the brain, chronic nicotine exposure causes increased dopamine and reduced serotonin levels (67).

Related to impulsive behavior are nicotine's effects on the GABA system, which could theoretically lead to behavioral disinhibition, similar to alcohol. In context, "behavioral disinhibition" means that even when we know we shouldn't smoke, we reach for the cigarette anyway. The bottom line is that nicotine is so addictive not only because it effectively activates the reward centers of our brain (dopamine), it also partially impairs our decision-making ability through its actions on 5-HT and GABA.

Because the dynamics of nicotine addiction span across more than one receptor system, treatment for nicotine addiction should be just as complex. Despite the fact that SSRI's by themselves do little to aid in smoking cessation (80), there is some evidence that they might be of benefit when used in conjunction with transdermal nicotine (81). Thus, a complete "shotgun approach" to quitting nicotine (in whatever form) would include the use of proven effective dopaminergics such as bupropion and/or deprenyl (82,83) along with an SSRI.

Toxicity

Neurotoxicity

Two opposing concepts confound the issue of nicotine's neurotoxicity: nicotine has a protecting effect in Alzheimer's and Parkinson's disease due to antioxidant properties (68), yet can induce cognitive impairments in the offspring of smoking mothers from oxidative cellular injury (69). So is nicotine neurotoxic? At first glance, it would appear that the answer is yes, since nicotine can decrease glutathione levels and increase oxidative markers such as malondialdehyde, lactate dehydrogenase, hydrogen peroxide, and superoxide ion (69,70).

However, evidence of increased oxidative stress is only evident when high dose nicotine is administered (1mM or 162mg and up). Lower dose nicotine appears to have free radical scavenging effects and protects against lipid peroxidation (71). It is also this "lower dose nicotine" (.1mM or 16mg) that most smokers are using, and in these quantities it seems to be protective against Alzheimer's and Parkinson's disease (72).

Cardiotoxicity

Carbon monoxide and other components of cigarette smoke are thought to pose a larger threat to cardiovascular health than nicotine administered on its own (73). However, given nicotine's stimulant profile, it's no surprise that it has several cardiovascular effects on its own. By inducing the release of vasopressin, nicotine causes constriction of vascular beds in the skin (74). In other parts of the body, such as skeletal muscle, vasodilation occurs due to increased cardiac output and epinephrine release (75).

In animals, nicotine has the ability to increase platelet aggregability, possibly by inhibiting the prostaglandin protacylin, which is an antiplatelet aggregation factor (76,77). While this might appear to pose a threat to cardiovascular health by increasing the risk for blood clots, human snuff users (who generally do not suffer the cardiovascular risks of smokers) show no evidence of platelet activation (77). Similar discrepancies between human and animal studies exist for nicotine's effect on cholesterol profiles. Squirrel monkeys show increased levels of LDL when administered nicotine (78), while humans do not (79).

Overall, adverse cardiovascular effects stemming from nicotine use derived from sources other than smoking is in humans far from conclusive.

Nicotine Delivery Systems

Cigarette

The nicotine content in cigarettes varies widely depending upon brand, but usually averages around 1mg per cigarette (56). The actual amount absorbed upon smoking will depend upon how the cigarette is smoked, as well as the presence and amount of other added ingredients. Compared to other delivery systems, nicotine levels from cigarettes peak within minutes and fall shortly thereafter. Because the half-life of nicotine is around 2 hours, those who smoke more than one cigarette over the course of a day will demonstrate accumulated nicotine levels in their plasma (1).

It should be noted that the highly addictive quality of cigarettes lies not within its nicotine content, but rather its nicotine pharmacokinetics. Cigarettes provide an immediate jolt of nicotine to the CNS, resulting in almost instant gratification. Delaying nicotine gratification with the use of slower delivery mechanisms should aid minimizing addictive potential.

Oral Snuff and Nicotine Gum

Since both snuff and gum are absorbed from the oral mucosa, they have similar pharmacokinetics. Levels of nicotine peak at 30 minutes and slowly decline over 2 hours. Nicotine gum comes in 2mg and 4mg strengths and has absorption rates of 53% and 72%, respectively (58). Oral snuff tobacco is comprised of approximately 0.4% nicotine (58). Of course, "pinch" size will vary from person to person, but 2.5g caused a peak nicotine level of around 15ng/ml, similar to that of cigarettes and gum (57).

Nicotine Patch

Nicotine patches come in varying strengths, from 14-22mg, delivering nicotine at a constant rate of approximately .9mg per hour; levels peak at anywhere from 4 to 9 hours after initial administration (3).

Nicotine Nasal Spray

Nicotine nasal spray delivers 0.5mg to each nostril in a single dose, and levels peak within 5-10 minutes (3).

Conclusions

Given Nicotine's pharmacology, it appears to be most useful during periods of intense dieting. By enhancing the actions of dopamine, serotonin and leptin, as well as partially inhibiting the actions of neuropeptide Y, nicotine can partially deceive the body into thinking it is fed-thereby decreasing appetite, mobilizing fat, and preserving lean body mass-even in the presence of a calorie deficit.

So, how would one ideally use nicotine while dieting? From our review of the literature, we know that higher doses are more effective than lower doses at regulating various factors such as neuropeptide Y (47). However, given that these values are based on mg/kg in rats, establishing conversion rates for optimal human usage is a little tricky. Nonetheless, if we return to our original observation that smokers generally weigh less than non-smokers, and suppose that a "smoker" uses approximately 20mg of nicotine a day (about 20 cigarettes, one pack), we can conclude that 20mg might be an appropriate dosage.

It should also be noted that there are a number of other compounds that might compliment a nicotine regimen. Already mentioned has been deprenyl (5-10mg a day), the use of which is aimed at potentiatiating dopaminergic activity. Similarly, caffeine can sensitize the dopaminergic response to nicotine (61). Because nicotine upregulates tyrosine hydroxylase while concurrently inducing catecholamine release, supplementing with L-tyrosine would ensure ample substrates for neurotransmitter formation. Finally, Spook suggested the addition of calcium supplements, as nicotine induces the release of calcitonin gene-related peptide (CGRP), which can deplete intracellular calcium stores (62).
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Originally Posted by goose4

Cyclicone `legal gear` that is truly Disgusting:lol:

I going to give this a try,Alex ;what do you think about the potential of the Nicotine patches,as this is an effective method to enter the blood stream.When you take the gum, the substance is absorbed from the gut and goes into the bloodstream, and the body slowly gets rid of it over the following hours. This results in fairly high levels of the drug in the blood shortly after taking the gum, which drop down again until the next dose is taken. Patches, on the other hand, result in a much more constant amount of the substance being in the blood stream for the time the patch is attached.As far as nicotine is concerned and the fat loss qualities , this means that there is a constant but small amount in your bloodstream,do you think this would result in better results? I was thinking of Combing the two for Superior results,it would be a 24 hour Blazing on your fat cells,what a nice way to cut to 4%:wg:

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actually the nicotine in gums is taken up by the oral mucosa.. i for myself use a rather safe approach of using 5 gums taken throughout the day with 100mg caffein each. if you do the math it is only 5-7mg nicotine per day. The recommend dosage in the article above is around 20mg/day so using nicotine patch with additional gums might indeed be the best way to use nicotine. I may add these to my regimen aswell. very good input goose!!

But the downside of patches is that nicotine dosage peaks after some hours.. I suppose highest peak concentration which could be achieved with one 20mg patch is 4-5mg. For persons who are not used to high nicotine exposure this will lead to vomitting for sure.. So i figured it might be best - for me as a non smoker - to ease the body in the nicotine treatment, and after a while (one week i had in mind) up the dosage, or simply apply patches as u suggested.

Another point which should not be left out is that it has been observed that nicotine patches have site specific fat burining properties.

Alex, you really got me thinking here, excellent thread. As a person who quit a 2 pack a day habit about 5 yrs ago I just don't want to risk it though, stuff nearly kicked my ass~Good luck and I look forward to your results.

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Originally Posted by AleX-69

actually the nicotine in gums is taken up by the oral mucosa.. i for myself use a rather safe approach of using 5 gums taken throughout the day with 100mg caffein each. if you do the math it is only 5-7mg nicotine per day. The recommend dosage in the article above is around 20mg/day so using nicotine patch with additional gums might indeed be the best way to use nicotine. I may add these to my regimen aswell. very good input goose!!

But the downside of patches is that nicotine dosage peaks after some hours.. I suppose highest peak concentration which could be achieved with one patch is 4-5mg. For persons who are not used to high nicotine exposure this will lead to vomitting for sure.. So i figured it might be best - for me as a non smoker - to ease the body in the nicotine treatment, and after a while (one week i had in mind) up the dosage, or simply apply patches as u suggested.

Another point which should not be left out is that it has been observed that nicotine patches have site specific fat burining properties.

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Well I was going to start an ECAY stack this week,but I`m going to give this a try,I think that`s a great concept of introducing the patches after around 8 days to boost the effect and combat any Tolerance.It`s on........

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Originally Posted by goose4

Well I was going to start an ECAY stack this week,but I`m going to give this a try,I think that`s a great concept of introducing the patches after around 8 days to boost the effect and combat any Tolerance.It`s on........

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:thumbsup: keep me updated on your results - positive and negative. I will do the same!

I used to chew a lot and I had better workouts when i chewed while working out. Not so much did it help me with strength, but endurance. I could do more reps for different exercises and when I ran I could go a lot longer.

what do you think that would be a safe daily dose so we wont become adicted to nicotine

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Originally Posted by Angelus

what do you think that would be a safe daily dose so we wont become adicted to nicotine

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it don't think this is dose dependent.. it has more to do nicotine absoprtion speed.

"It should be noted that the highly addictive quality of cigarettes lies not within its nicotine content, but rather its nicotine pharmacokinetics. Cigarettes provide an immediate jolt of nicotine to the CNS, resulting in almost instant gratification. Delaying nicotine gratification with the use of slower delivery mechanisms should aid minimizing addictive potential. "

The safest way is to ease the body into treatment with rather low dosages of nicotine gums (slow release time) and later add patches or up the dosage.
In the end no one can gurantee that you will no develop an addiction, but as said in my initial post the chance of becoming addicted due to the use of nicotine gums is really low..

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Originally Posted by AleX-69

they are not that expensive nark.. 100 chewing gums (2mg) cost approx 30$.. You actually NEED 2mg chewing gums, as only 50-70% of the dose contained within a cheweing gum is absorbed.

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I'm out of the USA.

I went looking for it yesterday tho... the pharmacist i use doesn't sell it.

I'd have to check out Big K's pharmacist

Nice thread indeed

just bought a load of the 4mg gum - will let you know how it goes - gonna use it in conjunction with my lipostabil experiment