NICOTINE: good or bad?

ssbackwards

Well-known member
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seems if you can use it without the harmful effects of smoking to get desired levels, it works well.

and is fairly safe

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this shows inhibition on 11b hsd and 21 hydroxylase which both effect cortisol and possible glucodcorticoid, granted in rats.

other studies use it for ulcerative colitis which colitis (itis meaning inflamation) which shows reduced inflammation.

Other studies showing it to aid in anti aromatase activities. reduce hunger (which is weird due to an enhanced NPY expression in rat hypothalamus Invalid Link Removed.). But this says opposite Invalid Link Removed

Granted there are certain negative effects. But nicotine in its purest form seems to be not bad aside from probably activating the CART or POMC in some way.

shed some light.
 
Effect on the CART system

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Effect on POMC
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Possible thyroidal effects?

seems inconclusive. Can be no effect or a big one depending on how it effects your appetite.
 
nicotine is poisonous though... isnt that why its in Raid?

How are you getting pure nicotine? through the patch or gum? Tobacco, not nicotine, is a vasoconstrictor which certainly doesnt help muscle.
 
ka0tik said:
nicotine is poisonous though... isnt that why its in Raid?

How are you getting pure nicotine? through the patch or gum? Tobacco, not nicotine, is a vasoconstrictor which certainly doesnt help muscle.
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poisonous is the bunch of CHEMICALS and CRAP they put it tobacco itself.
 
nicotine is a good stimulant and the only stimulant that calmes the nerves or relaxes (that I have ever heard of). the problem is the lack of human studies that use pure nicotine without tobacco.

"It is also true that a drop of pure nicotine can be deadly, and that if you concentrated the nicotine from a pack of cigarettes (or a can of snuff, or a box of pharmaceutical nicotine products) and put it into your body all at once, it would likely be fatal." Invalid Link Removed

how do you suppose you are going to take nicotine without the other chemicals? patches arent enjoyable, and the gum causes a burning sensation in your mouth...

and I dont mean to poke holes in your theory or hijack your thread... just conversing
 
ka0tik said:
nicotine is a good stimulant and the only stimulant that calmes the nerves or relaxes (that I have ever heard of). the problem is the lack of human studies that use pure nicotine without tobacco.

"It is also true that a drop of pure nicotine can be deadly, and that if you concentrated the nicotine from a pack of cigarettes (or a can of snuff, or a box of pharmaceutical nicotine products) and put it into your body all at once, it would likely be fatal." Invalid Link Removed

how do you suppose you are going to take nicotine without the other chemicals? patches arent enjoyable, and the gum causes a burning sensation in your mouth...

and I dont mean to poke holes in your theory or hijack your thread... just conversing
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either E cig, or the patch, or gum. looking into pure source for topical. seems like itll really aid in that area as well.

pure nicotine if given in the right amounts doesnt seem all that bad. when mixed with known carcinogens its horrible and causes a slew of inflammatory responces. but from this it seems that isnt an issue if given to obese people with UC. UC is inflammatory and obesity is inflammitory.

i seriously think there is something to be said for getting nicotine in small amounts throughout the day.
 
long time ago custom Capsule has a topical version of this if i remember correctly was Anthony Roberts who bring it.

"Nico-Lean"

Active Ingredients:

Serving Size: 1 Pump

Servings Per Container: 50

Caffeine 75mgs
Yohimbine HCL 50mgs
Nicotine 4mgs
 
I think ill stick to my green tea and ginsing
 
Interesting thread. Personally I'm not a huge fan of nicotine anymore. I stopped using Swedish snus three months ago, I just felt that I used too much of it so I had to stop.
 
"nicotine increases energy expenditure and could reduce appetite" PMID: 18400700

There also is some minor evidence on nicotines affects on 3aHSB and DHT so nicotine could be of benefit for those seeking to reduce the androgenic sides experienced on-cycle

" The results suggest that nicotine and cotinine are competitive inhibitors of the HSD, an important enzyme involved in the metabolism of DHT and produce an accumulation of DHT. " PMID: 3200111
 
Has anyone seen the DIY eliquid. You can specify how much nicotine per 60ml and it's diluted in a vegatable glycerin.
 
have not seen it but i got some evicerate im going to toss in like 100mg of aromasin in there aswell and if i can find some nicotine add that **** . but the aromasin is liquid, pretty thik consistency so not sure what thatll do.
 
Boy oh boy is this a thread that can get me into some trouble or what?!? I don't need anyone saying "Dr. Houser recommended nicotine therapy." Becuase frankly - I don't - and feel people are rationalizing their own use when trying to justify it's "positives." I will leave you with my own quotes from years ago on a different forum...

dinoiii said:
Well, I will save the speeches about how nicotine is bad for your health. I presume you have heard that one before.

There is evidence to suggest that nicotine supplementation of just 1mg per dose could be beneficial in increasing total calorie expenditure, through increases in metabolic rate and thermogenisis. Furthermore, it has been shown that the conjunctional ingestion of 50mg caffeine results in an approximate 100% increase in thermic response over nicotine alone, with no reported side effects.

BUT - HOLD THE PHONE, there is also a notion that nicotine may result in reductions in insulin secretion which may lead to an increase in the utilisation of fat, protein and glycogen together with a reduction in preference for sugary foods. This may not be the ideal post-workout scenario if trying to harbor the positive effects of the so-called "anabolic window," you would agree?

Also, nicotine clearly acts as an appetite suppressant. This fact is supported from many accounts of ex-smokers who find themselves gaining weight. There are MANY rationales hypothesized as to why this is (constant nicotinic acid receptor stimulation, stimulant effect, UCP-1 stimulation, and so on...).

So - when do we decide is a good time (if we happen to harbor the habit) to begin our ingestion of such products ... ideally - never, but you wouldn't expect a doctor to try and sell you on something alternate to that, would you?
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The reality is that about 50% of the active is absorbed and nicotine has about a 2-hour half life (inhaled, chewed, parenteral/IV administration are all the same). To take advantage of our anabolic window, this is usually quoted at 2 hours-ish (dependent upon the source) as well. So minimally...I would based on this and alternative elimination information decline use until 4 hours post-workout minimally, or you could be impeding your post-workout nutrition (and subsequent body comp changes) to some degree.



Aside: Understand that all bets are off on a cycle (especially C17 alkylated agents) as huge metabolic happenings occur in the liver and kidneys (major metabolite is something called cotinine and nicotine-1'-N-oxide and 3-hydroxycotininne as the major conjugated metabolites) and to me - this is an unacceptable level of risk.
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When asked...
Isn't this because of its aromatase inhibition? Couldn't this acutely translocate GLUT4?
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My response...
dinoiii said:
Actually, the mechanism is suggested more often to reside with stimulation of both cytokine and tumor necrosis factor stimulation. TNF has been shown to inhibit insulin-stimulated tyrosine-phosphorylation of both the insulin receptor and insulin receptor substrate, and to stimulate downregulation of the insulin-sensitive glucose transporter, GLUT-4 in adipocytes.

One thing we are keeping an eye on in the literature is the fact that nicotine has actually shown mixed review on androgenic production. Certainly some studies show increasing levels of T, whereas others show decreased. If the decreased is true, elevated androgens apparently also contribute to insulin resistance.

It is very interesting to note the relationships made lately between insulin resistance, the metabolic syndrome, and test deficiency exist considering this notion, no?

As far as an answer on your chronic vs. acute...I would likely want to suggest there is going to be a different response and due to a factor (as yet to be identified), there are people seeing different responses in regard to these parameters.
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D_
 
Also, if we are adding studies...

Am J Physiol Endocrinol Metab. 2007 Jul 3; [Epub ahead of print]Click here to read Links
Smoking impairs muscle protein synthesis and increases the expression of myostatin and MAFbx in muscle.
Petersen AM, Magkos F, Atherton P, Selby A, Smith K, Rennie MJ, Pedersen BK, Mittendorfer B.

Copenhagen Muscle Research Center, Copenhagen, Denmark.

Smoking causes multiple organ dysfunction. The effect of smoking on skeletal muscle protein metabolism is unknown. We hypothesized that the skeletal muscle protein synthesis rate is depressed in smokers compared with non-smokers. We studied eight smokers (>/=20 cigarettes/day for >/=20 years) and eight non-smokers matched for sex (4 men and 4 women per group), age (65+/-3 and 63+/-3y, respectively; means+/-SEM) and body mass index (25.9+/-0.9 and 25.1+/-1.2 kg/m(2), respectively). Each subject underwent an intravenous infusion of stable isotope-labeled leucine in conjunction with blood and muscle tissue sampling to measure the mixed muscle protein fractional synthesis rate (FSR) and whole-body leucine rate of appearance (Ra) in plasma (an index of whole-body proteolysis), the expression of genes involved in the regulation of muscle mass (myostatin, a muscle growth inhibitor; MAFBx and MuRF-1, which encode E3 ubiquitin ligases in the proteasome proteolytic pathway) and that for the inflammatory cytokine tumor necrosis factor-alpha (TNFalpha) in muscle, and the concentration of inflammatory markers in plasma which are associated with muscle wasting in other conditions. There were no differences between non-smokers and smokers in leucine Ra and plasma concentrations of inflammatory markers, or TNFalpha mRNA in muscle, but muscle protein FSR was much less (0.037+/-0.005 vs. 0.059+/-0.005 %/h, respectively; P=0.004) and myostatin and MAFBx (but not MuRF-1) expression was much greater (by ~33% and 45%, respectivley; P<0.05) in the muscle of smokers than of non-smokers. We conclude that smoking impairs the muscle protein synthesis process and increases the expression of genes associated with impaired muscle maintenance. Key words: muscle protein synthesis, stable isotope tracers, smoking.

PMID: 17609255 [PubMed - as supplied by publisher]
 
How bout the Aromatase Inhibition Dr. H.?

Bodybuilders are overtly a strange bunch in that they try and get me to thumb's up their alternate addictions in many instances and this is probably the second most common. Well, I won't codemn use per se, but I won't support it either.

The papers that suggest hormonal support offering are restricted to certain groups and even the 2-hydroxylation offering above is probably only seen in females as has tended to be the overt suggestion in the literature at large, but the steroidogenic pathways are extremely different in that regard when compared to males.

Also beneficial might be the observation that in dogs, nicotine inhibits 3 alpha-hydroxysteroid dehydrogenase, preventing metabolism of DHT to a less potent androgen. 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. This decrease might be due to nicotine's effect on increased ACTH release, leading to increased circulating coritcosteroids (i.e. - cortisol), which have been known to alter sex hormone synthesis (as I have pointed out countless times in my protocols for post-cycle cortisol control). While the in vivo action of nicotine on sex steroids might be less pronounced, those using nicotine with the purpose of aromatase inhibition should be aware of its other effects on steroidogenesis and because we oftentimes look to support our habits, this is unfortunately not done.

The lowering of bodyfat certainly can lower conversion to estrone through lowering the overall concentration of aromatic conversion by default, but this is pure pontification and that alone at present time. The problem that will continually plague this theory is that no systematic trials will ever be entertained because of the aforementioned problems to generalized health status - whether this is promoted by overt ciagrrette smoking or nicotine itself can be infinitely debated.



D_
 
Blergs said:
I think ill stick to my green tea and ginsing
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Well, I am an advocate of green tea in significant moderation if testosterone is your primary sought-after effect.

Green tea (at least in vitro and in rodent models) has been shown to increase levels of SHBG. Some will protest this effect ("because of their long-term use with success" - YAWN); but the reality is - you can pretty much get a negative out of most things; the data was enough for me to forget significant use. However, it's health benefits are so overwhelming that I highly encourage you to drink it anyway maybe a few times per week.

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D_
 
i was thinking of topically .

I dont see anything being bad in terms of cortisol production it is said to inhibit 11b hsd and 21 hydroxylase.

it definetly works as an AI and anti cortisol. i used it at the end of my cut, 6 cigs a day for 2 months. not healthy but i wasnt about to use the patch and i used to smoke ... long story.

anyway. i was thinkin 2-4mg 2-3x a day would suffice.

not from cigarette smoke, but from either gum patch or Ecig. I dont think anyone would take from you saying its good. because it effects the CART i assume thats where the addictive behavior comes from. and a decrease in cart over X amount of time leasd to less CART stimulation leading to more cigarettes or nicotine needed to illicit same responce.

whether you say its good or bad, people wont just do something because you say to.

i like your write up. but id like to know how you feel about it saftey wise for fat burning topically and orally.
 
dinoiii said:
Well, I am an advocate of green tea in significant moderation if testosterone is your primary sought-after effect.

Green tea (at least in vitro and in rodent models) has been shown to increase levels of SHBG. Some will protest this effect ("because of their long-term use with success" - YAWN); but the reality is - you can pretty much get a negative out of most things; the data was enough for me to forget significant use. However, it's health benefits are so overwhelming that I highly encourage you to drink it anyway maybe a few times per week.

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D_
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This study investigated the acute effects of green tea extract (GTE) and its polyphenol constituents, (-)-epigallocatechin-3-gallate (EGCG) and (-)-epicatechin (EC), on basal and stimulated testosterone production by rat Leydig cells in vitro. Leydig cells purified in a Percoll gradient were incubated for 3 h with GTE, EGCG or EC and the testosterone precursor androstenedione, in the presence or absence of either protein kinase A (PKA) or protein kinase C (PKC) activators. The reversibility of the effect was studied by pretreating cells for 15 min with GTE or EGCG, allowing them to recover for 1 h and challenging them for 2 h with human chorionic gonadotropin (hCG), luteinizing hormone releasing hormone (LHRH), 22®-hydroxycholesterol or androstenedione. GTE and EGCG, but not EC, inhibited both basal and kinase-stimulated testosterone production. Under the pretreatment conditions, the inhibitory effect of the higher concentration of GTE/EGCG on hCG/LHRH-stimulated or 22®-hydroxycholesterol-induced testosterone production was maintained, whereas androstenedione-supported testosterone production returned to control levels. At the lower concentration of GTE/EGCG, the inhibitory effect of these polyphenols on 22®-hydroxycholesterol-supported testosterone production was reversed. The inhibitory effects of GTE may be explained by the action of its principal component, EGCG, and the presence of a gallate group in its structure seems important for its high efficacy in inhibiting testosterone production. The mechanisms underlying the effects of GTE and EGCG involve the inhibition of the PKA/PKC signalling pathways, as well as the inhibition of P450 side-chain cleavage enzyme and 17-hydroxysteroid dehydrogenase function.
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whats always questionable about these types of studies (besides that it was on rats) is it was done in-vitro and directly on the leydig cells.

So now the question becomes, how much EGCG will realistically make it to your Leydig Cells?

My guess would be it is BARELY so unless people are worried about the test levels of their gut-bacteria then I doubt there really is any need of concern with drinking green tea or taking a EGCG supplement.
 
JudoJosh said:
whats always questionable about these types of studies (besides that it was on rats) is it was done in-vitro and directly on the leydig cells.

So now the question becomes, how much EGCG will realistically make it to your Leydig Cells?

My guess would be it is BARELY so unless people are worried about the test levels of their gut-bacteria then I doubt there really is any need of concern with drinking green tea or taking a EGCG supplement.
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I don't necessarily disagree with your comments, BUT that's the case with ALL oral supplementation, but we can certainly deduct some things from studies on tea flavonols and catechols from some other work...

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And if you're willing to write off bioavailability, why the hell take it anyway? Just because it may or may not have low bioavailability, you don't still take it for alternative properties with a terrible bioavailability...just because (that's slightly flawed logic I am afraid). THE SHBG is a serum offering produced by the LIVER and finds it's way to the bloodstream with some level of affinity for serum sex hormones, NOT solely testicular.

But still, bioavailability isn't presumed to be as bad as we once thought per a journal article from the journal Nutrition which approximates it closer to 40% from dismal initial serum predictive numbers (26% for mice and like 1.6% for rats. No other article evaluated it at all; it was simply predictive.

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PLUS, we're still forgetting that metabolites have activity YET STILL, it is NOT solely the molecule before glucuronidation but if you are concerned there, we still see increased bioavailability with added bioperine for those looking to get potentially better health benefit.

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D_
 
ssbackwards said:
also D

isnt nicotine broken down into nicotinic acid in the body?

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In part (yes)...a small amount, oxidation of nicotine will yield nicotinic acid (niacin), which is partly how the compound derived its name, BUT solely as a result of initial experiments in the 1800s with nicotine and subsequent understanding in prevention of pellagra was this ever considered significant and only briefly before other sources of niacin were found (i.e. - from corn through nixtamalization in 1951). When the biological significance of nicotinic acid was realized, it was thought appropriate to choose a name to dissociate it from nicotine, to avoid the perception that vitamins or niacin-rich food contains nicotine, or that cigarettes contain vitamins. The resulting name 'niacin' was derived from nicotinic acid + vitamin.

D_
 
would that be a safe replacement in a topical formula? would it have any effect similar to fat mobilization as nicotine or hardly any at all.
 
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