70 replies to this topic

[Dazzcat]

 

 

You are boring. Do you really believe that nicotine is so dangerous. I can't imagine a significant number of people chewing gum for fun. It's so not recreational. I assume chewing gum for smokers still is better than smoking gum.

 

 

I am boring, excuse me? At least I make some sense.

Of course NRT is better than smoking, but the contex of this thread is about nicotine as a "nootropic", why may imply long term use, especially if it becomes addictive.

 

[Major Legend]

 

Nornicotine nitrosation in saliva and its relation to endogenous synthesis of N'-nitrosonornicotine in humans.

Nicotine Tob. Res.

Nicotine Tob Res 2013 Feb 24;15(2):591-5. Epub 2012 Aug 24.

Aleksandar Knezevich, John Muzic, Dorothy K Hatsukami, Stephen S Hecht, Irina Stepanov

We recently reported that certain amounts of the carcinogen N'-nitrosonornicotine (NNN) can be formed endogenously from nicotine and/or nornicotine in some users of oral nicotine replacement therapy products. Although the acidic environment of the stomach creates the most favorable conditions for nitrosation, this reaction could also occur in the oral cavity in the presence of bacteria that catalyze nitrosation at neutral pH.
To test the hypothesis that endogenous formation of NNN could occur in the oral cavity, we investigated nitrosation of nicotine and nornicotine in human saliva. To specifically identify NNN as derived from precursors added to saliva, we incubated saliva samples with [pyridine-D(4)]nicotine and [pyridine-D(4)]nornicotine, with and without the addition of nitrite, and subsequently analyzed [pyridine-D(4)]NNN by liquid chromatography-tandem mass spectrometry.
Consistent with kinetic studies on nicotine and nornicotine nitrosation, incubation of saliva with [pyridine-D(4)]nornicotine alone produced detectable amounts of [pyridine-D(4)]NNN, whereas only traces of [pyridine-D(4)]NNN were found in samples incubated with [pyridine-D(4)]nicotine and sodium nitrite. Incubation of saliva samples from 10 nonsmoking volunteers with [pyridine-D(4)]nornicotine resulted in the formation of [pyridine-D(4)]NNN in 8 samples, with yields ranging from 0.003% to 0.051% of the added alkaloid.

Our results demonstrate that NNN can be formed from nornicotine in human saliva without deliberate addition of any other substance. Therefore, nornicotine, as present in tobacco or in nicotine replacement products, is a carcinogen precursor.

 

 

Presence of the Carcinogen N′-Nitrosonornicotine in the Urine of Some Users of Oral Nicotine Replacement Therapy Products

1. Irina Stepanov, 
2. Steven G. Carmella, 
3. Anna Briggs, 
4. Louise Hertsgaard,
5. Bruce Lindgren, 
6. Dorothy Hatsukami, and 
7. Stephen S. Hecht

+Author Affiliations

1. Masonic Cancer Center and Transdisciplinary Tobacco Use Research Center, University of Minnesota, Minneapolis, Minnesota

1. Requests for reprints:
   Irina Stepanov, Masonic Cancer Center, University of Minnesota, 420 Delaware Street SE-MMC 806, Minneapolis, MN 55455. Phone: 612-624-4998; Fax: 612-626-5135; E-mail:stepa011@umn.edu.

Abstract

N′-nitrosonornicotine (NNN) is a strong carcinogen present in unburned tobacco and cigarette smoke. We here analyze data obtained in two studies, in which a biomarker of exposure to NNN—the sum of NNN and its pyridine-N-glucuronide, called total NNN—was quantified in the urine of people who had stopped smoking and used various nicotine replacement therapy (NRT) products. In 13 of 34 nicotine gum or lozenge users from both studies, total NNN at one or more time points after biochemically confirmed smoking cessation was comparable with, or considerably higher than, the baseline levels. For most of the subjects who used the nicotine patch as a smoking cessation aid, urinary total NNN at all post–quit time points was <37% of their mean baseline levels. These results indicate that endogenous formation of significant amounts of NNN may occur sporadically in some users of oral NRT. Given the carcinogenicity of NNN and the frequent use of nicotine gum as a smoking cessation aid, further studies are needed so that preventive measures can be developed. [Cancer Res 2009;69(21):8236–40]

 

From FDA Site:

• 

Smoking cessation with NRT is advisable because levels of 

most toxicants decrease substantially.

• 

Use of oral NRT products results in exposure to NNN 

(mean 0.4 µg/day, range 0.1 µg – 1 mg) during use. 

• 

Long term use of NRT could present a significant 

carcinogenic hazard due to endogenous formation of NNN.

• 

NNN formation in rats treated with nornicotine and nitrite is 

inhibited by ascorbic acid, dihydroxyfumaric acid, and 

catechin ( D. Porubin et al., J. Agric. Food Chem . 55 7199 (2007 )).

• 

NRT products can probably be designed to minimize or 

eliminate NNN formation.

 

Case closed. ( at least for the gum)

 

Edited by Major Legend, 07 June 2014 - 08:33 PM.

[serp777]

 

 

 

So is there a doubt that nicotine is carcinogenic if it's pro angiogensis? or are the two processes not necessarily related.
 

 
I believe the real definition of nicotine is that it's a co-carcinogen, while it does not initiate cancer it promotes the growth of existing tumors. I never meant to imply that it alone is a carcinogen, but remember that it metabolizes into NNN when taken orally and the combination of the two could pose some real risks.
 
Until we see some long term human NRT studies, I would urge caution, especially in ex-smokers or those that are at higher risk of cancer due to age.

You are boring. Do you really believe that nicotine is so dangerous. I can't imagine a significant number of people chewing gum for fun. It's so not recreational. I assume chewing gum for smokers still is better than smoking gum.

 

 

"While no epidemiological evidence supports that nicotine alone acts as a carcinogen in the formation of human cancer, research over the last decade has identified nicotine's carcinogenic potential in animal models and cell culture.^{[49][50][51]"}

 

^{http://en.wikipedia....tine#Toxicology}
 

In addition, it has a significant addiction potential, which means you could convince yourself to start smoking cigs so you can get a bigger rush.

[Constantine Vorobyoff]

Significant addiction potential. Yea right. Start smoking coz nicotine patches won't work anymore. Gotta do a meme about it lol. While I can understand that it's may be cancerogenic and I value attention to detail of some of you, I don't believe it's any so significant that worth thinking about too long.

[Dazzcat]

 

 

From FDA Site:

• 

Smoking cessation with NRT is advisable because levels of 

most toxicants decrease substantially.

• 

Use of oral NRT products results in exposure to NNN 

(mean 0.4 µg/day, range 0.1 µg – 1 mg) during use. 

• 

Long term use of NRT could present a significant 

carcinogenic hazard due to endogenous formation of NNN.

• 

NNN formation in rats treated with nornicotine and nitrite is 

inhibited by ascorbic acid, dihydroxyfumaric acid, and 

catechin ( D. Porubin et al., J. Agric. Food Chem . 55 7199 (2007 )).

• 

NRT products can probably be designed to minimize or 

eliminate NNN formation.

 

Case closed. ( at least for the gum)

 

 

 

Thanks for that, interesting information. However it's not that practical chewing vitamin c each time before chewing gum. Manufacturers of gum could throw it into the mix but this may interfere with the absorption of nicotine (I believe nicotine requires an alkaline environment to absorb in mouth). Considering the formation of NNN is alarmingly high in oral NRT users, I'd say the safest bet is to avoid chronic oral nicotine use all together.

[Constantine Vorobyoff]

Btw patches came. It's good and unobtrusive.Tested with the iOS app called Lumosity: has a good effect on reaction time as well as math skills, I didn't notice immediate effects on short term memory within the app

Edited by Constantine Vorobyoff, 09 June 2014 - 03:40 AM.

[Major Legend]

 

 

 

From FDA Site:

• 

Smoking cessation with NRT is advisable because levels of 

most toxicants decrease substantially.

• 

Use of oral NRT products results in exposure to NNN 

(mean 0.4 µg/day, range 0.1 µg – 1 mg) during use. 

• 

Long term use of NRT could present a significant 

carcinogenic hazard due to endogenous formation of NNN.

• 

NNN formation in rats treated with nornicotine and nitrite is 

inhibited by ascorbic acid, dihydroxyfumaric acid, and 

catechin ( D. Porubin et al., J. Agric. Food Chem . 55 7199 (2007 )).

• 

NRT products can probably be designed to minimize or 

eliminate NNN formation.

 

Case closed. ( at least for the gum)

 

 

 

Thanks for that, interesting information. However it's not that practical chewing vitamin c each time before chewing gum. Manufacturers of gum could throw it into the mix but this may interfere with the absorption of nicotine (I believe nicotine requires an alkaline environment to absorb in mouth). Considering the formation of NNN is alarmingly high in oral NRT users, I'd say the safest bet is to avoid chronic oral nicotine use all together.

 

Unfortunately nicotine gum is the only nicotine delivery system that has nootropic effects for me. The formation of NNN happens in the stomach, when acidic conditions and nitrite is present. Nitrite is nullified by ascorbic acid (vitamin c). NNN only comes from nornicotine not nicotine. Probably why the FDA report said suppliers can probably change the formula to reduce the formation of nornicotine.

 

As for the saliva NNN, I believe the amounts is trace, but not impossible.

 

If 1 cigarette is 1-2 mg with gum coming in 1-4mg and people go through like 12 to 24 pellets a day.

 

I hope I am safe with 1 or 2 pellets every other day. Doesn't stop me from being paranoid about it. Nicotine has very unique nootropic effects on me that I don't find in other stimulants, it is not addictive as I can function normally without it, I only use nicotine in scenarios with high noise.

[Metagene]

I use Nicotine lozenges from time to time but this has been an area of oversight

 

 

Though the number of cigarette smokers in the United States has been steadily on the decline since the 1960s, an estimated 45.3 million Americans are still considered daily cigarette smokers (CDC 2010). An average cigarette yields approximately 1mg of absorbed nicotine, a stimulant alkaloid responsible for the addictive-properties of cigarette smoking (Connolly et al., 2007). Nicotine is a soluble small molecule that rapidly diffuses through the BBB and can interact directly with nicotinic acetylcholine receptors (nAChRs) on BECs (Le, 2003). Preclinical studies using rodent models of acute and chronic nicotine exposure reported compromised BBB integrity, marked by Evans blue or [14C] sucrose leakage into brain parenchyma. This BBB disruption occurred as early as 2h after acute nicotine and after 6weeks of chronic exposure (Lin et al., 1992; Uzum et al., 1999; Venisnik,2000;Hawkins et al., 2004, 2005). In vitro studies using either brain microvascular endothelial cells alone or in combination with C6 astrocytes revealed increases of FITC-Dextran and [14C]sucrose leakage across the cells after nicotine treatment (Schilling et al., 1992; Abbruscato et al., 2002). Nicotine also decreases transendothelial electrical resistance in an in vitro BBB model (Hutamekalin et al., 2008; Rodriguez-Gaztelumendi et al., 2011). This decrease in resistance is dose-dependent (0.1–100μM) and sufficient enough to produce a 60–150% increased invasion of Escherichia coli across brain microvascular endothelial cells (Chen et al., 2002). Whole animal studies also revealed nicotine-induced BBB dysfunction leading to increased transport from blood to brain of xenobiotics like squanivir, a protease inhibitor included in anti-retroviral therapy for HIV infection (Manda et al.,2010a). These studies offer added insight into the consequences of nicotine use relating to uptake of therapeutics into the CNS. Finally, both in vitro and in vivo studies report significant loss, or alterations in, tight junction proteins including ZO-1, claudin-3, JAMs, and occludin (Abbruscato et al., 2002; Hawkins et al., 2004; Hutamekalin et al., 2008; Manda et al., 2010b).

In addition to altering BBB tight junctions, nicotine affects transport and receptor systems involved in normal BBB function. Nicotine increases the activity of monocarboxylase and organic cation transporters while decreasing the functional activity of ion transporters like Na+, K+, 2Cl− co- transporter, and Na+, K+-ATPase on BECs (Wang et al., 1994; Abbruscato et al., 2004; Lockman et al., 2005; Paulson et al., 2006; Liou et al., 2007). Nicotine treatment produced a 22 and 17% decrease in Na+ and K+-ATPase activity in the microvasculature and brain, respectively (Wang et al., 1994). Nicotine also inhibited the activity of P-glycoprotein, an important efflux transporter responsible for impeding the entry of a range of compounds into the CNS (Manda et al., 2010a). Changes in transport mechanisms across the BBB can produce detrimental alterations in ion gradients and in the nutrients available to the brain (Paulson et al., 2006; Yang et al., 2006). Nicotine-induced alterations in ion transport are especially injurious as changes in ion gradients lead to brain edema lasting for up to 3weeks after nicotine exposure as well as increased cerebral ischemic injury (Wang et al., 1997; Paulson et al., 2010). nAChRs on cells within the BBB are also affected by nicotine. Chronic nicotine decreases nAChR surface expression as well as expression of certain nAChR subunits, particularly the α2 isoform, on BECs (Wang et al., 1994; Abbruscato et al., 2004; Lockman et al., 2005). While nicotine activity at nAChRs on BECs alters the BBB, treatment with nAChRs antagonists (e.g., mecamylamine, α-bungarotoxin, and hexamethonium) decreases nicotine-induced BBB dysfunction. This decrease in BBB disruption was identified by attenuation of [14C]sucrose leakage into the brain parenchyma, reversal of ZO-1 loss, and decreased Escherichia coli invasion in an in vitroBBB model (Abbruscato et al., 2002; Chen et al., 2002; Conklin et al., 2002; Hawkins et al., 2005; see Table ​Table44for a summary of the effects of nicotine on BBB function).

 

 

 

http://www.ncbi.nlm....les/PMC3386512/

 

[Major Legend]

Not really sure, so if mecamylamine was used with nicotine, would it cancel out nicotines concentration + nootropic effect.

 

Sounds horrific, I hope its over blown. 

[Metagene]

Not really sure, so if mecamylamine was used with nicotine, would it cancel out nicotines concentration + nootropic effect.

 

Sounds horrific, I hope its over blown. 

 

Yeah I think this mostly applies to smokers. Nicotine seems a lot less attractive as a nootropic though

 

http://pharmrev.aspe...nt/57/1/79.long

 

I'll look in to it later to be sure.

Edited by Metagene, 26 July 2014 - 12:34 AM.

[teacult]

Using Nicotine and smoking are not the same. Using stimulant and combining stimulants are not the same (with coffee or something else). Using stimulant energy for compensating bad diet or using it for extra stress adaptation and ergogenic purposes are not the same. Different brands of cigarettes or vaping chemicals are not the same. Reaction of different individuals due to their nature and nurture to that point are not the same. The diminishing return effects are not same for everyone (My father smokes 2 packs a day without any diminishing returns for 6 months and quits and smokes none for another six, same goes for whiskey and chocolate for him but he always combines things, whiskey chocolate , tea and smoking, nuts and bear, carbs and lemonade etc ...) 

My mother clearly benefits smoking for its hypothyroidic compensation effects, however her blood pressure is getting high and she has diagnosed with a dimmer version of hashimoto' s disease which I dont believe and still bet on sub clinical hypothyroid tweaked by smoking ...

General statistics shed light on your road for you to decide on whatever you are looking for, however you should try everything for yourself.

All I have mentioned above are one big word with lots of dependency and diversity in it. All is one, none are same.
That being sad, I wouldn't bother with commoners farm and street medicine ...

 

[EarthWaterAir]

yes, well done. you don't need to go looking to see if nicotine is a nootropic, it clearly is.

 

go on, smoke a cig or take nicotine gum. its extremely powerful.

[necrobytez]

It's alpha-7 nicotinic agonism, almost definitely.

There are a bunch of other drugs that do the same, including EVP-6124 and GTS-21.

One of the big issues with just plain nicotine is it desensitizes the alpha-7 nicotinic receptors fairly quickly, so the effects disappear and you have to stop taking it for a while for desensitization to reverse if you want to see the nootropic effects again. EVP-6124 should desensitize said receptors less quickly, if at all, than nicotine.

But yeah, nicotine definitely is a decent nootropic if you keep the doses low enough.

I've personally noticed taking nicotine orally in the form of carefully measured dilute e-cigarette fluid reduces tolerance buildup a lot. I suspect this is due to the fact that a large portion of it is being metabolized to cotinine before making it to the brain, which is a weaker nicotinic agonist that does not desensitize alpha-7 receptors as quickly. You just can't overdose on that like you did on Sunifiram and not expect another world of hurt, a couple ml of e-cig fluid is enough to kill you.

the literature on chronic tolerance to nicotine in humans is reasonably consistent in showing clear evidence of tolerance to subjective mood effects but little or no tolerance to cardiovascular, performance or other nicotine effects, within the limitations inherent in most human research on tolerance. What's this all about then?

 

(http://www.ncbi.nlm....ubmed/12521400)

[X_Danny_X]

i thought for sure Nicotine in small dosages (2mg or less)   were not enough to have any link to NNN or be potential to cause cancer directly or indirectly.

[Complexology]

I have been a chronic smoker, smoking 8 cigarettes at average a day for 8 months in time of stress. And it seems to me that smoking cigarettes significantly reduce brainpower and IQ. This claim is also made on scientific research, and my personal experience.

 

I highly recommend not smoking cigarettes for nicotine uptake.

 

I am now using nicotine gums, and I feel a tremendous increase in mental capacities. 

 

Have been a social smoker from July 2013 till now, september 2014. And I am strong enough to make it a habit to not experience nicotine addiction. I have smoked like 10 cigarettes in 2 days, and had little need for cigarettes, on those non-social times. The greatest reason was because I have enough reasons to HATE smoking, because I give a lot of value to brain power.

 

Nicotine addiction is for me more than 80% psychological, and 20% physical. Mind over matter.

 

So I recommed for non-smokers or people who have enough motivation and reasons to not smoke, to still use nicotine gums. Not recommended for people who are highly addicted to smoking in general, or belief in the nicotine myth.

[Covalencies]

Former smoker here (quit 3 years ago). Just started experimenting with 4mg lozenges after reading about the potential use of nictotine as a nootropic. Initial feeling was that it might be useful, but I'm not so sure now. Not much effect at 0.5mg/hour, so I upped it today to 1mg/hour to see what happens. Not much better at that dose; some alerting effect, but Cambridge brain science scores don't appear to be any different from baseline. Will ramp again tomorrow, but I'm not expecting much. Could be that I've smoked in the past. Then again, I haven't had much luck with any of the other noots I've tried this far, save Bacopa and maybe ISX-9 (need to try the latter again, but for more than a day), so it could just be me.

 

On the bright side, I haven't felt any withdrawl effects when I don't take it...

[Covalencies]

I'd like to revise my opinion on nicotine. It actually seems to work pretty well for improving motivation/focus. Memory is improved somewhat; both nicotine appears to give me an extra point over my plateu/average score in Cambridge Brain Science spatial search, and highest scores for a while on lumosity memory matrix were with nicotine. (Up higher now, but that's a different story.)

[X_Danny_X]

I surprise nobody has tried Pixotine....Nicotine toothpicks...things are powerful!   Only 2mg of nicotine

 

http://www.pixotine.com/

 

 

it is roughly $5 for a pack of 20 picks....there is a bigger pack for $50 or something for a big pack of toothpicks! 

[medicineman]

No one mentions nicotine here because it's benefits are common knowledge. Nicotine wards off Parkinsons, Alzheimer's, improves MCI in the elderly, etc.

Smoking is the worst route to go for. Whatever benefits you may hope to achieve via smoking will be offset by increased risk of CV disease among many others. I go for pastilles or patches.

[medievil]

 

So is there a doubt that nicotine is carcinogenic if it's pro angiogensis? or are the two processes not necessarily related.
 

 
I believe the real definition of nicotine is that it's a co-carcinogen, while it does not initiate cancer it promotes the growth of existing tumors. I never meant to imply that it alone is a carcinogen, but remember that it metabolizes into NNN when taken orally and the combination of the two could pose some real risks.
 
Until we see some long term human NRT studies, I would urge caution, especially in ex-smokers or those that are at higher risk of cancer due to age.

You are boring. Do you really believe that nicotine is so dangerous. I can't imagine a significant number of people chewing gum for fun. It's so not recreational. I assume chewing gum for smokers still is better than smoking gum.

he? a relation btw nicotine and boring? nico is boring, mdma now thats fun

[Constantine Vorobyoff]

 

 

 

 

So is there a doubt that nicotine is carcinogenic if it's pro angiogensis? or are the two processes not necessarily related.
 

 
I believe the real definition of nicotine is that it's a co-carcinogen, while it does not initiate cancer it promotes the growth of existing tumors. I never meant to imply that it alone is a carcinogen, but remember that it metabolizes into NNN when taken orally and the combination of the two could pose some real risks.
 
Until we see some long term human NRT studies, I would urge caution, especially in ex-smokers or those that are at higher risk of cancer due to age.

You are boring. Do you really believe that nicotine is so dangerous. I can't imagine a significant number of people chewing gum for fun. It's so not recreational. I assume chewing gum for smokers still is better than smoking gum.

he? a relation btw nicotine and boring? nico is boring, mdma now thats fun

 

 

 

It is. But for a short while. Nicotine is fun too for a bit. I find both unsustainable in the long run. Just cannot increase the dose everytime. Dose increase basically means that it's time to wrap up or side effects will show up

[ckendrick99]

I surprise nobody has tried Pixotine....Nicotine toothpicks...things are powerful!   Only 2mg of nicotine

 

http://www.pixotine.com/

 

This immediately made me think of nicotine dental floss - why not, two birds with one stone right?

 

From some quick Googling - it's been patented (of course), but no one appears to be selling it (yet).

[eon]

I would assume nicotine is a bad combo with an amphetamine Vyvanse since it's also a stimulant? I've considered using nicotine solely, the profile seem to work for people with ADHD, if I'm not mistaken.

 

Since if oral dose of nicotine has poor bioavailability according to someone on this thread, those nicotine gums sold at Walmart would be useless then? According to the article I just read below, the nicotine patch works better:

 

Hidden Benefits Of Nicotine on The Brain

 

http://mentalhealthd...e-on-the-brain/

 

"When used in the form of a standalone patch, a person is capable of attaining a psychological “buzz” or cognitive enhancement from nicotine, without the dangerous toxins associated with smoking cigarettes."

 

"For this reason, many people resort to smoking cigarettes or even just using nicotine patches as a way to remain calm and focused during cognitively demanding tasks.  Nicotine is considered a nootropic and can be used as a “smart drug” to maximize cognitive capacity, plus some evidence suggests that it may act as a neuroprotective agent.  Examples of tasks that people have found benefit from using nicotine include: solving complex mathematical equations, taking exams, and technical writing."

 

"There are a couple of exceptions to its nicotinic acetylcholine receptor agonism, specifically at the Alpha-9 and Alpha-10 nAChR receptors, where it functions as an antagonist.As a result of agonism at the nAChR receptors, nicotine increases stimulatory neurotransmitters including dopamine.  When inhaled as smoke, a monoamine oxidase inhibition effect can be observed as a result of harman and norharman."

 

Sounds like it could work for those with ADHD? Curious if the MAOI activity is only possible when inhaled or smoked and not so much when used as a patch or swallowed in pill form?

 

"Nicotine is considered a parasympathetic alkaloid derived from nightshade plants (Solanaceae).  It acts as a stimulant drug, speeding up activity in the central nervous system and brain, giving people increased physical and mental energy."

 

Considering some of the nightshade plants are used by some in rituals and has antidepressant properties such as Datura, etc. nicotine's profile is starting to look good to me.

 

 

 

 

 

Nicotine is also a fairly effective pesticide.

As is Caffeine.

Here's a thought, why don't some of these supplement companies go out and get some synthetic nicotine and add it in with one of their 'nootropic' proprietary cocktails, eh? Who likes it?

Nicotine has a very poor oral bioavaiblility (around or less than 20%). This means a small amount in a pill would be very ineffective, unless taken sublingually .

 

But it is largely metabolized to Cotinine, which IMO is actually the superior nootropic. Also much slower rise-time in blood concentration.

Also everyone claiming how addictive nicotine is, again is conflating nicotine with tobacco. It's specifically MAO-A inhibition that makes nicotine more addictive, which harman and norharman (two main MAOIs in tobacco) do.

 

 

Edited by eon, 01 June 2015 - 02:27 AM.

[Constantine Vorobyoff]

It's an effective nootropic. Sexual effets made me almost exclude it. Even 2 mg gum induces moderate to severe anorgasmia for a day. It will Côme back after daily use, like antidepressants but not to thé level as without it.

[eon]

Are you saying nicotine drops libido? I thought it would increase it considering smokers are IMO full of libido? Maybe I'm wrong? I don't smoke.

[gamesguru]

[eon]

But "smoking" is not exactly the same as putting a nicotine patch on me! Which would be my ideal route, that or taking it orally. Is the bioavailability really bad when taking oral nicotine gum? Where do I buy the patch the cheapest, does anyone have sources?

Edited by eon, 03 June 2015 - 07:40 AM.

[eon]

If anyone knows what dose does the nicotine patches come in, minimum to maximum? I have no clue really since I've never used them. As with anything I usually start off with low dosage. I would assume a nicotine patch product would have a standard minimum dose and a standard maximum dose. What are they?

[health_nutty]

I've tried nicotine patches for the nootropic / motivation effects.  Not as effective as caffeine and pretty expensive.  Not worth the health risk.  Btw at higher doses, i.e. full patch I was noticing vasoconstriction / lack of bloodflow issues.

[ricko321]

i like nicotine because it enhances alpha 7 nicotinic receptor, when i take it with other acetylcholine supplements i notice nootropic effects, are there any herbal alpha 7 nicotinic receptor enhancers?