Vaping for nicotine advantages?

[sofarsogood]

OP is awesome. I am contemplating how I can apply nicotine research in my nursing research class, my cohort is in the top tier of Indiana, hand selected by the state so we can get grants from the state. It's still a work in progress, but I am attempting to apply the subjective benefits people can feel such as cigarette addicts who have contraindicated gait, and are stuck with cravings while they are not allowed to smoke in the building, and how a nicotine relief can aid their comfort and be applied in a nursing setting.

Also about the OP, interesting you say the increased buzz with nicotine. Everytime I smoke hookah or my ecig when I have been drinking, I get a woozy drunken headbuzz like I had doubled down on shots for the night for about 1 minute, its an extreme alcohol/nicotine buzz then it goes back to what level of booze I was at prior to.

I know someone who smokes and had a hospital stay and while they were there they were given an ecig to use during their stay.

 

[mosspa]

I'm thinking hard about your point that the chemicals in cigarettes aren't very reinforcing (unlike some other psycho active substances we aren't supposed to mention by name in the e-cig forum)

Close, but I think that when one starts smoking cigarettes the nicotine does provide quite a bit of primary reinforcement. Think about the first time you smoked (for real). If it was like mine, it wasn't a particularly 'good' experience. However, persevering for a week or so (in my case, through peer pressure...(I walked to school each morning with a guy that was in 8th grade and had been passed over for a few classes so he was about three years older than I was. He always had cigarettes, so I smoked a couple with him on the way to school each morning). I was soon smoking regularly after that and I quickly adapted to the nausea and dizziness, and I guess I liked smoking for the way it made me feel. The rest of my story is explained as I described it previously. The short version is that after regular smoking became a part of my life, it continually got paired with many very pleasurable experiences. It got paired with drinking and smoking other things. It was there when I got laid the first time, and many times thereafter. I was an adolescent, getting reinforced by the things that reinforce the behavior of adolescence (e.g., having fun with my friends, underage drinking, civil disobedience, etc.). In thinking my position on why I smoked for 5 years, it now seems clear that it was the positive events that were paired with smoking that reinforced my behavior to smoke, and as more positive experiences got included in that list, more and more things became the actual reinforcers for my smoking behavior, and the nicotine, and whatever else that was the primary reinforcer lost effectiveness as other things provided reinforcement for my smoking behavior, By the time I decided to quit, the only thing I had to fight was the habit strength of smoking in all the situations that were continuing to be reinforced by the act of smoking, By the time I quit, (i.e., which was only five years after I started) I don't think it was that difficult to associate the reinforcers I was receiving from smoking to other things that were reinforcing my building smoking habit. Toward the end of my senior year of high school, I was dabbling in a lot of psychoactive substances and decided to quit them all, including smoking. I quit cold turkey, from many things in April 1972, and smoking was one of them (i.e., but i continued social drinking, and a couple years later, I took up minor psychostimulans as cognitive performance enhancers that I occasionally dabbled with during college,and less frequently in during grad school). During the summer between high school and college, I never smoked and my only 'vice' was drinking. Over that summer, and something that persisted for my first few few of college were a mild compulsion to smoke (which i never did) whenever I was in a dimly lit bar with a draugh beer in front of me. Two years after my smoking cessation, whatever the reinforcement properties of cigarettes were when I started, should have extinguished, and apparently did. However, I believe my brain still 'remembered' the good old times and provided me an impulse to smoke in the pretense of situations where smoking was highly correlated with positive experiences I hadn't when I had been smoking in the past. Bring me to the present, after 42 years had passed, smoking lost all of its reinforcer effectiveness, As i remarked previously, many of the persons in my classes have admitted quitting smoking without experiencing any urge to restart smoking, and out of more than 50 such students, none had said they ever experienced situations of smoking craving. Contrast that with long-time smokers who proceed to smoke as a part of their lives for 30-50 years. The experiencing of the smoking-while in reinforcing situations had persisted over decades and should have continued to allow cigarette smoking to be associated with the ups and downs of life. Estes wrote about habit strength acquired in this manner for many years. So, incorporating B.F. Skinner's principles of positive reinforcement, with Estes theory of habit strength, I have come up with an explanation for why young smokers, (i.e., those that don't continue smoking for more than, say 4-10 years, don't experience many symptoms of physiological dependence when they quit, but why people that smoke for multiple decades do. It is the habit of smoking that drives continual smoking, and as time goes on and nicotine plays less and less of a role. This would explain why 'the patch' has proven to be a poor method of smoking cessaton.

 

[mosspa]

To the original post...interesting concept and I tend to agree that I am sharper with nic...but I have never deduced if that was dependance or and advantage of the chemical.

It is the reason that I believe that nicotine doesn't really contribute much to the negative associations with going cold-turkey from cigarettes

 

[mosspa]

OP is awesome.

Wow,two awesomes in a row ...

I am contemplating how I can apply nicotine research in my nursing research class, my cohort is in the top tier of Indiana, hand selected by the state so we can get grants from the state. It's still a work in progress, but I am attempting to apply the subjective benefits people can feel such as cigarette addicts who have contraindicated gait, and are stuck with cravings while they are not allowed to smoke in the building, and how a nicotine relief can aid their comfort and be applied in a nursing setting.

Also about the OP, interesting you say the increased buzz with nicotine. Everytime I smoke hookah or my ecig when I have been drinking, I get a woozy drunken headbuzz like I had doubled down on shots for the night for about 1 minute, its an extreme alcohol/nicotine buzz then it goes back to what level of booze I was at prior to.

That's the effect I get, but it is much more short acting (< 20 sec max), and I think that I purposely induce it by not vaping fro at least 2-3 hrs before I begin drinking, and don't vape until I gave at least 4 drinks (.i.e a couple more hours). The first couple hits in those circumstances have been extraordinary .

PM me if you want some ideas you can play with in your nursing class

 

[ItsBroTime]

I just wanted to thank Mosspa for the interesting information that supports what I have read with regards to nicotine being a positive on cognitive performance. I couldn't seem to find that .zip file you mentioned earlier in the post that contained information on the efficacy of nicotine and Alzheimers... would you be able to share it once more for a budding young biologist?

 

[The Dog Guy]

I just wanted to thank Mosspa for the interesting information that supports what I have read with regards to nicotine being a positive on cognitive performance. I couldn't seem to find that .zip file you mentioned earlier in the post that contained information on the efficacy of nicotine and Alzheimers... would you be able to share it once more for a budding young biologist?

It was posted in a post brotime. No need for the zip

 

[ItsBroTime]

Ok in that case I'll get digging, thanks for the tip

 

[mosspa]

I just wanted to thank Mosspa for the interesting information that supports what I have read with regards to nicotine being a positive on cognitive performance. I couldn't seem to find that .zip file you mentioned earlier in the post that contained information on the efficacy of nicotine and Alzheimers... would you be able to share it once more for a budding young biologist?

It is pretty near the beginning (page 4-5, mayber). Also, somebody expanded the zip to a very long post that is all text. I'd re-post the zip but I'm not going to be in my office today.

 

[Robino1]

<snip>
Contrast that with long-time smokers who proceed to smoke as a part of their lives for 30-50 years. The experiencing of the smoking-while in reinforcing situations had persisted over decades and should have continued to allow cigarette smoking to be associated with the ups and downs of life. Estes wrote about habit strength acquired in this manner for many years. So, incorporating B.F. Skinner's principles of positive reinforcement, with Estes theory of habit strength, I have come up with an explanation for why young smokers, (i.e., those that don't continue smoking for more than, say 4-10 years, don't experience many symptoms of physiological dependence when they quit, but why people that smoke for multiple decades do. It is the habit of smoking that drives continual smoking, and as time goes on and nicotine plays less and less of a role. This would explain why 'the patch' has proven to be a poor method of smoking cessaton.

Precisely. Toward the end, actually for several years before finding e-cigs, I did NOT like or find enjoyable the act of smoking. I just disliked smoking intensely. It was the Habit that I couldn't get rid of. There was just something about taking that time to chill with a cigarette. I lost the ability to just sit and relax after 30+ years of smoking. That is a Very Long time to develop an ingrained habit.

This is really not news for us long time smokers. Most of us are very aware of why patches didn't work. They don't address the hand to mouth habit. That and the fact that the method of delivery is not very efficient. I managed to smoke while wearing the patch and not have any ill effects. Gum is just plain unpleasant. To use that in the method recommended, you place the gum between the jaw and cheek. Do you know how hard it is to keep there and good lord, you know people see that bump. Not to mention when you get a gross bunch of nic into the stomach. Blech!

 

[mmsjs5]

Here's the text.....

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1. Bioorg Med Chem Lett. 2014 Mar 15;24(6):1472-8. doi: 10.1016/j.bmcl.2014.02.008.
Epub 2014 Feb 14.

Evaluation of nicotine and cotinine analogs as potential neuroprotective agents
for Alzheimer's disease.

The currently available therapies for Alzheimer's disease (AD) and related forms
of dementia are limited by modest efficacy, adverse side effects, and the fact
that they do not prevent the relentless progression of the illness. The purpose
of the studies described here was to investigate the neuroprotective effects of
the nicotine metabolite cotinine as well as a small series of cotinine and
nicotine analogs (including stereoisomers) and to compare their effects to the
four clinically prescribed AD therapies.


2. J Mol Model. 2014 Mar;20(3):2109. doi: 10.1007/s00894-014-2109-8. Epub 2014 Feb
25.

Targeted studies on the interaction of nicotine and morin molecules with amyloid
β-protein.

Alzheimer's disease (AD) is a neurodegenerative disorder that occurs due to
progressive deposition of amyloid β-protein (Aβ) in the brain. Stable
conformations of solvated Aβ₁₋₄₂ protein were predicted by molecular dynamics
(MD) simulation using the OPLSAA force field. The seven residue peptide
(Lys-Leu-Val-Phe-Phe-Ala-Glu) Aβ₁₆₋₂₂ associated with AD was studied and reported
in this paper. Since effective therapeutic agents have not yet been studied in
detail, attention has focused on the use of natural products as effective
anti-aggregation compounds, targeting the Aβ₁₋₄₂ protein directly. Experimental
and theoretical investigation suggests that some compounds extracted from natural
products might be useful, but detailed insights into the mechanism by which they
might act remains elusive. The molecules nicotine and morin are found in
cigarettes and beverages. Here, we report the results of interaction studies of
these compounds at each hydrophobic residue of Aβ₁₆₋₂₂ peptide using the hybrid
ONIOM (B3LYP/6-31G**:UFF) method. It was found that interaction with nicotine
produced higher deformation in the Aβ₁₆₋₂₂ peptide than interaction with morin.
MD simulation studies revealed that interaction of the nicotine molecule with the
β-sheet of Aβ₁₆₋₂₂ peptide transforms the β-sheet to an α-helical structure,
which helps prohibit the aggregation of Aβ-protein.


3. Acta Neuropathol. 2014 Jan;127(1):53-69. doi: 10.1007/s00401-013-1210-x. Epub
2013 Nov 16.

Neuropathology of cigarette smoking.

Chang RC(1), Ho YS, Wong S, Gentleman SM, Ng HK.

It is well established that cigarette smoking is hazardous to health and is a
risk factor for many chronic diseases. However, its impact on the brain, whether
it be from prenatal exposure to maternal cigarette smoking, cerebrovascular
disease, Alzheimer's disease (AD) or Parkinson's disease, is still not very
clear. Neuroimaging and neuropathological investigations suggest that there are
heterogeneous effects of cigarette smoking on the brain. On the one hand, it is
quite clear that cigarette smoking causes damage to endothelial cells, resulting
in increased risk of cerebrovascular disease. On the other hand, it seems to be
associated with different Alzheimer's pathologies in post-mortem brains and
experimental models, despite the fact that epidemiological studies clearly
indicate a positive correlation between cigarette smoking and increased risk for
AD. Interestingly, cigarette smoking appears to be associated with reduced
Parkinson's pathology in post-mortem brains. However, although nicotine in
cigarettes may have some neuroprotective actions, the effects of all the other
toxic compounds in cigarettes cannot be ignored. It is, therefore, our aim to
summarize what is known about the neuropathology of cigarette smoking and, in
particular, its implications for neurodegenerative diseases.


4. Neuromolecular Med. 2013 Sep;15(3):549-69. doi: 10.1007/s12017-013-8242-1. Epub
2013 Jul 11.

Nicotine prevents synaptic impairment induced by amyloid-β oligomers through
α7-nicotinic acetylcholine receptor activation.

An emerging view on Alzheimer disease's (AD) pathogenesis considers amyloid-β
(Aβ) oligomers as a key factor in synaptic impairment and rodent spatial memory
decline. Alterations in the α7-nicotinic acetylcholine receptor (α7-nAChR) have
been implicated in AD pathology. Herein, we report that nicotine, an unselective
α7-nAChR agonist, protects from morphological and synaptic impairments induced by
Aβ oligomers. Interestingly, nicotine prevents both early postsynaptic impairment
and late presynaptic damage induced by Aβ oligomers through the
α7-nAChR/phosphatidylinositol-3-kinase (PI3K) signaling pathway. On the other
hand, a cross-talk between α7-nAChR and the Wnt/β-catenin signaling pathway was
revealed by the following facts: (1) nicotine stabilizes β-catenin, in a
concentration-dependent manner; (2) nicotine prevents Aβ-induced loss of
β-catenin through the α7-nAChR; and (3) activation of canonical Wnt/β-catenin
signaling induces α7-nAChR expression. Analysis of the α7-nAChR promoter
indicates that this receptor is a new Wnt target gene. Taken together, these
results demonstrate that nicotine prevents memory deficits and synaptic
impairment induced by Aβ oligomers. In addition, nicotine improves memory in
young APP/PS1 transgenic mice before extensive amyloid deposition and senile
plaque development, and also in old mice where senile plaques have already
formed. Activation of the α7-nAChR/PI3K signaling pathway and its cross-talk with
the Wnt signaling pathway might well be therapeutic targets for potential AD
treatments.


5. Ther Adv Chronic Dis. 2011 May;2(3):197-208. doi: 10.1177/2040622310397691.

Enhancement of nicotinic receptors alleviates cytotoxicity in neurological
disease models.

The common pathological mechanisms among the spectrum of neurodegenerative
diseases are supposed to be shared. Multiple lines of evidence, from molecular
and cellular to epidemiological, have implicated nicotinic transmission in the
pathology of the two most common neurodegenerative disorders, namely Alzheimer's
disease (AD) and Parkinson's disease (PD). In this review article we present
evidence of nicotinic acetylcholine receptor (nAChR)-mediated protection against
neurotoxicity induced by β amyloid (Aβ), glutamate, rotenone, and
6-hydroxydopamine (6-OHDA) and the signal transduction involved in this
mechanism. Our studies have clarified that survival signal transduction, the α7
nAChR/Src family/PI3K/AKT pathway and subsequent upregulation of Bcl-2 and Bcl-x,
would lead to neuroprotection. In addition to the PI3K/AKT pathway, two other
survival pathways, JAK2/STAT3 and MEK/ERK, are proposed by other groups. In
rotenone- and 6-OHDA-induced PD models, nAChR-mediated neuroprotection was also
observed, and the effect was blocked not only by α7 but also by α4β2 nAChR
antagonists. We also document that nAChR stimulation blocks glutamate
neurotoxicity in spinal cord motor neurons. These findings suggest that
nAChR-mediated neuroprotection is achieved through subtypes of nAChRs and common
signal cascades. An early diagnosis and protective therapy with nAChR stimulation
could be effective in delaying the progression of neurodegenerative diseases such
as AD, PD and amyotrophic lateral sclerosis.


6. Neurobiol Aging. 2011 May;32(5):834-44. doi:
10.1016/j.neurobiolaging.2009.04.015. Epub 2009 May 22.

Chronic nicotine restores normal Aβ levels and prevents short-term memory and
E-LTP impairment in Aβ rat model of Alzheimer's disease.

Alzheimer's disease (AD) is a devastating neurodegenerative disorder
characterized by increased deposition of beta-amyloid (Aβ) peptides and
progressive cholinergic dysfunction in regions of the brain involved in learning
and memory processing. In AD, progressive accumulation of Aβ peptide impairs
nicotinic acetylcholine receptor (nAChR) function by an unknown mechanism
believed to involve α(7)- and α(4)β(2)-nAChR blockade. The three approaches of
the current study evaluated the effects of chronic nicotine treatment in the
prevention of Aβ-induced impairment of learning and short-term memory. Rat AD
model was induced by 14-day i.c.v. osmotic pump infusion of a 1:1 mixture of 300
pmol/day Aβ(1-40)/Aβ(1-42) or Aβ(40-1) (inactive peptide, control). The effect of
nicotine (2 mg/(kg day)) on Aβ-induced spatial learning and memory impairments
was assessed by evaluation of performance in the radial arm water maze (RAWM), in
vivo electrophysiological recordings of early-phase long-term potentiation
(E-LTP) in urethane-anesthetized rats, and immunoblot analysis to determine
changes in the levels of beta-site amyloid precursor protein (APP)-cleaving
enzyme (BACE), Aβ and memory-related proteins. The results indicate that 6 weeks
of nicotine treatment reduced the levels of Aβ(1-40) and BACE1 peptides in
hippocampal area CA1 and prevented Aβ-induced impairment of learning and
short-term memory. Chronic nicotine also prevented the Aβ-induced inhibition of
basal synaptic transmission and LTP in hippocampal area CA1. Furthermore, chronic
nicotine treatment prevented the Aβ-induced reduction of α(7)- and α(4)-nAChR.
These effects of nicotine may be due, at least in part, to upregulation of brain
derived neurotropic factor (BDNF).


7. Front Biosci. 2008 Jan 1;13:492-504.

Neuroprotection via nAChRs: the role of nAChRs in neurodegenerative disorders
such as Alzheimer's and Parkinson's disease.

Epidemiological studies have identified a negative correlation between smoking
and the development of neurodegenerative disorders such as Parkinson's disease,
and in some studies, Alzheimer's disease. These findings have been attributed to
the ability of nicotine to act as a neuroprotective agent. A large number of
studies demonstrate that nicotine can protect against neuronal death in vitro and
in vivo, and the mechanisms underlying the ability of nicotine to protect against
excitotoxicity and amyloid-? toxicity are beginning to be elucidated. Despite the
compelling evidence that nicotine is neuroprotective, it is clear that nicotine
can be toxic under some circumstances. The balance between nicotine
neuroprotection and toxicity depends on dose, developmental stage and regimen of
administration. Therefore, a full understanding of the molecular and cellular
effects of nicotine on signaling pathways relevant to neuronal survival is
critical for informed drug discovery of nicotinic compounds to combat human
neurodegeneration. This review summarizes recent studies related to the
mechanisms underlying nicotine-mediated neuroprotection, and addresses issues
that are relevant to use of nicotine as a neuroprotective agent in vivo.


8. Psychopharmacology (Berl). 2006 Mar;184(3-4):523-39. Epub 2005 Oct 12.

Nicotinic effects on cognitive function: behavioral characterization,
pharmacological specification, and anatomic localization.

RATIONALE: Nicotine has been shown in a variety of studies in humans and
experimental animals to improve cognitive function. Nicotinic treatments are
being developed as therapeutic treatments for cognitive dysfunction.
OBJECTIVES: Critical for the development of nicotinic therapeutics is an
understanding of the neurobehavioral bases for nicotinic involvement in cognitive
function.
METHODS: Specific and diverse cognitive functions affected by nicotinic
treatments are reviewed, including attention, learning, and memory. The neural
substrates for these behavioral actions involve the identification of the
critical pharmacologic receptor targets, in particular brain locations, and how
those incipient targets integrate with broader neural systems involved with
cognitive function.
RESULTS: Nicotine and nicotinic agonists can improve working memory function,
learning, and attention. Both alpha4beta2 and alpha7 nicotinic receptors appear
to be critical for memory function. The hippocampus and the amygdala in
particular have been found to be important for memory, with decreased nicotinic
activity in these areas impairing memory. Nicotine and nicotinic analogs have
shown promise for inducing cognitive improvement. Positive therapeutic effects
have been seen in initial studies with a variety of cognitive dysfunctions,
including Alzheimer's disease, age-associated memory impairment, schizophrenia,
and attention deficit hyperactivity disorder.
CONCLUSIONS: Discovery of the behavioral, pharmacological, and anatomic
specificity of nicotinic effects on learning, memory, and attention not only aids
the understanding of nicotinic involvement in the basis of cognitive function,
but also helps in the development of novel nicotinic treatments for cognitive
dysfunction. Nicotinic treatments directed at specific receptor subtypes and
nicotinic cotreatments with drugs affecting interacting transmitter systems may
provide cognitive benefits most relevant to different syndromes of cognitive
impairment such as Alzheimer's disease, schizophrenia, and attention deficit
hyperactivity disorder. Further research is necessary in order to determine the
efficacy and safety of nicotinic treatments of these cognitive disorders.


9. Neuroscience. 2005;130(4):997-1012.

Repeated nicotine exposure in rats: effects on memory function, cholinergic
markers and nerve growth factor.


A decrease in the number of nicotinic-acetylcholine receptors (nAChRs) in the
brain is thought to contribute to the cognitive dysfunction associated with
diseases as diverse as Alzheimer's disease and schizophrenia. Interestingly,
nicotine and similar compounds have been shown to enhance memory function and
increase the expression of nAChRs and therefore, could have a therapeutic role in
the aforementioned diseases. Nicotine has also been shown to exert positive
effects on certain neurotrophins such as nerve growth factor (NGF), and therefore
could play a role beyond mere symptomatic therapy. However, to date,
comprehensive studies of nicotine's effects on the expression of specific
acetylcholine (ACh) receptor subtypes, key cholinergic proteins (that are
regulated by NGF) such as choline acetyltransferase (ChAT) and the vesicular ACh
transporter (VAChT) are lacking. Studies to further investigate the effects of
nicotine on NGF especially its high- and low-affinity receptors are also needed.
In the present study, male Wistar rats exposed a relatively low dosage of
nicotine (0.35 mg/kg every 12 h) for 14 days demonstrated improved memory
performance (assessed in two separate water maze testing methods) when compared
with controls. Autoradiographic experiments indicated that nicotine increased
[3H]-epibatidine, [125I]-alpha-bungarotoxin and [3H]-AFDX384, but not
[3H]-pirenzepine binding sites in several learning- and memory-related brain
areas. The expression of ChAT, VAChT, as well as tropomyosin-receptor kinase A
(TrkA) NGF receptors and phospho-TrK receptors was increased by nicotine in the
hippocampus. No changes were observed in the levels of the NGF peptide or low
affinity p75 neurotrophin receptors (p75NTR), however. These results suggest that
repeated exposure to nicotine results in positive effects on central cholinergic
markers and memory function, which may be mediated via effects on high-affinity
NGF receptors.


10. Brain Cogn. 2002 Jul;49(2):232-4.

Nicotine and sensory memory in Alzheimer's disease: an event-related potential
study.

The auditory mismatch negativity (MMN) event-related brain potential (ERP)
reflects the storage of information in acoustic sensory memory. Thirteen patients
with probable Alzheimer's disease (AD), 6 receiving treatment with the
cholinesterase inhibitor (ChEI) tacrine (..........aminoacridine, THA) and 7
receiving no treatment, were administered 2 mg of nicotine polacrilex and
placebo. MMNs were recorded with 1- and 3-s interstimulus intervals pre- and
postplacebo/nicotine administration. In nontreated patients, amplitudes were
decreased from pre- to postplacebo recordings but remained stable in THA-treated
patients. Comparison of pre- and postnicotine MMNs found amplitude increases with
nicotine in nontreated but not THA-treated patients. MMN latencies were shortened
by nicotine in both treatment groups. These exploratory findings suggest that
nicotine-improved strength of acoustic sensory memory traces and speed of
acoustic sensory discrimination in AD are differentially affected by chronic ChEI
treatment.


11. Curr Drug Targets CNS Neurol Disord. 2002 Aug;1(4):423-31.

Nicotinic treatment for cognitive dysfunction.

Nicotinic medications may provide beneficial therapeutic treatment for cognitive
dysfunction such as Alzheimer's disease, schizophrenia and attention deficit
hyperactivity disorder (ADHD). For development of nicotinic treatments we are
fortunate to have a well characterized lead compound, nicotine. Transdermal
nicotine patches offer a way to deliver measured doses of nicotine in a
considerably safer fashion than the more traditional means of administration,
tobacco smoking. We have found that transdermal nicotine significantly improves
attentional function in people with Alzheimer's disease, schizophrenia or ADHD as
well as normal nonsmoking adults. To follow-up on this proof of principal that
nicotinic treatment of cognitive dysfunction holds promise, it is important to
use animal models to determine the critical neurobehavioral bases for nicotinic
involvement in cognitive function so that more selective nicotinic analogues that
improve cognitive function with fewer side effects can be developed. We have
found with local infusion in rat studies that the hippocampus and amygdala are
important substrates for nicotinic effects on working memory function. Both
alpha7 and alpha4beta2 nicotinic receptors are involved in working memory.
Nicotinic interactions with dopaminergic and glutaminergic systems are also
important in the basis of cognitive function. Studies of the neural nicotinic
mechanisms underlying cognitive function are key for opening avenues for
development of safe and effective nicotinic treatments for cognitive dysfunction.


12. Biol Psychiatry. 2002 Nov 1;52(9):880-6.

Nicotine breaks down preformed Alzheimer's beta-amyloid fibrils in vitro.

BACKGROUND: Cerebral deposition of amyloid beta-peptide (Abeta) is a major
neuropathologic feature in Alzheimer's disease (AD). A consistent protective
effect of smoking on AD has been documented by many case-control studies. It has
been suggested that nicotine, a major component of cigarette smoke, protects
neurons against Abeta toxicity via the upregulation of nicotinic receptors, as
well as via the inhibition of beta-amyloid fibril (fAbeta) formation from Abeta.
METHODS: We used fluorescence spectroscopy with thioflavin T and electron
microscopy to examine the effects of nicotine, pyridine, and N-methylpyrrolidine
on the formation, extension, and disruption of fAbeta(1-40) and fAbeta(1-42) at
pH 7.5 at 37 degrees C in vitro.
RESULTS: Nicotine dose-dependently inhibited fAbeta(1-40) and fAbeta(1-42)
formation from fresh Abeta(1-40) and Abeta(1-42), respectively, as well as the
extension reaction of both fAbetas. Moreover, nicotine disrupted preformed
fAbeta(1-40) and fAbeta(1-42). These effects of nicotine were observed at
concentrations above 10 mmol/L and were similar to those of N-methylpyrrolidine.
CONCLUSIONS: The antiamyloidogenic effect of nicotine may be exerted not only by
the inhibition of fAbeta formation but also by the disruption of preformed
fAbeta. Additionally, this effect may be attributed to N-methylpyrrolidine
moieties of nicotine.


13. Aging Ment Health. 2002 May;6(2):129-38.

Nicotine's effect on neural and cognitive functioning in an aging population.

Tobacco is a dangerous and addictive drug being consumed by more than 13% of
Americans over the age of 65. Of the people in this cohort it has been estimated
that between 24% and 85% experience some form of age related cognitive decline
and 30-50% of the population will be diagnosed with Alzheimer's disease by the
age of 85. Recent advances in nicotine research have pointed to a number of
cognitive and neurological benefits that have been linked to the ingestion of
nicotine. These discoveries hold the potential of new drugs and therapies that
retain and improve upon nicotine's benefits while eliminating the negative impact
that both nicotine and tobacco possess. This article examines cognitive decline
in the elderly and looks at nicotine's potential role in ameliorating this
decline. In service to this, the neurological and cognitive actions of nicotine
are reviewed, as are theories on the neurological degeneration associated with
Alzheimer's disease (AD).


14. Eur J Pharmacol. 2000 Mar 30;393(1-3):141-6.

Development of nicotinic drug therapy for cognitive disorders.

Nicotine, as well as other nicotinic drugs, may provide useful therapeutic
treatment for a variety of cognitive impairments including those found in
Alzheimer's disease, schizophrenia and attention deficit hyperactivity disorder
(ADHD). We have found that nicotine skin patches significantly improve
attentional performance in people with these disease states as well as normal
nonsmoking adults. Animal models are critical for determining the neurobehavioral
bases for nicotinic effects on cognitive function. We have found in lesion and
local infusion studies with rats that the hippocampus is an important substrate
for nicotinic effects on working memory function. Both alpha7 and alpha4beta2
nicotinic receptors in the hippocampus are involved. Further work has
investigated the relationship of nicotinic systems with dopaminergic and
glutaminergic systems in the basis of cognitive function. Nicotine has proven to
be a useful prototypic compound for the family of nicotinic compounds. It
produces cognitive improvements in both animal models and clinical populations.
Recent work with more selective nicotinic receptor agonists and antagonists in
animal models is providing important information concerning the neural mechanisms
for nicotinic involvement in cognitive function and opening avenues for
development of safe and effective nicotinic treatments for clinical use.


15. Psychopharmacology (Berl). 1999 Apr;143(2):158-65.

Four-week nicotine skin patch treatment effects on cognitive performance in
Alzheimer's disease.

RATIONALE: Acute nicotine injections have been found to improve attentional
performance in patients with Alzheimer's disease (AD), but little is known about
chronic nicotine effects.
OBJECTIVE: The present study was undertaken to evaluate the clinical and
neuropsychological effects of chronic transdermal nicotine in Alzheimer's disease
subjects over a 4-week period.
METHODS: The double-blind, placebo controlled, cross-over study consisted of two
4-week periods separated by a 2-week washout period. Patients wore the nicotine
patch (Nicotrol) for 16 h a day at the following doses: 5 mg/day during week 1,
10 mg/day during weeks 2 and 3 and 5 mg/day during week 4. The eight subjects had
mild to moderate AD and were otherwise healthy.
RESULTS: Nicotine significantly improved attentional performance as measured by
the Conners' continuous performance test (CPT). There was a significant reduction
in errors of omission on the CPT which continued throughout the period of chronic
nicotine administration. The variability of hit reaction time (reaction time for
correct responses) on the CPT was also significantly reduced by chronic nicotine.
Nicotine did not improve performance on other tests measuring motor and memory
function.
CONCLUSIONS: The sustained improvement in attention found in this study with
nicotine dermal patches is encouraging. However, the lack of detected effects of
nicotine treatment on other cognitive and behavioral domains in this study leaves
questions concerning the clinical impact of nicotinic treatment in Alzheimer's
disease. The modest size of this study limited statistical power which may have
been needed to detect more subtle but clinically significant cognitive effects.
Higher doses of nicotine, other nicotinic ligands or combination treatment of
nicotine with other therapies may be efficacious for producing broader
therapeutic effects.


16. Biochemistry. 1996 Oct 22;35(42):13568-78.

Nicotine inhibits amyloid formation by the beta-peptide.

The 42-residues beta-(1-42) peptide is the major protein component of amyloid
plaque cores in Alzheimer's disease. In aqueous solution at physiological pH, the
synthetic beta-(1-42) peptide readily aggregates and precipitates as oligomeric
beta-sheet structures, a process that occurs during amyloid formation in
Alzheimer's disease. Using circular dichroism (CD) and ultraviolet spectroscopic
techniques, we show that nicotine, a major component in cigarette smoke, inhibits
amyloid formation by the beta-(1-42) peptide. The related compound cotinine, the
major metabolite of nicotine in humans, also slows down amyloid formation, but to
a lesser extent than nicotine. In contrast, control substances pyridine and
N-methylpyrrolidine accelerate the aggregation process. Nuclear magnetic
resonance (NMR) studies demonstrate that nicotine binds to the 1-28 peptide
region when folded in an alpha-helical conformation. On the basis of chemical
shift data, the binding primarily involves the N-CH3 and 5'CH2 pyrrolidine
moieties of nicotine and the histidine residues of the peptide. The binding is in
fast exchange, as shown by single averaged NMR peaks and the lack of nuclear
Overhauser enhancement data between nicotine and the peptide in two-dimensional
NOESY spectra. A mechanism is proposed, whereby nicotine ......s amyloidosis by
preventing an alpha-helix-->beta-sheet conformational transformation that is
important in the pathogenesis of Alzheimer's disease.


17. Br J Nurs. 1996 Oct 24-Nov 13;5(19):1195-202.

Does nicotine have beneficial effects in the treatment of certain diseases?

Although tobacco smoking has long been associated with diseases of the lungs and
cardiovascular system, numerous studies have demonstrated a negative association
between tobacco smoking and ulcerative colitis, and the neurodegenerative
diseases, Alzheimer's disease (AD) and Parkinson's disease (PD). The evidence
suggests that nicotine--the main pharmacologically active ingredient of
tobacco--appears to be responsible for this effect. Pure nicotine has no known
carcinogenic properties and can be administered in numerous ways including
transdermal patches and tablets. As a therapeutic agent, its association with
tobacco can be likened to morphine and opium smoking. There is ample clinical
evidence to suggest that nicotine could be beneficial in the treatment of some
patients with diseases. Pharmacologically, nicotine acts on cholinergic
(nicotinic-specific) receptors which are depleted in AD and PD. Nicotinic
receptors also interact closely with several neurotransmitters including
dopamine, which is implicated in both PD and Gilles de la Tourettes's syndrome.
There is no doubt that tobacco smoking can be harmful and no-one should be
encouraged to smoke. However, although nicotine has many harmful side-effects, it
may have therapeutic value or at the very least be a useful tool for future drug
development.


18. Pharmacol Ther. 1996;72(1):51-81.

Pharmacology of nicotine and its therapeutic use in smoking cessation and
neurodegenerative disorders.

During the last decade, nicotine has been used increasingly as an aid to smoking
cessation and has been found to be a safe and efficacious treatment for the
symptoms of nicotine withdrawal. This period has also seen significant advances
in our understanding of the mechanisms underlying the psychopharmacological
responses to nicotine, including, particularly, those that have been implicated
in nicotine addiction. This paper reviews this decade of progress in the specific
context of the therapeutic application of nicotine to the treatment of smoking
cessation. Other putative future applications, particularly in the treatment of
neurodegenerative disorders, are also reviewed.


19. Alzheimer Dis Assoc Disord. 1995;9 Suppl 2:43-9.

Alzheimer disease, attention, and the cholinergic system.

Recent neuropsychological studies suggest that, in addition to prominent mnemonic
dysfunction, attentional impairments are a core feature of Alzheimer disease
(AD). As is the case for memory, attention is not a unitary process, and only
certain components of attention are disrupted in mild AD, particularly sustained
and spatial attention. In this article we review evidence from both human and
nonhuman neuropsychopharmacology that leads us to suggest that (at least some of)
the attentional impairments seen in AD can be related to damage to the basal
forebrain cholinergic system (BFCS), in particular the nucleus basalis of Meynert
(nbM), which undergoes significant neuronal loss in AD. The BFCS provides the
major cholinergic innervation to the cortex and innervates brain regions such as
the thalamus, prefrontal cortex, and parietal lobes known to be involved in
attentional operations. In addition, studies conducted by our group suggest that
drugs acting to stimulate the cholinergic system, in particular tacrine and
nicotine, can significantly improve attentional function in patients with AD as
measured by improved performance on objective computerised cognitive tasks.
Furthermore, cholinergic drugs may also have some utility in other disorders with
attentional pathology, such as Parkinson's disease.


20. Neuroepidemiology. 1994;13(4):131-44.

Smoking and Alzheimer's disease: a review of the epidemiological evidence.

Overall evidence from 19 case-control studies of Alzheimer's disease (AD) and
smoking shows a highly significant (p < 0.001) negative association [ever/never
smokers, relative risk (RR) 0.64, 95% confidence interval (CI) 0.54-0.76]. Some
studies have apparent design faults but the association is clearly evident in
those which do not (RR 0.60, 95% CI 0.46-0.78). A report of a positive
relationship from a prospective study can be dismissed due to unreliability of AD
diagnosis on death certificates, and other study weaknesses. Although more data
are needed on dose response and to rule out possible confounding, the negative
association is consistent with other data suggesting nicotine protects against
AD.

Here it is ItsBroTime.

Ok in that case I'll get digging, thanks for the tip

 

[four2109]

The zip was post 50 or thereabouts.

 

[mosspa]

I did another quirky test today. I gave a sensory neuroscience lecture at 11:00 and a statistics lecture at 12:30. I didn't vape before the first class (abstinent since about midnight last night). I vaped (about 8 drags) as I walked between buildings to my second class. During the sensory lecture in the first class, I made three stumbles and had one 'senior moment'. I went through the second lecture flawlessly, and was quite animated, even though the stat lecture was much less of interest to me than the sensory systems one. Even if this is a placebo effect, I'll take it any day!

 

[sofarsogood]

I read somewhere that people with certain mental disorders are over represented among smokers and may be there is evidence they are medicating themselves with nic. When those people happen to be institutionalized the staff wants them to have their cigarettes for practical reasons and the staff people like the idea of e-cigs instead.

Once I stopped smoking, last November, I was able to have some persective not possible before. Staring in late summer of 2010 some of the circumstances of my life became very very stressful and those issues persist to this day. Part of the response to was to smoke more. Smoking more means health issues and those become a source of anxiety. Stress tends to be addative. Looking back I can say smoking too much was causing so much stress and I was smoking more to relieve the stress of smoking too much. Removing all the anxiety of being a smoker, by quiting, reduced the overall level of stress so significantly that all the other stuff is far more managable. The stress of occaisional cravings is less than the stress I felt about being a smoker.

 

[Nick N]

I smoked from about 12-13 until I was 22. 03-06-2002 was my quit date. My Wife, Mom, and Sister went to a hypnotist seminar to quit smoking. While they were gone I decided that I was tired of smoking and by quitting it would help my Wife since I wouldn't be tempting her. 3 days later she was back to smoking.

The first month was hard, but I stuck with it and never went back. She still smokes to this day, I roll her cigarettes on a daily basis. I used patches for the first 3 weeks as an insurance policy, then I stopped using them.

My brother-in-law decided to quit in June of last year, and I took a liking to the equipment, the flavors and how relaxing it is to vape, even 0mg. I had bought my Wife some gear (Spinner + Protank, later an MVP + Mega) thinking she would quit too, but she didn't.

So here I was with this nicotine infused juice and vaping equipment going to waste per se. I had already been tasting 12mg juice that my BIL had been buying, so I decided to fill up "my" gear with some juice. It was a huge rush at first and a little harsh, but the initial buzz subsided. I liked it.

As time went on I moved on to mods and drippers/tanks. I prefer unflavored 6-9mg juice that I make myself. I don't vape at work, so I go 8-9 hours without nicotine daily during the week. I must admit that I do look forward to the drive home. The first vape is just like the first time, an initial rush and a little harsh but subsides.

I also look forward to vaping with my morning coffee, and after dinner. Very similar to the "good ole days" when I smoked. I find it very relaxing but I do not get edgy when I can't vape and I have no problem focusing at work. I feel the same satisfaction after a meal, mid morning, and afternoon with a fresh hot cup of coffee as I do when I vape.

Even prior to vaping I drink about 6-8 large cups of black coffee per day, 3 of them at work. I like my coffee. [emoji6] This new "habit" reminds me of the old man enjoying a pipe in his study, a way to unwind and relax.

 

[mosspa]

I smoked from about 12-13 until I was 22. 03-06-2002 was my quit date. My Wife, Mom, and Sister went to a hypnotist seminar to quit smoking. While they were gone I decided that I was tired of smoking and by quitting it would help my Wife since I wouldn't be tempting her. 3 days later she was back to smoking.

The first month was hard, but I stuck with it and never went back. She still smokes to this day, I roll her cigarettes on a daily basis. I used patches for the first 3 weeks as an insurance policy, then I stopped using them.

That's interesting. At 22 you were about the same age as many of the ex-smokers in my class. However, you did smoke for eight years. I have no data on how long anybody in my classes smoked, but I think I will start gathering that data as well. However, I have yet to find any of my students that hat a difficult time quitting. I quit after 5 years, and I, too, started at 13.

 

[Ca Ike]

For those of you wanting to know the other side of nicotine here's a good article with citations of some studies. http://themindunleashed.org/2014/10/nicotine-are-we-wrong.html

There are more but I found this one really good

 

[vapero]

too long, didn't read

Long story short, I started at 24mg, then went down to 12mg but found out that my ADHD spiked so I upped my nic to 18mg and it has really helped me, I did like the lower nic taste and didn't need more nic so I did it just for medical reasons

but here are to interesting links
Nicotine, the Wonder Drug? | DiscoverMagazine.com
Will a Nicotine Patch Make You Smarter? [Excerpt] - Scientific American

 

[Cacique]

I noticed some time ago when trying flavors at a B&M that I felt more awake and less fuzzy in the head after leaving. I had tried a lot of juices that were 16mg, and I did 0 as I had quit years ago. I never did anything with it but I looked into all of the information gathered here (thanks!) and came to the conclusion it might help me. I picked up some 1% nic e-juice last night and over did it a bit to start and got a bit jittery, but it immediately gave me a clearer mind. Can't tell if it's the nic for sure but I do feel more awake and able to focus easier.

 

[ItsBroTime]

That's absolutely awesome, thanks a million! Much research ahead it seems, wish us luck! Thanks again to Mosspa, Shirtbloke for the collation and mmsjs5 for the repost.

 

[KDCart]

Here's an anecdotal story: I started vaping and quit smoking nearly a year ago. I used 12mg nicotine for quite a while, then tapered off to 6mg, then 3mg, then 0. I vaped nicotine-free juice for about 2 months. I really can't put my finger on it, but I just didn't seem like the same person. The way I felt was akin to what I imagine a mild case of depression would be like. I didn't miss the nicotine, but that was the only thing in my life that had changed. Recently, I went back to vaping 6mg nicotine liquid. I feel like an entirely new person. I feel like myself again. I don't know if it's bad for me or not, but I see myself using nicotine for the rest of my life. If it is relevant, I'm 48 years old, and smoked cigarettes for 32 years before quitting.