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" Is Nicotine Addiction Safe In The Long Term And You" : The Debate

Discussion in 'Nicotine' started by ShogaNinja, Jul 22, 2012.

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  1. ShogaNinja

    ShogaNinja Vaping Master ECF Veteran

    Feb 18, 2012
    I recently got in a debate with some veterans, ECF moderators, and CASAA activists about nicotine and the effects on the human body in the long term. I was received quite coldly, to be honest, but that doesn't stop my from my mission. Nicotine is a very toxic substance, and despite everyone here wanting to live in a happy land of rainbows and butterflies, I have done a bit of preliminary research and personally found that, in the long term, it can lead to your early demise - despite what I've read here at the ECF telling me that "it's as safe as a caffeine habit". This concerns me and I do believe that it merits a realistic discussion. Science hasn't proven much in this field of vaping, because it is so new, but I personally believe that EVERY doctor in the world will tell you that a non-smoker is healthier than a vaper 100 times out of 100. Nicotine, nay ANY addiction (be it legal or not), is a very serious matter that must be addressed if we are to live healthy lives. This thread is designed to do just that - address the issues that go with nicotine addiction, be they good or ill. Please, be kind to one another and do just that; discuss. Please do not accuse or attack.

    It was our original quest to quit smoking. We saw vaping as a tool to do that. Once we found out how easy it was it does not mean that our quest is over. After all, at the end of the day, we are here to lower our chances of getting cancer as much as possible despite the damage we have already done. I believe that this does not give us a license to vape ad infinitum carefree of the worries that nicotine is somehow a healthy substance to intake long term despite it being labeled a toxic substance of the highest order. I am creating this thread to open a realistic discussion on the effects of vaping whether what it may contain is what you want to hear, or not. I realize that this may be a hot topic, but I encourage each of you to respect each other and please provide only facts as you have found them. Please refrain from Ad Hominem attacks on each other and simply discuss what your OPINION is on this subject. Please back up this opinion with as much science as possible. Let the debate begin.

    A plea to the moderators, CASAA activists, website founders: Please recognize that this conversation must occur in a civil manner and I humbly request that you do not close this thread because it is somewhat controversial. I realize that people don't want to hear that the choices that they made may not have been perfect. I also recognize that sometimes we need to "pull off the bandaid, eat our peas" - President Barack Obama. This thread is for science. Please do not close it on account of it not being the answer that "we all want to hear". Thank you.
  2. Yves

    Yves Super Member Verified Member ECF Veteran

    May 23, 2012
    Matamata, New Zealand
    I think this thread had some very interesting information about nicotine.

    Dr Yaniv riz states clearly the damage that nicotine can do, as well as the merits of nicotine use.

    I think we all need to make a personnel choice as to nicotine use, taking into consideration, the good and the bad.

    I personally think it is not quite the same as caffeine from the information I have to date and I never use that analogy.
  3. ShogaNinja

    ShogaNinja Vaping Master ECF Veteran

    Feb 18, 2012
    Thanks for posting, Yves. I appreciate it. I did some basic google searches and some Wikipedia research and found that it MAY be responsible for the spread of cancer once you already have it (by up to 3 times more likely). From the research I have done I have found conflicting information that both states that it can cause cancer and that it cannot. I did not personally know what to make of such contradictory statements.
  4. ShogaNinja

    ShogaNinja Vaping Master ECF Veteran

    Feb 18, 2012
  5. Yves

    Yves Super Member Verified Member ECF Veteran

    May 23, 2012
    Matamata, New Zealand
  6. CES

    CES optimistic cynic Verified Member ECF Veteran

    Supporting member
    Jan 25, 2010
    Birmingham, Al
    Here are several references and abstracts that provide information about some of the potential positive effects of nicotine. There are others as well, but that would make this post even longer than it is. Each of these was published in peer-reviewed journals.

    Conners CK, Levin ED, Sparrow E, Hinton SC, Erhardt D, Meck WH, Rose JE, March J (1996) Nicotine and attention in adult attention deficit hyperactivity disorder (ADHD). Psychopharmacol Bulletin 32:67-73.
    Abstract: Nicotine, like the psychostimulants methylphenidate and dextroamphetamine, acts as an indirect dopamine agonist and improves attention and arousal. Adults and adolescents with attention deficit hyperactivity disorder (ADHD) smoke much more frequently than normal individuals or those with other psychiatric conditions, perhaps as a form of self-medication for ADHD symptoms. Nicotine might therefore have some value as a treatment for ADHD. The present study is an acute double-blind crossover administration of nicotine and placebo with smokers (n = 6) and nonsmokers (n = 11) diagnosed with adult ADHD. The drug was delivered via a transdermal patch at a dosage of 7 mg/day for nonsmokers and 21 mg/day for smokers. Results indicate significant clinician-rated global improvement, self-rated vigor and concentration, and improved performance on chronometric measures of attention and timing accuracy. Side effects were minimal. These acute results indicate the need for a longer clinical trial and a comparison with other stimulants in adult ADHD treatment

    De SR, jmone-Cat MA, Carnevale D, Minghetti L (2005) Activation of alpha7 nicotinic acetylcholine receptor by nicotine selectively up-regulates cyclooxygenase-2 and prostaglandin E2 in rat microglial cultures. J Neuroinflammation 2:4.
    Abstract: BACKGROUND: Nicotinic acetylcholine (Ach) receptors are ligand-gated pentameric ion channels whose main function is to transmit signals for the neurotransmitter Ach in peripheral and central nervous system. However, the alpha7 nicotinic receptor has been recently found in several non-neuronal cells and described as an important regulator of cellular function. Nicotine and ACh have been recently reported to inhibit tumor necrosis factor-alpha (TNF-alpha) production in human macrophages as well as in mouse microglial cultures. In the present study, we investigated whether the stimulation of alpha7 nicotinic receptor by the specific agonist nicotine could affect the functional state of activated microglia by promoting and/or inhibiting the release of other important pro-inflammatory and lipid mediator such as prostaglandin E2. METHODS: Expression of alpha7 nicotinic receptor in rat microglial cell was examined by RT-PCR, immunofluorescence staining and Western blot. The functional effects of alpha7 receptor activation were analyzed in resting or lipopolysaccharide (LPS) stimulated microglial cells pre-treated with nicotine. Culture media were assayed for the levels of tumor necrosis factor, interleukin-1beta, nitric oxide, interleukin-10 and prostaglandin E2. Total RNA was assayed by RT-PCR for the expression of COX-2 mRNA. RESULTS: Rat microglial cells express alpha7 nicotinic receptor, and its activation by nicotine dose-dependently reduces the LPS-induced release of TNF-alpha, but has little or no effect on nitric oxide, interleukin-10 and interleukin-1beta. By contrast, nicotine enhances the expression of cyclooxygenase-2 and the synthesis of one of its major products, prostaglandin E2. CONCLUSIONS: Since prostaglandin E2 modulates several macrophage and lymphocyte functions, which are instrumental for inflammatory resolution, our study further supports the existence of a brain cholinergic anti-inflammatory pathway mediated by alpha7 nicotinic receptor that could be potentially exploited for novel treatments of several neuropathologies in which local inflammation, sustained by activated microglia, plays a crucial role

    Heishman SJ, Kleykamp BA, Singleton EG (2010) Meta-analysis of the acute effects of nicotine and smoking on human performance. Psychopharmacology (Berl) 210:453-469.
    Abstract: RATIONALE AND OBJECTIVE: Empirical studies indicate that nicotine enhances some aspects of attention and cognition, suggesting a role in the maintenance of tobacco dependence. The purpose of this review was to update the literature since our previous review (Heishman et al. Exp Clin Psychopharmacol 2:345-395, 1994) and to determine which aspects of human performance were most sensitive to the effects of nicotine and smoking. METHODS: We conducted a meta-analysis on the outcome measures of 41 double-blind, placebo-controlled laboratory studies published from 1994 to 2008. In all studies, nicotine was administered, and performance was assessed in healthy adult nonsmokers or smokers who were not tobacco-deprived or minimally deprived (<or=2 h). RESULTS: There were sufficient effect size data to conduct meta-analyses on nine performance domains, including motor abilities, alerting and orienting attention, and episodic and working memory. We found significant positive effects of nicotine or smoking on six domains: fine motor, alerting attention-accuracy and response time (RT), orienting attention-RT, short-term episodic memory-accuracy, and working memory-RT (effect size range = 0.16 to 0.44). CONCLUSIONS: The significant effects of nicotine on motor abilities, attention, and memory likely represent true performance enhancement because they are not confounded by withdrawal relief. The beneficial cognitive effects of nicotine have implications for initiation of smoking and maintenance of tobacco dependence

    Huang LZ, Grady SR, Quik M (2011) Nicotine reduces L-DOPA-induced dyskinesias by acting at beta2* nicotinic receptors. J Pharmacol Exp Ther 338:932-941.
    Abstract: L-DOPA-induced dyskinesias or abnormal involuntary movements (AIMs) are a debilitating adverse complication associated with prolonged L-DOPA administration for Parkinson's disease. Few treatments are currently available for dyskinesias. Our recent data showed that nicotine reduced L-DOPA-induced AIMs in parkinsonian animal models. An important question is the nicotinic acetylcholine receptor (nAChR) subtypes through which nicotine exerts this beneficial effect, because such knowledge would allow for the development of drugs that target the relevant receptor population(s). To address this, we used beta2 nAChR subunit knockout [beta2(-/-)] mice because beta2-containing nAChRs are key regulators of nigrostriatal dopaminergic function. All of the mice were lesioned by intracranial injection of 6-hydroxydopamine into the right medial forebrain bundle. Lesioning resulted in a similar degree of nigrostriatal damage and parkinsonism in beta2(-/-) and wild-type mice. All of the mice then were injected with L-DOPA (3 mg/kg) plus benserazide (15 mg/kg) once daily for 4 weeks until AIMs were fully developed. L-DOPA-induced AIMs were approximately 40% less in the beta2(-/-) mice compared with the wild-type mice. It is interesting to note that nicotine (300 mug/ml in drinking water) reduced L-DOPA-induced AIMs by 40% in wild-type mice but had no effect in beta2(-/-) mice with partial nigrostriatal damage. The nicotine-mediated decline in AIMs was much less pronounced in wild-type mice with near-complete degeneration, suggesting that presynaptic nAChRs on dopaminergic terminals have a major influence. These data demonstrate an essential role for beta2* nAChRs in the antidyskinetic effect of nicotine and suggest that drugs targeting these subtypes may be useful for the management of L-DOPA-induced dyskinesias in Parkinson's disease

    Jarvik ME (1991) Beneficial effects of nicotine. Br J Addict 86:571-575.
    Abstract: Nicotine in tobacco brings illness and death to millions of people. Yet nicotine in its pure form has the potential to be a valuable pharmaceutical agent. Nicotine fairly specifically binds to the cholinergic nicotinic gating site on cationic ion channels in receptors throughout the body. This action stimulates the release of a variety of neurotransmitters including especially catecholamines and serotonin. When chronically taken, nicotine may result in: (1) positive reinforcement, (2) negative reinforcement, (3) reduction of body weight, (4) enhancement of performance, and protection against; (5) Parkinson's disease (6) Tourette's disease (7) Alzheimers disease, (8) ulcerative colitis and (9) sleep apnea. The reliability of these effects varies greatly but justifies the search for more therapeutic applications for this interesting compound

    Jones GM, Sahakian BJ, Levy R, Warburton DM, Gray JA (1992) Effects of acute subcutaneous nicotine on attention, information processing and short-term memory in Alzheimer's disease. Psychopharmacology (Berl) 108:485-494.
    Abstract: This single-blind, placebo controlled study reports on the effects of administering three acute doses of nicotine (0.4, 0.6 and 0.8 mg) subcutaneously to a group of Alzheimer's disease (DAT) patients (n = 22), young adult controls (n = 24), and normal aged controls (n = 24). The study extends our previous findings obtained using smaller groups of subjects. Drug effects were examined on three computerised tests: the first measuring rapid visual information processing, sustained visual attention and reaction time (RVIP task); a delayed response matching to location-order task measuring sustained visual attention and visual short-term memory (DRMLO task); and a finger tapping test measuring simple reaction time (FT task). The critical flicker fusion test (CFF) was used as a measure of perception and the WAIS digit span forwards (DS), of auditory short-term memory. Tests were graded in difficulty, titrated to avoid floor and ceiling effects so that meaningful, direct comparisons between groups could be made. Nicotine significantly improved sustained visual attention (in both RVIP and DRMLO tasks), reaction time (in both FT and RVIP tasks), and perception (CFF task--both ascending and descending thresholds). Nicotine administration did not improve auditory and visual short-term memory. There were no consistent, overall patterns of difference in performance between smokers and non-smokers in the control groups, or between males and females in any group. Despite the absence of change in memory functioning, these results demonstrate that DAT patients have significant perceptual and visual attentional deficits which are improved by nicotine administration.(ABSTRACT TRUNCATED AT 250 WORDS)

    Levin ED, Conners CK, Sparrow E, Hinton SC, Erhardt D, Meck WH, Rose JE, March J (1996) Nicotine effects on adults with attention-deficit/hyperactivity disorder. Psychopharmacology (Berl) 123:55-63.
    Abstract: Several lines of evidence suggest that nicotine may be useful in treating the symptoms of Attention-Deficit/Hyperactivity Disorder (ADHD). The current study was an acute, placebo-controlled double-blind experiment to determine whether nicotine might be useful as an alternative treatment of adults with ADHD symptomatology. Six smokers and 11 nonsmokers who were outpatient referrals for ADHD were diagnosed by DSM-IV criteria. Measures of treatment effect included the Clinical Global Impressions (CGI) scale, Hopkins' symptom check list (SCL-90-R), the Profile of Mood States (POMS), Conners' computerized Continuous Performance Test (CPT), the Stroop test, and an interval-timing task. The smokers underwent overnight deprivation from smoking and were given a 21 mg/day nicotine skin patch for 4.5 h during a morning session. The nonsmokers were given a 7 mg/day nicotine skin patch for 4.5 h during a morning session. Active and placebo patches were given in a counter-balanced order approximately 1 week apart. Nicotine caused a significant overall nicotine-induced improvement on the CGI. This effect was significant when only the nonsmokers were considered, which indicated that it was not due merely to withdrawal relief. Nicotine caused significantly increased vigor as measured by the POMS test. Nicotine caused an overall significant reduction in reaction time (RT) on the CPT, as well as, with the smokers, a significant reduction in another index of inattention, variability in reaction time over trial blocks. Nicotine improved accuracy of time estimation and lowered variability of time-estimation response curves. Because improvements occurred among nonsmokers, the nicotine effect appears not to be merely a relief of withdrawal symptoms. It is concluded that nicotine deserves further clinical trials with ADHD

    Levin ED, Conners CK, Silva D, Canu W, March J (2001) Effects of chronic nicotine and methylphenidate in adults with attention deficit/hyperactivity disorder Exp Clin Psychopharmacol 9:83-90.
    Abstract: Acute nicotine treatment has been found to reduce symptoms of attention deficit/hyperactivity disorder in adults (E. D. Levin, C. K. Conners, et al., 1996). In this study, chronic nicotine effects were compared with placebo and methylphenidate. Acute and chronic nicotine treatment significantly attenuated the rise in hit reaction time standard error over session blocks on the Conners Continuous Performance Test (C. K. Conners et al., 1996). Acute nicotine significantly reduced severity of clinical symptoms on the Clinical Global Impressions scale (National Institute of Mental Health, 1985). Nicotine caused a significant decrease in self-report of depressive mood as measured by the Profile of Mood States test (D. M. McNair, M. Lorr, & L. F. Droppleman, 1981). This small study (40 participants) provided evidence that nicotine treatment can reduce severity of attentional deficit symptoms and produce improvement on an objective

    Quik M, Huang LZ, Parameswaran N, Bordia T, Campos C, Perez XA (2009) Multiple roles for nicotine in Parkinson's disease
    Biochem Pharmacol 78:677-685.

    Abstract: There exists a remarkable diversity of neurotransmitter compounds in the striatum, a pivotal brain region in the pathology of Parkinson's disease, a movement disorder characterized by rigidity, tremor and bradykinesia. The striatal dopaminergic system, which is particularly vulnerable to neurodegeneration in this disorder, appears to be the major contributor to these motor problems. However, numerous other neurotransmitter systems in the striatum most likely also play a significant role, including the nicotinic cholinergic system. Indeed, there is an extensive anatomical overlap between dopaminergic and cholinergic neurons, and acetylcholine is well known to modulate striatal dopamine release both in vitro and in vivo. Nicotine, a drug that stimulates nicotinic acetylcholine receptors (nAChRs), influences several functions relevant to Parkinson's disease. Extensive studies in parkinsonian animals show that nicotine protects against nigrostriatal damage, findings that may explain the well-established decline in Parkinson's disease incidence with tobacco use. In addition, recent work shows that nicotine reduces l-dopa-induced abnormal involuntary movements, a debilitating complication of l-dopa therapy for Parkinson's disease. These combined observations suggest that nAChR stimulation may represent a useful treatment strategy for Parkinson's disease for neuroprotection and symptomatic treatment. Importantly, only selective nAChR subtypes are present in the striatum including the alpha4beta2*, alpha6beta2* and alpha7 nAChR populations. Treatment with nAChR ligands directed to these subtypes may thus yield optimal therapeutic benefit for Parkinson's disease, with a minimum of adverse side effects

    Richardson CE, Morgan JM, Jasani B, Green JT, Rhodes J, Williams GT, Lindstrom J, Wonnacott S, Peel S, Thomas GA (2003) Effect of smoking and transdermal nicotine on colonic nicotinic acetylcholine receptors in ulcerative colitis. QJM 96:57-65.
    Abstract: BACKGROUND: Ulcerative colitis (UC) is a disease largely of non-smokers, in which nicotine is of therapeutic value. The mode of action is unknown, but may involve nicotinic acetylcholine receptors (nAChRs) in the bowel wall. AIM: To investigate the presence of nAChRs in rectal mucosa, and the effect of smoking and nicotine on their expression. DESIGN: Prospective case-control study. METHODS: In situ hybridization (ISH) and immunocytochemistry (ICC) were used to show alpha3 nAChRs in colonic mucosa. Rectal mucosa was examined from controls (n=55) and patients with inactive UC (n=62), both smokers and non-smokers, by ICC, using two antibodies to show the density and distribution of receptors in the mucosa. Non-smokers with UC (n=43) were given transdermal nicotine or placebo patches for 6 months, and rectal biopsies, taken before and after treatment, were examined by ICC to show nAChRs. RESULTS: In normal colon, ISH and ICC showed alpha3 subunit in a wide variety of cells, including mucosal epithelium. In rectal biopsies, neither smoking nor nicotine influenced the expression of alpha3 immunoreactivity in epithelium, either in controls or UC. However, controls had a significantly greater density of immunodetectable mucosal epithelium alpha3 subunit, compared with UC patients. DISCUSSION: The presence of nAChRs in colonic epithelium may be pertinent to the beneficial effect of nicotine in UC, but since neither smoking nor nicotine treatment is associated with any change in the expression of epithelial alpha3 nAChRs, the effect may be due to functional changes in the receptor. The decreased number of alpha3 nAChRs in UC compared with controls may be related to an increased cell turnover in UC

    Sahakian B, Jones G, Levy R, Gray J, Warburton D (1989) The effects of nicotine on attention, information processing, and short-term memory in patients with dementia of the Alzheimer type. Br J Psychiatry 154:797-800.
    Abstract: Nicotine in patients with dementia of the Alzheimer type (DAT) produced a significant and marked improvement in discriminative sensitivity and reaction times on a computerised test of attention and information processing. Nicotine also improved the ability of DAT patients to detect a flickering light in a critical flicker fusion test. These results suggest that nicotine may be acting on cortical mechanisms involved in visual perception and attention, and support the hypothesis that acetylcholine transmission modulates vigilance and discrimination. Nicotine may therefore be of some value in treating deficits in attention and information processing in DAT patients

    Ward RJ, Lallemand F, de WP, Dexter DT (2008) Neurochemical pathways involved in the protective effects of nicotine and ethanol in preventing the development of Parkinson's disease: potential targets for the development of new therapeutic agents Prog Neurobiol 85:135-147.
    Abstract: In this short review, neurochemical targets are identified where nicotine, and possibly ethanol, may interact to prevent the occurrence of Parkinson's disease. These are (a) the nicotinic acetycholine receptors present in the nigrostriatal area or on the surface of microglia, (b) monoamine oxidases and (c) inducible nitric oxide synthase. If such induced changes can be verified in clinical studies, this may help in the design of new therapeutic drugs which may be of relevance to diminish the incidence and perhaps the progression of the debilitating condition of Parkinson's disease
  7. MickeyRat

    MickeyRat Vaping Master Verified Member ECF Veteran

    Mar 4, 2011
    Hickory, NC
    For the most part, the hazards of nicotine addiction are not really known separate from tobacco, if they exist at all. To ask is vaping safe is really the wrong question. The question for everyone on here is, is it safer than smoking? That's pretty well established. You might have an argument, if you could show that vaping increases the risk of cancer higher than smoking but, you don't.

    Everyone's afraid of cancer but, even with the elevated cancer risk from smoking, the vast majority of smokers don't get cancer. Just about all smokers get COPD. That's really the disease to fear. There's no evidence that vaping causes COPD.
  8. genelman

    genelman Super Member Verified Member ECF Veteran

    Mar 8, 2012
    Fairfax, Virginia
    This might be somehow personal, I have Cancer and I asked my Oncologist about Nicotine, he told me it is ok as long as I don't over do it, my oncologist is considered to be an authority in this matter, so I just simply don't over do it.
  9. JENerationX

    JENerationX Ultra Member Verified Member ECF Veteran

    Aug 25, 2011
    Rochester, NY
    My mother was going through a round of radiation when I came back to vaping. I went with her to her oncologist, and was told that nicotine in and of itself has never been proven to cause cancer. The carcinogens inhaled from smoking are separate from the nicotine itself. Nicotine may increase the rate of cancer in those that already have pre-cancerous cells. (Which makes a cigarette a perfect storm.)

    My own Dr. confirmed what the oncologist told me, and was thrilled when I showed him my PV. I have severe asthma, chronic bronchitis, allergies, insomnia, and anxiety. My asthma has improved. I now have only a rescue inhaler instead of that plus 2 others. I'm off prescription allergy medicine, my insomnia is slightly better because once I'm sleeping my breathing is better. When I try to drop my nicotine below 12mg, my anxiety gets worse. I was concerned about nicotine, my Dr. told me not to be. He'd rather I keep vaping a low level of nicotine than be smoking.

    Do I care if nicotine is completely safe? Not really. Unless I can grow all my own food without pesticides, and wear an oxygen mask to stop breathing the air, and find water I'm 100% sure contains no health risks, I'm pretty sure that my 12mg vape is probably the least of my worries. I'm willing to take my chances because I AM sure that vaping carries FAR less risk than the cigarette that would be hanging out of my mouth as I'm typing this if my PV wasn't an option.
  10. ricklynchcore

    ricklynchcore Super Member Verified Member ECF Veteran

    Jun 19, 2012
    Chicago, Il
    Every step taken in life leads towards the rot. Now, I can try to walk on tip toes, avoiding every crack in the pavement, constantly on vigil, ever worried I will make a mistake to hasten my end. I may choose instead, to stop once in awhile to enjoy the bounties of my surrounding, might this hasten my end, might, but with everything else from extreme stress, to extreme deprivation, I'll take the risk. I enjoy vaping. It keeps me safe from the far, far more reckless tobacco trap. I think it is what most of the health extremists miss. Vaping is the only technique I have found, keeping me from eventually falling back to tobacco. It is not a therapy to wind down my nicotine addiction, it is a replacement for my tobacco addiction, and the only one that has ever worked for this 59 year old.

    Sent from my cm_tenderloin using Tapatalk 2
  11. Cyrene

    Cyrene Senior Member ECF Veteran

    Jul 13, 2012
    Twin Lakes, WI
    This is how I look at it. Some people get on a bandwagon about one thing (and not talking about anyone in this thread), but they are the ones that don't see the whole picture of what you breathe & eat on a daily basis. The pollutants in the air, the water coming from your tap (or even bottled water - you can't believe everything you read on those), the food you eat. Heck, just stepping off a curb could be dangerous. Here we are choosing the less of the 2 evils. And vaping is a lot less dangerous than analogs for sure, and probably less dangerous than swimming in your local lake. Fight the big fights, look at the big picture, and don't blame health problems on one thing in your life. ;-)
  12. hlk

    hlk Senior Member ECF Veteran

    May 3, 2011
    Atlanta GA
    I am a nicotine addict.. But I would vastly prefer vaping to tobacco. Someday I would like to quit but for now, I feel much better that I have been vaping.. not smoking the past 2 years.
  13. markfm

    markfm Aussie Pup Wrangler Verified Member ECF Veteran

    Supporting member
    The times I've looked at this i get consistent information.

    The TSNA from smoking, not found in vaping, are the hardcore cancer causers.

    Other chemicals added to cigs, not found in vaping, are pretty nasty just on the face of it.

    The CO in smoking, again not in vaping, is another inherently not good thing, though the oxygen deprivation should be short lived.

    Nicotine may enhance cancerous conditions, but doesn't appear to be a direct cause.

    For me I DIY, to control the mix in my eliquids. I'm careful about flavorings, just because something is okay in food doesn't make it s swift move to vape.

    Any rational person would, I believe, agree that vapng is better than smoking, and that not vaping is better than vaping. I really don't have much of a feel for comparing vaping with, say, drinking coffee, though i have cut down my coffee consumption due to being able to vape in places i couldn't smoke, and am personally content with that trade.

    I do like the stimulant effects, in moderation, whether when doing intense work that takes concentration, long drives, whatever.

    I do hear you on the annoying level of some of the vaping advocates who blindly refuse to acknowledge any possible downside to vaping. They have lost sight of this being harm reduction, think/act as if this is harm removal. That mentality really doesn't help; sometimes I think of an old Chevy Chase line from SNL :) The "ignore" function on ecf can be good if a particular person consistently rubs you the wrong way.
  14. jeffreys

    jeffreys Senior Member Verified Member ECF Veteran

    Jun 23, 2012
    Omaha, Nebr
    I have a hard time believing that someone on a mission against nicotine is concerned about my health. Especially non-health professionals. Just think of other things they could fight against. Fighting against the hypocrisy of the FDA, ALA, and AHA for example would potentially improve the health of more people than a fight against nicotine.
  15. Underwhelmed

    Underwhelmed Account closed on request Verified Member ECF Veteran

    May 22, 2012
    I distrust anyone that is an activist/lobbyist. Lots of money to be made on either side of any issue people are passionate about.

    I don't see how being anti-anti immediately makes your position positive.

    Mostly I just ignore the bloviation from both sides since neither has the ability to make decisions for me.
  16. Malduk

    Malduk Super Member Verified Member ECF Veteran

    Mar 2, 2012
    I'd just like to point out the wrong premise in the original post: not everyones "original quest" was to quit smoking, or to live a perfectly healthy life. I tried it out of curiosity, and it just so happened that I liked it enough to dump the cigarettes. With that in mind, and pollution all around me that comes with living in a city in a 21st century, I have uglier things to worry about then nicotine.

    However, I do like to be informed and I'd love for this thread to be a discussion based on scientific data, rather than "mission against nicotine". Threads with words like "mission" or "quest" easily lose my interest.
  17. The Wiz

    The Wiz ECF Guru ECF Veteran

    Feb 14, 2009
    Whiskeyville USA
    Great thread! As Malduk mentioned,Many have used vaping as a way to quit while the majority(here at least),have used vaping as a smoking substitution(like myself).Nicotine and the addiction of hand to mouth are both hard to overcome IMO.

    I appreciate the posters who have contributed the medical info on the plus/negative effects of long term nicotine use. Nicotine is very missunderstood(Particularly by non-smokers) any way you look at it

  18. classwife

    classwife Admin
    Asst Classifieds Mgr
    Ask The Vets Mgr
    Admin Verified Member ECF Veteran

    Supporting member
    Moved to Nicotine:

    Nicotine in E-Cigarette Forum, All posts relating to nicotine and its effects on the body and mind go here.

    from General E-Smoking Discussion

  19. ShogaNinja

    ShogaNinja Vaping Master ECF Veteran

    Feb 18, 2012
    First of all I would like to thank everyone for their nice posts. I would also like to say sorry to classwife for missing the right category. There are so many to choose from!

    I pulled this straight from nicotine article on Wikipedia:

    Historically, nicotine has not been regarded as a carcinogen and the IARC has not evaluated nicotine in its standalone form and assigned it to an official carcinogen group. 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.[65][66] Nicotine has been noted to directly cause cancer through a number of different mechanisms such as the activation of MAP Kinases.[67] Indirectly, nicotine increases cholinergic signalling (and adrenergic signalling in the case of colon cancer[68]), thereby impeding apoptosis (programmed cell death), promoting tumor growth, and activating growth factors and cellular mitogenic factors such as 5-LOX, and EGF. Nicotine also promotes cancer growth by stimulating angiogenesis and neovascularization.[69][70] In one study, nicotine administered to mice with tumors caused increases in tumor size (twofold increase), metastasis (nine-fold increase), and tumor recurrence (threefold increase).[71]

    Though the teratogenic properties of nicotine may or may not yet have been adequately researched, women who use nicotine gum and patches during the early stages of pregnancy face an increased risk of having babies with birth defects, according to a study of around 77,000 pregnant women in Denmark. The study found that women who use nicotine-replacement therapy in the first 12 weeks of pregnancy have a 60% greater risk of having babies with birth defects, compared to women who are non-smokers.[citation needed]

    Effective April 1, 1990, the Office of Environmental Health Hazard Assessment (OEHHA) of the California Environmental Protection Agency added nicotine to the list of chemicals known to the state to cause developmental toxicity, for the purposes of Proposition 65.

    This is where I got that line about Nicotine helping spread cancer once you already have the cells in your body. I cannot seem to find a lot of information on it but I know that all nicotine comes from tobacco and as such they must contain TSNAs (tobacco specific nitrosamine). I get that this is created only in the curing process but I also understand economics to know that they are going to acquire tobacco in the cheapest way possible to do their extractions and that is going to be by the traditional means.

    Others mentioned that there isn't a lot of study on nicotine outside of tobacco. The best place to look for this information is in nicotine replacement therapies such as gum or patches. The whole thing that started this for me was I did a "quit smoking calendar" you know to see what has changed for the better since I quit. I noticed a particular entry that said if you are on the patch or gum that you are still at the same risk for pancreatic cancer and thus the debate began for me.

    Also, as a side note, on another thread I kept reading that people were scared of PG and only wanted 100% VG in their ejuice because of a nasty biocide called acrolein. This concerned me as well, to a minor degree, because according to the World Health Organization the safe oral intake of acrolein is 7.5mg per KG of body weight. It would be impossible to generate that much acrolein, and even more impossible to vape that much ejuice in a day, but it does concern me that they use this stuff to kill algae.
  20. Stubby

    Stubby Ultra Member ECF Veteran

    Apr 22, 2009
    Madison, WI USA
    The misstatement made is that it is not tobacco that causes the problem, it's smoking. Those are two very different things and it is best not to confuse them.

    As for the OP, in absolute terms perhaps nicotine is not the best thing to do if you are looking to lead some type of life of purity, but the harm caused by nicotine is extremely low compared to smoking. We actually do know the long term effect of nicotine from the long term studies on smokeless tobacco. If my memory serves me right, the long term use of smokeless tobacco from the US and Sweden will on average take about 15 days off a persons life. Compare that to the how-ever-many years smoking takes off. To try and say that nicotine use is even remotely related to the risk of smoking is to deny the decades of research already done.

    From being involved with ninjas other post about the dangers of nicotine I believe you are somewhat misguided as to what tobacco harm reduction is about and its history. Tobacco harm reduction did not start with e-cigs. It's not a new idea. E-cigs are just the new kid on the block. The questions about the safety of nicotine have been well thought through and studied for several decades. The many studies out of Sweden on snus, which date back to the 60's, has shown us that nicotine in a relatively pure form has a very low long term health risk. It is not harmless, but it is very low.
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