" Is Nicotine Addiction Safe In The Long Term And You" : The Debate
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.
Last edited by ShogaNinja; 07-22-2012 at 10:25 AM.
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.
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.
It is very hard to find information about nicotine without it being attached to smoking, Wikipedia includes e cigarettes under its nicotine information.
Nicotine - Wikipedia, the free encyclopedia
Last edited by Yves; 07-22-2012 at 11:10 AM.
Reason: adding link
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
Last edited by CES; 07-22-2012 at 11:44 AM.
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.
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.
Originally Posted by ShogaNinja
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.
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.
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