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Chapter 4: Use Rationalizations

Topics:  Inventing | One | Stress | Friend | Like | Little | Flavor | Coffee | Concentration | Boredom | Pleasure | Choice | Habit | Friendless | Healthy | Can't | Demons | Weight | Safer | Alcohol


"I vape e-cigs and they're vastly safer"


Female vaping an e-cigarette

While likely and hopefully true, we have little current appreciation as to what "safer" actually means. Thankfully, the e-cig is beginning to force research into health risks associated with cleaner forms of nicotine delivery.

The problem is that, as with cigarettes which doctors in advertisements once suggested were safe, it may take decades before enough of the vaping risk spectrum becomes known, clear and reliable enough to permit informed decision making regarding continued use.

Reserving the right to amend as quality risk data becomes available, contrasting long-term smoking to long-term vaping is akin to the risk of jumping from the top of a 5 story building (smoking) versus one that's 2 stories (vaping). Alternatively, imagine an automobile traveling 50 miles-per-hour (80 kph) being driven into a brick wall (cigarette smoking), compared to the same collision at 20 mph or 30 kph (e-cig vaping).

Obviously, contrasting the body's sudden deceleration tolerance to hourly lifetime chemical assaults is night and day. Still, the average long-term e-cig user would be wise to fully expect to sustain harm. They need to vape believing that they will eventually develop one or more vaping related diseases, with some as yet unknown and hopefully very low percentage paying the ultimate price, premature death.

Contrast that to nearly all lifetime smokers developing smoking related diseases, with roughly half failing to survive the above building fall or collision.

We're now watching as e-cig industry marketing takes as its starting point and builds upon decades of pharmaceutical industry marketing, advertising which continues to falsely imply that quitting without use of approved products is nearly impossible.

Putting risk, disease and death aside for a moment, ask yourself, why is nicotine delivery device transfer even necessary?

The underlying and unstated foundation of every e-cigarette advertisement is that you're hopelessly hooked, that you cannot quit, that it's simply too hard, that you're a failure, that a much safer alternative is available, so you should give up on giving up.

Now, now, I hear some of you. "John, you're totally missing the fact that vaping is fantastic!" Respectfully, I'm afraid that's the drug talking.

While clearly, there's no more deadly nicotine delivery device than analog cigarettes, fully arresting your addiction is vastly more do-able[1] and astonishingly more comfortable than your wanting for that next fix will suggest.

As reviewed in Chapter 1, nicotine addiction is a brain wanting disorder.[2] Nearly as unimaginable as giving up food, compromised dopamine pathways have assigned nicotine use the same priority as those pathways assign to eating food.[3]

According to Dr. Nora Volkow, director of the National Institute on Drug Abuse, nicotine addiction is a mental illness, a complex brain disease characterized by compulsive drug craving, seeking and use.[4]

Not only is nicotine compromised brain circuitry functioning as though nicotine is as crucial to survival as food, neo-nicotine industry marketing and advertising takes direct aim at wanting being generated inside a malfunctioning brain.

By June 2000, the cig industry became aware that replacement nicotine (NRT) undermines successful quitting. By then, it had in its hands a 200 page U.S. government "Guideline" containing evidence tables which combined and averaged the results from hundreds of different quitting studies.[5] Those tables shout that over-the-counter NRT is substantially less effective at 6 months than nearly all controls shared in all other study areas (7% vs. 10-11%).[6]

By now, new e-cigarette companies have awakened to the reality that successful cold turkey nicotine cessation threatens their future profits too, that frustrations born of highly ineffective quitting product attempts increase the likelihood of e-cigarette use. Sadly, it's a win-win for everyone but the addict.

Reality is, the tail has been wagging the dog. Only a tiny fraction of successful ex-smokers stopped smoking by using approved products (roughly 8 percent).[7]

Which is wiser, harm reduction or harm elimination?

Nicotine is a natural insecticide.[8] Anyone believing that addiction to inhaling a vaporized poison doesn't generate a host of serious health risks is residing in la la land.

Although nicotine is not believed to cause cancer, animal studies have implicated it in contributing to cancer promotion,[9] (including promotion of: breast cancer,[10] cervical cancer,[11] colon cancer,[12] esophageal cancer,[13] kidney cancer,[14] lung cancer,[15] lung cancer via cotinine,[16] oral cancer,[17] pancreatic cancer,[18] stomach cancer[19] and stem cell cancer).[20]

Nicotine is also believed to contribute to circulatory disease,[21] kidney disease and diabetes,[22] decreased sperm counts with DNA damage in men,[23] impaired follicular growth in women,[24] fetal harm,[25] (chromosome damage,[26] attention deficits,[27] impaired lung development,[28] asthma,[29] and impaired offspring ovarian function and fertility)[30] and in causing sudden infant death.[31]

On an emotional level, nicotine addicts live with greater anxiety[32], including stress induced urine acidification accelerating eliminiation of the alkaloid nicotine, causing the onset of early withdrawal to be added to stressful situations.[3]

While vaping is clearly safer than smoking, e-cig users deserve warning that they're acting as human guinea pigs.

For example, we know that it takes up to 10 years after ending cigarette use to reduce smoking lung cancer risks by 30 to 50%.[34] What we don't know is the long term consequences of inhaling vaporized nicotine into lungs and a body already damaged by years of smoking.

The cost of e-cig use promises to rise. While use costs are currently less expensive than smoking, the tobacco industry should be expected to continue to purchase major e-cig companies, in part to protect profits.

Expect both the tobacco and their pharmaceutical industry buddies to demand government regulation of e-cigarettes, nicotine e-juice, and canisters in order to limit competition, slow innovation and to protect existing product lines and profits.

Also expect concerns over e-cig use by youth and illegal drug users (already THC juice being vaped without smell) to motivate governments to either ban their sale, limit availability or impose sufficient excise taxes so as to raise prices high enough to discourage use by kids.

The good news is that current pen-type e-cigs are extremely inefficient at nicotine delivery without instruction or practice. Like trying to drink through a straw, they must be primed like a pump. Thus, most kids are able to experiment once or twice without getting hooked. The bad news is that technology (evolving tanks and mods) is a problem solver.

As for you, let's not kid ourselves. E-cig use is not about freedom but about keeping you hooked. It's not about arresting your dependence but about the novelty of using electricity and vapor to feed it.

What would it feel like to journey home, to begin going entire days without once thinking about wanting to use?

Those pushing e-cigs continue to insist on creating confusion. They co-opted the word "quitting" in describing nicotine dependency delivery device substitution, transfer and replacement. Real quitting doesn't involve handing the neo-nicotine industry our money.

In closing, sleep on this. If e-cigs do in fact greatly diminish smoking's premature death risks, if successful in transferring to them, once ready to end e-cig use, what remaining motivation would be substantial enough to keep you focused and dedicated long enough to arrive here on Easy Street?

On the postive side, obviously, you'd live longer, but as an hourly feeding addict.

There was always only one rule, that we cannot cheat a brain that's already been permanently compromised by nicotine. Like the alcoholic, when trying to break free, just one puff and we lose. The choice is ours: none or all, freedom or feed-em!



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References:

1. WhyQuit.com, Turkey's Triumphs, 2005 to present, http://whyquit.com/whyquit/turkeys.html
2. Blum K, et al "Liking" and "wanting" linked to Reward Deficiency Syndrome (RDS): hypothesizing differential responsivity in brain reward circuitry, Current Pharmaceutical Design, 2012, Volume 18(1), Pages 113-1188.
3. Blum K, et al, Reward circuitry dopaminergic activation regulates food and drug craving behavior, Current Pharmaceutical Design, 2011, Volume 17(12), Pages 1158-1167.
4. Polito JR, Addiction to smoking nicotine a mental illness, April 12, 2010, WhyQuit.com.
5. Fiore, MC et al, Clinical Practice Guideline, Treating Tobacco Use and Dependence, U.S. Department of Health and Human Services, June 2000.
6. Polito, JR Does the Over-the-counter nicotine patch really double your chances of quitting?, WhyQuit.com, April 8, 2002.
7. Polito, JR, Gallup Poll: cold turkey 48 times smarter than Nicorette, WhyQuit.com, August 26, 2013.
8. Steppuhn, A, et al, Nicotine's Defensive Function in Nature, PLoS Biol. August 17, 2004, 2(8): e217.
9. Russo P, et al, Nicotinic receptor and tobacco-related cancer Life Sciences, November 27, 2012, Volume 91(21-22):Pages 1087-1092.
10. Nishioka T, et al, Sensitization of epithelial growth factor receptors by nicotine exposure to promote breast cancer cell growth, Breast Cancer Research. 2011, Volume 13(6):R113
11. Calleja-Macias, et al, Association of single nucleotide polymorphisms of nicotinic acetylcholine receptor subunits with cervical neoplasia, Life Sciences, 2012 Nov 27;91(21-22):Pages 1099-1102.
12. Chu KM, et al, Nicotine and gastrointestinal disorders: its role in ulceration and cancer development, Current Pharmaucetial Design, 2013;19(1): Pages 5-10.
13. Zong Y, et al, Nicotine enhances migration and invasion of human esophageal squamous carcinoma cells which is inhibited by nimesulide, World Journal of Gastroenterology, May 20098, Volume 28;15(20): Pages 2500-25055.
14. Guo X, et al, Nicotine induces alteration of H3K27 demethylase UTX in kidney cancer cell, Humand and Experimental Toxicology, March 2014, Volume 33(3), Pages 264-269.
15. Guo L, et al, Mitochondrial reactive oxygen species mediates nicotine-induced hypoxia-inducible factor-1α expression in human non-small cell lung cancer cells, Biochim Biophys Acta. 2012 Jun;1822(6):852-61.
16. Nakada T, et al, Lung tumorigenesis promoted by anti-apoptotic effects of cotinine, a nicotine metabolite through activation of PI3K/Akt pathway, The Journal of Toxicological Science, 2012; Volume 37(3):Pages 555-563.
17. Salimi M, et al, Change in nicotine-induced VEGF, PGE2 AND COX-2 expression following COX inhibition in human oral squamous cancer, J Environ Pathol Toxicol Oncol. 2012;31(4):349-356.
18. Treviño JG, et al, Nicotine induces inhibitor of differentiation-1 in a Src-dependent pathway promoting metastasis and chemoresistance in pancreatic adenocarcinoma, Neoplasia. 2012 Dec;14(12):1102-1114.
19. Liu Y and Liu BA, Enhanced proliferation, invasion, and epithelial-mesenchymal transition of nicotine-promoted gastric cancer by periostin, World Journal Gastroenterology, 2011 Jun 7;17(21):2674-2680.
20. Yu MA, Nicotine promotes acquisition of stem cell and epithelial-to-mesenchymal properties in head and neck squamous cell carcinoma, PLoS One. 2012;7(12):e51967
21. Heeschen C, et al, Nicotine promotes arteriogenesis, Journal of the American College of Cardiology, 2003 Feb 5;41(3):489-496.
22. Jain G and Jaimes EA, Nicotine signaling and progression of chronic kidney disease in smokers, Biochemical Pharmacology, 2013 Oct 15;86(8):1215-23.
23. Kushwaha S and Jena GB, Effects of nicotine on the testicular toxicity of streptozotocin-induced diabetic rat: intervention of enalapril, Human and Experimental Toxicology, 2014 Jun;33(6):609-622.
24. Bordel R, Nicotine does not affect vascularization but inhibits growth of freely transplanted ovarian follicles by inducing granulosa cell apoptosis, Human Reproduction, 2006 Mar;21(3):610-617.
25. Ginzel, KH, et al, Critical Review: Nicotine for the Fetus, the Infant and the Adolescent?, Journal of Health Psychology, 2007, Volume 12(2), Pages 215–224.
26. The genotoxic effect of nicotine on chromosomes of human fetal cells: the first report described as an important study, Inhalation Toxicology, Nov.2011, Volume 23(13), Pages 829-834.
27. Bailey CD, et al, Chrna5 genotype determines the long-lasting effects of developmental in vivo nicotine exposure on prefrontal attention circuitry, Neuropharmacology. 2014 Feb;77:145-55.
28. Maritz GS and Harding R, Life-long programming implications of exposure to tobacco smoking and nicotine before and soon after birth: evidence for altered lung development, Int J Environ Res Public Health. 2011 Mar;8(3):875-98.
29. Rehan VK, et al, Perinatal nicotine exposure induces asthma in second generation offspring, BMC Med. 2012 Oct 30;10:129.
30. Holloway AC, et al, Fetal and neonatal exposure to nicotine disrupts ovarian function and fertility in adult female rats, Endocrine. 2006 Oct;30(2):213-6.
31. Slotkin TA, et al, Prenatal nicotine exposure in rhesus monkeys compromises development of brainstem and cardiac monoamine pathways involved in perinatal adaptation and sudden infant death syndrome: amelioration by vitamin C, Neurotoxicologyand Teratology, 2011 May-Jun;33(3):431-4.
32. Maurizio, C, et al, Acute nicotine induces anxiety and disrupts temporal pattern organization of rat exploratory behavior in hole-board: a potential role for the lateral habenula, Front Cell Neurosci. 2015; 9: 197.
33. Polito, JR, Use Rationalizations: "Use relieves stress and anxiety", Freedom from Nicotine - The Journey Home: Chapter 4.
34. Polito, JR, Stop Smoking Recovery Timetable , WhyQuit.com.



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Page created June 16, 2015 and last updated February 6, 2016 by John R. Polito