Thanks. Though, as aI before stated, my experience with vaping is that it is ironically worse on the lungs than cigarettes; at least for short term use. Vaping hardware is a cowboy market, and there is no priority on filtering out particulate in the vape smoke. In my opinion, vaping needs better filter technology. In addition, there isn't any research on the effect of glycerine vapor on the lungs. My lungs quickly recover after short term cigarette use. After my stint with vaping, my lungs took a few months to recover from noticeable impairment indicative of particulate in the lung.
I've started and quitted enough to know my addiction potential with tobacco. Also, I don't start and quit with any regularity. The last time that I did, before this time, was over a decade ago. My 'start/stop' cycles were more frequent in my twenties and it was never, ever a problem to stop. That being said, I have a hypothesis that addiction potential increases with decreased brain plasticity. A highly plastic, young brain might even have a tendency to reject anything but short term tobacco use due to tobacco's relative inability to decrease plasticity quickly. Whereas cocaine, for instance, likely works to quickly decrease plasticity and increase addiction quickly. However, as one gets older and plasticity decreases with age, cigarette addiction potential, from short term use, might increase.
As an aside, my last smoking daliance was after smoking a cigarette that was unkowingly abnormally high in free-base tobacco. Avoiding such cigarettes, for occassional smokers, is llikely crucial to avoidance of habit.
Last, just to reiterate, my primary point wasn't to address addiction and use cycles. I have no current inclination toward tobacco use.
My primary point was to continue and expand on a discussion of possible therapeutic useage of nicotine or even cigarettes in the very short term. That discussion could possibly be expanded to either pro-oxidant therapy or even more specific adaptive therapy using substances that are shown to cause specific disease states.
To begin, might short term use of a substance that is statistically shown to slowly lead to alzheimers, over years, create an anti-alzheimers adaptive response in the brain should the substance be used in the short term and then abandoned? I noticed very mild (hardly notieceable but I'm sensitive) cognitive impairment while smoking over the course of about one month recently. After quitting, my memory and resistance to the negative effects of cognitive abuse (sleep deprivation) continues to be noticeably greater weeks later (to a degree that transcends my relative sensitivity) than before I began the smoking. This is an effect that virtually no other substance mentioned or used on this forum has ever produced or has any chance of producing.
I'm not advocating smoking, but these anecdotal results might be a substrate for a discussion to include ramifications and strategies that may include but also extend beyond tobacco use. Again, as I before stated, personal risk and reward would be a consideration. To illustrate. if I have a cognitive impairment then short term lung damage might be an acceptable risk. These decisions are made all of the time by doctors. For instance, chemotheray tends to noticeably age anyone but young people, but the risk of such a thing is acceptable given the propsect of being free from cancer. Also, perhaps other such theoretical adaptive strategies can be found that avoid the emotional response in the average person that often accompanies discussion of tobacco use
Cigarette smoking is a risk factor for Alzheimer's Disease: an analysis controlling for tobacco industry affiliation.
Author information
- 1Department of Physiological Nursing, Gerontology, University of California, San Francisco, San Francisco, CA 94143-0610, USA. cataldo@nursing.ucsf.edu
Abstract
To examine the relationship between smoking and Alzheimer's disease (AD) after controlling for study design, quality, secular trend, and tobacco industry affiliation of the authors, electronic databases were searched; 43 individual studies met the inclusion criteria. For evidence of tobacco industry affiliation, http://legacy.library.ucsf.edu was searched. One fourth (11/43) of individual studies had tobacco-affiliated authors. Using random effects meta-analysis, 18 case control studies without tobacco industry affiliation yielded a non-significant pooled odds ratio of 0.91 (95% CI, 0.75-1.10), while 8 case control studies with tobacco industry affiliation yielded a significant pooled odds ratio of 0.86 (95% CI, 0.75-0.98) suggesting that smoking protects against AD. In contrast, 14 cohort studies without tobacco-industry affiliation yielded a significantly increased relative risk of AD of 1.45 (95% CI, 1.16-1.80) associated with smoking and the three cohort studies with tobacco industry affiliation yielded a non-significant pooled relative risk of 0.60 (95% CI 0.27-1.32). A multiple regression analysis showed that case-control studies tended to yield lower average risk estimates than cohort studies (by -0.27 +/- 0.15, P=0.075), lower risk estimates for studies done by authors affiliated with the tobacco industry (by -0.37 +/- 0.13, P=0.008), no effect of the quality of the journal in which the study was published (measured by impact factor, P=0.828), and increasing secular trend in risk estimates (0.031/year +/- 0.013, P=0.02). The average risk of AD for cohort studies without tobacco industry affiliation of average quality published in 2007 was estimated to be 1.72 +/- 0.19 (P< 0.0005). The available data indicate that smoking is a significant risk factor for AD.
Edited by golgi1, 08 October 2015 - 10:24 AM.