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Smoking is Good for You!

What are the differences between Epidemiology and Science? Why do politicians accept that Epidemiology is "science"?

Smoking is Good for You!

Postby Dee » Mon May 26, 2008 12:19 pm

Jay posted this on Mainerights


http://www.stahlheart.com/wispofsmoke/goodforyou.html

Smoking is Good for You!
AKA, Smokers' Paradoxes
Note that the studies referenced are what is known as "hard science" as opposed to the "soft science" of epidemological studies. Also, notice that the research here is not in tobacco literature or tobacco-funded literature; in fact, many of the studies cited are actually from antismoking literature funded by Big tobacco Control and/or Big Pharma. For more information, please see the Must Reads.
The miracle supplement (for skin, heart, brain rejuvenation) Coenzyme Q10 is extracted from tobacco leaf. WebMistress: Coenzyme Q10 is also essential in fighting cancer!!!
In Coenzyme Q10: A Miracle Vitamin , Dr. Ricjard A. Kunin extols the benefits of Coenzyme Q10. He also says:
The energy of oxidation in cells depends on CoQ in partnership with niacinamide (vitamin B3), riboflavin (vitamin B2), and minerals such as iron and copper to effect the movement of electrons and hydrogen protons in the power plant of cell, the mitochondrion.
...
Incidentally, tobacco leaf is the champion source, containing 184 mg in a quarter pound.
Note that the doctor follows with the disclaimer, "In fact, the Japanese companies make their CoQ from tobacco, however it is only released by means of bacterial fermentation not by smoking." The fact remains that CoQ 10 is a natural miracle for the human body and it's chief source is tobacco! Those MDs just can't get their heads around the fact that tobacco is a valuable gift from nature! Now take a look at what a pharmacy has to say about natural vs. synthetic CoQ10:
The natural CoQ10 in Qmelt is made via fermentation in which a microorganism (in the case of CoQ10, a bacterium or yeast) naturally produces CoQ10. The CoQ10 is then extracted from the organism and concentrated. It is termed natural since it is normally and naturally produced by the yeast or bacterium from which it was taken. This is different from synthetic CoQ10 which is made by taking a compound found in tobacco and then mixing it with other chemicals to form a similar structure of CoQ10. While tobacco is natural, CoQ10 is not taken from tobacco in this synthetic process….the only thing taken from the tobacco is a compound which is used as the starting material for chemically creating CoQ10. That is why it is referred to as a synthetic process. Tobacco or plants in general do not contain significant amounts of CoQ10
The pharmacy "information" is in direct contradiction of what is known by everyone else: (1) tobacco is the chief source of CoQ10 with an abundance of the enzyme and (2) the means by which CoQ10 is extracted is not chemical, although it might involve fermentation. (Note: The fermentation process might involve beets or fermented sugar cane.)
AN IMPORTANT NOTE: The doctor cited above comments on the importance of CoQ in partnership with other nutrients, including niacinamide, aka nicotinic acid, niacin and vitamin B3. This is a form of nicotine, which could result from the alteration of nicotine as it is very unstable. Please see Facts about Nicotine.
Smoking Reduces Parkinson's

Neurology. 1999 Sep 22;53(5):1158. Smoking and Parkinson's disease: a dose-response relationship Gorell JM, Rybicki BA, Johnson CC, Peterson EL
Department of Neurology, Henry Ford Health System, National Institute of Environmental Health Sciences Center in Molecular and Cellular Toxicology with Human Applications, Wayne State University, Detroit, MI, USA.
OBJECTIVE: To determine whether an inverse dose-response relationship exists between cigarette smoking and PD among ever-smokers and ex-smokers.
METHODS: Smoking and alcohol consumption were analyzed in 144 PD patients and 464 control subjects, who were frequency matched for sex, race, and age (+/-5 years), in a population-based case-control study of men and women > or =50 years old in the Henry Ford Health System.
RESULTS: With never-smokers as the reference category, there was an inverse association between current light smokers (>0 to 30 pack-years) and PD patients (odds ratio [OR], 0.59; 95% CI, 0.23 to 1.53), and a stronger inverse association of PD with current heavy smokers (>30 pack-years; OR, 0.08; 95% CI, 0.01 to 0.62). When former >30-pack-year smokers were stratified by the interval since quitting, there was an inverse association between those who stopped >20 years ago and PD (OR, 0.86; 95% CI, 0.42 to 1.75), and a greater inverse relationship with those who stopped 1 to 20 years ago (OR, 0.37; 95% CI, 0.19 to 0.72). Alcohol consumption had no independent, significant association with PD, but heavy drinking (>10 drink-years) had a greater effect than light-moderate drinking in reducing but not eliminating the inverse association between smoking and PD.
CONCLUSIONS: The inverse dose-response relationship between PD and smoking and its cessation is unlikely to be due to bias or confounding, as discussed, providing indirect evidence that smoking is biologically protective.
Also see Smoking lowers Parkinson's disease risk from Reuters (Mar 20, 2007).
From “Temporal relationship between cigarette smoking and risk of Parkinson disease” (NEUROLOGY 2007;68:764-768):
The lower risk of Parkinson disease among current and former smokers varied with smoking duration, intensity, and recentness. The dependence of this association on the timing of smoking during life is consistent with a biologic effect.
Osteo-arthritis reduced threefold (the most for knee arthritis in women)
IS OSTEOARTHRITIS IN WOMEN AFFECTED BY HORMONAL CHANGES OR SMOKING? from the journal for British Society for Rheumatology (1993).
Internal antioxidant SOD doubled (recent article labels the higher SOD "the elixir of eternal life" based on animal experiments)
From Scientists find elixir of eternal life - in a worm By Roger Highfield, Science Editor, "Detailed work showed that the gene can boost levels of proteins called SODs (superoxide dismutase) which mop up free radicals, harmful chemicals linked with ageing. The researchers think that this may be a defence mechanism that helps the creatures tolerate starvation."
Reduced MAO B enzyme (smokers in their 60s have MAO B of nonsmokers in their 20s; also here). Lowering of MAO B is the holy grail (deprenyl does it but not as well as tobacco) of life-extension and smart drug circles.
Explained very well by NightLight referencing The American Journal of Psychiatry illustrated by these graphs, and the National Academy of Sciences (September 8, 2003). More can be found on MAO and the importance of MAO-inhibitors in Turkish Journal of Medical Sciences, MAO Inhibitors in Aging: Can They Serve as Protective Agents in Cardiac Tissue Against Oxidative Stress?, Scholar Google and
The real eye-opener comes from theNational Institue on Drug Abuse! That's about as far as you can get from being a shill for Big Tobacco! Yet, this antismoking group's very own study, "Tobacco Smoke May Contain a Psychoactive Ingredient Other Than Nicotine" (NIDA News, Volume 13, Number 3, July, 1998), states plainly:
The amount of the enzyme, called monoamine oxidase (MAO), is reduced by 30 to 40 percent in the brains of smokers, compared to nonsmokers or former smokers, the brain scans show. The reduction in brain MAO levels may result in an increase in levels of dopamine, which scientists associate with the reinforcing effects of drugs of abuse.
A note needs to be on the research paper in the American Journal of Psychiatry, Maintenance of Brain Monoamine Oxidase B Inhibition in Smokers After Overnight Cigarette Abstinence. The Abstract includes these remarks:
OBJECTIVE: The authors’ goal was to replicate a previous finding that smokers have lower brain monoamine oxidase B (MAO-B) levels than comparison nonsmoking subjects ...RESULTS: Average MAO-B levels in smokers in the present study were similar to those found in the previous study and averaged 39% (SD=17) lower than those found in a comparison group of nonsmokers. Brain MAO-B levels did not differ between baseline levels and 10 minutes after smoking.
So, the authors of this study were replicating the results that MAO-B levels are lower in smokers!!!
This benefit of inhibiting MAO-B was known as long ago as 1987. From Irreversible inhibition of monoamine oxidase by some components of cigarette smoke, Life Science (1987 Aug 10;41(6):675-82), "Inhibitory activity towards monoamine oxidase has been found in a solution of cigarette smoke. The inhibition was irreversible."
Alas, one must an actual smoker to benefit. From the abstract of “Smoking a single cigarette does not produce a measurable reduction in brain MAO B in non-smokers” (PubMed):
Positron emission tomography (PET) studies with [11C]L-deprenyl-D2 have shown that brain monoamine oxidase (MAO) B is 40% lower in smokers than in non-smokers. …These results indicate that the reduction in MAO B in smokers probably occurs gradually and requires chronic tobacco smoke exposure.
Telomerase ("fountain of youth") much more active in smokers.
Smoking is associated with increased telomerase activity in short-term cultures of human bronchial epithelial cells, Cancer Letters 2007 Feb 8;246(1-2):24-33. Epub 2006 Mar 6--from the Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.
Glutathione (chief antioxidant in human body) and catalase (another key antioxidant which neutralizes alcohol damage, cyanide,...) doubled in smokers.
Also explained by NightLight.
From The Abstract of Normal alveolar epithelial lining fluid contains high levels of glutathione in the Journal of Applied Physiology (Vol 63, Issue 1, p. 152-157):
The epithelial cells on the alveolar surface of the human lower respiratory tract are vulnerable to toxic oxidants derived from inhaled pollutants or inflammatory cells. Although these lung cells have intracellular antioxidants, these defenses may be insufficient to protect the epithelial surface against oxidants present at the alveolar surface. This study demonstrates that the epithelial lining fluid (ELF) of the lower respiratory tract contains large amounts of the sulfhydryl-containing antioxidant glutathione (GSH). The total glutathione (the reduced form GSH and the disulfide GSSG) concentration of normal ELF was 140-fold higher than that in plasma of the same individuals, and 96% of the glutathione in ELF was in the reduced form. Compared with nonsmokers, cigarette smokers had 80% higher levels of ELF total glutathione, 98% of which was in the reduced form. Studies of cultured lung epithelial cells and fibroblasts demonstrated that these concentrations of reduced glutathione were sufficient to protect these cells against the burden of H2O2 in the range released by alveolar macrophages removed from the lower respiratory tract of nonsmokers and smokers, respectively, suggesting that the glutathione present in the alveolar ELF of normal individuals likely contributes to the protective screen against oxidants in the extracellular milieu of the lower respiratory tract.
More studies on antioxidants in people who smoke can be found in the Journal of Applied Physiology.
Selective increase of antioxidant enzyme activity in the alveolar macrophages from cigarette smokers and smoke-exposed hamsters. for American Review of Respiratory Disease, (1990 Mar, vol 141, no 3, p. 678-82).
http://www.imminst.org/forum/index.php? ... ntry170219
Nicotine suppresses cell death of neurons (it also promotes vascular growth factor, e.g. growth and branching of capillaries). (Another advantage of nicotine is that Nicotine Slays TB. The link to this mainstream article is prefaced by this comment, "This article was written in 2001 and since then the ban on smoking in public places and taxing tobacco has grown. Extremely-Drug-Resistant Tuberculosis strains will continue to spread and multiply. The resulting global XDR-TB epidemic will be an untreatable and unstoppable calamity.")
Low concentration carbon monoxide (as found in tobacco smoke) protects cells in harsh conditions, such as low oxygen and general cell death.
Nitric oxide stimulates peripheral circulation (this is the mechanism behind Viagra effect).
Raises youth hormones, e.g. DHEA, pregnenolone, testosterone,...
Relation of age and smoking to serum levels of total testosterone and dehydroepiandrosterone sulfate in aged men in Geriatrics & Gerontology International (Volume 6 Issue 1 Page 49-52, March 2006), which found these results, "Serum T did not decrease with age, and was significantly higher in smokers than for non-smokers. Serum DHEA decreased with age more sharply in non-smokers than for smokers."
Smoking reduces IGF-1 (insulin-like growth factor 1)--at least in males for sure. In animal experiments, lowered insuline growth factor IGF-1 change extends lifespan.

From Signals from the reproductive system regulate the lifespan of C. elegans (Nature. 1999 May 27;399(6734):308-9), "Mutants with reduced activity of the insulin/IGF-1-receptor homologue DAF-2 have been shown to live twice as long as normal". From Dietary and Lifestyle Correlates of Plasma Insulin-Like Growth Factor-I (IGF-I) and IGF Binding Protein-3 (IGFBP-3): The Multiethnic Cohort (Cancer Epidemiology Biomarkers & Prevention, Vol. 13, 1444-1451, September 2004), "In addition, we observed associations between current smoking and low IGF-I levels..."--and, on p. 1449, table 3 shows that smoking had strongest reduction effect on IGF-1 in males!
Hmmmmm.... So, IGF-1 is reduced in people who smoke and animals bred to have reduced IGF-1 have a tendency to double their life spans. That goes a long way toward explaining the reason that the people who have lived longest on this earth are all smokers!
Reduced Incidence of Colorectal Cancer--especially in women.
Cigarette Smoking and the Risk of Colorectal Cancer in Women (Journal of the National Cancer Institute, Vol. 80, No. 16, 1329-1333, October 19, 1988) states, "Colorectal cancer incidence rates for smokers, nonsmokers living with smokers (i.e., passive smokers), and non-smokers in smoke-free households were compared in a 12-year prospective study of 25, 369 women who participated in a private census conducted in Washington County, MD, in 1963. Women who smoked had a decreased relative risk of colorectal cancer compared with the risk for nonsmokers (age-adjusted relative risk, 0.76; 95% confidence interval, 0.52–1.10). The risk for passive smokers was similar to that for smokers. The relative risks were significantly reduced for older women; relative risks were 0.42 for smokers and 0.66 for passive smokers over age 65. The data suggest that older women who smoke have a lower risk of colorectal cancer than non-smokers. The effect may be mediated by an antiestrogenic effect of smoking." More evidence can be found in this scanned document
People who smoke fare better than nonsmokers when exposed to occupational hazards.
From Lack of combined effects of exposure and smoking on respiratory health in aluminium potroom workersBritish Medical Journal, Occupational and Environmental Medicine (Vol 56, 468-472, 1999):
Smokers in the potroom group had a lower prevalence of respiratory symptoms than never smokers or ex-smokers, which was significant for wheezing (2.6% v 17.4% and 28.6% respectively, both p < 0.01), whereas respiratory symptoms in controls tended to be highest in smokers (NS). No effects of potroom work on the prevalence of respiratory symptoms could be detected. In potroom workers, impairment of lung function due to occupational exposure was found only in non-smokers, with lower results for forced vital capacity (FVC) (98.8% predicted), forced expiratory volume in one second (FEV1) (96.1% predicted) and peak expiratory flow (PEF) (80.2% predicted) compared with controls (114.2, 109.9, and 105.9% predicted; each p < 0.001). Conversely, effects of smoking on lung function were only detectable in non-exposed controls (current smokers v non-smokers: FVC 98.8% v 114.2% predicted; p < 0.01; FEV1 95.5 v 109.9% predicted; p < 0.05)." (NOTE: The key result is that for the exposure controlled group (the potroom workers) the smoking reduced the risk of lung damage sixfold compared to never-smokers.)
Reduces schitzophrenia symptoms.
From “Investigating the Association Between Cigarette Smoking and Schizophrenia in a Cohort Study,” Am J Psychiatry (160:2216-2221, December 2003):
Cigarette smoking may be an independent protective factor for developing schizophrenia. These results are consistent with animal models showing both neuroprotective effects of nicotine and differential release of prefrontal dopamine in response to nicotine.
From Cancer in schizophrenia: is the risk higher or lower? in Schizophrenia Research (Volume 73, Issue 2, Pages 333-341) at http://www.schres-journal.com/article/P ... 0/abstract :
The incidence of cancer in patients diagnosed with schizophrenia was compared with the incidence in the general population. The results showed that the cancer standardized incidence ratios (SIRs) for all sites were significantly lower among men and women with schizophrenia, 0.86 [95% confidence interval (CI) 0.80–0.93] and 0.91 (95% CI 0.85–0.97), respectively. This reduced overall risk was clearest for those born in Europe–America, both men (SIR 0.85, 95% CI 0.74–0.97) and women (SIR 0.86, 95% CI 0.77–0.94).
Appetite Suppressant -- no citations. Common sense. Most stimulants are appetite suppressants, and nicotine does seem to be a stimulant.
Tobacco: the definitive link in healthy aging by Daniel John Richard Date.
Reduces incidence of Alzheimer's, among other degenerative diseases.
From The Straight Dope Classics:
"A statistically significant inverse association between smoking and Alzheimer's disease was observed at all levels of analysis, with a trend towards decreasing risk with increasing consumption" (International Journal of Epidemiology, 1991)
"The risk of Alzheimer's disease decreased with increasing daily number of cigarettes smoked before onset of disease. . . . In six families in which the disease was apparently inherited . . . the mean age of onset was 4.17 years later in smoking patients than in non-smoking patients from the same family" (British Medical Journal, June 22, 1991)
"Although more data are needed . . . [an analysis of 19 studies suggests] nicotine protects against AD" (Neuroepidemiology, 1994)
Nicotine injections significantly improved certain types of mental functioning in Alzheimer's patients (Psychopharmacology, 1992).
One theory: nicotine improves the responsiveness of Alzheimer's patients to acetylcholine, an important brain chemical.
“When chronically taken, nicotine may result in: (1) positive reinforcement [it makes you feel good], (2) negative reinforcement [it may keep you from feeling bad], (3) reduction of body weight [by reducing appetite and increasing metabolic rate], (4) enhancement of performance, and protection against: (5) Parkinson's disease, (6) Tourette's disease [tics], (7) Alzheimer's 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." ("Beneficial Effects of Nicotine," Jarvik, British Journal of Addiction, 1991)
See more on smoking and reduced incidence of Alzheimer's disease. In this compilation of 19 studies, 15 found a reduce risk in smokers, and none found an increased risk. Also noted is the fact that acute administration of nicotine improves attention and information processing in AD patients, which adds further plausibility to the hypothesis.
Smoking is Good for You: Absence, Presence, and the Ecumenical Appeal of Indian Islamic Healing Centers
In Shop owner says smoking 'doesn't cause disease' a shop owner "tells his customers that smoking calms the nerves and soothes the mind." This is in sync with what Albert Einstein stated upon becoming a lifetime member of the Montreal Pipe Smokers Club at the age of 71, "I believe that pipe smoking contributes to a somewhat calm and objective judgment in all human affairs."

A Few Words of Caution Concerning Filters
<TR>
From “Cigarettes with defective filters marketed for 40 years: what Philip Morris never told smokers” (Tobacco Control 2002;11:i51-i61):
Background: More than 90% of the cigarettes sold worldwide have a filter. Nearly all filters consist of a rod of numerous ( > 12 000) plastic-like cellulose acetate fibres. During high speed cigarette manufacturing procedures, fragments of cellulose acetate that form the mouthpiece of a filter rod become separated from the filter at the end face. The cut surface of the filter of nearly all cigarettes has these fragments. In smoking a cigarette in the usual manner, some of these fragments are released during puffing. In addition to the cellulose acetate fragments, carbon particles are released also from some cigarette brands that have a charcoal filter. Cigarettes with filters that release cellulose acetate or carbon particles during normal smoking conditions are defective.
and:
Conclusions: We have shown that: (a) the filter of today's cigarette is defective; (b) Philip Morris, Inc has known of this filter defect for more than 40 years; (c) the existence of this filter defect has been confirmed by others in independent studies; (d) many methods exist to prevent and correct the filter defect, but have not been implemented; and (e) results of investigations substantiating defective filters have been concealed from the smoker and the health community. The tobacco industry has been negligent in not performing toxicological examinations and other studies to assess the human health risks associated with regularly ingesting and inhaling non-degradable, toxin coated cellulose acetate fragments and carbon microparticles and possibly other components that are released from conventional cigarette filters during normal smoking. The rationale for harm assessment is supported by the results of consumer surveys that have shown that the ingestion or inhalation of cigarette filter fibres are a health concern to nearly all smokers.
From “A False Martyr?” from Surreality Times:
The "official" explanation for smokers developing less squamous tumors and more adenocarcinoma tumors, is that modern filters on cigarettes cause smokers to inhale more deeply which deposits irritants into the small airways deep in the lungs where adenocarcinomas develop. But - non-smokers don't inhale second-hand smoke through a filter!

The anti-smoking industry claims, smokers are now developing andenocarcinomas because they are inhaling cigarette smoke through modern filters, specifically. It's the filtering that makes the difference, in smokers, they claim. Non-smokers never inhale SHS through filters, they always inhale unfiltered smoke. That means, if SHS is causing lung cancer in non-smokers, they should be developing Squamous Cell tumours! Unfiltered tobacco smoke = squamous cell tumours, filtered tobacco smoke = andenocarcinoma tumours, according to the American Cancer Society.
Other health risks could be associated with the use of tobacco sheets in cigarette manufacturing. Although "authorities" and "experts" tell us that "there is no safe cigarette"--but then try to legislate for safer cigarettes—the fact is that whole leaf tobacco and organic tobacco are less hazardous. Moreover, whole leaf tobacco burns slower, thus reducing fire hazards.
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Postby nightlight » Mon May 26, 2008 9:38 pm

There is also an active thread with the same title on Smoking Ladies Board.
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Postby tnsmoker » Tue May 27, 2008 5:31 am

Glad to see you back, Nightlight!

Please continue to post links to these discussions you have on other boards.
Smoke'em if ya got'em!
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Postby Ariel » Tue May 27, 2008 9:42 am

Hey nightlight! *waving*

Glad to see you too. You should hang around more.
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Postby Dee » Tue May 27, 2008 11:58 am

Thanks for the link!
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Postby smallbird » Wed May 28, 2008 12:15 am

I've missed you too, nightlight!
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Postby nightlight » Wed May 28, 2008 5:09 am

Thanks folks for all for the nice words above. I am still quite busy at work, but I was so infuriated by the recent Fire-Safe "Cigarettes" mandated in my state (MA), I had to start doing something.

A friend of mine and a fellow smoker came by recently and offered me one of her FSC products, which outwardly appeared indistinguishable from my favorite cigarettes (Natural American Spirit). I had to put it out in disgust three puffs later. This change came in few months ago, but I didn't notice since I make my own from NAS rolling tobacco.

What we have here is stealthy de facto prohibition. Our regular product, cigarette has been banned and replaced by another one in a deceptively similar packaging, but which cannot be good for you (I was disgusted with it within seconds, as well as any other smoker I talked to). This sneaky prohibition is analogous to prohibiting alcohol again by mandating, under some safety or 'for the children' pretext, that all liquor manufacturers must add specific noxious additive to their products.

Time is unfortunately running out for the present ineffective methods of organizing and battling the antismoking scourge. Our first and most devastating enemy is our own ignorance, the void which the antismoking parasite has filled in with a paralyzing toxin of fear and guilt. Until we conquer this mightly enemy within each of us, we will have no strength or will to fight the enemies in the physical realm, the Big Pharma and the fat bureauracies which are pulling the strings of the visible antismoking puppets and drama queens. The latter two are of no consequence and should be completely ignored since they will perish as as soon as their string pullers have been dealth with.

It pains me to see FORCES and other good folks and fellow smokers squandering precious time and resources getting tangled up in arguing or trying to reason with and convince these inconsequential puppets, by writing and debating about SHS, against smoking bans and their economic impact, about eternal battle between liberty vs tyranny, even about global warming or some such. That is exactly what the puppetiers want us to do, knowing well that it will lead us nowhere and that in fact it only helps spread their mind-toxin among our fellow smokers. There is no time folks for it any more, we already have this stealthy prohibition upon us.

The only approach that will work is to urgently inject the antidote for these mind-toxins, which is expressed concisely as -- replicate as quickly as possible the understanding that "Smoking is Good for You" among our fellow smokers. It helps, of course, that the message carrying this understanding is true, scientifically and for each of us empirically, through our own experience. Without neutralizing the mind-toxins first, we cannot organize in order to exterminate the antismoking vermin.

The larger strategy on how to replicate this understanding still stands (see also here and here), except that this cannot wait. As for myself personally, due to present and transient time constraints, I can only spread the word informally and briefly, in different smoker forums, lighting thus the little fires in hope some will spread on their own after I have moved to the next one. Those who share or resonate with the priorities stated above and themselves have no time or resources to create and maintain a formal organization, ought to do the same -- visit all new pro-smoker sites and boards, post links to "Smoking is Good for You" materials and discuss a bit with folks there, ask others to join you in doing the same, then move on to the next unvisited place. Those with artistic talents and skills should create videos on this subject and post them on YouTube.

As for FORCES and other smoker organizations, lets hope their leaderships will think this through and refocus their efforts exclusively on formulating and delivering the antidote for the antismoking mind-toxins to the fellow smokers. The first and most potent enemy, the one within each of us, has to be dealt with first. Otherwise, there will be no hammering without a strong muscle (the 2+ billion world smokers) and a willing mind behind it, to hold and swing the hammer.
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Postby nightlight » Thu Jun 05, 2008 10:52 am

Dee wrote:Thanks for the link!


Here is another one for your reference -- on FreeRepublic site (where I posted on & off since 1997), a smoking thread got going and I asked if someone could show me a single experiment demonstrating that smoking causes lung cancer. So a guy brings up a 2005 paper claiming, judging by its abstract and intro section, to show just that on mice. After reading a bit down into the paper, it turns out the smoking mice lived significantly longer and kept their youthful figures into the ripe old age. This is despite the fact that they smoked at least 4 pack/day equivalent, all highly concentrated into 6 hour asphyxiating, no breaks, whole body smoke exosures, which is 15-20 times more concentrated and intense than a human smoker would experience.

Buried deep on page 2006, they admit in words the real finding on the effect of tobacco smoke on the health & longevity (the "sham-exposed" mice was the one exposed to HEPA filtered plain air):

"In spite of the higher lung tumor incidence and multiplicity in CS-exposed mice, survival of these mice was significantly longer than for the sham-exposed mice. Longer survival in the CS-exposed mice is likely a sequela of the lower incidence and delayed onset of other types of fatal neoplasia, in part due to the reduced body weight in these mice."

Here is the survival graph from that experiment:

Image
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lung cancer in people

Postby gary k » Thu Jun 05, 2008 11:51 am

I realize that there is some overlap in the cigarette and cigar smokers groups;but, I do not think it is enough to make a real difference.

Gary K.

Most lung cancer statistics lump smokers and all x-smokers together, this group is one of the very few that separates smokers/x-smokers/never smokers into individual entities.

http://www.lungcanceralliance.org/washi ... _sheet.htm

In fact, non-smokers now account for nearly 20 percent of all new
lung cancer cases and over 50% of new lung cancer patients are former smokers, many of whom quit decades ago, says the Alliance for Lung
Cancer (Alcase), a Vancouver, Wash.-based non-profit group.

http://stopsmoking.uchicago.edu/benefits.html
Chicago STOP Smoking Research Project

Benefits of Quitting Smoking
Health benefits from quitting smoking:

lung cancer death rate decreases by half in 5 years, and is similar
to that of nonsmokers after 10 years



The American Lung Association
http://www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=33568

Long-term Benefits of Quitting
At 10 years:
risk of lung cancer drops to as little as one-half that of continuing
smokers
At 15 years:
risk of death returns to nearly the level of people who have never
smoked(note: this statement would include Lung Cancer death!-Gary K
.)

http://apps.nccd.cdc.gov/brfss/Trends/trendchart_c.asp?
state_c=US&state=IL&qkey=10000&SUBMIT1=Go

http://www.statehealthfacts.org/compare ... d=80&cat=2

According to the CDC,there has actually been very little decrease in
the percentage of the population that smokes since about 1990.
1965 = 46% smoked
1990 = 23% smoked
2002 = 23% smoked
2006 = 20.1% smoked

About 90% of ex-smokers had quit by 1990.(23 of the 25.9%)

Thus, almost 90%of all ex-smokers would have the same risk for lung cancer as never smokers.

http://www.statehealthfacts.org/compare ... d=80&cat=2
Adult Smoking Rate(cigarettes)
United States 20.1%

ACS Cancer Report 2008:
In 2005, 6% of adults aged 18 and older had smoked
cigars in the past month.

I understand that pipe smokers are only 1% of the adult population.

There are about as many x-smokers as smokers. 10% of the x-smokers have a risk of lung cancer somewhat approaching smokers = 4.5 million.


There are about 225 million adults in the USA.
Cigarette smokers at 20.1% are 45.23 million.
X-smokers = number of smokers = 45.23 million.
Cigar smokers at 6% are 13.5 million.
Pipe smokers at 1% are 2.25 million.
X-smokers that quit with in the last 15 years are 10% of x-smokers = 4.5 million.

Total number of smokers plus x-smokers with about the same risk for lung cancer = 66 million.

66 million is 29.3% of the 225 million adults in the USA.

Thus we have 70.7% of the adults(non-smokers/x-smokers with same risk factor) getting 70% of the lung cancers and 29.3% of the adults(smokers/x-smokers with the same risk factor) getting 30% of the lung cancers.

This is rather close to the same ratio(1 to 1) for both groups of the adult population.

Conclusion: I respectfully submit that smokers have no greater risk of getting lung cancer than non-smokers
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Postby nightlight » Sat Jun 14, 2008 3:54 pm

Thanks Gary for all the useful data. Your and Stephanie's pages have become quite handy, informative destinatins to send people to from various smoking discussions on FreeRepublic and Liberty forum (see ongoing thread there).
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Postby Ariel » Wed Jun 25, 2008 7:02 pm

I was thinking about the "healthy smoker" effect. That's what they call it whenever epi smoking studies turn out the "wrong" way. That is, they argue that smokers have the better outcome because only relatively healthy people would continue to smoke and the "unhealthy" are weeded out of the smoking group. Ya know? (Nice to have all your bases covered smokers do better? "Healthy smoker effect" Smokers do worse? smoking is unhealthy.)

Whatever.

Anyway -- I came across this little tidbit ...

http://www.chestjournal.org/cgi/content/full/123/3/660

"A systematic review of cross-sectional epidemiologic studies of spirometric lung function showed consistently that healthy (ie, asymptomatic) smokers had higher lung function values than did their nonsmoking counterparts. "

(Gee.. but do they conclude from this that smoking enhances lung function? Of course not... )


"This may also be explained by a similar hypothesis that subjects with higher lung volumes are more likely to tolerate the acute effects of cigarette smoke and then go on to become long-term smokers. The missing piece in this intriguing puzzle is what determines the adverse effects of smoking that are observed in only about 20% of long-term smokers."

How interesting.
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Postby nightlight » Wed Jun 25, 2008 7:31 pm

The "healthy smoker effect came up in the thread at Dr. Siegel's blog, where I entered last week to criticize Doc's article and defend position "smoking is good for you." Having tossed the gauntlet at the residnet "experts", including the Doc himself, who all made careers out of antismoking scaremogering, after the 290+ posts of this interesting debate I haven't had to retract or back off on anything I said there. They don't have any real science on their side and they know it.
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Postby Ariel » Wed Jun 25, 2008 8:24 pm

I had forgotten that -- that it came up with regard to the potroom workers. in fact, I guess it's what started me thinking about it.

(I dislike Siegel's blog very much -- but I made an exception and have been posting just on that thread.)

"haven't had to retract or back off on anything I said there"

Noo.. but it's been quite circular (IMO). Good grief you have much patience, nightlight. I keep wondering, "How many times must one explain the same friggin thing?" (Okay, got that out of my system, whew!).

I know, explain til they finally get it, I guess.

Is it my paranoia?, or did he throw out a record(?) number of new blog posts real quickly to bury that thread?
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Postby Ariel » Mon Jun 30, 2008 1:45 pm

Forces reported on this AADT study a few days ago on the news page -- and I've been puzzling over it since.

I welcome anyone who cares to puzzle with me. Really, I'm trying to figure out what this is really saying. I also wish I had access to the original rather than just the report (as usual) but I don't.

http://www.medscape.com/viewarticle/575125

Among carriers, the risk of developing lung cancer was similar regardless of smoking history. The risk for lung cancer in carriers was 2.2 times the risk in noncarriers, after adjustment for confounders that included a history of unspecified COPD. [<--Note -- does this mean overall, or is this the figure for non-smokers?] Carriers who were light smokers had a risk for lung cancer that was more than 2 times greater than the risk for noncarriers; carriers who were moderate to heavy smokers had a risk 2.3 times greater than noncarriers.


What does "similar" mean? Was 2.3 significantly different from 2.0 or 2.2?

We also have this:

A history of COPD increased lung cancer risk 2.5- to 5.9-fold among smokers and nonsmokers, with the greatest influence in never smokers


Also, so COPD increased LC risk more in never smokers... and they adjusted for COPD in comparing carriers by smoking status...

Oh.. my brain is hurting....


The researchers estimated that AATD carrier status might account for 11% to 12% of the lung cancer in patients who participated in this study.



So that means if the "risk" was similar in carriers and non-carriers, then they are also admitting that 11-12% of LC's in smokers are unrelated to smoking? (I believe that the rest of them are unrelated to smoking too -- but 11-12% is a start).

Okay -- now, the next quote was earlier in the report -- but I'm having difficulty reconciling it with the above findings. Can anyone explain? It sounds like its presented as fact, rather than "we previously hypothesized..." -- but seems to contradict the actual findings?

AATD is one of the most common genetic conditions affecting people in the United States, particularly those of European descent. Among homozygous people, it can lead to early-onset of emphysema; heterozygous people might be unaware of their status as carriers and generally do not experience AATD-related diseases. However, carriers of AATD might be more vulnerable to the carcinogenic effects of tobacco smoke than the general population, especially when their levels of alpha1-antirypsin are compromised by physiologic stress or if they already have some degree of lung-tissue damage.

The authors note that the development of lung cancer is a complex and multistage process that involves numerous factors that are intrinsic and extrinsic to the host. Noxious substances in tobacco smoke can damage the DNA of cells and also stimulate an inflammatory response in the lung. Conversely, host mechanisms can inactivate harmful substances in tobacco smoke, remove or repair damaged DNA, and adapt the stimulants by structural changes in the lung tissue. The underlying mechanism of lung cancer encompasses an intricate interplay of these factors.



HELP?????
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Postby nightlight » Thu Jul 03, 2008 3:25 pm

Ariel wrote: Noo.. but it's been quite circular (IMO). Good grief you have much patience, nightlight. I keep wondering, "How many times must one explain the same friggin thing?" (Okay, got that out of my system, whew!).


The best and most useful discussions arise in politely hostile environments. Just few days ago, in another 'health forum', someone asked about 'remedy for aging'. Some local know-it-all offered a list of things to do or not do, which included advice not to smoke. Since tobacco smoke is the most potent youth elixir and life-extending substance known to humans, I couldn't resist but take him on and an interresting discussion errupted.
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