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 epidemiological 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. You can find previously
cited Therapeutic Effects of Smoking and Nicotine in the FORCES International
archives. An easy-to-read but well-referenced paper is ONE FEELS BETTER
TEMPERED: An Investigation Into The Beneficial Effects Of Smoking

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. Richard 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 its 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 aging. The researchers think that this may be a
defense 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 Institute 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?s=&act=ST&f=169&t=15654&st=20&#entry170219
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.

From CO-RMs: Therapeutic Carbon Monoxide Releasing Molecules (Monday, October 22, 2007;
medGadget, Internet journal of Medical Technologies):

Carbon monoxide (CO), a silent and powerful poison gas, might actually lend itself for a variety of
promising clinical applications, according to the researchers from Sheffield University in the UK.
Professor Brian Mann and colleagues from the University's Department of Chemistry and
hemoCORM Ltd, a spinout company, are working on water-soluble molecules that can deliver CO
to tissues to "reduce inflammation, widen blood vessels, increase blood flow, prevent unwanted
blood clotting and even suppress the activity of cells and macrophages which attack transplanted
organs," according to the university's press release.
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 insulin 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.)

For asbestos workers, "Effect of Smoking on Immunological Abnormalities in Asbestos Workers"

(Institute of Immunology and Experimental Therapy, Poland) by Lange, A.:

Smoking has a protective effect on immunological abnormalities in asbestos workers.

More for asbestos workers is found in "Cancer of the Lung Among Asbestos Factory Workers"
(University of London, School of Hygiene and Tropical Medicine), relative risk of lung cancer for
asbestos workers was "highest for those who had never smoked, lowest for current smokers,
and intermediate for ex-smokers. The trend was statistically significant. There was no
significant association between smoking and deaths from mesothelioma,"

And again in The Interaction of Asbestos and Smoking in Lung Cancer by G. BERRY1, and F. D.
K. LIDDELL (Oxford Journals, Medicine, Annals of Occupational Hygiene, Volume 48, Number 5,
p. 459-462, 2004):

Conclusion: The excess relative risk of lung cancer from asbestos exposure is about three
times higher in non-smokers than in smokers. The modified measure has been placed within a
more versatile model of interaction. If interaction is present the relative risk from asbestos
exposure changes only slightly between light and heavy smokers, but is higher in very light
smokers and non-smokers.

Many other studies show protective effects of smoking for asbestos workers. Similar effects are
found for other lung cancer risk factors, including radiation and chemical cancerogen exposures. For
example:

From "Lung Cancer Dueto Chloromethyl Ethers" (Hahnemann Medical College and Hospital,
Philadelphia) by Weiss, W., "Over the 22 years of follow-up, exposed workers have had a very
high risk of respiratory cancer, mostly of the lung. The risk has been dose related and has
been much higher in nonsmokers and ex-smokers than in current smokers. The epidemic
began to subside shortly after exposure to chloromethyl ethers ceased. The mean induction-
latency period was 17 years. Most of the lung cancers in the moderate and high dose groups
have been small cell carcinoma,"

From "Respiratory Effects of Exposure to Diesel Emissions in Underground Coal Miners" by Ames,
R.G. (DHHS, PHS, CDC, NIOSH. Funding: NIOSH), "Presence of chronic respiratory
symptoms at baseline was inversely related to cessation of smoking. Respiratory impairment
was positively associated with smoking cessation, but failed to reach statistical significance,"
Reduces schizophrenia 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/PIIS0920996404002130/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."
Evidence that smoking is protective against thyroid cancer

Prepublished from the American Journal of Epidemiology (Sep 2007). From the abstract of
pubmed's Alcohol Drinking, Tobacco Smoking, and Anthropometric Characteristics as Risk Factors
for Thyroid Cancer: A Countrywide Case-Control Study in New Caledonia. (Unité 754, INSERM,
Villejuif, France) by Guignard R, Truong T, Rougier Y, Baron-Dubourdieu D, Guénel P., quote
(emphasis added):

Exceptionally high incidence rates of thyroid cancer are observed in New Caledonia, particularly in
Melanesian women. To investigate further the etiology of thyroid cancer and to clarify the reasons
of this elevated incidence, the authors conducted a countrywide population-based case-control study
in this multiethnic population. The study included 332 cases with histologically verified papillary or
follicular carcinoma (293 women and 39 men) diagnosed in 1993-1999 and 412 population controls
(354 women and 58 men) frequency matched by gender and 5-year age group. Thyroid cancer was
negatively associated with tobacco smoking and alcohol drinking, but no inverse dose-response
relation was observed. Height was positively associated with thyroid cancer, particularly in men.
Strong positive associations with weight and body mass index were observed in Melanesian women
aged 50 years or more, with an odds ratio of 5.5 (95% confidence interval: 1.5, 20.3) for a body
mass index of 35 kg/m(2) or greater compared with normal-weight women, and there was a clear
dose-response trend. This study clarifies the role of overweight for thyroid cancer in
postmenopausal women. Because of the high prevalence of obesity among Melanesian women of
New Caledonia, this finding may explain in part the exceptionally elevated incidence of thyroid
cancer in this group.

A Few Words of Caution Concerning Filters

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.

Much of "addiction" propaganda is aimed at uneducated. While it is true that smoking causes
permanent changes in brain (and in other tissues), so does remembering you birthday or your last name
or your native tongue. Your entire life is an irreversible unfolding at biochemical, psychological,...
economic, social levels.

The relevant question is not whether changes are permanent (they mostly are) but whether the changes
in your biochemical network induced by tobacco smoking are good or bad for you. All the hard science
from antismoking research itself, indicates that tobacco smoking has protective, invigorating and
rejuvenating effects on the nervous systems, central and peripheral. In particular regarding the
"addiction" causing changes above, tobacco smoking does increase the numbers of nicotinic receptors
(which are one of the two main types of cellular receptors; these receptors exist in everyone, unrelated
to smoking despite historically accidental suggestive name).

These nicotinc receptors are vital for functioning of not just brain but of perhipheral nervous system and
ultimately of every cell and organ in your body. Their numbers and functionality decline with age, most
dramatically in people with dementias (such as Alzheimer's and Parkinson's). As with MAO levels
discussed in the first post (which increase with age, like a gunk in a high precision machinery), the
number of well functioning nicotinic receptors is another clock defining your real biological age -- the
more well functioning nicotinic receptors you have, the younger and more vital you are. The permanent
increase in number of these receptors induced (in the long run, not instantly) by tobacco smoke is most
certainly good for you.

What the antismoking propaganda refers to is the fact that nicotine itself occupies temporarily these
receptors, making thus fewer available for acetylcholine for a brief time. This is no different than if you
lift a weight, some of muscle cells are certainly temporarily occupied by lifting a "useless" weight. Yet,
lifting weights is good for your muscles since in response to periodic increase in their load, they
upregulate all biochemical systems needed to support greater load. Hence nicotine from tobacco smoke
is a workout for your receptor system, which strengthens it over time. Note that nicotine from patches
or other slow delivery systems peddled by pharmaceutical industry doesn't work here nearly as well,
since it acts more like getting hold of a weight and holding it up for 10 hours -- it is not a real weight
lifting exercise but something which will likely harm your muscles. The nicotine levels from smoking
tobacco oscillates and thus it is more like taking 20-30 exercise breaks every day, which is a much better
way to do it.

You will find the same sleight of hand used for most other effects of tobacco smoking, as illustrated
earlier on glutathione example (the same goes for CO and NO, neutrophyls, oxygen & blood supply to
heart,...) -- they take a momentary snapshot of some oscillatory effect of smoking, pick the most
convenient phase in the process and measure the change, such as decline in some resource and then
declare: this is what smoking does to this resource - it depletes it.

While it would certainly be bad for your were that were all that is happening to the resource, that is not
all that is happening -- the smoking causes oscillation on all such resources and with live systems this is
good for them, since it represents a workout of the production & support systems for the resource,
strengthening them and upregulating the supplies over time. The recent hoopla on negative
cardiovascular effects of secondary smoke after only 30 seconds of exposure is also the gimmick of this
kind -- they were talking about the transient mild reduction in reserves of blood carrying capacity to
heart, which is actually a very positive effect -- that's why people do aerobics in the first place, to reduce
the reserves temporarily so that the suppplies would get upregulated in the long run. Using this kind of
"logic" one could also "prove" that sleep is bad for you, since during sleep many of the systems we value
for our productive life reduce acitivity or shut down altogether.

Just as exercise is "addictive" or having a family is "addictive" or eating and breathing are "addictive" so
is the smoking -- people seek it because it is good for them. I wrote a bit more on the smoking
"addiction" on another forum.

quote:
I've come across information lately that has led me to believe that meat eating and smoking is more
analagous than most would probably believe. Humans began eating meat because it had a survival
benefit that boosted the evolutionary process. The high protein yielded from meat consumption gave
homo sapiens the muscular strength and endurance to prevail and survive. In other words,
hypothetically, if one were to look at it "naturally" at the time, one could say "humans aren't meant to
eat meat. Humans have always been herbivores."
...
In summary, the idea of something being "natural" should not have to meet the simple definition of
being "organically and historically pre-justified". Just because humans do it now and didn't do it before,
is not a reason to summarily dismiss anything. Humans don't just simply adapt to their environments,
but adopt them and carry them forward into future generations. One could further argue that humans
have become advanced enough to create greater complexities to adopt into themselves, thus carrying
the adoption of the symbiotic relationship into the next generation, and further, for a survival benefit.

In this way, what doesn't kill you, makes you, and those who follow you, stronger.

Nice observations. When I hear "humans aren't meant to..." from antismokers and other 'god
wannabes', I usually ask them whether human hand was "meant to" type on keyboards or just to hold
branches, pick fruits and insects and such. The major advances in any realm occur precisely when the
systems find a way around "what was meant" and do something which "was not meant" while
extracting the net benefit from it.

The deaths attributed to smoking are statistical deaths. The percentages attributed to smoking were
obtained by the ACS CPS study. This study followed over a million volunteers who filled out survey forms
about their smoking habits. When they died the cause of the death is determined from their death
certificate. This allows one to obtain the risk ratios which are used to calculate yearly Smoker Attributed
Mortality. The alternative would be to perform an expensive autopsy. It may be impossible for the
pathologist to determine whether a lung cancer death was due to environmental smoke, tobacco or a
chance mutation. An ideal statistical study would compare smokers, non smokers and former smokers.
As much as possible, everything else would be the same. For example, one would not want to compare
non-smoking doctors with smoking asbestos workers.

Data from the CDC and the NHTSA has shown that non-smokers do not live longer than smokers.

The average age of death from all causes was 71.1 years,
http://www-nrd.nhtsa.dot.gov/Pubs/98.025.PDF

The average age of death for smokers is about 72.

http://www.cato.org/pubs/regulation/regv21n4/lies.pdf

Smokers and never smokers are diagnosed with lung cancer at about the same age!!

http://jco.ascopubs.org/cgi/content/full/25/5/472
From the same study.
I found this interesting:

"Adenocarcinomas seem to be more common in never smokers, light smokers, and former smokers,
whereas squamous cell or other histologic types are more common in heavy smokers and current
smokers.27,33,34

Furthermore, the prevalence of adenocarcinoma among lung cancer patients increases with years since
quitting smoking.35

Likewise, our data show a higher proportion of adenocarcinoma among never smokers than among
former or current smokers (Table 2)."

Why would a former smoker be more likely to get the 'never smoker type lung cancer' if his former
smoking caused his lung cancer?

Smokers have a 50% less risk of Alzheimer's and a 73% less risk for Parkinson's Disease.

HEART DISEASE

What about heart disease, then? It's on the cigarette packet in capital letters:
SMOKING CAUSES HEART DISEASE.

The most authoritative study on this is certainly the Framingham Heart Study, which is known as the
Rolls Royce of studies.

When information about certain of the other 300 risk factors for heart disease were taken into account,
the relationship between smoking and heart disease was lost.

LUNG CANCER

Finch GL, Nikula KJ, Belinsky SA, Barr EB, Stoner GD, Lechner JF, Failure of cigarette smoke to induce or
promote lung cancer in the A/J mouse, Cancer Lett; 99(2):161-7 1996

No matter how much tobacco smoke they made poor animals inhale, even in equivalents of a carton or
more per day (through surgically implanted breathing tubes), the more they smoked the fewer lung
cancers they get. It just doesn't work and it even contradicts their "theory" so they just gave it up.

With humans, we can't force them to smoke, or even not to smoke, hence the next best thing, closest to
hard science, are randomized intervention trials -- you take a group of smokers, assign half of them
randomly into a 'quit group' (strongly advised not to smoke), and a 'control group' (left alone, to smoke
as they wish), then follow them up for some years or decades, observe the smoking rates (which are
normally lower in 'quit group') and check for lung cancers or other diseases.

That was done, of course, but only a handful of times in the early years of antismoking "science". As with
animal experiments, the results of these few randomized intervention trials,whenever they showed
anything at all, also went the "wrong way" -- the 'quit group' ends up with more lung cancers than the
'control group' (and generally higher death rates).

Professor Burch, in a letter to the British Medical Journal (March 1985) pointed out that in these two
studies:

In the low smoking intervention groups 56 cases of lung cancer were recorded in a total starting
population of 7,142 men (0.78%); the corresponding number for the more heavily smoking normal care
groups being 53 in 7,169 (0.74%).

Findings for cancer other than those of the lung were even more surprising.

Some 88 cases (1.23%) were recorded in the low smoking intervention groups, but only 60 cases (0.84%)
in the normal care groups. Thus in the category 'all cancers' there were 144 cases (2.02%) in the
intervention groups but 113 cases (1.58%) in the more heavily smoking normal care groups.

Reduced levels of smoking were associated with increases in cancer incidence.

Ever wondered how much of a cigarette's smoke we actually inhale?

Research using myself as the test subject:

There are about 28 puffs per cigarette(5 cigarette average).

I smoke 6 puffs per cigarette(10 cigarette average).

Mainstream inhalation is 21% of the total cigarette smoke(6 divided by 28).

I breathe 9 breaths per minute plus 1 smoke inhalation per minute.

Breathing in averages about 1.5 seconds.

Smoke inhalation is about 2 seconds.

Inhaling/breathing in take about 15.5 seconds per minute or about 25%, about 75% of the smoking
minute is spent exhaling or between breaths.

At two feet from an ashtray, SHS seems to dissipate to about 16% of it's original density.

(Note:smoke coming from the tip of a cigarette is a hot gas. Hot gases will expand to fill the space
around the point of origin. 4ft x 4ft x ft = 64 cubic ft.thus,smoke will be 1/64th as dense or 1.6% as
dense. I went to 16% to err on the side of caution and to make the math easier.)

I breath in only 25% of the time and thus get about 4% of the SHS.

Mainstream smoke of 21% plus SHS of 4% means that I inhale about 25% of the total smoke from a
cigarette.

What does this mean in the real world?

Please consider these facts.

According to a study done for the 'Mass. Dept. of Health', the total smoke(mainstream and sidestream)
from a cigarette contains 32 nanograms (ng) (ppb) of Arsenic.

I inhale 25% of this or about 8ng per cigarette.

The EPA says that a level of Arsenic equal to 10 ppb(ng) in drinking water is safe. This is 10ng per gram.
There are 28.35 grams per ounce;thus 283.5 ng per ounce is a safe level of exposure to Arsenic.

An 8oz glass of water could safely contain 2,268ng of Arsenic.

I would have to smoke 283.5 cigarettes to inhale enough Arsenic to be equal to the safe amount of
Arsenic that the EPA allows in drinking water.

That's a pack a day for 2 weeks!!

The FDA's safe level for Arsenic in eggs is 500ppb(ng).

This is 14,175 ng per ounce.

An egg weighs about 2oz and could safely contain 28,350ng of Arsenic.

At 8ng per cigarette, I would have to smoke 3,544 cigarettes to equal the amount of Arsenic the FDA
says is safe in an egg.

At a pack a day that would be 177 packs of cigarettes or about 25 weeks(over 6 months)worth.

A non-smoker sitting 2ft from a cigarette in an ashtray would be exposed to the same 4% of the SHS as
the smoker and thus be exposed to 1/4th the total amount of smoke as the smoker.

That non-smoker would have to be exposed to the SHS from 1,134 cigarettes to equal to the safe
amount of Arsenic in a glass of water and 14,176 cigarettes to equal the safe amount of Arsenic in one
egg.
(Note: their actual exposure is way less nad the cigarette equivalent much,much higher. I just do not
know how to figure it out. )

However, The surgeon General said there is no 'safe level of exposure' to SHS and we now have a
smoking ban in Illinois to show for it.

This message has been edited. Last edited by: gkayser30, Fri January 11 2008 04:32 PM

THE TRUTH ABOUT SMOKING CAUSED DISEASES:

TRENDS AND INCIDENCE RATES

If smoking was bad for us and caused heart disease and cancers, as the anti-smokers claim,; then, the
fact that smoking rates have decreased by 50% over the last 40 years should bring about an equal
decrease in heart disease and cancer incidence rates.

This decrease has not happened!!

http://www.nj.gov/health/ces/reports.shtml

Data,Statistics and Reports:

Trends in Cancer Incidence and Mortality in New Jersey, 1979-2002 [pdf 312k] (11/28/05)
NOTE: U.S. rates are also shown.

Tables 5+6,pages 46 and 47

Total cancer incidence rate- U.S.(per 100,000)
1979 male + female total = 861.5
2001 male + female total = 963.4
2004 male + female total = 970.9

www.cdc.gov.mill1.sjlibrary.org/nchs/data/hus/hus06.pdf[/URL]
Health,United States,2006
Page 229
Table 39 (page 1 of 3). Death rates for malignant neoplasms of trachea, bronchus, and lung, by age:
United States, selected years 1950–2004
[Data are based on death certificates]
All persons: Deaths per 100,000 resident population
All ages, age-adjusted
1970.........2004

37.1.........53.2

This is a 43% increase in lung cancer deaths!!

Smoking can not be the major cause of lung cancer!!

HEART DISEASE
http://www.proteinpower.com/drmike/uncategorized/cancer...disease-and-smoking/

The AHA doesn’t particularly want us to know about the incidence of heart disease; they just want us
to know that deaths from it are declining. To find the incidence you have to go to a table called Hospital
Discharges with Cardiovascular Disease as the First Listed Diagnosis.

Hospital Discharges With Cardiovascular Disease as the First Listed Diagnosis

United States: 1979-2003

1969 = about 3,200,000

2003 = 6,434,000

As you can see the rate of these discharges is increasing. When you correct for the increase in
population over the years, the line doesn’t increase as rapidly, but still increases slightly. What does
this mean? It means that despite a 50% decrease in smoking rates, that the number of people
developing heart disease hasn’t dropped at all. If anything it has increased.
Smoking can not be the major cause of Heart Disease!!!
This message has been edited. Last edited by: gkayser30, Sat February 23 2008 07:31 AMSat February 23
2008 07:31 AM

EMPHYSEMA and BRONCHITIS (COPD)

This is from the "American Lung Association(ALA)", we know that they would not lie as they are a public
health organization and only interested in our welfare.

TRENDS IN CHRONIC BRONCHITIS AND EMPHYSEMA MORBIDITY AND MORTALITY;

AMERICAN LUNG ASSOCIATION;

EPIDEMIOLOGY & STATISTICS UNIT;
RESEARCH AND PROGRAM SERVICES
MAY 2005

COPD Age Adjusted Death Rates Population, 1979-2002

Age-Adjusted Death Rate per 100,000 Persons
1979..... 2002
24.2.......42.0

NOTE: Smoking has gone DOWN by almost 50% over the last 40 years, over the last 20 plus years the
COPD death rate has GONE UP BY 74%.

Yet, the ALA and other health advocates say that smoking causes Emphysema!!!!

Clearly, smoking does not cause Emphysema and Chronic Bronchitis.

Smoking and the Asthma Epidemic:

The most recent study to exonerate smoking and tobacco smoke as a cause of asthma was published in
the British Medical Journal July 8, 2000.

In this 20-year, inter generational study, researchers found that the rate of asthma had doubled
between l976 and l996, even as the smoking rate dropped by half during that same period. Asthma
and hay fever increased for both smokers and non-smokers, but the increase was higher for non-
smokers. The steep rise in asthma was dramatically underscored by the fact that prescriptions for
steroid inhalants for treatment of the disease rose more than six-fold between l980 and l990 alone.

This pattern of precipitous increases in asthma coupled with significantly diminishing smoking rates is
not unique to the population described by the Scottish researchers in their BMJ article.
In the United States, too, the incidence of adult and childhood asthma has climbed to an unprecedented
high during the past twenty years, while smoking and exposure to environmental tobacco smoke [ETS]
have decreased significantly during the same period.

"...Between 1980 and l995, the number of people reporting asthma in the U.S. more than doubled (from
6.7 million to 13.7 million), a 75% increase in the rate per 100,000 population.
The Centers for Disease Control estimates the l998 rate at 17.3 million, a 150% increase since 1980.

"...Between l980 and l995, the adult smoking rate decreased from 33.2 to 24.7, a drop of 25%. In the
late l990s the overall smoking rate has remained steady at between 24 and 25 percent of the adult
population, far less than its peak of 42.6% in l966. The inverse relationship between asthma rates and
smoking and between asthma rates and exposure to ETS can be seen quite clearly.

Smoking and SHS cannot be causing Asthma!!

Smoking: addiction or habit? http://www.forestonline.org/output/page134.asp

USING the modern sense of the word 'addiction', it is now widely accepted (even by some tobacco
companies) that nicotine is 'addictive'.

Unfortunately the word is now used so often - in relation, for example, to sex or chocolate or even
television - that it is largely meaningless.

The late Professor Hans Eysenck, one of world's leading psychologists, argued that 'Smoking is not an
addiction because the term 'addiction' really has no scientific meaning ... You can call anything addictive
which a person does routinely and which he would be sorry to stop doing and which might have all sorts
of repercussions on his mental and physical life.'

Using the more traditional definition ('a habit that has become impossible to break', Chambers
Dictionary, 1992) it is even easier to argue that smoking is not addictive. Professor John Davis (University
of Strathclyde) put things in perspective when he said, 'What I don't agree with is the idea that people
who use nicotine become ... helpless addicts who have no say in the choice of this activity - that the
nicotine compels them to smoke.

The evidence is simply not there. People give up smoking all the time ...' Smoking and common
sense’

The February,2008, American Cancer Society Report

Cancer facts and Figures 2008
page 49

Among adults aged 18 and older in 2006, national or state data showed:

• An estimated 45.7 million adults were former smokers,representing 50.2% of persons who ever
smoked.

Dr Tage Voss, author of Smoking and Common Sense (1992), agrees. According to Voss, tobacco
consumption is a habit not an addiction because it doesn't conform to the criteria of addiction that
consumers exhibit 'social collapse, mental dissolution and require an escalation of dosage'.

In other words - and unlike alcohol or drugs such as heroin or cocaine - nicotine does not dramatically
change people's behaviour patterns. Unlike those who are addicted to heroin, for example, there is no
evidence that consumers of tobacco are so desperate for their next 'fix' that they have ever mugged
anyone for the money to pay for it.

Likewise, on an average Friday or Saturday night, it is alcohol not nicotine that is responsible for hospital
casualty departments being rather busier than usual.

Interestingly, in 1996 Dr Sandy Macara, the then chairman of the British Medical Association and a
former smoker, wrote (Western Daily Press), 'I don't accept that smokers are truly addicted to tobacco. I
think they have a habit ... I believe the majority of smokers could stop tomorrow - no, today - if they
really wanted to.' Language of addiction

Dr Macara was possibly influenced by his own experience of giving up and by a BMA handbook, 'Help
Your Patient Stop', which stated that 'A balance needs to be struck, acknowledging the potential
difficulties of stopping as well as the ease with which many smokers manage to stop.' That was
published in 1988 when 2,000 people a day were said to be giving up.

For once the evidence is in the statistics. In the 1950s 80% of all men smoked. Since then the figure has
dropped to just 28% of men and 26% of women.

In total eleven million people have given up smoking in Britain alone, hardly the sign of a nation
addicted to nicotine.

Why the addiction argument is so popular

There's a great deal of hypocrisy surrounding the addiction argument.

After all, if smoking is so addictive why does the anti-smoking lobby try so hard to ban smoking in all
public places? Surely, if smokers are as addicted as they say, prohibition is simply going to increase their
suffering.

No, the reason the addiction argument is so popular among anti-smokers is because it takes away the
important concepts of free choice and personal responsibility.

By arguing so vociferously that smokers are 'slaves to the weed', the anti-smokers are trying to
undermine the idea:

"that by choosing to smoke,adult smokers are old enough to decide their own lifestyle and are merely
exercising their own free will."

This in turn gives anti-smokers the excuse to insist that the state must apply the tightest restrictions on
smokers 'for their own good'.

What the killjoys cannot accept is that a great many people enjoy smoking and take pleasure from it.

The fact that they smoke has NOTHING to do with addiction.

quote:

the Japanese and Isreali people have very high smoking rates and much lower lung cancer death rates
than the US, economic and environmental factors have a much greater impact on LC incidence and
death rates than does smoking.

..............................

In case your are curious.

lung cancer death rate(lcdr)
http://www.kidon.com/smoke/percentages3.htm
Smokers Prevalence(%)- LCDR/100,000 smokers
MALE
Japan--- 59.0 ('94)-- --- 81.2
Israel---- 45.0 ('90)----- 84.7
USA ----- 28.1 ('91)---- 305.7
FEMALE
Israel---- 30.0 ('90)------- 40.3
Spain---- 25.0 ('93)------- 21.6
USA------ 23.5 ('91)------ 157.0

The real question is just how much does smoking contribute to Lung Cancer and Lung Cancer Deaths?

The answer= NOT MUCH!!!

This information is not for the antis, they believe what they want to believe and no amount of 'Truth'
will influence them.

This is for the smokers and will help to free them from the decades of propaganda and brain-washing
that they have received.
Gary K.

This is 'THE TRUTH-5'.

We will use the map above and female smoking rates from here.
http://www.statehealthfacts.org/comparetable.jsp?ind=81&cat=2

In 'The Truth-4', we saw that American Indians/Alaskan Natives had a 35% higher smoking rate and a
28% lower LC Death rate than white smokers.

These a just a few of the dose-response comparisons that can be done.

Using the map and female smoking rates,we find that New York has a lower smoking rate than
Penn.(18.1%-22.3%) and about a 200% higher LC death rate!!

The Penn. smoking rate is about 100% higher than Calif's(22.3%-11.3%) and Calif has LC death rate that
is about 200% higher!!

Iowa and Neb both have a smoking rate slightly higher than does Fla(19.1%-18.8%) and Fla has a LC
death rate about 100% higher!!

Utah and Calif have about the same smoking rate(9.3%-11.3%) and Calif has a LC death rate that is about
300% higher!!

Do the smokers living on the coast of No.and So. Carolina smoke more toxic cigarettes??
lung cancer death rate(lcdr)
http://www.kidon.com/smoke/percentages3.htm
Smokers Prevalence(%)- LCDR/100,000 smokers
MALE
Japan--- 59.0 ('94)-- --- 81.2
Israel---- 45.0 ('90)----- 84.7
USA ----- 28.1 ('91)---- 305.7
FEMALE
Israel---- 30.0 ('90)------- 40.3
Spain---- 25.0 ('93)------- 21.6
USA------ 23.5 ('91)------ 157.0

For females we see that both Spain and Israel have slightly higher smoking rates and the USA's LC death
rate is about 700% and 300% higher!!

This message has been edited. Last edited by: gkayser30, Tue February 26 2008 11:34 AMTue February
26 2008 11:34 AM