Nicotine Benefits 2

NICOTINE and SMOKING BENEFITSBy Wanda Hamilton Researchers have long been aware that fewer smokers get Alzheimer's and Parkinson's diseases than non-smokers. Up to April l992, of the 17 studies on Alzheimer's and smoking which had been published in peer-reviewed journals, 13 reported a reduced risk for smokers and only four found no difference between smokers and non-smokers. Similar findings have been published on the effect of smoking and Parkinson's disease. In an article in The Times of London (9/7/93), Dr. James Le Fanu provided an examination of the research on smoking and its apparent protective effect for certain diseases. Dr. Le Fanu stated unequivocally: "Smokers have a 50 per cent reduced risk of developing Alzheimer's--and the more smoked the greater the protection." He also noted that emerging research points to a similar effect of smoking on Parkinson's disease. So striking was the apparent protective effect of smoking on Alzheimer's and Parkinson's that increasingly biomedical researchers are experimenting with nicotine to treat the symptoms of these dread disease in-patients who have been diagnosed as having them. Results from these experiments have all showed promise in alleviating the symptoms of these diseases with the administration of nicotine. The mechanism by which the nicotine in tobacco works to protect smokers is that it increases the number of so-called "nicotinic" receptors in the brain, which in turn influence the production and release of the neurotransmitter acetylcholine. Those who come down with Alzheimer's show a marked loss of "nicotinic" receptors in their brains and thus have reduced levels of acetylcholine, which is necessary for memory and other brain functions. Research has shown that tobacco smoke (and the nicotine therein) inhibits the activity of monoamine oxidase B (MAOB). Experiments on mice which were genetically engineered to be without the gene for MAOB "were resistant to the neurodegenerative effects of MPTP, a toxin that induces a condition reminiscent of Parkinson's disease," (Dr. Jean C. Shih researcher at the University of Southern California, as reported in Reuters, 10/7/97, "Isoenzyme Inhibited by cigarette Smoke May Have Role in Aging and Neurodegeneration"). The findings of Dr. Shih and her colleagues point to a protective effect from smoking on the aging of the brain. Other diseases for which smoking and nicotine appear to be protective are ulcerative colitis, Tourette's Syndrome, and possibly rheumatoid arthritis and colorectal cancer. Below are excerpts from some recent articles and studies on nicotine, Alzheimer's, Parkinson's, cognitive abilities, Tourette's and ulcerative colitis.

"In human studies, reported performance improvements with post-trial administration of nicotine have all involved associated learning (Mangan and Golding l883; Colrain et al, l992; Warburton et al, l992).... Nicotine improves performance by increasing the attentional resources available for such strategic processing," [Rusted JM, et al, "Facilitation of memory by post-trial administration of nicotine: evidence for attentional explanation," Psychopharmacology, 108(4):452-5, l992]. "1. Nicotine improves attention in a wide variety of tasks in healthy volunteers. 2. Nicotine improves immediate and longer-term memory in healthy volunteers. 3. Nicotine improves attention in patients with probable Alzheimer's Disease," [Warburton D M, "Nicotine as a cognitive enhancer," Progress in NeuroPsychopharmacology and Biological Psychiatry, 16(2): 181-91, Mar l992]

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"Researchers observed lessening of tic frequency and severity 3 minutes after subjects chewed [nicotine] gum, even more so at 10 minutes." [Rickards E H, "Nicotine gum in Tourette's disorder," American Journal of Psychiatry, 149(3):417, Mar l992. Note: the subjects were all children with Tourette's disorder]. "In humans, nicotine-induced improvement of rapid information processing is particularly well documented.... Preliminary studies have found that some aspects of the cognitive deficit in Alzheimer's disease can be attenuated by nicotine." [Levin E D, "Nicotinic systems and cognitive function," Psychopharmacology, 108(4):417-31, l992] "Improvement in attention, learning, reaction time, and problem solving have been reported.... Different processes, including attention, stimulus evaluation, and response selection, appear to be involved in the effect of nicotine on human information processing." [Le Houezec J, Benowitz N L, "Basic and clinical psychopharmacology of nicotine," Clinics in Chest Medicine, 12(4):681-99, Dec l991]. "Despite the absence of change in memory functioning, these results demonstrate that DAT [Alzheimer's disease] patients have significant perceptual and visual attentional deficits which are improved by nicotine administration." [Jones G M, Sahakian B J, et al, "Effects of acute subcutaneous nicotine on attention, information processing and short-term memory in Alzheimer's disease," Psychopharmacology, 108(4):485-94, l992]. "When you look at people who smoke, and people who don't smoke...you find those who smoke cigarettes are about half as likely to get Parkinson's disease." [Dr. David Morens of the University of Hawaii School of Public Health as quoted in "Stunned docs discover cigarettes stop Parkinson's," by Roger Field, New York Post, 6/15/95. Dr. Morens and colleagues examined 34 studies on smoking and Parkinson's. Their study was published in the June, l995 issue of Neurology]. According to a study conducted at Surrey University and published in the journal Psychopharmacology, smokers are more mentally alert at night than non-smokers. Rosemary Brook, spokeswoman for Surrey University's psychopharmacology unit, said, "The results showed that smokers were subsequently able to perform various tests of reaction, memory recall and other related tasks consistently better than the nonsmokers," [Reported on the BBC News, 4/8/98, "Cigarettes 'keep you sharp after dark'." In a presentation at the 151st annual meeting of the American Psychiatric Association (June 8, l998 in Toronto), Dr. Paul Newhouse of the University of Vermont reported on his research on treating Parkinson's disease with nicotine. "Preliminary analysis shows improvements after acute nicotine administration in several areas of cognitive performance." These areas included reaction time and central processing speed. The researchers also reported that after chronic use of nicotine on Parkinson's patients, motor function and the ability to move also improved. [Reported by Reuters, 6/8/98, "Nicotine patch promising for Parkinson's"]. "The influence of smoking on the risk of developing ulcerative colitis is well documented. Compared with lifetime nonsmokers, the risk is reduced in smokers...." [Tysk C, Jarnerot G, "Has smoking changed the epidemiology of ulcerative colitis?" Scandinavian Journal of Gastroenterology, 27(6):508-12, Jun l992]. "When association between cigarette smoking and UC [ulcerative colitis] are examined, never-smokers are approximately three times more likely to develop UC than smokers. A consistent finding from study to study is that quitters have a mildly increased risk of developing UC which suggests that cigarette smoking may have a protective effect," [Lashner B A, "Inflammatory bowel disease: family patterns and risk factors," Comprehensive Therapy, 18(8):2-4, Aug l992]. "It is beyond doubt that smokers are protected against ulcerative colitis, and the more that is smoked the greater the protection--so those on 25 cigarettes a day or more have a risk as little as one-tenth that of nonsmokers," (Dr. Martin Osbourne, surgeon at the Royal Free Hospital in London, as quoted in the Daily Telegraph, 9/7/93).

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THE ANTI-SMOKERS LIED ABOUT OSTEOPOROSIS AND ABOUT ESTROGEN Antismokers grasping at straws: Lying at any cost, even when all the evidence is against them The media flooded the country with the anti-smoker claim that smoking increases osteoporosis (Danielle HW. Osteoporosis of the slender smoker. Arch Intern Med 1976;136:298-304). There was no publicity when the claim was later refuted (Jensen GF. Osteoporosis of the slender smoker revisited by epidemiologic approach. Eur J Clin Investig 1986;16:239-242). The Danielle study used two "ill-defined" patient populations; the second included all 70 year-old women in nine suburbs of Copenhagen, and had more cases, 180 versus 72. The first asserted that there was no relation between weight and bone mass in non-smokers, while the second, and most other studies, have found correlation in both. Most importantly, there was no difference between smokers and non-smokers in the frequency of definite osteoporotic or other fractures. The smokers actually had fewer. Since all the cases were the same age, there is no way to use age adjustment to manipulate the data. Referring to smoking, another researcher has admitted, "this factor is a more manipulable one than some of the other factors which have been shown to be important in the etiology of fracture." A number of studies have found that smokers have slightly higher bone mass and density than nonsmokers, both pre- or post-menopausal. "No association between bone mass and smoking was observed. A subgroup with patterns of substantial combined tobacco and alcohol use having a lower mean bone mass could not be identified" (MF Sowers et al. Prev Med 1985;14:585-596). "Smoking history in pack years did not correlate with bone density at either skeletal site," spine or forearm (MM Luckey et al. J Clin Endocrinol Metab 1989;69:762-770). In the Framingham Study, Felson et al found that "Cigarette smoking was not associated with risk of fracture in any analyses including models without alcohol." This was in 217 cases, 174 of them female, in an ongoing prospective of over 40 years' duration 1988;128(5):1102-1110). (Felson DT et al. Am J Epidemiol

And in a study the next year which separately analyzed radiographs of the white, middle class Framingham subjects, and poorer, more nonwhite HANES I subjects, Felson also found a borderline statistically significant protective association between smoking and osteoarthritis, which was strongest in the heaviest smokers (Arthr Rheum 1989;32:166-172).

However, true to their anti-smoker psychosis, they had to find something bad to say about smoking. Although they admitted that very few of their subjects ever used estrogen, they claimed that smokers did not benefit from estrogen therapy on the basis of a mere 29 ever-users, 8 of them smokers. Never mind that this claim was opposite to that of a large 1982 study which claimed both big risks of fractures, and big benefits from estrogen for smokers. With this study, the anti-smokers could simultaneously fear-monger against smoking and promote pharmacological intervention. But in the "Nurses Study," (D Hemenway, AJPH Dec 1988;78(12):1554-1558), which is possibly

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Smoking and Lung Cancer Though there seem to be strong links between smoking and lung cancer, anti-tobacco propaganda often infers that smoking is THE cause of lung cancer, with the implicit message that if smoking could be eliminated, so could lung cancer. This is, of course, false. Smoking is by no means the only risk factor for lung cancer, and in some occupations cigarette smoking appears actually to help protect against getting the disease. Lung cancer is acknowledged to be on the rise both in the U.S. and elsewhere despite the decline in cigarette smoking which began more than 25 years ago. Further, lung cancer among nonsmokers seems to be increasing, while the rate of lung cancer among smokers is decreasing, thanks to the advent of filtered cigarettes, which nearly every study has shown decreases risk anywhere from 20% to 30% (only one such study is listed here).

"Rising lung cancer mortality rates during 1953-1982 were similar for both sexes in all parts of Oregon; the steepest increases were among women living in the coastal counties." "Occupational risk differences among both sexes far exceeded those noted with other risk factors, suggesting that occupational exposures deserve primary emphasis in future efforts at lung cancer control." "Causes of lung cancer other than smoking which are associated with particular occupations will be identified in the hope of eventually reversing the epidemic trend of this disease." 1375. University of Oregon, School of Medicine. Morton, W.E. "epidemiology of Lung Cancer in Oregon." Methods: Following data have been collected:

(1) sex-specific, age-standardized, mean annual death rates for 5-year periods since 1953 for all counties [Portland-Vancouver area] (2) occupations from death certificates since 1963 (3) all cases occurring in the Portland metropolitan area during 1963-1977 by search of tumour registries and hospital record rooms (4) age-adjusted incidence rates by sex for geographic regions, socioeconomic strata, and occupational categories.

"Prospective contribution of pack-years to development of lung cancer was reduced by crosssectional adjustment, but remained significant." But more important than pack years was airflow obstruction. "Data suggest that smokers who will develop lung cancer may be recognized by prior development of ventilatory obstruction." 1006. Johns Hopkins University, School of Hygiene and Public Health. Tockman, M.S.; Anthoisen, N.R.; Wright E.C. "Airways Obstruction and the Risk of Lung Cancer."

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"AO was significantly associated with advanced age, male sex, PiZ allete, blood group A antigen, heavy coffee intake (> 3 cups/day) and first degree relationship to a patient with chronic obstructive pulmonary [lung] disease [genetical predisposition]" "Both AO and CB were associated with cigarette smoking and low socioeconomic status." 1005. Johns Hopkins University, School of Hygiene and Public Health. Tockman, M.S.; Khoury, M.J.; Cohen, B.H. "Different Risk Factor Distributions for Airways Obstruction [AO] and Chronic Bronchitis."

"A cross-geographical analysis of lung cancer mortality for white male residents of Harris County for 1979 to 1981 is being made to assess the contribution of air pollution." "Regression techniques will be used to examine the relationship between mortality rates and measures of air pollution while statistically controller for variables that are known to be linked with excess lung cancer mortality, including age, smoking, and socioeconomic status, [emphasis added]" Results not available at time of printing. 1472. University of Texas Health Science Centre, School of Public Health. Buffler, P.A.; Stallones, R. "Air Pollution and Lung Cancer in Harris County, Texas." Funding: EPA (CR807108-01) 10/79-4/84.

Results to date (Sept, 1976-May, 1981): "A possible flattening in the dose-response [between smoking and lung cancer] was found and a low relative risk in an area of the world with one of the highest recorded incidence of lung cancer. The flattening of the dose-response curve occurred with an above-average consumption of 20 cigarettes/day" [emphasis added] 0590. West of Scotland Cancer Surveillance Unit (Glasgow) and University of Michigan, School of Public Health. Gillis, C.R.; Hoie, D.J.; Hawthorne, VIM et al. "Retrospective Case Control Study of Smoking Habits and Lung Cancer in the West of Scotland." Funding: National Institutes of Health (N01-CP-05646).

"Excess risks of lung cancer found in miners and foundry workers could not be fully explained by the high prevalence of smoking among these occupations," [emphasis added]. 0495. University of Zurich, Institute of Pathology (Switzerland). Schuler, G. "Epidemiology of Lung Cancer in Switzerland."

Smoking has a protective effect on immunological abnormalities in asbestos workers. 0429. Institute of Immunology and Experimental Therapy (Poland). Lange, A. "Effect of Smoking on Immunological Abnormalities in Asbestos Workers.

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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," [emphasis added]. 0565. University of London, School of Hygiene and Tropical Medicine. "Cancer of the Lung Among Asbestos Factory Workers." [Many other studies show similar findings for asbestos workers].

"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," [emphasis added]. 1388. Hahnemann Medical College and Hospital (Philadelphia). Weiss, W. "Lung Cancer Dueto Chloromethyl Ethers."

Method: "A cohort of 125 workers (91 exposed to chloromethyl ethers) have been followed since 1963, and semi-quantitative estimates of degree of exposure and records of duration of exposure have been maintained. Information on smoking habits was obtained at the beginning of the observation period." "Marked atypia were found only in workers chemically exposed to BCME (4.8 percent of smokers and 6.2 percent of nonsmokers). The biological mechanism for increased injury in nonsmokers...has not yet been determined [emphasis added]." [Index number not recorded]. Labour Protection and Hygiene Centre, Laboratory of Cytology (Romania). Herivan, R.: Constantinescu, V.; Melinte, L. "BCME, Soot, Smoking and Lung Cancer.

"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," [emphasis added]. 1544. DHHS, PHS, CDC, NIOSH. Ames, R.G. "Respiratory Effects of Exposure to Diesel Emissions in Underground Coal Miners." Funding: NIOSH.

"Lung volume parameters were found to decrease with age, but there was no significant modification related to tobacco consumption."

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0241. Institut D'Etudes Et Recherches Pneumophtisiologiques (Institute of Studies on Tuber-culosis). France. Keisbauer, J.P. "Longitudinal Study of the Methods of Early Detection of Respiratory Diseases in a Population of Cab Drivers."

"Neither smokers nor nonsmokers showed any changes in bronchial responsiveness after smoking cigarettes." 0391. Yokohama City University, School of Medicine (Japan). Okubo, T; Suzuki, S; Sano, F. "Acute Effect of Smoking on Bronchial Responsiveness."

"Chronic bronchitis was found more often in suburban inhabitants than in rural inhabitants, a significant difference." "It is concluded that chronic bronchitis is twice as common in the city as in rural areas, however, in both areas, air pollution and cigarette smoking lead to higher incidence." 0427. Copernicus Academy of Medicine (Poland). Nikodemowicz, E.; Owsinski, J.M.; Chomicka, Z. et al. "Influence of Urban Factors on the Incidence of Chronic Bronchitis in Rural Populations."

Smoking and Heart Disease

The connection between smoking and heart disease is far more tenuous than that between smoking and lung disease. Though the medical establishment considers smoking to be a risk factor (among many risk factors) for heart disease, the fact remains that anywhere from 30 to 50% of those admitted to hospitals for coronary problems exhibit none of the known risk factors (including smoking), and that the research is by no means either consistent of conclusive in linking smoking the heart disease. It is true that deaths from heart disease, which is still the number one cause of death, are declining but most researchers attribute this to better surgical and medical techniques, not to a decline in smoking rates, since deaths from heart disease are declining world-wide, even in countries with high smoking rate.

"No statistically significant relationship was found in either community between smoking and coronary heart disease, hypertension or somatic complaints" [emphasis added] 1477. University of Texas School of Allied Health Sciences. Philips, B.U., Jr.; Bruhn, J.G. "Smoking Habits and Reported Illness in Two Communities With Different Systems of Social Support." FUNDING: Univ. of Texas; National Institute of Mental Health. 1981-83.

"Preliminary data indicate greater frequency of anterior infarctions among nonsmokers." "Among patients with unstable angina, smoking was associated with less persistent rest pain and a lower proportion of

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smokers had chronic angina of effort prior to hospital admission. Preliminary analysis suggests a marginally lower in-hospital mortality rate among smokers after controlling for age and other prognostic factors." [emphasis added]. 0298. St. Vincent's Hospital, Dept. of Preventive Cardiology and Cardiac Dept. (Dublin, Ireland). Cohort of 898 males and 415 female heart patients. 12/80-1/86.

"Preliminary data indicate a high prevalence of IHD [Ischemic Heart Disease] in South Wales. A significant association between white cell count and IHD defined cross-sectionally is not explained by smoking habits. Prevalent IHD is not explained by smoking habit" [emphasis added] 0598. Medical Research Council, Epidemiology Unit (Wales). Yarnell, J.W.G; Elwood, P.C.; Sweetnam, P.M. "Caerphilly Prospective Study of Ischemic Heart Disease." Cohort study of 2,400 men (aged 44-60) began in 1979. Two samples of women also studied.

"Recent secular trends in sex and age specific mortality from ischemic heart disease, both in the United Kingdom and in the United States, appear to be independent of changes in cigarette consumption." 0564. University of Leeds, Dept. of Medical Physics (England). Burch, P.R.J. "Tests of Causal, Constitutional and Mixed Hypotheses of Associations between Smoking and Disease in Man," 1972 and continuing. Funding: Univ. Leeds.

While smoking was more common among women who had myocardial infarction, "no such difference was observed between women with angina pectoris and other women." Also no significant differences were observed between smoking and nonsmoking women with respect to myocardial infarction and death during the 12-year follow-up. 0464. Sahlgrenska Hospital, Medical Dept. (Sweden). Bengtsson, C.: Lapidus, L; Hallstrom, T. "The Population Study of Women in Gothenburg, Sweden."

"In asymptomatic male aviators (aged 20 to 60), age and ratio of total cholesterol to high density lipoprotein cholesterol are most highly correlated with degree of coronary artery disease found on angiography. After removing the effect of age and this ratio, no statistically significant additional variance is explained by other risk factors [including smoking]." [emphasis added] 1465. Department of Defense, Department of the Air Force, School of Aerospace Medicine (Brooks Air Force Base, Texas). Tolan, G.D.; Honck, P.; Hickman, R. et al. "Multivariate Approaches to the Detection of Asymptomatic Coronary Artery Disease." Funded by USAF. 1971 - continuing.

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Pipe smokers have a higher intake of nicotine than cigarette smokers (as measured by serum and urinary cotinine levels). "Since pipe smokers have little excess risk of CHD [chronic heart disease], higher chronic nicotine exposure is unlikely to be the cause of the excess seen in cigarette smokers." 0534. Medical College of St. Bartholomew's Hospital. Dept. of Environmental and Preventative Medicine (England). Wald, M.J.; Bailey, A. "Nicotine and Heart Disease.".

ETS and Heart Disease

"No difference in prevalence of cardiovascular symptoms was found [between those living with smokers and those not]" 0591. West of Scotland Cancer Surveillance Unit, Ruchill Hospital (Scotland). Gillis, C.R.; Hole, D.J.; Hawthorne, V.M. "Health Effects of Exposure to ETS (Environmental Tobacco Smoke] in the West of Scotland." Cohort of 16,171 (45-64 years old) screened in 1972 and 1976.

Smoking and "Throat" Cancer (See also appended bibliography for additional studies on this)

"All countries experienced a sharp increase in lung cancer mortality; [but] laryngeal and oral cavity cancers showed divergent trends (10 countries had steady or decreasing rates). Results suggest that tobacco may not be the major causative factor for laryngeal and oral cavity cancers." [emphasis added] 0244. Institut National de Recherche et de Security (France). Moulin, J.J; Mur, J.M.; Cavelier, C. "Comparative Epidemiology, In Europe, of Tobacco-Related Cancers (Lung, Larynx, Pharynx, Buccal Cavity)." Data is from World Health Organization 1950-1977.

"Secular trends in mortality from oesophageal cancer in the United Kingdom are independent of secular changes in cigarette consumption, but well correlated with secular changes in alcohol consumption...alcohol acts as an indirect causal agent. The proximal causal agent is likely to be a precipitator, such as a microorganism. Genetic predisposition is also implicated" 0564. University of Leeds. Dept. of Medical Physics (England). Burch, P.R.J. "Tests of Causal, constitutional, and Mixed Hypotheses of Associations Between Smoking and Disease in Man." Funding: Univ. of Leeds. 1972 -

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continuing.

..."alcohol consumption was the dominant risk factor [for oesophageal cancer" [em. add.] Dept. of HHS, National Cancer Institute. Blot, W.J.; Brown, L.M.; Ershow, A. et al. "Epidemiologic Studies of Tobacco Use and Risk Cancer."

Smoking and Renal [Kidney] Cancer

"Preliminary results implicate relative weight in both men and women as a principal risk factor in renal cell carcinoma. Comparison with population controls failed to implicate cigarette smoking of beverage use as risk factors." [emphasis added] 1363. University of Oklahoma, Health Sciences Canter. Asal, N.R.; Geyer, J. "Risk Factors in Kidney Cancer." Oct. 1981 - Feb., 1985. FUNDING:< National Cancer Institute.

"A weak positive association with cigarette smoking has been found, but only after controlling for selection biases." "Findings appear to confirm previously observed associations with obesity, northeastern European ancestry, renal calculi [kidney stones], and use of phenacetin-containing analgesics." [emphasis added] 1060. Harvard University, School of Public Health, Dept. of Epidemiology. MacMahon, B; Maclure, K.M. "A Casa Control Study of Renal Adenocarcinoma." Method: Used Cancer registries, pathology logs and medical records at 37 participating hospitals in the Boston area and follow-up interviews by phone. FINDING: Harvard School of Public Health; National Cancer Institute.

ETS and Bladder Cancer

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"No association was found for exposure to side-stream smoke, coffee drinking, or artificial sweetener use. The association of several occupations with bladder cancer risk has been found in males..." 1216. American Health Foundation. Wynder, E.L.; Goodman, M.T.; Kabat, G.C., et al. "Studies in Tobacco-Related Cancers." FUNDING: National Cancer Institute.

Smoking and Endometrial, Ovarian and Breast Cancer

"Overall, smoking was not found to be associated with any of the cancers studied." Centres for Disease Control. Epidemiologic Studies Branch. Division of Reproductive Health. Rubin, G.; Tyler, C.W.; Franks, A.L.; Stroup, M. "Smoking and Endometrial, Ovarian, and Breast Cancer." FUNDING: NICHD.

"The risk of breast cancer does not appear to be influenced by cigarette smoking" 1039. Boston University Medical Centre. Drug Epidemiology Unit. Shapiro. S Rosenberg. L.; Kaufman. D. "Multiple Case-Control Study of the Long Term Effects of Drug, Use in the Treatment of Chronic Disease." FUNDING: FDA (U01 FD01222-03) and NICHD [National Institute nf Child Health & Human Development]. Emphasis added.

Smoking and Cervical Cancer

"Sexual Behaviour and socioeconomic indicators predict cervical cancer incidence, as has been demonstrated in numerous other studies.: [emphasis added]" University of Utah. School of Medicine. Lyon J.L. "Epidemiologic Investigation of Cervical Cancer in an Area of Low Incidence " FUNDING: NCI (Dept. of Health &HS)

Smoking and Pregnancy

Some studies have found a correlation between maternal smoking during pregnancy and lower birth weight in babies. However, there are many factors which correlate with low birth weight, and the dominant risk factors seem to be the mother's age and the mother's socioeconomic class. Even those studies which show a correlation between maternal smoking and low birth weight speak of weight differences in grams, not ounces, and one ounce = 28.35

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grams.

Risk factors associated with low birth weight (in rank order):

1. Mother's age (too young or too old) 2. First pregnancy 3. More than two previous stillbirths 4. Lower birth weight of older siblings 5. Small stature and weight of mother 6. Fewer examinations during pregnancy 7. Smoking by mother or father

0360. Department of Public Health. Jichi Medical School (Japan). Nagai. M.; Yanagawa. H.; Kawaguchi, T. et al. "A Study of the Factors Associated With low Birth Weight. A Case-Control Study in Togichi Prefecture Apr. 1982Dec. 1984.

"Women who smoke during pregnancy have full-term babies which, on the average are 5-6 grams [a fraction of an ounce] smaller than full-term babies born to nonsmoking mothers." 0755. University of Colorado. Health Sciences Centre. Moore. L.C. "Maternal O2 Transport During Pregnancy at High Altitude " [emphasis added]

1. Birth weight lower in the smoking group, but the incidence of smoking was higher in young, unmarried women of lower socioeconomic status. Perinatal death was also higher among young, unmarried, low income women. 2. "No differences in antepartum hemorrhage or congenital anomalies between the groups" 3. "Hypertension and postpartum hemorrhage were lower in smokers [emphasis added]."

0045. University of Tasmania, ( Queen Alexandra Hospital, Dept. of Obstetrics & Gynaecology. Correy, J.; Newman. N.: Currarn, J "An Assessment of Smoking in Pregnancy." Method: Since I974, this study was conducted on ALL patients in Tasmania (smoking data was collected since Jan.1981 ). Details of alcohol ingestion and drug use were also included. By 1984 information available on 90% of patients on average birth weight of infants, incidence of low birth weight (less than 2,500 grams), incidence of prematurity, congenital abnormalities, perinatal death antepartum hemorrhage and hypertension in pregnancy.

"The proportion of complications of pregnancy and delivery were similar in smokers and nonsmokers."

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University of Oslo (Norway). Dalaher, K.; Grunfeld, B.; Jansen, A.

"Data do not confirm the suggestion that changes in cord blood vessels similar to those of arteriosclerosis are brought about by maternal smoking during pregnancy. Pathological changes in the cord at term may be found in infants of healthy, nonsmoking mothers..." 0184. Universitat Freiburg, Anatomische: Institut (Germany). Staubesand, J.; Seydewitz, V.; Hugod, C. et al. "Effects of Maternal Smoking on the Neonatal Umbilical Cord."

Parental Smoking, ETS and Children

"...excess influenza virus infection was found for black infants and infants with at least one sibling (especially those with school-age siblings), and rhinovirus infection rates were highest among girls attending daycare. No convincing differences for viral infection or respiratory illness were seen with parental smoking as an isolated factor..." [emph. added] 1462. Baylor College of Medicine, Influenza Research Centre (Texas). Gardner, G.C.; Frank, A.L.; Taber, L.H. "Effects of Social and Family Factors on Viral Respiratory Infection and Illness in the First Year of Life." A longitudinal study,1975 - 1980. This study was published in the Journal of Epidemiology and Community Health 39 (1); 42-48, March, 1984.

"The correlation matrix revealed that maternal education was the variable most significantly inversely correlated with infection... Its statistical significance persisted in the presence of other added factors." "Maternal education appeared to have played a highly significant role in the health of the children studied." [emphasis added] 0878. University of Kansas, College of Health Sciences. Holmes. G.E.; Hassanein, K.M.; Miller. H.C. "Factors Associated with Morbidity Among Breast Fed and Formula Fed Babies." The incidence of infection in babies was studied with regard to a number of factors, including maternal smoking.

Nicotine and Smoking: Benefits

Though the risks of smoking are highly publicized, the medical benefits of smoking are rarely mentioned. The greatest risks of smoking come from the tars released during the combustion of tobacco, and these tars are implicated in lung cancer and other breathing disorders, though even the tar apparently has some beneficial effects in protecting the lungs from some noxious particulate matter (e.g. asbestos). According to many studies, the chief medical benefits of smoking are from the nicotine, which occurs naturally in tobacco as well as in certain vegetables such as tomatoes, potatoes, and red peppers, though in much smaller amounts. Interestingly, these three plants

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originated in the Americas so nicotine was essentially a "New World" substance. Native Americans were well aware of the curative properties of tobacco, and used it both medicinally and ceremonially. Numerous studies have shown the protective effects of smoking with regard to Parkinson's Disease and ulcerative colitis, and an increasing body of research indicates it also helps protect against Alzheimer's Disease and colo-rectal cancer. Since these effects are so well known, wehave not listed them below but have focused instead on a few more obscure medical benefits culled from the 1984-85 CDC bibliography. Brief documentation of the beneficial effects of smoking with regard to Parkinson's, ulcerative colitis, Alzheimer and colo-rectal cancer will appear in an attached appendix of some relevant studies from the 1991 CDC bibliography.

1. Smoking improves human information precessing. 2. Higher nicotine cigarettes produce greater improvements [in information processing] than low-nicotine cigarettes. 3. Nicotine tablets produce similar effects. 4. Nicotine can reverse the detrimental effects of scopolamine on performance 5. Smoking effects are accompanied by increases in EEG arousal and decreases in the latency of the late positive component of the evoked potential."

0574. University of Reading, Department of Psychology (England). Warburton., D.M.; Wesnes, K. "The Effects of Cigarette Smoking on Human Information Processing and the role of Nicotine in These Effects "

"In general, motor performance in all groups improved after smoking." 0530. London University, Institute of Psychiatry. O'Connor, K.P "Individual Differences in Psychophysiology of Smoking and Smoking Behaviour "

"Smokers in general are thinner than nonsmokers, even when they ingest more calories." [Numerous studies, but only two are listed below] 0885. Kentucky State University. Lee. C.J.: Panemangalore. M. "Obesity Among Selected Elderly Females In Central Kentucky." FUNDING: USDA 0942. University of Louisville. Belknap Campus School of Medicine. Satmford, B.A.; Matter, S.; Fell, R.D., et al. "Cigarette Smoking, Exercise and High Density Lipoprotein Cholesterol" FUNDING: American Heart Association.

"...all smokers had less plaque, gingival inflammation and tooth mobility than nonsmokers and similar periodontal pocket depth."

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Veterans Administration, Outpatient Clinic (Boston). Chauncey. H.H,; Kapur, K.K.; Feldmar, R S. "The Longitudinal and Cross-Sectional Study of Oral Health: in Healthy Veterans (Dental Longitudinal Study)

"Smokers have lower incidence of postoperative deep vein thrombosis than nonsmokers." Guy's Hospital Medical School (England). Jones, R.M. "Influence of Smoking on Peri-Operative Morbidity." Hypertension (High blood pressure) is less common among smokers.

"Hypertension prevalence rate among smokers was 3.94 percent; among nonsmokers the rate was 4.90 percent." 0146. Shanghai Institute of Cardiovascular Diseases. Chen, H.Z.; Pan, X.W.; Guo, G. et al. "Relation Between Cigarette Smoking and Epidemiology of Hypertension. AND

"Hypertension and postpartum hemorrhage were lower in smokers." 0045. University of Tasmania (Australia). Correy, J.; Newman, N. Curran, J. "An Assessment of Smoking in Pregnancy."

"RBCs [red blood cells] from cigarette smokers contain more glutathione and catalase and protect lung endothelial cells against O2 [dioxide] metabolites better than RBCs from nonsmokers." [emphasis added] 0759. University of Colorado. Refine, J.E.; Berger, E.M.; Beehler, C.J. et al. "Role of RBC Antioxidants in Cigarette Smoke Related Diseases." Jan 1980 - continuing.

(A number of studies in the 1991 CDC bibliography describe the apparent protective effect of smoking with regard to mouth ulcers).

APPENDIX Following are studies listed in the Centres for Disease control's Bibliography on Smoking and Health, 1991. Many newer studies appear in this more recent CDC bibliography which support the earlier studies listed in the foregoing selected bibliography, including a lower risk of breast cancer, lower risk of endometrial cancer in smoking women; the improvement of fine motor control for smokers; lower incidence of overweight in smokers; lower incidence of high blood pressure among smokers. Below are selected studies which demonstrate the protective effect of smoking in Parkinson's Disease and ulcerative colitis.

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"Several epidemiological studies have indicated that there may be an inverse relationship between smoking and Parkinson's disease." There is an "apparent protective effect of cigarette smoke." 1102. Carr, L.A.; Rowell, P.P. "Attenuation of 1methyl-4-phenyl-1,2,3,6-tetrahydrophyridine- induced neurotoxicity by tobacco smoke." Published in Neuro-pharmacology 29(3):311-4, Mar 1990.

"These results indicate that in sufficient doses chronic treatment with nicotine may be considered in the pharmacological treatment of Parkinson's disease. It remains to be demonstrated whether these protective actions can be extended to include also other injured neurons..." 1190. Janson, A.M.; Fuxe, K.; Agnati, L.F. Jansson, A. et al. "Protective effects of chronic nicotine treatment on lesioned nigrostriatal dopamine neurons in the male rat." Pub. in Progress in Brain Research 79:257-65, 1989.

"Several studies have reported an apparent protective effect of cigarette smoking for the risk of idiopathic Parkinson's disease (IPD). These observations are supported by neurochemical studies..." These findings suggest that the inverse association between smoking and IPD may apply to NIP [neuroleptic-indiced parkinsonism]." 4014. Decina, P.; Caracci, G.; Sandik, R.; Berman, W. et al. "Cigarette smoking and neuroleptic- induced parkinsonism." In Biological Psychiatry 28(6):502-8, Sept. 15, 1990

"There is a low prevalence of smoking in ulcerative colitis. The disease often starts or relapses after stopping smoking." 4101. Prytz, H.; Benoni, C.; Tagesson, C. "Does smoking tighten the gut?" In Scandinavian Journal of Gastroenterology 24(9):1084-8, Nov. 1989.

"These results indicate that nonsmokers and especially ex-smokers of cigarettes have greater risk of UC [ulcerative colitis] and thus confirm the results of other studies." 4134. Lorusso, D.; Leo, S.; Miscianga, G.; Guerra, V. "Cigarette smoking and ulcerative colitis. A case control Study." Hepato-Gastroenterology 36(4): 202-4, Aug. 1989.

Documentation for the protective effect of smoking on Alzheimer's may be found in the 11 studies reviewed in the International Journal of Epidemiology, 1991. There is also documentation for lower incidence of colorectal cancer in JAMA in the early 1980s

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ADDITIONAL BIBLIOGRAPHY Forces Canada wishes to thank Martha Perske for providing the following bibliography:

"...particular attention is paid to the consumption of ethanol [alcohol] which has a major impact on the incidence of human cancer" 91-2046. Doll, R. Lifestyle: An overview. Cancer detection and prevention. 14(6): 589-94, 1990

" There is little direct evidence that cancer prevention has led to any major reduction in cancer incidence or mortality." 91-2068. Claysdon, D.B. " An overview of current and anticipated methods for cancer prevention." Cancer Letters. 50(1):3-9, April 9, 1990.

"...the prevalence of mild and moderate disease [oesophageal cancer] was found to be positively associated with the consumption of burning hot beverages (odds ratio = 4.7), the prevalence of esophagitis among siblings (O.R. = 4.4) and family history (O.R. = 1.8) ... Weaker associations were seen for cigarette smoking and the use of cottonseed oil..." 91-2069. Chang-Claude, J.C.; Wahrendorf, J. et al. " An epidemiological study of precursor lesions of oesophageal cancer among young persons in a high risk population in Hulxian, China." Cancer Research 50(8):2266-74, April 15, 1990.

" The incidence of these cancers appear to be increasing rapidly in response to the increasing level of alcohol consumption in Denmark." 91-2130. Miller, H. "Changing incidence of cancer of the tongue, oral cavity, and pharynx in Denmark." Journal of Oral Pathology and Medicine. 18(4): 224-9, Apr. 1989.

" Cancers of the mouth or pharynx and oesophagus were independently and strongly related to alcohol consumption..."

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91-2147. Ferraroni, M.; Negri, E. et al. " Socioeconomic indicators, tobacco and alcohol in the aetiology of digestive tract neoplasms." International Journal of Epidemiology. 18(3): 556-62, Sep 1989.

"...Linxian, a rural country in North Central China with one of the world,s highest mortality rates for these tumours. Cancer rates tended to raise with increasing intake of wheat or corn... Few persons reported drinking alcoholic beverages. Smoking was reported by 61% of the male cases and was a mild risk factor, related more to cancer of the cardia than of the oesophagus. The risk was increased by 70% among those whose parents had oesophageal or stomach cancer..." 91-2180. Li, J.Y.; Brshow, A.G.; et al [including Blot, W.J.]. "A case-control study of cancer of yhe oesophagus and gastric cardia in Linxian [China]." International Journal of Cancer. 43(5) : 755-61, May 15, 1989.

Odds ratios for oesophageal cancer: Current smokers: 3.8 - Heavy drinkers: 6.0 91-2199 Franceschini, S.; Talamini, R., et al. "Smoking and drinking in relation to cancers of the oral cavity, pharynx, larynx, and oesophagus in Northern Italy." Cancer Research. 50(20) :6502-7, Oct. 15, 1990.

"Highly significant associations with frequent intake of Maize emerged for oral cancer, pharyngeal cancer, and oesophageal cancer (OR = 3.3, 3.2, and 2.8, respectively). The risk elevation could not be explained in terms of difference in education, occupation, tobacco use, or consumption of fresh fruits and vegetables. The unfavourable effect of Maize... was evident only in those individuals who reported heavy drinking... The present findings agree with previous observations from Africa, China, the U.S., and Italy." 91-2202. Franceschini, S.; Bidoli, E.; et al. "Maize (corn) and risk of cancer in the oral cavity, pharynx, and oesophagus in Northeastern Italy." Journal of the National Cancer Institute. 82(17) :1407-11, Sept. 5, 1990.

"The three risk factor showed a strong tendency to be related to cancer only in combination, adding new evidence to the theory that risk factors in cancer act in a synergistic fashion." 91-2322. Grossart-Maticek, R.; Eysenck, H.J. "Personality, smoking, and alcohol as synergistic risk factors for cancer of the mouth and pharynx." Phycological Reports. 67 (3 Pt. 1) : 1024-6, Dec. 1990.

Source: Bibliography On Smoking and Health, 1991. Centres for Disease Control and Prevention.

SMOKERS HAVE REDUCED RISKS OF ALZHEIMER'S AND PARKINSON'S DISEASE Patients with Alzheimer's disease (AD) have a considerably decreased life expectancy, with the entire course of the disease taking an average of about eight years. AD is defined by a specific combination of neuropathologic features that

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include neuronal loss in particular regions of the brain and a high density of senile plaques and neurofibrillary tangles. It is hard to distinguish during life because of other damage and dementias. As many as 80% of the cases may be unrecognized by general practitioners. Acute administration of low doses of nicotine improved mental processes and may be protective in AD. This possibility was first put forward by Appel, who noted that only 6 out of 30 patients had smoked at any time in their lives. Since that time, nineteen case control studies have been published and are considered here. The overall from these showed a clear negative association, 15 out of 18 studies reporting a lower risk of AD in men and women who had smoked. Of the 19 studies, 15 found a reduce risk in smokers, and none found an increased risk. And smoking is clearly associated with a reduced risk of Parkinson's disease, another disease in which nicotine receptors are reduced. The fact that acute administration of nicotine improves attention and information processing in AD patients adds further plausibility to the hypothesis.

"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 from the same family." (Conelia M. van Duljn MSC Albert Hoffman Md., Erasmus Univ. Md. School) STUDIES AND PUBLICATIONS

Amaducci LA, et al. A case-controlled study of an Italian population. Neurology, 1986, 36:922-931. Barclay L, Kheyfets S. Tobacco used in Alzeimer's disease. Prog. Clin. Bho. Res 0989, 317:189-194. Brenner DE, et al. Relationship between cig. smoking and Alz. disease. Neurology 1993, 43:293-300. Broe GA et al. A case -controlled study of alz. in Australia. Neurology 1990, 40:1698-1707. Chandra V. et al. Case study of the late on-set 'probable Alz. disease'. Neurology 1987, 37:1295-1300. Dewey ME, et al. Risk factors for Dementia. Liverpool, Int. Geriatric Psychiatry 1988, 3:245-249. Ferini-Strambi, et al. Clinical Aspect of Alz. Disease with pre-senile on-set. Neuro Epidem 1990, 9:3449. French LR, et al. Case-control study of dementia of Alz. type. Am J Epidemiol 1985, 121:414-421. Graves, AB, et al. Case controlled study of Alz. disease. Neurol 1990, 28:766-774.

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Grossberg, GT, et al. Smoking as a risk factor for Alz disease. Am. Geriatric Soc. 1989, 37:819. Hebert LE, et al. Relation of smoking and alcohol to Alz disease. Amer. J Epidemiol 1992, 135:347355. Heyman A, et al. Alz disease: a study of epidem aspects. Am Neurol 1984, 15:335-341. Hofman A, van Duijn. Alz disease, Parkinson's disease, and smoking. Neurobiol Aging 1990, 11:295. Jones GMM, et al. Smoking and dementia of Alz type. Neurol Neurosurg Psychiatry 1987, 50:1383. Joya CJ, et al. Risk factors in clinically-diagnosed Alz disease. SA Neuroniol Aging 1990, 11:296. Katzman R, et al. Develop of dementing ill. in 80 yr. old volunteer cohort. Am Neurol 1989, 25:317324. Kondo, K Yamashita I. Case study of Alz in Japan. Biol & Social advances. Excerpta Medica 1990, 49-53. Shalat SL, et. al. Risk factors for Alz. disease. Neurology 1987, 37:1630-1633. Soininen H, et al. Clinical and etiological aspects of senile dementia. Eur Neurol 1982, 21:401-410. Korten AE, et al. Control informant agr. in case control studies of Alz. Int. J Epidie. 1992, 21:11211131. Breteler MMB, et al. Epidemiology of Alz disease. Epidemiol Review 1992, 14:59-82. Lee PN Statistics, Sutto, UK.

ALZHEIMER'S DISEASE IS ASSOCIATED WITH NON-SMOKING Graves' pooled reanalysis found, "A statistically significant inverse relation between smoking and Alzheimer's disease was observed at all levels of analysis, with a trend towards decreasing risk with increasing consumption (p=0.0003). A propensity towards a stronger inverse relation was observed among patients with a positive family history of dementia." Only three studies have ever linked smoking with AD. The reanalysis, in which the author of one participated, noted, "Since veterans may be expected to smoke more than the general population, and since smokers have been found to respond less frequently to questionnaires than non-smokers, the positive result observed for this study may be spurious."

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Contrary to a claim that smokers got AD at a younger age, there was no difference in men. Female smokers were younger among both cases and controls, which proved it to be spurious. Over 4 million people suffer from AD, and annual costs are over $88 billion. There may be 73,000 excess cases per year among non-smokers, with $17.5 billion in excess costs.

Ferini-Strambi L, Smirne S et al. Clinical and epidemiological aspects of Alzheimer's disease with presenile onset: a case-control study. Neuroepidemiol 1990;9:39-49. 63 ADs, ever/never 0.47 (0.23-0.94).

Li G, Shen YC et al. A case-control study of Alzheimer's disease in China. Neurol 1992 Aug;42(8):1481-1488. 70 ADs, >10y 0.92 (0.45-1.87), >20y 0.87 (0.35-2.16).

Hebert LE, Scherr PA et al. Relation of smoking and alcohol consumption to incident Alzheimer's disease. Am J Epidemiol 1992;135(4):347-355. 76 ADs, ever/never 0.7 (0.3-1.4), 40 pyrs 0.8 (0.6-1.1).

Jones GMM, Reith M et al. Smoking and Dementia of Alzheimer type (letter). J Neurol Neurosurg Psychiatry 1987;50:1383. 81 ADs. ever/never 0.63 (from Graves: NON-smokers 1.58).

Grossberg GT, Nakra R et al. Smoking as a Risk Factor for Alzheimer's Disease (letter). J Am Geriatr Soc 1989;37:822. 144 ADs ever/never 0.33 unmatched OR (p/= 20c 29.7 [calculated relative risks 1-19c 0.70, >/= 20c 0.89].

Hemminki K, Mutagen P, Saloniemi T: Smoking and the occurrence on congenital malformations and spontaneous abortions: Multivariate analysis. Am J Obstet Gynecol Jan 1 1983; 145:61-66. Finnish Register. 521 musc/skel, any s 1.31/1.02 adj; 335 regular s 1.32/0.90 adj; 218 >/= 5c 1.36/0.75 adj.

Van Den Eeden SK, Karagas MR, Daling JR, Vaughan TL. A case-control study of maternal smoking and congenital malformations. Paediatr Perinatal Epidemiol 1990;4: 147-155. 571 skeletal (171 club foot, 95 poly-, 74 syn- & 14 adactyly, 35 other limb reduction, 215 hip dislocation) 1.1 (0.91.3).

Evans DR, Newcombe RG, Campbell H. Maternal smoking habits and congenital malformations: a population study. BMJ July 21 1979; 2:171-173. Cardiff. Crude rates/1000: 715 musc/skel )o 11.3, 1-9c 9.3, 10-19c 9.9, 20+c 10.4 [calculated relative risk 1-9c 0.82, 10-19c 0.88, 20+c 0.92].

Shiono PH, Klebanoff MA, Berendes HW. Congenital malformations and maternal smoking during pregnancy. Teratol 1986;34:65-71. Kaiser-Permanente prospective. 17 limb reductions 2.2 (0.9-5.8); 34 syndactyly 0.7 (0.3-1.5); 44 skull 1.1 (0.6-2.0); 71 hip dysplasia 0.6 (0.3-1.1); 73 polydactyly 1.0 (0.6-1.6); 80 other musculoskeletal 1.4 (0.9-2.2); 407 other limb 0.9 (0.7-1.1). 726 total.

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Malloy MH, Kleinman JC, Bakewell JM, Schramm WF, Land GH. Maternal smoking during pregnancy: No association with congenital malformations in Missouri. AJPH 1989 Sep;79(9):1243-1246. 3705 musculoskeletal 0.99 (0.92-1.06). Not shown on graph:

Heinonen OP, Slone D, Shapiro S, eds. Birth defects and drugs in pregnancy. Littleton, MA: Publishing Sciences Group, 1977. Collaborative Perinatal Project prospective. 404 musculoskeletal (including polydactyly) smoking nonsignificance in MLR, no detail.

SMOKING DOES NOT CAUSE MULTIPLE MYELOMA

When the Mills study of multiple myeloma among Seventh-Day Adventists claimed in 1990 that smokers had over three times the risk of non-smokers, the national media eagerly trumpeted it as yet another new danger of smoking. This was despite the fact that previous studies actually found a slightly reduced overall risk among smokers, and that Mills' 21 cases represented not even 3% of the multiple myeloma cases studied to that date. It's a classic "little tiny study with a great big headline." Just as important is the basic epidemiological principle that cases and controls should be as ALIKE as possible except in the condition or protocol being studies. Seventh-Day Adventists are not representative of the general population. Their drinking, smoking, dietary and exercise habits are well outside the parameters of the population at large. In effect, using them as a "control group" is not only scientifically unsound; it borders on the absurd.. What is more, even Mills et al. later admitted that "recent evidence from this study has indicated the presence of substantial 'healthy volunteer effect' during the first few years of follow-up, suggesting that it may be inappropriate to compare participants in a study such as this with the general population." Judging by its discrepant finding, which doesn't even agree in direction with others, it probably has a "healthy volunteer effect" operating internally as well, involving the from-birth Adventists more than the converts from whom most of the smokers and ex-smokers were drawn. Most importantly, this Adventist study has been the basis of major anti-smoking propaganda, namely the Repace and Lowrey claim of 5,000 deaths (Environ Int 1985;11:3-22). But the antismoker and the mainstream media have never retracted their false claim. * Mills PK et al. History of cigarette smoking and risk of leukaemia and myeloma: Results from the Adventist Health Survey. JNCI 1990;82:1832-1836. 21 cases /=20c 10.8. [calculated risk ratio 1-19c 0.79, >/=20c 1.29].

Himmelberger DU, Brown BW, Cohen EN. Cigarette smoking during pregnancy and the risk of spontaneous abortion and congenital anomaly. Am J Epidemiol 1978;108(6):470-479. Trace Anesthetic Study, retrospective mail survey of health professionals. 163 cardiovescular malformations, crude rates/1000: smokers 19.07, nonsmokers 13.65 [calc. rel. risk 1.4].

Shiono PH, Klebanoff MA, Berendes HW. Congential Malformations and Maternal Smoking During Pregnancy. Teratol 1986:34:65-71. Kaiser - Permanente Prospective. 62 ventricular septal 0.5 (0.2-096): 22 heart valves 0.3 (0.1-1.1): 92 ductus arteriosus 1.1 (0.7-1.6): 16 unspecified 0.8 (0.3-2.6): 8 transposition 0.4 (0.04-2.9): 9 atrial septal defect 0.7 ( 0.2-3.5): 5 fibroelastosis 1.7 (0.3-10.1): 6 coarctation of aorta 0.5 (0.1-4.3). [calculated overall odds ratio 0.78].

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Evans DR, Newcombe RG, Campbell H. Maternal smoking habits and congenital malformations: a population study. BMJ Jul 21 1979; 2: 171-173. Cardiff. 223 cardiovascular malformations, crude rates/1,000: non 3.6, 1-9c 2.9, 10-19c 3.0, 20+c 2.8. [calculated risk ratios 1-9c 0.81, 10- 19c 0.83, 20+c 0.78].

Fredrick J, Alberman ED, Goldstein H. Possible teratogenic effect of cigarette smoking. Nature 1971 Jun 25;231:529-530. British Perinatal Mortality Survey, retrospective, 34/86 (39.5%)s 1 wk pop, 81/204 (39.7%)s v 4626/15, 719 (29.4%)s CHD 3 mo pop sample. 290 incident, smokers 7.3%, nonsmokers 4.7% [crude risk ratio 1.55]

McDonald AD, Armostrong BG, Sloan M. Cigarette, alcohol, and coffee consimption and congenital defects. AGPH Jan 1992;82(1), 91-93. 3/18 cardiovascular 1-9c 1.03 (0.6-1.6), 10-19c 1.17 (0.8-1.7), 20+c 1.17 (0.9-1.6).

Kelsey JL, Dwyer T, Holford TR, Brecken MB. Maternal smoking and congenital malformations: an epidemiological study J Epidemiol Commun Health 1978; 32:102-107. Retrospective case- random control at "several hospitals in Connecticut" Relative risks: 52 abnormal heart valves 1- 1.3, 0.4; 106 other 0.9, 1.0; 213 septal defects 1.0, 1.4. No combined results.

Van Den eden SK, Karagas MR, Daling JR, Vaughan TL. A case-control study of maternal smoking and congenital malformations. Paediatr Perinatal Epidemiol 1990;4:147-155. 88 patient doctus arteriosus 1.0 (0.6-1.6); 582 other 0.9 (0.7-1.1); 655 total cardiac 0.9 (0.8-1.2).

Milloy MH, Kleinman JC, Bakewell JM, Schramm WF, Land GH. Maternal smoking during pregnancy, No association with congenital Malformations in Missouri. AJPH 1989 Sep; 79 (9): 1243-1246. 123 atrial septal 1.04 (0.70-1.55); 151, valvular 0.74 (0.50-1.09); 447 ventricular septal 0.87 (0.70-1.09); 756 other cardiovascular 1.01 (0.86-1.19); 1341 heart 0.92 (0.82-1.05). NOT SHOWN ON GRAPH:

HEINONEN OP, SLONE D, SHAPIRO S, EDS. Birth defects and drugs in pregnancy. Littleton, MA: Publishing Science Group, 1977, Collaborative Perinatal Project prospective. 404 congenital heart defects, smoking non significant in Multiple Logistic Regression, no details.

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WORLD'S LARGEST AND LONGEST HEART STUDY PRODUCES SOME SURPRISESEmbargoed to Monday August 24th 1998 12:30 Vienna time Press Conference: European Congress of Cardiology, ESC Press Conference Centre Messe Vien, WHO MONICA Project: preliminary analysis of final results 11:30 to 12:20, Monday 24th August 1998. Participants: Dr Hugh Tunstall-Pedoe:Chairperson (Dundee, GB), Dr A Evans (Belfast, GB), Dr Ingrid Martin (WHO Geneva, CH), Dr U Keil (Mnster, DE), Dr K Kuulasmaa (Helsinki, FI)

The European Congress of Cardiology in Vienna this week is seeing preliminary analyses of the final ten-year results of the largest collaborative study of heart disease ever undertaken. These results - on the effects of treatments and risk factors in determining trends in coronary heart attack rates and mortality - which include some early surprises, will create considerable discussion and controversy amongst the worlds experts, although further analyses remain to be done. The near completion of this World Health Organization (Geneva) initiative is a remarkable feat of international research collaboration. Background Twenty years ago investigators in 38 centres in 21 countries got together with the World Health Organization to answer key questions on coronary heart disease and stroke: Why were rates declining rapidly in some countries and increasing in others ? Were changes in disease rates driven directly by changes in factors known to be important in individuals - smoking, blood pressure, cholesterol and obesity ? How well could changing survival and mortality from heart attacks be related to changes in treatment ? o questions which are as topical today, when heart disease generates everincreasing burdens and costs to the worlds ageing populations, as they were when they were first posed.

The Project The resulting collaboration was called the WHO MONICA Project (from MONItoring CArdiovascular disease). Participants, who were locally funded, used standardized methods to study trends in heart disease (and optionally stroke), trends in its treatment, and trends in coronary risk factors in their local populations, but copied their results to a Data Centre in Helsinki, for central analysis. Procedures and results were scrutinized by designated quality control centres, and by panels of international experts. Performances were scored, ranked and circulated. Serious failure led to exclusion from the study, but most investigators worked together for over ten years submitting data which met WHO MONICA Project requirements. Preliminary results from 150 thousand heart attacks, and 180 thousand risk factor records were presented briefly at a "Hot-Line" session by Professor Hugh Tunstall-Pedoe (Dundee, Scotland, head of one of the quality control centres, and long-term member of the MONICA Steering Committee) on Sunday 23rd August and with his MONICA colleagues (named above) at a press conference on the next day. Heart disease rates are declining in most of the populations studied but there is more decline in fatal than in nonfatal attacks and in men than in women. Rates are increasing in some Eastern populations. Survival rates from heart attacks are improving but to a lesser extent than event rates.

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Effective treatments are being adopted at very different rates in different countries. Improving heart attack rates do not always go with better survival. Blood pressure is coming down in most populations, as is smoking but there are differences by sex and age group in the latter. Cholesterol levels are difficult to measure and follow accurately over time, but they are changing little in most MONICA populations. Obesity is increasing in most MONICA populations. AND WHEN THESE ARE PUT TOGETHER

Those populations which, during the period of study, showed the most rapid increase in new treatments tended to be those in which heart attack survival and mortality were improving most but this effect could be nonspecific. Many drugs were being adopted at the same time, and there were regional effects. It was therefore not possible in these preliminary analyses to say which treatments, if any, were the cause. Although there was more relationship in women than in men, changing rates of coronary heart disease in different populations did not appear to relate at all well to the change in the standard risk factors, considered one by one, or in a risk factor score. Large differences in the rate of decline occurred across populations with similar trends in risk factors.

Discussion and possible explanations The latter preliminary finding will cause surprise and controversy, as many had assumed a direct relationship. Professor Hugh Tunstall-Pedoe, speaking for the study, said: "The WHO MONICA Project was set up in the early 1980s to see whether the engines driving the changes in heart disease rates were those known at that time to determine risk in individuals smoking, blood pressure, cholesterol, and to a lesser extent, obesity. Our initial impression, - of no direct relationship overall in this study, despite reported results from individual centres- does not negate the importance of these factors to the individual and to health education. If you get eaten by a crocodile when you are expecting lions and tigers it does not mean that big cats have rubber teeth! We would not have done the study if we had been sure what it would show, and we needed international collaboration to make it possible. The preliminary results are a bit of surprise but not entirely so. "There are several possible explanations for our findings, including problems of measurement, the fact that rates were declining in most populations anyway, and lack of linearity in trends associated with possible time-lags for which preliminary analyses do not allow. Another interesting possibility is that in population terms the contribution of the classical risk factors is swamped by that of other, dietary, behavioural, environmental or developmental factors, of which several have been proposed since the study was launched. Although many enthusiasts will now be staking claims for their favourite candidates, we cannot pass judgement on factors which were not included in the agreed core set of data for the original study. Some of these factors have been looked at in local and MONICA optional studies but will not have the power of a 38 population and ten-year evaluation. Further more sophisticated analysis of the central data that we do have will continue beyond these preliminary findings and will involve more use of our quality scores to weight the results." Dr Ingrid Martin, responsible officer for cardiovascular diseases at the World Health Organization Headquarters in Geneva stated: "The World Health Organization has facilitated, co-ordinated and helped to manage this study since 1979. MONICA has spread best practice in the technology of population surveys and disease monitoring through four continents. It has trained many young people in population aspects of cardiovascular disease. The findings on risk factors in no way diminish their importance for individuals and for public health. That the classical risk factors make major contributions to individual risk has been shown repeatedly in numerous studies, many involving MONICA investigators. They feature in ongoing WHO sponsored prevention programmes. The WHO MONICA Project is adding to our understanding of what is going on, and not taking away anything that was known before. It has

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generated high quality data for local use on what is happening to cardiovascular disease and major risk factors, and created an invaluable international resource. It is a model for other international research collaborations." Enclosure: Press Pack consisting of: List of MONICA sites and principal investigators World Map to show MONICA sites *Ten-year trends in coronary death rates in MONICA populations using MONICA diagnostic criteria. *Ten-year trends in daily smoking in MONICA populations, smoking defined by MONICA criteria *Selected examples of WHO MONICA Project output

NOTE: 1: These findings will be the subject of a special evening discussion session outside the main Congress programme, organized by the WHO MONICA Project and by the European Society of Cardiology Working Group on Epidemiology and Prevention in Hall 16C Messe Vien, Tuesday 25th August 18:30-20:00 NOTE: 2 The WHO MONICA Project is sponsored and co-ordinated by the World Health Organization with contributions from NHLBI (USA) to data analysis and quality control, and European Union funding through BIOMED grants, plus donations from drug companies. The MONICA Data Centre has been supported by Finnish funds. Individual MONICA centres are funded by government bodies and by heart foundations. NOTE: 3 Press release and results have been sent to individual Principal Investigators who can now comment both on the study and on their own local results for their national media and may put out their own statements.

Nicotines effect on fluoride Nicotine, most know of it through smoking and tobacco use. I've always wondered why the US Government is so adamant with anti-smoking and tobacco usage. The carcinogenic properties are bad yes, i do condone smoking but only in small amounts and from organic of hand rolling tobacco, pipe tobacco or Cigars. I do however condone nicotine gum, or other nicotine treatments. Here is why.

Nicotine has an adverse effect on fluoride.

Remember how fluoride inhibits choleric activity? Nicotine excites them, rebounding and undoing fluorides effect. Nicotine is being used as a treatment for ADD and ADHD, Alzheimers, Parkinson's disease. I will not list the rest, for every single ailment fluoride is known to cause, nicotine has the reverse effect.

It makes you wonder, why people who smoke may find a considerably less effect from Prozac and other anti-depressants. Why most people with ADD and ADHD develop into smokers. WHY DO MOST DOCTORS SMOKE?

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Parkinson's disease is your brain's ability to receive and use dopamine from the blockage or death of brain cells in the motor regions. The cause is UNKNOWN. On a side note, Ill mention again how fluoride enters the brain tissue easily and deposits aluminum at will, which has a conspicuous effect of killing brain cells and clogging up dopamine receptors. The most common treatment is levodopa; a drug that increases dopamine levels, so that what receptors and brain cells you have left can receive a better supply of dopamine. Funny, nicotine has the same effect. On a large level. Large enough so that it becomes addictive. Your brain becomes used to the higher dopamine count, so when the dopamine stops coming, your brain says "hey, i want some more 'o' that."

There is a lot more info. Here are some links for your own further research. www.epa.gov, www.fluoridealert.org, Summation - Fluoride & Pineal Gland: Up until the 1990s, no research had ever been conducted to determine the impact of fluoride on the pineal gland - a small gland located between the two hemispheres of the brain that regulates the production of the hormone melatonin. Melatonin is a hormone that helps regulate the onset of puberty and helps protect the body from cell damage caused by free radicals. It is now known - thanks to the meticulous research of Dr. Jennifer Luke from the University of Surrey in England - that the pineal gland is the primary target of fluoride accumulation within the body. The soft tissue of the adult pineal gland contains more fluoride than any other soft tissue in the body - a level of fluoride (~300 ppm) capable of inhibiting enzymes. The pineal gland also contains hard tissue (hyroxyapatite crystals), and this hard tissue accumulates more fluoride (up to 21,000 ppm) than any other hard tissue in the body (e.g. teeth and bone). After finding that the pineal gland is a major target for fluoride accumulation in humans, Dr. Luke conducted animal experiments to determine if the accumulated fluoride could impact the functioning of the gland - particularly the gland's regulation of melatonin. Luke found that animals treated with fluoride had lower levels of circulating melatonin, as reflected by reduced levels of melatonin metabolites in the animals' urine. This reduced level of circulating melatonin was accompanied - as might be expected - by an earlier onset of puberty in the fluoride-treated female animals. Luke summarized her human and animal findings as follows: "In conclusion, the human pineal gland contains the highest concentration of fluoride in the body. Fluoride is associated with depressed pineal melatonin synthesis by prepubertal gerbils and an accelerated onset of sexual maturation in the female gerbil. The results strengthen the hypothesis that the pineal has a role in the timing of the onset of puberty. Whether or not fluoride interferes with pineal function in humans requires further investigation."

TOKYO - Life expectancy for Japanese women already the longest in the world has risen by nearly one year, the Health Ministry said Thursday, citing the latest census data. Female life expectancy increased to 85.52 years in 2005 from 84.60 years in 2000, Health Ministry official Morio Akimoto said.

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The latest figures were calculated based on the fixed census data taken in 2005. The census is taken every five years in Japan. Akimoto said Japanese women's life expectancy remained the world's longest for the 21st straight year, ahead of Hong Kong and Spain, according to U.N. demographic figures. For men, life expectancy rose to 78.56 years from 77.72 years, the fourth-longest in the world after Hong Kong, Iceland, Switzerland, Akimoto said. Japan has long been touted as one of the world's longest-living populations, but experts are worried that changing eating patterns from the traditional fish and ricebased diet to fast food such as hamburgers and instant noodles may soon change this. http://news.yahoo.com/s/ap/20070301/ap_on_he_me/japan_l...A63sOuYGwxibtivMWM 0F

ummm excuse me!! how can this be?? Isnt Japan one of the highest tobacco use rates in the world?? Greece also has massive amounts of smokers and also have extremely high life expectancies.

Interestingly, reading Whitby's book from that link (great reading btw), on page 58-59 (of the book; 30-40 on web page) I find that Co-enzime Q10, CoQ10, hailed as the miracle supplement, for heart, circulation, infections, cancers, Parkinson's,... and just about everything that can go wrong, is actually a tobacco leaf and is manufactured from tobacco. Naturally, it is not mentioned very often, but that is what it is and how it was discovered in 1950s. Now, that is interesting. After reading Whitby one can only say, yep, tobacco is a miracle medicine, as our elders always thought. From every angle one looks the actual facts behind the antismoking propaganda, from biochemistry to animal experiments and the randomized quitting trials, even the statistical rigging in the epidemiology, one arrives to this same conclusion -- tobacco is a miracle drug. No wonder Big Pharma is doing its best to destroy it.

Here is an interesting official confirmation I found abot smoking rodents. The source is the official repository of tobacco documents (obtained during MSA negotiations). On page 97 of the report there is the following study citation & conclusion excerpt:

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"Inhalation Bioassy of Cigarette Smoke in Rats" A. P. Wehrner, et al. (Battele Pacific Northwest Labs, Richland WA) Journal of Toxiology & Applied Pharmacology, Vol. 61: pp 1-17 (1981) The results show that the highest number of tumors occured in the untreated control [non-smoking] rats. The next highest number of tumors occurred in rats subject to sham smoking, i.e. rats which were placed in the smoking machine without smoke exposure, and the lowest number of tumors occurred in the smoke-exposed rats. Among the latter, the largest number of tumors occurreed in rats exposed to smoke from cigarettes having the lowest level of nicotine.

So, among the lab rats, the "full flavor" smokers had the fewest tumors, the "light cigrattes" smokers had more, the sham-smokers even more, and non-smokers had the most. The entire document (pdf file) is a gold mine with many hudreds of fascinating and little publicised reasearch "anomalies" (i.e. the studies in which the data went the "wrong" way) regarding the relation of cancers to smoking. Of course, there is no real anomaly (the reality is surely not perplexed by itself), provided one views the data from the perspective of tobacco smoking being protective against (instead of "the cause of") the diseases studied. The data is anomalous only from the perspectiva in which tobacco smoke is assumed to be the cause of those diseases.

Major Health Advocate Groups state that smoking causes heart disease and deaths;however,since they do not state "HOW", their statements are of little use or believability. Many studies,ie "WhiteHall 1","MRFIT","Framingham", and etc,state that smoking is not a risk factor for heart disease. Since they do not say why this is so,they are of little help either. -----

Lung Cancer and smokersLet's see; 70% of LC cases are ex-smokers, plus 15% LC cases are never smokers, that means that only about 15% of LC cases are current smokers!!! Not anywhere near the 90% you hear about. Since there are as many ex-smokers(70% of LC's) as current smokers(15% of LC's) in this country, don't quit!

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In Calif., ex's = 70%, non's = 30% = 100%. Smokers do not get LC in Calif. http://www.smokersclubinc.com/modules.php?name=News&file=article&sid=3752 Rise in lung cancer in nonsmokers puzzling MDs 9/30/06

Doctors who treat lung cancer are facing a puzzling trend: every week about 65 Canadians who have never smoked are being told they have cancer in their lungs.

According to the Canadian Cancer Society, an estimated 22,700 Canadians will be diagnosed with lung cancer in 2006 and 19,300 will die of it. Smoking has long been understood to be a key risk factor for lung cancer. But according to information CTV's Avis Favaro received from doctors at Princess Margaret Hospital and the Sunnybrook Regional Cancer Centre in Toronto, 10 to 15 per cent of new lung cancer cases diagnosed are in people who have never smoked. Many have never been exposed to second-hand smoke. Genetics, hormones, second-hand smoke, diet and air pollution are all possible factors. "Many of these people are young," said Dr. Natasha Leighl of the Princess Margaret Hospital. "They're women and this is a population that is increasing. In California, they believe the number of people with lung cancer who have never smoked may now be 30 per cent." Doctors suspect environmental pollution may trigger some cases. In others there may be a genetic link. Many agree the numbers of non-smokers developing long cancer is growing. Although quitting smoking decreases the risk of getting lung cancer, it doesn't mean you don't have to worry. Leighl said 70 per cent of diagnosed cases of lung cancer are in former smokers who said they quit 10 or 20 years ago. Antis;using CDC data that shows that Kentucky has a 32.6% smoking rate and a 223.9/100,000 cancer death rate compared to Utah's 12.8% smoking rate and 144.9/100,000 cancer death rate,claim that smoking causes cancer and thus, cancer

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deaths. Below is a chart using only CDC data. There are some very interesting datum in this chart. For instance;note that both Colorado and The Dist.of Columbia have a 20.4% smoking rate. However,DC ranks 14th on the chart and Colo. ranks 49th! DC has more politicians, it must be the politicians that are causing cancers. Mass.,with a 18.9% smoking rate, ranks 24th and Alaska, with a 29.3%(about 50% higher)smoking rate, ranks 32nd!! New Jersey, with a 19% smoking rate,ranks 22nd and Hawaii,with a 21% smoking rate, ranks 51st!!! Now consider Ky. and Ut. Let's just say that smoking causes all cancers, this is what the antis would say. Ky's 32.6% = 32,600/100,000. 32,600 divided by Ky's 223.9/100,000 death rate = 1 cancer death per 146 Ky smokers. Ut's 12.8% = 12,800/100,000. 12.800 divided by Ut's 144.9/100,000 death rate = 1 cancer death per 88 Ut smokers. 1/88 is much worse than 1/146. If a Ut smoker moved to Ky, he would reduce his risk of dying from cancer by 66%!! Must be the Ky whiskey that has the protective effect. This data may indeed prove something;but,it does not prove that smoking causes cancer deaths. Gary K.

Cancer Death Rates and 95% Confidence Intervals by State (Table 5.1.2MF) Available at http://www.cdc.gov/nchs/data/nvsr/nvsr54/nvsr54_13.pdf. Source: U.S. Cancer Statistics Working Group. United States Cancer Statistics: 2003 Incidence and Mortality. Atlanta (GA): Department of Health and Human Services, Centers for Disease Control and Prevention, and National Cancer Institute; 2007. Rankings by State: 2003, Male and Female, All Sites Rates per 100,000 57

Smoking Rates from CDC- BRFSS Data. http://apps.nccd.cdc.gov/brfss/Trends/trendchart_c.asp?...key=10000&SUBMIT1=Go DEATHS (smoker%-2002) (Deaths/Smokers) (2003 Rate) 1 Kentucky 32.6 1/146 223.9 2 Louisiana 23.9 1/107 222.6 3 Tennessee 27.8 1/131 212.9 4 Mississippi 27.3 1/129 212.0 5 West Virginia 28.3 1/134 211.6 6 Alabama 24.4 1/117 207.7 7 Indiana 27.7 1/134 207.2 8 Arkansas 26.3 1/128 205.5 9 Ohio 26.6 1/130 204.3 10 Maine 23.6 1/116 204.1 11 South Carolina 26.5 1/130 203.7 12 Nevada 26.0 1/128 203.0 13 Missouri 26.5 1/131 201.7 14 Dist.of Columbia 20.4 1/101 201.1 15 Delaware 24.7 1/123 200.4 16 Oklahoma 26.6 1/133 199.7 17 Pennsylvania 24.5 1/124 197.9 18 Virginia 24.6 1/125 197.6 19 Georgia 23.3 1/118 197.4 20 Illinois 22.8 1/116 197.0 21 North Carolina 26.2 1/134 195.6 22 New Jersey 19.0 1/97 195.1 23 Maryland 22.0 1/113 194.9 24 Massachusetts 18.9 1/98 193.0 25 Michigan 24.2 1/125 193.0 26 Oregon 22.5 1/117 192.7 27 United States 23.0 1/121 190.1 28 New Hampshire 23.2 1/122 189.9 29 Washington 21.5 1/113 189.6 30 Rhode Island 22.4 1/118 189.5 31 South Dakota 22.5 1/119 188.9 32 Alaska 29.3 1/155 188.5 33 Wyoming 23.7 1/126 188.4 34 Iowa 23.2 1/124 187.1 35 Texas 22.9 1/123 186.3 36 Kansas 22.1 1/119 185.5 37 Wisconsin 23.3 1/127 182.8 38 Connecticut 19.4 1/107 182.1 39 Vermont 21.2 1/117 181.8 58

40 Idaho 20.6 1/113 181.7 41 Montana 21.2 1/117 181.5 42 Florida 22.1 1/122 181.3 43 Minnesota 21.8 1/120 181.2 44 New York 22.3 1/125 178.6 45 Nebraska 22.7 1/127 178.3 46 North Dakota 21.5 1/121 178.3 47 California 16.4 1/95 172.5 48 Arizona 23.4 1/126 172.3 49 Colorado 20.4 1/120 170.1 50 New Mexico 21.3 1/125 169.8 51 Hawaii 21.0 1/136 154.3 52 Utah 12.8 1/88 144.9

The problem is that most smokers, including many posters in this forum, have been infested by guilt (for allegedly harming themselves) and thus lack drive to defend publicly something they consider a bad habit of their own. It is a clever scheme and until smokers discard the anti-smoker "science", every rotten scrap of it, and realize that tobacco is an ancient medicinal plant, cultivated over milenia for its beneficial and benevolent smoke, thus which is good for them, the smokers will remain at the mercy of the swindlers. Hence, the type of pro-smoker organization which can fight and win, will have to have as its central postulate that smoking is good for smoker. It is true of course that a blind statistics, especially in recent years, will find correlation between smoking and variety of health problems. But that kind of correlation doesn't differentiate which is the cause and which is the consequence. For example, if you observe use of feeding tubes, you will find that their use correlates with spinal injury i.e. among those with spinal injury the feeding tubes will be found more often than among general population. Does that mean the feeding tubes are cause of spinal injuries? Or that banning feeding tubes will reduce occurence of spinal injuries? With smoking, even in the smoker friendly era, some portion of those attracted to smoking were people self-medicating themselves. Thus people in stressful or unhealthy jobs always tended to smoke more. Smoking stimulates internal antioxidants, such as glutathione (essential antioxidant for internal detox from mercury, aluminum, lead...), it is a kind of excercise for the immune system. With the social engineering against smokers, the social and economic pressures have filtered out smokers population, so that those who didn't really need

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to smoke (e.g. those who did it for social reasons, peer pressure) have largely quit, while those still smoking are largely people self-medicating. Hence, the correlation between smoking and various health ailments has increased in recent years. For those still smoking, quitting would not reduce the ailments but would increase them. Asthma and allergies (for which traditionally smoking was considered helpful) have been rapidly rising, while smoking has been decreasing. Alzheimers and Parkinson, have been increasing, too. Smoking is strongly protective against Alzheimer's e.g. when you match people genetically and socio-economically, such as when comparing between family members, smokers have ten times lower risk of Alzheimer's than their nonsmoking relatives! Of course, if you don't match the samples, but compare within general population, the smoking appears only mildly negatively correlated with Alzheimer's, and in recent 5-10 years even slighlty positively correlated. Similarly, smoking is strongly positively correlated with schizophrenia - schizophrenics smoke 23 times more often than general population, and smoke much more heavily than general smokers. Unlike Alzheimer's, schizophrenia usually starts in teens, often well before person has started smoking (or has smoked very little), hence it is obvious that smoking is a form of self-medication among schizophrenics rather than its cause (this has been also shown more explicitly). Even for lung cancer, smoking among asbestos workers was shown to be protective (a non-smoking asbestos worker is much more likely to get asbestos related lung cancer). In famous study by Doll (which was the first to find correlation between smoking & lung cancers), it was found that while lung cancers correlate positively with smoking, it was also found that those who inhale smoke have much lower rates of lung cancers than those who don't inhale! Similar stong protective effects of smoking against lung cancer (induced by radiation) were also demonstrated in controlled experiments on mice. Among nations, Japanese men smoke 2-3 times more often than Americans, yet they have 6-8 times lower rates of lung cancer. Similar paradoxical relations hold among Europeans, where Greeks are the heaviest smokers and have the lowest lung cancer rates. In USA, lung cancer has been rising for decades (most rapidly among non-smokers), and is now at its all time high, while smoking has been declining and is now at its all time low (note that CDC had to rig their counting to hide this fact contradicting their ideology and $$$) . After studying various papers and books (see e.g. Ray Johnstone, Lauren Colby, FORCES), as well as observing myself, my family and people I know, I have concluded that the truth about health effects of smoking is precisely opposite from the presentday conventional wisdom -- smoking is good for smoker. Further, believing antismoker propaganda, even partially, is harmful to smoker (due to witch doctor effect,

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negative placebo). In summary, there is money on our side, the money being currently stolen from us (only few crumbs of which are used against us). Unfortunately, until enough smokers realize that their habit is good for them (despite financial burden from extortion), there won't be organized and effective resistance against the anti-tobacco swindle. The essential first step in getting organized is to neutralize the key psychological weapon used against our will to defend ourselves, the poisonous anti-smoker pseudoscience.

Thu February 21 2008 04:24 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

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Table 39 (page 1 of 3). Death rates for malignant neoplasms of trachea, bronchus, and lung, by age: United States, selected years 19502004 [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 doesnt 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 doesnt 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 hasnt dropped at all. If anything it has increased. Smoking cannot be the major cause of Heart Disease!!!

The Truth-part 2 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;

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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 t