Originally posted by: Fausto1
Originally posted by: Valinos
Originally posted by: ergeorge
LoL The Jpurnal of Theoretics is a quack operation if I ever saw one!
Take a look at some of the other articles (GUT, Antigravity, papers published from PO boxes.
That paper is a poster child for how to lie with statistics.
Can I get some substantial evidence that the Journal of Theoretics is a "quack operation?" As soon as you show me some unbiased proof that its not a reliable source then I'll retract my statement...until then, you still lose. Don't cry too hard that you had your feelings hurt on an Internet message board...its ok, I'm sure mom still loves you.
You want proof? Look at all the journal articles listed under the "1" reference.
J Cancer, JAMA, J Natl Cancer Inst.....all peer-reviewed, all highly creditable. What's laughable is that the author thinks he can utterly discount all these articles essentiallly on semantics alone. Sure, not everyone who smokes gets lung cancer....but it does greatly increase the likelyhood of developing various respiratory and cardiovascular diseases. The data is all there, he just chooses to ignore it. He even states that he believes the tobacco industry folks when they testified that they "didn't believe smoking causes cancer" (who have every reason in the world to lie their asses off), and yet he disagrees with data published in the most respected medical and scientific journals. The only place you'll find articles like his are on the "Unconventional Science" sites scattered around the internet. Strangely, you won't find any of this stuff on PubMed or Entrez searches. Why? Because it's crap that no real journal will publish.
Here are a few abstracts from the first page of journal articles brought up via a PubMed search for "smoking and cancer".
New approaches to lung cancer prevention.
McWilliams A, Lam S.
Lung Tumor Group, British Columbia Cancer Agency, University of British Columbia, 600 West 10th Avenue, Vancouver, BC, Canada V5Z 4E6. slam@ bccancer. bc.ca
Lung cancer is the most common cause of cancer death worldwide. The overall 5-year survival rate remains disappointing at 14% or less. Several clinician- and community-based interventions show promise for reducing lung cancer incidence through prevention and smoking cessation. However, long-term heavy smokers retain a significant lung cancer risk despite smoking cessation. Half of newly diagnosed lung cancers are now found in former smokers. An additional strategy of lung cancer control through chemoprevention needs to be developed. Advances in optical imaging technologies and genome science will continue to improve our ability to identify individuals with the highest risk of lung cancer for chemoprevention. More accurate surrogate endpoint biomarkers are becoming available for phase II trials of new agents. A number of promising agents are currently being tested in phase II and III trials for prevention of lung cancer.
Molecular epidemiology of smoking and lung cancer.
Shields PG.
Lombardi Cancer Center, Georgetown University Medical Center, The Research Building, W315, 3970 Reservoir Rd. NW, Washington, DC 20007, USA.
Lung cancer is the single most common cause of death, and almost all of it is due to tobacco smoking. Before the widespread use of cigarettes in this century, lung cancer was a rare illness. Tobacco smoke is a complex mixture of numerous mutagens and carcinogens. Over the last 40 years, the type of cigarettes most frequently used has been changing, namely the increased use of low tar and nicotine cigarettes. This has been accompanied by an increased risk of lung cancer due to a smokers' need to maintain blood nicotine levels, which in turn causes the need for smoking more cigarettes per day and deeper inhalation. This phenomena has led to the increasing rates of lung adenocarcinoma, compared to squamous cell carcinoma. It also probably explains, in part, the greater risk of lung cancer in women compared to men (in addition to some biological differences). The study of lung cancer involves many types of biomarkers, including those that measure exposure, the biologically effective dose and harm. The use of these has allowed us to understand many parts of lung carcinogenesis. Genetic susceptibilities play a large role in lung cancer risk. They govern smoking behavior (affecting dopamine reward mechanisms due to nicotine and nicotine metabolism), carcinogen metabolism and detoxification, DNA repair, cell cycle control and other cellular responses. The need for the study of lung cancer is highlighted by the need to improve cessation rates and reduce exposure among persons who cannot quit smoking, for better prevention strategies for former smokers and an understanding of environmental tobacco smoke risk. doi:10.1038/sj.onc.1205832
Polymorphic metabolizing genes and susceptibility to atherosclerosis among cigarette smokers.
Salama SA, Au WW, Hunter GC, Sheahan RG, Badary OA, Abdel-Naim AB, Hamada FM.
Department of Preventive Medicine and Community Health, University of Texas Medical Branch, Galveston, Texas, USA.
Atherosclerosis (AR) is the leading cause of morbidity and mortality in the US and cigarette smoking is a major contributing factor to the disease. Like cigarette smoking in lung cancer, genetic susceptibility may be an important factor in determining who is more likely to develop AR. However, the current emphasis has been on susceptibility based on altered cardiovascular homeostasis. In this investigation, we studied 120 AR patients and 90 matched controls to elucidate the association between polymorphisms in some metabolizing genes (GSTM1, GSTT1, CYP2E1, mEH, PON1, and MPO) and susceptibility to AR. We found that the GSTT1 null allele and the fast allele of mEH(*) (exon 4) are associated with risk for AR. Furthermore, the combined genotypes GSTM1 null/ CYP2E1(*)5B, GSTM1 null/mEH YY, and GSTT1 null/mEH YY are significantly associated with susceptibility to AR (OR = 15.42, 95% CI = 1.33-77.93, P = 0.021; OR = 3.48, 95% CI = 1.63-8.04, P = 0.0008; OR = 3.4; 95% CI = 0.99-17.38, P = 0.05; respectively). We have also conducted cytogenetic analysis to elucidate if induction of chromosome aberrations (CAs) is a biomarker of AR susceptibility. We found that among cigarette smokers (AR patients and smoker controls), individuals having the GSTM1 null allele had a significantly higher frequency of CAs compared to those with the normal allele (P < 0.05). This association was not found among nonsmokers. In addition, individuals who had inherited the CYP2E1(*)5B allele exhibited a significantly higher CA frequency (8.0 +/- 0.82) compared to those with the CYP2E1 wild-type genotype (4.31 +/- 0.35). Since the analysis of genetic susceptibility factors is still in its infancy, our study may stimulate additional investigations to understand the roles of genetic susceptibility and cigarette smoking in AR. Environ. Mol. Mutagen. 40:153-160, 2002. Copyright 2002 Wiley-Liss, Inc.
And finally, here's the rundown on smoking compliments of the
Morbidity and Mortality World Report
Cigarette smoking continues to be a leading cause of death in the Unites States, and imposes substantial measurable costs to society. From 1995?1999, smoking killed over 440,000 people in the United States each year.
Each pack of cigarettes sold in the United States costs the nation an estimated $7.18 in medical care costs and lost productivity.
Estimates show that smoking caused over $150 billion in annual health-related economic losses from 1995 to 1999 including $81.9 billion in mortality-related productivity losses (average for 1995?1999) and $75.5 billion in excess medical expenditures in 1998.
The economic costs of smoking are estimated to be about $3,391 per smoker per year.
Smoking caused an estimated 264,087 male and 178, 311 female deaths in the United States each year from 1995 to 1999.
Among adults, the study estimates that most deaths were from lung cancer (124,813), ischemic heart disease (81,976) and chronic airway obstruction (64,735).
Excluding adult deaths from exposure to secondhand smoke, adult males and females lost an average of 13.2 and 14.5 years of life respectively, because they smoked.
Smoking during pregnancy resulted in an estimated 599 male infant and 408 female infant deaths annually.
For men, the average number of annual smoking-attributable cancer and cardiovascular disease deaths in 1995?1999 fell while the number of respiratory disease deaths remained stable.
For women, the average number of annual smoking-attributable cancer and respiratory disease deaths in 1995?1999 rose while the number of cardiovascular deaths fell.
Smoking-attributable neonatal expenditures were estimated at $366 million in 1996 or $704 per maternal smoker.
And on and on and on and on. Kindly present us all with whatever you can dig up in
real journals that indicates smoking isn't as harmful as 99.9% of journal articles state and we'll stop calling your pathetic "Journal" quackery.