Health Benefits of Tobacco

Re-blogged from Gordon Vick on Facebook Anti-smoking Exposed, partly because it references The Black Lung Lie:

Health Benefits of Tobacco (with references)

1. Exposure to cigarette smoke was found to have a mitigating effect on radon daughter-induced tumours. 3
2. Smoking has a suppressive effect on radiation-induced pneumonitis.3
3. The risk of developing lung cancer from asbestos exposure was significantly decreased in smokers in six of the studies 5
4. Smokers showed a significantly decreased inflammatory reaction i.e., reduced levels of mast cells and lymphocytes, compared to both non-smoking controls and patients. 7
5. Miners who were heavily exposed to diesel fumes have three times the higher risk of dying from lung cancer compared with miners with low exposure. Whereas for non-smokers, the risk was seven times higher. 8
6. Doctors are unable to tell you from examining a lung whether or not its former host had smoked. 10
7. Nicotine stimulation plays a key role in suppressing cytokine production, can significantly down-regulate and delay inflammatory and autoimmune responses in the central nervous system, and could further attenuate neuro-inflammation. 13
8. Nicotine treated mice injected with lethal doses of influenza A virus infection also displayed longer survival rates when compared to control groups. 13
9. People who received nicotine performed better on almost every test despite whether they were smokers or not, and this was especially in areas of memory, speed, precision, focus and attention. 14
10. Nicotine users performed significantly better in other areas such as long-term memory, semantic memory, arithmetic & complex calculations, and gross motor skills. 14
11. Smoking delivered nicotine produces improvements in mental efficiency. 15
12. Smoking delivered nicotine is associated with lower levels of social withdrawal, better cognitive function, and blunted emotional and motivational responses. 16
13. Nicotine improves attention in a wide variety of tasks in healthy volunteers. 17
14. Nicotine improves immediate and longer term memory in healthy volunteers. 17
15. Nicotine improves attention in patients with probable Alzheimer’s Disease. 17
16. Smokers have significantly lower levels of both types of MAO’s (A and B), which means that smoking acts as a natural antidepressant – without any of the horrible side-effects common to many pharmaceuticals. 18
17. Smokers lungs have been found to contain 80% more glutathione than the lungs of non-smokers. 22 It plays a critical role in detoxification processes and is acknowledged as the “mother of all antioxidants. Higher concentrations of glutathione in the lungs offer increased protection against foreign material and pathogenic agents
18. Smoking up-regulates the glutathione adaptive response, COPD is caused by an under active “glutathione adaptive response”, 23 so smoking clearly doesn’t cause COPD. It would be logical to assume that smoking can actually prevent COPD.
19. Superoxide dismutase enzyme levels in the blood and saliva were significantly higher in smokers than in non-smokers and the controls. 24 This could possibly explain how tobacco smoke manages to prevent lung cancer in those inhalling radiation, exhaust fumes and asbestos.
20. Therapeutic efficacies of carbon monoxide at low concentration (such as in cigarette smoke) have been demonstrated in experimental models of several conditions, including lung injuries, heart, hepatic and renal I-R injuries, as well as inflammation, including arthritis. 26
21. Smokers in the aluminium potroom group had a lower prevalence of respiratory symptoms than never smokers or ex-smokers 27
22. Smoking can strongly decrease someone’s risk of developing osteoarthritis 28 and provide some level of protection
23. Smokers demonstrate significant protection at four sites commonly seen in OA patients (knee, spine, hand and foot)29
24. . Smoking also presents a negative correlation with large joint OA and has been shown to decrease the risk of OA in obese individuals30.
25. When compared with non smokers, former smokers had a 22% lower risk of developing Parkinson’s disease, while current smokers had a staggering 73% lower risk 32
26. The more a person smokes, the lower the chances are of contracting Parkinson’s disease. 33
27. The risk of Alzheimer’s disease decreases with increasing daily number of cigarettes smoked before onset of disease. 35
28. Schizophrenics, 90% of whom smoke, have been shown to be between 30-60% less likely to develop lung and other cancers. 37
29. Current smokers are associated with an approximately 42% reduced risk, of contracting ulcerative colitis, however former smokers are associated with increased risk when compared to non-smokers. 41
30. SIRT1 activity is consistently up-regulated in smokers. This increase in SIRT1 activity may serve as a protective effect against oxidative stress and DNA damage. 56
31. Most of the oldest people in the world were smokers. Example –
Jeanne Louise Calment who smoked from age of 21 until she quit at age 117 and died at age 122. 57


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3. Cross F, Palmer R, Filipy R, Dagle G, Stuart B. Carcinogenic Effects of Radon Daughters, Uranium Ore Dust and Cigarette Smoke in Beagle Dogs. Health Physics 1982;42:33-52.
4. Bjermer L, Cai Y, Nilsson K, Hellstrom S, Henriksson R. Tobacco smoke exposure suppresses radiation-induced inflammation in the lung: a study of bronchoalveolar lavage and ultrastructural morphology in the rat [Internet]. 1st ed. [cited 2016 Mar 10]. Available from:
5. Lee P. Relation between exposure to asbestos and smoking jointly and the risk of lung cancer. Occupational and Environmental Medicine 2001;58:145-153.
6. BERRY G. The Interaction of Asbestos and Smoking in Lung Cancer: A Modified Measure of Effect. Annals of Occupational Hygiene 2004;48:459-462.
7. Bjermer L, Franzen L, Littbrand B, Nilsson K, Angstrom T, Henriksson R. Effects of Smoking and Irradiated Volume on Inflammatory Response in the Lung of Irradiated Breast Cancer Patients Evaluated with Bronchoalveolar Lavage [Internet]. 1st ed. Cancer Research; 1990 [cited 2016 Mar 10]. Available from:
8. Silverman D, Samanic C, Lubin J, Blair A, Stewart P, Vermeulen R et al. The Diesel Exhaust in Miners Study: A Nested Case–Control Study of Lung Cancer and Diesel Exhaust [Internet]. 1st ed. Oxford University Press 2012; 2011 [cited 2016 Mar 10]. Available from:…/press_r…/silvermandjs034.pdf
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12. Segura G. Nicotine – The Zombie Antidote [Internet]. Signs Of The Times2012 [cited 2016 Mar 10];Available from:…/254745-Nicotine-The-Zombie-Antidote
13. Han Y, Lau Y. Nicotine, an anti-inflammation molecule. Inflammation and Cell Signaling 2014;
14. Heishman S, Kleykamp B, Singleton E. Meta-analysis of the acute effects of nicotine and smoking on human performance. Psychopharmacology 2010;210:453-469.
15. Wesnes K, Warburton D. Smoking, Nicotine and Human Performance [Internet]. 1st ed. Pergamon Press Ltd; 1983 [cited 2016 Mar 10]. Available from:…
16. Esterlis I, Ranganathan M, Bois F, Pittman B, Picciotto M, Shearer L et al. In Vivo Evidence for β2 Nicotinic Acetylcholine Receptor Subunit Upregulation in Smokers as Compared With Nonsmokers With Schizophrenia. Biological Psychiatry 2014;76:495-502.
17. Warburton D. Nicotine As A Cognitive Enhancer [Internet]. 1st ed. Department of Psychology, University of Reading: Pergamon Press ltd; 1991 [cited 2016 Mar 10]. Available from:
18. Fowler J, Volkow N, Wang G, Pappas N, Logan J, Shea C et al. Brain monoamine oxidase A inhibition in cigarette smokers. Proceedings of the National Academy of Sciences [Internet] 1996 [cited 2016 Mar 10];93:14065-14069. Available from:
19. Milgram N, Racine R, Nellis P, Mendonca A, Ivy G. Maintenance on L-deprenyl prolongs life in aged male rats. [Internet]. PubMed, NCBI1990 [cited 2016 Mar 10];Available from:
20. Yen T, Knoll J. Extension of lifespan in mice treated with Dinh lang (Policias fruticosum L.) and (-)deprenyl. [Internet]. PubMed, NCBI1992 [cited 2016 Mar 10];Available from:
21. Ballatori N, Krance S, Notenboom S, Shi S, Tieu K, Hammond C. Glutathione dysregulation and the etiology and progression of human diseases. Biological Chemistry 2009;390.
22. Cantin A, North S, Hubbard R, Crystal R. Normal alveolar epithelial lining fluid contains high levels of glutathione. Journal of Applied Physiology [Internet] 1987 [cited 2016 Mar 10];63:152-157. Available from:
23. Gould N, Min E, Gauthier S, Martin R, Day B. Lung glutathione adaptive responses to cigarette smoke exposure. Respiratory Research 2011;12:133.
24. Jenifer H, Bhola S, Kalburgi V, Warad S, Kokatnur V. The influence of cigarette smoking on blood and salivary super oxide dismutase enzyme levels among smokers and nonsmokers—A cross sectional study. Journal of Traditional and Complementary Medicine 2015;5:100-105.
25. Mccusker K, Hoidal J. Selective Increase of Antioxidant Enzyme Activity in the Alveolar Macrophages from Cigarette Smokers and Smoke-exposed Hamsters. Am Rev Respir Dis 1990;141:678-682.
26. Naito Y, Uchiyama K, Takagi T. Therapeutic Potential of Carbon Monoxide (CO) for Inflammatory Bowel Disease. Digestion 2015;91.
27. Radon K, Nowak D, Szadkowski D. Lack of combined effects of exposure and smoking on respiratory health in aluminium potroom workers. Occupational and Environmental Medicine 1999;56:468-472.
28. Felson D, Anderson J, Naimark A, Hannan M, Kannel W, Meenan R. Does smoking protect against osteoarthritis?. Arthritis Care Res 1989;32:166-172.
29. Wilder F, Hall B, Barrett J. Smoking and osteoarthritis: Is there an association? The Clearwater Osteoarthritis Study. Osteoarthritis and Cartilage 2003;11:29-35.
30. Sandmark H, Hogstedt C, Lewold S, Vingard E. Osteoarthrosis of the knee in men and women in association with overweight, smoking, and hormone therapy. Annals of the Rheumatic Diseases 1999;58:151-155.
31. Gullahorn L, Lippiello L, Karpman R. Smoking and osteoarthritis: differential effect of nicotine on human chondrocyte glycosaminoglycan and collagen synthesis. Osteoarthritis and Cartilage 2005;13:942-943.
32. Thacker E, O’Reilly E, Weisskopf M, Chen H, Schwarzschild M, McCullough M et al. Temporal relationship between cigarette smoking and risk of Parkinson disease. Neurology 2007;68:764-768.
33. Gorell J, Rybicki B, Johnson C, Peterson E. Smoking and Parkinson’s disease: A dose-response relationship. Neurology 1999;52:115-115.
34. Toulorge D, Guerreiro S, Hild A, Maskos U, Hirsch E, Michel P. Neuroprotection of midbrain dopamine neurons by nicotine is gated by cytoplasmic Ca2+. The FASEB Journal 2011;25:2563-2573.
35. van Duijn C, Hofman A. Relation between nicotine intake and Alzheimer’s disease. BMJ 1991;302:1491-1494.
36. Schizophrenia and smoking: an epidemiological survey in a state hospital. American Journal of Psychiatry 1995;152:453-455.
37. Hodgson R, Wildgust H, Bushe C. Review: Cancer and schizophrenia: is there a paradox?. Journal of Psychopharmacology 2010;24:51-60.
38. Nicotine Helps Schizophrenics with Attention and Memory [Internet]. Yale News2005 [cited 2016 Mar 10];Available from:…/nicotine-helps-schizophrenics-attent…
39. Zammit S, Allebeck P, Dalman C, Lundberg I, Lewis G. Investigating the Association between Cigarette Smoking and Risk of Developing Schizophrenia in a Cohort Study. Clin Sci 2003;104:41P.2-41P.
40. Lashner B. Inflammatory bowel disease: family patterns and risk factors. [Internet]. PubMed, NCBI1992 [cited 2016 Mar 10];Available from:
41. Bastida B, Beltrán G. Ulcerative colitis in smokers, non-smokers and ex-smokers. World Journal of Gastroenterology : WJG [Internet] 2011 [cited 2016 Mar 10];17:2740. Available from:
42. Thomas G. Role of smoking in inflammatory bowel disease: implications for therapy. Postgraduate Medical Journal 2000;76:273-279.
43. Chu J. The Genetics of Nicotine Addiction [Internet]. MIT Technology Review2007 [cited 2016 Mar 10];Available from:…/the-genetics-of-nicotin…/
44. Davies G, Soundy T. The genetics of smoking and nicotine addiction. S D Med [Internet] 2009;Available from:
45. Massudi H, Grant R, Guillemin G, Braidy N. NAD + metabolism and oxidative stress: the golden nucleotide on a crown of thorns. Redox Report 2012;17:28-46.
46. Anderson R, Bitterman K, Wood J, Medvedik O, Cohen H, Lin S et al. Manipulation of a nuclear NAD+ salvage pathway delays aging without altering steady-state NAD+ levels. Journal of Biological Chemistry 2013;288:24160-24160.
47. Yamauchi K, Nakajima J. Effect of coenzymes and thyroid hormones on the dual activities ofXenopuscytosolic thyroid-hormone-binding protein (xCTBP) with aldehyde dehydrogenase activity. European Journal of Biochemistry 2002;269:2257-2264.
48. Gomes A, Price N, Ling A, Moslehi J, Montgomery M, Rajman L et al. Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging. Cell 2013;155:1624-1638.
49. Prolla T, Denu J. NAD+ Deficiency in Age-Related Mitochondrial Dysfunction. Cell Metabolism 2014;19:178-180.
50. Imai S, Armstrong C, Kaeberlein M, Guarente L. Transcriptional silencing and longevity protein Sir2 is an NAD-dependent histone deacetylase. Nature [Internet] 2000 [cited 2016 Mar 10];Available from:
51. Ghosh H, McBurney M, Robbins P. SIRT1 Negatively Regulates the Mammalian Target of Rapamycin. PLoS ONE 2010;5:e9199.
52. Suh J, Sieglaff D, Zhang A, Xia X, Cvoro A, Winnier G et al. SIRT1 is a Direct Coactivator of Thyroid Hormone Receptor β1 with Gene-Specific Actions. PLoS ONE 2013;8:e70097.
53. Sabir M, Khan Z. Resveratrol and SIRT1 Are Novel Positive Modulators of Vitamin D Signaling Via Apparent Deacetylation of VDR : Late-breaking Bone, Calciotropic Hormones & Vitamin D III. Endocrine Society [Internet] 2015 [cited 2016 Mar 10];Available from:…/endo-meetings.2015.BCHVD.6.LBS…
54. Kotas M, Gorecki M, Gillum M. Sirtuin-1 is a nutrient-dependent modulator of inflammation. Adipocyte 2013;2:113-118.
55. Chalkiadaki A, Guarente L. Sirtuins mediate mammalian metabolic responses to nutrient availability. Nat Rev Endocrinol 2012;8:287-296.
56. Beane J, Cheng L, Soldi R, Zhang X, Liu G, Anderlind C et al. SIRT1 Pathway Dysregulation in the Smoke-Exposed Airway Epithelium and Lung Tumor Tissue. Cancer Research 2012;72:5702-5711.
57. WHITNEY C. Jeanne Calment, World’s Elder, Dies at 122 [Internet]. Nytimes.com2016 [cited 2016 Mar 10];Available from:…/jeanne-calment-world-s-elder-dies-…

About Frank Davis

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31 Responses to Health Benefits of Tobacco

  1. Lovely references. All that aside, smoking tobacco is just plain wonderful and makes me happy…

    • Harleyrider1978 says:

      Not that many do now since Obama basically went after all the doctors prescribing and stiff armed them with threats of medical listened if they didn’t stop scripts. Now people like the elderly go to the streets since they afford pain clinic costs and pharma raised the price on drugs so high even street opiates from pharma are now 20 bucks a pop in places. While cut heroine is way cheaper there’s even homemade opiate pills on the streets now more or less like bathtub gin concoctions where the buyer beware as the doses aren’t measured or even safe. All because Obama changed the schedules and had DEA shake down everyone in the medical profession.

  2. jaxthefirst says:

    One particularly nasty ailment which smokers also get significantly less often than non-smokers, which is often overlooked, is Motor Neurone Disease (MND) – a long-term, incurable, untreatable, horrifically drawn-out death sentence of an illness. MND gradually diminishes a person’s ability to control all their motor functions, including the most essential ones such as swallowing, speech, and blinking, whilst – most cruelly of all – still leaving their cognitive functions intact, often resulting, eventually, in the horrors of a form of “locked-in” syndrome. There is no known cure and little, if any, effective treatment and it is sufferers of Motor Neurone Disease who have been the most active campaigners in the courts, fighting for the rights of their families to assist them in ending their lives, simply because they know only too well what the future holds for them, and it ain’t pretty. Smokers, it seems, almost never get it – to the point that (and I wish I could remember where I heard/read the quote, but I can’t) “long-term smokers get it so rarely that they could essentially be described as ‘immune.’”

    • Frank Davis says:

      If you could remember, it could be added to the list. The great thing about it is that it’s got so many references.

      In fact, a quick search turned up lots of blaming it on smoking.

      There is plentiful literature that suggests prolonged heavy cigarette smoking and exposure to organic solvents and heavy metals as modifiable risk factors for MND.

  3. waltc says:

    Is there a typo in #3. Says decreased in non-smokers

    • Frank Davis says:

      It certainly contradicts all the rest. I’ve gone back to Facebook to point this out. I hope there’ll be a correction forthcoming.

      • Gordon Vick says:

        Thanks people. It was a slip of the typing finger. I have fixed it in the original post on Facebook. The item should read “3. The risk of developing lung cancer from asbestos exposure was significantly decreased in smokers in six of the studies

    • Cecily Collingridge says:

      There isn’t a clear cut picture in No.3 The abstract says:

      OBJECTIVES To review evidence about the joint relation of exposure to asbestos and smoking on the risk of lung cancer to answer three questions: (1) does asbestos increase risk in non-smokers; (2) are the data consistent with an additive model; and (3) are the data consistent with a multiplicative model?

      METHODS Analysis of 23 studies reporting epidemiological evidence on the joint relation. Comparison of risk of lung cancer in subjects unexposed to asbestos or smoking, exposed to asbestos only, to smoking only, or to both. Estimation of the relative risk associated with asbestos exposure in non-smokers and of statistics testing for additivity and multiplicativity of risk.

      RESULTS Eight of the 23 studies provided insufficient data on the risk of lung cancer in non-smokers to test for possible effects of asbestos. Asbestos exposure was associated with a significantly (p<0.05) increased risk in non-smokers in six of the remaining studies and with a moderately increased, but not significant, increase in a further six. In two of the three studies that found no increase, asbestos exposure was insufficient to increase risks in smokers. In 30 of 31 data sets analysed, risk in the combined exposure group was greater than predicted by the additive model. There was no overall departure from the multiplicative model, the proportional increase in risk of lung cancer with exposure to asbestos being estimated as 0.90 (95% confidence interval (95% CI) 0.67 to 1.20) times higher in smokers than non-smokers. For two studies significant (p<0.05) departures from a multiplicative relation were found in some, but not all, analyses. Reasons are presented why these may not indicate true model discrepancies.

      CONCLUSIONS Asbestos exposure multiplies risk of lung cancer by a similar factor in non-smokers and smokers. The extent to which it multiplies risk varies between studies, no doubt depending on the type of asbestos involved, and the nature, extent, and duration of exposure.

  4. Lepercolonist says:

    I congratulate Gordon Vick for his excellent compilation of research.

    • Gordon Vick says:

      Thanks Lepercolonist. Much as I would like to take the credit, this is a summary of a long post that a fellow forum member made on the forum at a post on smoking on All I did was summarise it into bullet points with references so people like us could more easily use it to refute the Tobacco Control Puritans lies.

  5. Rose says:

    A wonderful compilation, many of which I haven’t seen before, but I would wary of any attribution of the effects to nicotine in studies. Nicotine is the only chemical in cigarette smoke that some scientists appear to be aware of and in the search for understanding and new treatments for non-smokers, greater attention should be given to other components of a burning tobacco leaf like low dose Nitric Oxide, Carbon Monoxide, Nicotinic Acid/Niacin and the various derivatives of Solanesol.

    After all, who knew that the tobacco plant made Salicylic acid (from Latin salix, willow tree, from the bark of which the substance used to be obtained) in response to attack until very recently?

    Systemic acquired resistance (SAR)

    “The level of SA increases by several hundred fold in tobacco or cucumber after pathogen infection (Malamy et al. 1990, Rasmussen et al.1991), and this increase has been shown to correlate with SAR not only in tobacco and cucumber but also in many other plants (Malamy et al. 1990, Metraux et al.

    To unlock the properties of Tobacco nothing should be missed out.

  6. Cecily Collingridge says:

    To add to the list (specific to women), here is another example of a powerful study that confirmed a beneficial effect of smoking which was found by other researchers:

    “Alcohol consumption, cigarette smoking, and endometrial cancer risk: results from the Netherlands Cohort Study” by A Loerbroks, L J Schouten, R A Goldbohm, P A van den Brandt, Cancer Causes & Control, 2007 Jun; 18(5): 551–560.

    Their summary conclusion was “There is no association between alcohol consumption and endometrial cancer. Current smoking is associated with a reduced risk of endometrial cancer. This association is neither mediated by BMI nor by age at menopause.”

    • Rose says:

      From Anti-Tobacco in Australia

      3.28.3 Endometrial cancer and uterine fibroids

      “Epidemiological studies have consistently reported that active cigarette smoking is inversely associated with developing cancer of the endometrium (the membrane lining of the uterus) in women who have reached menopause.

      A recent meta-analysis found that cigarette smoking was significantly associated with a reduced risk, especially so among postmenopausal women, where a 29% reduction in risk was found (RR 0.71; 95% CI, 0.65–0.78). Very similar results have been reported from recent studies conducted in Poland”

      “The Polish researchers found that obese women showed the greatest risk reduction for current smoking (OR 0.47; 95% CI, 0.27–0.81)”

      Then goes on dispute or suggest other possible reasons for the findings they don’t like.

      • Cecily Collingridge says:

        At the end of the day, Rose, I don’t give a damn. I don’t live my life weighing up risk factors and I consider risk factor epidemiology has brought the whole field into disrepute. It’s a money-making industry for researchers. The focus on lifestyles is turning people in the developed world neurotic. Just look at our Chief Medical Officer’s OCD considering her breast cancer risk every time she reaches out for a glass of wine! I’m with Some Other Tom.,. smoking makes me happy.

        • Rose says:

          I quite agree, but lying by omission is unforgivable, people deserve much better.

        • Cecily Collingridge says:

          I agree with you there.

          But I do care about the quality of studies or experiments, irrespective of whether beneficial or detrimental effects are found. Most research is rubbish and Frank’s copied list is not exempt of bad examples. Conclusions should not be relied upon.

          As I have emphysema, I looked at the one mentioning COPD done in 2011 (Ref.23). A quick read through was already enough to find limitations. E.G.

          i) It incorporated an animal study – I do not consider animals acceptable proxies for humans.

          ii) The experiments were on the commonly used C57BL/6 mouse, aka Black-6 – Daniel Engber wrote an interesting three-part series of articles a few years ago on this mouse in which the description was:
          “He’s a teenaged, alcoholic couch potato with a weakened immune system, and he might be a little hard of hearing.”

          It’s usefulness is questioned by a number of scientists and I, personally, cannot identify with a teenaged, alcoholic mouse (!) as I have never had much tolerance for alcohol myself and I’m no spring chicken.

          iii) All the mice were male – All to many experiments are still sex-biased making them worthless as far as women are concerned. It goes against modern research guidelines. The WHO adopted sex parity in research back in 2000, I think.

          iv) The authors did not state how many mice were used. Sample size is important. Small samples can be worthless.

        • beobrigitte says:

          I don’t give a damn. I don’t live my life weighing up risk factors and I consider risk factor epidemiology has brought the whole field into disrepute. It’s a money-making industry for researchers.
          Hypothetical danger sells and fear kills common sense. Otherwise people would ask the first and most obvious question: WHO financed studies with what expected result?

          Epidemiology is only the tip of the iceberg…..

        • harleyrider1978 says:

          Epidemiologists Vote to Keep Doing Junk Science

          Epidemiology Monitor (October 1997)

          An estimated 300 attendees a recent meeting of the American College of
          Epidemiology voted approximately 2 to 1 to keep doing junk science!

          Specifically, the attending epidemiologists voted against a motion
          proposed in an Oxford-style debate that “risk factor” epidemiology is
          placing the field of epidemiology at risk of losing its credibility.

          Risk factor epidemiology focuses on specific cause-and-effect
          relationships–like heavy coffee drinking increases heart attack risk. A
          different approach to epidemiology might take a broader
          perspective–placing heart attack risk in the context of more than just
          one risk factor, including social factors.

          Risk factor epidemiology is nothing more than a perpetual junk science machine.

          But as NIEHS epidemiologist Marilyn Tseng said “It’s hard to be an
          epidemiologist and vote that what most of us are doing is actually harmful
          to epidemiology.”

          But who really cares about what they’re doing to epidemiology. I thought
          it was public health that mattered!

          we have seen the “SELECTIVE” blindness disease that
          Scientist have practiced over the past ten years. Seems the only color they
          see is GREEN BACKS, it’s a very infectious disease that has spread through
          the Scientific community with the same speed that any infectious disease
          would spread. And has affected the T(thinking) Cells as well as sight.

          Seems their eyes see only what their paid to see. To be honest, I feel
          after the Agent Orange Ranch Hand Study, and the Sl-utz and Nutz Implant
          Study, they have cast a dark shadow over their profession of being anything
          other than traveling professional witnesses for corporate hire with a lack
          of moral concern to their obligation of science and truth.

          The true “Risk Factor” is a question of ; will they ever be able to earn
          back the respect of their profession as an Oath to Science, instead of
          corporate paid witnesses with selective vision?
          Oh, if this seems way harsh, it’s nothing compared to the damage of peoples
          lives that selective blindness has caused!

        • Some French bloke says:

          Epidemiology is only the tip of the iceberg … for those with eyes to see, that is. I’d suggest that the bulk of the iceberg is economics (e.g. “WHO financed studies…”). What’s worse is that the machinations thereof are sufficiently globalised to be safely beyond the reach of national electorates, however enlightened (which is not much the case at present). :(

        • Gordon Vick says:

          This is a really interesting article on Research studies, actually written by an Epidemiologist. He basically says that almost all published research is rubbish. Well worth a read.

  7. jltrader says:

    How about this piece of junk ?
    Are There Ways to Prevent Earaches From Colds or Ear Infections?
    Avoid contact with second-hand tobacco smoke, which increases the frequency and severity of ear infections.
    Reviewed by Jennifer Robinson, MD on October 28, 2014

  8. smokingscot says:

    For those who give a toss, George’s stuck to the 2% escalator for manufactured cigarettes, but hiked the escalator for rolling tobacco to 5%. There’s also talk about a minimum price level, but no details yet (odd, given that the EU barred that sort of thing for booze).

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