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Carol A S Thompson Flambeau Micro Plastics
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The brains of persons thought to be suffering from incipient dementia temporarily release large amounts of ammonia, which declines to smaller amounts in advanced states. This is in contrast to normal brains, which take up a small amount of ammonia (Hoyer S et al. Ammonia is endogenously generated in the brain in the presence of presumed and verified dementia of Alzheimer type. Neurosci Lett 1990 Sep 18;117(3):358-362). The use only of data as last recorded 10 or more years before death, ostensibly "to avoid any material effect of the disease itself on smoking habits," also avoids any meaningful examination of any material effect of smoking on the disease process. This flagrant disregard of the pathogenesis of diseases in favor of simplistic comparisons of smokers versus nonsmokers is typical of the anti -smoking junk science embraced by the British Medical Journal, and of Doll & Peto in particular. In addition, a death certificate study concerning a disease which is known to be grossly underreported on death certificates, since more people die with it than of it, is not suitable for drawing conclusions about the onset rates of the disease. Finally, Alzheimer's disease has been associated with lower intellectual abilities much earlier in life (Snowdon DA et al. Linguistic ability in early life and cognitive function and Alzheimer's disease in late life. Findings from the Nun Study. JAMA 1996 Feb 21;275(7):528-532), and such persons are unlikely to become doctors. So, the study of Doll & Peto et al is flawed by a severe selection bias as well. |
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Eric Boyd University of Waterloo
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R Doll et al's findings that ‘persistent smoking does not substantially reduce the age specific onset rate of Alzheimer's disease or of dementia in general' is not surprising. The authors didn't compare smokers to non-smokers. By combining 'lifelong non-smokers and ex-smokers' in the 'non- continuing' group they effectively stopped comparing smokers to non smokers. To further complicate the issue the authors then note ‘As questionnaires were sent out only every six to 12 years, the mean time before death that the relevant smoking habits had been recorded was not 10 but 15 years'. In the end this study compares a group including non-smokers and ex- smokers who may have started smoking in the last 15 years to a group of smokers who may have quit in the last 15 years. Has the British Journal of Medicine fallen prey to the concerted and unrelenting efforts of ‘health organizations' determined to dictate an anti-smoking social policy rather than providing the honest and unbiased facts individuals need to make informed personal choices - or is the BMJ part of the team? |
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Joao Calinas-Correia, medical practitioner contact: 16 Roskear, Camborne, Cornwall TR14 8DN
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Iain Chalmers and Douglas Altman [1] analysed the work of Janerich et al. [2] regarding passive smoking and lung cancer. The authors focused on the effects on children, presenting an hypothesis which is contradicted by their own results (according to Chalmers and Altman), and fail to comment on the inverse relationship they found between social exposure to passive smoking and lung cancer. This is just an example of the kind of bias we are likely to suffer from when dealing with cigarette smoking in the current political environment. Doll and colleagues present another version of a politically engaged analysis [3]. While they found that smoking seems to protect against Alzheimer's disease, and eventually offering long-lasting protection as the ex-smokers presented a decrease in risk similar to current smokers, their final comment reorganises the data to affirm the opposite: while they present their results comparing current smokers against never smokers, ex-smokers against never smokers, and current against ex-smokers, on their final comparison with other studies, they create a different category, different from their discussion and different from the comparable studies - an originality! Is it prompted by their findings? No, it is not: they found a pattern where current and ex-smokers behave similarly, but aggregated ex-smokers to never smokers anyhow. With this trick, the difference they found between all smokers and never smokers was diluted and they could present the politically correct conclusion: no benefit. However, Doll et al. results reinforce the evidence for protection regarding Alzheimer's disease, with a risk rate of 0.83 for continuing smokers and 0.78 for ex-smokers, refining, but fundamentally agreeing, with the results they quote from Herbert et al. The power to assert significance may be discussed, but the exercise in denying the trends they found is a sign of the submission of research to the political agenda. J. Calinas-Correia MD(LicMed) DIMC RCSEd j_calinas@yahoo.co.uk 1 Chalmers I, Altman D. Systematic Reviews. London, 1995. BMJ books 2 Janerich DT, Thompson WD, Varela LR, et al. Lung cancer and exposure to tobacco smoke in the household. N Engl J Med 1990;323(10):632-636 3 Doll R, Peto R, Boreham J, Sutherland I. Smoking and dementia in male British doctors: prospective study. BMJ 2000;320:1097-1102 |
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William B Grant Newport News, VA, USA
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The paper by Doll et al. [1] seems to clearly establish that smoking does not affect the risk of developing Alzheimer's disease (AD). However, it may not since some of the likely risk factors for AD were not included in the study. During the past 3 years, diet has emerged as a high risk factor for AD. Grant [2], using an ecologic approach on prevalence of AD in 11 countries, found that a high-fat, high-energy diet was highly correlated with AD, while fish was inversely correlated. In addition, diet around the time of incidence of AD was most important. This point was supported by a case-control study reported by Smith et al. [3] in which diet after the age of 60 years was important while diet prior to that age was not. The mechanisms linking diet to the development of AD appear to be inflammation and oxidative stress, primarily from fatty acids but with support from high total energy, while fish oil reduces inflammation. A number of other studies published in the past 3 years have provided additional support to the dietary links for AD [4]. While the authors of [1] have retreated from the ecologic approach [5], they do admit that it is useful in developing hypotheses. Given the facts that smokers tend to have different diets than nonsmokers, with, for example, fewer antioxidants [6-8] and more fats [6], it could be that when the data presented in [1] are corrected for dietary factors, smoking may turn out to be a risk reduction factor for the development of AD after all. Indeed, it has been shown that tobacco use in normal elderly individuals is associated with increased alpha4 immunoreactivity in the cortex and lower densities of amyloid-beta plaques, opposite of what occurs in the development of AD [9]. It would be very interesting if the cohort study data in [1] could be reexamined in terms of diet shortly before development of AD as well as smoking habits. 1. Doll R, Peto R, Boreham J, Sutherland I. Smoking and dementia in male British doctors: prospective study. BMJ 2000; 320: 1097-1102. 2. Grant WB. Dietary links to Alzheimer's disease. Alz Dis Rev 1997; 2: 42-55 ( http://www.coa.uky.edu/ADReview/contents.htm) 3. Smith MA, Petot GJ, and Perry G. Diet and oxidative stress: A novel synthesis of epidemiological data on Alzheimer's disease. Alz Dis Rev 1997; 2: 58-59. 4. Grant WB. Dietary links to Alzheimer's disease: 1999 update. J Alz Dis 1999; 1: 197-201. 5. Doll R, Peto R, The Causes of cancer. JNCI 1981; 66: 1191-1308. 6. Birkett NJ. Intake of fruits and vegetables in smokers. Public Health Nutr 1999; 2: 217-222. 7. Cross CE, Traber M, Eiserich J, van der Vliet A. Micronutrient antioxidants and smoking. Br Med Bull 1999; 55: 691-704. 8. Ma J, Hampl JS, Betts NM. Antioxidant intakes and smoking status: data from the Continuing Survey of Food Intakes by Individuals 1994-1996. Am J Clin Nutr 2000; 71: 774-80. 9. Perry E, Martin-Ruiz C, Lee M, Griffiths M, Johnson M, Piggott M, Haroutunian V, Daniel Buxbaum J, Nasland J, Davis K, Gotti C, Clementi F, Tzartos S, Cohen O, Soreq H, Jaros E, Perry R, Ballard C, McKeith I, Court J. Nicotinic receptor subtypes in human brain ageing, Alzheimer and Lewy body diseases. Eur J Pharmacol 2000; 393: 215-222. William B. Grant, Ph.D.
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Zaffar Ul Hassan, Clinical Medical Officer in Old Age Psychiatry Farnham Road Hospital,Guildford,Surrey,GU2 5LX
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Dear Editor, I was amazed to see that Doll et al (1)has totally ignored the "stress" as a contributory factor of dementia. Medicine has always been considered as a highly stressing profession. The cause of excessive smoking in doctors and health professionals is increasing pressure of work and stress due to ever changing needs and demands of public. According to Ritter et al(2) smoking continues to be widespread in mental health care settings and exposure to cigarette smoke thought to contribute to stress and ageing because of the damage they do to body cells. He also mentioned that nurses also admitted to use alcohol and drugs to alleviate the stress. Another thing, which was worth mentioning and ignored, is the fact that stress precipitates hypertension thereby increasing the chances of cerebral infarction and vascular dementia. It also forces a person to change his life style, abandoning recreational activities, lack of exercise and thereby developing hypercholestraemia, all of which are known risk factors. This study did not specify the specialities of the doctors. A study by Newcomer et al (3) highlighted that prolonged stress can cause the memory to fail. Every day for 4 days, 51 human volunteers were given a dose of cortisol mimicking a mildly stressful event, a higher dose mimicking a major stress or a placebo. About 93% of those given the higher dose of hormone showed more cognitive impairment than those given low dose or placebo. The conclusion was that stress might cause some people to produce large amounts of cortisol thereby causing impact on memory. If smoking increases the chance of dementia then we are going to see more deaths from dementia due to "stress induced smoking". This is yet to be seen that how many deaths due to "dementia" are going to be related to "work related stress" thanks to the encouragement of back biting culture in the NHS, American style suit culture, un-supportive atmosphere from some of the colleagues and increasing demand to provide the best service with lack of resources. This study also did not say anything about the ethnic origin of those doctors. If it is not politically too damaging then it will also be worthwhile to research that whether stress related dementia bites more to ethnic minority doctors or their white counterparts. Dr.Zaffar Ul Hassan
References: - 1.Doll R, Peto R, Boreham J, Sutherland I. Smoking and dementia in male British doctors: prospective study. BMJ 2000;320: 1097-1102(22 April.) 2.Ritter S. A, Tolchard B, Stewart R. Coping with stress in mental health nursing. In: Carson J, Fagin L, Ritter S (eds) Stress and coping in mental health nursing. Chapman and Hall, London (1995) 3.Newcomer J W, Selke G, Melson A K, Hershey T, Craft S, Richards K , Alderson A L. Decreased memory performance in Healthy Humans induced by Stress-Level Cortisol treatment. Archives of General Psychiatry,1999;56:527-533(June) |
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Dennis Lynn, Lonesome Doc Kentucky, USA
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Run a search on Nicotine and Memory. There is no question it improves mentation and is protective against dementia. Smoking however is contaminated Nicotine and long term effects are deleterious. The microvascular damage and hypoxia are significant and counteract any benefit nicotine could have. Distill the good from the evil and benefit. |
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