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Rapid Responses: Rapid Responses published:
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Death, (indirect) taxes and chocolate
- Richard J Partington (14 March 2009)
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Can the effects of smoking be understood if the effects on blood flow are ignored ?
- Les O. Simpson (17 March 2009)
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The continuing underestimation of the risk of smoking
- Friedebert J Kunz, Christoph Pechlaner Professor, Research (27 March 2009)
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Richard J Partington, Foundation Year One Doctor Manchester Royal Infirmary M13 9WL
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A recent motion, the suggestion to tax chocolate, put forward at the Scottish Local Medical Committee Conference in Clydebank created significant national publicity. Alongside this, three population based studies published in the BMJ 14/03/09, added evidence to guide physicians when advising patients regarding lifestyle choices. They related that exposure to secondhand smoke may be a factor associated with increased odds of cognitive impairment 1. That male and female smokers in all social positions had poorer survival than those who had never smoked in even the lowest social positions 2. And that mortality risk was increased in men who were both overweight and obese in late adolescence as well as in those who smoked 3. Currently beer is taxed at a rate of £16.15 per hectolitre per cent of alcohol, cigarettes at a rate of 22 per cent of the retail price plus £112.07 per thousand cigarettes and chocolate at the standard rate of VAT (15%)4. The current level of taxation is high but clearly does not diminish the enthusiasm of the general populace in the consumption of these products. A recent meta-analysis showed a significant negative correlation between alcohol tax or price and indices of sales and consumption 5. Would it be unreasonable to suggest a taxation on ALL products high in saturated fats would not produce similar results? If the levies that currently exist are purely revenue streams rather than an attempt to guide public health, perhaps they should be repealed and the wealth they generated could be replaced with fairer direct taxation. If however they are part of a desire to improve the lifestyles of the general public then surely rather than being half hearted the taxes should be raised to punitive levels that would significantly reduce rates of consumption. The opposition this move would generate would be large to say the least but so could the numbers of lives saved. 1 Llewellyn D, Lang I, Langa KM, Naughton F, Matthews F. Exposure to secondhand smoke and cognitive impairment in non-smokers: national cross sectional study with cotinine measurement. BMJ 2009;338:b42 doi:10.113/bmj.b462 2 Gruer L, Hart CL, Gordon DS, Watt, GCM. Effect of tobacco smoking on survival of men and women by social position: a 28 year cohort study. BMJ 2009;338:b480 doi10.1136/bmj.b480 3 Neovius M, Sundstrom J, Rasmussen F. Combined effects of overweight and smoking in late adolescence on subsequent mortality: nationwide cohort study. BMJ 2009;338:b496 doi:10.1136/bmj.b496 4 http://customs.hmrc.gov.uk 5 Wagenaar AC,Salois MJ Effects of beverage alcohol price and tax levels on drinking: a meta-analysis of 1003 estimates from 112 studies. Addiction, Feb 2009, vol./is. 104/2(179-90), 1360-0443 Competing interests: None declared |
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Les O. Simpson, retired experimental pathologist Dunedin, New Zealand 9077
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This paper is one of three research papers involving smoking in the same issue of the BMJ. In none of those papers was there reference to the published information about how smoking increases blood viscosity and reduces red cell deformability. What does this undiscussed rejection of published information imply ? Is it arrogance on the part of the writers, who consider that the information does not warrant discussion ? A PubMed search for "Smoking and blood viscosity," produced 278 titles, which represents a sizeable body of information. How is it possible to disregard that information ? In 1984, we published the findings from a small study (1) which showed that the filterability of cigarette smoker's blood was related to the number of cigarettes smoked. When the prostaglandin E1 levels of the blood were raised by taking 2 grams daily of evening primrose oil, after two weeks blood filterability was increased significantly. With regard to "Passive smoking" in the English abstract of a Chinese paper it was noted that in non-smoking women exposed to smoking for 5 years, amongst other changes, "...fibrinogen, plasma and whole blood viscosity were higher than in non- passive smokers." As blood viscosity has been a research subject for more than a century, surely it is time to utilize the available information. Reference, 1. Simpson LO, Olds RJ, Hunter JA. Changes in rheological properties of blood in cigarette smokers taking Efamol: a pilot study. Proc Univ Otago Med Sch 1984;62:122-3. Competing interests: None declared |
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Friedebert J Kunz, Professor, Research Medical University, A 6020 Innsbruck, Austria, Christoph Pechlaner Professor, Research
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The risk of smoking may have been underestimated in „Combined effects of overweight and smoking in late adolescence on subsequent mortality : nationwide cohort study“(1), because the risk rates listed are based on the assumption of equal baseline characteristics of smokers and non-smokers, which has never been proven and is therefore not evidence-based. This assumption has been generally accepted without any discussion, although many investigations cast considerable doubts on it. This applies particularly to the main reason for mortality, ischaemic heart disease, in view of the many irreconcilable contradictions between the damages smoking inflicts on the coronaries of individuals and observations in collectives of smokers (2) culminating in the smokers paradox (3), the greater short-term postinfarction survival of smokers than of non-smokers. As reasons for this paradox the younger age, lower incidence of diabetes, better ejection fraction or angiographic scores or less atherogenic (and more thrombogenic) lesions of the smokers have been discussed (3-5). However, these explanations do not take into account, that all listed advantageous characteristics are associated with younger age and that therefore multiple adaptations for related characteristics have been carried out. Apart from the fact, that this over-adaptation is not justified, most authors observed a greater short-term survival of smokers also after adaptation for age and many of the other examined characteristics (3-5). This paradox can be explained by favourable baseline characteristics of smokers, which in fact we observed in those, who are starting to smoke early (2) and who are most likely to become permanent and heavy smokers (6). Particularly more efficient basal fibrinolysis (2,4) may be unmasked already by the short period of non-smoking after myocardial infarction, outweigh the damages caused by decades of smoking and thereby explain the smokers paradox including even the utter paradox of the association between the amount of cigarettes smoked and higher short-term post-infarction survival (3). Therefore the assumption of equal baseline coronary characteristics of smokers and non smokers cannot be upheld, which indicates, that smoking-associated mortality, essentially determined by cardiovascular mortality, is considerably greater than listed generally and also in the investigation presented (1). As a consequence, more research not only on the extent of the health risk of smoking, but particularly on novel strategies to reduce this risk is warranted. References
Friedebert Kunz MD, Prof, Christoph Pechlaner MD, Prof. Department of Internal Medicine Competing interests: The authors are also authors of a publication on the risk of smoking. |
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