2 Matching Annotations
  1. Jul 2018
    1. On 2016 Jun 02, Clive Bates commented:

      The measured markers are not a reliable proxy for disease risk

      The authors are careful not to attribute serious disease risk to these measured changes in vascular function. That caution is well-founded. It is worth pointing out that similar effects are observed in coffee drinkers. See for example:

      Papamichael CM, 2005 Effect of coffee on endothelial function in healthy subjects: the role of caffeine

      The study examined similar effects as they arise from coffee consumption and concluded:

      In conclusion, coffee exerts an acute unfavourable effect on the endothelial function in healthy adults, lasting for at least 1 h after intake. This effect might be attributed to caffeine, given that decaffeinated coffee was not associated with any change in the endothelial performance.

      A comparison with coffee would have made a worthwhile additional arm to this study and may have helped with interpreting whether there is a material risk of harm. If the effects are similar to those experienced by coffee drinkers, that might have provided valuable reassurance for smokers making an informed choice about quitting smoking by switching to e-cigarettes.

      The role of nicotine

      The authors suggest several possible mechanisms for the observed changes in vascular function, including changes induced by nicotine. This is a promising explanatory hypothesis because achieving a satisfactory nicotine dose is common to both smoking and e-cigarette use. One might expect, therefore, similar physiological changes to arise from both ways of taking nicotine if nicotine is the primary cause of these observations.

      However, that would also be reassuring to e-cigarette users. Nicotine has well-documented effects on the body but these effects have not been found to be a significant cause of the diseases attributed to smoking, including cardiovascular disease. The effect of nicotine separated from tobacco smoke exposure has been studied through assessments of medical nicotine replacement therapy (discussed on TreatTobacco.net) and snus, a form of smokeless tobacco that delivers high doses of nicotine - see Lee PN, 2013.

      The danger of over-interpreting these findings

      No one should underplay any potential risks from e-cigarettes. But neither should activists jump to exaggerations about disease risk based on these findings. Overstating the risks of e-cigarettes is logically and ethically equivalent to understating the risks of tobacco smoking. The latter was the practice of tobacco companies 30 years ago and it is essential to challenge the former in today's public health discourse.

      As an example, one campaigner has already declared that this study means "e-cigarettes could be half as dangerous as conventional cigarettes" here.

      I hope the authors will distance themselves from such extreme over-interpretation of their work. The authors could have pre-empted the need for that by explaining in the discussion that disease is not an inevitable consequence of these changed markers of vascular function.

      To be fair, the authors do point to the need for further studies, "to clarify the chronic vascular effects of E-cigarette smoking". To which they might have added "if any" for completeness.


      This comment, imported by Hypothesis from PubMed Commons, is licensed under CC BY.

  2. Feb 2018
    1. On 2016 Jun 02, Clive Bates commented:

      The measured markers are not a reliable proxy for disease risk

      The authors are careful not to attribute serious disease risk to these measured changes in vascular function. That caution is well-founded. It is worth pointing out that similar effects are observed in coffee drinkers. See for example:

      Papamichael CM, 2005 Effect of coffee on endothelial function in healthy subjects: the role of caffeine

      The study examined similar effects as they arise from coffee consumption and concluded:

      In conclusion, coffee exerts an acute unfavourable effect on the endothelial function in healthy adults, lasting for at least 1 h after intake. This effect might be attributed to caffeine, given that decaffeinated coffee was not associated with any change in the endothelial performance.

      A comparison with coffee would have made a worthwhile additional arm to this study and may have helped with interpreting whether there is a material risk of harm. If the effects are similar to those experienced by coffee drinkers, that might have provided valuable reassurance for smokers making an informed choice about quitting smoking by switching to e-cigarettes.

      The role of nicotine

      The authors suggest several possible mechanisms for the observed changes in vascular function, including changes induced by nicotine. This is a promising explanatory hypothesis because achieving a satisfactory nicotine dose is common to both smoking and e-cigarette use. One might expect, therefore, similar physiological changes to arise from both ways of taking nicotine if nicotine is the primary cause of these observations.

      However, that would also be reassuring to e-cigarette users. Nicotine has well-documented effects on the body but these effects have not been found to be a significant cause of the diseases attributed to smoking, including cardiovascular disease. The effect of nicotine separated from tobacco smoke exposure has been studied through assessments of medical nicotine replacement therapy (discussed on TreatTobacco.net) and snus, a form of smokeless tobacco that delivers high doses of nicotine - see Lee PN, 2013.

      The danger of over-interpreting these findings

      No one should underplay any potential risks from e-cigarettes. But neither should activists jump to exaggerations about disease risk based on these findings. Overstating the risks of e-cigarettes is logically and ethically equivalent to understating the risks of tobacco smoking. The latter was the practice of tobacco companies 30 years ago and it is essential to challenge the former in today's public health discourse.

      As an example, one campaigner has already declared that this study means "e-cigarettes could be half as dangerous as conventional cigarettes" here.

      I hope the authors will distance themselves from such extreme over-interpretation of their work. The authors could have pre-empted the need for that by explaining in the discussion that disease is not an inevitable consequence of these changed markers of vascular function.

      To be fair, the authors do point to the need for further studies, "to clarify the chronic vascular effects of E-cigarette smoking". To which they might have added "if any" for completeness.


      This comment, imported by Hypothesis from PubMed Commons, is licensed under CC BY.