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“A leader is best when people barely know he exists, not so good when
people obey and acclaim him, worse when they despise him....But of a good
leader who talks little when his work is done, his aim fulfilled, they
will say, "We did it ourselves.”
Clearly John Ashton’s aphorism mirrors Lao Tzu’s thoughts on
leadership, and is thus hard to argue against. However I think public
health practitioner...
“A leader is best when people barely know he exists, not so good when
people obey and acclaim him, worse when they despise him....But of a good
leader who talks little when his work is done, his aim fulfilled, they
will say, "We did it ourselves.”
Clearly John Ashton’s aphorism mirrors Lao Tzu’s thoughts on
leadership, and is thus hard to argue against. However I think public
health practitioners should indeed be “bothered… if we don’t get the
credit for our own ideas.” It precisely this self effacing stance that has
led to the current situation where public health is grossly undervalued
and under-resourced. It is hard enough trying to promote a negative – the
disease outbreak that didn’t happen – we only make it worse for ourselves
if we allow others to claim responsibility for all the visible successes.
Why should public health practitioners be employed if the successes are
due to the ‘exertions’ of politicians and generic bureaucrats? It is time
that we assembled the evidence of our many successes and market public
health and its practitioners aggressively. We need to attract the
attention of those who procure sickness services at ever increasing
expense and show them the folly of neglecting the protectors, promoters
and the preventers. Time to dispense with the bushel and let our lights
shine!
I have read with high interest the comments made by Petronis and
Anthony on my editorial.[1] I have also read their forthcoming article,[2] and
I believe they apply an analytical approach that seems to be, in my
opinion, a step in the right direction for research on contextual
influences and health that focus on investigation of clustering. I will be
very pleased of writing a larger comment and send i...
I have read with high interest the comments made by Petronis and
Anthony on my editorial.[1] I have also read their forthcoming article,[2] and
I believe they apply an analytical approach that seems to be, in my
opinion, a step in the right direction for research on contextual
influences and health that focus on investigation of clustering. I will be
very pleased of writing a larger comment and send it for consideration and
possible publication in the Journal.
Measuring clustering with the aim of obtaining substantive scientific
information is so far an uncommon approach in social epidemiology and most
multilevel analyses have in fact been plain “contextual analysis”[3] focused
on measures of association. This seems be true not only for studies using
GGE techniques but also for studies using multilevel hierarchical
regression. However, the original standpoint of multilevel hierarchical
regression analyses is the investigation of complex patterns of variation [4]
rather than dealing with residual correlation.
Regarding the use of “GEE2” and measurement of clustering, the
comment of Petronis and Anthony is certainly right.
From an epidemiological point of view the most interesting question
is the conceptual rather than the mathematical approach used. I agree with
Petronis and Anthony in their conceptual approach and I believe that they
put context back in epidemiology using “GEE2” techniques.[5] The Parwise
Odds Ratio and other techniques for measuring neighbourhood heterogeneity
and clustering like the Median Odds Ratio and the Interval Odds Ratio [6,7]
deserve more development and spreading.
References
(1) Merlo J. Multilevel analytical approaches in social epidemiology:
measures of health variation compared with traditional measures of
association. J Epidemiol Community Health 2003;57:550-2.
(2) Petronis KR,.Anthony JC. A different kind of contextual effect:
geographic clustering of cocaine incidence in the US. J Epidemiol
Community Health 2003;in press.
(3) Diez Roux AV. A glossary for multilevel analysis. J Epidemiol
Community Health 2002;56:588-94.
(4) Goldstein H. Multilevel Statistical Models. London: Hodder Arnold, 2003.
(5) Carey V, Zeger SL, Diggle P. Modelling multivariate binary data
with alternating logistic regressions. Biometrika 1993;80:517-26.
(6) Larsen K, Petersen JH, Budtz-Jorgensen E, Endahl L. Interpreting
parameters in the logistic regression model with random effects.
Biometrics 2000;56:909-14.
(7)Larsen K,.Merlo J. Appropriate assessment of neighborhood effects
on individual health -integrating random and fixed effects in multilevel
logistic regression. Working paper 2003.
This is indeed a strange disease. The epidemiology suggests it to be
of relatively low infectivity, but high severity.This in itself is odd,
especially if the causative agent is a virus and the principal mode of
spread by coughing/droplet.Also odd is the undoubted existence of
"superspreaders", who can infect very many of their contacts - I can't
think of any parallels to this in respiratory virology....
This is indeed a strange disease. The epidemiology suggests it to be
of relatively low infectivity, but high severity.This in itself is odd,
especially if the causative agent is a virus and the principal mode of
spread by coughing/droplet.Also odd is the undoubted existence of
"superspreaders", who can infect very many of their contacts - I can't
think of any parallels to this in respiratory virology.
Perhaps the SARS virus obeys the usual rules of droplet-transmitted
respiratory infections, and is of high infectivity. However, due to
shared antigens, a proportion of the population has an acquired resistance to the new virus, having already been exposed to another, relatively
innocuous, virus that provides immune protection. It is possible that the
proportion of humanity immune or partially immune to SARS could be as high as, say, 95% if the second virus were a very common one, e.g. one of the
coronaviruses that causes coryza.This would explain the seemingly low,
unexpectedly so, infectivity of the SARS agent.
Maybe this also explains "superspreaders". Picture humanity divided
into two categories:
1). Those who have met a common related coronavirus,
and consequently have a degree of immunity to SARS, say for the sake of
argument 95% of the population.
2). Those who have not met it, and have no immunity, 5%. If the defences of the first group are overwhelmed by
exposure to a huge SARS virus inoculum, perhaps they would contract a
modified form of the disease, quickly recruit their immune systems to
produce antibodies to a recognised infectious agent, be likely to recover,
not shed large amounts of virus, not be all that infectious.The second
group would get the disease in an exuberant form, excrete quantities of
infectious material, be likely to succumb before their immune system could
meet the challenge.....the superspreaders.
I believe that a coherent model of the SARS epidemic could be
constructed
from the above theory. This of course would not necessarily lend it
validity,
but it may be worth looking at.
We appreciate the comments from Cope et al on our paper reporting the
association between smoking cessation and smoking reduction and subsequent
risk of myocardial infarction (1). Specifically, Cope et al propose that
the lack of a beneficial effect of reduced smoking - in contrast to
smoking cessation - could be due to inaccuracy (underreporting) of the
self-reported tobacco consumption. In addition, Cope et al raise the...
We appreciate the comments from Cope et al on our paper reporting the
association between smoking cessation and smoking reduction and subsequent
risk of myocardial infarction (1). Specifically, Cope et al propose that
the lack of a beneficial effect of reduced smoking - in contrast to
smoking cessation - could be due to inaccuracy (underreporting) of the
self-reported tobacco consumption. In addition, Cope et al raise the
important question of which measurement method most accurately reflects
tobacco exposure in the individual smoker.
We agree that nowadays almost every study of smoking habits apply one
or more measurement of biochemical marker of smoking in addition to self-
report. It is also correct that in our paper the study participants are
divided into the different smoking categories on basis of self-reported
smoking and changes in smoking. However, as mentioned in the discussion,
measurements of expired carbon monoxide (CO) and serum cotinine were
undertaken in one of the follow-up examinations. We found increasing
levels of CO (Table 2) and cotinine (not shown) with increasing self-
reported tobacco consumption, indicating that underreporting of smoking
alone cannot explain our results, but clearly misclassification cannot be
ruled out in this observational study. Furthermore, a previous review and
meta-analysis (2) concluded that self-reported smoking is an accurate
measure of tobacco exposure in population based studies, whereas this is
not the case in intervention and clinical studies. Our data were based on
a sample of the general population; participants with known coronary heart
disease prior to study entrance were excluded. In addition, information on
smoking habits and changes in smoking were part of a large questionnaire
initiated in the late 1970's and the 1980's, thus minimizing the risk of
"social desirability bias" in this study.
Cope et al describe a pilot study using a urine cotinine test for
measuring nicotine intake. There are various methods of validating tobacco
intake including biochemical markers, and cotinine is one of the better
due to its relatively long half-life and the possible linear relationship
with number of cigarettes smoked. However, cotinine is not very useful in
smoking reduction studies since most of the participants in these trials
are supplied with nicotine replacement medications. Interestingly, the
intervention studies of smoking reduction all report that despite nicotine
replacement the percentage decline in amount of tobacco is followed by a
smaller decline in biochemical markers of smoking exposure.
Evidence of the effects of reduced smoking on risk of coronary heart
disease is limited. The few ongoing smoking reduction trials report
favorable changes in blood analyses of parameters of arteriosclerosis up
to two years after smoking reduction. Unfortunately, these studies have a
very high "drop-out" percentage, but it will be interesting to see the
clinical results of a long-term follow-up in this type of "risk reduction"
study.
In summary, we believe that the self-reported smoking habits in our
study are fairly precise. However, biochemical verification of smoking is
necessary in intervention and clinical studies although there are no ideal
markers of tobacco exposure specifically with respect to assessment of
smoking reduction.
(1) Godtfredsen NS et al. Smoking reduction, smoking cessation, and
incidence of fatal and non-fatal myocardial infarction in Denmark 1976-
1998: a pooled cohort study. J Epidemiol Community Health 2003;57:412-416.
(2)Patrick DL et al. The validity of self-reported smoking: a review
and meta-analysis. Am J Public Health 1994;84:1086-1093.
The recent editorial entitled "Multilevel analytical approaches in
social epidemiology: measures of health variation compared with
traditional measures of association" [1] offers an interesting critique of
the generalized estimating equations (GEE) analysis of a paper published
in the same issue of JECH (August 2003). In the editorial, the author
notes that the paper's GEE analysis treats "the intr...
The recent editorial entitled "Multilevel analytical approaches in
social epidemiology: measures of health variation compared with
traditional measures of association" [1] offers an interesting critique of
the generalized estimating equations (GEE) analysis of a paper published
in the same issue of JECH (August 2003). In the editorial, the author
notes that the paper's GEE analysis treats "the intra-neighbourhood
correlation as a 'nuisance' that needs to be adjusted in the analysis but
not explicity investigated" (p. 550).
The editorial then becomes a call for an alternative, more innovative
approach in social epidemiology: "Estimation of the extent to which
individuals within a given neighbourhood are correlated with one another
in relation to health (that is, the concept of intra-neighbourhood
correlation) has value in the context of ideas about the efficacy of
focusing intervention on places instead of people" (p.551). The finale is
a logical conclusion that studies of intra-neighbourhood correlation may
"...present themselves as a new epidemiological approach that may prove
very useful in social epidemiology" (p. 551).
The author is appartently speaking of first-order GEEs but the JECH
readership may not appreciate that second order GEEs (GEE2) treat the
intra-neighbourhood and inter-neighbourhood correlations into deliberate
objects of study and estimation [2]. Although we ourselves deserve
absolutely no credit for biostatistical innovations, the "alternating
logistic regressions" (ALR) approach [3] we employ in our forthcoming
article in JECH [4] is a computationally efficient alternative to GEE2 in
the case of a binary outcome. As such, it estimates the pairwise odds
ratio (PWOR), which quantifies the degree to which health conditions,
behaviors, or perceptions might cluster within neighbourhoods (or other
nested structures of community life) to a degree other than one might
expect if these health conditions, behaviors, or perceptions were
distributed at random across neighbourhoods.
Because we believe our work is responsive to the author's call for a
new approach in social epidemiology that measures intra-neighbourhood
correlation, we would welcome an editorial comment on the potential value
(and possible shortcomings) of the GEE/ALR approach we used in our
forthcoming article in JECH on clustering of cocaine incidence in the
United States. We hope you will
concur that our application of the ALR approach is a step in the right
direction for research on contextual influences and health.
References
(1) Merlo J. Multilevel analytical approaches in social epidemiology:
measures of health variation compared with traditional measures of
association. JECH 2003;57:550-552.
(2) Liang K-Y, Zeger SL. Regression analysis for correlated data.
Annu. Rev. Pub. Health;14:43-68.
(3) Carey V, Zeger SL, Diggle P. Modelling multivariate binary data
with alternating logistic regressions. Biometrika;80:517-26.
(4) Petronis KR, Anthony JC. A different kind of contextual effect:
geographic clustering of cocaine incidence in the U.S. JECH, in press.
We read the paper by Godtfredsen et al. with interest.[1]
The paper
reported on the effect of smoking reduction on the incidence of myocardial
infarction (MI) and found that although patients who stopped smoking had a
decreased risk of MI, those who reportedly reduced their smoking did not.
The conclusions drawn were that smoking reduction, rather than complete
cessation, did not produce...
We read the paper by Godtfredsen et al. with interest.[1]
The paper
reported on the effect of smoking reduction on the incidence of myocardial
infarction (MI) and found that although patients who stopped smoking had a
decreased risk of MI, those who reportedly reduced their smoking did not.
The conclusions drawn were that smoking reduction, rather than complete
cessation, did not produce any benefit with regard a reduction of risk of
MI.
The major drawback to this study is that the information about smoking was
totally reliant on self-reported smoking habit. There is abundant evidence
that patients who smoke, when questioned about a smoking-related illness,
frequently under-report their cigarette consumption or deny smoking
altogether. The more significant the effect smoking has, the greater the
‘social desirability bias’, so increasing the likelihood of denial. To
overcome this bias biochemical verification of smoking by measurement of
nicotine metabolites, specifically cotinine, has become almost obligatory.
To improve the accuracy of information about smoking and to facilitate
easier nicotine metabolite measurements we developed a 6-minute point-of-
care test called SmokeScreen.[2] The easy-to-use colorimetric urine test
can provide qualitative, semi-quantitative and quantitative measurements
of nicotine intake. Using this test we undertook an audit of smoking
habits of 154 new patients attending a large inner-city hospital
cardiology outpatient clinic, comparing the test identification of smoking
with self-completed questionnaire of current smoking habit. The results
identified 112 (72.7%) patients as non-smokers, 30 (19.5%) as confessed
smokers and 12 (7.8%) as ‘smoking deceivers’.
We followed this with another study of the same population (n=85, 33
smokers and 52 never-smokers) to examine the interaction of smoking and
risk factors associated with coronary artery disease, as assessed by a
biochemical screen and a blood count. Interestingly, none of the
parameters measured in the biochemical screen, such as cholesterol, HDL
and triglycerides; urea and electrolytes and liver function tests were
associated with smoking habit or quantitative assessment of nicotine
intake. Whereas white blood cell count (wbc) was significantly higher in
smokers (p=0.002), in particular, neutrophils (p=0.01) and eosinophils
(p=0.02). Lymphocytes, monocytes and basophiles were higher but failed to
reach significance. Quantitative assessment of nicotine intake of the
smokers further revealed a positive correlation with wbc (p<_0.0001 neutrophils="neutrophils" p0.001="p0.001" eosinophils="eosinophils" p0.004="p0.004" and="and" lymphocytes="lymphocytes" p0.02="p0.02" with="with" monocytes="monocytes" approaching="approaching" significance="significance" p="p"/>
It would seem from this pilot study that smoking or the amount of tobacco
consumed does not influence the biochemical risk factors for coronary
artery disease, such as cholesterol and HDL. However, smoking does appear
to increase many of the immune cells associated with both the formation
and destabilisation of the atheromatous plaque. It would seem logical
therefore that a reduction in nicotine intake would be accompanied by a
reduced risk of MI, as supported by our quantitative findings. One reason
for the poor association between smoking reduction and subsequent
myocardial infarction in the Godtfredsen et al. study [1] may be the
inaccuracy of self-report.
We suggest that identification of smokers with the point-of-care test is a
more valuable method of smoking assessment. Coupling this test with
subsequent advice on smoking cessation could have a significant impact on
reducing a major risk factor associated with coronary artery disease and
decrease cardiovascular events and mortality.
References
(1) Godtfredsen NS, Osler M, Vestbo J, Andersen I, Prescott E. Smoking
reduction, smoking cessation, and incidence of fatal and non-fatal
myocardial infarction in Denmark 1976-1998: a pooled cohort study. JECH
2003:57:412-416.
(2) Cope GF, Nayyar P, Holder R, Gibbons J, Bunce R. A simple near-patient
test for nicotine and its metabolites in urine to assess smoking habit. Clin Chim Acta 1996;256:135-149.
I noted with interest the article by Unal et al.[1] and wondered whether they had seen our population-based study describing the prevalence of IHD in what
is now Wandsworth PCT.[2]
We describe 6776 IHD patients in detail from a total population
of 378,021 and address many of the issues Unal et al.[1] raise in their paper. We are
about to collect a second round of data and will be taking...
I noted with interest the article by Unal et al.[1] and wondered whether they had seen our population-based study describing the prevalence of IHD in what
is now Wandsworth PCT.[2]
We describe 6776 IHD patients in detail from a total population
of 378,021 and address many of the issues Unal et al.[1] raise in their paper. We are
about to collect a second round of data and will be taking account of your
recommendations.
References
(1) B Unal, J A Critchley, and S Capewell. Missing, mediocre, or merely obsolete? An evaluation of UK data sources for coronary heart disease. J Epidemiol Community Health 2003;57:530-535.
(2) Carroll K, Majeed A, Firth C, Gray J. Prevalence and
management of coronary heart disease in primary care: population-based
cross-sectional study using a disease register. Journal of Public Health
Medicine 2003;25(1):29-35. http://www.pubmed.oupjournals.org/cgi/content/abstract/25/1/29
Morrison et al. examine the effect on questionnaire response of
feeding back research findings to participants.[1] As authors of the
systematic review [2] cited in their paper we would like to point out that
we had in fact identified eight such randomized trials.[3-10] The broad
strategy under which these trials had been classified in our review was
‘non monetary incentives’.
Morrison et al. examine the effect on questionnaire response of
feeding back research findings to participants.[1] As authors of the
systematic review [2] cited in their paper we would like to point out that
we had in fact identified eight such randomized trials.[3-10] The broad
strategy under which these trials had been classified in our review was
‘non monetary incentives’.
We are currently updating our systematic
review and have recently extended the search of databases to the beginning
of 2003 and have contacted the authors of potentially eligible trials. A
further two trials [11,12] have been identified and the total of 10 trials
have also been classified under the new strategy called ‘offer of research
findings’. These trials include a total of 13,642 participants. When the
results of these trials are pooled in a random effects meta analysis the
odds ratio for response with research findings is 0.92 (95% CI 0.75 to
1.11). Despite omitting to refer to these previous trials, Morrison et al.
were justified in conducting their trial: few of such trials have been
health-related and none has examined the effect this an intervention when
participants were resurveyed. However, even with the inclusion of their
new trial in our systematic review, uncertainty about the effect of
dissemination of research findings on questionnaire response remains.
The update to our systematic review now includes a total of 372
trials of methods to influence response to postal questionnaires,
classified under 98 strategies. Although many conclusions remain
unchanged our updated review presents the definitive account of the
evidence for which strategies may be used to improve response to postal
questionnaires. The updated review will appear in the Cochrane Library
later this year.
References
(1) Morrison DS, Thomson H, Petticrew M. Effects of disseminating research
findings on response rates in a community survey: a randomised controlled
trial. J Epidemiol Community Health 2003;57:536-7.
(2) Edwards P, Roberts I, Clarke M, et al. Increasing response rates to
postal questionnaires: systematic review. BMJ 2002;324:1183-5.
(3) Dommeyer CJ. Does response to an offer of mail survey results interact
with questionnaire interest? Journal of the Market Research Society
1985;27:27-38.
(4) Dommeyer CJ. Offering mail survey results in a lift letter. Journal of
the Market Research Society 1989;31:399-408.
(5) Glisan G, Grimm JL. Improving response rate in an industrial setting:
will traditional variables work? Southern Marketing Association Proc
1982;20:265-8.
(6) Green KE, Kvidahl RF. Personalization and offers of results: effects on
response rates. Journal of Experimental Education 1989;57:263-70.
(7) Jobber D, Sanderson S. The effect of two variables on industrial mail
survey returns. Industrial Marketing Management 1985;14:119-21.
(8) Kerin RA, Barry TE, Dubinsky AJ, Harvey MG. Offer of results and mail
survey response from a commercial population: a test of Gouldner's Norm of
Reciprocity. Proceeding of the American Institute of Decision Sciences
1981:283-5.
(9) Mullner RM, Levy PS, Byre CS, Matthews D. Effects of characteristics of
the survey instrument on response rates to a mail survey of community
hospitals. Public Health Reports 1982;97:465-9.
(10) Powers DE, Alderman DL. Feedback as an incentive for responding to a
mail questionnaire. Research in Higher Education 1982;17:207-11
(11) Thistlethwaite PC. The impact of selected mail response enhancement
techniques on surveys of the mature market: Some new evidence. Journal of
Professional Services Marketing 1993;8:269-76
(12) Wiseman F. Methodological bias in public opinion surveys. Public
Opinion Quarterly 1972;36:105-8.
During the days culminating in the US-British invasion of Iraq, I was working with a human rights attorney colleague,
exploring links and distinctions between health, equity, and human rights. These concepts thus have been in my thoughts,
and concern for each leads me to deplore the invasion of Iraq on several counts.
First, given the scale of suffering and
death that inevitably accompany war, it is unconscionable to...
During the days culminating in the US-British invasion of Iraq, I was working with a human rights attorney colleague,
exploring links and distinctions between health, equity, and human rights. These concepts thus have been in my thoughts,
and concern for each leads me to deplore the invasion of Iraq on several counts.
First, given the scale of suffering and
death that inevitably accompany war, it is unconscionable to embark on that course, even for a just cause, except as a
clearly demonstrated last resort. There is widespread international consensus that reasonable alternatives to war had not been exhausted in this case. The consequences of war include not only its direct effects but the massive after-shocks due to destruction of infrastructure (e.g. clean water) critical for survival and health; many more deaths occurred for this
reason in the wake of the first Gulf War than as a direct result of the military action itself. Moreover, this is not a just war; evidence linking Iraq and September 11 or Al Qaeda was never produced, and equally heinous regimes have been tolerated or supported
(as Saddam Hussein was previously) by the US. There are many reasons to suspect that the real motives for US interest in a regime change in Iraq have more to do with control of oil and empire than with fighting terrorism. Terrorism will surely
increase in light of the hatred this war and the ensuing occupation will provoke for generations to come, throughout the
Arab and Islamic worlds and among others who reject the disturbing vision of a hegemonic New World Order evoked by this
invasion.
Second, by setting the frightening dual precedents of pre-emptive military strikes and defiance of the United Nations, this
action drags the entire world backward toward the laws of the jungle, obliterating decades of work toward global
disarmament and 50-100 years of work toward international governance. The arrogance this reflects is in itself shocking.
Third, this war will exacerbate inequities. In Iraq, it undoubtedly is now taking and will continue in its aftermath to
take its heaviest toll on the poor and especially poor children. In the US, the costs of the war and its aftermath most
certainly will accelerate the dismantling of public services already initiated by the current administration's domestic
policies, thereby increasing social disparities in this country; and there will be less support for international
development outside the self-serving agenda for the Fertile Crescent.
Fourth and finally, this action represents a grave threat to human rights globally. By its explicit undermining of the
authority of the United Nations (UN), the Bush administration has implicitly undermined the force of international law overall
and specifically of human rights treaties and other agreements developed under UN auspices. We must publicly condemn
this unjustified war, find ways to help repair the damage, and develop new strategies to struggle for health, equity, and
human rights in a world that is far more brutal and violent than the world we had dared hope to encounter in the 21st
century.
I can make no pretence to pacifism. It was out of conviction that, a mere 18 years old in my native South Africa, I volunteered for service in World War II. And for the next five years I chose to serve in three successive services and on three successive fronts of the war. Nor have I ever regretted doing so, nor questioned that it was a right and necessary thing to do. That is to say, I believed then and believe now that there...
I can make no pretence to pacifism. It was out of conviction that, a mere 18 years old in my native South Africa, I volunteered for service in World War II. And for the next five years I chose to serve in three successive services and on three successive fronts of the war. Nor have I ever regretted doing so, nor questioned that it was a right and necessary thing to do. That is to say, I believed then and believe now that there can be just and necessary wars, one of which was the war against Nazi Germany.
Nor, in the present instance in Iraq, do I dissent from the view that Saddam Hussein is a thoroughly wicked man. He perpetrated much evil among his people, waged war without any justification whatever, used proscribed chemical weapons (in his unprovoked war with Iran and on his own Kurdish subjects), and violated the surrender agreements about UN weapons inspections after the 1991 war he precipitated. An article in Science cogently assembles what has been discovered about the vast chemical weapons program Iraq had going before and probably after the Gulf War.
Nonetheless, as an American citizen (one admittedly transplanted, but one who has enjoyed here something of a charmed life), I must declare that I am appalled by the war in Iraq. The crucial issues are clear. No one will claim that either character disorder (which may well afflict Hussein) or the putative threat Hussein poses as dictator are legitimate grounds for preemptive war. As for allegations that could constitute real grounds subsequent to the Gulf War, two charges have been made. First, as to the death and destruction wreaked by the attack of September 11, 2001 on the World Trade Towers (towers that I looked on each day out of my office window): no substantive evidence has yet been produced about Hussein's connection with the Al Quaeda onslaught. Second, as to weapons of mass destruction (which do indeed raise health questions): since Saddam Hussein stalled the UN inspections instituted after the Gulf War ended, no new evidence has been produced about Iraq's current possession or production of such weapons (although, very likely, only because of successful evasion by the Iraqi regime). Worse, by short-circuiting the search of the Security Council weapons team, the short fuse of Bush the Younger's ultimatum to Hussein precluded the possibility of their discovery. In doing so and bypassing the Security Council, a president elected with marginal legitimacy has gone far to undermine if not finally to destroy the world's best hope for an international instrument to maintain peace and law among nations, namely, an effective United Nations.
References
(1) Stone R. Peering into the shadows. Iraq's Bioweapons Program. Science 2002;297:110-1112.
Dear Editor
“A leader is best when people barely know he exists, not so good when people obey and acclaim him, worse when they despise him....But of a good leader who talks little when his work is done, his aim fulfilled, they will say, "We did it ourselves.”
Clearly John Ashton’s aphorism mirrors Lao Tzu’s thoughts on leadership, and is thus hard to argue against. However I think public health practitioner...
Dear Editor
I have read with high interest the comments made by Petronis and Anthony on my editorial.[1] I have also read their forthcoming article,[2] and I believe they apply an analytical approach that seems to be, in my opinion, a step in the right direction for research on contextual influences and health that focus on investigation of clustering. I will be very pleased of writing a larger comment and send i...
This is indeed a strange disease. The epidemiology suggests it to be of relatively low infectivity, but high severity.This in itself is odd, especially if the causative agent is a virus and the principal mode of spread by coughing/droplet.Also odd is the undoubted existence of "superspreaders", who can infect very many of their contacts - I can't think of any parallels to this in respiratory virology....
We appreciate the comments from Cope et al on our paper reporting the association between smoking cessation and smoking reduction and subsequent risk of myocardial infarction (1). Specifically, Cope et al propose that the lack of a beneficial effect of reduced smoking - in contrast to smoking cessation - could be due to inaccuracy (underreporting) of the self-reported tobacco consumption. In addition, Cope et al raise the...
Dear Editor,
The recent editorial entitled "Multilevel analytical approaches in social epidemiology: measures of health variation compared with traditional measures of association" [1] offers an interesting critique of the generalized estimating equations (GEE) analysis of a paper published in the same issue of JECH (August 2003). In the editorial, the author notes that the paper's GEE analysis treats "the intr...
Dear Editor
We read the paper by Godtfredsen et al. with interest.[1]
The paper reported on the effect of smoking reduction on the incidence of myocardial infarction (MI) and found that although patients who stopped smoking had a decreased risk of MI, those who reportedly reduced their smoking did not. The conclusions drawn were that smoking reduction, rather than complete cessation, did not produce...
Dear Editor
I noted with interest the article by Unal et al.[1] and wondered whether they had seen our population-based study describing the prevalence of IHD in what is now Wandsworth PCT.[2]
We describe 6776 IHD patients in detail from a total population of 378,021 and address many of the issues Unal et al.[1] raise in their paper. We are about to collect a second round of data and will be taking...
Dear Editor
Morrison et al. examine the effect on questionnaire response of feeding back research findings to participants.[1] As authors of the systematic review [2] cited in their paper we would like to point out that we had in fact identified eight such randomized trials.[3-10] The broad strategy under which these trials had been classified in our review was ‘non monetary incentives’.
We are curren...
During the days culminating in the US-British invasion of Iraq, I was working with a human rights attorney colleague, exploring links and distinctions between health, equity, and human rights. These concepts thus have been in my thoughts, and concern for each leads me to deplore the invasion of Iraq on several counts.
First, given the scale of suffering and death that inevitably accompany war, it is unconscionable to...
I can make no pretence to pacifism. It was out of conviction that, a mere 18 years old in my native South Africa, I volunteered for service in World War II. And for the next five years I chose to serve in three successive services and on three successive fronts of the war. Nor have I ever regretted doing so, nor questioned that it was a right and necessary thing to do. That is to say, I believed then and believe now that there...
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