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Sir,
I read with interest the article by Yu-Hung Chang et al.(1) Authors have articulated some limitations in their paper.
However, the findings are derived from purpose of the Elderly Nutrition and Health Survey in Taiwan (1999-2000), done to assess the diet, nutrition and health of persons aged 65 and above in Taiwan. One of the common and often forgotten limitation of such surveys is Survivor Bias.(2) People who go to shoppin...
Sir,
I read with interest the article by Yu-Hung Chang et al.(1) Authors have articulated some limitations in their paper.
However, the findings are derived from purpose of the Elderly Nutrition and Health Survey in Taiwan (1999-2000), done to assess the diet, nutrition and health of persons aged 65 and above in Taiwan. One of the common and often forgotten limitation of such surveys is Survivor Bias.(2) People who go to shopping might be those who are healthy and survived minor illness. Hence, Survival is a determinant of whether people remain active and whether they can go to shopping. Also, people who are debilitated, disabled and who have severe illness might not be able to go to shopping at all. It will be interesting to know whether authors have considered this limitation and if yes, why have they not chosen to discuss regarding this in their paper.
References:-
1. Chang Y-H, Chen RC-Y, Wahlqvist ML, et al. J Epidemiol Community Health (2011). doi:10.1136/jech.2010.12669
2. Giridhara R Babu.Do you see an elephant or just its trunk? The need of learning Modern Epidemiologic Methods: An introduction. The Internet Journal of Epidemiology. 2011 Volume 10 Number 1 (Under Print)
As a coffee-drinking virologist, I read Leung et al's report on
coffee consumption and risk of hepatocellular carcinoma (HCC) with
interest[1].
The authors excluded those "under medication for liver diseases". It
is a reasonable assumption that this means that patients who were
receiving antiviral therapy for hepatitis B virus (HBV), e.g. lamivudine,
entecavir etc. were excluded. Because patients...
As a coffee-drinking virologist, I read Leung et al's report on
coffee consumption and risk of hepatocellular carcinoma (HCC) with
interest[1].
The authors excluded those "under medication for liver diseases". It
is a reasonable assumption that this means that patients who were
receiving antiviral therapy for hepatitis B virus (HBV), e.g. lamivudine,
entecavir etc. were excluded. Because patients with a higher risk of
developing HCC tend to receive drug therapy for HBV[2], there is a risk
that the exclusion of HBV carriers on anti-HBV therapy may have introduced
a bias into the non-HCC control group.
Healthy HBV carriers in whom antiviral therapy is not indicated may
be fundamentally different from patients with HBV-related HCC. One would
expect patients who do not meet criteria for initiating antiviral therapy
to have a better prognosis i.e. are less likely to develop HCC.
Leung et al acknowledge some limitations of this study e.g. lack of
HBV viral load data and alanine transaminase (ALT) level. However,
patients' hepatitis B e antigen status, one measure of HBV infectivity and
an independent predictor for progression to HCC[3], is also missing. I
would suggest these limitations have been underplayed.
The absence of HBV viral load data, e antigen status and ALT levels
are significant omissions and linked to my first point about excluding
patients on "medication for liver disease". These variables are both
prognostic indicators and indicators for the necessity for HBV treatment.
Finally, it would be of interest to know the hepatitis C (HCV) and
HIV status of the patients studied, as these do affect the prognosis in
hepatitis B carriers. I concede that both HCV and HIV seem to be
relatively uncommon in Hong Kong[4,5]. As this information was not
provided, yet more potential confounding variables have been left
unaddressed.
The apparent exclusions and omissions detailed above leave
considerable room for doubt about the comparability of the cases and
controls and thus of the conclusions drawn.
The proposition that coffee consumption reduces the risk of HCC
developing in HBV carriers is a seductive one. It would be an almost ideal
public health intervention, as coffee is widely available, economical,
given that the cost is borne by patients and there are few significant
side effects with light or moderate consumption.
Unfortunately, it is difficult to concur with the author's conclusion
that moderate coffee consumption significantly reduces the risk of HCC in
HBV carriers based upon the findings of this study.
References:
1. Leung W W-M, Ho SC et al. Moderate coffee consumption reduces the
risk of hepatocellular carcinoma in hepatitis B chronic carriers: a case-
control study. J Epidemiol Community Health 2011;65:556-558
2. Sung JJ, Amarpurkar D et al. Treatment of chronic hepatitis B in
Asia-Pacific countries: is the Asia-Pacific consensus statement being
followed? Antivir Ther 2010;15(4):607-16
3. Yang HI, Lu SN, Liaw YF et al. Hepatitis B e antigen and the risk
of hepatocellular carcinoma. N England J Med 2002;347(3):168-74
4. Hong Kong Department of Health. Viral Hepatitis Preventive Service
website. http://www.info.gov.hk/hepatitis/english/hep_c_set.htm (accessed
18/7/11)
5. Hong Kong Department of Health. HIV/AIDS Situation in Hong Kong
(2005) factsheet. http://www.info.gov.hk/aids/pdf/g154.pdf (accessed
18/7/11)
The correlation (r = 0.73) between income inequality and prevalence
of mental illness reported by Pickett, James and Wilkinson (2006) was an
intriguing finding, but we should be extremely cautious interpreting it.
First, it was admittedly only a preliminary analysis and hence the
number of data points (countries) was small (n = 8). Consequently, the
correlation estimate will lack precision...
The correlation (r = 0.73) between income inequality and prevalence
of mental illness reported by Pickett, James and Wilkinson (2006) was an
intriguing finding, but we should be extremely cautious interpreting it.
First, it was admittedly only a preliminary analysis and hence the
number of data points (countries) was small (n = 8). Consequently, the
correlation estimate will lack precision and this is reflected in the
confidence intervals for the correlation estimate, 95% CI [0.03, 0.95].
Hence, the correlation estimate could be substantially lower.
Second, referring back to the raw data that originated from the UNDP
Human Development Report (2005) and Demyttenaere et al. (2004) I
discovered that data from the four developing countries (Mexico, Columbia,
Ukraine and Nigeria) was excluding from the original analysis. If we
recomputed the correlational analysis using the original data supplemented
by the data from the four developing countries we obtain a correlation of
0.07 (95% CI [-0.52, 0.62]).
Third, assuming that there are good reasons for excluding the
developing countries, a high correlation between income inequality and
prevalence of mental illness tells only part of the story. What is equally
important is the unstandardized slope of the linear regression line (i.e.,
simple effect size). This is because, though income inequality and
prevalence of mental illness may be highly correlated, the magnitude that
the prevalence of mental illness increases in relation to the income
inequality may be negligibly small. The unstandardized slope of the linear
regression line for the original data from Pickett et al (2006) is 3 (95%
CI [0.12, 5.87]). Therefore, as the income equality, measured in terms of
the ratio of the top 20% to the bottom 20% incomes increases by 1 the
prevalence of mental illness increases by 3%. But what we have to bear in
mind is that a ratio increase of 1 actually represents a 100% increase in
the difference between the top 20% and the bottom 20% incomes. Therefore,
the prevalence of mental illness increases by only 3% when the difference
between the top 20% and the bottom 20% incomes increases by 100%. Or in
other words 1% increase in the difference between the top 20% and the
bottom 20% incomes is associated with a 0.03% increase in the prevalence
of mental illness. Hence, the impact of income equality on the prevalence
of mental illness appears to be, as one would expect, relatively small.
References
Demyttenaere K, Bruffaerts R, Posada-Villa J, et al. (2004).
Prevalence, severity, and unmet need for treatment of mental disorders in
the World Health Organization world mental health surveys. JAMA, 291, 2581
-90.
Pickett, K.E., James, O.W., & Wilkinson R.G. (2006). Income
inequality and the prevalence of mental illness: a preliminary
international analysis. Journal of Epidemiology & Community Health,
60, 646-647.
United Nations Development Programme. (2005). Human Development
Report. New York: Oxford University Press. Retrieved from:
http://hdr.undp.org/en/media/HDR05_complete.pdf
We read with interest the article describing methods for modelling count data with excess zeros compared to standard count distributions, such as Poisson1. This topic has been extensively discussed in the statistical and epidemiological literature2-3. Didactic messages given by statisticians can often lack an appreciation of the epidemiological context and sadly this article has the same shortcomings.
The primary novelty is t...
We read with interest the article describing methods for modelling count data with excess zeros compared to standard count distributions, such as Poisson1. This topic has been extensively discussed in the statistical and epidemiological literature2-3. Didactic messages given by statisticians can often lack an appreciation of the epidemiological context and sadly this article has the same shortcomings.
The primary novelty is the context in which the issue is discussed: application to counts of Activities of Daily Living (ADL-s). It is laudable that methodological issues are tackled using practical examples, but our concern is that the novel context has been largely overlooked and an educational opportunity lost. The message is too narrow in scope and arguably misleading. The reader is told that the zero-inflated Negative Binomial is the most appropriate model for the ADL-s data, yet this is likely incorrect and could lead to inappropriate models being adopted in this domain.
The Binomial distribution deals with bounded data and is extended to yield the Beta Binomial, which accommodates overdispersion. Both the Binomial and Beta Binomial distributions have zero-inflated extensions (e.g. the "zero-inflated Binomial") to account for an excess of zeros4. We were surprised to see no mention of these alternative distributions since the Poisson distribution exhibits an infinite tail and predicts counts in excess of six, albeit with low probabilities. Allowing for over-dispersion, the Negative Binomial accommodates a longer tail for the same mean. Both distributions (whether zero-inflated or not) thus possess properties that are incongruent with the nature of the data in this context.
Any count distribution assumes an increment of one has the same meaning from one to two as from five to six; for zero-inflated extensions, the increment from zero to one may have a different meaning. As each ADL-s is unique, each is likely to have a different meaning. Hence, as individuals deteriorate in their condition, some activities may become a challenge before others. Consequently, an increment of one ADL may have different meaning along the scale and it is sensible to assume an ordinal outcome5, which also accommodates differences in the increment from zero to one.
Good agreement between observed and predicted outcomes is necessary but not sufficient. Disparity between models with regard to predicted outcomes can often be negligible whilst models differ substantially in parameterisation and hence interpretation. Likelihood-based model-fit criteria are only one facet of model development; context validity and interpretability must also have a bearing and researchers must appreciate the context in which data are generated. For this reason the best model may not yet have been found. We have not investigated the dataset, nor do we feel the need to do so when proposing the ordinal model and only with no compelling evidence that increments differed might we instead propose the zero-inflated Binomial or Beta Binomial for parsimony.
References
1. Zaninotto P, Falaschetti E. Comparison of methods for modelling a count outcome with excess zeros: application to Activities of Daily Living (ADL-s). J Epidemiol Community Health 2011; 65: 205-210.
2. Lambert D. Zero-inflated Poisson regression, with an application to defects in manufacturing. Technometrics 1992; 34:1–14.
3. Gilthorpe MS, Frydenberg M, Cheng Y, Baelum V. Modelling count data with excessive zeros: The need for class prediction in zero-inflated models and the issue of data generation in choosing between zero-inflated and generic mixture models for dental caries data. Statistics in Medicine 2009; 28: 3539-3553.
4. Vieira AMC, Hinde JP, Demetrio CGB. Zero-inflated proportion data models applied to a biological control assay. Journal of Applied Statistics 2000; 27:373–389.
5. Lall R, Campbell MJ, Walters SJ, Morgan K and MRC CFAS Co-operative. A review of ordinal regression models applied on health-related quality of life assessments. Stat Methods Med Res 2002; 11: 49-67.
There is much evidence linking learning and behaviour problems in
childhood to refined oils in the maternal diet during pregnancy and
lactation, particularly linoleic acid in both cis and trans forms which
may impair fetal brain development. A lower IQ in these children would
not be surprising.
I have seen no evidence, however, linking fresh natural fats to any
of these problems. Diets high in refined sugars...
There is much evidence linking learning and behaviour problems in
childhood to refined oils in the maternal diet during pregnancy and
lactation, particularly linoleic acid in both cis and trans forms which
may impair fetal brain development. A lower IQ in these children would
not be surprising.
I have seen no evidence, however, linking fresh natural fats to any
of these problems. Diets high in refined sugars tend to be high in
refined oils as well -- the two go together -- so I think it's important
to stress that "high fat" in this case refers only to processed oils, not
the healthy fats naturally present in fresh whole foods.
I would be pleased to provide references re linoleic acid and effects
on offspring to anyone wishing to contact me at the address above.
The authors conclusions that the media did not 'over-hype' the swine
flu nondemic are reached as a result of a methodology that directed them
towards that conclusion; an analysis solely of the UK print media.
I travelled to New Zealand on 11 May - two weeks after the first
cases emerged - and arrived in Melbourne on the 5th June, a time when this
was arguably the swine flu capital of the world. Yes...
The authors conclusions that the media did not 'over-hype' the swine
flu nondemic are reached as a result of a methodology that directed them
towards that conclusion; an analysis solely of the UK print media.
I travelled to New Zealand on 11 May - two weeks after the first
cases emerged - and arrived in Melbourne on the 5th June, a time when this
was arguably the swine flu capital of the world. Yes, it was apparent that
there was flu circulating and I fell victim to it, but the print media
response was far more measured and balanced than it was here. The joys of
the internet meant that I was following the print media in the UK closely,
as well as reading the major daily newspapers in both Australia and New
Zealand.
I suspect that an analysis of the UK print media v that of other
countries may expose our response to this nondemic for the hysteria that
it was.
There is much to like in the argument presented by Clare Bambra. Epidemiology (and public health generally) has much to learn from the social sciences and the reverse is also true. And Bambra is surely correct to raise concerns about the associated risks including the "engrained caution and purism of epidemiology" and the excessive deference to experimental research designs before acting.
However, in order to effectively mana...
There is much to like in the argument presented by Clare Bambra. Epidemiology (and public health generally) has much to learn from the social sciences and the reverse is also true. And Bambra is surely correct to raise concerns about the associated risks including the "engrained caution and purism of epidemiology" and the excessive deference to experimental research designs before acting.
However, in order to effectively manage and profit from "the interface between social science and epidemiology" it is essential that epidemiologists and their public health colleagues engage with the broad range of social science including, and perhaps especially, political science. In many discussion of the linkage between epidemiology and the social sciences there are repeated references to the insights of psychology, economics and sociology but few if any direct references are made to political science. This is ironic given the sheer size of the political science enterprise. It is also tragic insofar as the goal of much of the writing on the social and economic determinants of health is to encourage action on these determinants often, if not primarily, by means of the state. Political science has much to say about the why, what and how of state action.
Fore example, having highlighted the association between social inequality and poor health, while it is reasonable to call, as Bambra does, for income redistribution, this is but the start. Contemporary political science (including political theory) can offer a great deal of insight into why inequality is on the rise (e.g., Pierson, Paul, and Jacob S. Hacker. 2010. Winner-Take-All Politics: How Washington Made the Rich Richer--and Turned Its Back on the Middle Class. New York: Simon & Schuster.), why this varies between states, what alternative exist for ensuring more redistribution, and how to counter the inevitable arguments that this would be unfair or unwise (e.g., Cohen, G. A. 2008. Rescuing Justice and Equality. Cambridge, Mass.: Harvard University Press).
I suggest the findings of Xu, et al., are caused by increased
testosterone within urban populations. A report comparing rural areas and
a large city found that testosterone is higher in the large city (Folia
Histochem Cytobiol. 2001;39 Suppl 2:38-9).
It is my hypothesis that the "secular trend," the increase in size
and earlier puberty occurring in children, is caused by an increase in the
percentage of individu...
I suggest the findings of Xu, et al., are caused by increased
testosterone within urban populations. A report comparing rural areas and
a large city found that testosterone is higher in the large city (Folia
Histochem Cytobiol. 2001;39 Suppl 2:38-9).
It is my hypothesis that the "secular trend," the increase in size
and earlier puberty occurring in children, is caused by an increase in the
percentage of individuals of higher testosterone. More specifically, I
suggest this is due to an increase in the percentage of mothers of higher
testosterone with time within the population. This exposes more fetuses to
increased maternal testosterone with time within the population. This
causes permanent effects in the fetus which persist throughout the life
span. I suggest this is the cause of the parallel increases in morbidity
occurring within the population, such as obesity, cancer, breast cancer,
diabetes, etc., including prematurity, small for gestational age, etc.,
including less obvious gross effects which later contribute to "failing
schools" and other adverse behavioral outcomes in children.
I have come to the conclusion that the "increase in testosterone" may
partially be due to a reduction in "sex hormone binding globulin (SHBG)"
as a number of phenomena explained by the secular trend may be based on
changes in SHBG. A decrease in SHBG increases free testosterone levels.
I suggest increased testosterone may be higher in the lower
socioeconomic levels. Increased testosterone has been connected with
reduced learning ability, reduced impulse control, and sexuality. All of
these reduce the ability to obtain gainful employment and participation in
a society increasingly dependent upon advanced educational achievement and
personal control. This would concentrate this type of individual within...
I suggest increased testosterone may be higher in the lower
socioeconomic levels. Increased testosterone has been connected with
reduced learning ability, reduced impulse control, and sexuality. All of
these reduce the ability to obtain gainful employment and participation in
a society increasingly dependent upon advanced educational achievement and
personal control. This would concentrate this type of individual within
these levels and they would exhibit reduced intelligence and shorter life
spans.
I agree with the previous responder that the age of 5 and the battery
of tests used here seem inadequate to detect many of the impacts of
prenatal alcohol exposure.
Even so, I still find it remarkable that this study fails to find
statistically significant (after adjustment for confounders) impacts of
heavy maternal drinking in this sample to date.
This may have resulted from the relatively young age...
I agree with the previous responder that the age of 5 and the battery
of tests used here seem inadequate to detect many of the impacts of
prenatal alcohol exposure.
Even so, I still find it remarkable that this study fails to find
statistically significant (after adjustment for confounders) impacts of
heavy maternal drinking in this sample to date.
This may have resulted from the relatively young age of the study
group, inadequately sensitive measures, significant levels of 1st
trimester "before I knew I was pregnant" alcohol exposure in the "not
during pregnancy" group, optimistic self-reports of "light drinking," or
the obvious confounding effects of socioeconomic status and environmental
influences.
Regardless, if this study is unable to find a specific impact of
heavy drinking, how is it adequate to rule out impacts from light
drinking?
The authors do note some of these limitations in the discussion, but
frustratingly these have not come across so clearly in the media coverage.
From the press reports of this and the previous paper, it would seem that
FAPs (Fetal Alcohol Powers) have been discovered.
I think this conclusion, and even milder statements such as "At age
5, children of women who were light drinkers during pregnancy do not have
higher risk of socioemotional or cognitive deficits than those of women
who did not drink at all in pregnancy" are very premature, and in fact
irresponsible, in light of current knowledge of alcohol as a neurotoxin,
and one without a reliably described safe lower limit of exposure.
Can we please keep these concerns in mind when interpreting this
study, and future reports from this cohort, to the media?
Sir,
As a coffee-drinking virologist, I read Leung et al's report on coffee consumption and risk of hepatocellular carcinoma (HCC) with interest[1].
The authors excluded those "under medication for liver diseases". It is a reasonable assumption that this means that patients who were receiving antiviral therapy for hepatitis B virus (HBV), e.g. lamivudine, entecavir etc. were excluded. Because patients...
Dear Editor,
The correlation (r = 0.73) between income inequality and prevalence of mental illness reported by Pickett, James and Wilkinson (2006) was an intriguing finding, but we should be extremely cautious interpreting it.
First, it was admittedly only a preliminary analysis and hence the number of data points (countries) was small (n = 8). Consequently, the correlation estimate will lack precision...
There is much evidence linking learning and behaviour problems in childhood to refined oils in the maternal diet during pregnancy and lactation, particularly linoleic acid in both cis and trans forms which may impair fetal brain development. A lower IQ in these children would not be surprising.
I have seen no evidence, however, linking fresh natural fats to any of these problems. Diets high in refined sugars...
Sir,
The authors conclusions that the media did not 'over-hype' the swine flu nondemic are reached as a result of a methodology that directed them towards that conclusion; an analysis solely of the UK print media.
I travelled to New Zealand on 11 May - two weeks after the first cases emerged - and arrived in Melbourne on the 5th June, a time when this was arguably the swine flu capital of the world. Yes...
I suggest the findings of Xu, et al., are caused by increased testosterone within urban populations. A report comparing rural areas and a large city found that testosterone is higher in the large city (Folia Histochem Cytobiol. 2001;39 Suppl 2:38-9).
It is my hypothesis that the "secular trend," the increase in size and earlier puberty occurring in children, is caused by an increase in the percentage of individu...
I suggest increased testosterone may be higher in the lower socioeconomic levels. Increased testosterone has been connected with reduced learning ability, reduced impulse control, and sexuality. All of these reduce the ability to obtain gainful employment and participation in a society increasingly dependent upon advanced educational achievement and personal control. This would concentrate this type of individual within...
I agree with the previous responder that the age of 5 and the battery of tests used here seem inadequate to detect many of the impacts of prenatal alcohol exposure.
Even so, I still find it remarkable that this study fails to find statistically significant (after adjustment for confounders) impacts of heavy maternal drinking in this sample to date.
This may have resulted from the relatively young age...
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