As I illustrated earlier, all researches on the relation between type 16
and 18 HPV and cervical cancer, as well as its primary prevention with
anti HPV vaccine, although honestly performed in a worthy manner, are
fundamentally biased (1-14.
In fact, I have underscored a fundamental bias, overlooked distressingly
and suspiciously, in all researches on the relation between papillomavirus
(especially 16, 18...
As I illustrated earlier, all researches on the relation between type 16
and 18 HPV and cervical cancer, as well as its primary prevention with
anti HPV vaccine, although honestly performed in a worthy manner, are
fundamentally biased (1-14.
In fact, I have underscored a fundamental bias, overlooked distressingly
and suspiciously, in all researches on the relation between papillomavirus
(especially 16, 18 types) and cervical cancer. As a matter of fact,
Oncological Terrain "and" cervical cancer INHERITED REAL RISK , bedside
recognized rapidly with a stethoscope, are generally overlooked by both
physicians and mass-media all around the world, with some worthy
exceptions,due to a lot of well-known reasons (1-7, 14, 15) See
www.semeioticabiofisica.it.
As a consequence, in spite of its complications, readable in Literature,
vaccination campaign against HPV to prevent cervical cancer has to be
performed exclusively in young women, surely recognized as involved by
such as disorders. In Italy, as you surely know, is going on an expensive
campaign against Cervix Carcinoma by means of HPV vaccination, adviced in
ALL young women aged from 16 to 20 years. Really, NOT ALL individuals CAN
be involved by malignancy, according to Oncological Terrain and
Oncological Inherited Real Risk theory, largely accepted by farsighted,
open-minded Editors, analogously to diabetes and CAD (1-14). All inherited
real risks are characterized by microcirculatory remodelling, wherein
newborn-pathological, type I, subtype a) Oncological, and respectively,
subtype b) Endoarteriolar Blocking Devices play a central role (1-13).
Nowadays, doctor can bedside assess both Oncological Terrain and
Oncological Congenital Real risk in two minute, with the aid of a simple
stethoscope, as I have demonstrated in details in papers published in
famous peer-reviews (1-7, 14).
To advice young women, 16-20 year old, NOT involved by Oncological
Terrain and Inherited Oncological Real Risk in cervical tissue, to undergo
vaccination against type HPV aiming to prevent cervical cancer,
demonstrates that we are living in the Middle Age of Medicine (See
http://www.ilpungolo.com/leggi-tutto.asp?IDS=13; and
http://valorieliberta.wordpress.com/2008/01/18/spunti-di-comunicazione-sul
-papilloma-virus-umano/).
Sergio Stagnaro MD
Founder of Quantum Biophysical Semeiotics
Who's Who in the World (and in America)
since 1996 to 2009.
16039 Riva Trigoso (Genova) Europe.
Via Erasmo Piaggio 23/8
Ph. 0039-0185-42315
Cell. 3338631439
dottsergio@semeioticabifisica.it
www.semeioticabiofisica.it
References
1. Stagnaro-Neri M., Stagnaro S. Introduzione alla Semeiotica Biofisica.
Il Terreno Oncologico. Ed. Travel Factory, Roma, 2004.
http://www.travelfactory.it
2. Stagnaro Sergio. New bedside way in
Reducing mortality in diabetic men and women. Ann. Int. Med.2007.
http://www.annals.org/cgi/eletters/0000605- 200708070-00167v1
3. Stagnaro Sergio. Bedside Evaluation Tobacco's actions on Biological
Systems. The Lancet, October 13, 2007,
http://www.thelancet.com/journals/lancet/article/PIIS0140673607614822/comments?action=view&totalComments=2#1286
4. Stagnaro S. Genes and Cancer: a clinical view-point. The Oncological
Terrain. BioMed Central Informatics. http://www.biomedcentral.com/1471-
2105/5/21/comments#10454 2004
5. Stagnaro S., Stagnaro-Neri M.,
Oncological Terrain, conditio sine qua non of Oncogenesis:
http://www.gutjnl.com/cgi/eletters?lookup=by_date&days=60 2004
6. Stagnaro Sergio. "Genes, Oncological Terrain, and Breast Cancer", World
Journal of Surgical Oncology. 2005,
http://www.wjso.com/content/3/1/45/comments#205475 2005
7. Stagnaro Sergio. Cancer Risk Factors and Oncological Terrain. 2006.
http://www.wjso.com/content/4/1/74/comments#247528
8. Stagnaro Sergio. Without Oncological Terrain oncogenesis is not
possible. CMAJ. 23 March 2007 http://www.cmaj.ca/cgi/eletters/176/5/646
9. Stagnaro Sergio. GPs , Biophysical Semeiotics, and bedside cancer
diagnosis. 08 July 2007, International Seminar of Surgical Oncology,
http://www.issoonline.com/content/4/1/11/comments#281539
10. Stagnaro Sergio. Oncological Terrain and Inherited Oncological Real
Risk: New Way in Malignancy Primary Prevention and early Diagnosis.
International Seminars in Surgical Oncology, 2007.
http://www.issoonline.com/content/4/1/25/comments#290565
11. Stagnaro Sergio. Bedside Biophysical-Semeiotic Diagnosis of Breast
Cancer, since initial Stage. International Seminars in Surgical Oncology
2007, http://www.issoonline.com/content/4/1/21/comments
12. Stagnaro Sergio. What about Oncological Terrain. www.thescientist.com
2007. http://www.the- scientist.com/article/display/53938/
13. Stagnaro Sergio. Oncogenesis is possible exclusively in individuals
Oncological Terrain-positive. www.thescientist.com 2007. http://www.the-
scientist.com/blog/print/53498/
14. Stagnaro Sergio. Overloking Oncological Terrain and oncological Real
Risk, no paper is up-dated! 18 January 2008 Ann. Intern Med.
http://www.annals.org/cgi/eletters/147/11/775
15) Stagnaro Sergio. Quantum Biophysical Semeiotics and Cancer Inherited
Real Risk www.nature.com:
http://blogs.nature.com/nm/spoonful/2008/05/our_new_columns_narrowing_the.html#comments
, and specially
http://blogs.nature.com/nm/spoonful/2008/04/stress_as_a_therapy_1.html#comments
I read with interest the article by Bhattacharya [1] about the role
of the World Health Organization (WHO) in the development of the smallpox
eradication program. The author provides information about the inner
workings of the WHO in the 1960s and 1970s and described the various
political, economic, and social conditions under which WHO officials,
field managers, and public health workers attempted to...
I read with interest the article by Bhattacharya [1] about the role
of the World Health Organization (WHO) in the development of the smallpox
eradication program. The author provides information about the inner
workings of the WHO in the 1960s and 1970s and described the various
political, economic, and social conditions under which WHO officials,
field managers, and public health workers attempted to implement this
program on the global, national, and local levels.
I was amazed to read about the complexity of the smallpox eradication
program and the “behind the scene” activities we typically do not hear
about. It is true that most information about this program is described in
the literature in terms of clear strategies, organizational orders, and
unified actions on all levels in a multiplicity of international
locations. I appreciate that Bhattacharya [1] took the time to go through
the unpublished papers of the WHO in order to describe in detail how
difficult it is in reality to make a program of such magnitude work.
The eradication of the variola virus from human populations is
undoubtedly one of the greatest successes in the history of medicine and
public health [1-3]. However, the virus still exists on earth and many
fear it might be used as a germ warfare agent or in a bioterrorism attack
[4]. Although I strongly believe in the importance of the commemoration of
the 30th anniversary of smallpox eradication [5], we cannot afford to slow
down in developing the best programs possible to solve the many health
problems we face today. Publications like the one by Bhattacharya [1] keep
us alert and remind us to revisit our current public health strategies and
modify them as needed.
References
1. Bhattacharya S. The World Health Organization and global smallpox
eradication. J Epidemiol Community Health 2008;62:909-12.
2. Needham CA, Canning R. Global disease eradication: the race for
the last child. Washington, DC: American Society for Microbiology Press,
2003.
3. World Health Organization. Smallpox, 2009.
http://www.who.int/mediacentre/factsheets/smallpox/en/ (Accessed 1 Jan
2009).
4. Khardori N. Bioterrorism preparedness: medicine – public health –
policy. Weinheim, Germany: Wiley-VCH, 2006.
5. Centers for Disease Control and Prevention. Smallpox: 30th
anniversary of global eradication, 2007.
http://www.cdc.gov/Features/SmallpoxEradication/ (Accessed 1 Jan 2009).
Some forms of maternal morbidity may not kill mothers, but have the
ability to incapacitate them, enough to make them vertually non-existent,
as far as their infant is concerned e.g. Post Partum psychosis/depression
is one such, which is quite commonly observed in many mothers following
delivery, understood to be triggered by interplay of hormones due to
pregnancy related physiology during and immediat...
Some forms of maternal morbidity may not kill mothers, but have the
ability to incapacitate them, enough to make them vertually non-existent,
as far as their infant is concerned e.g. Post Partum psychosis/depression
is one such, which is quite commonly observed in many mothers following
delivery, understood to be triggered by interplay of hormones due to
pregnancy related physiology during and immediately after delivery.
Although the mother may be afflicted with the depression, but the
equal sufferer and unfortunate victim is ultimately her infant. The mother
in this condition, may refuse to breast feed her new born and may ignore
or even dis-own her kid. Even if mother is willing to breast feed, the
newborn is taken off from feeding, if the mother is put on anti-depressants. All of which deprives the new born of crucial nourishment and
more importantly the bonding in the initial weeks of birth and will have
to contend with external feed. Not to speak of tremendous damage done due
to loss of mother-child bonding and its after effects.
The above illustration is just to emphasise that the maternal
morbidity is very intimately linked with the infant’s morbidity n health,
therefore prompt and early public health intervention aimed at ante partum
and post partum partum depression during post partum period and
thereafter, will help not only in improving maternal health but also will
have a bearing on improving Infant health and hence, indirectly but
positively influencing both Maternal Mortality Rate and Infant Mortality
Rate.
It is my hypothesis that human evolution occurred because of
increases in testosterone (Rivista di Biologia / Biology Forum 2001; 94:
345-362). Testosterone is highest in humans and testosterone levels of the
great apes directly parallel relatedness to humans. According to my
explanation of human evolution, testosterone will periodically increase
within populations and periodically decrease. I suggest...
It is my hypothesis that human evolution occurred because of
increases in testosterone (Rivista di Biologia / Biology Forum 2001; 94:
345-362). Testosterone is highest in humans and testosterone levels of the
great apes directly parallel relatedness to humans. According to my
explanation of human evolution, testosterone will periodically increase
within populations and periodically decrease. I suggest many populations
are currently experiencing increases which are proving to be detrimental.
I suggest the "secular trend," the increase in size and weight and
earlier puberty occurring in children, is caused by an increase in the
percentage of individuals of higher testosterone within the population
with time. I think this is driven by increased reproduction of women of
increased testosterone. This increases exposure of their fetuses to
excessive testosterone which is producing increases in negative
consequences with the population, such as increasing obesity, diabetes
type 2, cancer, etc.
Where this trend occurs, pregnancy, especially in young women,
increases along with the consequences of the trend in offspring. Teenage
pregnancy is very high in the U.K. and, I suggest, is the reason for the
findings of Massó-González, et al., that diabetes type 2 is increasing in
the U.K. Many reports in the medical literature suggest that low
testosterone results in type 2 diabetes. However, other reports suggest
that excessive testosterone and anabolic steroids produce type 2 diabetes.
Evolution will select for increased testosterone in young women and the
current increases in type 2 diabetes are occurring at younger ages with
time within the population.
Most data on ethnic inequalities in health will have studied ‘first-
generation’ migrants from South Asia, as even the oldest second-generation
South Asians are only now in 2009 beginning to enter their 40s.
Smith et al’s[1] pertinent question is to ask whether the sons and
daughters of first-generation South Asians will be at equal risk of poor
health. The case of coronary disease is of particular importance
con...
Most data on ethnic inequalities in health will have studied ‘first-
generation’ migrants from South Asia, as even the oldest second-generation
South Asians are only now in 2009 beginning to enter their 40s.
Smith et al’s[1] pertinent question is to ask whether the sons and
daughters of first-generation South Asians will be at equal risk of poor
health. The case of coronary disease is of particular importance
considering the higher rate ratios for coronary mortality in men and women
from South Asia.[2-4] There is however conflicting evidence in studies
examining acculturation. Decreasing mortality with increasing duration of
residence in the new host country was observed for migrants from South
Asia in a study in a study in Australia,[5] perhaps due to cardio-protective
behavioural practices in the Australia. However, studies in the UK have
presented opposite results to the Australian work, with increasing
cardiovascular risk with length of residence among South Asian migrants.[6]
The interaction of behavioural practices and socio-economic patterns
will complicate matters. The coronary risk of a group of educated and
affluent second-generation South Asians may more resemble that of a
similarly educated and affluent white group, as opposed to a less educated
group and less affluent group of second-generation South Asians. It is
here that perhaps the heterogeneity of the South Asian group may become
increasingly important in the future. It is interesting that apart from
Indians, minority ethnic groups (including Pakistani/Bangladeshis) are
found to be more likely to engage in poor dietary behaviours in a study of
adolescent and parental lifestyles, with those born in the UK and girls
being more susceptible.[7] Thus, some subgroups may inherit (more so through
their behaviour than their genes) the diseases of their parents, whilst
others – like the offspring of some professional Indian classes – inherit
the disease profile of the majority white population.
Beyond socio-economic mechanisms, the influence of biology may
continue to adversely affect the children of South Asians. South Asians
have a smaller superficial subcutaneous adipose tissue compartment than
white people and a theory has been proposed that babies born to mothers of
South Asian descent are smaller and have less peripheral fat, and that
during subsequent growth and development immersed in the richer diet of
the developed world, this primary compartment reaches its capacity for fat
storage rapidly and the deep subcutaneous and visceral compartments become
more prominent, with adverse consequences for risks of diabetes and
coronary disease.[8] Early evidence of ethnic differences in coronary risk
has also been presented in a cross sectional comparison of British South
Asian and white children, with ethnic differences being present even in
these children aged 8 to 11 years – an increased tendency to insulin
resistance was observed in South Asian children, and the authors inferred
an increased sensitivity to adiposity as a result.[9]
These findings that second-generation minority ethnic groups in
England continue to report as poor a general health as their parents,
unaffected by changes in health behaviours,[1] suggests that continuing
investigation into ethnic inequalities in health – and into both
biological and socio-economic determinants - will be needed in the
progeny of first-generation migrants.
References
1. Smith NR, Kelly YJ, Nazroo JY. Intergenerational continuities of
ethnic inequalities in general health in England. J Epidemiol Community
Health 2009;63(March 1, 2009):253-258.
2. Harding S, Rosato M, Teyhan A. Trends for coronary heart disease
and stroke mortality among migrants in England and Wales, 1979-2003: slow
declines notable for some groups. Heart 2008;94(4):463-70.
3. Wild SH, Fischbacher C, Brock A, Griffiths C, Bhopal R. Mortality
from all causes and circulatory disease by country of birth in England and
Wales 2001-2003. J Public Health (Oxf) 2007;29(2):191-8.
4. Fischbacher CM, Steiner M, Bhopal R, Chalmers J, Jamieson J,
Knowles D, et al. Variations in all cause and cardiovascular mortality by
country of birth in Scotland, 1997-2003. Scott Med J 2007;52(4):5-10.
5. Gray L, Harding S, Reid A. Evidence of divergence with duration of
residence in circulatory disease mortality in migrants to Australia. Eur J
Public Health 2007;17(6):550-4.
6. Harding S. Mortality of migrants from the Indian subcontinent to
England and Wales: effect of duration of residence. Epidemiology
2003;14(3):287-92.
7. Harding S, Teyhan A, Maynard MJ, Cruickshank JK. Ethnic
differences in overweight and obesity in early adolescence in the MRC DASH
study: the role of adolescent and parental lifestyle. Int. J. Epidemiol.
2008;37(February 1, 2008):162-172.
8. Sniderman AD, Bhopal R, Prabhakaran D, Sarrafzadegan N, Tchernof
A. Why might South Asians be so susceptible to central obesity and its
atherogenic consequences? The adipose tissue overflow hypothesis. Int J
Epidemiol 2007;36(1):220-5.
9. Lampe FC, Morris RW, Walker M, Shaper AG, Whincup PH. Trends in rates
of different forms of diagnosed coronary heart disease, 1978 to 2000:
prospective, population based study of British men. BMJ
2005;330(7499):1046-.
Under-reporting of weight and over-reporting of height are problems
in estimating the prevalence of obesity. [1] However, many studies rely on
self-report methods. Dauphinot et al. suggested using BMI≥ 29.2 kg/m2
for the definition of obesity based on self-report height and weight in
Swiss population. [2]
Using data from North West Adelaide Health Study in Australia, [3, 4]
we as...
Under-reporting of weight and over-reporting of height are problems
in estimating the prevalence of obesity. [1] However, many studies rely on
self-report methods. Dauphinot et al. suggested using BMI≥ 29.2 kg/m2
for the definition of obesity based on self-report height and weight in
Swiss population. [2]
Using data from North West Adelaide Health Study in Australia, [3, 4]
we assessed the validity of the suggested cut-off by Dauphinot et al. In
our study, there are 1371 participants with both self-reported and
measured height and weight. The mean age of the participants was 44.9
years for men and 47.0 years for women. Using BMI≥30 as cut-off, the
prevalence of obesity based on measurement was 26.3% (26.2% in men and
26.5% in women) compared with 19.1% (18.6% in men and 19.6% in women),
using self-reported height and weight. With BMI≥29.2 as cut off for
obesity based on self-reported data, the prevalence of obesity was 23.2%
(24.0% in men and 22.3% in women). It was 3% lower than the measured
prevalence. The sensitivity, specificity and ROC were 81.3%, 96.9% and
0.89. Thus, the definition suggested by Dauphinot et al does not fit
Australian population.
The best BMI cut off for obesity based on self-reported height and
weight in our data was 28.5 for women and 29.0 for men. Based on this cut
off, the estimated prevalences of obesity were 25.0% in women and 26.5% in
men, which were similar to the measured prevalences. In women, the
sensitivity, specificity and ROC for this cut off were 85.1%, 94.3% and
0.90; in men the corresponding figures were 86.2%, 94.6% and 0.91. The
greatest over-reporting of height was found among participants ≥65 years.
For this age group, the cut off for obesity should be BMI≥28.0 for women
and BMI≥28.5 for men.
Based on 1995 Australian National Nutrition Survey data, Hayes et al.
presented a formula to correct self-reported height and weight. [5] Using
Hayes's formula, the estimated prevalence of obesity in our sample was
27.4% (26.3% in men, 28.4% in women). Compared with measured data, the
sensitivity, specificity and ROC were 88.0%, 93.2% and 0.91 (88.3%, 92.7%
and 0.90 in men; 87.6%, 93.7% and 0.91 in women). The correction gave a
reasonable estimation of the prevalence.
A clear, easy to use and population specific cut off for the
definition of obesity based self reported data is needed. Our suggested
cut off for the Australian population needs confirmation from other
studies in Australia.
References
1. Engstrom JL, Paterson SA, Doherty A, Trabulsi M, Speer KL. Accuracy of
self-reported height and weight in women: an integrative review of the
literature. J Midwifery Womens Health. 2003;48:338-345.
2. Dauphinot V, Wolff H, Naudin F, et al. New obesity body mass index
threshold for self-reported data. J Epidemiol Community Health.
2009;63:128-132.
3. Taylor AW, Dal Grande E, Gill TK, et al. How valid are self-reported
height and weight? A comparison between CATI self-report and clinic
measurements using a large cohort study. Aust N Z J Public Health.
2006;30:238-246.
4. Grant JF, Chittleborough CR, Taylor AW, et al. The North West Adelaide
Health Study: detailed methods and baseline segmentation of a cohort for
selected chronic diseases. Epidemiol Perspect Innov. 2006;3:4.
5. Hayes AJ, Kortt MA, Clarke PM, Brandrup JD. Estimating equations to
correct self-reported height and weight: implications for prevalence of
overweight and obesity in Australia. Aust N Z J Public Health. 2008;32:542
-545.
Editor - An improved understanding of the role of place for health is
one of the main challenges in social epidemiology [1]. To contribute to
this challenge, many studies are concerned with the identification of
environmental characteristics related to health. As a consequence of the
early phase of research in this field, a majority of these studies employ
a cross-sectional design. Recent papers in the Journal have descri...
Editor - An improved understanding of the role of place for health is
one of the main challenges in social epidemiology [1]. To contribute to
this challenge, many studies are concerned with the identification of
environmental characteristics related to health. As a consequence of the
early phase of research in this field, a majority of these studies employ
a cross-sectional design. Recent papers in the Journal have described how
methodological advances can contribute to understanding the role of place
for health, putting emphasis on improving causal inference [2, 3]. Without
denying the crucial importance of these methodological advances, studies
should also be grounded on theory about how environmental characteristics
are interrelated and temporally connected to each other. In absence of
clearly expressed thoughts, a recent study reported “little evidence that
better locational access to tobacco retail in New Zealand is associated
with individual-level smoking behaviour [4]”. A crucial element in
reaching this conclusion is an adjustment for neighbourhood-level
deprivation: before the adjustment, those with best access to supermarkets
and to convenience stores showed an increased probability of being a
smoker, but odds ratios attenuated to the null after the adjustment with
confidence intervals no longer including 1. The adjustment was justified
by the finding that deprived neighbourhoods may have a disproportionate
number of outlets selling tobacco, and that smoking is more prevalent in
deprived neighbourhoods. Thus, neighbourhood deprivation was
conceptualized as a classical confounder for which one needs to adjust in
order to gain insight into the influence of “retail availability, other
things being equal”. However, it is likely that owners of retail outlets
know and want to be close to where most clients are, and that the
disproportionate number of outlets in deprived neighbourhoods is due to
the level of deprivation. To the extent this is true, it would have been
justified not to adjust for neighbourhood deprivation. This results in a
substantially different conclusion: better locational access to tobacco
retail provision is associated with individual-level smoking behaviour in
New Zealand.
References
1. Kaplan GA. What's wrong with social epidemiology, and how can we
make it better? Epidemiol Rev 2004;26:124-35.
2. Fleischer NL, Diez Roux AV. Using directed acyclic graphs to guide
analyses of neighbourhood health effects: an introduction. J Epidemiol
Community Health 2008;62:842-6.
3. Kawachi I, Subramanian SV. Neighbourhood influences on health. J
Epidemiol Community Health 2007;61:3-4.
4. Pearce J, Hiscock R, Moon G, et al. The neighbourhood effects of
geographical access to tobacco retailers on individual smoking behaviour.
J Epidemiol Community Health 2009;63:69-77.
We are grateful to Faeh and al. for having applied the reduced
obesity threshold that we proposed on their data. Our purpose was not to
define an universal cut-off of 29.2 kg/m2 as a new definition of obesity,
but rather to demonstrate that using the simplest correction method i.e.
reducing the obesity threshold, was effective in estimating the true
obesity prevalence in our population samples, rather than usi...
We are grateful to Faeh and al. for having applied the reduced
obesity threshold that we proposed on their data. Our purpose was not to
define an universal cut-off of 29.2 kg/m2 as a new definition of obesity,
but rather to demonstrate that using the simplest correction method i.e.
reducing the obesity threshold, was effective in estimating the true
obesity prevalence in our population samples, rather than using previously
proposed corrective equations based on complementary data [1].
Any threshold can be criticized, in particular because of the association
of the self-report with population characteristics such as sex, age and
socio-economic conditions. This is one of the limits that we identified in
our article. The application of threshold remains nevertheless useful. We
also have to keep in mind that in adult people, the generally accepted
threshold for obesity of 30kg/m2 does not take into account other
subjects’ characteristics, even if in practice, the reality of obesity is
not limited to the application of this threshold.
When we determined an optimal threshold based on self declared data
in the French validation sample only, we found values close to the ones
proposed by Faeh and al. (29.0 for men and 28.4 for women), but the
representativity of this French sample was not insured because of the
subjects selection method. This is why we used a study population whose
representativity of the Geneva population (Switzerland) was previously
shown [2]. After application of this threshold in the French sample, the
obesity prevalence was corrected even if it did not reach the true value
of the obesity prevalence. And the new corrected prevalence in the French
sample was not statistically different from the true prevalence. It would
have been useful if Faeh and al. provided in their comment whether using
the threshold we proposed leaded to a statistically different corrected
obesity prevalence compared to the true one in their population study.
This comment illustrates several points, discussed in our article. We
agree with Faeh and al. when they question if an ubiquitary BMI threshold
can be identified. Ideally, measurement should be performed whenever
possible, and with the same procedure in order to allow comparison between
studies. Otherwise, an optimal threshold could be determined in each
population if the measurement is available only for a part of the
population. And if no measurement is available at all, we face the choice
of not correcting the estimation, knowing that we underestimate the
obesity prevalence or adopting a pragmatic approach such as using a
reduced BMI threshold.
The magnitude of the reduction to apply and the necessity of
distinguishing gender have still to be precised by further studies.
References
[1] Visscher TJ, Viet AL, Kroesbergen JH, Seidell JC. Underreporting
of BMI in adults and its effect on obesity prevalence estimations in the
period 1998 to 2001. Obesity 2006; 14(11):2054-2063.
[2] Wolff H,
Delhumeau C, Beer-Borst S, Golay A, Costanza MC, Morabia A. Converging
prevalences of obesity across educational groups in Switzerland. Obesity
2006;14(11):2080-8.
Proposed obesity body mass index correction for self-reported data
may not be appropriate
David Faeh and Matthias Bopp
Institute of Social and Preventive Medicine (ISPM), University of
Zurich, Hirschengraben 84, 8001 Zurich, Switzerland
The study published by Dauphinot et al. in the February issue of the
Journal of Epidemiology and Community Health compared self-reported and
measured BMI in a...
Proposed obesity body mass index correction for self-reported data
may not be appropriate
David Faeh and Matthias Bopp
Institute of Social and Preventive Medicine (ISPM), University of
Zurich, Hirschengraben 84, 8001 Zurich, Switzerland
The study published by Dauphinot et al. in the February issue of the
Journal of Epidemiology and Community Health compared self-reported and
measured BMI in a sample of the general population of Geneva (Switzerland)
and a smaller French sample [1]. In order to account for underestimation
of BMI arising from self-reports, the authors proposed an universal cut-
off of 29.2 kg/m2 instead of 30 kg/m2 for the definition of obesity. In a
previous study, we compared the obesity prevalence based on measured and
self-reported BMI in ten population-based studies carried out in
Switzerland between 1977 and 2003 (N=54,315) [2]. As shown in the figure,
we found considerably higher (1.6 times) prevalence of obesity in the five
studies using measured BMI (black solid line and squares) compared to the
five surveys with self-reports (grey solid line triangles, for details see
[2]). The use of the Dauphinot cut-off in our data suggests that this
could indeed improve estimates of obesity. However, the proposed cut-off
of 29.2 kg/m2 (dotted line, diamonds) may not sufficiently account for
self-report bias and for sex-differences. The latter is supported by
figure 1 in the Dauphinot publication and by the majority of population
studies included in the review of Connor Gorber et. al [3]. According to
our data, a cut-off of 28.6 kg/m2 in men and 28.2 kg/m2 in women (dashed
line, crosses) could be more appropriate. Probably, persons participating
in the Geneva study have a lower body weight than inhabitants of other
Swiss areas. For example, in the CoLaus population based study carried out
in Lausanne, the obesity prevalence was 15.6% (vs 12.6% in the Geneva
population).[1, 4] Furthermore the validation with the French study may be
problematic, since the BMI underestimation mainly arose from an
overestimation of height in that population, while it predominantly
resulted from an underestimation of weight in the sample from Geneva.[1]
Finally, it is questionable whether an ubiquitary valid BMI threshold can
be derived. This is also suggested by the rather large differences between
studies (see [3]) and by the fact that rounding of height strongly depends
on cultural affiliation.[5] Nevertheless, all lines derived from linear
regression are quite parallel (particularly in men) suggesting that a
single threshold for self-reported BMI works independently of time.
Figure. Mean (%) prevalence of obesity with trend line (obteined with
linear regression) by study.
References
1. Dauphinot V, Wolff H, Naudin F, et al. New obesity body mass index
threshold for self-reported data. J Epidemiol Community Health
2009;63(2):128-32.
2. Faeh D, Marques-Vidal P, Chiolero A, et al. Obesity in Switzerland: do
estimates depend on how body mass index has been assessed? Swiss Med Wkly
2008;138(13-14):204-10.
3. Connor Gorber S, Tremblay M, Moher D, et al. A comparison of direct vs.
self-report measures for assessing height, weight and body mass index: a
systematic review. Obes Rev 2007;8(4):307-26.
4. Firmann M, Mayor V, Vidal PM, et al. The CoLaus study: a population-
based study to investigate the epidemiology and genetic determinants of
cardiovascular risk factors and metabolic syndrome. BMC Cardiovasc Disord
2008;8:6.
5. Bopp M, Faeh D. Who gives me five? Rounding preference for self
reported height depends on language. BMJ 2008;337(a2950):1463.
Whilst not disputing the originality of the review of community-based participatory research by Cook, and published in the August 2008 edition of JECH, it does raise questions about what the agreed minimum methodological requirements are for JECH to describe a review as “systematic”.[1]
Specifically, the Cook review meets none of the criteria which are widely considered to differentiate systemati...
Whilst not disputing the originality of the review of community-based participatory research by Cook, and published in the August 2008 edition of JECH, it does raise questions about what the agreed minimum methodological requirements are for JECH to describe a review as “systematic”.[1]
Specifically, the Cook review meets none of the criteria which are widely considered to differentiate systematic reviews (SRs) from traditional literature reviews (Table 1).[2] Most notably, the Cook study employed a very minimalist search strategy not least as in terms of the electronic searches, only MEDLINE was searched. This is widely considered as inadequate for SRs, particularly public health ones, as many relevant studies are missed.[3, 4] Further, citation follow-ups, hand searching and author contact, all considered important aspects of a sound SR search strategy, are absent.[2, 5] Clear descriptions of study inclusion, data extraction and quality appraisal were similarly lacking. Indeed, quality appraisal seems limited to a description of the various study designs employed by the included studies. No quality appraisal criteria are presented. As table 1 demonstrates, transparency is lacking in many other aspects of the review methodology and it is unclear why studies are included (or indeed excluded). In addition, there is only one author of the review (Cook). This is very rare for a SR, as having a second reviewer to independently check judgements is an important component of the rigour of SRs – minimising bias and enhancing reproducibility. [2, 5] Indeed all other SRs published in JECH since 2000 have had more than two reviewers.
It is therefore highly misleading to describe the Cook literature review as a “systematic” review.[1] Doing so within the pages of JECH undermines the extensive efforts (time, cost, management) put in by actual SR teams, ignores the evidence of the benefits of taking a systematic approach to evidence synthesis,[2-5] and brushes aside the extensive guidelines developed about the good conduct of SRs.[5] The essential methodological elements of SRs (transparency, rigour, reproducibility, quality appraisal), not only differentiate them from traditional reviews, but they are also what gives SRs their high status within the hierarchy of evidence and makes them such a valuable source of research evidence. The Cook review lacks the methodological rigour which characterises a SR and cannot be fairly described as such: it is a traditional literature review and JECH readers should re-consider its findings in this context.
Clare Bambra
References
1. Cook, WK. Integrating research and action: a systematic review of community-based participatory research to address health disparities in environmental and occupational health in the USA. J Epidemiol Comm Heal. 2008, 62: 668-676.
2. Petticrew, M. Systematic reviews from astronomy to zoology: myths and misconceptions. Brit Med J. 2001, 322;98-101.
3. Suarez-Almazor, ME., Belseck, E., Homik, J., et al. Identifying clinical trials in the medical literature with electronic databases: MEDLINE alone is not enough. Control Clin Trials 2000, 21: 476.87.
4. Ogilivie, D., Hamilton, V., Egan, M., et al Systematic reviews of health effects of social interventions: How far should you go? J Epidemiol Comm Heal. 2005, 59: 804-808.
5. Higgins, JPT., Green, S. (eds). Cochrane Handbook for Systematic Reviews of Intervention Studies (v5.0). 2008. Available at: http://www.cochrane-handbook.org/ [accessed 20/08/08]
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David Faeh and Matthias Bopp
Institute of Social and Preventive Medicine (ISPM), University of Zurich, Hirschengraben 84, 8001 Zurich, Switzerland
The study published by Dauphinot et al. in the February issue of the Journal of Epidemiology and Community Health compared self-reported and measured BMI in a...
Dear Editor
Whilst not disputing the originality of the review of community-based participatory research by Cook, and published in the August 2008 edition of JECH, it does raise questions about what the agreed minimum methodological requirements are for JECH to describe a review as “systematic”.[1]
Specifically, the Cook review meets none of the criteria which are widely considered to differentiate systemati...
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