The idea that the diseases of the future will increasingly have their
aetiological roots in 'comfort' is at first sight an appealing and
powerful one. However, to accept this idea uncritically could in fact be
part of the problem. Just to take one example for brevity: the idea that
everyone desperately wants to confine themselves to moving around in a
motor car. I often have arguments with people who cl...
The idea that the diseases of the future will increasingly have their
aetiological roots in 'comfort' is at first sight an appealing and
powerful one. However, to accept this idea uncritically could in fact be
part of the problem. Just to take one example for brevity: the idea that
everyone desperately wants to confine themselves to moving around in a
motor car. I often have arguments with people who claim that the car is a
precious guarantor of 'freedom'. One thing that argues against this is the
difference in the effects on the prices of houses when it is proposed to
build a road nearby versus what happens when improvements in local public
transport take place. In the former case, house prices plummet. In the
latter case, they generally tend to shoot upwards. In this way the market
gives us a clear signal about preferences if people are really given a
choice. The type of 'comfort' disease that arises from our ever
diminishing levels of exercise is in part the result of an unholy alliance
between the oil and motor vehicle industries, and governments who would
rather not deal with unionised skilled labour forces needed to run
transport systems. A furtive privatisation of transportation, by cutting
services and forcing people into cars, took place long before what was
left was officially privatised. A recent ONS report shows that households
now spend on average over £50 per week on their motor cars, one of most
expensive items in overall living costs, and around 1/3 of the total
guaranteed income level for pensioner households. So I do not really think
the pervasiveness of the car can be regarded in any simple way as the
result of the human attachment to comfort.
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-.
The Journal of Epidemiology and Community Health has recently
published two papers by Knox[1,2] which conclude that “childhood cancers
are strongly determined by prenatal or early postnatal exposures to oil
based combustion gases especially from engine exhausts. 1,3-butadiene, a
known carcinogen, may be directly causal”. This is a strong conclusion
for a study whose novel analysis uses only the birth...
The Journal of Epidemiology and Community Health has recently
published two papers by Knox[1,2] which conclude that “childhood cancers
are strongly determined by prenatal or early postnatal exposures to oil
based combustion gases especially from engine exhausts. 1,3-butadiene, a
known carcinogen, may be directly causal”. This is a strong conclusion
for a study whose novel analysis uses only the birth and death addresses
of childhood cancer cases and which uses atmospheric emissions data from
2001 as a surrogate for exposure that may have occurred as early as 1937
in the first report, or as early as 1955 in the second report.
Furthermore, Knox notes that the basic method of the study, and all the
results, depend upon a premise of a “migration equilibrium” among the
general child population. Strong claims are also made about the studies
in two accompanying editorials in the journal.[3,4] One editorial
acknowledges the lack of a proper control group, but still claims that the
papers contain “striking evidence relating atmospheric contaminants, and
mostly emissions derived from engine exhausts, with increased risk for
children of dying from leukaemia and other cancers”.[3] A second
editorial describes the work as “unique in its capacity to combine in a
meaningful way a series of routinely collected data on births, deaths,
residences, sources of exposure, and specific exposures”.[4] However,
this letter will demonstrate that a migration equilibrium cannot be
assumed and that Knox’s estimate of relative risk largely reflects the
relative likelihood of families living in the inner and outer exposure
zones to move house. Consequently the studies provide no meaningful
results and the findings should be disregarded.
The two reports by Knox aim to identify specific causal agents for
childhood cancer using methodology that links the birth and death
addresses of fatal child cancers (pre 1980) to current emissions hotspots
for specific chemicals. Knox has developed a methodology based on the
proximity of migrant children to pollution sources at birth and death
which he notes was initially dictated by the absence of a suitable set of
non-cancer controls in the study from which the case material was
extracted. For a particular definition of exposure (for example, living
within 1.0 km of an emissions hotspot), Knox estimates the relative risk
among the subset of children whose birth and death addresses differ in
respect of exposure by calculating the ratio of outward migrations (birth
address exposed and death address unexposed) to inward migrations. This
letter focuses on this estimator of relative risk because it has some
plausibility and the approach has been likened to a case-crossover study
design.[4] However, Knox also states that the ratio of births to deaths
is an adequate estimator of relative risk for short distances around
emissions hotspots although this clearly gives results that are
inconsistent with the migration ratio unless all families move house.
Knox acknowledges that the validity of his approach depends upon the
premise of a short term migration equilibrium among the general child
population and the second report[2] claims that this has been validated
in the earlier report.[1] However, Knox presents no data to test the
validity of this critical premise in either report and he only presents a
calculation of the scale of demographic movement that would be necessary
to explain the migration ratios that he has observed. In the case of 1,3-butadiene, Knox calculates that there would have to have been a net
general migration rate among children sufficient to have depopulated all
the exposed zones over the study period. However, this argument is
patently wrong as it overlooks the fact that the numbers of children in
the exposed areas will also be replenished by children born in these
areas. Knox’s premise of migration equilibrium is not only untested, it is
also readily apparent that is not valid as it completely ignores the
contribution of births (and deaths to a much lesser extent in the case of
children) to the maintenance of a population equilibrium. For example,
consider the housing stock at the foot of the housing ladder that is
rented or purchased by many young couples before they start a family. Many
of these couples will move to larger properties in better residential
areas after they start their families. Other families with young children
are unlikely to move into the properties and replace the children that
have left. However, the area will not become depopulated of children as
couples without children will move into the properties and start their
families as the cycle repeats. In contrast, many children living in larger
properties in better residential areas will grow up there and move out as
adults, and their parents are likely to be replaced at some point by
families with young children.
Kogevinas and Pearce[4] correctly identify that the findings of
Knox’s studies will be invalid if there is not a short term migration
equilibrium among the general child population or if there is a specific
tendency for families to move away from environmental hotspots after the
diagnosis of cancer in the child. However, they incorrectly state that
Knox attempted to address these two assumptions by restricting his
analysis to short migrations of less than 1.0 km. Knox did not perform
such an analysis in either report and most of Knox’s analyses are
restricted to migrations that were more than 1.0 km in distance. However,
there is sufficient information in tables 1, 2 and 5 of Knox’s first
report[1] to perform the analysis suggested by Kogevinas and Pearce for 7
of the 8 exposures that had the highest migration ratios in the analysis
of migrations greater than 1.0 km. The short distance migration ratio for
benzo(a)pyrene (BAP) could not be calculated because Knox gives different
numbers of hotspots in tables 1 and 5 for BAP (the lower limit for BAP
hotspots given in table 2 of Knox’s first report is also higher than the
figure given in the National Atmospheric Emissions Inventory (NAEI)
emissions maps[5]). However, the other 7 migration ratios for short
migrations (less than 1.0 km) range from 1.43 (1,3-butadiene, 33 outward
and 23 inward migrations) to 0.67 (benzene, 10 outward and 15 inward
migrations) with a median of 1.02 (PM10, 44 outward and 43 inward
migrations). Hence, the migration ratios for migrations of less than 1.0
km provide no evidence of an association between exposure and childhood
cancer.
Table 5 of Knox’s first report[1] also provides information about
the proportions of children born in the inner (within 1.0 km of a hotspot)
and outer exposure regions that migrated (any distance). For all the
exposures in Knox’s table 5, the proportions of children that migrated
were much higher for the inner exposure regions than the outer regions.
The largest difference is seen for 1,3-butadiene (inner migration rate =
80.1%, outer migration rate = 59.3%) and the smallest for BAP (inner
migration rate = 74.1%, outer migration rate = 65.1%). These differences
are strongly related to the magnitude of Knox’s estimate of relative risk
for exposure (based on migrant children with discordant birth and death
addresses). Knox obtained the highest estimate of relative risk for 1,3-
butadiene (3.73) and the lowest estimate of relative risk for BAP (1.92).
Furthermore, if the inner and outer migration rates are used to calculate
the odds ratios for exposure when comparing migrant and non migrant
children, then these are similar in magnitude to Knox’s estimate of
relative risk for an exposure. For example, 1,3-butadiene has an odds
ratio for migration of 2.73 and BAP has an odds ratio for migration of
1.53. However, there is absolutely no reason to expect any relationship
between a child moving house and their exposure. Knox’s estimate of
relative risk is largely a measure of the relative likelihood of a family
to move house in the inner and outer exposure zones and almost certainly
reflects differences between the type of housing to be found within the
inner and outer exposure regions. This is readily apparent when one looks
at the NAEI emissions maps.[5] Most of the exposures with high
outward/inward migration ratios have exposure hotspots that are mainly
situated alongside busy roads and/or in inner city areas. The housing in
these areas is often the sort of housing that families with young children
will try to move away from i.e. small terraces and flats. Nitrogen oxides
(NOx), 1,3-butadiene, benzene and PM10 are examples of such emissions and
the emissions map for NOx
(http://www.naei.org.uk/images/mapping_2002/6_large.png) is typical of
this group of emissions. In contrast, the locations of hot spots for
emissions with a high inward/outward migration ratio are very different. A
good example is the emissions map for nickel
(http://www.naei.org.uk/images/mapping_2002/16_large.png) with many of
the hotspots on the edges of urban areas situated close to housing areas
that are attractive to families. This also explains the surprising fact
that Knox obtained similar results in analyses of the different tumour
classes. Even if some of these agents are the cause of childhood cancer,
it is biologically implausible that they will affect all tumour classes.
It has been demonstrated that the outward/inward migration ratios are
not measuring the carcinogenic effect of substances or the non-specific
emissions from certain types of site as claimed by Knox. However, it
would also be very surprising if the 2001 modelled NAEI emissions data are
a good surrogate for exposure that occurred between 21 and 64 years
earlier (21 to 46 years in the second report). Knox focuses on 1,3-
butadiene, but this is one of the compounds for which the 2001 NAEI
emissions data are least likely to be representative of exposures so many
years earlier. Stationary source emissions for 2002 have now replaced the
information for 2001 on the NAEI website, but the emissions spreadsheet
for 2002 shows that there were 200 tonnes of emissions from 1134
stationary sources. Over 80% of the emissions occurred at just two
locations (97% from 8 locations). Most of the 1134 sites (96%) are
motorway service stations and supermarket filling stations that would not
have existed when the majority of the children in these studies were born.
Of the total of 3.5 ktonnes of 1,3-butadiene estimated to have been
emitted in 2002, 2.6 ktonnes were due to road transport activity.
Motorways and major roads are clearly shown as hotspots on the NAEI
emissions map. However, none of the motorways existed when the first
children in the studies were born and many did not exist when the last
children died in 1980 (although proximity to a motorway is also one of the
individual exposures studied by Knox).
It should also be noted that Knox is incorrect in two respects when
he states that the workplace exposure standard for 1,3-butadiene is 1 part
per billion (ppb), a limit which he says is not designed to prevent
childhood cancers. In fact, workplace exposure is limited to a maximum of
10 parts per million and the 1 ppb standard that Knox refers to is the
current UK standard for 1,3-butadiene in urban air (a running annual
average). This is a standard that is meant to protect all of the
population, including children, and it has been recently reviewed by the
UK Expert Panel on Air Quality Standards (EPAQS) who concluded that
“concentrations of 1,3-butadiene in the ambient atmosphere of 1 ppb
constitute so small a risk to the population as to be undetectable by any
feasible study”.[6]
In conclusion, it is clearly evident that Knox’s underpinning
assumption is not met and hence that the study has no control group and
the results are not interpretable. However, even if Knox had included a
comparison group of children who did not develop cancer, it is debatable
whether the results would have had much value because of the lack of valid
exposure information. An analysis restricted to short migrations of less
than 1.0 km which is less dependent upon the migration equilibrium
assumption,[4] shows no evidence of an association between childhood
cancer and birth proximity to Knox’s pollution hotspots. The studies are
fatally flawed and there is no basis for Knox’s conclusions and the
assertions made in the editorials that “studies such as this clearly
indicate the potential importance of specific environmental exposures in
the causation of cancer in children”[4] or that “Knox’s findings should
be seriously taken into account by decision makers concerned with
environmental emissions’ limits and control” [3]. On the contrary, these
reports clearly indicate the dangers of conducting epidemiological
research without a proper comparison group and sound exposure assessment
methodology, and the need to challenge arguments that are presented with
no supporting evidence.
Competing interests: The author provides consultancy services to a
range of customers including the chemical industry. The author reviewed
these publications on behalf of the Lower Olefins sector group of the
European Chemical Industry Council (Cefic). However, the opinions
expressed in the letter are entirely those of the author.
References:
1. Knox EG. Childhood cancers and atmospheric carcinogens.
J Epidemiol Community Health. 2005;59:101-5.
2. Knox EG. Oil combustion and childhood cancers.
J Epidemiol Community Health. 2005;59:755-60.
3. Garcia AM, Alvarez-Dardet C. A journal for evidence based
policies. J Epidemiol Community Health. 2005;59:716-7.
4. Kogevinas M, Pearce N. Geographically based approaches can
identify environmental causes of disease. J Epidemiol Community Health.
2005;59:717-8.
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).
This is a response to the e-letter sent by Dr Wenbin Liang. We
appreciate the comments and found them highly valuable.
Point 1. "The subjects of the study are collected from several
geographical clusters, and peoples health in the same hospital could be
strongly related....A small flu spreading among staff may affect the
incidence of medically certified sickness absence in one local emp...
This is a response to the e-letter sent by Dr Wenbin Liang. We
appreciate the comments and found them highly valuable.
Point 1. "The subjects of the study are collected from several
geographical clusters, and peoples health in the same hospital could be
strongly related....A small flu spreading among staff may affect the
incidence of medically certified sickness absence in one local employment
rate strata greatly".
Response: There are some points to be considered here. First, all
workplaces in municipalities and to some extent in hospitals are
physically spread across the town; in our data there are over 3000
different working units. Second, below are listed the different diagnostic
categories in explaining the medically certified sickness absence
incidence (>9 days) in Finland:
Musculoskeletal disorders 32%
Mental health disorders 15%
Injuries 13%
Cardiovascular diseases 7%
Respiratory diseases 6%
Disorders in digestive system 5%
Neurological diseases 4%
Tumours 4%
Pregnancy 3%
Urinary and venereal diseases 2%
Infectious diseases 1%
Other diseases 8%
Our results on the association between high local unemployment rate
and long-term (>8 days) medically certified sickness absence in women
were similar to those obtained for all medically certified absences. Thus,
common cold or other infections are unlikely to explain the present
results. In contrast, infectious diseases may have a great contribution to
self-certified sickness absence (of 1 to 3 days' duration).
Point 2: "The cloud could be cleared if the original data showed no
great variation of "medically certified sickness absence incidence in
different hospitals/municipalities which are within the same local
unemployment rate strata".
Response: As suggested, we re-analysed our data and found that there
was variation in the incidence of medically certified sickness absence
between the workplaces (10 municipalities and 15 hospitals). However,
there was statistically significant (p<.001) variation within all local
unemployment rate stratum (high, decreasing and low). However, the
workplace accounted only for 1-2% of the variation in sickness absence
incidence.
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.
This study showed a nice way to estimate income level.[1] However in
the paper it stated that there was a 24% changed of the increased risk
among unskilled workers after “adjusting for GHI”—(1.55-1.42)/(1.55-1)=0.236, if estimating in the same way, the difference between the lower
cut off point of the “CI”—1.24 and the point estimated hazard ratio—1.55
is (1.55-1.24)/0.55=56% of “the increased risk”,(...
This study showed a nice way to estimate income level.[1] However in
the paper it stated that there was a 24% changed of the increased risk
among unskilled workers after “adjusting for GHI”—(1.55-1.42)/(1.55-1)=0.236, if estimating in the same way, the difference between the lower
cut off point of the “CI”—1.24 and the point estimated hazard ratio—1.55
is (1.55-1.24)/0.55=56% of “the increased risk”,(data from table 3)[1] and
therefore it may not be suitable to consider there is a “real” reduction
in the “increased risk” as the reduction is much less than 56% of the
“increased risk”. Nevertheless if there was an effect of income on the
risk of MI that was unrelated to occupation, an effect of income might be
observed within the same occupation category.
Moreover when family income is also being investigated, it is
possible that the occupation of other family members may play an important
role on both of the family income and the life style of the family, and
further “link” income with “MI” risk.
Reference:
1. Andersen, I., et al., Income as mediator of the effect of
occupation on the risk of myocardial infarction: does the income
measurement matter? J Epidemiol Community Health, 2005. 59(12): p.1080-5.
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.
I most certainly agree with the “reviewer’ comments” cited by the
authors in the text of their paper; “The paper is timely and can be
potentially useful for health policy makers” (p. 1032). However, “timely”
in this case is a bit of an oddity. In response to a recent critique of
progress that I had written (Betts, 2005) a rather noted philosopher, who
is kind enough to review scholarly work for me fro...
I most certainly agree with the “reviewer’ comments” cited by the
authors in the text of their paper; “The paper is timely and can be
potentially useful for health policy makers” (p. 1032). However, “timely”
in this case is a bit of an oddity. In response to a recent critique of
progress that I had written (Betts, 2005) a rather noted philosopher, who
is kind enough to review scholarly work for me from time to time, asked
me; “I would think that this language [of Progress] is pretty hollow now.
Do your colleagues really believe it?” The point is, that serious
thinkers have not “believed” in Progress since – well perhaps since
Nietzsche (1990) suggested that;” “Mankind surely does not represent an
evolution toward a better or stronger or higher level, as progress is now
understood. This ‘progress’ is merely a modern idea, which is to say, a
false idea.” (p. 4), over a century ago. Though, certainly since Ivan
Illich gave the term iatrogenesis a whole new meaning. And yet virtually
all of our social and political institutions, particularly those of health
and welfare, are founded, perhaps even premised on the idea of Progress.
One wonders then, why it has taken so long for many of us, who generally
consider ourselves to be health practitioners of one kind or another, to
catch on to this serious problem of Progress? Could it be that we have
subscribed so heavily to a techno-rational science model, again
particularly in the health and welfare industry, that all of our, so
highly advertised, critical faculties have become stuck in a paradigm of
delusion? Indeed, in a recent article by Roy (2005), a chemist by the
way, aptly titled in my view; Scientism and Technology As Religions he
claims that; “Science-and-technology is the most powerful force under
human control; hence, scientific fundamentalism is the most dangerous.”
(p. 836). Of course Roy isn’t the first to suggest that techno-
rationalism (or scientism) may well constitute a religion of sorts, in
fact, once again a century ago, Nietzsche claimed something similar, as
have many others. In fact, more recently, Schaler (2002) has proposed
that health itself had indeed become a religion, with “the medical
profession as a priestly caste.” (p. 67).
Those of us who do the work of healthcare (be it diagnosis, intervention, education, promotion and what not) must now begin some serious thinking, or at any rate begin to pay
attention to some of the serious (anti-modern if you will) thinking that
has characterized the 20th century. Perhaps we might begin with a
question of the profoundest sort that has already, and again recently,
been proposed by Joseph Heath (2004); “Is it possible to emulate many of
the attractive features of western societies, while avoiding the social
pathologies?” (p. 665-6). While I do agree with the authors’ claim that;
“Public health needs to be more passionate about health issues associated
with human progress and adopt a health promotion stance.” (p. 1033), we
must also be careful for at least two reasons. The first concerns what
both Fitzgerald (1994) and Fitzpatrick (2001) refer to as The Tyranny of
Health, while the second is perhaps best summed up by Ulrich Beck
regarding his theory of reflexive modernity (or second modernity); “Due to
the close link between institutions that depend on one another to exist,
it can be assumed that processes of change and transformation in
particular parts of the structure will trigger problems in other parts
(the side-effects of side-effects)…” (Beck & Lau, 2005, p. 533).
Indeed, side effects are the order of the day, and nothing happens without
them happening. The problem then, for those who claim to be engaged in
the fixing of problems, is which side effects are good and which are bad.
Or put differently, which are acceptable and which are not. Moreover,
these are socio-political and socio-cultural issues of value, and they are
anything but scientific. Finally, in the spirit of the authors’ well put
claim that; “public health has to become more assertive and politically
aware…” (p. 1033), with, perhaps, a continuing attention to Foucault, let
us begin a plea for the progress of serious thinking about health, rather
than maintaining the modern course of unhealthy Progress.
References
Beck, U. & Lau, C. (2005). Second modernity as a research agenda:
Theoretical and empirical explorations in the ‘meta-change’ of modern
society. British Journal of Sociology, 56(4), 525-557.
Betts, C. E. (2005). Progress, epistemology and human health and
welfare: What nurses need to know and why. Nursing Philosophy, 6, 174–188
Fitzgerald F. T. (1994). The tyranny of health. N Engl J Med, 331,
196-198.
Fitzpatrick M. (2001). The tyranny of health: Doctors and the
regulation of life style. Routledge: New York.
Heath, J. (2004). Liberalization, modernization, westernization.
Philosophy and Social Criticism, 30(5-6), 665-690.
Nietzsche F. (1990) The Anti-Christ (tr. R.J. Hollingdale). Penguin,
New York.
Roy, R. (2005). Scientism and technology as religions. Zygon, 40(4), 835-844.
Schaler, J. A. (2002). Moral Hygiene. Society, May/June, 63-69.
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Point 1. "The subjects of the study are collected from several geographical clusters, and peoples health in the same hospital could be strongly related....A small flu spreading among staff may affect the incidence of medically certified sickness absence in one local emp...
Dear Editor
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...
Dear Editor,
This study showed a nice way to estimate income level.[1] However in the paper it stated that there was a 24% changed of the increased risk among unskilled workers after “adjusting for GHI”—(1.55-1.42)/(1.55-1)=0.236, if estimating in the same way, the difference between the lower cut off point of the “CI”—1.24 and the point estimated hazard ratio—1.55 is (1.55-1.24)/0.55=56% of “the increased risk”,(...
Dear Editor
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...
Dear Editor,
I most certainly agree with the “reviewer’ comments” cited by the authors in the text of their paper; “The paper is timely and can be potentially useful for health policy makers” (p. 1032). However, “timely” in this case is a bit of an oddity. In response to a recent critique of progress that I had written (Betts, 2005) a rather noted philosopher, who is kind enough to review scholarly work for me fro...
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