Editorials represent the opinions of the authors and not
necessarily those of the BMJ or BMA EDITORIALS
For the full versions of these articles see bmj.com
Screening for prostate cancer
PSA testing should be tailored to individual risk
Screening based on prostate specific antigen (PSA) measure-
MIKE ALBANS/NY DAILY NEWS ARCHIVE/GETTY IMAGES
ment has contributed to a dramatic increase in the number of
prostate cancer cases diagnosed. In addition, most tumours
are now smaller and clinically localised at diagnosis, whereas
before the introduction of screening, tumours were often
clinically advanced or overtly metastatic at diagnosis. How-
ever, the effects of screening on overall mortality and mor-
tality from prostate cancer were unclear and variable in two
large randomised trials.1  2 The American PLCO study found
no benefit on mortality, whereas the European ERSPC trial
showed a 20% reduction in prostate cancer specific mortality
after 10 years in men who underwent PSA based screening.
RESEARCH, pp 593, 594 In the linked systematic review and meta-analysis,
Gerald L Andriole Jr chief of Dj­ulbegovic and colleagues comprehensively assessed the
urologic surgery, Washington effects of screening for prostate cancer. The analysis of six
University School of Medicine, randomised controlled trials, including the PLCO and ERSPC
4960 Children’s Place, Campus
Box 8242, St Louis, MO 63110, studies, found that screening increased the probability of
USA being diagnosed with prostate cancer (relative risk 1.46, 95%
andrioleg@wustl.edu confidence interval 1.21 to 1.77) but had no significant effect
Competing interests: The author
has completed the Unified
on mortality from prostate cancer (0.88, 0.71 to 1.09) or over-
Competing Interest form at all mortality (0.99, 0.97 to 1.01). The authors concluded that
www.icmje.org/coi_disclosure. insufficient evidence is available to support the routine use
pdf (available on request from
of prostate cancer screening.3
the corresponding author) and
declares: no support from any In addition to the uncertain benefit on mortality, the human
organisation for the submitted and economic costs associated with PSA based screening are
work; he has had specified
substantial, mainly as a result of “overdiagnosis” and “over-
relationships with Aeterna
Zentaris, Amgen, Augmenix, treatment.”4  5 This occurs because repetitive PSA based screen-
Cambridge Endo, Caris, EMD ing detects all types of prostate cancer—indolent small volume
Serono, Envisioneering,
tumours as well as aggressive lesions that have a high potential
Ferring Pharmaceuticals,
France Foundation, GenProbe, to cause harm. To date, methods of reducing overdiagnosis and
GlaxoSmithKline, Johnson & overtreatment of indolent tumours have included the use of 5α
Johnson, Myriad Genetics, NCI, reductase inhibitors6  7 as an adjunct to PSA testing and “active
NIDDK, Nema Steba, Onconome,
Ortho Clinical Diagnostics, Veridex surveillance”8 programmes for small “low risk” tumours. By
LLC, and Viking Medical in the eliminating dihydrotesterone, 5α reductase inhibitors reduce
previous three years; no other the development or growth (or both) of low grade prostate
relationships or activities that
could appear to have influenced tumours. In clinical trials, about 25% fewer cases of low grade
the submitted work. prostate cancers were seen in treated men who were followed
Provenance and peer review: for four to seven years. Active surveillance requires close
Commissioned; not externally
peer reviewed.
follow-up of men with low grade tumours, with frequent PSA
testing and biopsy every year or so. In well selected patients,
Cite this as: BMJ 2010;341:c4538 often elderly men or those with an anticipated short overall
doi: 10.1136/bmj.c4538
survival, this strategy has helped avert aggressive treatment in
those who are likely to die of other conditions. Neither of these
strategies is widely practised at the moment.
A second linked study by Vickers and colleagues assessed
the potential of another strategy to improve the efficacy and
reduce the costs of PSA based screening.9 They correlated
PSA concentration at age 60 to the lifetime risk of a clinical
diagnosis of prostate cancer, prostate cancer metastasis,
and death from prostate cancer. PSA concentration at age 60
BMJ | 18 SEPTEMBER 2010 | VOLUME 341 563
was strongly associated with prostate cancer and death from
prostate cancer. Men with a PSA concentration below 1 ng/ml
(about half of the population studied) had negligible rates of
metastasis or death. Although only a minority of men with
a PSA concentration greater than 2 ng/ml developed fatal
prostate cancer, 90% (78% to 100%) of deaths from prostate
cancer occurred in these men. Thus, men with a PSA less than
1 ng/ml could be exempted from repetitive testing, which
would reduce overdiagnosis and overtreatment. Conversely,
men with higher PSA concentrations at age 60, who have the
highest risk for prostate cancer metastases or death, could
be followed more intensively and might be more compliant
with screening and treatment recommendations and with risk
reduction strategies, such as drugs and lifestyle adjustments.
These findings need to be validated in additional studies.
Studies should also look at different racial and ethnic groups,
in whom the risk of prostate cancer may correlate with dif-
ferent PSA thresholds, and investigate whether a similar risk
stratification can be carried out in a younger cohort—for exam-
ple, men in their late 40s and early 50s. However, ultimately,
early detection of prostate cancer relies on finding more
specific biomarkers. Sadly, none has yet emerged, although
recently there have been some promising developments.10  11
Identification of cancer specific genes in cells sloughed into
the urine after prostatic examination, which is now feasible
with the commercially available PCA3 test, may reduce the
number of benign biopsies in men whose increased PSA con-
centration is caused by benign prostatic hyperplasia, and
identification of aggressive prostate cancer by its molecu-
lar signature should help clinicians decide which prostate
c­ancers need aggressive treatment.
For now, clinicians are best advised to individualise their
approach to PSA based screening. Young men at high risk of
prostate cancer, such as those with a strong family history
and higher baseline PSA concentrations, should be followed
closely and could also be considered for “risk reduction”
approaches with 5α reductase inhibitors or dietary and life-
style modifications (or both). Conversely, elderly men and
those with a low risk of disease could be tested less often, if at
all. Approaches such as these will hopefully make the next 20
years of PSA based screening better than the first 20.12
1 Andriole GL, Crawford ED, Grubb RL III, Buys SS, Chia D, Church TR, et
al; for the PLCO Project Team. Mortality results from a prostate-cancer
screening trial. N Engl J Med 2009;360:1310-9.
2 Schröder FH, Hugosson J, Roobol MJ, Tammela TL, Ciatto S, Nelen V, et
al. Screening and prostate-cancer mortality in a randomized European
study. N Engl J Med 2009;360:1320-8.
3 Djulbegovic M, Beyth RB, Neuberger MM, Stoffs TL, Vieweg J, Djulbegovic
B, et al. Screening for prostate cancer: systematic review and meta-
analysis of randomised controlled trials. BMJ 2010;341:c4543.
4 Draisma G, Etzioni R, Tsodikov A, Mariotto A, Wever E, Gulati R, et al.
Lead time and overdiagnosis in prostate-specific antigen screening:
importance of methods and context. J Natl Cancer Inst 2009;101:374-83.
 EDITORIALS
RESEARCH, p 595
Peter A Bampton head of luminal
gastroenterology and associate
professor in gastroenterology,
Flinders Medical Centre and
Flinders University, Bedford Park,
SA 5042, Australia
peter.bampton@flinders.edu.au
Competing interests: All authors
have completed the Unified
Competing Interest form at
www.icmje.org/coi_disclosure.
pdf (available on request from
the corresponding author) and
declare: no support from any
organisation for the submitted
work; no financial relationships
with any organisations that might
have an interest in the submitted
work in the previous three years;
no other relationships or activities
that could appear to have
influenced the submitted work.
Provenance and peer review:
Commissioned; not externally
peer reviewed.
Cite this as: BMJ 2010;341:c4667
doi: 10.1136/bmj.c4667
564 BMJ | 18 SEPTEMBER 2010 | VOLUME 341
5 Etzioni R, Penson DF, Legler JM, di Tommaso D, Boer R, Gann PH, et al.
Overdiagnosis due to prostate-specific antigen screening: lessons from US
prostate cancer incidence trends. J Natl Cancer Inst 2002;94:981-90.
6 Kramer BS, Hagerty KL, Justman S, Somerfield MR, Albertsen PC,
Blot WJ, et al. Use of 5-alpha-reductase inhibitors for prostate cancer
chemoprevention: American Society of Clinical Oncology/American
Urological Association 2008 clinical practice guideline. J Clin Oncol
2009;27:1502-16.
7 Andriole GL, Bostwick DG, Brawley OW, Gomella LG, Marberger M, Montorsi
F, et al. Effect of dutasteride on the risk of prostate cancer. N Engl J Med
2010;362:1192-2002.
8 Klotz L, Zhang L, Lam A, Nam R, Mamedov A, Loblaw A. Clinical results of
long-term follow-up of a large, active surveillance cohort with localized
prostate cancer. J Clin Oncol 2010;28:126-31.
Non-endoscopic screening for Barrett’s oesophagus
Might help identify biomarkers that can predict a higher risk of developing
adenocarcinoma
Barrett’s oesophagus is characterised by the development of
columnar line oesophageal mucosa and is thought to be a
premalignant condition that increases the risk of adenocarci-
noma of the oesophagus 30-40-fold. Adenocarcinoma of the
oesophagus has a poor five year survival (0-13%). The inci-
dence has increased from 7.6 to 12.8 per 100 000 men and
4.2 to 5.7 per 100 000 women over the past three decades in
England and Wales,1 and from 0.7 to 3.2 per 100 000 in the
United States.2 Cohort studies suggest that survival is longer
in people with adenocarcinoma detected by surveillance
than in those presenting with symptoms, and surveillance
is recommended by all major gastroenterology societies,
although evidence from randomised controlled trials to
support this practice is lacking.3 In the linked study, Kadri
and colleagues assessed whether non-endoscopic screening
for Barrett’s oesophagus, using an ingestible oesophageal
sampling device (Cytosponge) coupled with immunocyto-
chemisty for trefoil factor 3, was accurate and acceptable
to patients.4
The ability of any community screening programme to
reduce mortality and morbidity rates from a disease depends
on four factors. Firstly, whether a screening test that has
adequate sensitivity to detect the target disease is available.
Secondly, whether the test is accessible to the population
screened. Thirdly, whether the test is acceptable to the
screening population, to ensure that participation rates are
sufficient. And lastly, whether the benefits of the screening
programme are worth the cost, especially in a condition that,
once identified, needs ongoing surveillance.5
Screening for Barrett’s oesophagus followed by sur-
veillance by endoscopy fails most, if not all, of the above
criteria. Although endoscopy is the gold standard for the
detection of Barrett’s oesophagus, it is expensive and
requires the resources of the endoscopy suite, many of
which are currently over burdened by the demands of
colorectal cancer screening. Endoscopy, as a screening
test for Barrett’s oesophagus in primary care, is also poorly
accepted by patients, with participation rates of less than
20%.6 In addition, a recent review of cost-benefit analyses
of an endoscopic approach to screening and surveillance
found that this approach could not be justified.7
Alternative approaches to screening for Barrett’s oesopha-
9 Vickers AJ, Cronin AM, Björk T, Manjer J, Nilsson PM, Dahlin A, et
al. Prostate specific antigen concentration at age 60 and death
or metastasis from prostate cancer: case-control study. BMJ
2010;341:c4521.
10 Jansen FH, van Schaik RHN, Kurstjens J, Horninger W, Klocker H, Bektic
J, et al. Prostate-specific antigen (PSA) isoform p2psa in combination
with total PSA and free PSA improves diagnostic accuracy in prostate
cancer detection. Eur Urol 2010;57:921-7.
11 Demichelis F, Fall K, Perner S, Andrén O, Schmidt F, Setlur SR, et al.
TMPRSS2:ERG gene fusion associated with lethal prostate cancer in a
watchful waiting cohort. Oncogene 2007;26:4596-9.
12 Welch HG, Albertsen PC. Prostate cancer diagnosis and treatment after
the introduction of prostate-specific antigen screening: 1986-2005.
J Natl Cancer Inst 2009;101:1325-9.
gus have included non-sedated narrow bore endoscopy
and video capsule endoscopy. Both of these approaches are
expensive, however, and the first is probably less acceptable
to patients than standard endoscopy while the second does
not enable sampling of the mucosa for histopathology.7
The approach by Kadri and colleagues, however,
shows a possible way forward.4 They describe the use of
a C­ytosponge, which is swallowed by the patient and then
withdrawn. The retrieved Cytosponge samples are then
immunostained for trefoil factor 3, a biomarker for intes-
tinal metaplasia. All patients then had an endoscopy to
explore the sensitivity and specificity of this biomarker for
the detection of Barrett’s oesophagus.
The Cytosponge test had an acceptable sensitivity and
specificity for Barrett’s oesophagus (73.3% and 93.8%,
respectively), was easily accessible to patients (because it
is performed in primary care by a practice nurse), and was
tolerated well by most participants. However, the study did
not assess cost so future studies are awaited.
Kadri and colleagues focused on patients with a record
of being prescribed acid suppressants and they found a
3% prevalence of Barrett’s oesophagus. However, whether
screening of this select group of patients will reduce popula-
tion mortality from Barrett’s oesophagus depends on the pro-
portion of Barrett’s oesophagus in the community that will be
detected by this approach. In patients with oesophageal ade-
nocarcinoma, 30-40% of patients do not report bothersome
reflux symptoms in the five years or more before the diagnosis
of cancer.8 To have an effect on population mortality from
Barrett’s oesophagus the screening strategy would therefore
Cytosponge capsule

IMAGEBROKER/ALAMY
RESEARCH, p 596
Bjørn Blomberg associate
professor of infectious diseases,
Institute of Medicine, University of
Bergen, 5021 Bergen, Norway
bjorn.blomberg@med.uib.no
Nina Langeland professor of
infectious diseases, Institute of
Medicine, University of Bergen, 5021
Bergen, Norway
Competing interests: Both
authors have completed the
Unified Competing Interest form
at www.icmje.org/coi_disclosure.
pdf (available on request from the
corresponding author) and declare:
no support from any organisation
for the submitted work; no financial
relationships with any organisations
that might have an interest in the
submitted work in the previous
three years; no other relationships or
activities that could appear to have
influenced the submitted work.
Provenance and peer review:
Commissioned; not externally peer
reviewed.
Cite this as: BMJ 2010;341:c4677
doi: 10.1136/bmj.c4677
BMJ | 18 SEPTEMBER 2010 | VOLUME 341 565
need to be expanded to the whole population or patients with
other risk factors for the development of B­arrett’s oesophagus
such as male sex, white race, and obesity.7
Perhaps the most exciting aspect of the Cytosponge is its
potential for accessing tissue for use in identifying biomark-
ers that might predict which patients with Barrett’s oesopha-
gus are at risk of developing oesophageal cancer. Several
such biomarkers have been described (such as abnormalities
in the tumour suppressor genes CDKN2A and TP53 and the
presence of aneuploidy in epithelial cells). Although larger
studies are needed to validate these and other markers,
future screening and surveillance for Barrett’s oesopha-
gus might use a two step approach, with endoscopy being
reserved to confirm the diagnosis (in the screened popula-
tion) and to survey patients with confirmed disease who
have been identified as having a high risk of progression on
the basis of clinical risk factors and tissue biomarkers.9
Tuberculous meningitis and resistance to isoniazid
Higher case fatality rate should prompt prudent use of antituberculous drugs
In the linked study, Vinnard and colleagues assess whether
initial resistance to isoniazid is associated with death during
the treatment of tuberculous meningitis.1 Central nervous
system tuberculosis accounts for about 1% of the estimated
9.4 million annual cases of tuberculosis worldwide.2 Tuber-
culous meningitis is a medical emergency and in the past
was usually lethal, although better chemotherapy, starting
with streptomycin in 1947, has improved survival dramati-
cally.3 None the less, even with modern treatment almost a
third of patients die, and case fatality rate approaches two
thirds in patients with HIV.4 Half of those who survive have
neurological sequelae.5
Because delayed treatment increases case fatality rate,6
it is unfortunate that tuberculous meningitis is so difficult
to diagnose. In high income countries, patients may die
because of the delay in diagnosis—culture of Mycobacterium
tubercu­losis requires special medium and takes many weeks.
In developing countries, clinicians make a presumptive
diagnosis by combining clinical data and simple laboratory
results,7 but they struggle to confirm the diagnosis because
spinal fluid microscopy has low sensitivity and culture
and susceptibility testing are available in only a few major
medical centres.
Early treatment is crucial because most deaths from the
effects of tuberculosis on the central nervous system occur
during the first month of treatment.8 Unfortunately, culture
and susceptibility testing by standard methods may take one
to two months. Thus, even in advanced Western hospitals,
most cases of tuberculous meningitis are treated empiri-
cally during the crucial initial phase.5 These regimens must
therefore provide a reasonable chance of effectively curing
the infection.
Most authorities recommend treating tuberculous
meningitis with the standard quadruple treatment recom-
mended by the World Health Organization—rifampicin,
isoniazid, pyrazinamide, and ethambutol—but to extend
EDITORIALS
1 Newnham A, Quinn MJ, Babb , Kang JY, Majeed A. Trends in oesophageal
and gastric cancer incidence, mortality and survival in England and Wales
1971-1998/1999. Aliment Pharmacol Ther 2003,17:655-64.
2 Devesa SS, Blot WJ, Fraumeni JF Jr. Changing patterns in the incidence
of oesophageal and gastric carcinoma in the United States. Cancer
1998:83:2049-53.
3 Sharma P. Barrett’s oesophagus. N Engl J Med 2009;361:2548-54.
4 Kadri SR, Lao-Sirieix P, O’Donovan M, Debiram I, Das M, Blazeby JM, et al.
Acceptability and accuracy of a non-endoscopic screening test for Barrett’s
oesophagus in primary care: cohort study. BMJ 2010;341:c4372.
5 Watson JMG, Junger G. Principles and practice of screening for disease.
WHO Public Health Papers No 34, WHO, 1968.
6 Ronkainen J, Aro P, Storskrubb T, Johansson SE, Lind T, Bolling-Sternevald
E, et al. Prevalence of Barrett’s oesophagus in the general population: an
endoscopic study. Gastroenterology 2005;129:1825-31.
7 Barbiere JM, Lyratzopoulos G. Cost-effectiveness of endoscopic
screening followed by surveillance for Barrett’s esophagus: a review.
Gastroenterology 2009;137:1869-76.
8 Lagergren J, Bergstrom R, Lindgren A, Nyren O. Symptomatic gastro-
oesophageal reflux as a risk factor for oesophageal adenocarcinoma.
N Engl J Med 1999;340:825-31.
9 Prassad GA, Bansal A, Sharma P, Wang KK. Predictors of progression in
Barrett’s oesophagus: current knowledge and future directions. Am J
Gastroenterol 2010;105:1490-502.
the c­ontinuation phase with rifampicin and isoniazid to
nine to 12 months in total.9 Rifampicin and isoniazid, the
most bactericidal drugs, are essential for treating most
forms of tuberculosis. Unfortunately, rifampicin does not
readily cross the blood-brain barrier. Isoniazid is the only
first line antituberculous drug that has bactericidal activ-
ity throughout the treatment period and penetrates freely
into the central nervous system. The first trials of strepto-
mycin more than 60 years ago showed that monotherapy
for tuberculosis leads to treatment failure and development
of resistance.3 This has led clinicians to suspect that isoni-
azid resistance would aggravate the outcome of treatment of
tuberculous meningitis. Tuberculous meningitis caused by
multi-drug resistant tuberculosis (resistant to isoniazid and
rifampicin) is associated with increased case fatality rates.10
Studies assessing outcomes in relation to resistance to isoni-
azid or streptomycin (or both) have shown slower bacterial
clearance from spinal fluid in resistant cases,11 but they have
not shown conclusively that the case fatality rate is higher.6
Vinnard and colleagues’ study shows that isoniazid resist-
ance is associated with increased case fatality rate in tubercu-
lous meningitis.1 Despite the relative rarity of the condition,
the study is unique in including a large number of cases. Of
the 3114 cases of tuberculous meningitis registered during
13 years on the Center for Disease Control’s database, 1896
patients with positive cultures for M tuberculosis and known
isoniazid susceptibility results were analysed. Among cases
with positive cultures from spinal fluid, case fatality rate was
significantly higher in those with isoniazid resistant tuber-
culosis than in those with susceptible tuberculosis (39%
(43/109) v 29% (433/1505); odds ratio 1.61, 95% confidence
interval 1.08 to 2.40). The association remained strong in an
analysis of patients who received standard quadruple treat-
ment. The association was not significant when cases of clini-
cal meningitis with positive cultures from non-central nervous
system sites only were included. However, this should not
 EDITORIALS
Joy Lawn director, global evidence
and policy, Saving Newborn Lives/
Save the Children USA, Cape Town
7405, South Africa
joylawn@yahoo.co.uk
Competing interests: All authors
have completed the Unified
Competing Interest form at www.
icmje.org/coi_disclosure.pdf
(available on request from the
corresponding author) and declare:
no support from any organisation
for the submitted work; no financial
relationships with any organisations
that might have an interest in the
submitted work in the previous
3 years; no other relationships or
activities that could appear to have
influenced the submitted work.
Provenance and peer review:
Commissioned, not externally peer
reviewed.
Cite this as: BMJ 2010;341:c5045
doi: 10.1136/bmj.c5045
566 BMJ | 18 SEPTEMBER 2010 | VOLUME 341
affect the main conclusion because verification by spinal fluid
culture is a highly specific criterion and cases not confirmed in
this way are more likely to be misclassified. In the multivariate
analysis, missing data are dealt with using imputation, where
estimated values are substituted for missing values. Although
imputation may introduce bias, when used appropriately it
can be better than complete case analysis.12
Difficult and costly to treat multi-drug resistant tubercu-
losis accounts for almost half a million cases of tuberculo-
sis, and extensively drug resistant tuberculosis (resistant
to several additional second line drugs) has emerged on all
continents. Considering this escalating drug resistance, it is
worrying that even simple isoniazid resistance worsens the
outcome of tuberculous meningitis.
Vinnard and colleagues’ study resolves one uncertainty
but poses new questions. Regional data on resistance
should be considered when developing recommendations
for treatment of tuberculous meningitis. In areas with sub-
stantial isoniazid resistance, further studies are needed to
assess the value of adding bactericidal second line drugs
with good bioavailability in the central nervous system,
such as fluoroquinolones, to the empirical regimens. The
findings confirm the need for improved and more rapid
diagnostic tools. Most importantly, the study emphasises
the fundamental importance of taking actions to contain
the emerging drug resistance, firstly by prudent use of anti­
tuberculous drugs.
Are the millennium development goals on target?
Successes and shortfalls so far make 2010 a tipping point especially for maternal
and neonatal survival
At the United Nations Millennium Summit in 2000, 189
member states, including 147 heads of state, committed
to the Millennium Development Goals (MDGs). These eight
interlinking goals tackle the global plagues of poverty, hun-
ger, lack of education, and ill health and provide a unique
opportunity to accelerate progress for the world’s poorest
families (fig). On 20-22 September 2010, world leaders meet
to assess progress over the past decade and set priorities for
the five years before the MDG deadline of 2015.
Multiple reports have been published throughout the year,
but are the promises of the MDGs connecting to progress?1 At
the heart of the MDGs are goals 4 for child survival and 5 for
maternal survival. Are fewer mothers, newborns, and chil-
dren dying? Is essential health care improving for the poor-
est? Or are the numbers themselves a battleground? Maternal
statistics have become as political as HIV/AIDS statistics were
in the past.2
Despite superficial differences, common themes exist
in the new data—a mixture of success and shortfalls. The
good news is that progress for child mortality is accelerat-
ing. Although fewer children died this year than last year,
it is unacceptable that each year 8.8 million children still
die, including 3.6 million newborns.3 However, progress for
neonatal and maternal mortality seems to be lagging, with
successes such as China being the exception rather than the
rule. The proportion of deaths in under 5 year olds accounted
1 Vinnard C, Winston CA, Wileyto EP, MacGregor RR, Bisson GP. Isoniazid
resistance and death in patients with tuberculous meningitis: retrospective
cohort study. BMJ 2010;341:c4451.
2 WHO. Global tuberculosis control. A short update to the 2009 report.
WHO/HTM/TB/2009.426. 2009. www.who.int/tb/publications/global_
report/2009/update/tbu_9.pdf.
3 Medical Research Council. Streptomycin treatment of tuberculous
meningitis. Lancet 1948;1:582-96.
4 Thwaites GE, Duc Bang N, Huy Dung N, Thi Quy H, Thi Tuong Oanh D, Thi
Cam Thoa N, et al. The influence of HIV infection on clinical presentation,
response to treatment, and outcome in adults with Tuberculous meningitis.
J Infect Dis 2005;192:2134-41.
5 Bidstrup C, Andersen PH, Skinhoj P, Andersen AB. Tuberculous meningitis
in a country with a low incidence of tuberculosis: still a serious disease and
a diagnostic challenge. Scand J Infect Dis 2002;34:811-4.
6 Thwaites GE, Chau TT, Caws M, Phu NH, Chuong LV, Sinh DX, et al. Isoniazid
resistance, mycobacterial genotype and outcome in Vietnamese adults with
tuberculous meningitis. Int J Tuberc Lung Dis 2002;6:865-71.
7 Thwaites GE, Chau TT, Stepniewska K, Phu NH, Chuong LV, Sinh DX, et al.
Diagnosis of adult tuberculous meningitis by use of clinical and laboratory
features. Lancet 2002;360:1287-92.
8 Afghani B, Lieberman JM. Paradoxical enlargement or development of
intracranial tuberculomas during therapy: case report and review. Clin Infect
Dis 1994;19:1092-9.
9 WHO. Treatment of tuberculosis guidelines. WHO/HTM/
TB/2009.420. 4th ed. 2010. http://whqlibdoc.who.int/
publications/2010/9789241547833_eng.pdf.
10 Thwaites GE, Lan NT, Dung NH, Quy HT, Oanh DT, Thoa NT, et al. Effect of
antituberculosis drug resistance on response to treatment and outcome in
adults with tuberculous meningitis. J Infect Dis 2005;192:79-88.
11 Thwaites GE, Caws M, Chau TT, Dung NT, Campbell JI, Phu NH, et al.
Comparison of conventional bacteriology with nucleic acid amplification
(amplified mycobacterium direct test) for diagnosis of tuberculous
meningitis before and after inception of antituberculosis chemotherapy.
J Clin Microbiol 2004;42:996-1002.
12 Van der Heijden GJ, Donders AR, Stijnen T, Moons KG. Imputation of
missing values is superior to complete case analysis and the missing-
indicator method in multivariable diagnostic research: a clinical example.
J Clin Epidemiol 2006;59:1102-9.
for by newborn deaths has increased from 37% in 2000 to
41% in 2008. Yet few UN documents on MDG 4 even mention
neonatal care.4 Each year upwards of 342 900 women die,5
depending on which report is subscribed to. Each year 60
million births occur at home and this is a critical determinant
for maternal and newborn survival.6
An independent data and accountability movement called
Countdown to 2015 tracks progress in the 68 countries with
over 95% of maternal and child deaths.7 For MDG 4 towards
child survival, 19 countries are now on track and 47 have
accelerated progress since 2000. Even some of the poorest
countries are now on track, including four low income coun-
tries in sub-Saharan Africa—notably Botswana and Malawi,
although both have a high prevalence of HIV. Understanding
why these countries have succeeded will hold many lessons
for their neighbours and for what now must be repeated for
maternal and neonatal survival.
Health outcome gaps are increasing between the rich-
est and poorest countries. Some countries are being left far
behind, especially in Africa. With only 11% of the world’s
population, Africa carries more than half of all maternal
and child deaths, two thirds of the global AIDs burden, and
90% of deaths from malaria.8 Within countries there are also
important gaps for the poorest—if all the families in Nigeria
had the same neonatal mortality rate as the richest 20%, then
127 000 fewer newborns would die each year.9 Governments

Priorities to speed up progress for maternal, newborn, and child survival
What is progressing?
Progress for mortality in children under 5
(postneonatal and years 1-5 part of MDG 4)
Malaria interventions, especially insecticide treated bed nets (MDG 6)
Prevention of mother to child transmission of HIV (MDG 6)
Safe drinking water (MDG 7)
What are priorities to accelerate progress?
Neonatal mortality (now 41% of MDG 4)
Maternal mortality (MDG 5)
Family planning (linked to MDG 5 and MDG 4)
Africa (now accounts for more than half of MDG 4 and most of MDG 5)
Coverage of skilled care at birth, especially in sub-Saharan Africa and South Asia
Curative care especially for pneumonia and other neonatal and childhood infections
The poorest families in most low income countries (more data needed to track and target gaps)
should be held to account for reaching their poorest and the
most vulnerable citizens. The latest UNICEF Progress for
Children publication has an important focus on equity and
closing gaps for the poorest.10
Reducing these needless deaths is dependent on high and
equitable coverage of basic interventions. Rapid increases in
coverage have been achieved for some well funded and verti-
cally delivered interventions such as immunisations, preven-
tion of mother to child transmission of HIV/AIDS, and malaria
interventions. Almost 200 million bednets were distributed
between 2007 and 2009, more than half of the 350 million
required.10
However, progress remains too slow for some interven-
tions, including the highest impact interventions, such as
safe care at birth and treatment of neonatal and childhood
illness. Family planning and contraception are at risk of fall-
ing off the agenda despite being rapid and cost effective ways
to reduce maternal and child deaths and accelerate develop-
ment.7 Many UN documents focus on the interventions that
already receive the most attention11 rather than those with
the greatest potential effect in the next five years.
Donor funding for health has increased by 105% since
2003, and funding for maternal and child health has kept
pace, but still does not reflect the size of the burden.12 For
example, the combined HIV, tuberculosis, and malaria bur-
den of around 3 million deaths (including 201 000 deaths
from AIDS and 732 000 from malaria in children under 53)
is only a third of the size of the burden of maternal, newborn,
and child death, yet it receives vastly more funding. The UN
Secretary General’s Joint Plan of Action for Women and Chil-
dren aims to redress this investment gap and involve wider
stakeholders, such as civil society and private sector.
So what are the key priorities in the next crucial five years?
The first is to use data at national or ideally subnational level,
considering the main causes of death, coverage, and quality
and equity gaps, and to focus on implementing the interven-
tions with the greatest impact especially for care at birth and
the first few days after birth. Rapid reductions in mortality
are possible even with 20% increases in coverage of targeted
interventions.8 National7 and subnational9 data are a key to
designing programmes and tracking their progress.
The second priority is to innovate, especially for service
delivery. Most of the countries with the highest mortality rates
have fewer than 0.5 skilled health personnel per 1000 popu-
BMJ | 18 SEPTEMBER 2010 | VOLUME 341 567
EDITORIALS
SAVE THE CHILDREN/MICHAEL BISCELGIE
lation, compared with over 10 per 1000 in the UK. This will
require task shifting within the health system and bringing
care closer to home—for example, using community health
workers to manage how antibiotics are used. The third prior-
ity is to target the poor and remove financial barriers such as
user fees for maternity and child services, and not to leave
lessening disparity to chance and “trickle down” philoso-
phies. The final priority is to strengthen accountability for
donor governments, for low income country governments,
and for all partners including the UN.
The year 2010 is a tipping point. We are the first genera-
tion to have the tools and the funding to transform lives for
the world’s poorest families. Why should a mother in rural
Nigeria die giving birth? Why should a baby in India die of
birth complications? Why should a child in Ethiopia die of
pneumonia? The underlying question is whether the world’s
leaders, and all of us, will deliver on our promises.
1 United Nations report of the Secretary General. Keeping the promise: a
forward-looking review to promote an agreed action agenda to achieve
the Millennium Development Goals by 2015. Report of the follow-up to the
outcome of the Millennium Summit. United Nations, 2010. www.un.org/
ga/search/view_doc.asp?symbol=A/64/665.
2 Horton R. Maternal mortality: surprise, hope, and urgent action. Lancet
2010;375:1581-2.
3 Black RE, Cousens S, Johnson HL, Lawn JE, Rudan I, Bassani DG, et
al. Global, regional, and national causes of child mortality in 2008: a
systematic analysis. Lancet 2010;375:1969-87.
4 Shiffman J. Issue attention in global health: the case of newborn survival.
Lancet 2010;375:2045-9.
5 Hogan MC, Foreman KJ, Naghavi M et al. Maternal mortality for 181
countries, 1980-2008: a systematic analysis of progress towards
Millennium Development Goal 5. Lancet 2010;375:1609-23.
6 Darmstadt GL, Lee AC, Cousens S, Sibley L, Bhutta ZA, Donnay F, et al.
60 million non-facility births: who can deliver in community settings to
reduce intrapartum-related deaths? Int J Gynaecol Obstet 2009;107(suppl
1):S89-112. www.ijgo.org/issues/contents?issue_key=S0020-
7292%2809%29X0010-X.
7 Countdown to 2015. Countdown to 2015 decade report (2000-2010):
taking stock of Maternal, Newborn and Child Survival. WHO and UNICEF,
2010. www.countdown2015mnch.org/reports-publications/2010-report.
8 Friberg IK, Kinney MV, Lawn JE, Kerber KJ, Odubanjo MO, Bergh AM, et
al. Sub-Saharan Africa’s mothers, newborns, and children: how many
lives could be saved with targeted health interventions? PLoS Med
2010;7:e1000295.
9 Federal Republic of Nigeria Ministry of Health. Saving newborn lives in
Nigeria: situation analysis and action plan for newborn health in the
context of the integrated MNCH strategy. FMOH, 2009. http://www.
healthynewbornnetwork.org/resource/saving-newborn-lives-nigeria-
situation-analysis-and-action-plan-newborn-health-context-inte.
10 UNICEF. Progress for children: achieving the MDGs with equity. UNICEF,
2010. www.unicef.org/publications/index_55740.html.
11 UNDP. What will it take to achieve the MDGs? UNDP, 2010. http://content.
undp.org/go/cms-service/stream/asset/?asset_id=2620072.
12 Pitt C, Greco G, Powell-Jackson T, Mills A. Countdowm to 2015: assessment
of the official development assistance to maternal, newborn and child
health, 2003-08. Lancet [forthcoming].
 EDITORIALS
TONY LILLEY/ALAMY
Elizabeth Dowler registered
public health nutritionist and
professor of food and social
policy , Department of Sociology,
University of Warwick, Coventry
CV4 7AL
elizabeth.dowler@warwick.ac.uk
Competing interests: All authors
have completed the Unified
Competing Interest form at
www.icmje.org/coi_disclosure.
pdf (available on request from
the corresponding author) and
declare: no support from any
organisation for the submitted
work; ED is in receipt of financial
support from Defra for her work
at Warwick University on low
income and food in the UK; ED is
in preliminary discussion with the
authors of the minimum income
standards report about future
work on “sustainable” minimum
income standard calculations and
will be seeking research grant
funding for this work.
Provenance and peer review:
Commissioned; not externally
peer reviewed.
Cite this as: BMJ 2010;341:c4070
doi: 10.1136/bmj.c4070
568 BMJ | 18 SEPTEMBER 2010 | VOLUME 341
Income needed to achieve a minimum standard of living
The standards will now not be reached by households on low incomes in the UK
As the new coalition government in the United Kingdom calls
for ideas on cutting public expenditure, the Joseph ­Rowntree
Foundation has published the latest annual update of its
“minimum income standards” (MIS). These standards pro-
vide a measure of how much various types of households
need to earn to reach what members of the public think is a
minimum acceptable standard of living.1
The data enable a relatively objective view of what society
thinks is essential for a decent standard of living and what
it costs to achieve such a standard, taking tax and benefit
changes into account. The report gives details of MIS and
their components for different family household types—
single adult or couple, with or without dependent children,
and pensioners—and it enables households to calculate their
own MIS, by adjusting for their own circumstances.2
The results are surprising and sobering. For example, in
contrast to official inflation over the past decade of 23%,
minimum budget costs have risen by 38% over that period,
largely because of increased costs of food (37%), bus fares
(59%), and council tax (67%). This demonstrates the often
cited reality that price inflation for goods that dominate the
budgets of poorer households is greater than for the aver-
age household’s budget; this is important because the offi-
cial inflation figure is used to update all state benefits, and
these form a higher proportion of income for people on the
lowest incomes. The data allow assessment of the effects of
national or local government policies or personal changes
in circumstances on the likely wellbeing of different types
of household.
Specifically, a single person who could just manage in
2000, and whose income has only kept pace with infla-
tion, will by April 2010 have been nearly £20 (€24; $31) a
week short of what he or she needs to meet the minimum
budget. What will these people have had to go without to
avoid getting into debt? If they are unemployed, as 29% of
UK single adults of working age are, the basic out of work
benefits provide less than half the MIS a single adult needs.
For unemployed couples with children benefits provide
about two thirds of what they need. Working couples with
two children now need an income of £29 700 a year to afford
a basic but acceptable standard of living (including childcare
costs). This equates to £7.60 an hour, but the minimum wage
is only £5.80 an hour, and around 23% of full time workers
and 39% of part time workers aged 22 and above were paid
less than £7 an hour in 2009,3 so low pay must affect the
wellbeing of many households.
The construction of MIS is crucial to their legitimacy. There
is a long history in the UK and elsewhere of trying to establish
how much money people need to live decently.4  5 Since 2008,
research on MIS by the Centre for Research in Social Policy,
Loughborough University, and the Family Budget Unit,
­University of York, has integrated two separate approaches to
establishing budget standards: the “consensual” negotiation
of budgets by panels made up of members of the public, and
budgets based on research evidence and expert judgments.
Thus, groups of ordinary people from mixed socioeconomic
backgrounds, including those in the relevant demographic
category (for example, parents decide the minimum for par-
ents), specify “baskets” of goods and services needed by
different types of household both to meet basic needs and
be able to participate in society. These specifications are
supported by advice from relevant experts, who check that
criteria for adequacy in nutrition, heating, and other require-
ments are met.
MIS do not set out to measure poverty but do continu-
ally check what people think is essential. Despite two years
of recession and rising prices, particularly fuel and food,
the 2010 report shows that people have not lowered their
expectations. Alongside physical needs for shelter, warmth,
and food, people still list things that enable social partici-
pation, such as the ability to travel, celebrate birthdays and
key festivals, and meet friends or family, in addition to a
week’s holiday in the UK, as essential. These views highlight
the importance of social determinants of health, and they
support the recent international6 and national7 strategic
reviews of inequalities, where the need for minimum income
standards for health are proposed policy recommendations.8
Without sufficient money, people are more likely to consume
inadequate diets; live in damp, poorly heated, overcrowded
housing, with few amenities and services; and to give up
social activities.
MIS must be more widely recognised and under-
stood; they should be used to ensure that households
have enough money to live on. At national government
and local levels, the effects of fiscal changes (in taxes,
tax allowances, and benefits) and changes in wages
can be calculated on the basis of MIS. The Living Wage
­campaign already draws on MIS; successes in London
and ­elsewhere in implementing a living wage have been
good for ­businesses and the wellbeing and health of
­employees (see case studies at www.livingwageemployer.
org/). MIS should also be used as a reference point for
debt ­repayment and levels of fines for defaulters.
MIS allow fairer discussions on wages, taxes, and benefits
and provide transparency on the effects of the many current
changes. Getting to grips with inequality needs robust evi-
dence on the monetary costs of minimum standards of living
and the effects of government and employer practice through
taxes, benefits, and wages: MIS provide that evidence.
1 Davis A, Hirsch D, Smith N. A minimum income standard for the UK in
2010. Joseph Rowntree Foundation, 2010. www.jrf.org.uk/sites/files/
jrf/MIS-2010-report_0.pdf.
2 Minimum Income Standard for the UK. www.minimumincomestandard.org/.
3 The Poverty Site. Numbers in low pay. www.poverty.org.uk/51/index.shtml.
4 Bradshaw J, Sainsbury R, eds. Getting the measure of poverty: the early
legacy of Seebohm Rowntree. Ashgate, 2000.
5 Bradshaw J, Sainsbury R, eds. Researching poverty. Ashgate, 2000.
6 WHO. Closing the gap in a generation: health equity through action
on the social determinants of health. Final Report of the Commission
on Social Determinants of Health. 2008. www.who.int/social_
determinants/thecommission/finalreport/en/index.html.
7 Marmot M, Allen J, Goldblatt P, Boyce T, McNeish D, Grady M, et al. Fair
society, healthy lives: strategic review of health inequalities in England
post 2010. Marmot review, 2010. www.ucl.ac.uk/marmotreview.
8 Morris J, Donkin A, Wonderling D, Wilkinson P, Dowler E. A minimum
income for healthy living. J Epidemiol Community Health 2000;54:885-9.