Abstract:
We welcome the comments by
Jin Zhang and colleagues on our
study,1 which reported the strong
role of alcohol consumption
in oesophageal squamous cell
cancer (ESCC) in east Africa. Our
findings, which showed that alcohol
consumption was a risk factor for
ESCC, are consistent with the IARC
monographs.2
In Kenya and Tanzania,
we found that a large proportion
of male patients with ESCC was
attributable to alcohol consumption.
Public health actions to reduce
harmful alcohol consumption will
benefit not only cancer prevention
but also prevention of other NCDs
and alcohol-associated harms in
society.
Zhang and colleagues highlight
investigations to further refine
the association between alcohol
consumption and risk of ESCC. Many
of these suggestions are already in
the pipeline, given that the ESCCAPE
study is contributing to a genomewide association study of ESCC in
Africa.3
Genetic influences on alcohol
metabolism—notably polymorphisms
of ADH and ALDH2 genes—are
known to influence concentrations
of acetaldehyde and risk of ESCC,
and have been well studied in Asian
populations, but not in African
populations. We have not been able
to investigate such effect modification
without genotyping because there
is no known accessible proxy, such
as self-reported alcohol flushing,
in African populations. Although
interactions between genes and
the environment will be studied,
investigating the primary effect of
a main exposure is an important
first step. A genetic-based precision
component is unlikely to benefit or
be feasible for primary prevention
strategies tackling alcohol; however,
such a component might help to refine
the identification of individuals at high
risk for early detection.
Zhang and colleagues speculate
that genetic differences between
ethnic groups might contribute to
heterogeneity in the magnitude of
the relationship between alcohol
consumption and risk of ESCC. We
do not expect genetic effects to be
the driving factor behind the absence
of association in Malawian men
because any genetic modification
to the effect of alcohol on ESCC risk
would probably affect both sexes,
and a positive association was seen
in Malawian women. Therefore, we
considered reporting biases to be a
more plausible explanation for the
sex differences. Effect modification
of the relationship between alcohol
consumption and risk of ESCC by
tobacco use was presented and was
found to be present in Kenya, as has
been previously published.4
However,
the pattern of alcohol consumption
and tobacco use is such that the power
to detect interactions is reduced
because there are few smokers who
have never consumed alcohol.
The priorities in our analytical
approach acknowledge that the
research needs, priority questions,
and status of existing knowledge
in aetiological cancer epidemiology
are not homogenous worldwide.
Building a solid foundational
knowledge on major environmental
and lifestyle risk factors remains
a necessary research priority to
support cancer control plans in subSaharan Africa. Risk refinements will
be made as research investments,
which include prospective studies and
improved exposure assessments and
biobanking, are made