Articles
Global burden of cancer attributable to high body-mass
Lancet Oncol 2015; 16: 36–46
Published Online
November 26, 2014
http://dx.doi.org/10.1016/
S1470-2045(14)71123-4
See Comment page 3
*Contributed equally
Section of Cancer Surveillance
(M Arnold PhD, J Ferlay MSc,
D Forman PhD,
I Soerjomataram PhD),
Biostatistics Group
(G Byrnes PhD), and Nutrition
and Metabolism Section—
Epidemiology Group
(I Romieu PhD), International
Agency for Research on Cancer,
Lyon, France; School of
Population Health, University
of Queensland, Brisbane, QLD,
Australia (N Pandeya PhD);
Faculty Institute of Cancer
Sciences, University of
Manchester, Manchester
Academic Health Science
Centre, Manchester, UK
(Prof A G Renehan PhD);
Department of Health
Statistics and Information
Systems, WHO, Geneva,
Switzerland (G A Stevens DSc);
MRC-PHE Centre for
Environment and Health and
Department of Epidemiology
and Biostatistics, School of
Public Health, Imperial College
London, London, UK
(Prof M Ezzati FMedSci);
CRONICAS Centre of Excellence
in Chronic Diseases and School
of Medicine, Cayetano Heredia
University, Lima, Peru
(J Jaime Miranda PhD); and
Department of Epidemiology,
Tata Memorial Hospital,
Mumbai, India (R Dikshit PhD)
Correspondence to:
Dr Melina Arnold, Section of
Cancer Surveillance,
International Agency for
Research on Cancer, 69372 Lyon,
France
arnoldm@fellows.iarc.fr
36
index in 2012: a population-based study
Melina Arnold*, Nirmala Pandeya*, Graham Byrnes, Andrew G Renehan, Gretchen A Stevens, Majid Ezzati, Jacques Ferlay, J Jaime Miranda,
Isabelle Romieu, Rajesh Dikshit, David Forman, Isabelle Soerjomataram
Summary
Background High body-mass index (BMI; defined as 25 kg/m² or greater) is associated with increased risk of cancer.
To inform public health policy and future research, we estimated the global burden of cancer attributable to high BMI
in 2012.
Methods In this population-based study, we derived population attributable fractions (PAFs) using relative risks and
BMI estimates in adults by age, sex, and country. Assuming a 10-year lag-period between high BMI and cancer
occurrence, we calculated PAFs using BMI estimates from 2002 and used GLOBOCAN2012 data to estimate numbers
of new cancer cases attributable to high BMI. We also calculated the proportion of cancers that were potentially
avoidable had populations maintained their mean BMIs recorded in 1982. We did secondary analyses to test the
model and to estimate the effects of hormone replacement therapy (HRT) use and smoking.
Findings Worldwide, we estimate that 481 000 or 3·6% of all new cancer cases in adults (aged 30 years and older after
the 10-year lag period) in 2012 were attributable to high BMI. PAFs were greater in women than in men (5·4% vs
1·9%). The burden of attributable cases was higher in countries with very high and high human development indices
(HDIs; PAF 5·3% and 4·8%, respectively) than in those with moderate (1·6%) and low HDIs (1·0%). Corpus uteri,
postmenopausal breast, and colon cancers accounted for 63·6% of cancers attributable to high BMI. A quarter (about
118 000) of the cancer cases related to high BMI in 2012 could be attributed to the increase in BMI since 1982.
Interpretation These findings emphasise the need for a global effort to abate the increasing numbers of people with
high BMI. Assuming that the association between high BMI and cancer is causal, the continuation of current patterns
of population weight gain will lead to continuing increases in the future burden of cancer.
Funding World Cancer Research Fund International, European Commission (Marie Curie Intra-European Fellowship),
Australian National Health and Medical Research Council, and US National Institutes of Health.
Copyright ©2014. World Health Organization. Published by Elsevier Ltd/Inc/BV. All rights reserved.
Introduction increase in risk of these cancers due to high BMI ranges
High body-mass index (BMI; defined as 25 kg/m² or from 3% to 10% per unit increase in BMI.14 A recent
greater) is a known risk factor for various chronic estimate from Global Burden of Disease (GBD) study15
diseases and mortality. Although prevalence varies showed that 3·9% of cancer mortality in 2010 could be
widely, overweight and obesity have been increasing attributed to high BMI. However, this estimate did not take
worldwide, raising concerns about their effect on health. into account the lag time necessary for high BMI to lead to
Recent statistics showed that 35% of the adult population the development of a new cancer. Additionally, relating risk
(aged 20 years and older) worldwide is overweight (BMI factors to mortality in the estimation of disease burden can
≥25 kg/m²), including 12% that is classified as obese be problematic because of the potential role of reverse
(BMI ≥30 kg/m²).1 The prevalence of high BMI ranges causation.16 Potential confounders and effect modifiers of
from about 10% in many Asian and African countries to the association between BMI and cancer, such as the use of
more than 90% in Pacific island nations such as the Cook hormone replacement therapy (HRT) and smoking, also
Islands and Nauru. According to recent estimates,1,2 the need to be taken into account.17,18
global prevalence of excess bodyweight in adults In this study, we aimed to estimate the global population
increased by 27·5% between 1980 and 2013, although the attributable fraction (PAF) of cancer incidence in 2012
increase has slowed in recent years in some European attributable to high BMI in 2002, acknowledging the time
countries and the USA.3–7 lag between the exposure (high BMI) and outcomes
Continuous updates of the scientific literature have (cancer incidence). We also aimed to test the robustness of
confirmed the association between high BMI and risk of the estimates in a series of sensitivity analyses, including
oesophageal adenocarcinoma and colon, rectal, kidney, assessment of the role of smoking and HRT use as
pancreas, gallbladder (women only), postmenopausal potential effect modifiers or confounders of the association
breast, ovarian, and endometrial cancers.8–13 The estimated between high BMI and cancer incidence.
www.thelancet.com/oncology Vol 16 January 2015

Methods
Study design
In this population-based study, we quantified the effect of
high BMI on cancer incidence in the adult population
worldwide, tested the effect of various model
assumptions, and assessed the effect of confounders and
effect modifiers. We applied PAFs according to sex, age,
cancer site, and country to national estimates of cancer
incidence estimates, using data for mean BMI, cancer
incidence, and corresponding risk estimates.
We used the BMI estimates reported by Global Burden
of Metabolic Risk Factors of Chronic Diseases
Collaborating Group.1 The details of the applied model
and its assumptions in the estimation of mean BMIs
have been reported elsewhere.19 For this study, we
obtained the annual estimates of mean BMI and the
corresponding SDs for adults aged 20 years and older
for each country by sex and age group (20–34, 35–44,
45–54, 55–64, 65–74, and ≥75 years) in 1982 and 2002
(appendix pp 2–7).
In our primary analysis, we included only cancers
reported by the World Cancer Research Fund (WCRF) as
having sufficient evidence to be associated with high
BMI.8–13 These include oesophageal adenocarcinoma and
colon, rectal, kidney, pancreatic, gallbladder, post-
menopausal breast, corpus uteri, and ovarian cancers,
collectively defined here as high-BMI-related cancers. In
view of the differences in risk of colon and rectal cancer
associated with obesity, we estimated PAFs for these two
cancer sites separately. Similarly, only adenocarcinoma of
the oesophagus was included because of the absence of an
association between excess bodyweight and oesophageal
squamous-cell carcinoma.
The sex-specific relative risks (RRs) for the sites included
in the analysis were obtained from the standardised meta-
analysis estimates by Renehan and colleagues14 and the
WCRF Continuous Update Project.8–13 In these meta-
analyses, risk estimates were pooled from from cohort
studies that mainly used cancer incidence as an outcome
(apart from pancreatic cancer, for which studies included
mortality as an outcome). In a secondary analysis we
included thyroid cancer and non-Hodgkin lymphoma as
additional cancer sites, which might be associated with
high BMI,14,20 but were not listed by WCRF as having
sufficient evidence. The exact sources and sizes of RRs are
described in the appendix (pp 8–9).
Calculation of PAF
We calculated PAFs on the basis of the approach
suggested by the Comparative Risk Assessment
Collaborative Group, using the formula:21
∫RR(x)P(x)dx – ∫RR(x)P*(x)dx
PAF=
∫RR(x)P(x)dx
where P(x) is the population distribution of BMI, P*(x) is
the distribution of theoretical minimum BMI, RR(x) is
www.thelancet.com/oncology Vol 16 January 2015
Articles
the RR of cancer associated with BMI, and dx indicates
that the integration was done with respect to BMI. The
theoretical minimum distribution of BMI was defined as
a BMI distribution with a mean of 22 kg/m² and an SD
of 1 kg/m², at which the disease burden is assumed to be
lowest at the population level.15,22
We used a log-logit function to characterise the shape
of the RR across BMI units. Furthermore, we assumed
no risk for BMI less than 22 and no risk increase for BMI
greater than 40, since estimates of RR beyond these
points were scant. A pictorial illustration and a more
detailed description of these assumptions of the risk
function are presented in the appendix (pp 8–9).
We calculated age-specific, sex-specific, and country-
specific PAFs for individual high-BMI-related cancer
sites. We then derived the number of cancer cases
attributable to high BMI by multiplying age-specific, sex-
specific, country-specific, and cancer-specific PAFs by the
corresponding numbers of incident cancers in 2012. We
calculated overall national, regional, and global estimates See Online for appendix
of the total attributable proportion of cancer related to
high BMI by summing the numbers of attributable
incident cases and dividing them by the total number of
cancer cases in each subgroup.
We estimated 90% uncertainty limits for PAFs using
Monte Carlo simulation. We also computed a counter-
factual scenario (ie, a model of incidence if mean BMIs
had remained at their 1982 values) to provide a more
realistic view about the preventable proportion of the
current burden of cancers caused by high BMI. The
analysis was done by replacing the theoretical minimum
distribution with the BMI distribution that was reported
in in 1982, an attainable value in the past in each country
and probably a more realistic goal for prevention than
the mean BMI of 22 kg/m² used in our main analysis.
Using this approach, we estimated what the PAF would
be if population mean BMIs had stayed constant at their
1982 values. A more detailed description of PAF inputs
and calculation is presented in the appendix (pp 31–33).
Cancer incidence and attributable cancer burden
The numbers of incident cancers in 2012 by age (in adults
aged 30 years and older after 10-year lag period), sex, and
country were obtained from GLOBOCAN 2012.23
Countries were grouped into 12 geographical regions
(appendix pp 34–40): sub-Saharan Africa (eastern, middle,
southern, and western Africa); Middle East and north
Africa (western Asia and northern Africa); Latin America
and the Caribbean (central and south America and the
Caribbean); North America; east Asia (eastern Asia,
including China); southeast Asia; south-central Asia
(southern Asia, including India); eastern Europe;
northern Europe; southern Europe; western Europe; and
Oceania (including Australia and New Zealand).24
Furthermore, countries also were grouped by 2012
human development index (HDI; very high, high,
moderate, or low).25 Because the separate incidences of
37
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Oesophageal adenocarcinoma Colon Rectum Pancreas Kidney Total
Articles

PAF n PAF n PAF n PAF n PAF n n PAF high BMI* PAF all†
Region
Sub- 15·5% 125 5·0% 330 2·6% 144 4·3% 175 5·9% 94 867 4·6% 0·4%
Saharan (10·9–21·0) (88–169) (3·6–6·9) (235–457) (1·8–3·5) (103–199) (3·2–5·5) (132–227) (4·3–8·2) (68–129) (625–1181) (3·3–6·3) (0·3–0·5)
Africa
Middle 34·3% 391 16·1% 2111 8·1% 631 10·8% 697 19·5% 1150 4980 14·5% 2·0%
East and (28·4–40·5) (323–462) (13·9–18·2) (1831–2395) (7·1–9·3) (547–719) (9·4–12·2) (608–788) (17·3–21·7) (1018–1282) (4327–5646) (12·6–16·4) (1·7–2·2)
north
Africa
Latin 35·6% 1193 15·4% 4058 7·6% 1099 10·0% 1294 19·0% 2366 10 009 14·4% 2·0%
America (31·7–39·1) (1063–1312) (13·4–17·4) (3520–4590) (6·6–8·6) (953–1248) (8·7–11·4) (1123–1470) (16·7–21·2) (2080–2639) (8739–11 258) (12·6–16·2) (1·7–2·2)
and the
Caribbean
North 44·4% 4293 21·0% 11 453 10·9% 2792 14·2% 3390 25·0% 9801 31 729 20·8% 3·5%
America (46·0–49·6) (4456–4804) (19·9–22·0) (10 861–12 002) (10·3–11·5) (2638–2941) (13·4–15·0) (3208–3578) (23·7–26·2) (9307–10 270) (30 470–33 595) (19·9–22·0) (3·4–3·7)
East Asia 17·9% 1390 6·9% 9120 3·4% 3386 4·4% 2625 8·2% 4878 21 398 6·0% 0·9%
(15·4–20·4) (1200–1587) (5·9–8·0) (7797–10 534) (2·9–4·0) (2888–3926) (3·8–5·1) (2246–3041) (7·0–9·4) (4201–5632) (18 332–24 720) (5·1–6·9) (0·8–1·1)
Southeast 13·8% 91 4·2% 951 2·1% 301 2·6% 165 5·6% 248 1756 3·6% 0·5%
Asia (9·9–19·3) (66–128) (2·9–5·8) (659–1325) (1·4–2·9) (208–421) (1·8–3·7) (111–234) (4·0–7·6) (177–337) (1221–2444) (2·5–5·0) (0·3–0·7)
South- 9·7% 389 4·2% 997 1·7% 353 2·8% 255 5·1% 481 2474 3·7% 0·4%
central Asia (6·6–13·1) (266–527) (3·1–5·3) (736–1277) (1·2–2·3) (246–476) (2·0–3·6) (185–332) (3·7–6·6) (350–623) (1783–3235) (2·6–4·8) (0·3–0·5)
Eastern 38·2% 637 16·0% 6082 8·2% 2586 10·3% 1829 18·7% 4382 15 517 13·8% 3·1%
Europe (32·9–42·9) (549–716) (13·6–18·5) (5141–7021) (6·8–9·6) (2144–3049) (8·7–12·0) (1538–2130) (15·9–21·4) (3744–5016) (13 115–17 931) (11·7–15·9) (2·6–3·6)
Northern 44·0% 2262 18·4% 3756 9·5% 1337 12·2% 845 21·8% 2042 10 242 18·3% 3·8%
Europe (41·6–46·0) (2139–2369) (16·9–19·8) (3447–4046) (8·7–10·3) (1221–1452) (11·1–13·3) (769–919) (19·9–23·5) (1867–2202) (9443–10 989) (16·9–19·6) (3·5–4·1)
Southern 43·0% 527 18·1% 7002 9·4% 1930 12·0% 1379 21·1% 3206 14 044 16·1% 3·3%
Europe (39·5–46·0) (484–564) (16·3–19·9) (6295–7667) (8·4–10·4) (1717–2142) (10·6–13·3) (1223–1533) (18·9–23·1) (2873–3514) (12 593–15 421) (14·5–17·7) (3·0–3·6)
Western 42·6% 1911 18·7% 8536 9·7% 2847 12·5% 1959 21·8% 4984 20 236 17·2% 3·3%
Europe (38·0–46·4) (1705–2083) (16·6–20·7) (7586–9447) (8·6–10·8) (2529–3167) (11·1–13·9) (1742–2178) (19·5–24·0) (4461–5488) (18 023–22 364) (15·3–19·0) (3·0–3·7)
Oceania 44·2% 361 19·1% 1212 9·9% 399 12·8% 233 22·6% 600 2804 17·9% 3·4%
(41·7–46·5) (340–379) (17·9–20·4) (1131–1292) (9·2–10·6) (371–427) (11·9–13·7) (216–250) (21·1–24·0) (560–637) (2619–2985) (16·7–19·1) (3·2–3·6)
HDI group
Low HDI 7·8% 175 3·3% 341 1·5% 127 2·5% 117 3·9% 134 895 3·1% 0·3%
(2·9–14·6) (64–326) (1·6–6·2) (165–634) (0·7–2·9) (61–239) (1·3–4·2) (63–199) (1·8–7·0) (62–243) (414–1642) (1·4–5·7) (0·1–0·5)
Medium 16·4% 1703 5·9% 7399 2·8% 2778 4·1% 2340 7·6% 4365 18 584 5·3% 0·7%
HDI (13·7–19·1) (1425–1991) (4·8–7·1) (6037–8894) (2·3–3·4) (2268–3346) (3·4–4·9) (1939–2788) (6·4–9·0) (3675–5135) (15 343–22 154) (4·4–6·4) (0·6–0·8)
High HDI 34·2% 1735 14·5% 8533 7·4% 3104 9·6% 2717 17·4% 5437 21 527 13·0% 2·1%
(30·1–38·0) (1527–1926) (12·4–16·6) (7289–9775) (6·2–8·6) (2610–3620) (8·2–11·1) (2312–3132) (15·0–19·7) (4695–6178) (18 433–24 630) (11·1–14·9) (1·8–2·4)
Very high 43·2% 9955 16·8% 39 335 8·4% 11 795 11·2% 9672 21·3% 24 295 95 052 15·9% 3·2%
HDI (41·9–47·1) (9664–10857) (15·3–18·3) (35 748–42 749) (7·6–9·3) (10 626–12 963) (10·1–12·2) (8787–10 560) (19·5–22·9) (22 275–26 213) (87 100–103 344) (14·6–17·3) (2·9–3·4)
World
Total 33·3% 13 569 13·0% 55 608 6·2% 17 804 8·4% 14 845 16·6% 34 231 136 058 11·9% 1·9%
(31·1–37·0) (12 680–15 100) (11·5–14·5) (49 239–62 052) (5·4–7·0) (15 565–20 168) (7·4–9·5) (13 100–16 680) (14·9–18·3) (30 707–37 769) (121 291–151 769) (10·6–13·3) (1·7–2·1)

Data are population attributable fractions (PAFs) or numbers of cancer cases (n), both reported with 90% uncertainty intervals. BMI=body-mass index. HDI=Human Development Index. *PAF high BMI=proportion of high-BMI-related cancers
attributable to high BMI. †PAF all=proportion of all cancer (excluding non-melanoma skin cancers) attributable to high BMI.

Table 1: Estimated PAFs and numbers of cancer cases associated with high BMI in men in 2012

www.thelancet.com/oncology Vol 16 January 2015

 Oesophageal Colon Rectum Gallbladder Pancreas Breast Corpus uteri Ovary Kidney Total
adenoarcinoma (postmenopausal)
PAF n PAF n PAF n PAF n PAF n PAF n PAF n PAF n PAF n n PAF PAF
high all†
BMI*
Region
Sub- 27·3% 151 4·8% 302 2·2% 128 20·4% 279 5·6% 216 6·1% 2759 24·8% 2142 2·3% 252 11·1% 184 6413 7·6% 2·0%
Saharan (22·0– (122– (3·7– (235– (1·6– (96– (14·3– (195– (4·6– (176– (4·6– (2079– (19·4– (1678– (1·6– (178– (7·7– (127– (4886– (5·8– (1·5–
Africa 32·9) 182) 6·1) 381) 2·8) 167) 27·3) 373) 6·8) 262) 7·8) 3526) 30·3) 2619) 3·0) 339) 15·3) 252) 8102) 9·6) 2·5)
Middle 43·9% 172 11·1% 1254 5·6% 334 53·2% 1501 11·8% 514 14·7% 6760 47·7% 4609 6·4% 617 34·7% 1256 17 018 18·2% 7·0%
East and (39·0– (153– (10·2– (1145– (5·1– (304– (48·3– (1364– (10·8– (470– (12·8– (5912– (45·0– (4346– (5·7– (547– (32·6– (1181– (15 421– (16·5– (6·4–
north 48·4) 189) 12·1) 1359) 6·2) 366) 57·7) 1631) 12·7) 556) 16·5) 7598) 50·5) 4881) 7·2) 691) 36·8) 1332) 18 602) 19·9) 7·7)
Africa
Latin 41·2% 507 9·3% 2670 4·6% 603 48·4% 4930 9·5% 1377 12·1% 12 401 41·6% 8022 5·5% 900 30·3% 2269 33 678 15·8% 6·4%

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America (38·4– (473– (8·4– (2415– (4·2– (546– (44·2– (4504– (8·7– (1255– (10·7– (11 024– (38·5– (7424– (4·9– (811– (28·1– (2102– (30 553– (14·3– (5·8–
and the 43·6) 537) 10·2) 2913) 5·0) 662) 52·6) 5361) 10·3) 1497) 13·4) 13 797) 44·4) 8554) 6·0) 991) 32·4) 2425) 36 736) 17·2) 6·9)
Caribbean
North 48·2% 706 11·1% 6052 5·6% 1009 53·4% 3131 11·2% 2625 14·3% 29 741 47·8% 26 082 6·8% 1554 34·5% 8084 78 984 19·2% 9·4%
America (46·8– (686– (10·6– (5801– (5·4– (963– (50·5– (2959– (10·8– (2527– (13·1– (27 095– (46·6– (25 397– (6·4– (1469– (33·5– (7848– (74 746– (18·2– (8·9–
49·3) 723) 11·5) 6276) 5·9) 1053) 56·5) 3311) 11·6) 2715) 15·5) 32 111) 48·9) 26 677) 7·1) 1633) 35·4) 8296) 82 796) 20·1) 9·8)
East Asia 21·5% 582 3·9% 4229 2·0% 1228 25·0% 10 285 3·9% 1796 5·1% 8143 19·6% 16 920 2·2% 965 13·8% 4045 48 192 8·3% 3·0%
(19·4– (524– (3·5– (3807– (1·8– (1103– (21·9– (9018– (3·6– (1617– (4·5– (7105– (17·5– (15 093– (1·9– (852– (12·4– (3657– (42 775– (7·4– (2·6–
23·4) 632) 4·3) 4668) 2·2) 1360) 27·9) 11 500) 4·4) 1981) 5·8) 9252) 21·4) 18 511) 2·4) 1087) 15·1) 4445) 53 435) 9·2) 3·3)
Southeast 22·5% 54 3·5% 694 1·8% 174 22·7% 819 3·5% 200 4·8% 2959 18·9% 2842 2·2% 399 12·9% 321 8465 6·2% 2·2%
Asia (18·4– (45– (3·0– (581– (1·5– (146– (17·1– (616– (2·9– (166– (4·0– (2447– (16·0– (2415– (1·8– (333– (10·9– (271– (7019– (5·2– (1·9–
26·5) 64) 4·2) 820) 2·1) 208) 28·7) 1034) 4·1) 238) 5·7) 3511) 21·7) 3265) 2·6) 473) 15·0) 375) 9987) 7·4) 2·6)
South- 17·6% 289 3·4% 636 1·4% 227 13·2% 2249 3·2% 237 4·1% 4736 16·5% 3241 1·5% 540 12·4% 526 12 682 5·4% 1·7%
central (14·4– (237– (2·8– (529– (1·1– (182– (10·0– (1708– (2·6– (191– (3·2– (3755– (13·2– (2593– (1·2– (426– (10·3– (440– (10 061– (4·3– (1·3–
Asia 21·0) 346) 4·0) 754) 1·8) 278) 17·2) 2916) 3·9) 288) 5·0) 5796) 19·9) 3908) 1·9) 667) 14·5) 617) 15 569) 6·6) 2·1)
Eastern 46·4% 228 10·7% 4543 5·3% 1371 52·5% 3450 10·7% 1796 13·3% 13 337 44·7% 18 745 5·9% 1639 32·8% 5317 50 425 18·2% 9·9%
Europe (42·6– (209– (9·7– (4121– (4·7– (1216– (47·7– (3133– (9·6– (1622– (11·6– (11 582– (41·2– (17 264– (5·3– (1450– (30·2– (4906– (45 503– (16·4– (8·9–
49·6) 243) 11·6) 4939) 5·9) 1527) 56·9) 3737) 11·7) 1961) 15·0) 15 010) 47·7) 19 981) 6·6) 1827) 35·2) 5705) 54 931) 19·8) 10·7)
Northern 43·8% 579 9·4% 1829 4·8% 441 47·3% 656 9·6% 695 11·8% 7513 41·5% 5707 5·5% 544 30·0% 1728 19 693 14·9% 7·9%
Europe (42·2– (558– (8·8– (1716– (4·4– (413– (43·8– (607– (9·0– (654– (10·6– (6790– (39·6– (5440– (5·1– (504– (28·5– (1640– (18 321– (13·9– (7·4–
45·2) 598) 9·9) 1936) 5·1) 471) 51·0) 707) 10·1) 733) 12·9) 8246) 43·3) 5947) 5·9) 584) 31·4) 1808) 21 031) 15·9) 8·4)
Southern 44·3% 111 9·6% 2943 4·9% 647 48·9% 2193 9·8% 1122 11·9% 9096 41·1% 8013 5·3% 672 29·8% 2231 27 028 15·3% 8·1%
Europe (42·0– (105– (8·9– (2737– (4·5– (596– (45·2– (2027– (9·1– (1042– (10·6– (8103– (38·6– (7509– (4·8– (610– (27·9– (2089– (24 818– (14·1– (7·5–
46·3) 116) 10·2) 3138) 5·3) 698) 52·6) 2356) 10·4) 1197) 13·2) 10 074) 43·4) 8452) 5·8) 733) 31·5) 2359) 29 123) 16·5) 8·7)
Western 42·1% 416 9·3% 3707 4·7% 875 48·7% 2631 9·5% 1533 11·4% 14 582 40·5% 9562 5·3% 758 28·7% 3791 37 854 14·5% 7·8%
Europe (39·3– (388– (8·5– (3416– (4·3– (802– (45·1– (2438– (8·8– (1420– (10·1– (12 956– (37·9– (8951– (4·8– (687– (27·3– (3603– (34 662– (13·3– (7·1–
44·9) 443) 10·0) 4019) 5·1) 956) 52·6) 2843) 10·3) 1654) 12·7) 16 283) 43·0) 10 162) 5·8) 835) 31·1) 4105) 41 301) 15·8) 8·5)
Oceania 43·5% 67 9·8% 592 5·0% 122 49·1% 222 9·9% 158 12·4% 1740 42·4% 1287 5·7% 108 30·7% 428 4722 15·2% 7·2%
(41·8– (64– (9·3– (561– (4·7– (115– (46·1– (208– (9·4– (150– (11·2– (1575– (40·5– (1231– (5·3– (101– (29·5– (411– (4416– (14·2– (6·7–
45·3) 70) 10·3) 622) 5·3) 129) 52·5) 237) 10·4) 165) 13·6) 1908) 44·1) 1339) 6·1) 116) 31·9) 445) 5031) 16·2) 7·6)
HDI group
Low HDI 13·8% 150 2·9% 253 1·4% 104 11·7% 882 3·3% 138 4·4% 2980 17·3% 2005 1·6% 301 9·3% 234 7048 5·5% 1·5%
(7·9– (86– (1·6– (143– (0·8– (60– (5·9– (444– (2·0– (84– (2·9– (1955– (11·1– (1289– (0·9– (174– (5·4– (136– (4370– (3·4– (0·9–
20·3) 221) 4·4) 384) 2·1) 158) 18·5) 1394) 4·8) 202) 6·2) 4152) 23·8) 2755) 2·4) 455) 13·9) 350) 10 070) 7·8) 2·1)
Medium 22·6% 850 4·0% 4112 1·9% 1279 23·2% 10 150 4·3% 1774 5·6% 15 466 20·6% 21 979 2·2% 1814 14·3% 4052 61 478 8·2% 2·7%
HDI (20·2– (760– (3·5– (3615– (1·7– (1119– (20·1– (8776– (3·8– (1561– (4·8– (13 194– (18·2– (19 414– (1·9– (1563– (12·7– (3622– (53 624– (7·2– (2·4–
24·8) 932) 4·5) 4644) 2·2) 1452) 26·4) 11 546) 4·8) 1996) 6·5) 17 864) 22·7) 24 325) 2·6) 2084) 15·8) 4500) 69 342) 9·3) 3·1)
(Table 2 continues on next page)
Articles

39
 Articles

colon and rectal cancers and the incidence of oesophageal

7·8%

5·4%
7·5%
(6·8–

(4·9–
(7·2–
8·2)

5·9)
8·3)
PAF
cancer by histological subtypes are not reported in
all†
GLOBOCAN,23 we estimated the numbers of these

Data are population attributable fractions (PAFs) or numbers of cancer cases (n), both reported with 90% uncertainty intervals. BMI=body-mass index. HDI=Human Development Index. *PAF high BMI=proportion of high-BMI-related cancers
16·6%

15·5%

13·1%
(185 876– (14·4–

(313 180– (11·9–

(15·1–
cancers by subtypes using country-specific and sex-

213 731) 16·5)

376 644) 14·3)

18·1)
BMI*
high
PAF

specific proportions of subtypes reported in Cancer

Incidence in Five Continents volume X (appendix p 10).26,27
(69 310–
76 626

200 003

345 154
83 501)
Total

The precise time lag between development and

n

duration of high BMI and the occurrence of cancer is not

(28·5– (18 401–

(24·3– (28 273–

well established. However, the general perception is that
6604

29·8% 19 288

25·9% 30 179

32 162)
20 251)
(29·3– (6115–
7061)

excess bodyweight does not initiate cancer, but rather

n

promotes of cancer to clinical presentation over several

31·6%
Kidney

years. Renehan and colleagues28 assumed a 10-year lag

33·8)

27·6)
31·3)
PAF

time on the basis of the scientific literature, wherein the

average follow-up time of 10 years showed the beneficial
(3·5– (7967–
(2160–

(5·0– (4071–

9978)
2424

5·4% 4409

4·0% 8948
2691)

4749)

effect of weight loss on subsequent cancer risk.29,30 With

n

no additional information available, we chose to assume

Ovary

5·7%
(5·0–

a 10-year lag period in this study, mapping high BMI

4·4)
5·8)
6·3)
PAF

prevalence in 2002 (by sex, age, and country) to cancer

(99 342–
(23 184–

114 297)
(39·9– (55 455–

incidence in 2012.
25 125

41·8% 58 061

107 172
26 784)

60 433)
Corpus uteri

Sensitivity analyses
43·6%

34·0%
(40·2–

(31·5–

In estimating the PAFs of cancers attributable to high

46·5)

36·3)
43·5)
PAF

BMI, we made several assumptions about the population

BMI distribution and the RRs function. To assess their
(100 424–
(postmenopausal)

(11·0– (63 936–

(11·0– (21 339–

127 111)
24 317

71 005

10·2% 113 767

77 866)
27 228)

effect on the results, we repeated the analyses while

changing the following assumptions: exposure definition
n

(categorical vs continuous BMI; appendix pp 13–14); BMI

12·5%

12·2%
Breast

14·0)

(9·0–
11·4)
13·3)
PAF

distribution (normal vs log-normal; appendix pp 15–16);

shape of the RR (linear or log-linear vs log-logit; appendix
attributable to high BMI. †PAF all=proportion of all cancer (excluding non-melanoma skin cancers) attributable to high BMI.
(11 289–
13 248)
2692

7665

7·8% 12 269
(2446–

(7198–

pp 17–19); and region-specific versus global RR estimates

2927)

8123)

(appendix pp 20–23). Because smoking31–34 and use of

n
Pancreas

HRT8,11,35 are known effect modifiers of the association

10·0%

9·0%

Table 2: Estimated PAFs and numbers of cancer cases associated with high BMI in women in 2012
10·9)

(8·4–
(9·1–

(7·1–
8·4)
9·5)
PAF

between bodyweight and cancer, we estimated PAFs

stratified by current smoking status (for pancreatic
(28·7– (28 776–
(38·2– (13 823–
6285

41·5% 15 029

16 244)

32·3% 32 346

36 007)

cancer) or HRT use (for postmenopausal breast cancer,

(44·7– (5732–
6823)

ovarian cancer, and endometrial cancer) and assessed the

Gallbladder

bias that might have occurred when these interactions

49·0%

44·9)

35·9)
53·2)

were ignored (appendix pp 24–27). Furthermore, because

PAF

studies have shown a protective effect of high BMI on

(3·2– (6480–
(4·1– (3654–
(4·4– (1647–

premenopausal breast cancer,8,14,36 we also assessed the

5·0% 1845

4·4% 3933

3·6% 7160
2043)

4221)

7874)

potentially adverse effects of decreasing population BMI

n
Rectum

on the incidence of premenopausal breast cancer and its

3·9)
4·7)
5·5)
PAF

effect on the total PAF (appendix pp 28–30).

(27 065–
(17 361–
19 696)

31 824)
(5945–
9·9% 6539

8·9% 18 547

7·6% 29 451

Role of the funding source

7100)

The funders of the study had no role in study design,

n

data collection, data analysis, data interpretation, or

Colon

10·8)
(9·0–

(8·3–

(7·0–
9·4)

8·2)
PAF

writing of the report. The corresponding author had full

access to all the data in the study and had final
(Continued from previous page)
adenocarcinoma

(31·2– (3564–
(42·3– (1976–

4144)
2148)
796

44·2% 2066

33·8% 3862
(38·6– (741–
844)

responsibility for the decision to submit for publication.

Oesophageal

41·5%

Results
46·0)
43·9)

36·2)
PAF

Worldwide, our result show that an estimated 481 000 or

3·6% of all new cancers (or 12·8% of all high-BMI-
Very high
High HDI

related cancers) in adults in 2012 were attributable to

World
Total
HDI

high BMI. By sex, 136 000 (1·9%) new cancers in men

(table 1) and 345 000 (5·4%) in women (table 2) were

40 www.thelancet.com/oncology Vol 16 January 2015

 Articles

attributable to high BMI. The attributable burden was
larger in countries with very high and high HDIs (PAF
5·3% and 4·8%, respectively) than in those with
moderate (1·6%) and low (1·0%) HDIs.
Region-specific estimates show that all three Asian
regions and sub-Saharan Africa had the lowest PAFs,
ranging from 0·4% to 0·9% of total cancers (3·6% to
6·0% of total high-BMI-related cancers) in men and
1·7% to 3·0% of total cancers (5·4% to 8·3% of total
high-BMI-related cancers) in women. North America
had the highest PAFs, at 3·5% of total cancers (20·8% of
high-BMI-related cancers) for men and 9·4% of total
cancers (19·2% of high-BMI-related cancers) for women.
For the remaining regions (Middle East and north Africa,
Latin America and the Caribbean, Oceania, and all
European regions), the PAF ranged from 2·0% to 9·9%
of total cancers (14·4% to 18·2% of high-BMI-related
cancers) in both sexes.
With respect to the regional contribution to new high-
BMI-related cancers in 2012, the North American region
contributed the most (111 000 or 23·0% of the total
worldwide cases attributable to high BMI), and sub-
Saharan Africa the least (7300 or 1·5%; tables 1, 2).
Eastern Europe had the greatest share of attributable

Men

PAF (%)
3·1–<5·5
2·0–<3·1
1·0–<2·0
0·3–<1·0
0·0–<0·3
No data

Women

PAF (%)
8·5–<12·7
6·6–<8·5
3·9–<6·6
1·6–<3·9
0·4–<1·6
No data

Figure 1: PAF of new cancer cases in 2012 caused by high BMI in men and women, by country
PAF=population attributable fraction.

www.thelancet.com/oncology Vol 16 January 2015 41

 Articles
North America 153·8 26·7
Northern Europe 160·0 24·9
Western Europe 166·3 24·3
Oceania 164·8 25·2
Southern Europe 153·2 21·4
Eastern Europe 143·3 17·4
Latin America and the Caribbean 63·6
Middle East and north Africa 53·9
East Asia 80·7
Southeast Asia 44·4
Sub-Saharan Africa 20·6 1·0
South-central Asia 22·1 0·8
200 100
Figure 2: Age-standardised incidence rate of high-BMI-related cancers and high-BMI-related cancers attributable to high BMI (per 100 000 people) in 2012
Incidence data are age-standardised to the world standard population. Light bars show total incidence rates of high-body-mass-index (BMI)-related cancers, and dark
bars show those attributable to high BMI.
burden among the European regions (66 000 or 33·8% of
the total European cases attributable to high BMI).
Despite the low PAF (1·8%), the east Asia region had the
second largest number of cases attributable to high BMI
(70 000) after North America, because of its large
population size.
Country-specific PAFs for men and women are shown
in figure 1 and in the appendix (pp 34–40). In men, the
highest PAF of 5·5% was in the Czech Republic,
followed by 4·5% in Jordan and Argentina, and 4·4% in
the UK and Malta. The greatest between-country
differences within a region were in Latin America and
the Caribbean, where the PAF ranged from 4·5% in
Argentina to 0·7% in Haiti and Jamaica. In women,
Barbados had the highest PAF, with 12·7% of cancers
attributable to high BMI, followed by the Czech
Republic (12·0%) and Puerto Rico (11·6%). As for men,
between-country differences were largest in Latin
America and the Caribbean, where the PAF ranged
from 12·7% in Barbados to 1·6% in Haiti. Countries in
sub-Saharan Africa had consistently lower overall PAFs
than those in other regions, of less than 2% in men and
less than 4% (with the exception of Mauritius and South
Africa) in women.
PAF also varied greatly by cancer site, ranging from
6·2% for rectal cancer to 33·3% for oesophageal
adenocarcinoma in men and from 3·6% for rectal cancer
to 34·0% for cancer of the corpus uteri and oesophageal
adenocarcinoma in women (tables 1, 2). Despite having a
large estimated PAF of more than 30%, oesophageal
adenocarcinomas accounted for only 14 000 (or 10·0%) of
the total worldwide cancer cases attributable to high BMI
in men and 4000 (or 1·1%) in women. Colon cancer in
men and postmenopausal breast cancer in women
contributed the largest number of cancer cases
attributable to high BMI. In men, colon and kidney
cancer together contributed about two-thirds of the new
cancer cases attributable to high BMI (90 000). In women,
42
58·2 352·4
42·7 330·6
38·7 315·9
40·0 299·0
35·2 269·2
38·5 250·1
8·1 23·4 170·7
6·9 21·8 140·4
4·6 9·7 125·6
1·5 6·5 109·7
6·2 86·2 Men
3·9 76·1 Women
0 100 200 300 400
Incidence rate
postmenopausal breast cancer and cancer of the corpus
uteri contributed about two-thirds of the new cancer
cases attributable to high BMI (221 000).
We noted substantial differences between men and
women in PAFs for colon cancer (13·0% vs 7·6%). Sex
differences in the numbers of attributable cases were
largest for colon cancer and oesophageal adeno-
carcinoma, with 56 000 and 14 000 attributable cases,
respectively in men and only 29 000 and 4000 attributable
cases in women (tables 1, 2). The incidence of high-
BMI-related cancers attributable to high BMI was
relatively higher for women than for men in all regions
(figure 2). Particularly, in regions with a fairly low
incidence of high-BMI-related cancers, such as Asia and
sub-Saharan Africa, the proportion of new cancer cases
attributable to high BMI was two to three times greater
for women than for men.
In our counterfactual scenario, we calculated that if
BMI had remained as recorded in 1982, about a quarter
(118 000 cases) of cases of high-BMI-related cancers in
2012 could have been averted. In other words, a quarter of
all high-BMI-related cancers could be attributed to the
increase in BMI between 1982 and 2002 (appendix
pp 31–33). About 0·9% (0·5% in men and 1·3% in
women) of all cancers diagnosed in 2012 could therefore
be regarded as realistically avoidable by prevention of
high BMI. The realistically attributable fraction was
greatest in countries with a very high or high HDI, where
83·2% of these potentially avoidable cancers occurred. In
a high-burden region such as North America, this
proportion translated into more than 40 000 cases, or
35·6% of all attributable cancer cases that could be linked
to the increase in BMI since 1982. With respect to specific
cancer sites, about 10·7% of all oesophageal adeno-
carcinomas (5600), 8·5% of all corpus uteri (27 000),
4·9% of all kidney (15 000) and 2·5% of all postmenopausal
breast cancers (28 000) could have been avoided if BMI
had not increased between 1982 and 2002.
www.thelancet.com/oncology Vol 16 January 2015

When PAF for pancreatic cancer was corrected for
smoking status, we estimated that it ranged between 0·6%
and 18·3% for both men and women (appendix pp 24–25),
dependent on country. Compared with the unadjusted
PAFs, this adjustment increased the PAF by 0–5 percentage
points in men and 0–9 percentage points in women. This
difference was largest in the UK for both men and women.
HRT non-users had substantially higher PAFs than HRT
users; PAFs for HRT non-users ranged from 50·4% to
65·0% for corpus uteri cancer and from 8·3% to 12·4%
for postmenopausal breast cancer and ovarian cancer,
dependent on country. For HRT users, we noted PAFs
between 8·6% and 20·8% for corpus uteri cancer and
PAFs below 0% for postmenopausal breast and ovarian
cancers, because of slightly protective RRs (appendix
pp 26–27). When comparing the PAFs corrected for HRT
use to the unadjusted PAFs, the difference was small for
most countries, ranging from 0 to 14 percentage points for
corpus uteri cancer and from 0 to 5 percentage points for
postmenopausal breast and ovarian cancers. The difference
was larger in countries where the prevalence of HRT use
was low (<55%) and a large proportion of women had high
BMI—eg, Germany and Russia.
The results for thyroid cancer, non-Hodgkin lymphoma,
and premenopausal breast cancer are reported in the
appendix (pp 28–30). In the sensitivity analyses, the
choice of BMI data type and distribution did not
substantially affect the results (appendix pp 13–16),
although PAFs changed with the use of different RR
functions (appendix pp 17–19) and region-specific RRs
(appendix pp 20–23).
Discussion
Our results show that about 3·6% of all new cancers in
adults aged 30 years and older (excluding non-melanoma
skin cancer) in 2012, or 12·8% of high-BMI-related
cancers, could be attributed to high BMI. These figures
are equivalent to an estimated 481 000 new cancers that
might have been caused by high BMI. Postmenopausal
breast, corpus uteri, and colon cancer accounted for
72·5% of the total attributable cases in women, whereas in
men kidney and colon cancers accounted 66·0% of all
attributable cases. 63·5% of the global cancer cases related
to high BMI were in the North American and European
regions, although the PAF was also large in Oceania, Latin
America and the Caribbean, and the Middle East and
north Africa. Assuming that the association between high
BMI and cancer is causal, the continuation of current
patterns of population weight gain will lead to continuing
increases in the future burden of cancer. Most importantly,
about one quarter of the total cases attributable to high
BMI (118 000 cancers) could potentially have been avoided
if the global population mean BMI had remained the
same as was recorded in 1982.
Our results show that the issue of cancer burden related
to high BMI mainly affects higher-resource regions,
particularly North America and Europe. Besides the
www.thelancet.com/oncology Vol 16 January 2015
Articles
unequal distribution of cancer cases attributable to high
BMI worldwide, we noted substantial differences within
regions; for example, in Latin America and the Caribbean
PAFs for women ranged from 12·7% in Barbados to 1·6%
in Haiti. Although high-BMI-related cancers have become
a global issue,37 the transition from increasing, to
stabilising, to possibly decreasing obesity prevalence
occurs at different rates in different countries and
regions. In a few countries such as the UK and the USA,
where BMI increased substantially in the 1980s and
1990s, the BMI increase has since slowed, but in most
countries the average BMI has continued to increase
steadily since the 1980s.2
The results of our secondary analysis, in which historical
BMI was used as an achievable population mean BMI,
could be used to measure the changing effect of BMI on
the burden of cancer. Taking into account both current
population mean BMIs and their changes over time, the
increase in PAF has been greatest in the Middle East and
north Africa, Latin America and the Caribbean, North
America, and Oceania. By contrast, eastern Europe
maintained a similar (high) population mean BMI
between 1982 and 2002, so despite the large current PAF,
only very few cases are attributable to the change in BMI in
that period. The varying pattern in BMI distribution and
trends across countries emphasises the need for future
research into the cumulative effects of overweight and
obesity on the burden of cancer and other chronic diseases.
Investigators of independent pooled studies31–33 have
reported an attenuated risk of high BMI in smokers for
pancreatic and thyroid cancers. In our study, taking into
account the differential effect by smoking status produced
different estimates, dependent on a country’s smoking
prevalence. In high-income countries such as the UK and
the USA, because of the high past prevalence of tobacco
smoking38 and high present BMI,1 the PAF of pancreatic
cancer related to high BMI was slightly underestimated in
our uncorrected analysis. By contrast, in low-income
countries such as Ghana, where smoking prevalence has
only started to rise,39 the effect of high BMI on pancreatic
cancer was slightly overestimated or was not large enough
to be appreciable. Another important effect modifier in
the relation between BMI and cancer is HRT use, wherein
the risk of female hormone-driven cancers related to high
BMI is largely attenuated or even eliminated among HRT
users.8,11,35 In our sensitivity analysis, we showed that most
postmenopausal breast, ovary, and corpus uteri cancers
attributable to high BMI occurred among HRT non-users.
The falling use of HRT since the early 2000s40,41 has
contributed to a decrease in breast cancer incidence in
countries where use was high; this decrease in use will
probably translate into a higher proportion of cases being
attributable to high BMI and therefore amenable to
prevention by weight loss.
This study adds important insights to the contribution
of lifestyle and exogenous risk factors on cancer risk.
Previous studies have quantified the global cancer burden
43
 Articles
attributable to infections (2 million new cases in 2008,
PAF 16·1%)42 and smoking (1·4 million cancer deaths in
2000, PAF 21%).43 Ours is the most comprehensive study
so far reported to provide worldwide estimates of the
burden of cancer due to high BMI (panel).
A report from the GBD study15 provided estimates of
the burden of cancer due to high BMI, but those results
are not directly comparable to ours because PAF was
presented as a proportion of deaths or disability-adjusted
life years attributable to high BMI, whereas incidence was
the outcome in our study. Furthermore, in the GBD study,
information about high BMI prevalence and cancer
mortality was obtained for the same year, not allowing for
a lag between the exposure and cancer development and
mortality. A few other studies have provided estimates of
cancer incidence associated with high BMI,17,28,44–46 but
these were limited to European populations. For example,
Renehan and colleagues28 estimated that 2·5% of all
cancer cases in men and 4·1% in women were related to
high BMI. Our estimates for the European regions ranged
between 3·1% and 3·8% in men and between 7·8% and
9·9% in women. Such differences in estimates are to be
expected, since our estimates are based on more recent
data for both the prevalence of high BMI and the
incidence of cancer, both of which have increased greatly
over the past decade.19,47
Another strength of this study is the use of age-specific,
sex-specific, and country-specific estimates of BMI and
the latest available estimates of cancer incidence.
Although these data were estimates and therefore careful
interpretation of the results is advised, the best available
estimates were used. We made many assumptions when
estimating the PAFs; however, our sensitivity analyses
Panel: Research in context
Systematic review
We searched Medline for articles published in any language up to Jan 1, 2014, using the
search terms “obesity”, “body-mass index”, “cancer risk”, “cancer incidence”, “attributable
fraction”, “avoidable”, and “preventable”. We identified several studies that provided
estimates of the burden of cancer attributable to high body-mass index (BMI) in specific
countries or regions,17,28,44–46 as well as a report15 from the Global Burden of Disease study
that included estimates of deaths or disability-adjusted life years attributable to high BMI.
However, no previous study had provided global estimates of cancer incidence
attributable to high BMI.
Interpretation
Our results show that 3·6% of all new cancers in adults in 2012 (a total of 481 000 cases)
are attributable to excess bodyweight. This finding emphasises the need for a global effort
to abate the continuing increases in overweight and obesity worldwide. Assuming a
causal link between high BMI and cancer incidence, if the current pattern of population
weight gain continues, it will lead to further increases future burden of cancer, especially
in regions such as Latin America and the Caribbean and north Africa, where the largest
increases in the prevalence of obesity have occurred in the past three decades.2 Our results
should be used to inform health policy in terms of targets for prevention programmes,
while emphasising existing gaps in our knowledge about the association between BMI
and cancer.
44
showed that changing these assumptions made little
difference to the reported PAFs. One of the assumptions
that we tested was related to the evidence of non-linear
associations between BMI and several cancers—eg,
oesophageal, colon, breast, and endometrial cancers.44
We opted for a log-logit RR function for all cancer sites
included in this study instead of a linear function, which
partly addressed this issue. In the sensitivity analyses, we
tested different RR functions, which had only small
effects on the final PAF estimates.
Alongside point estimates for the PAF, we presented
90% uncertainty intervals to provide a measure of
reliability. However, these uncertainties do not take into
account uncertainties in the cancer data from the
GLOBOCAN 2012 database, which provides a qualitative
ranking of data quality for each country-specific estimate.23
Quantification of this uncertainty and incorporation of
additional uncertainties from the modelling and
estimation processes remains a major challenge and
therefore was not attempted in our analysis.48,49
Another limitation of this study includes the
assumption of constant RRs across very diverse popu-
lations. The risks of some cancers associated with excess
bodyweight have been reported to vary by ethnic group
and geographical location.14,50 Variation exists in the
distribution of body fat between ethnic groups and how
this is reflected in the BMI measure. For example, within
the USA, African-American and Hispanic women are
more likely to be obese than white and Asian-American
women, yet white and Asian-American women have
higher body fatness at similar BMIs.51 Other
anthropometric measures, such as waist circumference
or waist-to-hip ratio, have been suggested as better
predictors of obesity-related health outcomes than
BMI.52,53 Furthermore, rural and urban differences in the
prevalence of obesity have been reported.54–56 In our study,
some variation in the distribution of BMI between ethnic
groups might have been captured by our use of country-
specific BMI estimates. However, residual variation—ie,
within countries—was not accounted for in the models.
Because very little information is available for subnational
populations such as ethnic groups and because of the
absence of comparable global prevalence data for other
anthropometric measures and their risk estimates, we
could not do additional analyses to address these issues.
Another drawback is the assumption of the absence of
time-dependent effects of high BMI on cancer risk,
which cannot be completely captured by age-specific
BMI data and lag time. We assumed a 10-year lag in our
modelling, but we recognise that the time-related effects
of excess adiposity are likely to vary between cancer types.
Results from some studies57,58 have shown that the risk of
cancer from high BMI accumulates with the number of
years lived with excess weight, suggesting that the risk
can better be predicted from years of life lived with high
BMI. Longer duration of obesity has also been linked to
other diseases and conditions, such as coronary artery
www.thelancet.com/oncology Vol 16 January 2015

calcification, a precursor of coronary heart disease.59
Although this finding is in line with the biological
mechanisms underlying the association between obesity
and the development cancer, studies examining this
aspect of obesity are a recent development and neither
risk estimates nor the exposure information are available
for every type of high-BMI-related cancer.
Lastly, the estimation of the PAF is based on the
assumption that the association between high BMI and
each cancer type included in our study is causal.60 We
thus assume that reducing BMI will lead to a reduction
in the incidence of these cancers. Excess bodyweight has
been shown to increase circulating levels of oestrogens
and bioactivity of IGF-1, hence promoting the
development of cancer.61 However, epidemiological
studies that report risk associations between BMI and
cancer are prone to several limitations. Residual
confounding might account for the association between
obesity and some types of cancer, and this possibility was
not accounted for in our analysis. We have tried to
overcome this issue by exclusively using risk estimates
based on large meta-analyses that included only high-
quality studies and, whenever possible, only cohort
studies.
Based on our results, historical and continuing
increases in the global prevalence of high BMI, especially
in younger cohorts, are expected to translate into further
increases in cancer burden in the future. Changes in the
prevalence of strong effect modifiers such as HRT use
are likely to increase the proportions of cancers
attributable to high BMI, particularly among women.
The large burden of cancers attributable to high BMI in
North America, Europe, Oceania, Latin America and the
Caribbean, and the Middle East and north Africa points
to the importance of weight-control programmes in these
regions. Our results should inform health policy in terms
of targets for prevention programmes, while emphasising
existing gaps in our knowledge about the association
between BMI and cancer. It also emphasises the need for
research into effective interventions to control weight
gain to avoid further increases in the burden of cancer
related to high BMI.
Contributors
MA, NP, and IS contributed to data collection, study design, analysis,
and wrote the first draft of the report. GB and AGR contributed to study
design, analysis, and finalising the report. GAS and ME contributed to
study design, data collection, analysis, and finalising the report. JF
contributed to data collection and finalising the report. DF, RD, IR, and
JJM contributed to study design and drafting of the report. All authors
read and approved the final report.
Declaration of interests
We declare no competing interests.
Acknowledgments
This project was funded by the World Cancer Research Fund
International (grant number SG 2012/619). NP was funded by the
Australian National Health and Medical Research Council (NHMRC
project 31691). IS was funded by a Marie Curie Intra-European
Fellowship from the European Commission (project number 302050).
We would like to thank Rachel Thompson and Martin Wiseman from
www.thelancet.com/oncology Vol 16 January 2015
Articles
World Cancer Research Fund International for their crucial input at
several stages of the project. JJM is with the CRONICAS Centre of
Excellence in Chronic Diseases at Cayetano Heredia University (Lima,
Peru), supported by federal funds from the US National Heart, Lung
And Blood Institute (National Institutes of Health, Department of
Health and Human Services), under contract number
HHSN268200900033C. GAS is a staff member of WHO. Data for
body-mass index by hormone replacement therapy status were collected
by the WHO MONICA investigators and have been made available for For the WHO MONICA
this publication by the WHO MONICA project. The views expressed in investigators see http://www.
this report are those of the authors and do not necessarily represent the thl.fi/publications/monica/
decisions, policy, or views of WHO, nor the views of individual investigators.htm
investigators from the WHO MONICA project.
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