Body mass index/CR and cancer

[Guest guest]

Hi All,

The pdf-available below excerpted paper may suggest that cancers, at least some

cancers, are related to our body mass indices/CR.

A prospective study may have been a better strategy for such a study.

Rousseau MC, Parent ME, Siemiatycki J.

Comparison of self-reported height and weight by cancer type among men from

Montreal, Canada.

Eur J Cancer Prev. 2005 Oct;14(5):431-8.

PMID: 16175048

Among men there is epidemiological evidence for an association between obesity

and

increased risk of renal cell carcinoma, colon cancer and adenocarcinoma of the

oesophagus. The evidence for other cancer sites remains inconsistent. We

conducted a

large population-based, multi-site, case-control study of environmental causes

of

cancer among males in Montreal, Canada. Among the many questionnaire items

collected

by interview were height and usual weight. We compared height, weight and body

mass

index (BMI) among individuals with 11 different cancer types (combined N=3016)

and

population-based controls (N=509). Linear regression was used to model the

relationship of the disease status with each of three dependent continuous

variables

(height, weight and BMI), while adjusting for covariates. For most cancer

groups,

weight and BMI were lower than among population controls. Because of potential

information bias and reverse causality bias, we focused on the comparisons among

cancer types. The lowest BMI values were observed among men with squamous cell

carcinoma of the oesophagus, lung and stomach cancers. The highest BMIs were

reported by men with prostate and kidney cancers, and oesophageal

adenocarcinoma.

Inconsistencies in the epidemiological literature on obesity and cancer risk

could

be related to the difficulties in obtaining unbiased reports of pre-disease

weight

and to publication bias.

Introduction

Most of the evidence on excess weight and its relation to cancer development

derives

from experimental studies in which restriction of energy intake prevented

adult-onset obesity in animals. The resulting protection against several tumour

types, both spontaneous and chemically induced, was observed among numerous

laboratory species (Kritchevsky, 1999; Hursting and Kari, 1999; Hursting et al.,

2003). Increased energy expenditure through physical activity has also resulted

in

decreased tumour incidence in animals (Kritchevsky, 1999). Several physiological

mechanisms have been postulated for the association between obesity and cancer

risk,

but very few have been verified in humans. They include a decreased endogenous

production of reactive oxygen species and oxidative DNA damage in situations of

energy restriction, alterations in carcinogen metabolizing enzymes and changes

in

endogenous hormone metabolism such as sex steroids, insulin and insulin-like

growth

factor 1 (IGF-1) (Dunn et al., 1997; Hursting and Kari, 1999; Bianchini et al.,

2002; Hursting et al., 2003). It is not yet clear if and how all these pathways

are

involved in obesity-mediated carcinogenesis, and whether the mechanisms vary

according to the organ studied or the source of energy deficit (energy

restriction

or physical activity).

.... Table 5 Comparison of the mean body mass index (BMI) by cancer type in our

study

with previous literature on an association between BMI and specific cancers

among

men

==================

----Published literature a

Cancer type Mean BMI in Montreal study b----Number of studies c Median RR d

Interquartile range of RR d

==================

[Population controls 25.5 – – –]

Oesophagus (squamous cell carcinoma) 23.6 – – –

Lung 24.5 7 0.7 0.6–0.9

Stomach 24.6 – – –

Bladder 24.8 – – –

Colon 25.1 11 1.8 1.4–2.2

Pancreas 25.1 3 1.4 1.1–1.5

Rectum 25.2 4 1.4 1.0–2.0

Non-Hodgkin’s lymphoma 25.2 – – –

Melanoma 25.3 – – –

Prostate 25.6 25 1.0 1.0–1.2

Kidney 26.1 16 1.6 1.3–2.0

Oesophagus (adenocarcinoma) 26.4 6 2.7 e 2.4–3.1

=================

a These studies are cited in the exhaustive review by Vainio and Bianchini

(2002).

b From lowest to highest BMI.

c Number of studies included in calculation of median and interquartile range.

Studies listed in (Vainio and Bianchini, 2002), tables 23 (colon, rectum), 31

(prostate), 32 (kidney), 33 (lung), 34 (oesophagus), 35 (pancreas), where

estimates

were provided for men, and for which the exposure was BMI or relative weight.

For

those cancers with no studies listed there were either no informative studies

published, few studies and inconsistent results, or the weight of the evidence

indicated no association with BMI.

d RR signifies the relative risk as assessed by comparing the highest with the

lowest BMI category.

e For adenocarcinoma and gastric cardia.

.... Dunn SE, Kari FW, French J, Leininger JR, Travlos G, R, Barrett JC.

Dietary restriction reduces insulin-like growth factor I levels, which modulates

apoptosis, cell proliferation, and tumor progression in p53-deficient mice.

Cancer Res. 1997 Nov 1;57(21):4667-72.

PMID: 9354418

Hursting SD, Kari FW.

The anti-carcinogenic effects of dietary restriction: mechanisms and future

directions.

Mutat Res. 1999 Jul 15;443(1-2):235-49. Review. No abstract available.

PMID: 10415442

Hursting SD, Lavigne JA, Berrigan D, Perkins SN, Barrett JC.

Calorie restriction, aging, and cancer prevention: mechanisms of action and

applicability to humans.

Annu Rev Med. 2003;54:131-52. Epub 2001 Dec 3. Review.

PMID: 12525670

Kritchevsky D.

Caloric restriction and experimental carcinogenesis.

Toxicol Sci. 1999 Dec;52(2 Suppl):13-6. Review.

PMID: 10630585

Al Pater, PhD; email: old542000@...

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