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Quoted message said:
Well, do you have cites for it? I have a little collection of various
abstracts etc, and this would be a great addition.i
Here's a start:
Cancer Causes Control 2002 Apr;13(3):255-61 Related Articles, Links
Nutrient intake and ovarian cancer: an Italian case-control study.
Bidoli E, La Vecchi C, Montella M, Maso LD, Conti E, Negri E, Scarabelli C,
Carbone A, Decarli A, Franceschi S.
Epidemiology Unit, Centro di Riferimento Oncologico, Aviano, Italy.
[email hidden]
OBJECTIVE: The role of selected macronutrients, cholesterol, and fatty acids in
the etiology of epithelial ovarian cancer was analyzed using data from a
case-control study carried out in five Italian areas between January 1992 and
December 1999. METHODS: Cases comprised 1,031 women with incident,
histologically confirmed epithelial ovarian cancer, admitted to the major
teaching and general hospitals of the study areas. Controls comprised 2,411
women admitted for acute, non-neoplastic conditions to the same network of
hospitals. Information on dietary habits was elicited using a validated
food-frequency questionnaire including 78 food groups and recipes. Odds ratios
(OR) and their corresponding 95% confidence intervals (CI) were computed by
subsequent quintiles of nutrient intake. RESULTS: Direct associations with
ovarian cancer emerged for starch intake (OR = 1.4 in the highest vs the lowest
quintile of intake; 95% CI 1.1-1.8), while inverse associations emerged for
monounsaturated (OR=0.7; 95% CI 0.5-0.9), and polyunsaturated (OR = 0.7; 95% CI
0.5-0.9) fatty acids. Among fatty acids, oleic (OR = 0.7; 95% CI 0.5-0.9),
linoleic (OR = 0.7; 95% CI 0.5-0.9), and linolenic (OR = 0.8; 95% CI 0.6-1.0)
acids were inversely related to ovarian cancer. When, however, six
macronutrients were included in the same model, only the adverse effect of high
starch intake remained significant. Results were consistent in separate strata
of menopausal status, parity, and energy intake. CONCLUSIONS: Starch was
directly associated, and unsaturated fatty acids were inversely associated,
with ovarian cancer risk.
PMID: 12020107 [PubMed - indexed for MEDLINE]
Ann Oncol 2003 Jan;14(1):78-84 Related Articles, Links
Dietary glycemic index, glycemic load and ovarian cancer risk: a case-control
study in Italy.
Augustin LS, Polesel J, Bosetti C, Kendall CW, La Vecchia C, Parpinel M, Conti
E, Montella M, Franceschi S, Jenkins DJ, Dal Maso L.
Servizio di Epidemiologia, Centro di Riferimento Oncologico, Istituto Nazionale
Tumori, Aviano, Italy.
BACKGROUND: Dietary carbohydrates vary in their ability to raise blood glucose
and insulin levels, which, in turn, influence levels of sex hormones and
insulin-like growth factors. We analyzed the effect of type and amount of
carbohydrates on ovarian cancer risk, using the glycemic index (GI) and the
glycemic load (GL) measurement in a large case-control study conducted in
Italy. MATERIALS AND METHODS: Cases included 1031 women with incident,
histologically confirmed epithelial ovarian cancer, from four Italian regions.
Controls included 2411 women admitted to the same hospital networks for acute,
non-neoplastic conditions. Average daily GI and GL were calculated from a
validated food frequency questionnaire. Odds ratios (OR) and the corresponding
95% confidence intervals (CI) were computed using multiple logistic regression.
RESULTS: Ovarian cancer was directly associated with dietary GI (OR for highest
versus lowest quartile = 1.7, 95% CI 1.3-2.1) and GL (OR = 1.7, 95% CI
1.3-2.1). The associations were observed in pre- and postmenopausal women, and
they remained consistent across strata of major covariates identified.
CONCLUSIONS: This study supports the hypothesis of a direct association between
GI and GL and ovarian cancer risk and, consequently, of a possible role of
hyperinsulinemia/insulin resistance in ovarian cancer development.
PMID: 12488297 [PubMed - in process]
The largest and most comprehensive study on diet and breast cancer to
date, studying over 5,000 women between 1991 and 1994, showed that
women with the lowest intake of dietary fat had a significantly higher
incidence of breast cancer than the women with the highest intake of
dietary fat. It also found that women with the highest intake of
starch had a significantly higher incidence of breast cancer than the
women with the lowest intake of starch. The study found no evidence
that saturated fat had any effect one way or the other on breast
cancer, and that unsaturated fat had a significantly protective effect
against breast cancer. (Franceschi S et. al. Intake of macronutrients
and risk of breast cancer. Lancet; 347(9012):1351-6 1996)
"We found no evidence of a positive association between total dietary
fat intake and the risk of breast cancer. There was no reduction in
risk even among women whose energy intake from fat was less than 20
percent of total energy intake. In the context of the Western
lifestyle, lowering the total intake of fat in midlife is unlikely to
reduce the risk of breast cancer substantially." (Hunter, DJ et. al.
Cohort studies of fat intake and the risk of breast cancer - A pooled
analysis. New England Journal of Medicine, 334: (6) FEB 8 1996)
Susan
CEBP -- Abstracts: Muti et al. 11 (11): 1361
Cancer Epidemiology Biomarkers & Prevention Vol. 11, 1361-1368, November 2002
Fasting Glucose Is a Risk Factor For Breast Cancer
A Prospective Study1
There is some evidence that glucose and other factors related to glucose
metabolism, such as insulin and insulin-like growth-factors (IGFs) may
contribute to breast cancer development.
The present study analyzed the hypothesis that serum glucose, insulin levels,
and IGF-I pattern are associated with breast cancer using a nested case-control
study. Between 1987 and 1992, 10,786 women ages 35–69 were recruited in a
prospective study in Italy. Women with history of cancer and on hormone therapy
were excluded at baseline. At recruitment, blood samples were collected after a
12-h fast between 7:30 and 9:00 a.m. from all of the study participants.
After 5.5 years, 144 breast cancer cases were identified among the participants
of the cohort. Four matched controls were chosen for each breast cancer case
from members of the cohort who did not develop breast cancer during the
follow-up period.
In premenopausal women, glucose was associated with breast cancer risk: the
age, body mass index, and reproductive variable adjusted relative risk (RR) for
the highest quartile of serum glucose versus the lowest was 2.8 (that's 280%
higher). . .
Insulin showed a weaker association with breast cancer, the adjusted RR of the
highest quartile versus the lowest was 1.7, . . . whereas the adjusted RR of
the highest quartile of IGF-I was 3.1 . . .
Increased levels of insulin-like growth factor binding protein-3 (IGFBP)-3
were related to breast cancer risk: the adjusted RR for the highest quartile
was 2.1 , . . .
In POSTmenopausal women, the associations of glucose, insulin, and IGF-1
pattern were associated with breast cancer risk in heavier subjects
characterized by a body mass index higher than 26.
These results indicate that chronic alteration of glucose metabolism is related
to breast cancer development.