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Obesity, endogenous hormones, and endometrial cancer risk: a synthetic review.

Abstract

Endometrial cancer is a disease of the affluent, developed world, where epidemiological studies have shown that > or =40% of its incidence can be attributed to excess body weight. An additional proportion may be because of lack of physical activity. Alterations in endogenous hormone metabolism may provide the main links between endometrial cancer risk, and excess body weight and physical inactivity. Epidemiological studies have shown increased endometrial cancer risks among pre- and postmenopausal women who have elevated plasma androstenedione and testosterone, and among postmenopausal women who have increased levels of estrone and estradiol. Furthermore, there is evidence that chronic hyperinsulinemia is a risk factor. These relationships can all be interpreted in the light of the "unopposed estrogen" hypothesis, which proposes that endometrial cancer may develop as a result of the mitogenic effects of estrogens, when these are insufficiently counterbalanced by progesterone. In our overall synthesis, we conclude that development of ovarian hyperandrogenism may be a central mechanism relating nutritional lifestyle factors to endometrial cancer risk. In premenopausal women, ovarian hyperandrogenism likely increases risk by inducing chronic anovulation and progesterone deficiency. After the menopause, when progesterone synthesis has ceased altogether, excess weight may continue increasing risk through elevated plasma levels of androgen precursors, increasing estrogen levels through the aromatization of the androgens in adipose tissue. The ovarian androgen excess may be because of an interaction between obesity-related, chronic hyperinsulinemia with genetic factors predisposing to the development of ovarian hyperandrogenism.

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  • Authors+Show Affiliations

    ,

    Hormones and Cancer Group, International Agency for Research on Cancer, 69372 Lyon, France. kaaks@iarc.fr

    ,

    Source

    MeSH

    Age Distribution
    Aged
    Androgens
    Endometrial Neoplasms
    Estrogens
    Female
    Gonadal Steroid Hormones
    Humans
    Insulin
    Middle Aged
    Obesity
    Prevalence
    Prognosis
    Risk Assessment
    Risk Factors
    Sex Hormone-Binding Globulin

    Pub Type(s)

    Journal Article
    Research Support, U.S. Gov't, Non-P.H.S.
    Research Support, U.S. Gov't, P.H.S.
    Review

    Language

    eng

    PubMed ID

    12496040

    Citation

    Kaaks, Rudolf, et al. "Obesity, Endogenous Hormones, and Endometrial Cancer Risk: a Synthetic Review." Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored By the American Society of Preventive Oncology, vol. 11, no. 12, 2002, pp. 1531-43.
    Kaaks R, Lukanova A, Kurzer MS. Obesity, endogenous hormones, and endometrial cancer risk: a synthetic review. Cancer Epidemiol Biomarkers Prev. 2002;11(12):1531-43.
    Kaaks, R., Lukanova, A., & Kurzer, M. S. (2002). Obesity, endogenous hormones, and endometrial cancer risk: a synthetic review. Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored By the American Society of Preventive Oncology, 11(12), pp. 1531-43.
    Kaaks R, Lukanova A, Kurzer MS. Obesity, Endogenous Hormones, and Endometrial Cancer Risk: a Synthetic Review. Cancer Epidemiol Biomarkers Prev. 2002;11(12):1531-43. PubMed PMID: 12496040.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Obesity, endogenous hormones, and endometrial cancer risk: a synthetic review. AU - Kaaks,Rudolf, AU - Lukanova,Annekatrin, AU - Kurzer,Mindy S, PY - 2002/12/24/pubmed PY - 2003/4/5/medline PY - 2002/12/24/entrez SP - 1531 EP - 43 JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology JO - Cancer Epidemiol. Biomarkers Prev. VL - 11 IS - 12 N2 - Endometrial cancer is a disease of the affluent, developed world, where epidemiological studies have shown that > or =40% of its incidence can be attributed to excess body weight. An additional proportion may be because of lack of physical activity. Alterations in endogenous hormone metabolism may provide the main links between endometrial cancer risk, and excess body weight and physical inactivity. Epidemiological studies have shown increased endometrial cancer risks among pre- and postmenopausal women who have elevated plasma androstenedione and testosterone, and among postmenopausal women who have increased levels of estrone and estradiol. Furthermore, there is evidence that chronic hyperinsulinemia is a risk factor. These relationships can all be interpreted in the light of the "unopposed estrogen" hypothesis, which proposes that endometrial cancer may develop as a result of the mitogenic effects of estrogens, when these are insufficiently counterbalanced by progesterone. In our overall synthesis, we conclude that development of ovarian hyperandrogenism may be a central mechanism relating nutritional lifestyle factors to endometrial cancer risk. In premenopausal women, ovarian hyperandrogenism likely increases risk by inducing chronic anovulation and progesterone deficiency. After the menopause, when progesterone synthesis has ceased altogether, excess weight may continue increasing risk through elevated plasma levels of androgen precursors, increasing estrogen levels through the aromatization of the androgens in adipose tissue. The ovarian androgen excess may be because of an interaction between obesity-related, chronic hyperinsulinemia with genetic factors predisposing to the development of ovarian hyperandrogenism. SN - 1055-9965 UR - https://www.unboundmedicine.com/medline/citation/12496040/full_citation L2 - http://cebp.aacrjournals.org/cgi/pmidlookup?view=long&pmid=12496040 DB - PRIME DP - Unbound Medicine ER -