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Re: High Fat Diet During Pregnancy = Bad news?

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Hi folks:

This particular paper does not seem to be in PubMed yet. But here is another

paper by the same author, on a similar tack, published four years ago. For a

guess the new study, just published, was likely undertaken because of the

findings of this paper from 2006:

Ann N Y Acad Sci. 2006 Nov;1089:14-35.

Timing of dietary estrogenic exposures and breast cancer risk.

De Assis S, Hilakivi-e L.

Department of Oncology, town University, Research Building E407, 3970

Reservoir Road NW, Washington, DC 20057, USA.

Abstract

The same dietary component, such as fat or phytochemicals in plant foods, can

have an opposite effect on breast cancer risk if exposed in utero through a

pregnant mother or at puberty. Dietary exposures during pregnancy often have

similar effects on breast cancer risk among mothers and their female offspring.

High fat intake and obesity are illustrative examples: excessive pregnancy

weight gain that increases high birth weight is associated with increased breast

cancer risk among mothers and daughters. High body weight during childhood is

inversely linked to later breast cancer risk. The main reason why the age when

dietary exposures occur determines their effect on breast cancer risk likely

reflects the extensive programming of the mammary gland during fetal life and

subsequent reprogramming at puberty and pregnancy. Programming is a series of

epigenetic/transcriptional modifications in gene expression that can be

influenced by changes in the hormonal environment induced, for example, by diet.

Because epigenetic modifications are inherited by daughter cells, they can

persist throughout life if they occur in mammary stem cells or uncommitted

mammary myoepithelial or luminal progenitor cells. Our results indicate that the

estrogen receptor (ER), mitogen-activated protein kinase (MAPK), and the tumor

suppressors BRCA1, p53, and caveolin-1 are among the genes affected by

diet-induced alterations in programming/reprogramming. Consequently, mammary

gland morphology may be altered in a manner that increases or reduces

susceptibility to malignant transformation, including an increase/reduction in

cell proliferation, differentiation, and survival, or in the number of terminal

end buds (TEBs) or pregnancy-induced mammary epithelial cells (PI-MECs) that are

the sites where breast cancer is initiated. Thus, dietary exposures during

pregnancy and puberty may play an important role in determining later risk by

inducing epigenetic changes that modify vulnerability to breast cancer.

PMID: 17261753

Rodney.

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