by Virginia Hopkins on 18/11/09 at 4:19 pm
Let’s have some straight talk and commonsense around the mammography controversy that has erupted this week. Thebottom line is, this controversy has nothing to do with concern over women’s health, and everything to do with money and politics.
 
On Monday (Nov 16), the U.S. Preventive Services Task Force (PSTF), part of the government’s Agency for Healthcare Research and Quality, released a report that recommends against routine mammography screenings for women ages 40 to 49. They recommend that women ages 50 to 74 have a mammogram every two years.
 
 
Women kick the PremPro habit and live to tell the tale.
 
In November 2006, research was released by cancer centers around the U.S. showing that breast cancer rates have dropped dramatically since 2002. Most doctors and researchers agree that the drop was created when millions of women suddenly stopped using hormone replacement therapy (HRT) after the Women's Health Initiative (WHI) study group announced, in the summer of 2002, that HRT users had an increased risk of breast cancer, stroke and heart disease. Estimates are that as many as 50 percent of women using HRT stopped taking it within six months after the WHI results came out.
How large was the drop in breast cancer? It depends on who's reporting the statistics and how they're interpreting the numbers. Most of the data came from the National Cancer Institute's (NCI) cancer registry.
 
 
It's pretty hard to get goose bumps reading a scientific review article, but as I was reading "Pregnancy, progesterone and progestins in relation to breast cancer risk," by a group of Italians led by Carlo Campagnoli, my hair stood on end. Here, in one eloquently worded, organized and argued paper was the same basic argument that Dr. Lee, Dr. Zava and myself made our 2002 book, What Your Doctor May Not Tell You about Breast Cancer about why progesterone is protective against breast cancer and progestins cause it. However, since the article was written four years after our book, it cited even more good research to prove the point.
 
 
Although male breast cancer only accounts for less than one percent of all breast cancer, the fact that it increased in the U.S. by 26 percent between 1973 and 1998 is cause for concern. Breast cancer tumors in men tend to be detected later in life and at a later and more aggressive stage. The research, done at The University of Texas M. D. Anderson Cancer Center, will be published in the July 1 issue of the journal Cancer. Men are also more likely to have estrogen receptor positive tumours.
 
Although it’s difficult to do good research on male breast cancer with such a small number of cases, there’s every indication that excess estrogen is the primary culprit in men’s breast cancer, as it is in women’s breast cancer. Past studies have shown that men with gynecomastia, an enlargement of the male breast, have a higher than normal oestrogen to androgen ratio, and others have hinted at an association between gynecomastia and breast cancer. The strongest risk factors for breast cancer in men are obesity and lack of exercise, which makes sense since fat cells in both men and women produce estrogen, and the more fat you have, the more estrogen you’ll make.
 
 
Carlo Campagnoli, , Chiara Abbà, Simona Ambroggio and Clementina Peris. First published 24 October 2005
Unit of Endocrinological Gynecology,“Sant’Anna” Gynecological Hospital, Corso Spezia 60, 10126 Torino, Italy 
Abstract
In the last two decades the prevailing opinion, supported by the “estrogen augmented by progesterone” hypothesis, has been that progesterone contributes to the development of breast cancer (BC). Support for this opinion was provided by the finding that some synthetic progestins, when added to estrogen in hormone replacement therapy (HRT) for menopausal complaints, increase the BC risk more than estrogen alone. However, recent findings suggest that both the production of progesterone during pregnancy and the progesterone endogenously produced or exogenously administered outside pregnancy, does not increase BC risk, and could even be protective. The increased BC risk found with the addition of synthetic progestins to estrogen in HRT seems in all likehood due to the fact that these progestins (medroxyprogesterone acetate and 19-nortestosterone-derivatives) are endowed with some non-progesterone-like effects which can potentiate the proliferative action of estrogens. The use of progestational agents in pregnancy, for example to prevent preterm birth, does not cause concern in relation to BC risk.
 
Presented at the European Progestin Club Scientific Meeting, Amsterdam, The Netherlands, 05 October, 2004.
 The Journal of Steroid Biochemistry and Molecular Biology 
Volume 97, Issue 5 , December 2005, Pages 441-450 
European Progestin Club Scientific Meeting: Progesterone and Progestins in Human Pregnancy and Breast Cancer