Many people believe that estrogen causes breast cancer. They’ve heard this from their friends, or have read it in women’s magazines, or their doctors may even have told them that taking estrogen will increase their risk of breast cancer. And, if a woman is diagnosed with breast cancer, the first thing her doctor does is stop her hormone therapy. On top of this, estrogen is listed as a carcinogen on the American Cancer Society’s web page, right alongside arsenic, benzene, and mustard gas!
As a result, many women are reluctant to consider HRT because of this issue. But, does estrogen actually cause breast cancer? The answer is not straightforward.
- Many studies show that short-term use of estrogen alone (up to 5 years) does not increase one’s risk of breast cancer, and some (including the WHI) show a decreased risk.
- Studies of women on long-term HRT have been mixed, some showing a slight increased risk over time; others showing no effect.
- High-dose estrogen has actually been found effective in treating some women with advanced breast cancer.
- There is considerable data showing that women who do develop breast cancer, who have taken estrogen, have a lower risk of dying from it.
So what does this imply? To get a better understanding it is helpful to review how cancer develops in the first place. Every time one of our cells divides, its DNA duplicates providing the blueprint for each new cell. With surprising frequency this is not an exact process and an error can occur. In fact, it is these slight mishaps that can alter the characteristics of a cell and its future generations that is the basis for evolution. Some of these genetic “accidents” are beneficial, allowing an organism or creature to survive more successfully. But in some cases, these errors affect a cell’s self control – causing it to replicate in an unrestrained fashion, which is the hallmark of cancer. The cells keep dividing uncontrollably and eventually grow into a tumor.
The more frequently cells divide, the greater the likelihood of cancerous changes. Therefore, anything that promotes cell division promotes cancer. This is what likely occurs with hormone therapy. During a woman’s adolescent and reproductive years there is ongoing stimulation of the breast tissue by the presence of our female hormones. Once a woman reaches menopause, however, the breast cells become somewhat “dormant” and the breast ducts and glands shrink. If a woman takes HRT there continues to be some stimulation – so there is a higher probability that at some point a cancerous defect could occur.
You may question then, why don’t we see more cancer in younger women when hormone levels are quite high? That is a good question and is a little puzzling, but it is likely due to the fact that aging cells are more likely to undergo genetic mutations, and also are more susceptible to an external agent, such as radiation, that can initiate a cancerous change. It is also becoming increasingly apparent that synthetic progestogens may have properties that increase the risk of breast cancer. These were the agents used in the bulk of the studies that have shown a correlation between HRT and breast cancer.
Once a breast cell transforms into a malignant one, taking hormones can stimulate it and accelerate its growth. This is why women with a diagnosed cancer should not take hormones. This can also be a factor in studies that show a higher rate of cancer in women placed on HRT compared to those on a placebo. Both groups of women may have had the same number of cancers, but the cancers in the women on HRT may have grown faster and been diagnosed earlier. In these situations, HRT did not cause the cancers, but promoted them. In fact, it is estimated that in the WHI, over 90% of the cancers that appeared during the 5 years of the study likely were pre-existing.
So where are we in our current understanding?
Estrogen does not appear to cause breast cancer, but over time may promote its development because the breast cells remain active and dividing. However, studies have shown that women who do develop breast cancer while taking estrogen have a decreased risk of dying from it. This seems counterintuitive and research in the future will hopefully explain this. It may be that taking estrogen somehow prevents the more aggressive cases of breast cancer from developing.
It is not clear whether one form of estrogen is less likely to promote cancer than another. Estradiol, especially the transdermal preparations, appear to behave identically to our natural estrogen. Conjugated equine estrogens (such as Premarin), when taken without a progestogen, did not increase breast cancer in the WHI study. It is possible that this form of estrogen may have some anti-cancer properties.
Natural progesterone appears to have a neutral effect on the development of breast cancer. It may be the optimal choice if combined therapy is needed because some of the synthetic progestogens appear to increase the risk of breast cancer. However, it should be noted that this risk is very small, especially when HRT is taken for less than 5 years. In the WHI, women on combined hormone therapy increased their risk by one additional case of breast cancer per 1,000 women per year.
Finally, whatever the potential risk HRT plays in increasing breast cancer, it should be weighed against the potential benefits estrogen bestows – such as improvement in quality of life, protection against heart disease and osteoporosis, and other less known benefits such as a decreased risk of diabetes.
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