How does hormone replacement therapy (HRT) increase the risk for cancer?

The explanation for why hormone replacement therapy (HRT) seems to promote cancer lies in the fact that hormones work as chemical signals. The body produces them in a gland, such as the pituitary gland, and sends them out in the bloodstream to give instructions to other parts of the body. In order for these other parts of the body to "hear" the signal, they must have a specifically attuned place -- a receptor -- where the chemical signal is able to attach and transmit its message.

Just as important as estrogen are the estrogen receptors. Without them, the body wouldn't be able to respond to the signal. The subject of estrogen and estrogen receptors is a complicated one, and many types of estrogen receptors that have been identified so far.

For the purposes of our discussion, there are three that I consider important to understand. For simplicity's sake I will call them estrogen-1 (E1), estrogen-2 (E2), and estrogen-3 (E3) receptors. Let's assume that E1 receptors are located in breast and uterine tissue and are linked to the development of female traits such as breast enlargement, menstruation, and a high-pitched voice.

The interaction between estrogen and the E1 receptors appears to promote breast, ovarian, and uterine cancers, apparently by initiating tissue growth. Estrogen-2 receptors are linked to the cardiovascular system, and in test-tube studies, these receptors have made it possible for estrogen to have a protective cardiovascular effect. Finally, E3 receptors allow bones to strengthen.

When a woman takes estrogen supplements after her body has stopped producing high levels of estrogen, she is extending the period of her body's exposure to estrogen, and this increases her risk of E1 receptor stimulation and breast and uterine cancer.

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