The perils of postmenopausal hormonal profile.

Last update and review: November 11, 2019.
 

Physiologically literate people have solid reasons to be optimistic about male reproductive hormones in mature men:

There is a piece of Physiological Literacy that should inspire optimism in every man who learns it. Indeed, it turns out that not only total testosterone, but even sperm production and quality remain largely unchanged in men during their eighth decade of life.

Physiological Literacy, Male Longevity: Even flawed medical textbooks represent overall correctly the fact the men at 80 continue producing the same amount of sperm, 100% of the maximal level. The same is true for testosterone in healthy.
Physiological Literacy, Male Longevity: Even flawed medical textbooks represent overall correctly the fact the men at 80 continue producing the same amount of sperm, 100% of the maximal level. The same is true for testosterone in healthy.

Unfortunately, the picture is a lot more complicated in women. Premenopausal women do better than men. Indeed, high estrogen levels in premenopausal women are considered “protective” from cardio-metabolic diseases. To support this statement, we could produce an endless number of references from the published literature. On very complex and overstudied subjects, however, references are often of inferior quality.

There are, however, several very informative graphs that we encountered in the published literature at different times. They seem to confirm the presumed protective action of estrogen.

The figure below is from a recent study of liver fat and liver iron content in a large group of the German population. In that study, the researchers used magnetic resonance imaging (MRI) technology to assess liver fat and liver iron content. The graph A on the figure below shows how women are “protected” from the accumulation of liver fat up to the age of 40. This “protection” may well be attributed to high estrogen levels in premenopausal women.

 

The graph A shows how women are “protected” from accumulation of liver fat up to the age 40. Sex-specifc relationships between, A, age and liver fat content (PDFF), B, waist-to-height ratio and PDFF, and, C, age and waist-to-height ratio. Graphs show functions of restricted cubic splines. From Kuhn, 2017.
After menopause, estrogen levels in females fall dramatically. While the levels of total estrogen in men remain unchanged. The graphs from a 1998 study by Khosla et al. provides a good illustration of this.
Serum total estrogen (A) and bioavailable estrogen (B) levels as a function of age among an age-stratified sample of Rochester men (solid lines, squares) and women (dashed lines, circles). See Table 1 for correlation coefficients with age.” From Khosla et al., 1998.

From studies in men, we also know that (from Finkelstien, 2012):

“Estradiol > 10 pg/ml and testosterone > 200 ng/dl were generally sufficient to prevent increases in bone resorption and decreases in bone mass density in men.”

A quick analysis of the above suggests that to prevent osteopenia, postmenopausal women should maintain their levels of estradiol at a certain level. One of the ways to achieve the required levels of estradiol is supplementation with exogenous estrogens.

At the same time, the dominant opinion among the researchers in cancer is that even slightly higher levels of estrogen in postmenopausal women cause an increased risk of breast cancer.

From James et al., 2011 (2):

“Recent studies suggest that elevated endogenous estrogens are associated with increased risk of both estrogen receptor-positive and receptor-negative breast cancers in postmenopausal women.”

Also, depressingly, (from Fuhrman et al., 2013 (1)):

“Breast cancer is the leading cancer diagnosis among women worldwide.”

Thus, it would seem that if we restore estrogen levels in postmenopausal women to the levels necessary to prevent osteopenia and osteoporosis, the risk of breast cancer would also increase. Physiologically illiterate PhD Colin Champ has no doubt about this.

At a lecture at IHMC in 2018, Colin Champ says “fat cells secrete estrogen” and this increases the risk of cancer in postmenopausal women:

18:14 “…we have mechanisms to explain that (an increase in the risk of breast cancer with an increase of body weight). Body fat secretes estrogen. Estrogen binds to cells and tells them to grow. It can cause breast cancer.”

At a lecture at IHMC in 2018, Colin Champ says "fat cells secrete estrogen".
At a lecture at IHMC in 2018, Colin Champ says “fat cells secrete estrogen” and increase the risk of cancer in postmenopausal women.

Why do we call Colin Champ illiterate? There are a lot of questionable or outright incorrect statements in his lecture. Here, we will only point out that Colin is at least careless with his words when he says “fat cells secrete estrogen”. Fat cells do not “secrete estrogen”. Fat cells, like many other tissues in human body, express an enzyme called aromatase. This enzyme converts testosterone, most of which is produced by female ovaries, into estrogens.

From Fuhrman, 2013 (11):

“aromatization of androgens accounts for most postmenopausal estrogens”

Further in his lecture, Colin Champ gives a gloomy picture of hormone replacement therapy in women. But we will leave a more detailed examination of hormone replacement therapy in women and debunking of Colin Champ for our future articles.

So, on one hand, insufficient levels of estradiol in postmenopausal women cause osteopenia and osteoporosis as well as a whole host of other serious diseases. Alzheimer is arguably one of them. On the other hand, if we maintain higher levels of estrogen, the risk of the most common cancer in women, breast cancer, increases.

What to do?

If you are a medical practitioner and can propose a reasonable approach to solving the dilema discussed above, we invite you to get in contact with us (see our Contact page). This will be of great help to our consulting clients.

People who need advice and/or want to support our research in this area, including our search for competent medical practitioners, are also invited to get in contact with us (see our Contact page).


Selected References:

1. Fuhrman et al., Nutr J. 2013; 12: 25.

2. James et al., Cancer Prev Res (Phila) 2011;4(10):1626–1635.

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