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Estrogen and Progesterone 101

Estrogen and progesterone levels change in perimenopause. The declining supply of eggs in the ovaries initiates these changes to hormonal patterns.

What is a Hormone?

Hormones, like estrogen and progesterone, are chemical messengers that are made in an endocrine gland (e.g. the ovary, the pituitary gland) and act either on another endocrine gland or an organ. A hormone often stimulates another cell to make more or less of a hormone. In this way, hormones are part of a vast cellular communication system in our bodies.

Estrogen, progesterone, FSH and LH govern the menstrual cycle.

Where is it made?

Primarily in the ovaries, but also in the adrenal glands and fat tissue.

Where does it work?

There are over 400 estrogen receptor sites throughout the body, which is why the effects of low or high estrogen have significant repercussions. Receptor sites include the brain, muscles, gut, uterus, ovaries, vagina, breasts, eyes, heart, lungs, and blood vessels.

What does it do?

Estrogen does many things, but think of estrogen primarily as a growth promoter affecting the many receptor sites. Estrogen fosters the growth of the uterine lining each month, promotes growth in breast tissue, increases the water content of your skin, and increases blood flow.

When there is not enough estrogen, which begins in the later phase of perimenopause, women experience symptoms like vaginal dryness and dry skin. When there is too much estrogen — which is characteristic of the early phase of perimenopause — women experience breast tenderness, headaches, cramps, and heavy flow.

Where is it made?

It is made in the ovaries while a woman is still ovulating. After menopause, it’s made in the adrenal glands in smaller quantities.

Where does it work?

Progesterone receptors are found throughout the body, in all the same places estrogen receptors are present. The brain, lungs, skin, eyes, breasts, and bones all have progesterone receptors.

What does it do?

Progesterone has two primary roles: first, each month, progesterone serves to thicken the endometrial lining following ovulation in preparation for a potential pregnancy.

Second, it acts as an inhibitor and maturation factor to estrogen’s growth-promoting actions. Each month during a normal cycle, estrogen encourages the growth of the endometrial lining. In the absence of a fertilized egg, progesterone gives the signal to stop this growth, which leads to a period.

Whereas estrogen causes the production of cervical mucus that enhances the ability of sperm to reach an egg, progesterone stops the production of this mucus. And where estrogen is said to have an excitatory effect on the brain (making us possibly anxious or irritable when there is too much), progesterone is said to be calming. In summary, estrogen causes the growth of cells, and progesterone causes those cells to mature to their fully functioning state.

Where is it made?

Follicle stimulating hormone (FSH) is released from the anterior pituitary gland, a part of the endocrine system, located in the brain.

Where does it work?

In the ovaries.

What does it do?

Follicle-stimulating hormone, or FSH, stimulates the growth of follicles in the ovary during the first half of the menstrual cycle, which is aptly called the “follicular phase.” Between 3-30 follicles typically mature each month. Each of the maturing cells produces estrogen, which causes estrogen levels to rise in the first half of the cycle.

Where is it made?

Luteinizing hormone, or LH, is found in the anterior pituitary gland, which is a part of the endocrine system and located in the brain.

Where does it work?

In the ovaries.

What does it do?

The buildup of estrogen in developing follicles causes the rise of LH. At peak levels, LH triggers ovulation at midcycle and facilitates the development of the corpus luteum — the burst sac from which a mature egg is released. The corpus luteum is the main source of progesterone production and produces estrogen for the second part of the cycle.

Note: Both men and women make all three sex hormones (testosterone, estrogen and progesterone) — just in different quantities.

Hormones act all over our bodies — far beyond our ovaries!

We were amazed to learn how many places in the body have active receptor sites for estrogen and progesterone. When these hormones are fluctuating, it’s no wonder it can cause such a wide array of symptoms, and we feel off-kilter!

MEET HORMONE WOMAN
why some women experience symptoms as hormones change

When the number of eggs left in the ovary reaches a certain level, changes to hormonal patterns start.

Many of us never fully consider the whole history of our follicle (egg) supply — how many eggs we start with and how many naturally mature or die each month. It turns out that when a certain level of eggs remain, it causes hormonal patterns to start to change.

Approximate Egg Reserve Across the Lifespan

A female baby is born with 1,000,000 eggs.1

At puberty, there are about 500,000 eggs.2,4,5

By the late 30s, there are an average of between 10,000 and 50,000 eggs left.2,4,5

A low level of follicles (eggs) kicks off hormonal changes around age 37.3

The median age at menopause is 52.5 years in North America.6

REFERENCES
  1. Block, E. A quantitative morphological investigation of the follicular system in newborn female infants. Acta Anat (Basel). 1953; 17(3):201-6.
  2. Sonya M. Schuh-Huerta, Nicholas A. Johnson, Mitchell P. Rosen, Barbara Sternfeld, Marcelle I. Cedars, and Renee A. Reijo Pera. Genetic markers of ovarian follicle number and menopause in women of multiple ethnicities. Hum Genet. 2012 Nov; 131(11): 1709–1724. Published online 2012 Jun 13. doi: 10.1007/s00439-012-1184-0
  3. Faddy MJ, Gosden RG, Gougeon A, Richardson SJ, and Nelson JF. Accelerated disappearance of ovarian follicles in mid-life: implications for forecasting menopause. Hum Reprod. 1992 Nov; 7(10):1342-6.
  4. Hansen KR, Knowlton NS, Thyer AC, Charleston JS, Soules MR, Klein NA. A new model of reproductive aging: the decline in ovarian non-growing follicle number from birth to menopause. Hum Reprod. 2008 Mar; 23(3):699-708.
  5. Richardson SJ, Senikas V, Nelson JF. Follicular depletion during the menopausal transition: evidence for accelerated loss and ultimate exhaustion. J Clin Endocrinol Metab. 1987 Dec; 65(6):1231-7.
  6. Santoro N, Johnson J. Diagnosing the Onset of Menopause. JAMA. 2019 Aug 27;322(8):775-776.
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