Polycystic ovary syndrome

Video summary

Polycystic ovary syndrome or just PCOS, refers to a set of symptoms due to excessive androgen production in women. Signs and symptoms of PCOS include irregular or no menstrual periods, heavy periods, excess body and facial hair, acne, pelvic pain, trouble getting pregnant, and patches of thick, darker, velvety skin. Associated conditions include type 2 diabetes, obesity, obstructive sleep apnea, heart disease, mood disorders, and endometrial cancer. Management for PCOS may involve lifestyle modifications such as diet and exercise, hormone therapy, and medications.

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Introduction0:00–0:34

Before we begin, a quick terminology update. In 2026, an international group of patient advocacy and professional organizations introduced a new name for the condition previously known as polycystic ovary syndrome or PCOS.
PCOS is transitioning to polyendocrine metabolic ovarian syndrome, or PMOS. The new name was introduced because the condition involves much more than just the ovaries and can affect body weight, metabolism, mental health, skin, and reproductive function.

Physiology0:34–3:22

The old name emphasized ovarian cysts rather than the broader endocrine and metabolic features of the condition, which may have contributed to misunderstanding, delayed diagnosis, and inadequate treatment.
As you watch the video, keep in mind that any references to PCOS refer to the condition newly named PMOS. The underlying disease process and management discussed in this video remain the same.
In polycystic ovary syndrome, poly means many, and cystic refers to cysts. So you might think that having many ovarian cysts is a crucial part of polycystic ovary syndrome.
But while some people with polycystic ovarian syndrome do have ovarian cysts, ovarian cysts are no longer a necessary characteristic of the condition.
Instead, polycystic ovarian syndrome is a dysfunction in the hypothalamic pituitary ovarian axis. Which are the hormones that regulate the menstrual cycle.
A normal menstrual cycle can be divided into two phases the follicular phase, which takes place before ovulation, and the luteal phase, which takes place after ovulation.
During the follicular phase, the hypothalamus secretes gonadotropin releasing hormone, or GNRH. GNRH makes the anterior pituitary gland secrete two other hormones called gonadotropins in roughly equal amounts which it releases in pulses.
One of gonadotropins is a luteinizing hormone or LH. The other is a follicle stimulating hormone or FSH.
LH and FSH travel to the follicles in the ovaries. The follicles are small clusters of tca and granulosa cells that protect the developing oocyte or egg.
The Theca cells develop LH receptors which allow them to bind to LH and in response, they secrete a hormone called androstidione.
Granulosa cells develop FSH receptors, which allow them to bind to FSH and produce an enzyme called aromatase, which converts the androstidione to 17 beta estradiol, a member of the estrogen family.
As follicles grow, the level of 17 beta estradiol in the blood increases, and it acts as a negative feedback signal. That is, it tells the pituitary to secrete less FSH.
Less FSH in the blood means there's only enough to stimulate one follicle. The follicle that has the most FSH receptors grows the quickest and becomes the dominant follicle.

Pathophysiology3:22–5:30

At this point, about midway through the follicular phase, the granulosa cells also begin to develop LH receptors. As that happens, the dominant follicle keeps secreting estrogen, and the rising estrogen levels make the pituitary more sensitive to the pulsatile action of GNRH from the hypothalamus.
Blood estrogen levels start to climb, and now the estrogen from the dominant follicle becomes a positive feedback signal.
That is, it makes the pituitary secrete a whole lot of FSH and LH in response to GNRH. This happens a day or two before ovulation, and the massive surge of FSH and LH binds to the granulosa and theca cells, which help facilitate rupture of the ovarian follicle and release of the oocyte, while the rest of the theca and granulosa cells degenerate and die off, and now fully matured ooocyte breaks away from the dominant follicle and pops out of the ovary.
The egg begins its journey down the fallopian tube to the uterus, and the luteal phase begins. Now, while polycystic ovarian syndrome affects the whole menstrual cycle, it really starts with a breakdown in this follicular phase.
In polycystic ovarian syndrome, the anterior pituitary makes too much LH, at least double the amount as FSH. Excessive LH causes the Thecus cells to produce excess amounts of androstyndium, way too much for those granulosis cells to convert.
The excess androstyndion flows into the blood. And some of it gets converted into estrone by aromatase in fat or adipose tissue.
Estrone, like estradiol, is a member of the estrogen family, stopping the anterior pituitary from releasing FSH. Because LH levels are really high, there is no LH surge to trigger the dominant follicle to break away from the ovary, so it may remain there, appearing as a cyst, or it may degenerate with the other follicles.

Symptoms5:30–6:16

The bottom line is that ovulation doesn't occur. Now what causes the anterior pituitary to make so much LH is not well understood, but because the majority of those with polycystic ovarian syndrome have insulin resistance, it's thought that insulin resistance somehow disrupts the menstrual cycle.
Insulin resistance happens when the cells in your liver, adipose tissue, and muscles become insensitive to insulin and the cells become less willing to pull in glucose from the bloodstream, and this can develop into diabetes mellitus, not when to give up.
The persistent pancreas secretes more and more insulin until it can get those cells' attention. As a consequence, some people develop hyperinsulemia or too much insulin in the blood.
Theca cells have insulin receptors, so excess insulin can bind to the Theca cells, causing them to grow and divide, and over time that means having too many LH receptors.

Diagnosis6:16–6:38

It's thought that the hypothalamus responds by speeding up its pulses of GNRH so that more LH is made by the pituitary. High levels of androsthenone from polycystic ovary syndrome can cause hirsutism or hair growth on the chin and upper lip, chest, and back.

Treatment6:38–7:26

It can also lead to male pattern baldness, meaning a thinning of the hair starting from the crown of the head, as well as acne on the face, chest, and back.
Lack of ovulation causes amenorrhea, meaning an absence of menstruation, or oligomemenorrhea, meaning infrequent and irregular menstrual periods, both of which can lead to infertility.
Those with insulin resistance may be overweight or obese and may develop acanthosis nigricans, which are dark velvety patches in the creases of the neck, groin, and underarms.
A diagnosis of polycystic ovarian syndrome typically is made when there's a high ratio of luteinizing hormone to follicle stimulating hormone, as well as high levels of androstenion in the blood.

Review7:26–8:56

A pelvic ultrasound may reveal follicles on one or both ovaries that look like small cysts, but these aren't necessary for the diagnosis.
Weight loss, especially by eating foods with a low glycemic index, can help reduce insulin resistance and can help improve the symptoms of polycystic ovary syndrome.
Metformin can also increase insulin sensitivity. Spironolactone can be used to treat hirsutism, but because it's teratogenic, some form of contraception is required.
Oral contraceptives can also help regulate the menstrual cycle. Clomiphene citrate can help induce ovulation.
A procedure called ovarian drilling, which involves puncturing a cystic ovary, can induce ovulation, though it's not recommended for everyone because it can damage the ovary and it doesn't resolve the overall hormonal imbalance.
All right, as a quick recap, polycystic ovary syndrome is marked with symptoms related to excess androgen production, like hirsutism, acne, insulin resistance, and irregular or absent menstrual cycle.
Polycystic ovary syndrome is associated with an overproduction of the luteinizing hormone by the pituitary gland and also with insulin resistance.