What is polycystic ovarian syndrome?

Polycystic ovarian syndrome is the condition where typically, small cysts form on a woman’s ovaries. As cysts aren’t always present, it is a condition in which hormonal dysregulation causes a variety of symptoms. It is a condition which affects roughly 10% of women within reproductive age and 70% of women with PCOS also have insulin resistance.

What are the types of PCOS?

– Anovulation (lack of ovulation), increased testosterone and insulin resistance

– Anovulation, increased testosterone and no issues with insulin resistance.

– Anovulation, normal testosterone levels, obesity and insulin resistance

– Normal ovulation, increased testosterone and milk insulin resistance.

– Normal ovulation, increased testosterone and no issues with insulin resistance.

As you can see PCOS is very diverse so there is no one cause and the condition is very individual.

What are the symptoms of PCOS?

• Less than 8 periods per year
• Irregular periods
• Amenorrhea for longer than 4 months (w/ pregnancy or menopause)
• Infertility
• Ovarian cysts
• Excessive bleeding
• Adult acne, back chest neck shoulders
• Hirsuitism (excess hair growth in places you don’t want!)
• Hair thinning
• Acanthosis nigricans
• Weight gain (especially around the middle)

What happens during the menstrual cycle?

Your ovaries contain your egg supply, which before maturation, are stored in follicles.

Follicular phase Days 1-13

The hypothalamus releases GnRH (gonadotropin releasing hormone) which stimulates the pituitary gland in the brain releases gonadotropins which is, a little LH (luteinising hormone) and FSH (follicle stimulating hormone) which travel to the ovaries via the blood stream. These hormones stimulate the follicles to mature and expand. During this, the follicles secrete oestrodial (oestrogen) and the uterus begins to build a thickening of blood vessels and tissue called the endometrium.

Ovulation phase Day 14

Once oestrodial reaches a certain level, the pituitary suppresses FSH and sends more LH to the follicles. LH stimulates progesterone to surge which triggers ovulation and the most mature follicle will rupture and release the ova. The remaining follicles will dissolve and the released ova will travel down the fallopian tube with the help of cilia (hair like fibres) ready for fertilisation.

Luteal phase 15-28

After that the progesterone is going to decline. The LH declines gradually which will still stimulate the follicle (now called the corpus luteum) slightly and the corpus luteum is now responsible for maintaining oestrogen and progesterone production for the thickening and integrity of the endometrium (within the uterus). Once progesterone and oestrogen decline menstruation begins again.

Menstrual stage 1-5

The uterus sheds the lining and menstrual fluid is released. Cramping can occur due to the contraction of the uterine and muscles to expel the fluid.

In PCOS that have cysts, follicles can remain as fluid filled sacks.

What is insulin resistance?

When an individual eats food, glucose levels rise and the pancreas (organ situated behind the stomach) releases a hormone called ‘insulin’ which has a lock and key mechanism to open up cells to allow glucose inside. Glucose is needed by the body for energy; organs like the brain rely heavily on glucose for a fuel source. In insulin resistance, the insulin receptors don’t receive insulin so this mechanism is reduced. This may be due to overuse or even a genetic factor. The pancreas however continues to release insulin and herein comes into effect with PCOS.

PCOS and Insulin

There are many ways that PCOS can develop including a genetic risk factor. Insulin however is multifaceted in it’s effects.

PCOS patients tend to present with high free testosterone levels. Increased insulin will stimulate the release of androgens like testosterone, androstenedione and DHEA from the ovaries and adrenal glands which could have an effect on follicular development and therefore halt ovulation.

Not only does insulin increase testosterone, but it decreases sex hormone binding globulin (SHBG) which is needed to bind and deliver hormones. Circulating hormones in the body are ‘bound’ or ‘free’ at a 4:1 ratio. Testosterone when elevated, can disrupt this balance and circulate freely. It can get inside hair follicles and cause acne by increasing sebum production and the presence of unwanted hair growth.

High insulin results in the additional increases in LH release and suppresses FSH which disrupts the ratio of LH to FSH.

In the last stage of follicular maturation there is supposed to be a surge in estradiol (cyclic oestrogen – which is the strongest form) driven by FSH. In PCOS there may be a negative feedback of the HPG axis (Hypothalamus, pituitary, gonads) where the presence of oestrone (acyclic oestrogen produced by fat tissue or adrenals) can trick the pituitary into thinking there is enough circulating estradiol and therefore no need to produce FSH. FSH’s role is to develop the follicle, so suppression is inhibitive of this step and LH is instead increased which is why PCOS patients may show high levels of LH.

Being overweight can potentiate the PCOS condition. When insulin doesn’t facilitate glucose entering the cell, it eventually builds up and has to be stored as adipose tissue (fat). Blood levels of triglycerides increases and HDL levels decrease. Insulin’s androgen stimulating effects on ovaries and adrenals will increase the presence of androgens in fat tissue. Here it can be converted to oestrone via the enzyme aromatase (aromatisation) and again, high levels of oestrone will tell the pituitary there is no need to release FSH for stimulation of follicles.

Insulin and a hormone called insulin-like growth factor (IGF-1) stimulate the MAP-K pathway which causes cell replication in the follicles leading to cyst formation.

So you see, there is a vicious cycle with PCOS and insulin which is hard to break. Insulin resistance can cause weight gain, and within the adipose tissue, further hormonal dis-regulation occurs.

If you think you may suffer from PCOS, see your doctor.