Polycystic ovarian syndrome (PCOS) is an endocrine disorder that causes an increase in androgen hormone production in women. It affects 5 -10% of premenopausal women, and genetics play a large role in whether you have PCOS.
No one gene causes PCOS, but there are genetic variants in several hormonal pathways that increase the risk for it. Researchers estimate that PCOS is about 70% heritable.[ref] Understanding which genetic variants you carry may help you figure out the most effective way for you to manage your PCOS.
Members will see their genotype report below, plus additional solutions in the Lifehacks section. Join today.
Symptoms of PCOS
PCOS symptoms include irregular menstrual cycles, high androgen hormones, and cysts in the ovaries. Other hallmarks of PCOS include weight gain, insulin resistance, and elevated luteinizing hormone (LH) levels.[ref]
The excess of androgen hormones may cause facial or back hair as well as male pattern baldness. Skin problems include hormonal acne.
PCOS is a ‘syndrome’, meaning that not all symptoms have to be present to have PCOS.
Also, not everyone with PCOS has ovarian cysts — and not everyone with ovarian cysts has PCOS.[ref]
Let’s take a deep dive into what causes PCOS… and then look at your specific genetic susceptibility.
The three main physiological changes that we will look at include:
- hormone dysregulation
- insulin resistance and hyperinsulinemia
- circadian rhythm changes
Hormonal Dysregulation in PCOS:
Before diving into what goes wrong with PCOS, let’s first look at the hormonal processes that generally go on during a menstrual cycle.
The start of menstruation (your period) is considered the beginning of the menstrual cycle. Estrogen and progesterone levels are both low at this point.
Follicle-stimulating hormone (FSH) rises a bit, causing the development of the new follicle (containing an egg) in the ovary. The follicle produces estrogen, causing estrogen to rise over the next week.
Around day 12 – 14, ovulation occurs, releasing the egg. During ovulation, the pituitary gland releases luteinizing hormone (LH) and FSH at higher levels. This spike in LH and FSH hormone levels coincides with a fall in estrogen levels and an increase in progesterone. The follicle that has released the egg cell will form a corpus luteum, a hormone-secreting structure that produces high levels of progesterone.
What does your body need to make all these reproductive hormones? The molecular basis for these steroid hormones is cholesterol, which is converted into pregnenolone, which is the precursor for other hormones.
There are two ways that pregnenolone can be converted into other hormones. The enzyme CYP17A1 can eventually convert pregnenolone into DHEA. Alternatively, the enzyme 3B-HSD can convert pregnenolone into progesterone.
DHEA can then be converted into testosterone or other androgens — or it can convert to estrone and other estrogens.
Insulin resistance and androgen hormone production:
A number of different hormone pathways can be involved in PCOS. Androgen hormones in women usually convert to estrogen. Higher estrogen levels feedback to the pituitary gland, causing an increase in LH (luteinizing hormone) during ovulation.[ref]
Thus, when levels of androgen hormones are too high and not appropriately converted to estrogen, it interferes with ovulation or the release of the egg. It causes what looks like cysts in the ovaries when the immature egg follicles aren’t released.
Women with PCOS often have problems with insulin resistance and higher blood glucose levels.
Insulin increases the production of androgens in women. For this reason, women’s increased testosterone levels show associations with insulin resistance. The system works both ways – giving women testosterone can increase insulin resistance. These hormones are all interrelated. In the ovaries, insulin stimulates the production of testosterone.[ref][ref]
About 20 – 30% of women with PCOS have high DHEA levels. DHEA is a precursor for androgens and estrogens.[ref]
Circadian rhythm disruption as a cause of PCOS:
New research shows that circadian rhythm disruption may play a key role in causing PCOS.[ref]
Quick background: What is circadian rhythm?
Your circadian rhythm is the built-in 24-hour clock that drives many processes in the body. The first thing that pops to mind is your sleep/wake cycle, but your body’s circadian clock is far more than just sleep.
Over a 24-hour period, your body’s metabolic and cellular functions rise and fall. Some processes take place at night, and others during the day. For humans (and almost all animals), this 24-hour rhythm is synchronized by light.
Circadian rhythm disruption is tied to many chronic diseases, including obesity, heart disease, and dementia. Think about what jet lag feels like — your brain’s not working right, your stomach is not feeling right, and everything’s just out of sync.
Circadian disruption on a smaller scale happens each time you stay up later than usual in an area with bright lights. This shift is called social jet lag.
The body’s circadian clock is driving the rise and fall of some key proteins — and these oscillations are synchronized by light. Electric lighting has been around now for more than a century, but that is a drop in the bucket compared to the human and animal history of only having sunlight or firelight. Thus, it is easy to see how circadian rhythm disruption is a modern mismatch of lifestyle vs. innate biological function.
Back to PCOS:
Researchers have used animal models to show that circadian rhythm disruption can cause the same alterations to hormones as are seen in PCOS. For a couple of decades, it was known that altering circadian rhythm could alter insulin sensitivity and androgen production. But this new research lays out and produces the PCOS phenotype simply by altering circadian rhythm.
The researchers used changes in light to show that alterations to the circadian clock genes caused the downstream effects on the hormones involved in PCOS.[ref]
Pregnancy with PCOS:
Women with PCOS are more likely to have problems with ovulation, which is a common cause of infertility.
In-vitro fertilization (IVF) is a common solution for PCOS infertility.[ref] There are also medications that your doctor can prescribe that alter your hormones at the right time in your cycle.
Overall statistics are hard to come by regarding the percentage of women with PCOS and infertility. Larger population studies point to women with PCOS being more likely to have fewer children but having similar overall fertility rates when looking only at women with 1 – 2 children.[ref]
Is PCOS reversible with diet?
There are a lot of websites that claim to have a dietary solution for PCOS symptoms. Most focus on healthy foods, and some claim a ketogenic diet works.[article][article]
Other medical-based websites claim that all you can do is manage the symptoms of PCOS and that there is no cure.[article]
I’ll add specific recommendations in the Lifehacks section below that integrate genetics with some research-based suggestions for diet, supplements, and exercise.
One thing that is not clear is whether weight loss (through whatever type of diet) will cure PCOS. A ‘risk factor’ for PCOS is obesity, so your doctor may tell you to lose weight. With this in mind, research points to weight gain is caused by PCOS instead of obesity as a cause of PCOS. Chicken or the egg.[ref]
Insulin sensitivity, rather than fad diets, may be better for managing PCOS through nutrition.
Hashimoto’s and PCOS:
Researchers have found autoimmune thyroid diseases, such as Hashimoto’s thyroiditis, at much greater levels in women with PCOS. Thus, if you or your doctor suspects that you have a thyroid problem, it is recommended to also test for autoimmune thyroid antibodies.[ref]
Related article: Thyroid hormones and your genes
Genetics and PCOS:
Twin studies show that PCOS is about 70% hereditary, with the rest due to various environmental or dietary causes.
PCOS is considered an ‘evolutionary paradox’ since it is common (10% of the population), highly heritable, and also can cause infertility. Scientists want to know why the genetic variants involved in PCOS have continued to be passed on to a large part of the population – especially since evolutionary theory says that it should be weeded out. Some theories on this include that women with PCOS are more ‘metabolically thrifty’ and likely to live through a famine. Others theorize that women who only have a few children are better mothers and the children are more likely to survive.
Evolutionary theorizing aside, understanding which genetic variants you carry may help you to find the right solution for your PCOS symptoms.
PCOS Genotype Report
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LHCGR gene: luteinizing hormone receptor
Variants in the luteinizing hormone/choriogonadotropin receptor (LHCGR) gene are associated with an increased risk of PCOS and variations in the insulin response. The LHCGR is the receptor for both luteinizing hormone (LH), which triggers ovulation, and human chorionic gonadotropin (hCG), which maintains pregnancy.
Check your genetic data for rs13405728 (23andMe v4, v5; AncestryDNA)
- A/A: typical
- A/G: increased insulin levels in PCOS, but decreased overall risk of PCOS in Asian pops
- G/G: increased insulin levels in PCOS[ref], but decreased overall risk of PCOS in Asian pops.[ref]
Members: Your genotype for rs13405728 is —.
Check your genetic data for rs2293275 (23andMe v4, v5; AncestryDNA):
- T/T: increased risk (3 – 4-fold) of PCOS[ref][ref][ref]
- C/T: increased risk for PCOS
- C/C: typical risk of PCOS
Members: Your genotype for rs2293275 is —.
DENND1A gene: Androgen hormone synthesis
Too much DENND1A increases androgen hormone synthesis in the cells in the ovaries.
Check your genetic data for rs10818854 (23andMe v4, v5; AncestryDNA):
Members: Your genotype for rs10818854 is —.
FSHB gene: Follicle-stimulating hormone
The luteinizing hormone to follicle-stimulating hormone (LH:FSH) ratio is important in PCOS. Higher LH:FSH ratio can disrupt ovulation.
Check your genetic data for rs11031006 (23andMe v4, v5; AncestryDNA):
- A/A: increased LH levels[ref]
- A/G: increased LH levels
- G/G: typical LH levels
Members: Your genotype for rs11031006 is —.
FSHR gene: receptor for FSH
The FSHR gene codes for the follicle-stimulating hormone receptor.
Check your genetic data for rs6166 (23andMe v4, v5; AncestryDNA):
Members: Your genotype for rs6166 is —.
ADIPOQ gene: regulating insulin
Adiponectin (ADIPOQ) is created by fat cells and helps to regulate energy metabolism and insulin.
Check your genetic data for rs2241766 (23andMe v4, v5):
- T/T: (most common genotype) higher (1.9x) risk of PCOS[ref]
- G/T: lower risk of PCOS (compared to T/T)
- G/G: lower risk of PCOS
Members: Your genotype for rs2241766 is —.
Check your genetic data for rs1501299 (23andMe v4, v5; AncestryDNA):
- T/T: decreased risk of PCOS[ref]
- G/T: typical risk of PCOS
- G/G: typical risk of PCOS
Members: Your genotype for rs1501299 is —.
MTNR1B gene: melatonin, insulin resistance, and circadian rhythm
The melatonin receptor 1B is part of regulating your body’s circadian rhythm. Melatonin is essential in regulating insulin release at night and can play a significant role in fasting glucose levels.
Check your genetic data for rs10830963 (23andMe v4, v5; AncestryDNA):
- C/C: typical
- C/G: increased risk of higher insulin levels; PCOS
- G/G: increased risk of higher insulin levels; PCOS[ref][ref]
Members: Your genotype for rs10830963 is —.
TNF gene: encodes TNF alpha, an inflammatory cytokine
Check your genetic data for rs1799964 -1031T>C (23andMe v4, v5; AncestryDNA):
- C/C: (usually) higher TNF-alpha levels[ref][ref], increased risk of PCOS[ref]
- C/T: somewhat higher TNF-alpha levels, increased risk of PCOS
- T/T: typical – generally not at higher risk for inflammatory diseases
Members: Your genotype for rs1799964 is —.
Check your genetic data for rs4645843 (23andMe v4; AncestryDNA):
- T/T: increased risk of PCOS[ref]
- C/T: increased risk of PCOS
- C/C: typical risk
Members: Your genotype for rs4645843 is —.
Lifehacks
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Updated May 15, 2020