polycystic ovarian syndrome

Concerned About PCOS? Know These Common Myths

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pcosAs a medical student, one of the conditions that was hardest for me to get my head around was PCOS (polycystic ovarian syndrome). It took me several years of advanced training to understand the ins and outs of the syndrome.

PCOS is a complex hormonal condition that involves multiple organs systems. It’s is a clinical diagnosis, meaning that doctors diagnosis patients with PCOS based on symptoms – not on a specific lab test that is “positive of negative” for the condition. PCOS is diagnosed if a woman has two or more of the following symptoms:

  • Signs of too much male hormone (excess dark hair growth on chin, cystic acne or elevated  testosterone on blood tests)
  • Menstrual cycles > 35 days apart
  • Enlarged ovaries on ultrasound

As hard as it was to grasp in med school, and as challenging as it is to explain it to my patients in a 10-minute office visit, it’s not surprising that there are a lot of misunderstandings about PCOS floating around.

Myth #1 “PCOS is caused by your ovaries”

PCOS is caused by a full body hormonal miscommunication – the actual polycystic ovaries are merely a symptom. There are many different metabolic issues going on that contribute to PCOS. The brain sends the ovary mixed signals causing it to secrete excess male hormones, which affects the delicate fluctuations of female hormone that trigger ovulation. At the same time, fat cells contribute to the problem by resisting insulin, triggering the body to make excess insulin when carbs are eaten. This insulin increase not only prompts the ovary to produce too much male hormone, but also causes weight gain. The ovaries can’t manage to ovulate because the hormones are all wrong.

Myth #2 “Women with PCOS are infertile”

Women with PCOS can have difficulty getting pregnant, but the infertility associated with PCOS is often easy to treat. Women who have PCOS and are overweight can often begin to ovulate regularly with very modest weight loss of even 10% of their body weight. Medication can also help; 50% of women with PCOS will conceive with clomiphene treatment (an inexpensive ovulation-inducing pill). Of women who conceive on clomiphene, the majority conceive within 4 months, so it should not be taken for an extended amount of time.

Myth #3″PCOS causes pain”

During a normal menstrual cycle, the chosen egg of the month begins to grow within a small follicle cyst on the ovary. When ovulation occurs, the egg escapes the cyst and makes a run for the fallopian tube, and its former cyst usually dissolves over time. In PCOS the ovaries are trying to ovulate but because of the body’s confused hormones, the ovulation cyst gets stuck and is unable to fully develop to the point it can spit out the egg, hence the ovary becomes swollen with underdeveloped cysts. These cysts cause the ovaries to become enlarged, but the cysts do not usually rupture or cause pain.

Myth #4 “Women with PCOS are overweight”

PCOS is often associated with obesity, but not always. At one time, PCOS was defined as having all three symptoms plus obesity, but we now recognize that there are different “types” of PCOS. You only need two of the three symptoms of PCOS to have the condition. The treatment of PCOS is based on the sub-type and your goal (for example, birth control pills do an excellent job of controlling the irregular cycles and treating the abnormal male hormone of PCOS, but would not be the best option for someone try to conceive). For overweight PCOS patients, a low carb diet with regular exercise is recommended. (My personal recommendation is the nutrition plan in  The Obesity Code by Dr. Jason Fung)

Myth # 5 “PCOS patients have very high risk pregnancies”

I often have patients worry that since PCOS makes it challenging to get pregnant, it will also put them at super high risk during pregnancy. Once pregnant, PCOS patients are at an increased risk of gestational diabetes and high blood pressure, but most go on to have normal pregnancies. They do not have an increased risk of miscarriage as previously thought.

Around 10% of women meet the criteria for PCOS worldwide and our understanding of the condition and treatments has evolved over the last 20 years. If you have symptoms of PCOS, don’t get discouraged by the myths. Instead, talk to doctor about customized treatment of your condition.

Children with Psoriasis Carry High Comorbidity Risks

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Children with psoriasis are significantly more likely to develop obesity, hyperlipidemia, hypertension, diabetes, metabolic syndrome, polycystic ovarian syndrome, liver disease, and elevated liver enzymes than are children without the disease, according to a retrospective review of insurance claims data.

These risks are independent of obesity status: in non-obese children with psoriasis, the risk of comorbidities was 40% to 75% higher than in children without psoriasis, reported Megha M. Tollefson, MD, of the Mayo Clinic in Rochester, MN, and colleagues. But even in children without psoriasis, obesity was a much stronger contributor to comorbidities.

“In recent years, it has become increasingly clear that psoriasis is more than a ‘skin-deep’ condition and that it may frequently be associated with other systemic comorbidities, even in children,” the researchers wrote online in JAMA Dermatology. “While the association in adult patients is well established, the patterns and predictors of the risk of comorbidities in children with psoriasis are still not clear.

“There is mounting evidence that children with psoriasis are more likely to be obese than children without psoriasis, but this finding begs the question of whether the systemic comorbidities that are seen in children with psoriasis are attributable to obesity, or whether psoriasis is actually an independent risk factor for these comorbidities.”

In this study of claims from Optum Laboratories Data Warehouse, a Massachusetts-based Mayo Clinic partner, the researchers studied de-identified records of 29,957 children with psoriasis (affected children) and 29,957 children without psoriasis, matched for age, sex, and race, from 2004 through 2013.

The children, all under age 19, were divided into four groups:

  • Non-obese without psoriasis (reference cohort)
  • Non-obese with psoriasis
  • Obese without psoriasis
  • Obese with psoriasis

The average age of the children was 12.0, and 53.5% of the total were girls. At baseline, more affected children were obese than non-obese (2.9% versus 1.5%; P<0.001).

The average follow-up period for both groups was about 3 years. During this time, pediatric psoriasis patients were significantly more likely to develop comorbidities than those without psoriasis, with non-alcoholic liver disease, diabetes, and hypertension showing the highest risks.

Among non-obese children, the risk of comorbidities was significantly higher in those with psoriasis; these included elevated lipid levels (HR 1.42), hypertension (HR 1.64), diabetes (HR 1.58), metabolic syndrome (HR 1.62), polycystic ovarian syndrome (HR 1.49), non-alcoholic liver disease (HR 1.76), and elevated liver enzyme levels (HR 1.46).

Even in children without psoriasis, obesity was a much stronger contributor to comorbidities, carrying an 18-fold higher risk of non-alcoholic liver disease, a 16-fold higher risk of metabolic syndrome, a seven-fold higher risk of hypertension, a six-fold higher risk of hyperlipidemia, an almost three-fold higher risk of diabetes, and a 2.3-fold higher risk of elevated liver enzyme levels than the reference group; there was also a six-fold higher risk of polycystic ovarian syndrome in girls.

When the researchers analyzed the interaction between obesity and psoriasis, they found none, suggesting that while both obesity and psoriasis contribute to the development of pediatric comorbidities, the effect is additive, not exponential.

Asked for her perspective, Amy Paller, MD, chair of the Department of Dermatology at Northwestern Medicine Feinberg School of Medicine in Chicago, who was not involved with the study, noted that several studies have clearly demonstrated the association of obesity and pediatric psoriasis, and a large recent study also linked a high waist circumference to height ratio to more severe pediatric psoriasis. “The association of a variety of other ‘metabolic syndrome’ comorbidities has been controversial, however, and whether it is the obesity or psoriasis itself that increases the risk remains unknown.

“While there are issues with the use of a claims database, especially given the frequent misdiagnosis of psoriasis by non-dermatologists, several metabolic-related disorders were shown to be significantly increased in risk,” she said, adding that the fact that the associations were seen even among non-obese psoriasis patients suggests that early systemic intervention might lower risks.

The study has several limitations, Tollefson and colleagues noted. For example, it relies on data from administrative claims, and the diagnoses were not confirmed by medical record review. Also of possible concern are undercoding and misclassification of comorbidities. Extremely obese children would be more likely to have a corresponding obesity code than those with a body mass index of 25 to 40, the researchers added. “The lower prevalence of obesity in our cohort than in some others suggests that obesity may have been undercoded as a whole, with the resulting contribution from psoriasis being slightly overestimated.”

In addition, systemic medications used to treat psoriasis potentially might have influenced the risk of some comorbidities.

Risk for PCOS in women with European ancestry linked to genetic variants.

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After discovering three loci that present a risk for polycystic ovary syndrome in Han Chinese women in a genome-wide association study, researchers replicated risk variants and found that women with European ancestry were also at risk for the disorder.

“Previous studies have demonstrated association between variants in more than 70 candidate genes and risk for PCOS, although the majority of these have not been replicated,” the researchers wrote.

Corrine K. Welt, MD, a researcher in the reproductive endocrine unit at Massachusetts General Hospital, and colleagues conducted a case-control study at deCODE Genetics in Iceland and two academic medical centers in the United States.

They examined 376 Icelandic women, 565 women in Boston and 203 women in Chicago, all of whom were diagnosed with PCOS according to NIH criteria. Control groups were 16,947 women in Iceland, 483 women in Boston (aged 18-45 years with regular menses between 21 and 35 days and no hyperandrogenism) and 189 (healthy reproductive-aged women, aged at least 18 years) in Chicago.

Researchers replicated two strongly correlated Han Chinese PCOS risk variants on chromosome 9q33.3: rs10986105[C] (OR=1.68; P=.00033) and rs10818854[A] (OR=1.53; P=.0019) in samples of European ancestry.

Other risk variants at alternate chromosomes were not related to PCOS, the researchers wrote. Additionally, the same allele of rs10986105[C], which increased the risk for PCOS, also put women without PCOS from Iceland at risk for hyperandrogenism and displayed a heightened risk for PCOS according to NIH criteria rather than Rotterdam criteria, the researchers wrote.

They said the variants found may be involved in the hyperandrogenism and irregular menses associated with PCOS. Despite impressive findings linking women with European ancestry to risk for PCOS based on variants found in this study, further studies should be considered to determine the role of the variant in the pathogenesis of PCOS.

Disclosure: Four of the 12 researchers are employed by deCODE Genetics. All other researchers report no relevant financial disclosures.

Perspective

 

Andrea Dunaif

  • This is the second study that has replicated findings in a genome-wide association study done in Chinese women with polycystic ovary syndrome. What’s exciting is that the Chinese study confirmed what’s been hypothesized now since the early ‘90s; that there is a genetic susceptibility to PCOS by mapping a couple of gene regions. To then replicate it in a distinct ethnic population in European women suggests that some of the same susceptibility variants are contributing to the disease in two very different populations.

It was suggested many years ago, in 1998, in a landmark paper by Rick Legro and colleagues (Legro RS. Proc Natl Acad Sci USA. 1998;95:14956-14960), that elevated testosterone levels were the underlying trait in PCOS families that most likely had a genetic basis. In this current study, they find that the gene variants are associated with testosterone levels in these populations.

The syndrome has been a disorder that we still don’t know the etiology of. We know that there’s a genetic component, and this is showing how genetic analyses can focus on what is causing all the other features, and again suggesting maybe it’s the testosterone and elevated androgen levels rather than the way the ovaries look.

Could we now do a genotype in a girl and predict whether or not she was going to have PCOS? Could it be used for personalized medicine? Unfortunately, none of these genes in these common, yet complex diseases have enough of the effect. Even if you had these variants that were associated with a 50% to 60% increased risk, that’s still not really enough to say that you’re going to have a disease or not. So, we really can’t use these gene variants for prediction. However, they’re very helpful in beginning to understand causality.

The strength of these studies is that they’re using rigorous new technology, the appropriate statistics, and these are meaningful findings, and hopefully, we’ll be seeing more of these related to other endocrine diseases of interest. This has certainly been the approach that’s been used in type 1 and 2 diabetes, where a number of genetic variants have been discovered.

    • Andrea Dunaif, MD
    • Professor of Endocrinology and Metabolism
      Vice Chair for Research in the Department of Medicine
      Northwestern University, Feinberg School of Medicine
  • Source: Endocrine Today