Friday, November 13, 2015

My CBAC series on Science and Sensibility

This month, we are talking about Cesarean Birth After Cesarean, or CBAC.

CBAC is the preferred term for when a mother works for and wants a VBAC but ends up with another cesarean. Medical researchers usually call this a "failed" VBAC or a "failed trial of labor after cesarean" but this terminology is insensitive. Women who did not get a VBAC are not failures. The reality of birth is much grayer than a black-or-white, success-or-failure binary equation.

I had a CBAC with my second child, as I wrote about on this blog last week. Although I did go on to have two VBACs afterwards, the CBAC experience left a strong imprint on my soul, and pointed out to me the need to improve our emotional support for women who experience one.

In honor of this topic, I wrote a 3-part series on Supporting Women When VBAC Doesn't Happen, and it was published over on the childbirth blog, Science and Sensibility. The different posts include:
  • Part One: A Unique Grief - discusses how a CBAC is not the same as a primary cesarean or a planned repeat cesarean that was gladly chosen, as well as the vacuum of support that many CBAC mothers experience from care providers, friends and family, and the birth community 
  • Part Two: The Forgotten Mothers - discusses how CBAC mothers are largely ignored in medical research, reviews what little research there is on CBAC, and discusses what we can learn from it and from CBAC mothers' experiences
  • Part Three: Supporting CBAC Mothers - discusses concrete suggestions on how birth professionals and friends/family can support CBAC mothers

There is also a new brochure on CBAC that I helped write for the International Cesarean Awareness Network. This gives birth professionals something concrete to give to new CBAC mothers. (There are other ideas for supporting CBAC mothers available in Part 3 of the Science and Sensibility series linked above.)

In addition, I helped write a new CBAC support website, using materials brainstormed by CBAC moms for a workshop I did at an ICAN conference.

I am also offering two webinars on CBAC for ICAN this month (they will be listed with ICAN once they have been recorded; members can access them afterwards). One is for folks in the birth field to learn how to support CBAC women more effectively, and the other is for CBAC mothers themselves.

When I had my CBAC so many years ago, there was a real dearth of information on supporting CBAC mothers. No one knew how to help, and I got precious little support. Eventually we built a community of CBAC moms who helped each other. Together we brainstormed what kind of support was and was not helpful. We built the support network that we needed. It didn't take the pain and disappointment away of course, but it helped ease the process of coming to terms with it.

Far too often, there is still a dearth of support for CBAC mothers because few people know what support resources exist. My hope is that this Science and Sensibility series, the new brochure, the new website, and the webinars can help fill in gap, along with ICAN's Facebook support page.

But this shouldn't be the end of it. We need to continue to dialogue on what's needed to improve support for CBAC moms. However, that dialogue won't happen if other folks in the birth community are not aware of these concerns or have no concrete ideas on how to help.

So please, go check out the series and "like" or "share" it on Facebook and other social media. Make sure that people in the birth field, whether care providers, doulas, advocates, or moms themselves, have access to the message about improving support for CBAC moms.

Let's make sure that women who don't get a VBAC know that they are not alone and that all the work they put in their pregnancy and towards their birth still counts. ALL women deserve support; let's raise awareness of the needs of CBAC mothers and reach out to them with kindness and empathy as they work towards emotionally processing the experience and integrating it into their lives. 

Wednesday, November 4, 2015

Cesarean Birth After Cesarean, 18 Years Later

Image from Wikimedia Commons, here
  Remember, no effort that we make to attain something beautiful is ever lost. –Helen Keller

This month, we are focusing on CBAC, or Cesarean Birth After Cesarean. The following was expanded from an article written for the Spring 2015 Clarion, a publication of the International Cesarean Awareness Network (ICAN), now appearing on the ICAN blog

My CBAC Story

Eighteen years ago, my second child was born. He was born by repeat cesarean after a long, hard “trial of labor” which included 5 hours of pushing with no progress because he was big and posterior with an upright (“military”) head position.

I’ve second-guessed that birth for many years. It’s possible that if we’d pushed even longer, his head would have molded enough to fit through my pelvis and turn anterior on the perineum, as many posterior babies do. However, at that point, I was absolutely exhausted, in a lot of pain, and was worried about the wisdom of continuing when things had gone so long without progress. I knew a non-progressing labor was a risk factor for rupture, plus my baby had experienced some issues with his heart rate. They resolved, but I didn’t want to go into a repeat cesarean in true emergency mode because of a rupture or fetal distress, and emotionally I needed to make sure that I didn’t have an anesthesia failure like I did with my first cesarean.

At that point, I just had a strong sense of Inner Knowing that it was time to be prudent and stop before things became a real emergency. I believe I made the right decision, but it was hard to communicate that to my husband and support team. My doula treated me like I had wimped out and thrown in the towel too easily. I never heard from her again after the cesarean. It was clear she viewed me as a failure.

I dreaded having to go back to my VBAC groups and tell them I’d had a CBAC, but I gritted my teeth and did it anyway. I got some sympathetic responses, but mostly I got a lot of silence or tepid responses that felt judgmental. No one knew how to reply to someone who hadn’t gotten their VBAC . 

Over the years, there was a lot of armchair quarterbacking about my decisions. People meant well, but I was left feeling pretty unsupported. And I didn’t feel I could really emotionally process the birth fully in birth spaces because I was afraid of discouraging new mothers or those planning their VBACs. No one wants to hear about when VBAC doesn’t work out.

Eventually I was able to access some resources that helped me emotionally process my first two births. It took a lot of hard, emotionally grueling work, but in time I came to peace with those births, and I did have two VBACs afterwards. 

In some ways, the CBAC was healing from my highly traumatic first cesarean, but in other ways it would always remain hard, even though I felt like it was a prudent and wise call under the circumstances. My consolation was my precious child, but his birth would always remain bittersweet to me in some ways, especially because of the initial lack of support. And that led me to trying to improve support for other women who had difficult or traumatic births, especially CBAC mothers. 

Expanding CBAC Support

If about 75% of labors after cesarean end up with a VBAC, that means that about 25% of these labors end with another cesarean. Where is the support for women who have an undesired second cesarean? Where is the acknowledgement of all the work they put in towards a VBAC, the hours of labor, the pain, the worry? Does all that preparation and work not count if you don’t end up with a VBAC? 

In time, I began to realize there was a vacuum of support for the mothers who didn’t VBAC. It wasn’t just about my own experience anymore, but also about other moms. How could we make it so that all mothers felt supported, regardless of outcome? Shouldn't we offer emotional support after any cesarean, whether it’s your first or another one?

I wasn’t the only one, of course. A number of us shared this experience of another unwanted cesarean, including people in the leadership of ICAN, and we began to talk about how to offer better support. One of the first things we did was ditch the terms used in the medical literature, terms like “Failed VBAC” or “Failed Trial of Labor After Cesarean.” We felt this was too judgmental and insensitive. We were not “failures,” we did not fail, and we should not have been on trial.

We created the term Cesarean Birth After Cesarean (CBAC) as a more mother-friendly alternative. It refers to a cesarean that occurs when the mother really wanted and worked for a VBAC but didn’t get one. These women had different emotional needs than those who wanted a repeat cesarean, and terminology needed to reflect that difference. So we used “CBAC” to differentiate another unwanted cesarean from Elective Repeat Cesarean Section (ERCS), where women truly wanted another cesarean and voluntarily chose it. Neither one is good or bad; they are simply different experiences.

There are many shades of CBAC. Most of the time, it refers to someone who labored and ended with another cesarean, but it can also refer to a cesarean performed before labor for medical reasons, because the mother had no choice, or because the mother was coerced or scared into a repeat cesarean. Some women prefer "CSAC" (Cesarean Surgery After Cesarean) because they consider the term “birth” too emotionally loaded. Women get to choose the term that seems right for their own experience. The important thing is to acknowledge and validate the range of feelings that women have over this experience.

Of course, all CBAC mothers are not alike. Having the shared experience of a CBAC doesn’t mean other details of our situations are similar. Each CBAC is unique, and each carries its own particular color and resonance of pain. 

Some had disappointing or traumatic experiences, and some didn't. Some felt very betrayed by their caregivers, while others had very supportive caregivers. Some felt they had a “prudent CBAC,” where although it was difficult, a repeat cesarean felt like the right choice under the circumstances. Some had an “empowered CBAC,” where even though there was disappointment and sadness, there was powerful learning and healing too.  

Some CBAC mothers go on to have a VBAC eventually, while others never do. Some have multiple CBACs, each with their own emotional resonance. Some have a VBAC and then a CBAC, which has its own particular pain. A few have had the bitter experience of having lasting physical and emotional damage from their CBAC, including uterine rupture, hysterectomy, and damage to or loss of their baby. As always, each person’s experience is different and unique, and each CBAC mother needs safe space to process all the varying feelings about those experiences. But this can be difficult to do within regular birth forums.

Some people don’t think there needs to be any separate support for CBAC mothers (“a cesarean is a cesarean”), and to this day, many of us with CBACs still have our decisions questioned and second-guessed in birth forums. Although many doubters have come around to offer more support, CBAC still remains a topic of friction at times within the birth community. This needs to change. 

New CBAC Resources

Over the years, we have tried to expand resources for CBAC mothers. We have offered several CBAC sessions at ICAN conferences and at local chapter meetings, and until recently we had a Yahoo group for online support. 

In 2011, I offered a CBAC workshop at the St. Louis ICAN conference. The session was derived from discussions by mothers on the Yahoo CBAC Support Group, and many graciously consented to sharing their thoughts and quotes to help others. At that session, we brainstormed ways to offer further support for CBAC moms. 

One of the main ideas was to have an online website devoted to CBAC support and information. So last year, Melek Speros, Catherine Kowalik Harper, and I created a CBAC Support website, based on my material from the 2011 workshop and suggestions I got there. On this site, we share CBAC research, websites where CBAC moms can go for emotional healing, information on the unique emotional needs of CBAC mothers, suggestions for processing a CBAC, CBAC birth stories, inspirational quotes for healing, and suggestions for birth professionals to help them better support CBAC mothers. 

ICAN has also created a new online support group via a Facebook page for CBAC mothers. This is a closed group; you have to be a CBAC mother to join. It offers intensive, personal support for those dealing with the aftermath of a CBAC. 

ICAN is also about to publish a brand-new brochure on CBAC. It is intended for ICAN leaders and other birth professionals who may encounter a woman who has recently had a CBAC and is in need of extra support. We encourage birth professionals to include this brochure in a resource packet that they can send to women shortly after a CBAC so these mothers realize that they are not alone, that others have walked the CBAC trail and survived, and that there are resources for further support if they want it. 

In future years, I hope we can create even more ways to help support CBAC mothers. If you have other suggestions for how we can do that, please add them in the comments section. 

Final Thoughts

Eighteen years after my own CBAC, it remains a potent memory. My sweet little boy is a strong and independent man now, flying off on new adventures, but his birth is still a touchstone for many different emotions. Although I did eventually go on to have 2 VBACs after the CBAC, those experiences didn’t "fix" the CBAC or make it go away. They simply are different entities – not better or worse, just different. Although there are things I still mourn about my CBAC, I have learned to honor all my birth experiences, difficult or easy, because they are a big part of the person I am today.

The lessons I learned from my CBAC remain powerful and still resonate in my life. My CBAC helped me to be more compassionate about other people’s births, to recognize that sometimes there are just things that are beyond our control in the moment. It helped me to realize that sometimes birth is more about the willingness to heal and change; that birth is more about the journey and less about the destination. 

In time I learned to honor both the disappointment and the joy in all my births, to remember that what counts most is the parenting we do throughout life rather than how we birth, but also that how we feel about our births counts, even years later. Our deep love for our children is a different and separate thing from our emotions about their births, and while these things intertwine, one does not take away from the other. We can honor the disappointment and mourn the difficulty of a birth while still celebrating and fiercely loving the child that came from that birth. 

I found that out of my suffering came the ability to transform pain into advocacy. I found my voice in a new and potent way, and I have endeavored to channel the power of that voice to create change, as well as to create and hold safe space for other women and their unique experiences.

A CBAC is never an easy thing. The pain and disappointment of it stays with you forever, but like other grief, it does ease some and you find a way to live with it, just as you find a way to live with other disappointments in your life. You can celebrate certain aspects of it, you can mourn parts of it, you can still be upset that it occurred, but you honor what it has brought to your life, both difficult and wonderful. 

You also learn that in time, out of the pain and conflicting emotions that accompany a difficult experience, there can also come great growth and power to create change for yourself and others. Just give yourself the gift of time and space for that healing. It will come.

Monday, November 2, 2015

A Discussion of the Barriers to VBAC

Dr. Mark Landon
The majority of women who have a cesarean in one pregnancy go on to have cesareans in subsequent pregnancies. Sometimes it's because that's what they want (which is perfectly fine), but often it's because they are not given any choice in the matter. That's not fine.

Sadly, many hospitals or caregivers will not "allow" Vaginal Births After Cesarean (VBACs). Some say they allow it, but in the end the caregiver ends up scaring or pressuring the mother out of VBAC, or put so many restrictions on it that it's practically a miracle if the mother gets one.

There are risks to VBAC that are real and must be considered, but there are also real risks to repeat cesareans, especially multiple repeat cesareans. The rise in the incidence of placenta previa and placenta accreta, both life-threatening conditions, is tied to the rise in cesareans, especially repeat cesareans. Yet women are often not being adequately counseled about the risks of cesareans.

The "trial of labor" (TOL) rate for VBACs in the United States now is much lower than in Europe, and much lower than it used to be here in the U.S. The U.S. medical community, by and large, turned its back on VBAC in the early 2000s. While the rules around VBAC were loosened a bit a few years ago in order to help make it more available to women, this hasn't really happened. Many providers and hospitals still do not allow women to choose VBAC, even though about 70% of women who try for a VBAC will have one.

The following article is an excellent overall summary on the barriers to VBAC in the U.S. from one of the leading experts on VBAC, Dr. Mark Landon. If you haven't had a chance to read it yet, definitely check it out. 

Friday, October 23, 2015

Metformin Does NOT Lower Birthweight Among Non-Diabetic Obese Mothers

Although most higher-BMI women have average-sized babies, larger women have a higher percentage of big babies. This is one of the biggest reasons care providers intervene in the pregnancies of women of size.

Although most big babies do just fine, bigger babies do have higher rates of issues like shoulder dystocia, cesarean birth, and low blood sugar after birth. So care providers have long searched for ways to lower the rate of big babies among women of size.

Whether that's justified or not is a debate for another day. The point is that many care providers are willing to go to extreme lengths for this goal.

A few years ago there was a large public campaign pushing the prescription of metformin (brand name: Glucophage) for reducing birthweights among non-diabetic "obese" mothers.

We've written about this before. The study was called EMPOWaR and was a randomized, controlled study at 15 different U.K. hospitals.

The theory was that insulin resistance and/or borderline blood sugars were probably at the root of a higher incidence of large infants among high-BMI women, and that lowering blood sugar and insulin resistance even in non-diabetic obese mothers might improve outcomes.

While the publicity campaign noted that they were just investigating this possibility ─ really! ─ the publicity push around a study that hadn't even been done yet suggests that the investigators really had ulterior motives.

Pushing Unproven Agendas Through Publicity 

This is one of my pet peeves about research on obesity in pregnancy; it is often publicized now before the study is even done. One suspects that the researchers are trying to promote unproven high-intervention protocols for this group, trying to raise their own public profiles, or maybe even create a new market for certain medications or programs.

Why else would researchers publicize a study not yet even done?

Publicizing a research trial before it's done creates an expectation in the reading public, including other doctors, that a particular protocol or medication is THE way to manage a particular population or problem. It does an end run around the usual research procedures and starts promoting protocol changes in the minds of the public without having to wait for any pesky results.

We've seen it before in a Kaiser study that promoted zero weight gain in obese pregnant women before the study had even been done. Best guess is that it was part of a push from some doctors to lower prenatal weight gain guidelines because they didn't think the 2009 guidelines (11-20 lbs. for obese women) were low enough.

Certainly, doctors can campaign for changes to national guidelines because of strongly-held beliefs that a particular approach might improve outcomes. However, a pet theory is not enough; any changes need to be supported by actual evidence.

It is medically unethical for doctors to be promoting changes to policy without having clear data that shows a need for such changes and conclusive proof of a lack of harm of such changes.

And guess what? There is good reason for demanding such proof of lack of harm before guideline changes. Turns out that there IS harm in minuscule weight gains.

recent meta-analysis of 18 cohort studies concluded that "gestational weight gain below the guidelines cannot be routinely recommended" in obese women because of an increase in too-small infants and premature births.

THAT is why you need to show proof of a lack of harm of proposed changes and why no one should be publicizing studies before they are done. Doctors all over the country ─ outside of the research trials ─ took that publicity push seriously and are currently promoting minuscule gains, zero gain, and even weight loss in obese pregnant women. How many premature babies and too-small babies have been the result?

Promote healthy eating and lifestyle? Absolutely. And some larger women naturally gain very little in pregnancy, even with normal eating. That's okay; those women generally do okay. But to deliberately manipulate the diet so that weight gains are minuscule or non-existent? Unwise.

Too many care providers have jumped on the minuscule weight gain bandwagon because of the publicity push promoting it before these protocols were examined adequately for harm.

The Metformin Study

A similar questionable publicity campaign surrounded the British study using metformin to hopefully lower birth weights in babies of obese women. Some publicity articles used scare tactics and hyperbole about pregnancy risks in obese women to justify using this medication experimentally and implied that taking metformin would keep "overweight" women from having "overweight" babies. Basically, it was implied that obese women would be irresponsible if they didn't comply with this experiment.

The study had other issues; it used birthweight as a surrogate marker for the future ill-health of obese mothers' offspring. To me this is a very questionable assumption, since it is difficult to untangle cause and effect of metabolic issues like PCOS, lipedema, thyroid disturbances, and genetic contributions to a child's health vs. birthweight alone. In addition, big babies don't automatically become unhealthy adults, and there is plenty of evidence that too-small babies have more health problems than bigger ones.

The publicity campaign fanned the anti-obesity hysteria in the U.K., created a climate where women in the study probably felt they had little choice about taking such drugs (even though their use in this context was experimental), and created an expectation among care providers that metformin was the standard of care even in the pregnancies of non-diabetic obese women.

So I didn't love the premise of the study or the means by which they pressured women into it, even though I thought it would be interesting to see if metformin had an effect on birthweight.

Well, the study results are in, and metformin did NOT reduce birthweight among obese mothers. Birthweights were similar between the metformin and placebo groups. The ponderal index (a measure of length and weight, kind of like a BMI for babies) was similar between groups as well. In other words, metformin not only didn't lower average birthweight, it didn't make the babies any skinnier for their lengths either.

Nor did metformin improve other outcomes of pregnancy in obese women. The metformin group did not have lower prenatal weight gains, nor did they have fewer cesareans.

Basically, the researchers could not show any meaningful improvements in outcome from taking metformin.

There were a few minor differences between groups that did not rise to statistical significance. The metformin group did develop fewer cases of gestational diabetes, but only marginally. There were some small improvements in blood sugar and insulin in the metformin group at 28 weeks, but not at 36 weeks. Some inflammatory markers were lessened but the significance of this is unclear and didn't seem to have any bearing on immediate outcomes.

The metformin group did develop more pregnancy-induced hypertension, pre-eclampsia, and pre-term birth, but again only marginally. The difference did not rise to statistical significance.

Interestingly, there was a stronger tendency towards more poor outcomes (miscarriage, termination, stillbirth, or neonatal death) among the metformin group (3% vs. 1%), but the confidence interval crossed 1.0 and these results could have been mere coincidence rather than a real result of metformin. Given the rarity of such poor outcomes, the study group probably was not large enough to determine whether a real relationship between metformin and poor outcomes in non-diabetic mothers exists. In the study's defense, the description of the poor outcomes does not seem to indicate that they were due to metformin. The bottom line is that the study did not find a statistically significant increase in poor outcomes among those taking metformin.

It IS important to note that metformin is probably a relatively safe drug to use in pregnancy and is used with significant benefit in some diabetic mothers and women with PCOS, but its safety and efficacy in other mothers is less established.

Now we know that it really doesn't lower the birthweight of babies nor improve other outcomes in non-diabetic high BMI mothers. That led the study authors to conclude:
Metformin should not be used to improve pregnancy outcomes in obese women without diabetes.
Further Details

The fact that the study found no real benefit from metformin use in non-diabetic obese women disproved the authors' hypothesis that metformin would improve outcomes. However, the study's authors speculate that an impact on birthweight was not seen because of several possibilities.

First, the medication was not started until 12-16 weeks, rather than early in pregnancy or pre-conception. They theorized that perhaps the programming of fetal size takes place so early that starting it at 12-16 weeks was too late. However, since most women aren't seen in pregnancy until the end of the first trimester, it is unlikely most obese pregnant women would be able to be started earlier anyhow.

Second, they wondered if the doses may not have been high enough to be effective. They started at 500 mg per day and slowly increased the dosage until the "maximum tolerable dose" was reached ─ i.e., until woman experienced too many side effects like nausea, vomiting, diarrhea to tolerate continuing to increase the dose. Still, about 2/3 of the metformin arm received 2000 mg, very near the maximum dosage of 2500 mg, so the argument that the dose wasn't high enough is weak. This was an adequate test.

Third, the authors speculate that the real benefits of taking metformin during the fetal period would likely show in other ways as the child grew up instead of affecting birthweight. They cite an animal study that suggests less visceral fat in the offspring of mothers that received metformin during gestation. As a result, they are planning a follow-up study to monitor metformin-exposed children and see if they have less obesity and/or metabolic issues as they grow up.

This last theory is one that a lot of doctors are fixating on. This is the idea of fetal programming, that the window of time during gestation is one in which fat women "program" their babies to be larger and to have poorer long-term health, and therefore we needed to be extremely proactive about intervening in the pregnancies of obese women. One commentator noted:
The bold idea that what we do to the fetus during the short and finite period of pregnancy could change and even improve lifelong outcomes of offspring validates the whole concept of prenatal care. If this concept is true, this tiny window of opportunity should not be wasted.
This is an alarming statement to me. Yes, if we could change things during the fetal period that would improve that child's health long-term, that would be an exciting possibility. However, the potential for abuse here is quite high. I worry that researchers are SO excited about "preventing" obesity that their common sense will go out the window and they will start using even more scorched-earth ─ and unproven ─ tactics.

What if we intervene and change the child's long-term health negatively? I worry that scorched-earth protocols to get smaller babies through gestational weight loss or medications may actually backfire and create ripples those care providers don't anticipate. Where are the safety protocols to ensure lack of harm from such interventions?

The in-utero time is a powerful time, it's true. But that means we must be very VERY careful in how we intervene, if we intervene at all. And we certainly shouldn't be publicizing a particular approach until it has been proven both beneficial and harmless.


Big mothers tend to have bigger babies on average. This leads many care providers to institute major interventions and scorched-earth protocols to lower birth weight.

The most common intervention is to limit prenatal weight gain. While women of size probably need to gain less weight in pregnancy than other women, how much weight they should (or shouldn't) gain is more controversial. Even more controversial is what should be done to try to achieve that lower gain.

Too much weight gain is clearly linked to larger babies, and perhaps to other poor outcomes. As a result, many care providers have pushed to see the 2009 guidelines reduced even further. However, as noted, too-small gains during pregnancy have unacceptable trade-offs in more too-small babies and premature births. The harms are not worth the potential benefits.

Similarly, some care providers have begun to promote the idea of putting non-diabetic obese women on metformin prophylactically to try to prevent big babies. Although this can modestly reduce birthweight in women with gestational diabetes or full-blown diabetes, this study shows that metformin does not reduce birthweight in non-diabetic obese women.

This research effectively disproves the Pederson Hypothesis, which is that big babies are the result of maternal high blood sugar and responding high insulin levels in the baby. Although this feedback loop can cause fetal overgrowth in diabetic women, this study shows that higher birthweights in non-diabetic obese women are NOT because of borderline high blood sugar. There must be something else going on here to cause the bigger babies, which is something I've been saying for years. The authors suspect high lipid levels, but I'm dubious about that one too. Whatever the mechanism is, it's important to go cautiously and avoid jumping to conclusions based only on assumptions about fat people.

This study shows that metformin does not improve outcomes in non-diabetic obese women and should NOT be used for that purpose. Too bad the publicity push around the trial has already created a market for this, and some providers are pushing its use for all their obese patients. Two more trials like this one are already occurring.

Sadly, even though this research was completed and published this past summer, the trial's publicity website has not been updated to show the negative study results or conclusion. Although a bit of publicity about the negative findings has appeared in some medical publications, a large publicity push does not appear to have been done. How many care providers all over the world still have the impression that metformin should be the standard of care of obese women, regardless of blood sugar status?

Researchers, stop promoting a particular approach before the research is even done. A management protocol needs to be proven to be effective and safe in multiple trials before it should be publicized and promoted. Duh.

At least now we know that metformin, while helpful under certain circumstances, is not a cure-all for preventing complications in all high-BMI women or for preventing big babies. Care providers need to restrict its use to situations where it's actually appropriate and needed.


Lancet Diabetes Endocrinol. 2015 Oct;3(10):778-86. doi: 10.1016/S2213-8587(15)00219-3. Epub 2015 Jul 9. Effect of metformin on maternal and fetal outcomes in obese pregnant women (EMPOWaR): a randomised, double-blind, placebo-controlled trial. Chiswick C1, Reynolds RM2, Denison F1, Drake AJ2, Forbes S2, Newby DE3, Walker BR2, Quenby S4, Wray S5, Weeks A5, Lashen H6, Rodriguez A7,Murray G7, Whyte S1, Norman JE8. PMID: 26165398  Full text available here.
BACKGROUND: Maternal obesity is associated with increased birthweight, and obesity and premature mortality in adult offspring. The mechanism by which maternal obesity leads to these outcomes is not well understood, but maternal hyperglycaemia and insulin resistance are both implicated. We aimed to establish whether the insulin sensitising drug metformin improves maternal and fetal outcomes in obese pregnant women without diabetes. METHODS: We did this randomised, double-blind, placebo-controlled trial in antenatal clinics at 15 National Health Service hospitals in the UK. Pregnant women (aged ≥16 years) between 12 and 16 weeks' gestation who had a BMI of 30 kg/m(2) or more and normal glucose tolerance were randomly assigned (1:1), via a web-based computer-generated block randomisation procedure (block size of two to four), to receive oral metformin 500 mg (increasing to a maximum of 2500 mg) or matched placebo daily from between 12 and 16 weeks' gestation until delivery of the baby...FINDINGS: Between Feb 3, 2011, and Jan 16, 2014, inclusive, we randomly assigned 449 women to either placebo (n=223) or metformin (n=226), of whom 434 (97%) were included in the final modified intention-to-treat analysis. Mean birthweight at delivery was 3463 g (SD 660) in the placebo group and 3462 g (548) in the metformin group. The estimated effect size of metformin on the primary outcome was non-significant (adjusted mean difference -0·029, 95% CI -0·217 to 0·158; p=0·7597). The difference in the number of women reporting the combined adverse outcome of miscarriage, termination of pregnancy, stillbirth, or neonatal death in the metformin group (n=7) versus the placebo group (n=2) was not significant (odds ratio 3·60, 95% CI 0·74-17·50; p=0·11).  INTERPRETATION: Metformin has no significant effect on birthweight percentile in obese pregnant women. Further follow-up of babies born to mothers in the EMPOWaR study will identify longer-term outcomes of metformin in this population; in the meantime, metformin should not be used to improve pregnancy outcomes in obese women without diabetes

Monday, October 12, 2015

Pregnancy and Infant Loss Awareness Month

October is Pregnancy and Infant Loss Awareness Month.

Sadly, I have had a number of dear friends and acquaintances who have had miscarriages, whose babies were born still, or who did not live through their first year. These losses have left their footprints in my heart too.

You simply cannot work in the birth field for 20+ years and not know people whose precious babies have died. Miscarriage is more common than you might think, and while stillbirth and infant mortality is rare, it does still happen. These losses are absolutely devastating and go unspoken of far too often.

To any in my reading audience who might have experienced a loss like these, my heart goes out to you. To my dear friends who have been through this difficult experience, I hold you and your babies forever in my heart. It may seem like no one remembers, but you might be surprised how often I think of them, and you too. So much love to you.

Monday, October 5, 2015

Lipedema, self acceptance, and trolls

Image from this article
This is a really interesting article by Courtney Mina about dealing with the fat hate that often accompanies being open about lipedema or being body-positive in any way online.

She posted some pictures of herself in only undergarments on Instagram, Twitter (#biglegs), and Facebook to see if people would continue to be body-positive towards someone with large legs. She was open with people about having lipedema, what that meant, and how it has affected her life, all while still being body-positive.

Gratifyingly, many people were body-positive and supportive of her. This shows that body-positivity campaigns are making a difference and the message is being heard. 

However, there were also haters. Some of it was the open, in-your-face really vicious hate so common on the internet (yep, I get it too). Ugh. But that's such an obviously biased and obnoxious response that you mostly just have to let that roll off of you. Some people are just trying to stir up trouble and some people are just outright misogynists. None of us should be subject to such hatefulness, it's wrong wrong wrong for sexism like this to be so prevalent and our society needs to target this misogyny, but some individuals are so hateful they are simply lost causes. I refuse to lose sleep over them.

Of course there was also the poisonous "concern trolling" ─ I'm-just-worried-about-your-health stuff. This is the kind of stuff fat people get bombarded with by people we care about (because obviously you are simply in denial if you are fat and not trying to lose weight). They can't see how much they've bought into harmful untruths about weight and health, and they find it difficult to acknowledge that there really are medical conditions that can cause fatness. They think that since their bodies work a certain way, all bodies must therefore work that way, even when evidence for a disease process is presented to them. They mean well, but it's still hurtful.

And of course, sometimes the worst people of all are the "plus-size police," the women of size who so hate their own bodies that they try to police other fat women's bodies too. The self-hate they have is just palpable and so sad. The absolute worst are the ones who are in the honeymoon period during or just after weight loss before the regain begins, or the ones who are chronic dieters. They are in the "high" phase of the dieting addiction and they want everyone to join them on this drug. No one is allowed to rain on their parade, gainsay their experience, or present an alternative approach like Health At Every Size®. Anyone who approaches it differently is just "in denial."

Sadly, even some in the fat-acceptance movement have wanted to deny the medical reality of lipedema, a medical condition that often leads to heavier-than-average legs, hips, and arms. It's as if they think that any acknowledgement of a possible biological condition underlying weight means we are making excuses for it to appease the haters, rather than embracing our size with acceptance. [Nope, you can acknowledge the biological causes and still be part of fat acceptance.]

I thought this post had many thought-provoking things to say. Definitely check it out. I was encouraged that many people were supportive of her, but I have to wonder how many were supportive because she is young and beautiful. There's a heck of a lot less supportiveness out there for middle-aged and older fat women, but I have hopes that this, too, will improve with time. Body positivity should not be only for the young and beautiful but for people of all ages and looks.

Tuesday, September 29, 2015

PCOS Treatment: Anti-Androgen Medications

September is Polycystic Ovarian Syndrome (PCOS) Awareness Month. PCOS is a condition that affects many people of size, yet it is often under-diagnosed and under-treated. It's important to bring more awareness to this condition and its treatment choices, so every year I post something about a particular aspect of PCOS.

Here are some of the previous entries in our periodic continuing series on PCOS:
Now we are discussing common treatment protocols for PCOS (and the pros and cons of each) ─ from a size-friendly point of view (meaning no diet talk or weight loss promotion). We've already discussed:
Today, we discuss anti-androgenic medications, especially their use for common PCOS symptoms like hirsutism (excess facial and body hair), alopecia (hair loss), or acne.

Disclaimer: I am not a health-care professional. This information is not a complete explanation of all the risks and benefits of a particular medication, nor is it medical advice. Always do your own research and consult your healthcare provider before making decisions about your care.

Trigger Warning: Passing mention of the possible weight effects of several medications.

Anti-Androgen Medications

Since one of the major issues in PCOS is androgen excess, one of the major goals of treating it is to reduce the levels of androgens (male hormones) in the blood ─ or at least to reduce its effects.

As we have seen in previous posts, some birth control pills can have a major anti-androgenic effect and lessen many PCOS symptoms, which is why they are the most commonly prescribed medication for PCOS. However, there are some drawbacks.

Not all oral contraceptives have an anti-androgenic effect, and some significantly worsen androgens. Combined oral contraceptives also increase the risk for blood clots, particularly the anti-androgenic ones, and may have lower birth control efficacy in high-BMI women. Some argue that they merely put a band-aid on symptoms while not adequately addressing the underlying causes of PCOS issues.

Thus while birth control pills can be one option for PCOS, it's important to have other options as well. One of these choices can be an anti-androgen. These medications either prevent the body from making as many androgens, or they limit the activities and effects of androgens. Treatment with anti-androgenic medications may help:
  • Lower androgen levels
  • Reduce hirsutism
  • Reduce acne 
  • Minimize hair loss issues
While anti-androgens can reduce some PCOS symptoms, it's vitally important to know that they can also cause birth defects and must be taken with an extremely reliable form of birth control, even in women with fertility issues. 

Occasional spontaneous ovulation does happen even in those struggling with infertility, and the chance of birth defects is high in women who take anti-androgen medications. As a result, anti-androgens are often taken with oral contraceptives in order to make sure pregnancy is prevented. Sometimes the combination works even better than alone, giving it an added bonus.

As with insulin-sensitizing medications, anti-androgens are not FDA-approved for the treatment of PCOS. Research reviews note the poor quality of research on these drugs, so the best anti-androgen for treating PCOS symptoms is not yet known, nor is the best combination of anti-androgen and oral contraceptive. Women who want to use any of these drugs should be extremely cautious and discuss all pros and cons thoroughly with their health care provider.

Finally, it is important to note that it takes a long trial of treatment (6-18 months) before it is clear whether a particular anti-androgen drug is impacting your symptoms. Because the hair growth cycle is long, improvement is generally slow and gradual. You must be patient before you decide whether or not an anti-androgen drug is helping.

And remember, the drug's benefits last only as long as you are taking the drug, and the risk of side effects with some drugs is substantial. If the drug's benefits are only modest, some people may feel they are not worth the long-term risk of side effects.

Most Common Anti-Androgen Medications

There are a number of choices of anti-androgen medications for PCOS. These include:
  • Spironolactone (brand name: Aldactone)
  • Flutamide (brand name: Drogenil or Eulexin)
  • Finasteride (brand name: Propecia or Proscar)
  • Bicalutamide (Brand name: Casodex, Calutide)
  • Certain combination oral contraceptives
  • Drosperinone
  • Cyproterone Acetate (CPA; brand names: Androcur and Cyprostat)
  • Insulin-Sensitizing Medications
Let's look at each of these a bit more in detail.

Spironolactone (brand name: Aldactone)

Spironolactone is the most common anti-androgen drug used for women with PCOS. It is a potassium-sparing diuretic, usually prescribed for treating edema (excess fluid) or high blood pressure. It is also an aldosterone antogonist. Its use for PCOS symptoms is off-label but has been going on for years.

Spironolactone is thought to help in the following way:
Spironolactone inhibits the testosterone secreted by the body, and also competes for hormone receptors in the hair follicles. Receptors are sites on cells which allow hormones or chemical to bind to them, creating a reaction. If another chemical is in the receptor site, androgens cannot bind to them and stimulate the reaction causing hair growth.
Spironolactone has been shown to significantly lessen facial hirsutism in women with PCOS. A recent Cochrane meta-analysis suggests that 100 mg daily is quite effective against hirsutism, although it noted that the quality of this evidence was low and more research is needed. Other OB guidelines have suggested that higher doses may be needed in some women, but that it's best to build dosage up slowly over time.

Some recent research also suggests that spironolactone might also help women with hair loss, either with or without accompanying minoxidil (Rogaine). Some women report that it slows down hair loss, but most do not report that it restores hair that has been lost. Although it does not seem particularly effective against alopecia, it is another option that can be tried since responsiveness varies between patients.

Its use for acne, however, is even less clear. A 2009 meta-analysis notes that studies on its use for acne are scarce and very small. More research is needed.

For many women with significant hirsutism, spironolactone is the medication of choice. However, again, spironolactone can cause significant birth defects, so it must always be used with a form of extremely reliable birth control in women who have even the smallest chance of becoming pregnant. This usually means the Pill, since oral contraceptives are one of the most effective forms of birth control. Since some types of the Pill can also help with hirsutism, the combination of the Pill and spironolactone can be particularly effective for many women with PCOS. However, not all find it effective.

Because spironolactone is a diuretic, you will need to be monitored to make sure you don't build up too much potassium in the blood. Nausea, fatigue, headache, lightheadedness, indigestion, thirst, and excessive urination are common side effects; heart arrhythmias can occur if potassium levels spike. Liver enzymes must be monitored regularly for signs of hepatotoxicity.

You can read more about the uses, side effects, and cautions for spironolactone here and here. Guidelines for its use with acne are discussed here.

Flutamide (brand name: Drogenil or formerly Eulexin)

Another medication that works similarly to spironolactone is flutamide. From one website:
Flutamide is a non-steroidal antiandrogen that is devoid of other hormonal activity. It most likely acts after converting to 2-hydroxyflutamide, which is a potent competitive inhibitor of dihydrotestosterone (DHT) binding to the androgen receptor.
A few studies have found that flutamide helps restore regular menstrual cycles and ovulation in women with PCOS, but it is most useful against hirsutism. It is available in the United States, but is usually prescribed for men with prostate cancer, not women with PCOS. As a result, most of the hirsutism research on it is European.

Flutamide can have significant liver toxicity, so some organizations recommend against it use. Flutamide can also result in significant gastrointestinal upset, as well as issues with dry skin. Because of these side effects, flutamide is generally considered unsuitable for the treatment of acne and other skin problems where its benefit is only minimal.

Because it is more effective for hirsutism, the benefit/risk ratio for this is more controversial. A recent Cochrane meta-analysis suggests that flutamide (250 mg, twice daily) is "effective and safe" against hirsutism, although it noted that the quality of this evidence was low. Another recent meta-analysis disagreed, stating:
Due to its risk for hepatotoxicity, flutamide is not considered a first-line therapy. If used, the lowest effective dose should be administered with careful monitoring of liver enzymes.
Flutamide may be somewhat effective for slowing down the progress of alopecia (hair loss). It likely does not restore thinned hair but may slow down or stop the process from continuing. Again, more research is needed.

Some care providers feel that flutamide is relatively safe with careful monitoring. Close monitoring of liver function via regular blood tests is very important. The chance for birth defects is quite high with Flutamide, so again, a very reliable form of birth control must be used, or it may be prescribed only for women with no childbearing potential.

You can read more about Flutamide here, here, and here.

Finasteride (brand name: Propecia or Proscar)

Finasteride is a 5 alpha-reductase inhibitor. It is FDA-approved for the treatment of baldness and/or Benign Prostatic Hyperplasia (BPH) in men. It has a relatively good safety profile and is well tolerated by most men, but it is quite expensive. It is not approved for use with PCOS or with women.

Finasteride has been shown in some research to be effective against hirsutism, though not for hair loss in women. It works by preventing the androgens from getting into the cells. However, the recent Cochrane meta-analysis notes that the research on finasteride is inconsistent and therefore conclusions cannot be reached. It does not appear to be effective against hair loss in women.

Finasteride can cause headaches and depression. It is associated with a very high risk of birth defects (pregnancy drug category X), so it is not used in women who have even the smallest chance of becoming pregnant. Some doctors consider it an option, however, for women who have no childbearing potential anymore.

You can read more about finasteride here.

Bicalutamide (brand name: Casodex, Calutide)

A fairly new anti-androgen option is bicalutamide. It is a 5 alpha-reductase inhibitor, like finasteride. Its mechanism of action is as follows:
Bicalutamide acts as a pure antiandrogen by binding to the androgen receptor and preventing its activation and subsequent upregulation of androgen-responsive genes by androgenic hormones. In addition, bicalutamide accelerates the degradation of the androgen receptor.
Although it can impact liver function, bicalutamide is considered to be less likely to cause damage than some other anti-androgen drugs, which is a big advantage.

Like finasteride, it is associated with a high risk of birth defects and is contraindicated in women with any chance of becoming pregnant. However, there is some minimal research on its use in women.

You can read more about bicalutamide here.

Combination Oral Contraceptives

As we have discussed before, certain combination oral contraceptives (using both estrogen and progestin) have strong anti-androgen effects. As a result, they are often the first-line treatment for PCOS and for hirsutism in general.

One OB website sums up the mechanism of action:
Oral contraceptives...suppress pituitary production of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which in turn suppress ovarian androgen production. OCs also may reduce adrenal androgen production, although the mechanism of action is unclear. 
The estrogen component in OCs increases hepatic production of sex hormone-binding globulin (SHBG), thereby decreasing free testosterone levels. The progestin component antagonizes 5α-reductase and the androgen receptor; it also may increase hepatic metabolism of testosterone and can increase SHBG when the OC has low androgenic activity.
However, the strength of anti-androgenic effect in oral contraceptives varies. Some birth control pills (second generation, especially those involving levonorgestrel) have strong androgenic effects, which can make symptoms worse in some women with PCOS.

Many of the later oral contraceptives (third- and fourth-generation) have a stronger anti-androgenic effect. These can be used on their own or in combination with other anti-androgenic drugs (usually spironolactone) to treat hirsutism and acne.

Unfortunately, the oral contraceptives with the strongest anti-androgenic effects tend to have the strongest risk of blood clots, particularly for women of size and/or women with PCOS. Each woman's unique medical history and risk factors must be considered very carefully before use of these oral contraceptives. You can read more about these risks herehere, and here.

Here are further details of two of the most commonly-prescribed anti-androgenic oral contraceptives, those using droperinone and those using cyproterone acetate.


Drosperinone (also known as 1,2-dihydrospirorenone) is a synthetic steroidal progestin which has weak anti-androgenic properties. Structurally, it is similar to spironolactone.

When combined with ethinyl estradiol, it becomes the combination birth control pill called Yasmin, sometimes called a "fourth-generation" oral contraceptive. It has a modest effect against hirsutism and acne. (In a slightly different formulation, drosperinone plus estradiol is called Angeliq, and is sometimes used for menopausal symptoms.)

Yasmin is contraindicated in people with a history of liver, kidney, or adrenal insufficiency. Potassium levels must be carefully monitored in anyone on this medication.

Some research suggests that the risk for blood clots is significantly increased in people on Yasmin, both compared to those not on any birth control pills at all, and in those on other types of birth control pills. Certain risk factors (obesity, high blood pressure, family history of blood clots, diabetes, etc.) may raise the risk even more. Still, doctors point out that the absolute risk remains relatively low, and certainly lower than the risk of blood clots during pregnancy.

Cyproterone Acetate (CPA; brand names: Androcur and Cyprostat, among others)

CPA is another progestin that has anti-androgenic properties and may be used alone or as part of certain birth control pills. It inhibits production of androgens in ovarian theca cells, and also competes with androgens at receptor sites.

From its Wikipedia entry:
Cyproterone a synthetic steroidal antiandrogen drug with additional progestogen and antigonadotropic properties. Its primary action is to suppress the activity of the androgen hormones such as testosterone and its more potent metabolite dihydrotestosterone (DHT) in the body, effects which it mediates via competitive antagonism of the androgen receptor and inhibition of enzymes in the androgen biosynthesis pathway.
CPA is most often used as an anti-androgen treatment for men with prostate cancer. In PCOS women, it is an effective treatment for significant hirsutism and acne. It may be even more effective for this when combined with metformin. 

CPA may also slow the rate of hair loss in women with alopecia but this is not as well-researched. On the other hand, there are a number of anecdotal stories of women who say their hair loss greatly increased after stopping oral contraceptives with CPA. The true influence of CPA on alopecia remains to be figured out.

In the U.K. and Canada, CPA has been combined into the oral contraceptives known as Dianette and Diane-35. CPA and the Diane birth control pills are not available in the U.S.

The amount of CPA in most birth control pills is fairly small, and has only a modest effect on hirsutism. Higher doses of CPA tend to have more impact on hirsutism. However, it takes quite a while for the CPA in birth control pills to affect hirsutism; a trial of at least 6 months is needed, and often the maximum effect is not attained until 2-3 years later.

CPA can have significant liver toxicity. Liver enzymes, cortisol and electrolyte levels must be monitored when on CPA. A woman's ability to absorb vitamin B12 may also be impaired, while iron-binding abilities may be enhanced. B12 and ferritin levels should be monitored when on this medication long-term.

Nausea, vomiting, headache, depression, weight changes, edema, increased blood pressure, gallstones, and skin spots are potential side effects. Again, birth defects can occur with this drug, so effective birth control is needed, which is why it is usually administered in oral contraceptive form.

Blood clots are also a significant risk; women on birth control pills with CPA have a higher risk for blood clots than women on certain other types of the Pill, but some OB organizations feel that they can be worth the risk. Like Yasmin, the absolute risk of a blood clot is fairly low, but may be increased in women with certain risk factors.

If you consider use of CPA, a CPA oral contraceptive (like Dianette), or a drosperinone oral contraceptive (Yasmin), be sure to consult with your care providers carefully about your health history, risk factors, and the benefit/risk ratio of these medications. 

You can read more about Dianette oral contraceptives here and the newer oral contraceptives in general here.

Insulin-Sensitizing Medications

Insulin-sensitizing drugs are not anti-androgen drugs per se. However, by reducing insulin levels, they may have some anti-androgenic effects and can be somewhat effective against hirsutism or acne. Since they have the distinct advantage of being effective against multiple PCOS symptoms at the same time, some providers will prescribe insulin sensitizers first in women with PCOS.

Metformin (brand name Glucophage) is the most commonly used insulin-sensitizing medication in PCOS. TZDs like Actos and Avandia may be somewhat effective against hirsutism but because of concerns over their safety, are not used as commonly as metformin. You can read more about TZDs here.

Metformin has been shown in some past research to be as good as or somewhat better than oral contraceptives alone in reducing hirsutism in women with PCOS. A 2009 literature review for the American Academy of Family Physicians notes that past research showed that metformin was as effective for treatment of hirsutism as many oral contraceptives, although later research did not confirm its effectiveness.

Nowadays, metformin and other insulin-sensitizers are not considered to be first-line drugs for use alone against hirsutism. One recent review said:
Monotherapy with an insulin sensitizer does not significantly improve hirsutism. While insulin sensitizers improve important metabolic and endocrine aberrations in polycystic ovary syndrome, they are not recommended when hirsutism is the sole indication for use.
More recent research suggests that metformin modestly increases the effectiveness of other anti-hirsutism medications, particularly oral contraceptives and spironolactone. In other words, while metformin probably shouldn't be prescribed by itself for hirsutism, it may well be prescribed in combination with an anti-androgen medication (probably spironolactone) or an oral contraceptive.

Herbs for Anti-Androgenic Effects

In addition to traditional medicines, there are herbs that are reputed to have anti-androgenic effects.  

For example, herbal spearmint tea has long been used as an anti-hirsutism treatment in Middle Eastern cultures. Research suggests that spearmint tea may have mild anti-androgenic effects and may be helpful with hirsutism, but longer studies are needed to evaluate this.

Other possible herbal agents may include red reishi (a mushroom used in Chinese medicine), licorice root, Chinese peony, green tea, black cohosh, and saw palmetto extract. Many women with PCOS use chaste tree/vitex in particular. More information on the (rather sparse) research behind these possibilities can be found here.

Some of the most distressing symptoms of PCOS are the ones that affect a woman's appearance. Most (though not all) women with PCOS experience excess facial and body hair. Many experience cystic acne, and some also experience thinning hair on the head. Add in the obesity common to PCOS, and symptoms strike right at the heart of a woman's self-esteem.

Although most clinicians focus more on menstrual cycle and insulin resistance, the majority of women with PCOS actually seek treatment for cosmetic issues or fertility concerns. Distressing cosmetic issues are often the biggest priority because of the impact on social lives and self-esteem.

Most clinicians utilize oral contraceptives as the first-line treatment for symptoms of androgen excess like hirsutism. If there is not enough improvement after about 6 months, they may add in an insulin-sensitizing medication or an anti-androgen drug as well. Patients are often counseled to consider cosmetic solutions as well (such as electrolysis, laser treatment, or eflornithine for hirsutism).

Anti-androgen drugs have been shown to be reasonably effective against hirsutism and acne, but are not very effective in slowing down hair loss and usually do not restore hair that is already gone. CPA may show some promise for alopecia but more research is needed, and it is also not uniformly available. It also carries significant risks for blood clots, and withdrawal from the medication may make hair loss worse.

The efficacy of anti-androgen medications varies strongly from person to person. Some women get very effective help from these drugs, while others get little relief at all.

Some only get results when combining anti-androgen drugs with birth control pills and/or metformin. Others get better relief from herbs, or a combination of herbs and cosmetic treatments. Still others never get much effect at all, whatever the combination of treatments. As always, the key is to experiment with various treatment protocols and see what works for you.

Again, because the risk for blood clots, birth defects, and toxicity with these anti-androgen drugs is very high, be sure you thoroughly research the pros and cons of each choice, consult carefully with a healthcare provider about your risk factors, get baseline and follow-up blood tests, and have a foolproof plan for birth control in place.

Anti-androgen drugs can be an effective tool in the PCOS toolbox. Some women find them very helpful, while others prefer to avoid them. They do carry significant risks so consider all the pros and cons thoroughly before you decide on whether to make them part of your PCOS toolbox.


Anti-Androgen Medications, General Information

Cochrane Database Syst Rev. 2009 Apr 15;(2):CD000194. doi: 10.1002/14651858.CD000194.pub2. Spironolactone versus placebo or in combination with steroids for hirsutism and/or acne. Brown J1, Farquhar C, Lee O, Toomath R, Jepson RG. PMID: 19370553
AUTHORS' CONCLUSIONS: From the studies included in this review, there is some evidence to show that spironolactone is an effective treatment to decrease the degree of hirsutism but there was no evidence for effectiveness for the treatment of acne vulgaris. Studies in this area are scarce and small. Individual study data indicates some superiority of spironolactone over other drugs but results cannot be generalised.
J Endocrinol Invest. 2005 Jan;28(1):49-53. Spironolactone in the treatment of polycystic ovary syndrome: effects on clinical features, insulin sensitivity and lipid profile. Zulian E et al.  PMID: 15816371
...Twenty-five patients...were studied at baseline and then received oral spironolactone (100 mg/die) for 12 months...The efficacy of spironolactone on the androgenic clinical aspects of PCOS has been confirmed in this study. Furthermore, our data show that long-term treatment with spironolactone exerts no negative effects on lipoprotein profile and glucose metabolism; more relevant beneficial effects on glucose and lipid metabolism were observed when the antiandrogen was associated with weight loss in overweight PCOS women.
Dermatol Clin. 2010 Jul;28(3):611-8. doi: 10.1016/j.det.2010.03.011. Innovative use of spironolactone as an antiandrogen in the treatment of female pattern hair loss. Rathnayake D1, Sinclair R. PMID: 20510769
...Although androgens play a key role in the pathogenesis of male pattern hair loss (MPHL), the role of androgens in female pattern hair loss (FPHL) is less well established. Satisfactory treatment response to antiandrogen therapy supports the involvement of androgens in the pathogenesis of FPHL...Spironolactone both reduces adrenal androgen production and exerts competitive blockade on androgen receptors in target tissues. Spironolactone has been used off-label in FPHL for over 20 years. It has been shown to arrest hair loss progression with a long-term safety profile. A significant percentage of women also achieve partial hair regrowth....

Arch Gynecol Obstet. 2009 Mar;279(3):321-7. doi: 10.1007/s00404-008-0719-z. Epub 2008 Jul 8. The risk of hepatotoxicity during long-term and low-dose flutamide treatment in hirsutism. Dikensoy E1, Balat O, Pence S, Akcali C, Cicek H. PMID: 18607612
OBJECTIVE: Flutamide is an effective drug in treatment of hirsutism. Hepatotoxicity occasionally may occur with therapeutic doses (750-1500 mg/day), 3 months after initiation of treatment. Monitoring of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels is recommended to obviate serious hepatotoxicity. MATERIALS AND METHODS: Two hundred and fourteen patients with mean age of 20.9+/-2.34 years suffering from hirsutism were included in the study...Fifty-seven patients with PCOS (group 1) were given flutamide 125 mg/day + oral contraceptive. Sixty patients with PCOS (group 2) were given flutamide 250 mg/day + oral contraceptive. Forty-seven patients with IH (group 3) were given flutamide 125 mg/day alone, and 50 patients with IH (group 4) were given flutamide 250 mg alone. Thirty women in control group (group 5) were given placebo only...RESULTS: No incidence of increase in AST or ALT levels (>or= 45 U/L) was observed in any of the groups...CONCLUSION: We conclude that flutamide in a dosage of 125 or 250 mg daily is a safe drug in the long-term treatment of hirsutism. The follow-up of patients receiving flutamide can be done by monitoring AST or ALT levels for hepatotoxicity.
Ginekol Pol. 2013 Apr;84(4):258-62. Clinical efficacy of low dose flutamide plus Diane-35 in the treatment of idiopathic hirsutism and polycystic ovary syndrome. Boztosun A1, Açmaz G, Ozturk A, Müderris II. PMID: 23700857
...26 polycystic ovary syndrome and 24 idiopathic hirsutism patients were evaluated...All patients received 125 mg Flutamide once a day and Diane 35 tablets for 21 days of each month, for 12 months...The decreases in Ferriman-Gallwey scores were significant in both groups in the 6th and 12th month of therapy. Combined treatment significantly decreased total and free testosterone, DHEAS and significantly increased SHBG levels in both groups and additionally decreased levels of LH, androstenodione and LH/FSH ratio in the polycystic ovary syndrome group. CONCLUSION: Combined treatment was effective and safe in the treatment of hirsutism. Combined regimens have additional effects on the treatment of hirsutism.

Gynecol Endocrinol. 2003 Feb;17(1):57-63. The benefits of finasteride for hirsute women with polycystic ovary syndrome or idiopathichirsutism. Lakryc EM, et al.  PMID: 12724020
...The aim of this study was to evaluate the clinical and hormonal effects of finasteride on hirsute women with idiopathic hirsutism or polycystic ovary syndrome. Twenty-four women were randomly divided into two groups: those given placebo and those given finasteride 5 mg/day. The treatment period was 6 months. All patients were evaluated before the beginning of treatment (baseline) and after 3 and 6 months of treatment...All the patients treated with finasteride perceived a reduction in hirsutism after 6 months. In conclusion, our data suggest that finasteride may be effective for the treatment of the hirsute woman with idiopathic hirsutism or polycystic ovary syndrome.

Gynecol Endocrinol. 2002 Feb;16(1):63-6. New alternative treatment in hirsutism: bicalutamide 25 mg/day. Müderris II1, Bayram F, Ozçelik B, Güven M. PMID: 11915584
The efficacy of low-dose bicalutamide (25 mg/day) in the treatment of hirsutism was investigated in this study...42 women with hirsutism...received 25 mg/day bicalutamide... Clinical improvement in the degree of hirsutism was observed in all patients by the same author. The modified Ferriman-Gallwey scores decreased from a mean of 22.0 +/- 5.1 to 8.6 +/- 3.5 (p < 0.0001). The reduction in hirsutism scores was 41.2 +/- 11.4% at 3 months and 61.6 +/- 11.1% at 6 months. In conclusion, bicalutamide at 25 mg/day is an effective drug in the treatment of patients with hirsutism.
Comparisons of Different Anti-Androgen Medications

Cochrane Database Syst Rev. 2015 Apr 28;4:CD010334. doi: 10.1002/14651858.CD010334.pub2.
Interventions for hirsutism (excluding laser and photoepilation therapy alone). van Zuuren EJ1, Fedorowicz Z, Carter B, Pandis N. PMID: 25918921
...AUTHORS' CONCLUSIONS: Treatments may need to incorporate pharmacological therapies, cosmetic procedures, and psychological support. For mild hirsutism there is evidence of limited quality that OCPs are effective. Flutamide 250 mg twice daily and spironolactone 100 mg daily appeared to be effective and safe, albeit the evidence was low to very low quality. Finasteride 5 mg daily showed inconsistent results in different comparisons, therefore no firm conclusions can be made. As the side effects of antiandrogens and finasteride are well known, these should be accounted for in any clinical decision-making. There was low quality evidence that metformin was ineffective for hirsutism and although GnRH analogues showed inconsistent results in reducing hirsutism they do have significant side effects. Further research should consist of well-designed, rigorously reported, head-to-head trials examining OCPs combined with antiandrogens or 5α-reductase inhibitor against OCP monotherapy, as well as the different antiandrogens and 5α-reductase inhibitors against each other....
Beigi A, Sobhi A, Zarrinkoub F. Finasteride versus cyproterone acetate-estrogen regimens in the treatment of hirsutism. International Journal of Gynaecology and Obstetrics. 2004; 87: 29-33. PMID: 15464773
...Forty hirsute women were enrolled in a prospective randomized trial. Twenty-nine had polycystic ovary syndrome (PCOS) and 11 had idiopathic hirsutism. Patients were randomly treated with finasteride (5 mg/day; n=20) or CPA plus EE2 [CPA (25 mg/day on days 5-14) plus EE2 (20 microg/day on days 5-25) n=20] for 9 months... CONCLUSION: Finasteride and CPA plus EE2 are equally effective in decreasing hirsutism, despite significantly different effects on serum hormone levels.
Calaf J, Lopez E, Millet A, et al. Long-term efficacy and tolerability of flutamide combined with oral contraception in moderate to severe hirsutism: a 12-month, double-blind, parallel clinical trial. Journal of Clinical Endocrinology and Metabolism. 2007; 92: 3446-3452. PMID: 17566093
OBJECTIVE: Our objective was to test the efficacy and tolerability of three doses of flutamide (125, 250, and 375 mg) combined with a triphasic oral contraceptive (ethynylestradiol/levonorgestrel) during 12 months to treat moderate to severe hirsutism in patients with polycystic ovary syndrome or idiopathic hirsutism. DESIGN: We conducted a randomized, double-blind, placebo-controlled, parallel clinical trial...A total of 119 patients were included in the intention-to-treat analysis... CONCLUSIONS: Flutamide at 125 mg daily during 12 months was the minimum effective dose to diminish hirsutism in patients with polycystic ovary syndrome or with idiopathic hirsutism.
Moghetti P, Tosi F, Tosti A, et al. Comparison of spironolactone, flutamide and finasteride efficacy in the treatment of hirsutism: a randomized, double blind, placebo-controlled trial. Journal of Clinical Endocrinology and Metabolism. 2000; 85: 89-94. PMID: 10634370
To compare objectively the efficacies of spironolactone (100 mg/day), flutamide (250 mg/day), and finasteride (5 mg/day) in the treatment of hirsutism, 40 hirsute women were randomly assigned to double blind treatments with 1 of these 3 drugs or placebo for 6 months...spironolactone, flutamide, and finasteride are all effective in the treatment of hirsutism. After a 6-month course of therapy, the clinical efficacies of these drugs, at least at the doses used, are similar.
Anti-Androgen Effects of Various Oral Contraceptives 

Fertil Steril. 2012 Jul 13. Comparative study of the therapeutic effects of oral contraceptive pills containing desogestrel, cyproterone acetate, and drospirenone in patients with polycystic ovary syndrome. Bhattacharya SM, Jha A.  PMID: 22795636
OBJECTIVE: To compare the effects of oral contraceptive pills containing desogestrel, cyproterone acetate, and drospirenone, in polycystic ovary syndrome (PCOS), after 6 and 12 months of therapy. DESIGN: Double-blind randomized controlled trial... PATIENT(S): Women (n = 171) with PCOS (Androgen Excess Society criteria, 2006). INTERVENTION(S): The three-arm trial involved 58, 56, and 57 cases in desogestrel, cyproterone acetate, and drospirenone groups, respectively... CONCLUSION(S): No difference in effects after 6 months. At 12 months, cyproterone acetate showed the strongest antiandrogen activities. Effects on metabolic parameters were identical. 
Arch Gynecol Obstet. 2014 Aug;290(2):321-8. doi: 10.1007/s00404-014-3217-5. Epub 2014 Mar 28. Comparison of two oral contraceptive forms containing cyproterone acetate and drospirenone in the treatment of patients with polycystic ovary syndrome: a randomized clinical trial. Kahraman K1, Sükür YE, Atabekoğlu CS, Ateş C, Taşkın S, Cetinkaya SE, Tolunay HE, Ozmen B, Sönmezer M, Berker B. PMID: 24676694
PURPOSE: To compare the effects of combined oral contraceptives (OCs) containing cyproterone acetate and drospirenone in the treatment of polycystic ovary syndrome (PCOS). METHODS: Fifty-two patients with PCOS were randomized in two groups: group A (n = 26) received 0.035 mg ethinyl estradiol + 2 mg cyproterone acetate and group B (n = 26) received 0.03 mg ethinyl estradiol + 3 mg drospirenone-containing OCs for 12 months...CONCLUSIONS: Cyproterone acetate containing OCs seem to be more effective to treat clinical hirsutism in patients with PCOS after 12 months of treatment.

Ther Clin Risk Manag. 2008 Apr;4(2):487-92. Use of ethinyl estradiol/drospirenone combination in patients with the polycystic ovary syndrome. Mathur R, Levin O, Azziz R.   PMID: 18728832   Free full text available here.
...One of the main issues in COC [combined oral contraceptive] therapy is choosing the most appropriate progestin component to provide the greatest anti androgenic effects. Drospirenone, a relatively new progestin, has shown benefit in the PCOS population when used in conjunction with ethinyl estradiol. We now review the role of COCs in PCOS, focusing specifically on drospirenone. Controversy over metabolic effects of COCs in PCOS is also discussed. 
Cyproterone Acetate (CPA) 

See Mathur 2008 above for CPA information also
Gynecol Endocrinol. 2008 Oct;24(10):590-600. The effects of Diane-35 and metformin in treatment of polycystic ovary syndrome: an updated systematic review. Jing Z, et al. PMID: 19012104
...A systematic review and meta-analysis were conducted. Randomized controlled studies applying Diane-35 and metformin for treating PCOS were included. The primary outcome was hirsutism...CONCLUSIONS: Diane-35 is superior to metformin in reducing androgens, but inferior to metformin in reducing insulin. Whether Diane-35 deteriorates lipid metabolism and insulin resistance is still unclear.
Treatment of Hirsutism
General Review of PCOS Treatments

Clin Evid (Online). 2009 Jan 15;2009. pii: 1408. PCOS. Cahill D. PMID: 19445767  Free full text available here.
...CONCLUSIONS: In this systematic review we present information relating to the effectiveness and safety of the following interventions: finasteride, flutamide, metformin, spironolactone, cyproterone acetate-ethinylestradiol (co-cyprindiol), interventions to achieve weight loss, ketoconazole, and mechanical hair removal.
Am Fam Physician. 2009 Apr 15;79(8):671-676. Drug Treatment for Polycystic Ovary Syndrome. Radosh, L. American Academy of Family Physicians. Free full text available here