Bonehead Ideas: High Cholesterol Equals High Cesarean Rates in Obese Women

Periodically, the obstetric world comes up with some bizarre theories as to why "obese" women have higher cesarean rates than women of average size.

The reasons behind higher rates is a valid question, but the way in which the obstetric world examines the question reveals much of their biases and assumptions around obesity.

One of their more persistent theories is the "Fat Vagina" theory, where they theorize that the vaginas of high-BMI women are lined with fat pads that will prevent a baby from getting out. Sadly, many doctors and midwives are still taught this theory as if it is established fact, when in truth, there is no data to back it up.

And of course, the current favorite among many providers is the "High Prenatal Weight Gain" theory, where women who gain more than the approved amount of weight are blamed for cesareans. And since any gain at all in obese women is considered "too much" by many providers, this may play a particularly potent role in the cesarean rate in women of size. But providers making a causal connection between high gains and cesareans completely ignore the role that fear and bias around high gains can play in many labors. It may not be high gains per se that cause more cesareans but rather the fears and interventions common in high-gain women (especially "high" gain obese women) that result in more cesareans.

One of the more ludicrous theories that doctors have come up with in recent years to excuse abysmally-high cesarean rates in fat women is the "Cholesterol Inhibits Myometrial Activity" theory.

Sadly, this theory gained a lot of mention in obstetric literature in recent years, despite very limited and dubious evidence to support it.

High Cholesterol Causes Cesareans?

In the Cholesterol Theory, high cesarean rates in fat women are supposedly caused by high cholesterol rates (since, you know, all fat women have high cholesterol) because high cholesterol rates supposedly impair the contractility of the uterine muscle.

Say what? Yeah, I know, that was my reaction too.

But yes, it was an actual theory put forward by a number of researchers in recent years. (And its kissin' cousins, that leptin or some other substance are the guilty parties instead.)

Because, you know, all fat women are defective and this explains how.

So the theory goes, if we give fat pregnant women statin medications, maybe that will cut their cesarean rate. Yes, there are actually doctors who have proposed doing this.

Fortunately, there is a recent study out that casts serious doubt on this bonehead Cholesterol Theory.

Problems with the Cholesterol Theory

I've written about this issue before, pointing out that the Cholesterol Theory has a number of problems.

First of all, many fat women do NOT have high cholesterol at all. (I'm one of them.) Many fat women have perfectly normal cholesterol levels, particularly during childbearing years. The fact that researchers assume that nearly all fat people have high cholesterol is symbolic of the typical assumptions researchers make about fat people and how these impact their ability to reach sound conclusions.

Second, the studies on "poor contractility" in obese women are quite small. This certainly raises the question of how whether the findings could be related to coincidence or confounding factors, rather than showing a true causal relationship. But virtually no one raises this question. They are happy to just jump to conclusions.

Third, please note that many of the studies supposedly showing "poor contractility" in obese women were done on women having planned cesareans with NO labor. How does this prove how they might have labored in real life? They took samples of the uteri before labor even started, and then did some lab tests on them, testing "contractility" in the lab.

Sorry, this is hardly indicative of real-life labor and birth, and since they did pre-emptive cesareans on these women, how can they prove that these in vitro "contractility" tests really have any relationship to how labor would have gone? There is just no way that this proves that there is something wrong with fat women's uteri.

Furthermore, they did not look for any other explanations for lower contractility in vitro. Studies show that fat women tend to have longer menstrual cycles and longer pregnancies. Planned cesareans like these were often done at 38 or 39 weeks, and if obese women tend to go into spontaneous labor closer to 42 weeks (either due to inaccurate dating from longer cycles or because of a tendency towards longer pregnancies), doing such an early cesarean would not reliably show whether their uteri were inherently "less contractile." Rather, it would simply suggest that these obese women were not even close to spontaneous labor yet and therefore less responsive to stimulants.

The bottom line is that these studies have a lot of issues.

While it's not wrong to propose a hypothesis for an observed problem, you have to be careful about jumping to conclusions too quickly. These studies relied on very small sample sizes, speculated about an obese woman's response to labor based on in vitro testing from a pre-labor cesarean, didn't explore alternate causes for the findings, and generalized assumptions about obesity and cholesterol levels in a very broad and questionable manner.

The Cholesterol Theory is FAR from a proven connection, although you'd never know it, based on the way many researchers discuss it. And the research certainly does not support routinely putting fat women on statin medications.

The Newest Study on Cholesterol and Cesareans

My biggest question last time I wrote about this issue was whether they had done any studies to see if the fat women who delivered vaginally had better cholesterol levels than the ones who had cesareans, or whether thin women with high cholesterol had more cesareans.

Well, finally we have a study directly addressing some of this. A recent study from New Zealand compared delivery method (cesarean vs. vaginal birth) with women's cholesterol levels at 14-16 weeks to see if there was a correlation between high cholesterol and cesareans.

They found there was NO correlation between the mother's cholesterol levels in early pregnancy and her delivery method. 

However, surprise surprise, they found that induction of labor was connected to cesareans. Imagine!

They concluded:

Elevated maternal cholesterol in early pregnancy is not a risk factor for first stage caesarean for failure to progress in overweight/obese women. 

Conclusion

This "High Cholesterol Causes Cesareans in Obese Women" theory is the kind of bad science that makes fat people so distrustful of medicine and doctors.

So often, it's all just based on ASSUMPTIONS about fat people and not on any real detailed study or logical questioning of theories.

Furthermore, the fact that several years ago they publicized this theory without having proven it and were even marketing the idea of giving statins was absolutely irresponsible.

Statins are CONTRAINDICATED in pregnancy; they are category "X" and may cause birth defects. Cholesterol and lipids play a very important role in fetal development. There is a reason why a pregnant woman's cholesterol rises during pregnancy; the baby needs it for development. Artificially lowering these levels may have devastating effects on the baby.

Critics responded that they were "only" suggesting putting fat women on statins in the last few months of pregnancy, so therefore there would be no risk of birth defects. But if these drugs can be so dangerous in early pregnancy, who knows what kind of harm they might cause late in pregnancy as well? There are other harms that can be caused to babies besides birth defects during organogenesis.

No one knows for sure what critical roles cholesterol and lipids play during late pregnancy. Pregnant women's cholesterol levels rise through pregnancy, suggesting that it has an important biological role to play in the end of pregnancy. Putting women on statins at the end of pregnancy may be just as harmful as at the beginning of pregnancy, just perhaps with more subtle problems than birth defects.

What it boils down to is that they were proposing using fat women's babies as lab rats to experiment on, based on extremely flimsy theories. This is UNACCEPTABLE.

There is completely insufficient evidence to support the idea that high cholesterol is the cause of the high cesarean rate in fat women, and the safety of statins in pregnancy at ANY stage is highly questionable. To suggest treatment with statins for anyone during any stage of pregnancy is risky and BAD science.

Furthermore, to be running stories in the media suggesting statin use in fat pregnant women before suitable research was done substantiating the Cholesterol Theory was reprehensible. It smacks of a few researchers looking for a "hook" to gain name recognition and funding (or a drug company looking for new revenue streams), rather than serious and responsible scientists pursuing a legitimate investigation.

You can read more about the original story here.

It is time for researchers to stop jumping to conclusions about fat women and pregnancy, time for them to examine their own faulty assumptions about obesity and how this distorts their research, time for them to stop using fat women's babies as lab rats for their own personal theories, and time for researchers to stop prematurely "spinning" preliminary research in order to get name recognition and research funding.

It's far too easy for care providers to blame the high cesarean rate in obese women on Fat Vaginas, High Cholesterol, High Prenatal Weight Gain or whatever other boogeyman is currently popular in the obstetric literature. This blames the victim and conveniently absolves themselves of blame.

It is long past time for obstetric researchers to stop blaming women and do the uncomfortable job of examining how their own practices and biases raise the cesarean rate in obese women.


References

BMC Pregnancy Childbirth. 2013 Jul 9;13:143. doi: 10.1186/1471-2393-13-143. Elevated maternal lipids in early pregnancy are not associated with risk of intrapartum caesarean in overweight and obese nulliparous women. Fyfe EM, Rivers KS, Thompson JM, Thiyagarajan KP, Groom KM, Dekker GA, McCowan LM; SCOPE consortium. PMID: 23835080 Full text available here.

BACKGROUND: Maternal overweight and obesity are associated with slower labour progress and increased caesarean delivery for failure to progress. Obesity is also associated with hyperlipidaemia and cholesterol inhibits myometrial contractility in vitro. Our aim was, among overweight and obese nulliparous women, to investigate 1. the role of early pregnancy serum cholesterol and 2. clinical risk factors associated with first stage caesarean for failure to progress at term. METHODS: Secondary data analysis from a prospective cohort of overweight/obese New Zealand and Australian nullipara recruited to the SCOPE study. Women who laboured at term and delivered vaginally (n=840) or required first stage caesarean for failure to progress (n=196) were included. Maternal characteristics and serum cholesterol at 14-16 weeks' of gestation were compared according to delivery mode in univariable and multivariable analyses (adjusted for BMI, maternal age and height, obstetric care type, induction of labour and gestation at delivery ≥41 weeks). RESULTS: Total cholesterol at 14-16 weeks was not higher among women requiring first stage caesarean for failure to progress compared to those with vaginal delivery (5.55 ± 0.92 versus 5.67 ± 0.85 mmol/L, p= 0.10 respectively). Antenatal risk factors for first stage caesarean for failure to progress in overweight and obese women were BMI (adjusted odds ratio [aOR (95% CI)] 1.15 (1.07-1.22) per 5 unit increase, maternal age 1.37 (1.17-1.61) per 5 year increase, height 1.09 (1.06-1.12) per 1cm reduction), induction of labour 1.94 (1.38-2.73) and prolonged pregnancy ≥41 weeks 1.64 (1.14-2.35). CONCLUSIONS: Elevated maternal cholesterol in early pregnancy is not a risk factor for first stage caesarean for failure to progress in overweight/obese women. Other clinically relevant risk factors identified are: increasing maternal BMI, increasing maternal age, induction of labour and prolonged pregnancy ≥41 weeks' of gestation.

Theories on Cholesterol, Leptin, and Myometrial Contractility

Med Hypotheses. 2011 May;76(5):755-60. doi: 10.1016/j.mehy.2011.02.018. Epub 2011 Mar 5. Proposed biological linkages between obesity, stress, and inefficient uterine contractility during labor in humans. Lowe NK, Corwin EJ. PMID: 21382668

Cesarean delivery has reached epidemic proportions in contemporary western healthcare. For otherwise healthy first-time (nulliparous) women at term gestation with a single fetus in a head down position, the most common clinical diagnosis prompting cesarean delivery is dystocia, including clinical terms such as uterine dysfunction, failure to progress, arrest of dilation and/or arrest of descent of the fetal head. In 2006, the cesarean rate for this lowest risk population of childbearing women was 26% in the United States despite the goal of Healthy People 2010 to reduce this rate to 15% from a baseline of 18% in 1998. While multiple lines of evidence suggest that the nulliparous uterus is particularly vulnerable to a diagnosis of uterine dysfunction during labor, pathophysiologic explanations for this dysfunction have not been well described. The acute stress response has been implicated as one factor in this dysfunction for many years, while more recently the growing epidemic of adiposity among women of childbearing age has been suggested as an additional pathway by which myometrial cell function may be disrupted. Using both clinical and in vitro evidence, we hypothesize a combined model in which pathways of acute stress and changes associated with maternal adiposity, particularly exaggerated levels of cholesterol and leptin, may independently and synergistically impair the contractile apparatus of the myocyte leading to the clinical diagnosis of uterine dystocia and subsequent cesarean delivery.

Am J Obstet Gynecol. 2006 Aug;195(2):504-9. Epub 2006 May 2. Inhibitory effect of leptin on human uterine contractility in vitro. Moynihan AT, Hehir MP, Glavey SV, Smith TJ, Morrison JJ. PMID: 16647683

OBJECTIVE: The purpose of this study was to investigate the effects of leptin on human uterine contractility in vitro. STUDY DESIGN: Biopsies of human myometrium were obtained at elective cesarean section (n = 18). Dissected myometrial strips suspended under isometric conditions, undergoing spontaneous and oxytocin-induced contractions, were exposed to cumulative additions of leptin in the concentration range of 1 nmol/L to 1 micromol/L. Control strips were run simultaneously...RESULTS: Leptin exerted a potent and cumulative inhibitory effect on spontaneous and oxytocin-induced contractions compared to control strips...There was an apparent reduction in both frequency and amplitude of contractions. CONCLUSION: This physiologic inhibitory effect of leptin on uterine contractility may play a role in the dysfunctional labor process associated with maternal obesity, and the resultant high cesarean section rates.

Reprod Sci. 2007 Jul;14(5):456-66. Contractility and calcium signaling of human myometrium are profoundly affected by cholesterol manipulation: implications for labor? Jie Zhang, Kendrick A, Quenby S, Wray S. PMID: 17913965

The authors elucidate cholesterol's effect on human uterine contractility and calcium signaling to test the hypotheses that elevation of cholesterol decreases uterine activity and that oxytocin cannot augment contraction when cholesterol is elevated...Elevated cholesterol is deleterious to contractility and Ca2+ signaling in human myometrium. Cholesterol may contribute to uterine quiescence but could cause difficulties in labor in obese/dyslipidemic women, consistent with their increased cesarean delivery rates.

Obesity and Contractility

BJOG. 2007 Mar;114(3):343-8. Epub 2007 Jan 22. Poor uterine contractility in obese women.
Zhang J, Bricker L, Wray S, Quenby S. PMID: 17261121

OBJECTIVE: The aim of the study was to elucidate the reason for the high rate of caesarean section in obese women. We examined the following hypotheses: (1) obese women have a high incidence of complications related to poor uterine contractility--caesarean section for dysfunctional labour and postpartum haemorrhage. 2) The myometrium from obese women has less ability to contract in vitro. DESIGN: First, a clinical retrospective analysis of data from 3913 completed singleton pregnancies was performed. Secondly, in a prospective study the force, frequency and intracellular [Ca(2+)] flux of spontaneously contracting myometrium were related to the maternal body mass index. SETTING: Liverpool Women's Hospital and University of Liverpool. POPULATION: The clinical study involved all women who delivered in one hospital in 2002. The in vitro study myometrial biopsies were obtained from 73 women who had elective caesarean section at term. RESULTS: Maternal obesity carried significant risk of caesarean section in labour that was highest for delay in the first stage of labour (OR 3.54). The increased risk of caesarean section in obese women largely occurred in women with normal- and not with high-birthweight infants. Obese women delivering vaginally had increased risk of prolonged first stage of labour and excessive blood loss. Myometrium from obese women contracted with less force and frequency and had less [Ca(2+)] flux than that from normal-weight women. CONCLUSIONS: We suggest that these findings indicate that obesity may impair the ability of the uterus to contract in labour.