Saturday, January 10, 2015

Test Those Smoke Detectors Frequently

Last week, my husband almost burned down our house while cooking dinner.

The good news is that he didn't actually burn down the house. It was all smoke, albeit pretty thick smoke; I caught it before it turned into flames.

The bad news is that it probably ruined a beloved pan I got from my mother, and the house still smells a bit like scorched metal. Hopefully that will disappear soon.

The unsettling news is that this was a good check of our smoke detectors ─ and we found that they totally FAILED the test. Ulp! So now we are working on fixing that issue.

My husband is a great guy with many many sterling qualities, but he has a bad habit of putting something on the stove and then leaving the room, forgetting about the item on the stove. I've rescued many scorched things over the years, and have had to throw out more than a few. (I have to be fair ─ I've been known to put something on the stove and forget about it once in a while. You really shouldn't leave the room if you have anything on the stove.)

Well, that's what he did last week. He put a pot of beans on the stove to boil, then took the kids out, forgetting the pan on the stove. I stayed behind to work on the computer but he didn't tell me that he was cooking anything.

Thank goodness I stayed home! After quite a while I smelled the burning pot and went to investigate. Sure enough, there was the pot of beans on the stove, scorching like crazy. Luckily, I got to them before any flames actually began, but it was obviously only a matter of time before that had happened too. If I hadn't been at home, it might well have happened.

The most alarming part was that the house was filled with smoke, yet not a single smoke detector was going off. 

Sometimes there's not enough smoke to really set off a detector, even though it looks pretty smoky. But that's not what happened here. Nope, there was more than enough smoke to warrant a smoke detector going off this time, but not one did. Uh-oh.

We usually check our smoke detectors during daylight savings time changes in fall and spring. But sometimes I ask him to do that and he says he's done it, yet it turns out he didn't really do it. (Does your spouse ever do that?) That's what happened this year.

When we checked, it turns out that there wasn't a single smoke detector on the main floor of the house that was working properly. Doh!

And not only that, you're supposed to check the batteries on smoke detectors every six months (at the time changes) and change the batteries every year ─ PLUS you are supposed to test the smoke detectors every month. We were only testing them every six months (and apparently not always even then). Oops.

Thank goodness we hadn't had a fire. We would have been out of luck.

As a parent, I'm all about preparing for emergencies, as long-time readers of the blog know. Mostly I prepare for scenarios involving weather issues (snowstorms, windstorms), power outages, or earthquakes (we live in a major earthquake zone). Although I joke about the Zombie Apocalypse, I don't really get too concerned about the scenarios that many preppers worry about, honestly. I can't say I'm not concerned, but honestly I don't think most are very likely.

But natural disasters? Those happen regularly. It makes much more sense to focus your prepping on the kinds of scenarios that statistics show every area encounters periodically, rather than focus obsessively on a rare something that might or might not happen someday.

Yet you should always focus on fire safety first and foremost, because FIRE is the life-threatening emergency scenario you are most likely to face in your life. 

The Red Cross notes that, on average, 7 people die every day from a home fire. Fires kill more Americans each year than all other natural disasters combined.

But having a working smoke detector cuts the risk of dying in a home fire in half.

The Red Cross estimates that nearly 900 lives a year could be saved if only every home had working smoke detectors.

So go now, go check your smoke detectors. While you're at it, add some Carbon Monoxide detectors too. 

And don't forget to push the button regularly and test to see if these detectors actually work.


For more information:

Sunday, January 4, 2015

Recent Studies on Inositol for PCOS

Here are the abstracts of some new studies on the use of inositol (d-chiro-inositol or myo-inositol) in women with Polycystic Ovarian Syndrome (PCOS).

Inositol is a naturally-occurring substance in our foods that helps us process insulin properly. Normally, our bodies convert substances in plants and animals into several different forms of inositol. Two of these inositols are used in insulin-signaling pathways. However, some research suggests that women with PCOS do not use inositol properly, leading to insulin-signaling problems. 

These defects in insulin signaling means that the body has to over-produce insulin to compensate. The insulin that is produced does not get used properly, causing excess amounts to stay in the body.

This in turns stimulates the production of androgens ("male" hormones), leading to an imbalance in hormones in the body and many of the distressing symptoms of PCOS (including hirsutism, alopecia, acne, and difficulty ovulating).

And because the body struggles to use its insulin properly, this can lead to increased blood sugar issues over time. This is why many women with PCOS become diabetic at some point in their lives.

Now, however, emerging research suggests that supplementing the body with these inositols may help insulin signaling, thus lowering insulin resistance and improving blood sugar. It may even help lessen PCOS symptoms.

We've discussed inositols before in detail, here, which can be read for a good start on the subject. But right now let's take a look at some of the latest thinking on inositols, as well as on studies that have been released since that original post or were not cited in it.

How Inositols Work in Insulin Signaling

First, a little background for those new to the topic.

Inositols act as "second messengers" in insulin signaling. They play a very important role in how we use insulin.

Insulin produced by the body binds to insulin receptors on the cell walls. From there, the receptor generates second messengers (inositolphosphoglycans, or IPGs) to relay and amplify the signal to help the body use the insulin effectively.

But women with PCOS seem to have a defect in their second messenger pathway. This could explain why they have such strong insulin resistance. One PCOS resource simplifies it this way:
When we eat foods (mostly carbohydrates), they get converted into glucose in our blood stream. We need the glucose to enter our cells to be used for energy. When blood glucose levels rise, a signal (imagine a doorbell is rung) is sent from the cell door to the nucleus telling it to open up. However, with PCOS, the doorbell on the cell door may be defective. This means that it takes longer for the cells to open its doors to glucose resulting in higher amounts of insulin needing to be secreted. Secondary messengers acts to repair the doorbell so that the cell doors open in response to glucose, resulting in less insulin needing to be secreted. 
Improving this second messenger pathway could also become a radical new way of treating PCOS. As one review noted:
The discovery that the impairment in the insulin signalling could be due to a defect in the inositolphosphoglycans (IPGs) second messenger pathway opened a new horizon in the clinical management of PCOS. IPGs are known to have a role in activating enzymes that control glucose metabolism. In PCOS women, a defect in tissue availability or altered metabolism of inositol or IPGs mediators may contribute to insulin resistance
So the problem in PCOS may simply be errors in the second messenger insulin signaling pathway, and treating women with some form of inositol may help bridge the errors in this pathway.

The question is, which is the most effective form of inositol and should the type/dosage used depend on its purpose?

Which Form of Inositol Works Best?

Two forms of inositol get the most attention in PCOS research:
  • myo-inositol (MI or MYO)
  • d-chiro-inositol (DCI)
Both are forms of inositol, just slightly different stereoisomers. Both play important roles in insulin signaling; their roles are different but complementary.

MI is usually seen as a precursor to DCI; evidence suggests that the body converts myo-inositol to d-chiro inositol. Another inositol stereoisomer, d-pinitol, is also thought to convert into DCI in the body, but MI is thought to be the more important source.

However, many women with PCOS seem to have difficulty with the conversion from MI to DCI, suggesting that PCOS may be caused (or at least influenced) by errors in inositol metabolism. 

So, the theory goes, if we supplement the body directly with inositol, that might help help replace what's missing or make it work more efficiently.

As a result, people have been experimenting with inositol supplements, either myo-inositol or d-chiro-inositol. And the results of these experiments have been promising so far, both in research and anecdotally.

One of the most important questions that has yet to be answered is whether myo-inositol or d-chiro inositol (or some combination of the two) is the best treatment for women with PCOS and what the best dosage/treatment regimen would be.

MI is the form of inositol that is cheapest and easiest to use. It can be bought in capsules over the counter in many health food stores or in bulk powder over the internet. The thought is that if you take enough of it, then the body will convert more of it into DCI and improve insulin signaling, thus decreasing PCOS symptoms and health issues.

On the other hand, DCI is the form that seems to work best on improving hyperandrogenism and possibly insulin resistance. If some women have difficulties converting MI to DCI, why not skip to the chase and supplement directly with DCI?

Early studies on DCI had excellent results and so DCI was the focus of most research at first. However, subsequent studies were not able to replicate these results, so the drug companies largely abandoned DCI as a line of inquiry in 2002. DCI seemed discredited at that point.

What the research since then has suggested is that the initial follow-up studies didn't replicate the studies exactly ─ they increased the dosage in hopes of even better effect. But it seems that they increased the DCI dosage too much ─ apparently, there is a point of diminishing returns with DCI, beyond which it ceases to be helpful, particularly with fertility concerns. So the reason the follow-up studies didn't validate the original studies was because they used a too-high dosage, not because DCI was not potentially useful.

After the supposed "discrediting" of DCI, research on inositols was minimal and mostly focused on MI. Once researchers realized that a too-high DCI dosage was counter-productive and that MI also had benefits, research began to increase on both inositols.

Since myo-inositol is much cheaper and easier to produce, research still often focuses on MI. But some providers still feel that a moderate dose of DCI is a better choice. Still others feel that a combination of MI and DCI should work better, since both work on insulin signaling in different ways.

So what we do know is that there is no clear consensus on inositols yet but that data is emerging and it's important to keep up on the latest research.

Current research seems to suggest that MI is the inositol of choice for PCOS women with fertility issues (it especially seems to improve egg quality) and that MI works better than DCI for fertility treatment.

On the other hand, DCI may be better for those PCOS women with major hyperandrogenism issues and for whom fertility is not a major concern.

The jury is still out on which form is better for significant blood sugar/insulin resistance issues; there is research to support either MI and DCI (or both) for this purpose.

The very latest trend seems to be having women with PCOS take both MI and DCI in a 40:1 ratio (MI to DCI). This usually translates to MI (2-4 grams) and DCI (50-100 mg), but exact dosages will vary from person to person.

Recent research suggests this combination seems to be more effective than either MI or DCI alone. This is logical if they do indeed work on insulin signaling in different ways.

But it may be that the best treatment regimen may differ from woman to woman because the degree of impaired conversion may differ from person to person.

Remember, PCOS tends to have a spectrum of severity. Some have only mild symptoms while others have very severe symptoms. This may reflect a spectrum of efficiency in conversion of MI to DCI. As one resource speculates:
Considering the spectrum of human genetic diversity (take height for example), why should this trait be black/white, yes/no, or on/off? With a little imagination, we can see this impaired conversion of myo-inositol to D-chiro-inositol as a spectrum. Some women make the conversion efficiently, and they have no symptoms of PCOS. Others may make the conversion with some degree of efficiency, but not quite enough to have an optimal MYO/DCI ratio. Their symptoms may be mild. At the other end of the spectrum some people would be completely unable to make this conversion, and they would consequently present with the most severe symptoms. And, as part of the human tapestry, there would be everything in between as well.

Which brings us to the question of which inositol is right for me? Along this spectrum, people who are completely unable to convert myo-inositol to D-chiro-inositol are only going to benefit from supplementation with D-chiro-inositol. Other people who make the conversion, but with less than optimal efficiency, may benefit from large doses of myo-inositol. And, folks in between, might see the best results from a blend of the two.
In other words, some women with PCOS seem to convert MI to DCI pretty well, in which case they probably don't need to take supplemental DCI, just MI. However, others probably do not convert MI to DCI very well and may benefit more from just DCI. Still others may do best with a combination of both.

How are we to know which treatment regimen to try? As always, we need bigger and more qualitative studies to guide our choices.

But in the end, it may also be that each woman (in concert with her care provider) has to experiment and find the right regimen and dosage for her unique needs. 


More and more research is being done on the use of the inositols for PCOS, and most of this research so far is very encouraging. Some researchers are even suggesting that:
...the combined administration of MI and DCI in physiological plasma ratio (40:1) should be considered as the first line approach in PCOS overweight patients.
As we have seen, the most important benefit of inositols may be in improving insulin signaling, thus reducing insulin resistance and lessening PCOS symptoms. If insulin resistance is the major issue with PCOS and research continues to be promising, then inositols may become the key element to treating it. They may be especially useful for those who cannot tolerate metformin.

But there may be other benefits beyond improving the insulin-signaling pathway. For example, inositols are thought to also help the liver to metabolize fat, which may be helpful to those PCOS women with NAFLD (Non-Alcoholic Fatty Liver Disease).

In addition, inositols act as "signal transduction systems" in ways beyond insulin signaling pathways. They may also be related to the activation of serotonin receptors. Some research suggests that high doses of MI may reduce the risk of depression, which may be more common in people with PCOS.

There is only limited data on the use of inositols during pregnancy but some research suggests that use of myo-inositol may significantly lower the risk for the development of gestational diabetes in women with PCOS, in women with diabetic relatives, or in those who are at otherwise high risk for gestational diabetes.

However, keep in mind that most of the research trials on inositols have been very small, quite short-term, and are highly variable in methodological quality. Most are done in Italy and are not taken very seriously by many care providers in the U.S. or U.K. As a result, some researchers don't feel that any of the inositols have been adequately proven yet. And some care providers haven't even heard of inositols, so it can be difficult to find a provider supportive of trying this therapy.

Bottom line, we need more and better trials to know if long-term use of the inositols is safe and effective and to help care providers feel more comfortable with their use.

In particular, there are a few pressing safety questions that need to be addressed:

  • Some sources suggest that women who are on anti-depressants or medications for bipolar disorder may need to avoid inositols or use them only with great care since inositols may affect serotonin receptors
  • Some resources recommend that DCI not be used in conjunction with anti-androgen medications like spironolactone because the two together may be too effective against androgens and a certain amount of androgens are actually needed by the body
  • We need more data proving conclusively that inositols are safe in pregnancy
  • We need more data examining potential interactions with other drugs since many women with PCOS take other medications as well

In short, research on the use of inositols for PCOS is emerging and it behooves us to keep a close watch on emerging research to keep up with the latest developments.

The good news is that the results so far are promising. Below are the abstracts from some of the more important recent studies on inositol use.

*You can read more about the use of the inositols for treatment of PCOS herehere, here, and here. My original blog post about the use of inositols for PCOS can be found here



Eur Rev Med Pharmacol Sci. 2014 Jul;18(13):1896-903. Inositol: history of an effective therapy for Polycystic Ovary Syndrome. Bizzarri M1, Carlomagno G. PMID: 25010620 Free full text here.
Inositol is a physiological compound belonging to the sugar family. The two inositol stereoisomers, myo-inositol and D-chiro inositol are the two main stereoisomers present in our body. Myo-inositol is the precursor of inositol triphosphate, a second messenger regulating many hormones such as TSH, FSH and insulin. D-chiro inositol is synthetized by an insulin dependent epimerase that converts myo-inositol into D-chiro-inositol...In [PCOS] patients myo and/or D-chiro-inositol administration improves insulin sensitivity while only myo-inositol is a quality marker for oocytes evaluation. Myo-inositol produces second messengers for FSH and glucose uptake, while D-chiro inositol provides second messengers promoting glucose uptake and glycogen synthesis. The physiological ratio of these two isomers is 40:1 (MI/DCI) and seems to be an optimal approach for the treatment of PCOS disorders.
d-chiro inositol

Gynecol Endocrinol. 2014 Jun;30(6):438-43. doi: 10.3109/09513590.2014.897321. Epub 2014 Mar 7. Modulatory role of D-chiro-inositol (DCI) on LH and insulin secretion in obese PCOS patients. Genazzani AD1, Santagni S, Rattighieri E, Chierchia E, Despini G, Marini G, Prati A, Simoncini T. PMID: 24601829
...Since it has been demonstrated a high incidence of insulin resistance in PCOS patients, our study aimed to evaluate the efficacy of the integrative treatment with D-chiro-inositol (DCI) (500 mg die, per os, for 12 weeks) on hormonal parameters and insulin sensitivity in a group of overweight/obese PCOS patients (body mass index; BMI > 26). After the treatment, interval several endocrine parameters improved (luteinizing hormone [LH], LH/follicle stimulating hormone [FSH], androstenedione and insulin), insulin response to oral glucose tolerance test reported the significant improvement of insulin sensitivity as well as the gonadotropin-releasing hormone (GnRH)-induced (10 µg, in bolus) LH response. BMI decreased, though no lifestyle modification was requested. When data were analyzed according to the presence or absence of first-grade diabetic relatives, PCOS patients with diabetic relatives showed greater improvement after DCI administration. In conclusion DCI administration is effective in restoring better insulin sensitivity and an improved hormonal pattern in obese hyperinsulinemic PCOS patients, in particular, in hyperinsulinemic PCOS patients who have diabetic relatives.
Arch Gynecol Obstet. 2014 Nov 22. [Epub ahead of print] Evaluation of ovarian function and metabolic factors in women affected by polycystic ovary syndrome after treatment with D-Chiro-Inositol. Laganà AS1, Barbaro L, Pizzo A. PMID: 25416201
...We enrolled 48 patients, with homogeneous bio-physical characteristics, affected by PCOS and menstrual irregularities. These patients underwent treatment with 1 gr of D-Chiro-Inositol/die plus 400 mcg of Folic Acid/die orally for 6 months...We evidenced a statistically significant reduction of systolic blood pressure, Ferriman-Gallwey score, LH, LH/FSH ratio, total Testosterone, free Testosterone, ∆-4-Androstenedione, Prolactin, and HOMA Index; in the same patients, we noticed a statistically significant increase of SHBG and Glycemia/IRI ratio. Moreover, we observed statistically significant (62.5 %; p < 0.05) post-treatment menstrual cycle regularization. CONCLUSIONS: D-Chiro-Inositol is effective in improving ovarian function and metabolism of patients affected by PCOS.
Gynecol Endocrinol. 2015 Jan;31(1):52-6. doi: 10.3109/09513590.2014.964201. Epub 2014 Sep 30. The menstrual cycle regularization following d-chiro-inositol treatment in PCOS women: a retrospective study. La Marca A1, Grisendi V, Dondi G, Sighinolfi G, Cianci A. PMID: 25268566
...The objective of this study was to retrospectively analyze the effect of DCI on menstrual cycle regularity in PCOS women. This was a retrospective study of patients with irregular cycles who were treated with DCI. Of all PCOS women admitted to our centre, 47 were treated with DCI and had complete medical charts. The percentage of women reporting regular menstrual cycles significantly increased with increasing duration of DCI treatment (24% and 51.6% at a mean of 6 and 15 months of treatment, respectively). Serum AMH levels and indexes of insulin resistance significantly decreased during the treatment. Low AMH levels, high HOMA index, and the presence of oligomenorrhea at the first visit were the independent predictors of obtaining regular menstrual cycle with DCI. In conclusion, the use of DCI is associated to clinical benefits for many women affected by PCOS including the improvement in insulin resistance and menstrual cycle regularity. Responders to the treatment may be identified on the basis of menstrual irregularity and hormonal or metabolic markers.

Gynecol Endocrinol. 2014 Sep 26:1-5. [Epub ahead of print] Ovulation induction with myo-inositol alone and in combination with clomiphene citrate in polycystic ovarian syndrome patients with insulin resistance. Kamenov Z1, Kolarov G, Gateva A, Carlomagno G, Genazzani AD. PMID: 25259724
...The aim of the present study is to evaluate the effectiveness of myo-inositol alone or in combination with clomiphene citrate for (1) induction of ovulation and (2) pregnancy rate in anovulatory women with PCOS and proven insulin resistance. Patients and methods: This study included 50 anovulatory PCOS patients with insulin resistance. All of them received myo-inositol during three spontaneous cycles. If patients remained anovulatory and/or no pregnancy was achieved, combination of myo-inositol and clomiphene citrate was used in the next three cycles. Ovulation and pregnancy rate, changes in body mass index (BMI) and homeostatic model assessment (HOMA) index and the rate of adverse events were assessed. Results: After myo-inositol treatment, ovulation was present in 29 women (61.7%) and 18 (38.3%) were resistant. Of the ovulatory women, 11 became pregnant (37.9%). Of the 18 myo-inositol resistant patients after clomiphene treatment, 13 (72.2%) ovulated. Of the 13 ovulatory women, 6 (42.6%) became pregnant. During follow-up, a reduction of body mass index and HOMA index was also observed. Conclusion: Myo-inositol treatment ameliorates insulin resistance and body weight, and improves ovarian activity in PCOS patients.
Gynecol Endocrinol. 2013 Apr;29(4):375-9. doi: 10.3109/09513590.2012.743020. Epub 2013 Jan 22. Endocrine and clinical effects of myo-inositol administration in polycystic ovary syndrome. A randomized study. Artini PG1, Di Berardino OM, Papini F, Genazzani AD, Simi G, Ruggiero M, Cela V. PMID: 23336594
...50 overweight PCOS patients...underwent hormonal evaluations and an oral glucose tolerance test (OGTT) before and after 12 weeks of therapy (Group A (n¼10): MYO 2 g plus folic acid 200 mg every day; Group B (n¼10): folic acid 200 mg every day). Ultrasound examinations and Ferriman-Gallwey score were also performed... RESULTS: After 12 weeks of MYO administration plasma LH, PRL, T, insulin levels and LH/FSH resulted significantly reduced. Insulin sensitivity, expressed as glucose-to-insulin ratio and HOMA index resulted significantly improved after 12 weeks of treatment. Menstrual cyclicity was restored in all amenorrheic and oligomenorrheic subjects. No changes occurred in the patients treated with folic acid. CONCLUSIONS: MYO administration improves reproductive axis functioning in PCOS patients reducing the hyperinsulinemic state that affects LH secretion.
Combined Therapy (MI plus DCI)

J Clin Pharmacol. 2014 Oct;54(10):1079-92. doi: 10.1002/jcph.362. Epub 2014 Jul 18. The rationale of the myo-inositol and D-chiro-inositol combined treatment for polycystic ovary syndrome. Dinicola S1, Chiu TT, Unfer V, Carlomagno G, Bizzarri M. PMID: 25042908
...Two inositol isomers, myo-inositol (MI) and D-chiro-inositol (DCI) have been proven to be effective in PCOS treatment, by improving insulin resistance, serum androgen levels and many features of the metabolic syndrome. However, DCI alone, mostly when it is administered at high dosage, negatively affects oocyte quality, whereas the association MI/DCI, in a combination reproducing the plasma physiological ratio (40:1), represents a promising alternative in achieving better clinical results, by counteracting PCOS at both systemic and ovary level.
Eur Rev Med Pharmacol Sci. 2013 Feb;17(4):537-40. The Combined therapy myo-inositol plus D-Chiro-inositol, in a physiological ratio, reduces the cardiovascular risk by improving the lipid profile in PCOS patients. Minozzi M1, Nordio M, Pajalich R. PMID: 23467955
BACKGROUND: ...The aim of the present study was to evaluate whether the combined therapy myo-inositol plus D-chiro-inositol (in a in a physiological ratio of 40:1) improve the metabolic profile, therefore, reducing cardiovascular risk in PCOS patients. PATIENTS AND METHODS: Twenty obese PCOS patients [BMI 33.7 ± 6 kg/m2 (mean ± SD)] were recruited. The lipid profile was assessed by measuring total cholesterol, LDL, HDL and triglycerides before and after 6 months treatment with the combined therapy. Secondary end points included changes in BMI, waist-hip ratio, percentage of body fat, HOMA-IR and blood pressure. RESULTS: The combined therapy myo-inositol and D-chiro-inositol improved LDL levels (3.50 ± 0.8 mmol/L versus, 3 ± 1.2 mmol/L p < 0.05), HDL (1.1 mmol/L ± 0.3 versus 1.6 mmol/L ± 0.4 p < 0.05) and triglycerides (2.3 ± 1.5 mmol/L versus 1.75 ± 1.9 mmol/L p < 0.05). Furthermore, significant improvements in HOMA-IR were also observed. CONCLUSIONS: The combined therapy myo-inositol plus D-chiro-inositol is able to improve the metabolic profile of PCOS women, therefore, reducing the cardiovascular risk.
Monotherapy vs. Combined Therapy

Eur Rev Med Pharmacol Sci. 2012 May;16(5):575-81. The combined therapy with myo-inositol and D-chiro-inositol reduces the risk of metabolic disease in PCOS overweight patients compared to myo-inositol supplementation alone. Nordio M1, Proietti E. PMID: 22774396
...In this study, we aim to verify whether the two molecules have a synergistic action by acting on their specific cellular pathways. The effectiveness in reducing the risk of metabolic syndrome as well as in enhancing the ovarian functions of a combined therapy with MI and DCI was compared to a mono therapy in a randomized controlled trial. METHODS: Fifty overweight women with PCOS were enrolled and divided in two groups to receive MI and DCL (MI+DCI group) or MI alone (MI group) for a period of six months. Baseline measurements were repeated at three months (T1) and at the end of the treatment (T2). RESULTS: At the end of the treatment, both MI and MI+DCI groups showed an improvement of the metabolic parameters and no significant differences were found. As expected, the combined supplementation with MI and DCI resulted to be more effective, compared to the MI group, after three months of treatment. CONCLUSIONS: The combined administration of MI and DCI in physiological plasma ratio (40:1) should be considered as the first line approach in PCOS overweight patients, being able to reduce the metabolic and clinical alteration of PCOS and, therefore, reduce the risk of metabolic syndrome.
Arch Gynecol Obstet. 2013 Dec;288(6):1405-11. doi: 10.1007/s00404-013-2855-3. Epub 2013 May 25. The combined therapy myo-inositol plus D-chiro-inositol, rather than D-chiro-inositol, is able to improve IVF outcomes: results from a randomized controlled trial. Colazingari S1, Treglia M, Najjar R, Bevilacqua A. PMID: 23708322
PURPOSE: The present study aims to investigate the effects of the combined therapy myo-inositol (MI) plus D-chiro-inositol (DCI) or D-chiro-inositol treatment in oocyte quality. METHODS: Polycystic ovary syndrome (PCOS) women undergoing IVF-ET were treated with myo-inositol combined with D-chiro-inositol in the physiological ratio (1.1 g myo-inositol plus 27.6 mg of D-chiro-inositol; INOFOLIC combi Lo.Li.pharma) or D-chiro-inositol alone (500 mg; Interquim, s.a., Barcelona, Spain) to evaluate the umber of morphological mature oocytes, total International Units (IU) of recombinant FSH administered and the number of grade 1 embryos. RESULTS: The data clearly showed that only the combined therapy was able to improve oocyte and embryo quality, as well as pregnancy rates, in PCOS women undergoing IVF-ET. CONCLUSION: The present paper further supports the hypothesis that MI plays a crucial role in the ovary in PCOS women. In particular, due to the physiological role played by MI and DCI, the combined therapy should represent a better choice.

Monday, December 22, 2014

Happy Holidays

Image by Viggo Johanson,Wikimedia Commons
I'm taking some much-needed time off to spend with my family during the holiday, so the blog will be taking a brief break.

I hope you have a wonderful Christmas (or whatever holiday you celebrate). Many blessings to you and yours!

Friday, December 12, 2014

Honey for Cesarean Wound Healing?

We've discussed honey for wound healing before, and specifically for cesarean wound healing.

We talked about the mechanics of how honey (medical grade honey, not supermarket honeymight help healing and what studies there were on the topic.

As one review notes:
Honey has anti-oxidant, anti-bacterial and anti-inflammatory properties. It can be used as a wound dressing to promote rapid and improved healing. These effects are due to honey's anti-bacterial action, secondary to its high acidity, osmotic effect, anti-oxidant content and hydrogen peroxide content. The use of honey leads to improved wound healing in acute cases, pain relief in burn patients and decreased inflammatory response in such patients...There is biological plausibility.
Mixed Results

While honey has "biological plausibility" as a healing agent, results from use of medical grade honey have been encouraging in some situations and discouraging in others. Results were not very good for venous ulcers, for example, but on some wounds there are better results.

A recent Cochrane review found decidedly mixed results, depending on what type of wound was being studied, and cautioned against its routine use until more data is available. So it's hard to know just how useful medical grade honey really is, and how much is just hype.

The problem is that much of the honey-based research is sponsored by the companies that make medical-grade honey, so the results are at high risk for bias.

Bottom line.....better data is needed. But given the positive results in some studies and its relatively low cost, why haven't there been more well-controlled studies done by independent groups by now?

Medical-Grade Honey for Cesarean Healing

Sadly, there's not a lot of data on using honey for cesarean wound healing. There are a couple of older studies done in third-world countries, but they had small data sets and uncontrolled conditions. As a result, using medical honey on a cesarean wound has not been been embraced in Western countries.

Now there's a new study on the use of honey for abdominal wound healing after cesarean. The data set is still very small and still from a third-world country, but at least the study design is randomized and blinded. The results from this study were encouraging.

This doesn't prove honey is a healing agent of choice for cesarean wounds, but it certainly points to the need for bigger and better studies to further examine the question. 

I would particularly like to see medical-grade honey investigated in the treatment of cesarean wound infections of "obese" women (who are substantially more at-risk for wound infection than other women).

About 15-30% of high-BMI women will experience a wound infection after a cesarean, and sometimes these infections last for months. Wound infections like this can be devastating to a new mother, can interfere with breastfeeding, and are costly to treat.

Many cesarean wound infections in obese women can likely be lowered by using more appropriate dosages of antibiotics, but medical grade honey might give another weapon in the arsenal against infections in this group of women.

Of course, the best treatment is prevention of the cesareans in the first place whenever possible, which is why the 40-80% cesarean rate in "morbidly" and "super obese" women is so completely unacceptable.

But sometimes cesareans truly are necessary. When cesareans do occur in this group of women, more tools are needed to help prevent or treat the wound infections that will result in some of them.

Medical-grade honey might be yet another tool in the toolbox for this situation. And it's past time for Western medicine to investigate this possibility more thoroughly.


Oman Med J. 2014 Jul;29(4):255-9. doi: 10.5001/omj.2014.68. The effect of honey gel on abdominal wound healing in cesarean section: a triple blind randomized clinical trial. Nikpour M1, Shirvani MA2, Azadbakht M3, Zanjani R4, Mousavi E5. PMID: 25170405
OBJECTIVE: To assess whether honey can accelerate the wound healing in women undergoing cesarean section. METHODS: This was a triple blinded randomized prospective clinical trial. Women with cesarean section were randomly designated as drug (37 cases) and placebo (38 cases) groups. The drug group received local honey gel 25% while the placebo group received similar free-honey gel on abdominal cesarean incision twice a day for 14 days. REEDA scale (Redness, Edema, Ecchymosis, Discharge and Approximation of wound edges) was used to assess wound healing. RESULTS: The mean REEDA was 2.27 ± 2.46 and 3.91 ± 2.74 (p=0.008) on the 7(th) day and 0.47 ± 0.84 and 1.59± 1.95 (p=0.002) on the 14(th) day for the drug and placebo groups, respectively. Redness, edema and hematoma in the drug group were significantly lower on the 7(th) and 14(th) days. CONCLUSION: Honey was effective in healing the cesarean section incision. Using topical honey is suggested as a natural product with rare side effects in order to reduce the complications of cesarean wounds.

Friday, December 5, 2014

Widespread Misconceptions About Obesity

I recently stumbled across an article by pure coincidence. It's called "Widespread Misconceptions About Obesity."

It was written by several doctors and researchers, and it was published last month in the journal, Canadian Family Physician. You can read the full text of the article here.

In the meantime, here are some good quotes from the article (my emphasis):
  • Although obesity can be a serious health threat, we lack effective strategies to address this condition on an individual and a societal level. Myths and misconceptions about obesity are pervasive in the media, popular culture, and scientific literature
  • It is very common to hear that obese people are lazy and should get off the couch. This discriminatory bias against those with excess weight is not only widespread among the lay public but also among health professionals, even those in regular contact with patients with obesity
  • Physicians should remember that obesity is not a choice
  • Obesity management should focus on promoting healthier behaviour rather than simply reducing numbers on the scale
  • It might be time to shift the focus away from body weight to health and wellness in public health interventions
Here is their list of 7 common misconceptions about obesity:
  1. Obesity is primarily caused by a lack of physical activity or by unhealthy dietary habits
  2. Obese individuals are less active than their normal-weight counterparts
  3. Diets work in the long term
  4. Weight loss does not have significant adverse effects
  5. Exercising is better than dieting to lose weight
  6. Everyone can lose weight with enough willpower
  7. A successful obesity management program is measured by the amount of weight lost
The article is not perfect, of course, and I have some nitpicks here and there.

But I was especially pleased to hear them mention shifting the focus from numbers on a scale to health habits. We may not all be able to become a "normal" BMI, but we can all improve our health behaviors, and that will help health, regardless of where your BMI is.

This is right in line with the Health At Every Size® philosophy (even if they don't mention that concept by name), which is starting to gain more traction in mainstream research. Hopefully these authors would support eliminating obesity stigma in public health campaigns as well.

On the whole, this article is a welcome change to the dialogue about obesity. How heartening that at least some family doctors are starting to "get it."

Now if we could only get the word out to medical schools and obesity researchers, where weight stigma runs rampant and largely unchecked.

For example, did you see the recent blog post about professional obesity researchers making fun of fat people and cracking fat jokes during their conference? No less a major journal than The Lancet published a piece about it, which concluded:
In line with guidelines for publishing in obesity and journals of other disciplines that adhere to the standards of the Committee on Publication Ethics, authors should avoid bias and stereotypical language, which should apply to all dissemination activity including academic conferences. Hence, obesity researchers should adhere to these standards.
Amen to that! Hard to believe how unprofessional these researchers were. But frankly, that kind of behavior goes hand in hand with the utter contempt that so many in the obesity field have towards their study population. Kudos to authors Stuart W. Flint and Sophie Reale for having the professional courage to shine a light on this disgusting behavior.

So, on the whole, it was a week of encouragement and discouragement in some ways. It was encouraging to see the Canadian Family Physician article addressing common misconceptions about obesity, but it was frustrating to hear about professional academics resorting to fat jokes and put-downs about the very people they study and are supposed to be "helping." At least The Lancet published a letter calling them on the carpet for it, I guess.

One step forward, two steps back. Sigh.


Chaput, J. P., Ferraro, Z. M., Prud’homme, D., & Sharma, A. M. (2014). Widespread misconceptions about obesity. Canadian Family Physician, 60(11), 973-975. PMID: 25392431 Full text available here

Flint, S. W., & Reale, S. (2014). Obesity stigmatisation from obesity researchers. The Lancet, 384(9958), 1925-1926. Full text available here.

Saturday, November 29, 2014

Labor Length in "Obese" Women: Dig Deeper

Here's the abstract of an interesting study suggesting that the first stage of labor (dilation) is longer in "obese" women and that this ought to be taken into account when diagnosing labor arrest needing a cesarean in this group.

This is not the first study to find a longer length of labor in higher-BMI women. As a result of these differences, one study concluded:
It is critical to consider differences in labor progression by maternal prepregnancy BMI before additional interventions are performed.
I agree that a possible longer labor length ought to be taken into account before resorting to a cesarean. As we've discussed before, many cesareans are done for "Failure to Wait" rather than for a true emergency, and many cesareans in women of all sizes could probably be avoided if care providers were a little more patient during labor.

In fact, a recent joint statement from the American College of Obstetricians and Gynecologists and the Society for Maternal-Fetal Medicine suggested that women be allowed a longer time in early ("latent") labor, that women not be considered to be in "active labor" until 6 cm (instead of 4 cm), and that they be given more time both in active labor and in the pushing stage before the doctor starts thinking cesarean.

This may be especially meaningful for high BMI women, as there tends to be a lower surgical threshold for women of size. In one study, labor in obese women was terminated by cesarean an hour earlier on average than in other women. This shows that some doctors are nervous in the labors of obese women and jump to a surgical solution far too quickly.

On the one hand, it is understandable that doctors are nervous about doing a truly emergent cesarean in obese women, since accessing the baby takes longer and the surgery is more difficult. On the other hand, if doctors jump to cesareans too quickly, many obese women who might have given birth vaginally are exposed to the substantial risks of surgery. And since many women of size these days are strongly discouraged from VBAC, this often means further cesareans, which is even more risky.

It's important to acknowledge that it can be difficult for providers to judge whether or not labor should continue in obese women with slow labors. However, provided the fetus is doing well, this study suggests that care providers should be more patient in the labors of women of size. 

Yes! That's something I've been saying for a while now.

Digging Deeper

However, I'd also like researchers to dig even further into why our labors may be longer.

There is some research to suggest that women of size have higher rates of posterior (OP) babies, and OP babies often have prolonged labors. I wish this study's database had fetal position recorded so they could have checked out this possibility.

Do obese women really have more posterior babies? Is that why they tend to have longer labors and more cesareans for dystocia? Or is it a relative lack of responsiveness to oxytocin, as some authors have suggested?

A number of older studies on obesity and pregnancy noted higher rates of fetal malpositions, particularly OP. Most newer studies have not looked for a connection, although the study linked above does note higher OP rates in obese women. Anecdotally, my own birth stories and the birth stories of many fat women I've received over the years for my website seems to support the idea of a higher rate of malpositions as well. All this suggests a connection, but of course we need data to back that up.

I would love to see someone, somewhere research the fascinating question of whether women of size have more malpositioned babies and whether this is one factor behind slower labor rates in this group. I'm sure it's not the only factor, but I would guess that it is a significantly underestimated factor.

If you are a woman of size reading this post, don't panic and think you're doomed to have a really long labor just because you are heavier. On average, our labors tend to be longer, but there's no way to predict labor length for any one person.

SO MUCH of labor length has to do with the position of the baby, whether or not labor is induced, how ripe the woman's cervix is, whether the woman can be mobile in labor, and many other factors. I've known fat women who have had 2 hour labors, and I've known fat women who have had very long labors. My own four labors varied from 8 hours to nearly 20 hours ─ same-sized woman every time but the difference was well-positioned babies vs. OP babies. So labor length really can be highly variable, even within the same person's experiences.


A combination of a tendency towards longer labor and a lower surgical threshold for cesarean, along with more inductions, is probably why the cesarean rate in high BMI women has risen so high. Because obese women have more complications with cesareans, it is important to discover how to lower this rate.

The take-away message from this study is that, on average, the labors in high BMI women were longer, and their care providers probably should take that into account and wait a little longer before diagnosing a labor arrest disorder and doing a cesarean.

If you are a woman of size, find a care provider who truly believes that you can have a vaginal birth and who is willing to be more patient in labor before resorting to a cesarean. (Generally speaking, midwives tend to be more willing to wait, although some OBs are great about this too. Don't depend on a title but ask careful questions to better understand a provider's practice style.)

If you are a researcher, dig a little deeper and explore why women of size have longer labors, including whether or not there is a higher rate of fetal malpositions. I suspect there is but I'd love to see recent data to confirm this.

If there are more OP babies in heavier women, then there are things that women of size can do that might help lower their chances of a malpositioned baby before labor (chiropractic care is what helped me). Additionally, there are things a care provider can do during labor to help turn a malpositioned baby if needed (research on manual rotation is very promising). And of course, sometimes all that's needed for an OP baby is to have a little more patience in labor.

Whether it's being more patient in labor, doing fewer inductions, or being more proactive about fetal position in women of size, there are things we can do to lower the cesarean rate in this group. It's about time we start doing them. 


Eur J Obstet Gynecol Reprod Biol. 2013 Nov;171(1):49-53. doi: 10.1016/j.ejogrb.2013.08.021. Epub 2013 Aug 29. Maternal body mass index and duration of labor. Carlhäll S1, Källén K, Blomberg M. PMID: 24041847
OBJECTIVE: To evaluate whether the duration of the active phase of labor is associated with maternal body mass index (BMI), in nulliparous women with spontaneous onset of labor. STUDY DESIGN: Historical prospective cohort study including 63,829 nulliparous women with a singleton pregnancy and a spontaneous onset of labor, who delivered between January 1, 1995 and December 31, 2009. Data were collected from the Perinatal Revision South registry, a regional perinatal database in Southern Sweden. Women were categorized into six classes of BMI. Overweight and obese women were compared to normal weight women regarding duration of active labor. Adjustments were made for year of delivery, maternal age and infant birth weight. RESULTS: The median duration of labor was significantly longer in obese women (class I obesity (BMI 30-34.9) = 9.1h, class II obesity (BMI 35-39.9) = 9.2h and class III obesity (BMI > 40) = 9.8h) compared to normal-weight women (BMI 18.5-24.9) = 8.8h (p < 0.001). The risk of labor lasting more than 12h increased with increasing maternal BMI: OR 1.04 (1.01-1.06) (OR per 5-units BMI-increase).The risk of labor lasting more than 12h or emergency cesarean section within 12h, compared to vaginal deliveries within 12h, increased with increasing maternal BMI. Duration of the second stage of labor was significantly shorter in obese women: in class III obesity the median value was 0.45 h compared to normal weight women, 0.55 h (p < 0.001). CONCLUSION: In nulliparous women with a spontaneous onset of labor, duration of the active phase of labor increased significantly with increasing maternal BMI. Once obese women reach the second stage they deliver more quickly than normal weight women, which implies that the risk of prolonged labor is restricted to the first stage of labor. It is clinically important to consider the prolonged first stage of labor in obese women, for example when diagnosing first stage labor arrest, in order to optimize management of this rapidly growing at-risk group of women. Thus, it might be reasonable to adapt the considered upper limit for duration of labor, according to maternal BMI.

Friday, November 21, 2014

Increase in Cesarean Rate in Morbidly Obese Women Over Time

Here's the abstract of an interesting new study. I haven't seen the full text yet but it appears to show that while the cesarean rate has gone up over time in all sizes of women, it's gone up the most in the higher BMI categories.

In other words, a high BMI woman is far more likely to have a cesarean now than she was in 1990.

This shows that the high cesarean rate in obese women is not just about obesity itself, but also how obese women are managed in labor and the lowering of the surgical threshold for performing cesareans in high BMI women.

I've been saying this for years. Some care providers like to pretend that the high cesarean rate in obese women is only about the woman's fatness, as if this somehow prevents a fat woman from giving birth vaginally (the classic "fat vagina" theory).

But if it was really only about physical barriers, then you would see a relatively consistent cesarean rate in this group over time, and you DON'T. This study shows that there used to be much lower cesarean rates in women of size than there is today, and older studies show that the cesarean rate wasn't always higher in obese women than in average-sized women.

Critics would point out that the cesarean rate has increased in all groups over time, not just in obese women. Sad, but true.

But the cesarean rate has not increased equally in every group, as this study points out. Look at their comparison of cesarean rates between 1990 and 2012 by BMI group*:

                              1990                     2012                   Increase

Underweight         14.4%                   27.9%                  13.5%
Normal                  16.1%                   31.4%                  15.3%
Overweight           19.5%                   38.8%                  19.3%
Obese I                 22.3%                   45.1%                  22.8%
Obese II                25.0%                   50.2%                  25.2%
Obese III               26.9%                   55.2%                  28.3%

The increase in cesarean rates was not uniform across BMI categories. The increase in "normal" weight women was 15.3%, but the increase in Obese Class III women was nearly twice that at 28.3%.

In 1990, Obese class III women had a 26.9% cesarean rate in 1990....just over 1 in 4.

In 2012, Obese Class III women  had a 55.2% cesarean rate instead, or more than 1 in every 2 "morbidly obese" women.

In just 22 years, the cesarean rate in Class III Obese women went from 26.0% to 55.2%. How far will it go in the next 20 years?

Something has changed...and that something is probably how those women are managed in labor (more interventions), the exaggeration of fear around their pregnancies, and the resulting lowering of the surgical threshold for a cesarean in that group.

Similarly, research shows that cesarean rates in the same BMI group can vary dramatically between locations. For example, recent studies from Tennessee and Kentucky show an abysmal cesarean rate of nearly 60% in "morbidly obese" women. One particularly appalling study from Michigan shows a cesarean rate of over 80% in women with a BMI over 50.

Yet a large study from the U.K. shows a cesarean rate of about 30% in the same population.

This shows that practice variation is an issue not only in the overall population, but perhaps particularly in high BMI women.

It's time for care providers to examine not only how to prevent questionable cesareans in women across the board, but also to focus on how to prevent questionable cesareans in high-BMI women. Given that cesareans carry more risks in women of size, especially multiple repeat cesareans, it's inexcusable to be exposing so many of these women to these risks unnecessarily.

The cesarean rate is high is women of size, but the variation in rates over time and between locations shows it doesn't have to be, and that there are things we could be doing to bring the cesarean rate down in this group.

It's long past time to be looking into that question. Some researchers are starting to ask these questions or propose solutions, but few have actually tested these theories.

Where are the researchers and providers willing to actually study how to lower the cesarean rate in women of size?


J Perinat Med. 2014 Jun 10. pii: /j/jpme.ahead-of-print/jpm-2014-0126/jpm-2014-0126.xml. doi: 10.1515/jpm-2014-0126. [Epub ahead of print] Impact of maternal body mass index on the cesarean delivery rate in Germany from 1990 to 2012. Kyvernitakis I, Köhler C, Schmidt S, Misselwitz B, Großmann J, Hadji P, Kalder M. PMID: 24914711
ABSTRACT AIMS: Maternal obesity is a risk factor for cesarean delivery (CD). The aim of this analysis was to determine the association between early-pregnancy body mass index (BMI) and the rate of CD over the past two decades. METHODS: We retrospectively analyzed data from the perinatal quality registry of singleton deliveries in the state of Hesse in Germany from 1990 to 2012. We divided the patients into groups according to the WHO criteria for BMI: underweight (<18.5), normal weight (18.5-<25), overweight (25-<30), obese class I (30-<35), obese class II (35-<40), and obese class III (≥40). RESULTS: The analysis included 1,092,311 patients with available data regarding maternal BMI and mode of delivery. The CD rates for underweight (<18.5), normal weight (18.5-<25), overweight (25-<30), obese class I (30-<35), obese class II (35-<40), and obese class III (≥40) women increased from 14.4%, 16.1%, 19.5%, 22.3%, 25%, and 26.9% in the year 1990 to 27.9%, 31.4%, 38.8%, 45.1%, 50.2%, and 55.2% in the year 2012, respectively (P<0.001). CONCLUSION: Maternal BMI in early pregnancy is linearly associated with the incidence of CD. We found a disproportionate increase of CD in morbidly obese women compared with the CD incidence in the reference BMI population over the past two decades.

* Standard BMI classifications: 

  • "Underweight" = BMI less than 18
  • "Normal" weight = BMI 18-24.9
  • "Overweight" = BMI 25-29.9
  • Class I Obese = BMI 30-34.9
  • Class II Obese = BMI 35-39.9
  • Class III Obese = BMI of 40 plus
  • "Super Obese" = BMI of 50 plus

Thursday, November 13, 2014

See my Practice Variation Post at Science and Sensibility

My recent post on Practice Variation in Cesarean Rates went a bit viral. (Thank you to those of you who shared it on Facebook!)

The blog, Science and Sensibility (Lamaze International’s “Research Blog About Healthy Pregnancy, Birth & Beyond”), picked it up and asked to run it since it's very topical right now, what with the recent important study on Practice Variation.

I revised my very-quick original post and expanded on a few points, added some new research, reformatted it a bit, and generally prettified it up. (I spent all my time on that, so no new post here till next week.)

In the meantime, the revised post is now up on Science and Sensibility. You can go and read it here.

Sunday, November 2, 2014

Practice Variation in Cesarean Rates: Not Due to Maternal Complications

Photo courtesy "Angela"
There's a new study out that discusses the variation in cesarean rates between hospitals in the United States.

Practice variation is a serious problem in obstetrics. Women are often far more at risk for a cesarean in certain hospitals than in others, even when the hospitals serve the same geographical area and population.

Of course, care providers protest that some hospitals have higher cesarean rates because they serve higher-risk patients. This is a valid point, but it still doesn't explain the wide variation in rates between many hospitals.

For example, in the study above, the mother's risk status and diagnoses did not explain the variation in cesarean rates between hospitals:
We found that the variability in hospital cesarean rates was not driven by differences in maternal diagnoses or pregnancy complexity,” said [lead study author] Kozhimannil. “This means there was significantly higher variation in hospital rates than would be expected based on women’s health conditions. On average, the likelihood of cesarean delivery for an individual woman varied between 19 and 48 percent across hospitals.”
There were several key points highlighted in the article about the study, including:
  • Among lower risk women, likelihood of cesarean delivery varied between 8 and 32 percent across hospitals.
  • Among higher risk women, likelihood of cesarean delivery varied between 56 and 92 percent across hospitals.
  • Hospital variability did not decrease after adjusting for patient diagnoses, socio-demographics, and hospital characteristics.
This shows that practice variation in cesarean rates is real, substantive, and not just a reflection of the mother's risk level. 

Perhaps now we can stop playing the mother blame-game when we talk about cesarean rates?

This study is not the first to show that the culture of a hospital, their policies, and their routine practices all help determine how likely a woman is to "need" a cesarean in that hospital.

This is important because while cesareans can be life-saving at times, they present more risk for infection, bleeding, pain, neonatal breathing problems, and complications in future pregnancies. It matters where and with whom a woman gives birth.

But many women naively choose their care provider for pregnancy based mostly on convenience and location, not realizing that their chances of surgical birth may vary greatly depending on which hospital and caregiver they use

One leading consumer education site points out, "Research suggests that the same woman might have a c-section at one hospital but a vaginal birth if she gave birth at another, just because of the different policies and practices of those hospitals. One of the most effective ways to lower your chance of having a c-section is to have your baby in a setting with a low c-section rate."

Yet it is not always easy to find out the cesarean rates* of local hospitals in some states, and many hospitals remain largely unaccountable for sky-high cesarean rates, although we are beginning to see marginal progress in some places towards accountability. But even when a cesarean is truly necessary, there can be large discrepancies in complications afterwards between hospitals. How is a woman to know which hospital to choose?

Bottom line, more transparency and accountability are needed. As the lead author of the study states: 
Women deserve evidence-based, consistent, high-quality maternity care, regardless of the hospital where they give birth...and these results indicate that we have a long way to go toward reaching this goal in the U.S.

**An additional suggestion: Researchers should start examining cesarean practice variations in obese patients too. Research strongly suggests there are major practice variations in cesarean utilization for "obese" mothers between hospitals, yet this is a topic that is rarely broached in research. More exploration of this dichotomy might help reduce the cesarean rate in this group.

***Post received minor reference and picture edits on 11/6/14.


*See for hospital level cesarean rates in most U.S. states. Consumer Reports also has a recent article with some hospital-level c-section rates in the U.S.

PLoS Med. 2014 Oct 21;11(10):e1001745. doi: 10.1371/journal.pmed.1001745. eCollection 2014. Maternal Clinical Diagnoses and Hospital Variation in the Risk of Cesarean Delivery: Analyses of a National US Hospital Discharge Database. Kozhimannil KB1, Arcaya MC2, Subramanian SV2. PMID: 25333943
BACKGROUND: Cesarean delivery is the most common inpatient surgery in the United States, where 1.3 million cesarean sections occur annually, and rates vary widely by hospital. Identifying sources of variation in cesarean use is crucial to improving the consistency and quality of obstetric care. We used hospital discharge records to examine the extent to which variability in the likelihood of cesarean section across US hospitals was attributable to individual women's clinical diagnoses. METHODS AND FINDINGS: Using data from the 2009 and 2010 Nationwide Inpatient Sample from the Healthcare Cost and Utilization Project-a 20% sample of US hospitals-we analyzed data for 1,475,457 births in 1,373 hospitals. We fitted multilevel logistic regression models (patients nested in hospitals). The outcome was cesarean (versus vaginal) delivery. Covariates included diagnosis of diabetes in pregnancy, hypertension in pregnancy, hemorrhage during pregnancy or placental complications, fetal distress, and fetal disproportion or obstructed labor; maternal age, race/ethnicity, and insurance status; and hospital size and location/teaching status. The cesarean section prevalence was 22.0% (95% confidence interval 22.0% to 22.1%) among women with no prior cesareans. In unadjusted models, the between-hospital variation in the individual risk of primary cesarean section was 0.14 (95% credible interval 0.12 to 0.15). The difference in the probability of having a cesarean delivery between hospitals was 25 percentage points. Hospital variability did not decrease after adjusting for patient diagnoses, socio-demographics, and hospital characteristics (0.16 [95% credible interval 0.14 to 0.18]). A limitation is that these data, while nationally representative, did not contain information on parity or gestational age. CONCLUSIONS: Variability across hospitals in the individual risk of cesarean section is not decreased by accounting for differences in maternal diagnoses. These findings highlight the need for more comprehensive or linked data including parity and gestational age as well as examination of other factors-such as hospital policies, practices, and culture-in determining cesarean section use.
Am J Obstet Gynecol. 2007 Jun;196(6):526.e1-5. Variation in the rates of operative delivery in the United States. Clark SL1, Belfort MA, Hankins GD, Meyers JA, Houser FM. PMID: 17547880
OBJECTIVES: This study was undertaken to examine the national and regional rates of operative delivery among almost one quarter million births in a single year in the nation's largest healthcare delivery system, using variation as an arbiter of the quality of decision making. STUDY DESIGN: We compared the variation in rates of primary cesarean and operative vaginal delivery in facilities of the Hospital Corporation of America during the year 2004. RESULTS: In 124 facilities representing almost 220,000 births during a 1-year period, the primary cesarean and operative vaginal delivery rates were 19% +/- 5% (range 9-37) and 7% +/- 4% (range 1-23). Within individual geographic regions, we consistently found variations of 200-300% in rates of primary cesarean delivery and variations approximating an order of magnitude for operative vaginal delivery. CONCLUSION: Within broad upper and lower limits, rates of operative delivery in the United States are highly variable and suggest a pattern of almost random decision making. This reflects a lack of sufficient reliable, outcomes-based data to guide clinical decision making.
Neonatology. 2014 Oct 4;107(1):8-13. [Epub ahead of print] Women Are Designed to Deliver Vaginally and Not by Cesarean Section: An Obstetrician's View. Visser GH. PMID: 25301178
Worldwide, there is a rapid increase in deliveries by cesarean section. The large differences among countries, from about 16% to more than 60%, suggest that the cesarean delivery (CD) rate has little to do with evidence-based medicine. In this review, the background for the increasing CD rate is discussed as well as the limited positive effects on neonatal outcome in both term and preterm neonates. Negative effects of CD, including direct maternal morbidity, complications of subsequent pregnancies and iatrogenic early delivery resulting in increased neonatal morbidity, are discussed in addition to long-term implications for the offspring involving altered development of the immune system. The 'battle' to lower the CD rate will be difficult, but we should not forget that women are designed to deliver vaginally and not by cesarean section. 

Tuesday, October 21, 2014

A Weight-Inclusive Approach to Health

J Obes. 2014;2014:983495. doi: 10.1155/2014/983495. Epub 2014 Jul 23. The weight-inclusive versus weight-normative approach to health: evaluating the evidence for prioritizing well-being over weight loss. Tylka TL1, Annunziato RA2, Burgard D3, Daníelsdóttir S4, Shuman E5, Davis C2, Calogero RM6. PMID: 25147734 Free full text available here.
Using an ethical lens, this review evaluates two methods of working within patient care and public health: the weight-normative approach (emphasis on weight and weight loss when defining health and well-being) and the weight-inclusive approach (emphasis on viewing health and well-being as multifaceted while directing efforts toward improving health access and reducing weight stigma). 
Data reveal that the weight-normative approach is not effective for most people because of high rates of weight regain and cycling from weight loss interventions, which are linked to adverse health and well-being. Its predominant focus on weight may also foster stigma in health care and society, and data show that weight stigma is also linked to adverse health and well-being. 
In contrast, data support a weight-inclusive approach, which is included in models such as Health at Every Size for improving physical (e.g., blood pressure), behavioral (e.g., binge eating), and psychological (e.g., depression) indices, as well as acceptability of public health messages. 
Therefore, the weight-inclusive approach upholds nonmaleficience and beneficience, whereas the weight-normative approach does not. We offer a theoretical framework that organizes the research included in this review and discuss how it can guide research efforts and help health professionals intervene with their patients and community.