Tea for two?

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I am a scientist. But I also work in Berkeley, CA. And it was only a matter of time before these worlds collided…

Let’s talk about the science behind a very popular pregnancy herbal supplement – Raspberry Leaf Tea.

(My prenatal yoga instructor is not going to be happy with me.)

Though I proudly bought my Prenatal Vitamins, Ovulation tests, and pregnancy pee sticks, I hid my “Mother to Be” tea underneath a red pepper on the supermarket conveyor belt the other day.  Yes, I bought the tea but I am still conflicted about buying into the concept that a tea can magically (uh, I mean biologically) strengthen a uterus.

In addition to the gushing words from my yoga instructor, the internet offers up unlimited gems about the stuff.  These words of wisdom range from the very appealing –  “It strengthens the uterus and pelvic muscles which leads to shorter and easier labors” to the anecdotal –  “…my sister’s sister took it at 35 weeks and had her baby within 48 hours” to the very confident “Has been shown to concentrate the effects of contractions to make them more effective”

Alright then, challenge accepted! Time to dig up some scientific evidence for these claims.

So, can raspberry leaf tea do all these amazing things the internet claims it can: strengthen the uterus, shorten labor, decrease assisted delivery, and so on?

Well, despite this supplement being a fan favorite over in the midwife community (63% of American midwives recommend this supplement to stimulate labor [1]), overall it seems like the jury is still out as to its pro’s and con’s.

A very comprehensive scientific literature search by Holst et al. in 2009 [2] found only six studies testing the effects of the tea in a lab, with non-human or petri dish subjects, and only five studies that took place in the clinic. I do want to note that the small number of studies unveiled was not for lack of trying – these authors including an obscure paper from 1941 that only included three women!  Anyway, the lab studies were mixed.  Overall, raspberry leaf tea was shown to facilitate more rhythmic contractions in uterine tissue but also showed conflicted toning and relaxing effects.  The five clinical studies did not reveal any strong effects of the elixir (positive or negative) in humans.  Some studies did show a shorter first or second stage of labor but the tea only knocked off a few minutes (wow!) and one study showed shorter gestation length… but only by a couple of days (insert more sarcastic enthusiasm).

After Holst and colleagues published their efforts combing the literature, another lab study [3] was conducted to directly test uterine contractions in the presence of raspberry leaf tea in vitro (outside the body).  When applied directly to uterine tissue from non-pregnant rats, raspberry leaf tea had no effect on uterine contractibility.  However, when the researchers stuck a pregnant rat’s uterus in a petri dish with some the tea – BAM! – the cellular response rivaled that of Oxytocin.  Oxytocin, among the many wonderful things it can do during birth, is the main hormone in charge of making sure the uterus steps up and does its job to help get baby out into the world.  The researchers then tested whether raspberry leaf tea played Oxytocin’s little helper in this process.  With only six test subjects, however, they found results split in two directions:  half of the test subjects showed that oxytocin-induced contractions were augmented with raspberry leaf tea, but the other half showed the same augmentation followed by inhibition of contractions.  Hmmmm.  At the end of the day, though, the authors did not even want to put weight into their own findings (which I actually found quite promising so I was a bit bummed).  They concluded that since humans are unlikely to get the same dose that they used on their rat uteri, this effect is probably not translatable to the intact, in vivo uterus of your average pregnant women.

Now for the potential adverse effects.  Well, fortunately, there were mostly no adverse effects noted. However, there was one study that found odd trans-generational effects [4].  That’s right, drinking raspberry leaf tea while pregnant may affect your baby and your baby’s baby.  In this study, mother rats were fed raspberry leaf extract every day from conception to weaning.  The babies of these mother rats showed signs of early puberty and the babies’ babies showed greater growth restriction.  Important to point out, though, these rats were consuming raspberry leaf extract throughout the entire pregnancy.  I cannot put a percentage on the number of female humans consuming the tea throughout pregnancy but I am guessing more women are taking it primarily when they start to hit that “holy crap, I have to push out a screaming child!” stage.  My unscientific analysis of pregnant friends puts this stage somewhere between the second and third trimester but rarely during the first, when the developing womb baby is most likely to be affected by what we are putting into our bodies and when these effects may affect the womb baby’s egg babies.  Of course, more studies are needed before we can conclude that this is or is not a scary potential result of raspberry leaf consumption.

As for those benefits –

Sorry, internet, but I have to side with the scientist buzzkills, Holst and colleagues, when they state – “The fact that the product has been in traditional use for decades does not constitute evidence”.  There simply are not enough studies to back up the claims that raspberry leaf tea is a pregnancy super juice.  

With that said, in honor of full disclosure, I must admit that I have a steaming pot of “Mother to Be Tea” sitting next to me as I write this.

Yup, there will always be a tiny part of me swayed by the fact that it worked for somebody’s sister’s sister.

1. McFarlin, B. L., M. H. Gibson, et al. (1999). “A national survey of herbal preparation use by nurse-midwives for labor stimulation: Review of the literature and recommendations for practice.” Journal of Nurse-Midwifery 44(3): 205-216.

2. Holst, L., S. Haavik, et al. (2009). “Raspberry leaf – Should it be recommended to pregnant women?” Complementary Therapies in Clinical Practice 15(4): 204-208.

3. Zheng, J., M. J. Pistilli, et al. (2010). “The Effects of Commercial Preparations of Red Raspberry Leaf on the Contractility of the Rat’s Uterus In Vitro.” Reproductive Sciences 17(5): 494-501.

4. Johnson, J. R., E. Makaji, et al. (2009). “Effect of Maternal Raspberry Leaf Consumption in Rats on Pregnancy Outcome and the Fertility of the Female Offspring.” Reproductive Sciences 16(6): 605-609.

The nose knows

WELCOMING ANOTHER NEW CONTRIBUTOR!

Fellow scientist and good friend, Dr. C, has already made her way through this whole pregnancy thing and has been my sounding board for all things bump related.  I must admit, I am extremely jealous of those pregnancy superpowers – super smell, super taste – bestowed upon many a pregnant lady that seem to have missed my expanding body.  But then again, if this oversight also provided that sweet bypass from the cookie-tossing gods, I will take it. 

Dr. C., however, was lucky… or not so lucky… to have experienced the full on rewire –

pregnose

It’s a bird! It’s a plane! No, it’s a heightened rhinological olfactory manifestation!

Or, in plain English, a heightened sense of smell…

Honestly, I think my nose knew I was pregnant before I did.

It was a beautiful, San Diego Saturday. I was relaxing on the couch working on my computer (a.k.a. guiltily watching the latest reality show…), when my husband decided to make himself a tuna fish sandwich.

Within moments of opening the tuna can, the fishy aroma hit me like a Mack truck. I ran for the bathroom and promptly threw up in the toilet. And a little around it.

“Whoa. It must have been something I ate,” I said to a very surprised husband…

It wasn’t until weeks later I figured out that I was pregnant.  By then, I could, from our apartment, smell what our neighbors three doors down were having for dinner.

Was I imagining it?

Much like a spider bite gave spiderman his spidey sense, did a German shepherd bite me?

Target knew I was pregnant before I did, too. I started to get all these coupons for diapers and nursery furniture. I have no idea what changed in my buying habits to tip them off, but one secret experts posit is that expectant moms tend to opt for the scent-free lotions! [1]

So, what is it about smell that changes for pregnant women?

In a study by the National Geographic Smell Survey [2], a whole bunch of women (290,838 women to be exact, of whom 13,610 were pregnant) reported on their sense of smell. The pregnant women claimed they couldn’t smell as well as those that were not pregnant, yet they performed better on one of the smell tests they took.  More recent studies showed that women did self-report to have a better sense of smell while pregnant [3] [4], or at least experienced a change in smell [5].

But what yours truly says to all of those studies is: brave be the soul that can endure the smell of pungent fish while pregnant.

So, how and why do we get these super smell powers when we’re expecting?

During pregnancy, the hormone estrogen increases to help with a whole host of events that occur.  It’s been shown that it is this increase in estrogen that activates that crazy smell superpower.

Why? Back when we were all running away from the dinosaurs (ok, that never really happened, but a looong time ago), a heightened sense of smell may have been beneficial to the health of mama and baby. Those that ate the stinky, spoiled foods or other such toxic agents got very sick, couldn’t maintain pregnancy, or even died. Those that could smell out bad food and avoid it lived, passed on this beneficial smell trait to their daughters, who had daughters that could smell, who had daughters that could smell, and so on.

Because of this, women in general, as compared to men who maintain lower levels of estrogen, are supposed to have a better sense of smell and of taste. After all, taste is very much linked with smell [6].  Think about it – your nasal passageways and your mouth are connected – which you most likely tested unknowingly as a child when you drank chocolate milk, laughed, and it came out of your nose.

With that appetizing thought…

Have you ever watched the Food Channel? Whenever they have those awesome cooking competitions, sometimes the women judges disagree with the guy judges about which competitors’ pistachio-encrusted crème brulee tasted better. The women judges will proclaim themselves, because they are women, as having the more sensitive palate (and thus are right about their choice of most delectable brulee).

Gentlemen, I’m afraid the ladies have you on this one. Ten points for estrogen!

So, in this sense, when women get pregnant and have what an old science teacher of mine called “oodles and gobs” of estrogen, their smelling and tasting powers cannot be rivaled.

In fact, my pregnant ladies, you make the best wine tasters! Now, stay with me here – wine connoisseurs from Tesco’s HQ in Hertfordshire claim pregnant women make the best tasters [7]. They even put out a nationwide call for pregnant women to help them with in-store tasting and called it, Operation: Cot du Rhone!

Of course, some doctors came out of the woodwork shouting, “Alcohol BAD!” [8];

But back to the big picture: whether a pregnant woman’s heightened estrogen and associated sense of smell leads her to puke at a whiff of tuna or become the greatest wine connoisseur in the land, I think we all can genuflect in awe and wonder for these newly (and temporarily) acquired superpowers of the Nose.

 

1. Hill, K. How Target figured out a teen girl was pregnant before her father did. 2012. Forbes.

2. Gilbert, A.N., Wysocki, C.J. 1991. Quantitative assessment of olfactory experience during pregnancy. Psychosom Med. 53:693-700.

3. Cameron, E.L. 2007. Measures of human olfactory perception during pregnancy. Chem Senses. 32:775-782.

4. Ochsenbein-Kolble, N., von Mering, R., Zimmermann, R., Hummel, T. 2007. Changes in olfactory function in pregnancy and postpartum. Int J Gynaecol Obstet. 97:10-14.\

5.  Nordin, S., Broman, D.A., Olofsson, J.K., Wulff, M. 2004. A Longitudinal Descriptive Study of Self-reported Abnormal Smell and Taste Perception in Pregnant Women.” Chemical Senses. 29:391-402.

6. Kuga, M., Ikeda, M., Suzuki, K., Takeuchi, S. 2002. Changes in Gustatory Sense During Pregnancy. Acta Otolaryngol. 122:146-153.

7.  Sample, Ian. 2004. Do pregnant women really make the best wine tasters? The Guardian.

8. Tesco wine tasting plans slammed. 2004. BBC.

Mmmm, sweet sweet orange-flavored diagnosis

I drank the Kool Aid last week.

Crossed over into the third trimester and went in for the oh-so-pleasant glucose tolerance test to check for gestational diabetes.

As I choked down 75 grams of orange flavored liquid glucose, I thought to myself – “Who the hell came up with this pregnant woman torture test?  You want me to fast and then drink something thick and sugary, continue to not eat or drink for two hours all the while pricking me like a pin cushion?  Can’t you see that I’m pregnant?  And, wait…why am I doing this again?”  Really, how good is this one test at diagnosing and providing information for treatment?

To answer that first question – we can thank John B. O’Sullivan and Claire Mahan for developing the criteria to use with the oral glucose tolerance test in 1964 to screen for Gestational Diabetes Mellitus (GDM).  And yes, forty years later, we still pretty much use the same test and the same criteria.

For the second question – digging through the scientific literature on this quest was a bit overwhelming and unsatisfying. Luckily, the National Institutes of Health recently put together a panel of experts for a Diagnosing Gestational Diabetes Mellitus Conference to tackle the scientific literature and give their expert opinion on the current status of diagnosing this disease in pregnant women.

From the statement issued, it seems that the discussion centered on whether or not to universally adopt a newer test pushed by the International Association of Diabetes and Pregnancy Study Groups (IADPSG).

Two main tests are currently used across the world:
Two-step test – Pregnant woman drinks 50g glucose drink and has a single blood draw after an hour. If her glucose rides high, she has to go back and get the 3hr 100g test.  This second test is strictly on an as-needed basis; only 14-23% of patients will need this diagnostic follow-up.
One-step test (promoted by IADPSG) – Pregnant woman goes in fasting, gets blood drawn, drinks 75g glucose drink, gets blood drawn at 1 hour and 2 hours.  If any of her glucose levels ride high, for any of the three time points, she is diagnosed with GDM.  This is the test that I was given.

For the two-step test, 5-6% of mamas-to-be will get diagnosed with GDM.
The one-step test is more prone to false positives.  With only a one day, one time snapshot of sugar levels, this test does not exactly take into account the fact that results from the same woman can vary as much as 25% at different times. It is expected that this one-step test, with its current criteria, will diagnose 15-20% of pregnant women with GDM.

Considering this difference between the tests, the NIH panel statement focused on weighing the costs of underdiagnosing versus overdiagnosing GDM.

What are the risks of underdiagnosing?

First, what are the general risks of GDM?  A study published in The New England Journal of Medicine entitled “Hyperglycemia and Averse Pregnancy Outcomes” by the HAPO Study Cooperative Research Group compiled data from over 25,000 pregnant women from 15 birth centers across 9 countries. All the women were given the one-step test and their glucose levels at any of the three sample points (fasting, 1 hr post glucose, 2 hrs post glucose) were correlated to primary risks (e.g. birth weight >90th percentile) and secondary risks (e.g. birth injury). They found that increasing relative glucose at any of the time points increases the likelihood of birth weight above the 90th percentile and the likelihood of c-peptide levels in the cord blood (a marker for insulin resistance in the baby) being above 90th percentile.  There was also an increased risk of premature labor, preeclampsia, and birth injury.

Two things to consider though.  One, these relationships are observational – correlations rather than causal effects. Therefore, outcomes cannot be clearly attributed to the increased glucose levels in the mother.  Second, these increased risks and likelihoods have a linear relationship with glucose levels. There is no threshold so there is no easy cutoff point above when these levels cross into risky territory. Where do you draw the line for diagnosis?

Considering this diagnostic moving target, would all women at any range of GDM benefit from treatment?

Back to the NIH panel members, who pored over the literature for evidence and found…. well, there is really no consensus on the benefits of treating diagnosed GDM.

For the mother, treating GDM can decrease hypertensive disorders by 40% (one plus).  For the baby, treatment decreases the likelihood of bigger babies (also a plus, BUT, at a 6% decrease, I’m not too impressed).  Beyond these effects, there is no conclusive evidence that treatment decreases the other risks.  Also important to note, these studies are based on treatment of women diagnosed by the more stringent two-step test.  These are not women with mild GDM.  We have no freaking clue how/if treatment will benefit those falling in the “hmmm…maybe” range.

What are the risks of over-diagnosing?

For one, being told that you’re pregnancy isn’t going as swimmingly as you thought and that you have to be on high alert, pricking your finger all the time to test your blood sugar could certainly cause a bit of anxiety.

Additional concerns discussed by the NIH panel:
One, this diagnosis has been linked to higher induction rates.  Two, having “Gestational Diabetes Mellitus” on your chart could send you down a C section spiral – increased fetal and maternal monitoring which can then lead to increased false alarms which can lead to increased failed induction which can lead to increased cesarean section.  Three, it can result in increased neonatal care, separating mama from baby unnecessarily.  And, four, with all the heightened intervention, it can lead to increased direct and indirect health care costs.

Overall, the NIH panel warns that “overdiagnosis of GDM may lead to the ‘medicalization of pregnancy’ which transforms an otherwise normal pregnancy into a disease”

Verdict?  

As the panel concluded, it is too early to universally adopt the one-step approach. Increased diagnosis will lead to increased cost and intervention without a clear cut benefit to the patient.

Basically, the answer to my second question is – the jury is still out.  

I’m not sure how much say a woman can have in the type of test she is administered.  If I had known all of this before, I might have asked if the two-step test was an option.  Luckily my levels were totally normal.  But I guess I could have just been caught on a good day at a good time….  Phew!

Overall, I agree with the NIH panel, why risk unnecessarily stressing out a pregnant woman?  We have the rest of our lives to stress about all the ways we will screw up our kid!

Worrying about Whooping Cough

Recently, one of my mom’s friends had a new grandchild and this friend’s daughter, who works in a neonatal care unit, requested that all family members get a Pertussis vaccine.

My mom wanted to know if this was something she needed to worry about too.

Pertussis is the fancy name for Whooping Cough.  And, until a few years ago, I honestly thought that Whooping Cough was a thing of the past.  Something that your computer game children caught and died from when electronically traveling on the Oregon Trail.
And then there was an outbreak of the disease in California (and other parts of the country) in 2010.  Thousands of children got sick. Ten infants died.  Frightening stuff and no longer bound to the confines of a pixelated computer screen.

In the US, Whooping Cough outbreaks are actually more common that I would have thought. And this disease is cyclical: outbreaks tend to occur every 3-4 years.  I guess we’re due!  Yikes.

So, back to the query from my mother.

Do I (and my family) have to get vaccinated for Whooping Cough/Pertussis?

An info sheet about the Tdap vaccine (Tetanus-Diptheria-Pertussis) that I received from my doctor addresses this question very vaguely.  The info sheet only suggests women who “have never had a dose of Tdap” get one.  Well, my mom definitely made sure I got all of my shots as a child and I know that I have had a tetanus booster in the last 10 years (I am accident prone… especially around sharp metal objects!) but I cannot tell you the last time I had a booster that covered all three.

Taking a less ambiguous approach, the CDC recommends that ALL pregnant women get a Tdap vaccine during the 3rd trimester. As the CDC notes 30-40% of the cases involving infected infants in the 2010 outbreak could be directly attributed to the mother.  70+% could be attributed to any family member.  The “cocooning” strategy that my mom’s friend was subjected to addresses this level of prevention.  “Cocooning” is when all persons who may be coming into contact with the pre-vaccine baby (this vaccination series starts at 6-8 weeks of life) also gets vaccinated.  Apparently, vaccination as a child is not enough, your immunity to the disease starts to wear thin after about 10 years so you may still catch the disease and unknowingly pass it along to the non-vaccinated baby.

But the cocooning method seems a bit extreme to me.  And I feel justified in saying that given that an article in Clinical Infectious Diseases entitled “Infant Pertussis: Is cocooning  the answer?” appears to agree.  The authors note that cocooning just isn’t practical and a bit too “logistically complicated” to provide the benefits that a simple maternal immunization would allow [1].  So, I think I just might take the “don’t come around if you are sick” and “don’t cough on my baby” approach instead of making everyone around me double check their vaccination history.

You are off the hook, mom.

But what about that maternal immunization/booster?

The recommendation for all pregnant women to get the shot before or immediately after having the baby is a straightforward approach to making sure the mother will not catch and transmit Whooping Cough to the new bundle.  Holding off on the vaccine to watch and wait for an outbreak isn’t the most effective strategy – it takes about two weeks for the antibodies to build up to amounts that would effectively fight the illness and limit its spread.

But there is another reason to get the shot during pregnancy.  Recent research has suggested that a Tdap vaccination during the third trimester can actually confer some degree of protection to the infant for when it enters this dangerous, disease ridden world.  Studies have shown evidence for increased Pertussis antibodies in the cord blood and in the circulation of infants whose mother’s were vaccinated as compared to infants of unvaccinated mothers [2].  Effectively, this allows a brand new baby to have some antibody fighting power against Whooping Cough even before the first vaccine series initiates baby’s self-built antibody stockpile.

Important to note, though, there does appear to be a Goldilocks sweet spot for the timing of getting this shot:  post-birth may be too late but before the third trimester may be too early.  Getting the vaccine pre-conception or early in the pregnancy does not confer the same placenta-hopping-antibody benefits [3].  That’s right, if you are cooking up your second, third, fourth baby, you will still need to get that arm poked if you want to potentially pass along the benefits of the vaccine.

What about negative side effects?  An extensive review of reports sent in to an oversight body, VAERS (Vaccines Adverse Event Reporting System) turned up absolutely nothing of concern for maternal/infant/fetal outcomes post Tdap vaccine [4]..

So, I’m pretty convinced.  I think that passing along a bit of immune system fightin’ power against any potential Whooping Cough outbreaks seems more practical than hanging a sign around the baby’s neck that reads “Please do not cough on my baby”.

 

But, seriously, please do not cough on my baby.

 

 

1. Munoz F, Englund J,. Infant pertussis: is cocooning the answer? CID 2011;53:893–6.

2. Leuridan E, Hens N, Peeters N, de Witte L, Van der Meeren O, Van Damme P. Effect of a prepregnancy pertussis booster dose on maternal antibody titers in young infants. Pediatr Infect Dis J 2011;30:608-10.

3.Healy CM, Rench MA, Baker CJ. Importance of timing of maternal combined tetanus, diphtheria, and acellular pertussis (Tdap) immunization and protection of young infants. Clin Infect Dis 2013;56:539-44.

4. Zheteyeva YA, Moro PL, Tepper NK, et al. Adverse event reports after tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccines in pregnant women. Am J Obstet Gynecol 2012;207:59, e1–7.

Banking on cord blood

Well, the internet knows I’m pregnant.

Maybe it’s my lazy way of shopping for maternity clothes.  Maybe it’s all those searches for silly pregnancy advice.  Whatever it is, the internet knows I’m pregnant and now pregnancy related ads follow me everywhere.

The latest – Umbilical Cord Blood Banking.

I didn’t even realize this was an industry!

With tags like “Could One Day Be a Lifeline of Hope for Your Child” and “Saving More Cells-Saving More Hope”,  how can one pregnant lady resist?

Yes, promising to save my unborn child from leukemia AND save me $300 if I sign up now is very enticing.  Apparently, there are 80+ diseases that I could rescue this baby from by simply bagging up the umbilical cord and paying a company to safeguard until later use. Still not convinced, until I saw a point about it being used as a cure for Type 1 Diabetes.  Really?  This disease has the best likelihood of actually affecting my family, I paused and thought about it – should I bank my cord blood?

Although perfect in nearly every way, my husband is defective (love you, honey).
If not for the wonders of modern medicine, nature would have killed him off around 14 years of age when Type 1 Diabetes caused him to become completely dependent on insulin injections.  Because this disease is genetic, there is a good chance our little bundle will be carrying this defect and either developing Type 1 Diabetes or passing it along.

A brief overview of the disease – Type 1 Diabetes occurs when certain cells in the immune system (white blood cells called T lymphocytes) decide to gang up on little groups of cells in the pancreas called islet β cells.  What triggers these T cells, normally defenders of the realm, to turn into maniacal bullies targeting their own kind is still a bit of a mystery  But what we do know is that these crazed T cells are very effective in their islet β cells annihilation.  Type 1 Diabetes is no longer fatal if treated but it is chronic – all patients have to pick up the slack for their islet cell lacking pancreases and provide their bodies with every drop of insulin their body will need to deal with sugar appropriately throughout the day, every day for the rest of their lives.

Where does umbilical cord blood come in?  Well, cord blood is rich with stem cells.  And stem cells, especially the unique ones found in cord blood, have yet to be programmed, they don’t have a strict plan for their cellular destiny.  This makes them naive enough to be tricked into becoming any number of cell types across the body – perhaps even…. insulin-producing cells!  So, could stem cell rich cord blood actually be the answer to treating this baby’s possible Type 1 Diabetes?  Could my husband be treated with this magic blood and be cured?

Back to reality – the problem with stem cell therapy for Type 1 Diabetes is that even if you get those islet cells regenerated, the T cell bullies are still hanging around, waiting to beat them down. How could stem cells from cord blood be any different?

This is where I found some really freaking cool science.

As pointed out in a paper in Autoimmunity Reviews by Zhao and Mazzone in 2010, there are three main things that cord blood stem cells will have to accomplish to cure a Type 1 diabetic: 1) bulk up the stock of insulin-producing cells, 2) protect any introduced/re-grown islet β cells and 3) get the patient’s T cells back in line so they won’t attack and destroy.  And this research team may have found a way to tackle all of these points using cord blood stem cells using a very unexpected approach.

Zhao’s team followed up this tease of a review with a study published in BMC Medicine in 2012.  Rather than trying to introduce or re-grow insulin-producing cells, the team used the cord blood stem cells to educate the bad T lymphocytes.

That’s right! The baby cells are basically sitting this old guys down and saying “Listen up, its time to shape up and stop bullying the islet cells!”

How?  Well, this is a bit more complicated that I can even fully wrap my head around, but the gist of it is this:  lymphocytes are isolated from the patient’s blood and cycled through a column of petri dishes that are coated with the cord blood stem cells.  These stem cells have an added bonus property of sticking really well to the petri dish such that the lymphocytes feeding through the petri dish stacks simply bounce along the top of the stem cells, which are attached tightly to the dish.  As they bounce along, the lymphocytes hang out in the presence of the stem cells long enough for the stem cells to bestow their baby wisdom upon them.  What is this baby wisdom you may ask?  A micro environment created by different secreted molecules and molecules on the surface of the stem cells that alters how the patient’s lymphocytes respond to immune challenge.  Let’s just call this the “happy place”.

Once the patient’s lymphocytes visit the “happy place”, they are returned into the patients blood stream.  These lymphocytes have been schooled, educated, seen the light and turned away from the dark side.

As tested on a small number of patients (12 receiving treatment, 3 placebo), either showing a degree of islet β cells activity (group A = 6 patients) or absolutely no activity (group B = 6 patients), this Stem Cell Educator therapy was able to return insulin regulation capabilities.  Group A patients, who went in with subpar insulin responses, regained normal levels of insulin activity within 4 weeks of treatment.  Group B patients, who went in with no insulin activity whatsoever, were already progressing to normal insulin activity within 12 weeks and nearly matching normal levels at the end of the study (40 weeks).

To reiterate:  Group B patients went into the clinic with no insulin activity suggesting they had absolutely not a single working insulin-secreting cell in their bodies.  After one treatment with the cord blood stem cells educating the patient’s lymphocytes, insulin activity was nearly regained.  This suggests that either even these patients have a population of islet β cells struggling to survive or have other unidentified insulin-producing cells waiting in the wings, but the crazy T lymphocytes are constantly playing whack-a-mole to keep the numbers down.  Educate the lymphocytes, let these cells bounce back, BAM, Type 1 Diabetes cured?  Maybe someday.

To get back to why this relates to me and my pregnancy – I have decided that I am going to try my damndest to donate my cord blood.  I am sure this is only one of many amazing scientific pursuits cord blood stem cells are currently being used for and it seems a shame to let those precious precious cells get incinerated in a sad medical waste facility.

I’m still weighing my options, but I did find a helpful list of cord blood banks (public and private).

Maybe those cells will go on to save someone’s life.
Maybe a researcher will use them to cure Type 1 Diabetes.

Maybe this is just my way of making this baby a little scientist in utero.
“What are you up to, baby?”
“You know, just culturing some miracle cells inside the womb”.

The Deal with DHA

WELCOMING A NEW CONTRIBUTOR!

Dr. E is a fellow scientist and good friend of mine who has recently begun to navigate the crazy world of babymaking.   Naturally, her impulse is also to question all the advice and plugs and extra crap they try to sell us during this vulnerable time in our lives.  Such questions, in addition to the goings on in our female form, make for some fun and strange conversation topics – from our mutual obsession with placentas to questions such as “Wait, why are we taking DHA supplements?”. 

To start, Dr. E investigates the DHA mystery.

ImageImage

When I first started looking at prenatal vitamins I was pretty intimidated by all the ‘extras’ needed to keep baby healthy while in utero.  I was familiar with the need to increase intake of iron, vitamin D, and folic acid during pregnancy (and when trying to get pregnant, just to be safe).  Due to the fairly high rate of unplanned pregnancies in the U.S., and based on how early folic acid is needed in baby’s development, the CDC and NIH recommend all women of childbearing age to take 400 mg of folic acid daily.  What was unclear to me was how many other supplements touted as “important for prenatal development” actually were that, and how many were added to increase vitamin sales.

One of these supplements that came up time and time again was DHA, or Docosahexaenoic Acid. 

Maybe it’s like anything else, you attach the word “wedding” or “baby” to a product and it doubles in price.  So, is DHA a pricey additive designed to get you to shell out more for some vitamins?  Or is it a baby super-drug?

DHA is an essential omega-3 fatty acid that can only be obtained from the diet.  Our bodies are pretty awesome and make many of the fatty acids that we need (18/20), but this is not one of them.  DHA makes up polyunsaturated fatty acids (PUFAs) in the membranes of neurons (40%) and the retina (60%).   These PUFAs are involved in critically important membrane functions, neuronal development and plasticity, and receptor-mediated signaling among many other important tasks.

And while most of us can eat seafood or flaxseed oil to get our daily DHA requirements, pregnant women are advised to eat 2 servings or less of fish a week due to mercury concerns, and thus might not be getting enough DHA for themselves and the baby.  Hence the need for a DHA supplement.

Interest in DHA as a supplement during pregnancy began in the 1980’s when it was noted that babies born to women on the Faroe islands were born 4 days later and were on average 194 grams heavier than babies born to women in Denmark [1].  When these differences were linked to omega-3 fatty acid consumption (DHA), studies into the effects of DHA on birthweight and gestation length began.

Many studies validate the claims that DHA can increase birthweight and gestation length, including one published in the American Journal of Clinical Nutrition in 2013.  Supplement of 600 mg DHA/day to white, Hispanic, and black women in the last half of pregnancy resulted in gestation lengths 2.87 days longer than the placebo group.  Babies born to the women receiving DHA were on average 172 grams heavier and .7 cm longer [2]

SOLD!  Babies born earlier and smaller often have many more health problems and complications, so it’s a good bet to take DHA to increase gestation length and birthweight.

Additionally, DHA is critically important in neural development and childhood brain function and behavior.  From animal studies we know that lack of DHA in the diet of moms produces babies with reduced visual acuity and reduced performance on a variety of memory and learning tasks (Reviewed nicely in [3]).  These studies, however, generally cut DHA completely out of the diet, which is not realistic in humans.  We are generally consuming SOME DHA.  So does that mean DHA supplementation to our regular diet is necessary during pregnancy?

Babies from rat-moms supplemented with DHA during gestation did not perform better on the classic Morris water maze, a test of rat spatial memory and learning [4].

Similarly, a 2010 study published in the Journal of the American Medical Association had 2300 pregnant Australian women take a DHA capsule (or vegetable oil control) daily in the last half of pregnancy.  The percentage of women with depressive symptoms did not differ between the two groups, and at 18 months of age the babies born to these women did not differ in their scores on the Bayley Scales of Infant and Toddler development, which measures cognitive and language development [5]

So while consuming a DHA supplement during pregnancy is unlikely to produce brilliant genius super-spawn, my opinion is that the effects on birth weight and gestation length alone are worth spending a little extra to supplement your diet in the latter half of pregnancy.

Still, taking that extra DHA is also going to help me feel a little more secure in the fact that I’ve done everything possible to ensure babies brain development.

You know, until that kid comes out and starts running into walls.

Dr. E

  

1. Olsen SF, Hansen HS, Sorensen TI, et al. Intake of marine fat, rich in (n-3)-polyunsaturated fatty acids, may increase birthweight by prolonging gestation. Lancet. 1986;2:367-369.
2. Carlson SE, Colombo J, Gajewski BJ, Gustafson KM, Mundy D, Yeast J, Georgieff MK, Markley LA, Kerling EH, Shaddy DJ. DHA supplementation and pregnancy outcomes. Am J Clin Nutr. 2013:97:808-15
3. McCann JC, Ames BN. Is docosahexaenoic acid, an n-3 long-chain polyunsaturated fatty acid, required for development of normal brain function? An overview of evidence from cognitive and behavioral tests in humans and animals. Am J Clin Nutri 2005:82:281-95
4. Wainwright PE, Xing HC, Ward GR, et al. Water maze performance is unaffected in artificially reared rats fed diets supplemented with arachidonic acid and docosahexaenoic acid. J Nutr 1999;129:1079–89.
5. Makrides M, Gibson RA et al. Effect of DHA Supplementation During Pregnancy on Maternal Depression and Neurodevelopment of Young ChildrenA Randomized Controlled Trial JAMA. 2010:304(15):1675-1683

About that placenta…

De formato foetu liber singularis (1626) [1]     

I spent last Monday morning on a doctor’s table with goo on my belly, spying on the womb baby.
We found out the sex and about this baby’s love for doing flips and refusing to sit long enough in profile to get a money shot for the grandmas.

We also found out that I have a low-lying placenta.

“Oh, don’t worry about it”, says the sonographer, “they usually move away from the cervix as the uterus grows.  And if it doesn’t move, you’ll just have a c-section”.

What?  It’s not a big deal, we’ll just cut the baby out?

Sorry, I don’t take that as reassurance.  So, of course, I did a little bit of reading.

First, definitions – A low-lying placenta is defined by the location of its edge being < 2 cm from the opening in the cervix (baby’s escape hatch).  A more serious condition is when the placenta is actually covering this opening; this is called placenta previa.  It comes in two flavors – complete and incomplete.  The terminology specifies the degree of overlap of the cervix with complete placenta previa being the worst case scenario.  A placenta blocking the birth canal can result in hemorrhage and other scary outcomes, which can be avoided by c-section.

So, back to my selfish scenario – what about me?  What are my risks?

Hitting up the always helpful internet for advice, I found that I could decrease my risk of having a low-lying placenta and placenta previa by:   1) not smoking (check);  2) being younger (hmm… can’t do much about this one);  3) not having a previous c-section (check);  and 4) not hitting the crack pipe (big time check).

Not helpful. Plus, it is too late anyway.  The little bugger has already set up shop in this uterus of mine, now it just has to move its blood supply bag out of the way.

The sonographer and my nurse told me that as the uterus grows, the placenta will go with it, moving up and away from the cervix.  Reassuring, yes, but catching a ride on the expanding uterus might not be the true travel mode for the placenta.  Rizos et al. in 1979 note that 90% of placenta previa diagnosed during the 2nd trimester actually migrate to a normal location by term [2].

Wait, migrate?  The placenta can move on its own!?

My research mission:  1) what the hell does placental migration mean?  and 2) What is the likelihood that my anterior low-lying placenta will jump on this train and get out of the way by the time this baby wants out?

Placental migration –  So, we don’t really know how the placenta is doing this magic move technique, but there are are few hypotheses.  The two that rise to the top are the Dynamic Placentation hypothesis and the Trophotropism hypothesis.

Dynamic Placentation is based on the idea that placental attachment points are constantly forming and re-forming [3]. The rearrangement is in response to uterine growth as well as placental growth such that as the lower uterine wall forms and the muscles stretch, the stress causes the attachments in this area to degrade.  As those attachments degrade, new attachment points are formed higher in the uterus in areas that are not subjected to this same kind of growth stress. The placenta creeps along through growth, degradation and re-formation.

Trophotropism – ok, brace yourself, this one is pretty cool (if you are a huge nerd like me).  Picture the placenta as a plant seeking sunlight – plants need sun, placentas need a maternal blood supply.  Phototropism is when plants bend to bask in the best sun beam. Trophotropism is when the placenta migrates to find the best blood supply [4].  A growing uterus means that the bottom portion of the uterine wall gets stretched and, as a result, the blood supply thins.  The placenta then seeks greener pastures, moving away from this thin blood supply and towards the thicker upper uterine wall.  And here we have the same effect – over time, the placenta moves up and away from the cervix.

A different research group suggested that the trophotropism hypothesis would explain why centrally located placenta previa (sitting smack on the cervix) often do not end up migrating during the pregnancy [5].  The cervix has a healthy blood supply – why move?

So what is the prognosis for my anterior (in the front) low-lying placenta? –
A study by Cho and colleagues found that, for the studied cases of anterior low-lying placenta and incomplete placenta previa, nearly all cases showed placental migration away from the cervix (28 out of 29) [5].  And the one anterior low-lying placenta that didn’t budge, did not require a c-section at term. The migration, however, was not as strong in those placentas located posterior (in the back).  Migration was noted for 1 out of 7 posterior complete placenta previa cases, 15 out of 22 for incomplete placenta previa, and 36 out of 40 for posterior low-lying placentas.  These data suggest that there is a pretty good chance that my front-sitting placenta is already on the move.

Great!

But more importantly, who would win in a placenta race?  Anterior incomplete placenta previa takes that medal with the swift speed of 4.1mm/week. For comparison, the slow pokes include anterior low-lying placenta at 2.2 mm/week and posterior low-lying placenta at 1.4 mm/week.

While I am planning to save the deeper wonders of the placenta for a later post, I wanted to throw in one more tidbit – how the hell does the little ball of cells know where to implant itself?

There are many studies addressing this (and I hope to include them in that later post) but one simple study suggests that we might have good ‘ol gravity to blame [6].  The authors found that women who preferred to sleep on their right side, were more likely to show right-sided placentas.  The opposite held true for the left-sided sleepers.  The authors, publishing their findings in Military Medicine, were very concerned about zero gravity insemination.

Add this one to the list of things to decrease the risk of a misplaced placenta – 5) don’t get pregnant in space.

Check.

 

1De formato foetu liber singularis (1626)

2Rizos N, Doran TA, Miskin M, et al. (1979) “Natural history of placenta previa ascertained by diagnostic ultrasound.“ Am J Obstet Gynecol. 133: 287.

3King DL. (1973). “Placental migration demonstrated by ultrasonography.” Radiology 109:167. 19.

4Benirschke K, Kaufmann P. (1990) The pathology of the human placenta. New York: Springer-Verlag; p 202.

5 Cho, J. Y., Y. H. Lee, et al. (2008). “Difference in migration of placenta according to the location and type of placenta previa.” Journal of Clinical Ultrasound 36(2): 79-84.

6 Magann, E. F., W. E. Roberts, et al. (2002). “Dominant maternal sleep position influences site of placental implantation.” Military Medicine 167(1): 67-69.

 

UPDATE: Not only did my placenta move by 28 weeks (woohoo!), I revisited the data and re-wrote this post over on Preg U recently. Check it out – Placenta Previa and the Magic of Placental Migration.

A bit of respect for toxoplasmosis

Toby is my 17lb ball of feline lovin’.  He loves to cuddle and has taken a special interest to sleeping across my stomach these last few months.
I like to say to my husband “Hey, look!  Toby is already trying to smother the baby!”
For some reason he doesn’t find that as funny as I do.

One of the best things about being a pregnant cat owner is that you are expected to lay off the dirty chore of litter cleaning.  Fear of a parasite living in the poo called Toxoplasma gondii. And while I actually wanted to be very afraid of little Toxo, and continue to get out of litter duty, from what little I knew about the life cycle of this parasite, I realized that I might not have a valid excuse.

Before I dive into why Toxoplasmosis is a hard infection to catch in my Toby-specific scenario and why Toxoplasma gondii  could possibly be one of the coolest freaking parasites on the planet, I should probably start with the scary part.

Being exposed to toxoplasmosis during pregnancy is very bad.  In a 2005, American Journal of Medicine review entitled “Toxoplasmosis in Pregnancy”, authors Kravetz and Federman, lay out the risks and the recommendations for pregnant women.  The risks include miscarriage, mental retardation, microcephaly, hydrocephalus, and seizures.   Yikes.

Enough scary stuff, onto the cool part.

First, here is the life cycle of Toxo:

Toxoplasmosis_life_cycle_en.svg_

Quick summary of this pretty confusing figure:

Let’s start with the rodent (or really any small warm-blooded creature) – once an animal is infected, the parasite infects cells across the body and replicates until the host’s immune system realizes what is going on.  At that point, Toxo puts up the shields and lives on as cysts throughout the body.  Although the parasite can hang out in the host for quite some time, it cannot complete its life cycle until it is inside the intestines of a feline.  Toxo can only sexually reproduce inside a cat so in order to spread its genes (every creature’s basic goal in the grand scheme of evolution), it must get itself into a feline digestive tract.

It’s not a stretch to expect rats to be ok eating parasite-laden cat poo, or that rats will occasionally be eaten by a cat, but from the perspective of Toxo, wouldn’t be a hell of a lot more convenient if the rat you hitched a ride on and built lots and lots of copies of yourself within, was guaranteed to be eaten?

And this is exactly what Toxo does.

In normal rodents, there is an instinct to avoid cats at all costs. However, in Toxo infected rodents this aversion to feline predators disappears.  Even more fascinating is the mode by which it does this.  Toxo infection appears to target specific signaling pathways in the brain to switch the lovely and pungent scent of cat urine from a “holy crap, stay away!” signal to a “ooh, that’s a sexy smell!” signal [1].  Yes, the infected rodents are actually attracted to cat pee!  The authors who first made this finding actually called this a “fatal attraction” [2] – the parasite essentially manipulates its host’s brain chemistry to make that host more likely to be eaten by the one creature that will house and nurture the part of its parasitic life cycle required to spread its genes.

But wait, there’s more!  Toxo is also a sexually transmitted disease, spread between infected males and uninfected females and their resulting pups.  Normally, females have a sense to steer clear of sick males. However, in a stroke of evolutionary brilliance, Toxo makes these infected males more sexually attractive to females [3].  What?  That is bananas!

Ah, the wonders of evolution.

So, why am I not afraid of Toby’s litter box?  Well, the way I see it, the only way I could get infected would be if this indoor cat, who is pretty lazy and not a very good mouser, manages to get out and back in without my realizing it, have amazing luck to come upon a Toxo infected rodent, and eat it without leaving any evidence behind.  And at that point, I would still have to get his poo into my mouth somehow.  Yum.

Even Kravetz and Federman would agree with me. When the authors of the “Toxoplasmosis in Pregnancy” article carefully evaluated the findings from the scientific literature as to the causes for Toxoplasmosis, they note that it is really raw meat that we should be afraid of.  Toxo is lurking in our beef (8%), pork (20%), and lamb (20%) but luckily heating and freezing kills it quite effectively.  Of the seven recommendations the authors offer about how to avoid Toxoplasmosis, the top three are related to raw meat handling, the fourth is about washing vegetables, the fifth is about working in soil, and the last two are about house cats.  But even these last two, do not state “Get rid of your cat!  Never touch a litter box!” just advise keeping them inside and washing your hands or wearing gloves when handling litter.

(Important update from 7/3:  As noted by Dr. Tell in the comments, we are only at risk for toxoplasmosis infection if this is the first encounter with the Toxo parasite.  A good number of us are actually immune to toxoplasmosis since we have probably already been infected in our lifetime!  Kravetz and Federman note that 15% of women of childbearing age actually have signs of previous Toxo infection and Dr. Tell notes that the CDC says 22.5% of adults have been previously infected. Since after a primary infection, your immune system knows what it is looking for and is able to fight it very effectively, it is pretty unlikely that the second/third/fourth time Toxo comes around you will actually get toxoplasmosis.  I figure I am probably carrying around quite a few anti-Toxo antibodies given my childhood love for cats and sandboxes…another reason I probably don’t have to worry!)

So, I’ll cook my meat, wash my veggies, garden with gloves on but I’ll continue to change the litter box… and make sure to wash my hands really well afterwards, cause, well, you never know.

I still get the “Oh, you have a cat!?  Well, you shouldn’t be cleaning the litter” and my reply to that is often “Actually, I’m not that concerned.  Wanna hear about how freaking cool the Toxo parasite is?”

This usually ends in puzzlement.

And then acknowledgement that I am a total nerd.

1. Vyas A, Kim S-K, Giacomini N, Boothroyd JC, Sapolsky RM (2007) Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proc Natl Acad Sci USA 104: 6442–6447.

2. Berdoy, M., Webster, J. P. and Macdonald, D. W. (2000). Fatal attraction in rats infected with Toxoplasma gondii. Proc. Biol. Sci. 267, 1591-1594.

3. Dass, S. A.,Vasudevan, A., Dutta, D., Soh, L. J., Sapolsky, R. M. and Vyas, A. (2011). Protozoan parasite Toxoplasma gondii manipulates mate choice in rats by enhancing attractiveness of males. PLoS ONE 6, e27229.

Pregnancy – an excuse to stop running?

I hate running.

But I like to stay in shape and, well, running is the most convenient, cheapest form of exercise.  So, I lace up and run.

When I first got  pregnant, I thought:  “Sweet, now I have an excuse to stop running!”.  But, alas, the inner athlete in me refuses to die with this expanding belly.

But running falls into the same trap as with most pregnancy “advice” (both solicited and unsolicited) – one person will say “you need to slow down!” and the next will say “didn’t so-and-so run a marathon when she was 8 months pregnant?”.

The wide world of internet advice seems to stay a bit vague on this issue.  More than once, I have seen or overheard the magic number of “140” (bpm for maternal heart rate) floating around despite the fact that a little bit of investigation suggests that this recommendation was nixed in 1994 by the American College of Obstetricians and Gynecologists. But mostly, the advice is simple:  if you are overheating, if you are throwing up, if you are bleeding or passing out, stop your workout. Really? No shit.

Ok, on to the science.

A lengthy 2003 review by Artal and O’Toole in The British Journal of Sports Medicine scanned the data available throughout the scientific literature and found evidence (and lack of evidence) for the pregnant exercise dilemma.  The authors conclusion:  “exercise has minimal risk and confirmed benefits for most women”.

Wait, do I fall into the category of “most women”?  Not going to flatter myself, I probably do, but just in case…

A 2012 study by Szymanski and Satin published in the American Journal of Obstetrics and Gynecology categorized women into their exercise regiments and measured parameters of both mama and womb baby.  Pregnant ladies ranging from 28-32 weeks were split into three groups: inactive, moderately active, and highly active.  They were then tested before and after moderate and vigorous exercise (luckily for inactive group, they weren’t pushed to the vigorous stage so this category only contains those who exercised a bit before the test).  Measuring maternal heart rate (MHR), fetal heart rate (FHR), and indices of circulation making it between the two (via measurements from fancy Doppler sonography), the authors reached the conclusion that moderate exercise, even for the inactive preggos, does not change a single thing for the baby.  Only vigorous exercise caused changes – slight increase in FHR but a decrease in Doppler indices. Interestingly, this decrease actually indicates improved circulation to the baby, making this change “not clinically significant”.

Here’s a category that I definitely do not fit into:  elite athlete.  But just in case, I checked out an article entitled “Fetal Wellbeing May be Compromised During Strenuous Exercise Among Pregnant Elite Athletes”, a 2012 study by Salvesen et al, published in The British Journal of Sports Medicine. However, I quickly lost attention when I realized that this study was conducted on SIX women and the only result they found (increased FHR) occurred when these Olympians, training for endurance events, were pushed to >90% of their maximal heart rate.  So, if you are training to run a marathon in 2 1/2 hours, you might want to shoot for a 3 hr pace instead when you are running for two.

I guess I don’t have to worry about that one.

And… it looks like I have no excuse.

Time to get off my butt and lace up.

To cheese or not to cheese

at the cheese farm

My husband and I recently moved back from 2+ years living in Belgium.  My mom was absolutely convinced we would have babies over there, but my response – “no way, I like non-pasteurized cheese FAR too much”.  I just wasn’t quite ready to sacrifice the amazing experience of driving up to a random cheese farm in France and tasting their fare.

I certainly love my gooey, stinky, moldy cheese.

And this was, of course, another big concern when I got pregnant – none of my favorite cheeses for 9 months?

Here is what we are afraid of lurking soft cheeses:  a little bacteria called Listeria monocytogenes that causes listeriosis. And I am going to start this post by saying – listeriosis is a serious, SCARY infection to expose a developing fetus to.  A paper titled “Do We Really Need to Worry about Listeria in Newborn Infants?” by Oikike, Lamont, and Heath in The Pediatric Infectious Disease Journal  concluded with a strong yes.  Fatality risk is high and for babies that survive there is some evidence for long term disabilities.  So, yes, there is absolutely cause for concern.

But, back to the cheese.
Really, what are these odds that this nightmare bug is hanging out in the wheel of brie you just picked up from Whole Foods?

First of all, check the label.  It was probably pasteurized.  Pasteurization was designed to kill bugs and it does this very effectively.  So unless the cheese maker or the guy behind the cheese counter took a perfectly good piece of pasteurized cheese and slathered in in Listeria infected dirt, it is probably safe from bacteria.

To be safe – Stay away from unpasteurized cheese.  I know, this is not new. Every pregnant lady, her friends, acquaintances, and every other person who likes to offer pregnant women unsolicited health advice knows this tidbit.

But why the scare about ALL soft cheeses and blue cheeses and moldy rinded cheeses in the name of just-to-be-safe?

New scenario – a friend is hosting brunch and serving fresh goat cheese on a baguette with a dribble of honey.  It looks delicious.  Do you have to decline just-to-be-safe?

Let’s consider the odds that this cheese is actually carrying Listeria.

In the US, sale of raw milk and its products is pretty widely against the law.  California, along with 10 other states, does appear to allow retail of raw milk products but judging from the cheese available at my favorite cheese shop, even this legal status is limited. Check in on your state here: http://www.farmtoconsumer.org/raw_milk_map.htm#.

Ok, so I’m in California, land of limited cheese governance, do I have to be concerned?

In that previously mentioned article by Oikike et al., the authors openly admit that neonatal listeriosis is rare:  1.3/100,000 in the Netherlands, 5/100,000 in the UK, and 8.6/100,000 in the US.   See something strange, though?  The US, land of pasteurized cheese, has the highest low rate of infection where the Netherlands, a country that has absolutely no problem selling non-pasteurized cheese, is far behind.

Let’s focus on France, where it can be illegal to pasteurize cheese (as in the case of Roquefort) and the citizens and fromagers generally think Americans are silly when it comes to our fear of raw milk cheese.  In a 2012 paper, published in Clinical Infectious Diseases, Goulet and colleagues surveyed the incidence of neonatal listeriosis from 2001-2008 in France.   During this time, the rate of infection in pregnant women was 5.6/100,000 (still behind the US!).  Yes, the authors note that pregnant women should avoid “specific at-risk foods” but they mostly point fingers at prepared foods, smoked fish, etc.; absolutely no mention of non-pasteurized cheese.  Again, this is in France.

Focusing on the US, a 2012 paper by Langer and colleagues in Emerging Infectious Diseases titled “Nonpasteurized Dairy Product, Disease Outbreaks, and State Laws – United States, 1993-2006”, mined 13 years of CDC outbreak data.  Their goal: to demonstrate that non-pasteurized dairy products are dangerous to our health. From this 13 year data set, a whopping total of 73 disease outbreaks were directly attributed to non-pasteurized milk products.  Of these, 3, yes, 3, were from Listeria.  And this number is not cheese specific.

Quick mental math:  it appears that the risk of neonatal listeriosis is insanely low.
And those 8.6/100,000 cases of neonatal listeriosis in the US?  most likely, not cheese related.

That goat cheese at brunch?  Safer than leaving your house in the morning to get to brunch.

Advice to myself, I am going to continue to pass on the bologna and smoked salmon, but I will not hesitate to dig into a gooey, stinky block of slightly aged goat cheese that I love so much.

My recommendation?  Try to find yourself some Bonne Bouche from Vermont Creamery…

 don’t worry, its pasteurized.