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 ), 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  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  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 . 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.
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.
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”
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!
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.
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 . 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 
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 ). 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 .
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 
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.
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
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.
I started drinking coffee far too early. I blame it for my short stature (nothing to do with my 4’11” grandmother).
And more so than alcohol, the one thing I knew I would miss in these months ahead would be that morning (and sometimes afternoon) cup of coffee.
But do I have to ditch my daily dose of caffeine because I am growing a little human?
The general reviews and advice seem mixed – varying widely from “Oh god no!!!!!” to “hmmm… it’s not so bad”. Yeah, kind of a big range.
The websites attempting to answer this question rationally seem to suggest negative consequences but settle on the jury-is-still-out, limit-your-intake-just-in-case approach.
I decided to look a bit closer at some of the science covering the main concerns on those “Oh, god, no!” sites. Since this post is a bit lengthy, I bolded the categories so that you can fast-forward to the bits you are actually interested in.
A lot of the pregnancy websites offer the strongest evidence for and against caffeine based on two opposing scientific papers that specifically address risk of miscarriage.
First, a 2008 paper by Weng and colleagues published in American Journal of Obstetrics and Gynecology found an association between caffeine consumption and rate of miscarriage. But an article published in Epidemiology by Savitz and colleagues, also in 2008, found that caffeine consumption had no effect on increased risk of miscarriage.
So, what gives? Why such drastically different results. Ah, tis the nature of science, I suppose – so many variables can differ! One potential difference stood out to me – the amount of caffeine that is actually in the “high caffeine intake” group.
How to determine caffeine consumption –
Weng and colleagues (caffeine=BAD) asked the women to recall their overall caffeine consumption since becoming pregnant – essentially “how much caffeine have you had since your last menstrual period?”
Savitz and colleagues (caffeine=OK) asked women to recall how much they consumed before getting pregnant, since becoming pregnant, and at that very moment of the interview.
Can you recall every cup of coffee you have had since getting pregnant?
Pregnant lady population-
Weng et al. included women who came into the hospital to confirm a pregnancy and continue on from there.
Savitz et al. study included women who started visiting a clinic for prenatal care and were planning for pregnancy.
Could the women in Savitz’s study already be limiting their caffeine intake in anticipation of becoming pregnant?
Caffeine consumption classification-
Weng et al. blocked the women into 3 groups: no caffeine, low caffeine (<200 mg/day -pretty much a small cup of coffee a day), and high caffeine (>200 mg/day of caffeine – if you order a tall at Starbucks on a daily basis, this includes you!).
Savitz et al. also classified total caffeine consumption but assigned the “groups” according to the median of overall caffeine consumption for each time point. This actually ended up working out to about <200 mg/day and >200 mg/day for the during-pregancy point.
Hmmm… still pretty similar (although there are a dozen + other small differences between the women included in each study)
One thing that Savitz et al. points out about the limitations of their study is that the women included (remember, these are women that have been actively seeking prenatal care) did not show a high range of caffeine intake (>300-400 mg/day). And this high exposure range is the range that has been suggested to increase risk of miscarriage (discussed in a review by Signorello et al. in Epidemiology in 2004).
So, could the difference simply be that the “high caffeine” group in the Weng et al. study included women who were exposed to higher doses of caffeine than their counterparts in the Savitz et al. study?
(Unfortunately, I couldn’t find this sort of data point in the Weng et al. paper).
Ok, so the advice on this one seems to be – caffeine might be ok… in moderation.
What about other aspects? Growth? Development? Behavioral problems? Cancer?
Growth and development
A 2009 paper by Jahanfar and Jaafar, published in Obstetrics and Gynecology, looked at the outcome of decreasing the amount of caffeine pregnant women drank in the 2nd and 3rd trimester. In this paper, the authors describe a study conducted with a cohort of women who drank A LOT of caffeine (3 cups a day!). Half of these women were tricked into decreasing their intake via decaf coffee while letting the other half continue on feeding their caffeine addiction. Comparing the babies at the end? No effect on birth weight, no effect on length of gestation.
This outcome was also suggested by Jarosz and colleagues in a 2012 paper in the European Journal of Obstetrics & Gynecology and Reproductive Biology who found no association between caffeine and birth weight or risk of premature birth. All women considered in this study consumed less than 300 mg/day.
So contrary to some of the warnings about caffeine – at least from these two studies – it appears that caffeine hooked mama’s don’t birth smaller babies earlier.
Behavior problems later
A 2012 study by Loomans et al. published in Pediatrics found absolutely no evidence for increased risk of behavioral problems in children (5-6 years old) born to mothers who hit the coffee pot.
A 2013 in Cancer Causes Control paper by Bonaventure et al. found increasing risk of childhood acute leukemia with the mother’s caffeine consumption. This risk increase was most evident when comparing mother’s who drank two cups of coffee versus none. Uh oh.
But something to consider – there is a 0.04% chance your child will be diagnosed with acute leukemia and two cups of coffee raises this risk to 0.06%.
Ok, ok, my PhD still doesn’t give me any authority to dispense medical advice to myself or to any of you pregnant readers out there.
But, personally, I’m standing by my morning cup of coffee….
but I’ll keep it small… and stick to single shot lattes.
I was a vegetarian for about 12 years. I didn’t expect to keep up that self-imposed dietary constraint when I went off to college. But, alas, I found myself in vegetarian heaven – Ithaca, NY. Lets just say, ever since then, I love my tofu.
So after a healthy dose of soy last night, it occurred to me –
“Oh, crap, soy = phytoestrogens.”
Quick definition: phytoestrogens are plant-based compounds that have a similar structure to the estrogens that our own endocrine system produces. This similarity allows such compounds to go galavanting around, hitting up the estrogen receptors strategically placed throughout our bodies, mimicking estrogen or blocking our own estrogen. This is not actually entirely a bad thing in adults – there is quite of bit of research coming out showing the beneficial properties of phytoestrogens on aging and cancer and alleviating other health problems.
Back to my pregnancy question.
What is the protocol for eating (or not eating) soy during pregnancy? Am I dosing the seahorse (our affectionate nickname for the growing fetal form) with estrogenic compounds and screwing with the development of this little thing’s reproductive system? Its reproductive behavior? All the other developing systems that are primed and ready to respond to an estrogenic signal?
First, to Google where this gem rose to the top:
Ugh, really? If you didn’t click on the link, don’t bother. The post is USELESS. The papers they cite are OLD and have NOTHING to do with eating soy during pregnancy. Just scary points from studies dosing up babies with soy formula. And, no, I didn’t even bother clicking through the “For a thorough discussion of the dangers of soy products…” link.
Ok, onto the scientific literature.
I searched quite a bit and wasn’t completely satisfied with what I found.
In one paper by Yu et al. published in Behavioural Pharmocology in 2010, the researchers found a masculinizing effect on female behavior for those females exposed to phytoestrogens in utero.
Another paper from 2002 by Klein et al. in Molecular Medicine showed increased spleen and thymus weight for male rat pups born from mothers fed super high concentrations of phytoestrogens. They also found lower testosterone in the male pups even if their mother rats were fed low doses.
But, wait, these are rats. Rats fed chow laced with the compounds being studied. They have no other choice than to eat this every day. What about humans? On a normal human diet? Even I don’t eat tofu every day!
I found the most promising data set in a 2012 paper by Jarrell and colleagues published in Obstetrics and Gynecology International. The researchers were mainly interested in the overall presence of phytoestrogenic compounds that could reach baby from mama. They measured phytoestrogen content in the amniotic fluid during pregnancy and in umbilical cord blood and mother’s plasma at birth.
Phytoestrogens were detectable in the cord blood but at concentrations 3x lower than levels in the mom’s plasma.
But this measurement includes all women measured, whether or not they were active soy-eaters.
For those mamas who disclosed their soy intake, only those eating soy on a daily basis showed any difference in the amniotic fluid as compared to the pregnant ladies who claimed to never eat soy (no comparison shown for cord blood). Even those mamas who ate soy on a weekly basis showed absolutely no difference from the I-never-eat-soy group. A 24 hour clearance? A limited ability of the phytoestrogens to build up in the amniotic fluid with reduced intake? For future research to determine….
Also important to note, ALL the pregnant women, even those in the I-never-eat-soy group, had measurable amounts of phytoestrogens in the amniotic fluid. The cord blood data suggests the same since it is impossible to tease out who is who from the data provided.
So, even if you don’t enjoy a good tofu pup every now and again, you are probably still getting some soy sneaking into your diet.
Interestingly, those mamas carrying female nuggets had higher phytoestrogen content in the amniotic fluid than those carrying male nuggets. How that one works out physiologically is still a mystery.
My take home from this – Unless you manage to eat that tofu just at the precise moment when an estrogenic spike would screw up a key estrogen dependent fetal programming step, you are probably in the clear.
On the positive side of soy consumption – A 1998 paper from Fritz et al. in Carcinogenesis found that rat mothers chowing on a “physiological dose” of a phytoestrogenic compound actually conferred benefits to their daughters. Female rat pups dosed in the womb had reduced susceptibility to developing cancer in their mammary tissue. In humans this could translate to decreased risk of breast cancer!
Advice to myself – I will keep eating tofu… in moderation.