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Science interrupted ... by motherhood

This time on Science interrupted I’m going to talk about how my adventures in science were interrupted by my transition to motherhood.

Throughout the entirety of my pregnancy, I was so excited. Not because I was going to have a baby (well, not ONLY because I was going to have a baby), but because I was going to find out first hand what it was like to experience genetic conflict. The origins of thinking about genetic conflict are deeply rooted in thinking about trade-offs pregnant women make during pregnancy1. These trade-offs primarily deal with two questions: how quickly and how big will the fetus grow before it is born? In general, we call this maternal-fetal conflict2. Here I was poised to be able to both research and experience these trade-offs simultaneously. I was convinced I was going to gain some kind of magical insight during my pregnancy and my research was going to take off in new and exciting directions, looking at relationships that no one had even considered before.

And of course, that didn’t happen. I mean, I did see some pretty cool connections between my research and real-life experiences, but nothing that was particularly groundbreaking.

For the rest of this to make sense, remember that I study genetic conflict and how the “disagreements” between our genes influence the way we think and behave. Most of the time I think about this conflict within individuals3. But genetic conflict can also happen between individuals. Pregnancy is the clearest example of this. You are probably going “waaaaaah?! Shouldn’t pregnancy be cooperative? Both the fetus and mother have the same goal, right?” Wait to have your mind blown friend!

When I started experiencing pregnancy sickness (also known as morning sickness), I thought about how cool it was that my daughter was making me feel sick. And yes, you read that right. There are a few theories about why fetuses cause moms to feel nausea (it’s a byproduct of the hormones needed to help the fetus grow4, it’s more a byproduct of the placenta developing5,6, it’s caused by the fetus telling the mom what not to eat7–10), but ultimately the nausea is caused by genetic conflict.

When I started having pregnancy cravings (I drank a ton of milk), I thought even more about how genetic conflict might be influencing what I wanted to eat. This is an area of research that I have some expertise in, so I spent a lot of time trying to analyze my own eating early in my pregnancy. I eventually gave this up because I was driving myself crazy.

Remember earlier I told you that during pregnancy, the genetic conflict between mom and the fetus focuses on how quickly and how big the fetus grows before it is born. This sets the stage for competing “interests”, “wants”, and “desires”. It is important to remember when I talk like this, it doesn’t mean these differences are intentional or conscious. It is just the easiest way to talk about competing interests.

So how does genetic conflict translate to changed eating behavior? I’ve written about this before11, but basically mom and fetus don’t agree on how quickly the fetus should grow or how big it will be. It is in the fetus’ best interest to grow as big as it can before it is born. Mom’s perspective is a little different. Yes, it is in the mom’s best interest if the fetus is born healthy. But it is also in the mom’s best interest if the fetus doesn’t grow too large to be born.

If we take this idea about conflict over how big and fast to grow, this implies that there are two different preferred diets during pregnancy. One diet helps the fetus grow big quickly by prioritizing the consumption of sugars (think sugars, soft drinks, etc.) while all other necessary nutrients are taken from mom’s stores (calcium from bones12, protein from muscles, etc.). The other diet contains foods that take longer to digest and contain more complex nutrients (think complex carbohydrates, starches, grains, etc.). The fetus prefers the first diet because the diet contains mostly sugars that allow it to grow big quickly. The mom generally prefers the second diet because the diet contains complex nutrients and sugars so growth is at a slower and controlled pace. These two diet preferences are then combined to make the actual diet a woman eats while pregnant. To add more complexity to the mix, the fetus (through its placenta) can secrete hormones to tell the mom she is hungry13,14 and alter mom’s taste preferences during pregnancy15,16. (I told you the placenta is the coolest organ you know nothing about)

My research suggests that this conflict over diet might actually help doctors predict which women may be at risk for specific kinds of pregnancy complications. Take the example of high blood pressure and preeclampsia (which is high blood pressure on steroids). Fetuses get the nutrition they need to grow by extracting the nutrients from their mom’s blood. If the fetus needs more nutrients, it can increase maternal blood pressure17 so that it gets more nutrients quicker. So, if the fetus doesn’t have enough access to sugars to start growing big, it can 1) tell mom she is hungry, 2) change the way things taste so sweet food tastes the best, and 3) increase blood pressure so it has more access to sugars. If this goes unchecked, it is possible that a woman can develop high blood pressure or preeclampsia during pregnancy, both of which can make labor and delivery difficult, if not life threatening.

This research is still relatively new, but it has the potential to impact a lot of lives. Currently, there aren’t many good explanations for why some women have pregnancy complications while others don’t. Doctors can test for them, but we mainly use a “wait and see” approach. If my research is correct, then maybe someday doctors can start predicting which women are more at risk for complications and perform interventions before pregnancy complications become too serious.

You can probably see why thinking about this drove me a little crazy. My daughter and I are both fine and healthy, for those who were wondering. But I would have slept better if my doctor could have used my craving for milk to reassure me that we both would be fine.

Stay curious my friends,

JDA

In case you are interested, here are some of the articles that I read and thought about while writing this.

1. Haig, D. Genetic conflicts in human pregnancy. Q. Rev. Biol. 68, 495–532 (1993).

2. Fowden, A. L. & Moore, T. Maternal-fetal resource allocation: co-operation and conflict. Placenta 33 Suppl 2, e11–5 (2012).

3. Werren, J. H. Selfish genetic elements, genetic conflict, and evolutionary innovation. Proc. Natl. Acad. Sci. U. S. A. 108 Suppl 2, 10863–10870 (2011).

4. Furneaux, E. C., Langley-Evans, A. J. & Langley-Evans, S. C. Nausea and vomiting of pregnancy: endocrine basis and contribution to pregnancy outcome. Obstet. Gynecol. Surv. 56, 775–782 (2001).

5. Huxley, R. R. Nausea and vomiting in early pregnancy: its role in placental development. Obstet. Gynecol. 95, 779–782 (2000).

6. Lin, L. S., Roberts, V. J. & Yen, S. S. Expression of human gonadotropin-releasing hormone receptor gene in the placenta and its functional relationship to human chorionic gonadotropin secretion. J. Clin. Endocrinol. Metab. 80, 580–585 (1995).

7. Flaxman, S. M. & Sherman, P. W. Morning sickness: adaptive cause or nonadaptive consequence of embryo viability? Am. Nat. 172, 54–62 (2008).

8. Sherman, P. W. & Flaxman, S. M. Protecting Ourselves from Food: Spices and morning sickness may shield us from toxins and microorganisms in the diet. Am. Sci. 89, 142–151 (2001).

9. Sherman, P. W. & Flaxman, S. M. Nausea and vomiting of pregnancy in an evolutionary perspective. Am. J. Obstet. Gynecol. 186, S190–7 (2002).

10. Flaxman, S. M. & Sherman, P. W. Morning sickness: a mechanism for protecting mother and embryo. Q. Rev. Biol. 75, 113–148 (2000).

11. Un-happily ever after? How your genes are fighting about who you are. https://nutribites.blog/2020/06/15/un-happily-ever-after-how-your-genes-are-fighting-about-who-you-are/ (2020).

12. Kovacs, C. S. & Kronenberg, H. M. Maternal-fetal calcium and bone metabolism during pregnancy, puerperium, and lactation. Endocr. Rev. 18, 832–872 (1997).

13. Pérez-Pérez, A. et al. Leptin action in normal and pathological pregnancies. J. Cell. Mol. Med. 22, 716–727 (2018).

14. Forhead, A. J. & Fowden, A. L. The hungry fetus? Role of leptin as a nutritional signal before birth. J. Physiol. 587, 1145–1152 (2009).

15. Bowen, D. J. Taste and food preference changes across the course of pregnancy. Appetite 19, 233–242 (1992).

16. Brown, J. E. & Toma, R. B. Taste changes during pregnancy. Am. J. Clin. Nutr. 43, 414–418 (1986).

17. Kristiansson, P. & Wang, J. X. Reproductive hormones and blood pressure during pregnancy. Hum. Reprod. 16, 13–17 (2001).

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