Can What Mothers Eat Affect Their Babies’ Health?

Obesity is a huge problem in the United States, partly because many easily available foods have a lot of fat. Right now, more than half of the women in the United States are overweight or even obese around the age when they can get pregnant [1]. This could be dangerous, since scientists around the world have found that when moms are obese while they are pregnant, their babies have a higher risk of health problems throughout their lifetimes [1–5]. However, scientists do not yet know exactly why this happens. Even though obesity has many causes, an unhealthy, high-fat diet is one of the reasons some people are obese. This makes scientists ask: what changes happen in the baby when the mom eats a lot of fat?

Our hypothesis was that maybe, when moms eat a high fat diet, their babies will have different bacteria that may cause trouble in their intestines. This makes sense because when adults eat a lot of fat, their own gut bacteria change. Scientists believe this is because the fat encourages the growth of certain bacteria that break down the fat and allow the body to absorb more of it, making them gain more weight. With this in mind, we wondered if the bacteria of babies born to mothers on high-fat diets (60% saturated fat) can change, too [6].

Why do the bacteria in the intestines matter? These bacteria can affect the immune cells that can make the gut sensitive to damage and lead to a lot of problems. Even though the role of immune cells is to protect the body, they can also harm the body if they are too active or are activated by certain bacteria, resulting in inflammation [7]. One of the problems resulting from gut inflammation caused by specific bacteria is called necrotizing enterocolitis, which can cause babies born too soon (prematurely) to have to stay in the hospital for an extended period after they are born.

How did we test this idea? The bodies of mice have a lot of similarities with the human body, so we used mice in an experiment. Specifically, we gave some pregnant mice a diet with a lot of fat, and some mice a regular diet, with less fat. Then we looked at the guts of each of their babies to see if there were any differences. First, we looked at the babies’ gut bacteria. Second, we tested their intestinal inflammation by looking to see if they had more cells called type 3 innate lymphoid cells (ILC3 cells). These cells cause inflammation by secreting a molecule that irritates the gut and can make inflammation worse. So if we see a lot of these cells, it indicates that the mice have more gut inflammation.

What Happened to the Babies’ Gut Health?

After the pregnant mice had been on the unhealthy high-fat diet, we looked at their babies’ feces (poop) and found that the bacteria present were very different from those in the poop of the babies born from mice on a regular (healthy) diet (Figure 1).

We also looked at the immune cells in the babies’ intestines after they were born, and we found that ILC3 cells were increased in babies from moms that ate a high-fat diet (Figure 2). The test we used for this is called flow cytometry, in which we can identify cell types by the characteristic patterns they have on their surfaces. ILC3 cells can produce a molecule called IL-17A, which can hurt the intestine when inflammation is present.

Can We Protect the Babies From Intestinal Damage?

At this point, we knew that baby mice from mothers that ate an unhealthy, high-fat diet had a different pattern of gut bacteria and more dangerous ILC3 cells than babies from moms who ate a healthy diet. We wondered if we could protect the inflammation-prone babies from intestinal damage, so we did an experiment to see if we could stop the effect of the ILC3 cells—and it worked (Figure 3)! To do this, we checked the intestine of the baby mice after they had a substance that could cause inflammation to the intestine.

What was interesting was that, when we blocked the effect of the ILC3 cells by neutralizing IL-17A, we found we could save these babies from inflammation. This showed us that the mom’s high-fat diet changed the numbers of ILC3 cells in the babies’ intestines and caused more injury due to a higher production of IL-17A by those cells.

Mom’s Diet Matters!

This research taught us that what mothers eat while they are pregnant can affect their growing babies, even after they are born. Of course, mice are not humans, and this is a limitation of the study. However, mice are mammals, as are humans, and we can learn a lot from studying them. These experiments in mice showed us that the high-fat diet during pregnancy changed the immune cells and bacteria in the guts of the baby mice. Our findings could mean that eating healthy and avoiding high-fat foods when pregnant is very important for humans, too. A healthy diet does include some fat, but not an excessive amount. Eating healthy is all about getting a balance of all the nutrients that we need in our bodies, including vitamins, carbohydrates, proteins, healthy fats, and minerals.

Glossary

Intestine: ↑ A part of the gut where food is broken down and absorbed. Many bacteria live in the intestine.

Saturated Fat: ↑ A type of fat, that can be eaten, that has a high proportion of fatty acid molecules and is considered unhealthy.

Immune Cells: ↑ Cells that help protect the body from dangerous invaders such as harmful bacteria and viruses.

Inflammation: ↑ The state that results when immune cells are activated and cause damage to other cells. Inflammation appears as redness, swelling, heat, and pain.

Necrotizing Enterocolitis: ↑ A disease in which the intestines of babies that are born too soon (premature) are damaged, causing the babies to stay in the hospital for a while.

Type 3 Innate Lymphoid Cells: ↑ A type of immune cell present in the intestine that can produce the cytokine IL-17A.

Flow Cytometry: ↑ A technology that uses lasers to analyze single cells based on the molecules on their surfaces.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Acknowledgments

This research was originally funded by NIH K08 (DK100545), a Young Investigator Grant for Probiotic Research and a Children’s Medical Center Foundation Grant to JM. We would also like to acknowledge Sameera Chiruvolu (Ursuline Academy of Dallas) for her help in editing the manuscript.