Diet not obesity defines body’s microbiome communities
Consuming a high fat diet during pregnancy and breast feeding persistently alters the structure of an infant’s microbiome -- the small organisms that live in and on our bodies that help cells carry out their function – said researchers from Baylor College of Medicine and Oregon Health & Science University in a new study that appeared today in the journal Nature Communications.
“We know the human microbiome plays a pivotal role in human health and disease,” said Dr. Kjersti Aagaard, lead investigator and corresponding author on the report and an associate professor of obstetrics and gynecology at Baylor. “It is critically important that we understand how the microbiome changes from one person to the next, and what drives those individual changes. Part of that process is looking at how the microbiome is established early on during infant development, and what impacts these earliest microbiome communities, that will bear an impact throughout the rest of their life.”
For several years, there have been reports linking the microbiome with obesity, but there are limitations in both humans and mice where “cause” versus “mere association” have yet to be teased apart, she said.
Diet primary driver
Aagaard and her colleagues at OHSU’s Oregon National Primate Research Center have focused for several years on the role a high fat maternal diet, rather than just obesity, plays on the health of the infant. They have shown that in the primate the diet is the primary driver which perturbs the developing infant’s epigenome (the molecules and chemical modifications that decorate the human genome after the basic pattern of genomic DNA is established.)
In the study using non-human primates, the team observed dams and their offspring (both lean and obese) exposed to a high fat diet, and compared them to control diet exposed animals for up to 1 year of age.
“This enabled us to differentiate the impact of maternal obesity versus high fat diet on the developing fetus,” said Aagaard. “We observed an interesting phenomenon, about 1/3 of the dams did not become obese despite many years of exposure to a high fat diet.”
Building on these findings, Aagaard and her colleagues now sought to distinguish whether it was the diet or obesity which appeared to drive changes in the dams and their offspring’s microbiome. They found that it was a high fat diet, rather than obesity, that defined the microbiome communities of the gut.
High fat, low fat diet
The finding is key, she said. “A woman can more easily alter her diet from high fat to low fat, but safely and realistically cannot change her obesity status in the short course of pregnancy.”
Additionally, the team observed that Campylobacter (bacteria attributed to diarrheal illness in humans) was eradicated in the offspring with either maternal or post-natal, high-fat diet.
“In humans, this group of bacteria causes diarrheal illnesses, but in primates many species are commensal (neutral, not disease causing),” said Aagaard. “This suggests that a bacteria being pathogenic or disease causing may not always be because it mutates or changes, but rather our dietary changes over time evolve our microbial community such that what was once harmless becomes harmful.”
Pregnancy and lactation may be crucial windows for establishing the earliest colonizers in our microbiome, she said.
More importantly, it suggests that the association between obesity and the microbiome is more affect than cause.
“Based on our well-grounded observations in primates, it appears that a high fat diet drives changes in the intestinal microbiome. This in turn is associated with obesity some—but not all—of the time,” said Aagaard. “In fact, even lean animals on a high fat diet were observed to have an altered microbiome. Importantly, being born and breastfed to a high fat diet fed mom persistently and significantly changes the offspring’s microbiome. This is true even when a healthy control diet is given after weaning.”
Other authors on this report include: Jun Ma, Amanda L. Prince, David Bader, Dr. Min Hu, Dr. Radhika Ganu, Dr. R. Alan Harris, all of Baylor; Karalee Baquero, Peter Blundell, Dr. Antonio E. Frias and Dr. Kevin L. Grove, all of the Oregon National Primate Research Center at Oregon Health & Science University in Beaverton.
Funding for this work was provided by the National Institutes of Health (P51 OD011092, DP21DP2OD001500, NR014792, R01DK079194 and R01DK089201).
Aagaard is also a physician at the Texas Children’s Pavilion for Women.