Evolve BioSystems: We’re facing a ‘generational loss’ of critical gut bacteria in infants

By Elaine Watson contact

- Last updated on GMT

Picture: istockphoto-NataliaDeriabina
Picture: istockphoto-NataliaDeriabina
Research into the gut microbiome suggests that the ‘generational loss’ of a specific variety of beneficial bacteria - B. infantis - in the infant gut could increase the risk for a range of health problems later in life, from allergies to obesity. But to what extent can this risk be reduced through dietary interventions, and are these interventions only effective if we make them at a certain life stage?

To find out, FoodNavigator-USA caught up with David Kyle, PhD, CEO of California-based Evolve BioSystems,​ which is about to launch products containing activated B. infantis​ that can be mixed with breast milk to re-colonize infants’ intestinal tracts with this beneficial bacteria.

The rate of bifidobacteria colonization of infants in the US and other industrialized countries is low in part due to the prevalence of formula feeding, c-sections and antibiotic use, according to Evolve BioSystems,  a spinoff from the Foods for Health Institute at the University of California, Davis.

B infantis​ is passed from mother to baby during vaginal birth through fecal/oral transfer (Moms poop during birth), explaining why babies delivered via c-section are not exposed. Meanwhile, breastmilk contains human milk oligosaccharides (prebiotics) that provide food for the B infantis​ in the baby’s gut and help it flourish, explaining why the gut microbiome of formula-fed babies are also less likely to contain B infantis, ​says Dr Kyle.

This is a western world issue that is probably a generational loss

However, even breastfed babies delivered vaginally may still​ have low/zero levels of B infantis​ today because their Moms may have undergone several courses of antibiotics in their lifetime such that they no longer have any B infantis​ to pass on, says Dr Kyle.

“Even if you’re doing everything right ​[from the perspective of the microbiome] in the sense that you’re breastfeeding and you have a vaginal birth, babies born today can still be dysbiotic because they are not being inoculated with B infantis from their Moms.

 “Millennial Moms today from the time they are born to the time they have their first baby have had on average 15-20 courses of antibiotics, so this organism is just gone. But babies in Rwanda, Bangladesh or the Amazon are chock-a-block full of B infantis.

“This is a western world issue that is probably a generational loss. What really surprised us in our ​[latest clinical] trial ​[with 70 babies in California] is that while 80% of the c-section-delivered babies had no bifidobacteria at all, this was also​ the case with more than 50% of the vaginally delivered breastfed babies.”

Now that we understand what’s happening, we can put things right again

Dr Kyle stresses that how babies are delivered and fed are decisions driven by medical need coupled with pressure to go back to work soon after birth [making breastfeeding challenging for many women]. Similarly, antibiotics have “saved many lives​,” so this isn’t about making value judgments or suggesting we eliminate c-sections and stop taking antibiotics, he observes.

Evolve BioSystems is simply recognizing that we are where we are, and is therefore on a mission to recolonize the infant gut with B infantis​, one baby at a time, says Dr Kyle, who raised $9m in Series A funding​ in 2015, and is currently closing another funding round.

“Now that we understand what’s happening, we can put things right again.”

Evolve’s first product - launching in the next couple of months - is a refrigerated sachet (that can be stored frozen) containing activated B infantis​ that breastfeeding Moms can mix with breastmilk and give to babies via a dropper.  

Babies born in the US don’t have the microbiome that they did 100 years ago

He adds: “The discovery of the link between B infantis and the oligosaccharides in human breast milk has been profound. That combination creates what we call the ‘natural microbiome’ in babies, which is not what you find in the vast majority of babies born today, which don’t have the microbiome that scientists observed 100 years ago.

“This micro-organism ​[B infantis​] converts the human oligosaccharides in breast milk into short chain fatty acids that lower the pH of the microbiome. The stool pH of babies was around pH 4.8-5.0 for babies born in the 1920s, whereas babies born today have a stool pH of around 6.00-6.2.”

In its latest US clinical trial with 70 babies (the first segment of the write up, which focuses on safety and tolerance, has just been accepted for publication), Evolve showed that supplementation with activated B. infantis​, along with consumption of breast milk, restored the fecal pH back to those slightly more acidic levels, and led to stable colonization of B infantis​ in the infant gut at levels comparable to what it was in the 1920s in America,* or what it is in less industrialized countries today, he says.

Correlation vs causation

He adds: “We know that the immune system develops in the first six months of life, so it wouldn’t be surprising that mistakes are made in developmental pathways of the immune system ​[if the health of the gut microbiome is already compromised at that early stage]. So if you miss the open window for programming, you may not have the chance to reset.”

But do we really know that restoring the newborn gut to its ‘natural’ state during this early ‘window of opportunity’ [the first few weeks and months of life] will actually reduce the risk of allergies or type 1 diabetes, for example?

Not with 100% certainty, or course, although we know that the “correlation is definitely there​,” he says, noting that there is a six times higher incidence of allergies in children with lower levels of bifidobacteria,** six times higher incidence of type 1 diabetes in children with lower levels of bifidobacteria,** and a trend toward unhealthy body weight in children who had lower levels of bifidobacteria during infancy.***

*Norton and Stohl (1926) American Journal of Diseases of Children  32, 183-191

**Vatanen T. et al., Cell, 2016 

***Kalliomaki M. et al., American Journal of Clinical Nutrition 2008

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