The First 1,000 Days of Gut Health: A Parent's Guide to Neonatal Intestinal Dysbiosis

Table of Contents

• Key Points
• Introduction: The Microscopic World Inside Your Baby's Gut
• How the Gut Microbiome Develops in Early Life
• How Common Is Dysbiosis in Newborns?
• What Causes Intestinal Dysbiosis in Newborns?
• Measuring Dysbiosis: The Dysbiosis Index
• Health Problems Associated with Intestinal Dysbiosis
• How Dysbiosis Causes Disease: The Role of Short-Chain Fatty Acids
• What This Means for Patients and Families
• What This Study Couldn't Prove
• Recommendations for Parents
• Frequently Asked Questions
• Source Information

Key Points

• Intestinal dysbiosis in newborns is an alteration of gut microbes linked to disease, often marked by low Bifidobacteria and high Enterobacteriaceae.
• The first 3 years of life are critical for microbiome development; disruptions can have lasting health consequences.
• Breastfeeding supports beneficial Bifidobacteria; antibiotics for over 4 days in preterm infants may increase NEC risk.
• Acid-blocking medications in infants are associated with dysbiosis and increased NEC risk in preterm babies.
• Dysbiosis is linked to many conditions, but causation is proven for only a few, including type 1 diabetes and allergic disease.

Introduction: The Microscopic World Inside Your Baby's Gut

Inside every human intestine lives an enormous community of microorganisms — trillions of them. While bacteria are the most abundant members of this community, archaea, fungi, and viruses are also present in healthy individuals. Together, they form the intestinal microbiota, a living ecosystem that coexists with its human host.

This microbial community is far from passive. It actively:

• Competes for and generates nutrients that the body needs
• Influences and is shaped by the body's innate and adaptive immune systems
• Protects against some diseases while potentially triggering others

Researchers have discovered that gut microbes influence mucus production, the maturation and continuity of the epithelial layer (the thin barrier separating the intestinal contents from the rest of the body), the quality of inflammatory responses, and overall physiological balance. Particularly important, the interactions between gut microbes and the developing immune system appear to be most critical in early life.

The scientific understanding of these microbes has evolved. Previously, scientists categorized intestinal microbes as symbionts (where both host and microbe benefit), commensals (where the microbe benefits and the host is unharmed), or pathogens (where the microbe benefits and the host is harmed). This simple framework no longer holds. Many intestinal microbes are now better described as pathobionts — organisms capable of causing harm in some situations while being tolerated, or even beneficial, in others. This is because the cooperative factors that allow harmless microbes to colonize the gut share essential qualities with the virulence factors that drive disease.

When this delicate balance is disturbed, the result is intestinal dysbiosis — an alteration in the intestinal microbiota associated with disease. In some cases, the change can be traced to a small group of microbes, and causality can be tested in animal models by transferring the microbiota to see if the disease follows. In other cases, the relationship is more complex: dysbiosis might be the result of a disease, merely a coincidence, or — especially in newborns — an early warning sign of problems that may not appear until much later in childhood.

How the Gut Microbiome Develops in Early Life

Just as an injury to an organ during its formation (morphogenesis) can affect that organ's recovery and the systems that depend on it, disruptions during the "formative years" of the microbiome can have lasting consequences. The first 3 years of life are the most important period of microbiome development, with age-dependent shifts in the dominant types of bacteria driven by environment, diet, and medications.

Key insights come from studies of animals raised in completely germ-free conditions. These experiments reveal just how profoundly the microbiome shapes development:

• Offspring of germ-free mothers are at high risk for metabolic syndrome even if raised in normal conditions afterward — suggesting the microbiome's influence begins before birth
• Germ-free mice have poor growth, decreased weight, and reduced mucosal surface area in the small intestine
• They have decreased intestinal motility (movement of food through the digestive tract)
• They produce increased mucus and have an enlarged cecum (the pouch at the beginning of the large intestine)
• They experience mild diarrhea
• They show altered neurodevelopment, including deficiencies in stress responsivity, anxiety-like behaviors, sociability, and cognition

When germ-free animals are colonized with single microbes or known microbial communities (a state called gnotobiotic, meaning "known microbiota"), researchers can directly observe the effects. Comparisons of germ-free, gnotobiotic, and normal (wild-type) animals demonstrate that the intestinal microbiota plays an essential role in intestinal development. These models have established a causal role for intestinal dysbiosis in several conditions, including severe acute malnutrition, obesity, nonalcoholic liver disease, Alzheimer's disease, and colitis-associated colorectal cancer. Importantly, disrupting the microbiome during the early-life window in animals causes specific immune and health alterations that are not seen when the same disruption happens at a mature age — highlighting a critical "window of opportunity" in infancy.

The human immune system develops in parallel with the microbiome. The intestinal immune system is shaped by both the structural components of microbes and the products of their metabolism.

How Common Is Dysbiosis in Newborns?

To understand how common dysbiosis is, scientists first need to define what a "normal" infant microbiota looks like — and that definition is still incomplete. However, the article offers some reasonable starting assumptions: microbial communities are dynamic and shaped by host factors, environmental factors, and available nutrients; the ancestral infant gut was shaped by the mother's vaginal, fecal, oral, and milk microbiota, as well as by horizontal transmission within families and small communities; and modern practices — hygiene, antibiotics, antiseptics, Western-style high-fat/high-sugar diets, and infant formula — have fundamentally changed the human intestinal microbiota from that of our ancestors.

The earliest descriptions of breastfed infants' fecal bacteria were published by Tissier and Logan, who both found a predominance of Gram-positive, anaerobic, Y-shaped, non-motile bacteria in healthy infants. These were initially classified as a single species, Lactobacillus bifidus, until the 1960s, when they were grouped under the genus Bifidobacterium. Different Bifidobacterium species have specialized abilities: some produce the enzymes (glycosidases) needed to digest plant oligosaccharides (complex carbohydrates), while others digest milk oligosaccharides found in human breast milk. Microbes capable of consuming milk components have a competitive advantage in the infant gut.

Here is a striking finding from the article: A review of 14 studies published between 1926 and 2017, including more than 300 healthy breastfed infants, documented that over that time period, the average fecal pH of breastfed infants rose from 5.0 to 6.5. This change is consistent with a decrease in Bifidobacteriaceae (which produce lactic acid and lower fecal pH) and increases in Clostridiaceae and Enterobacteriaceae (both associated with higher fecal pH).

That matters because Enterobacteriaceae are Gram-negative facultative anaerobes that include two species well known to neonatologists: Escherichia coli and Klebsiella pneumoniae. Their virulence factors include flagella (for motility), fimbriae (for attaching to host cells), and toxins (that interfere with normal cellular function). An abundance of Enterobacteriaceae is considered one hallmark of dysbiosis.

For healthy term infants, recognizable patterns of fecal microbiota emerge, though with high individual variation. A "first wave" of bacterial colonization is influenced by delivery mode:

• Vaginally delivered babies: dominated by Enterobacteriaceae
• Cesarean-delivered babies: dominated by Staphylococcaceae

A "second wave" is influenced by feeding type:

• Breastfed infants: dominated by Bifidobacteriaceae
• Formula-fed infants: a more diverse population including Staphylococcaceae, Clostridiaceae, Enterococcaceae, Bifidobacteriaceae, and Bacteroidaceae

In very preterm infants, the pattern is more complex: initial colonization with Staphylococcaceae is followed by Enterobacteriaceae and then Clostrideaceae, with Bifidobacteriaceae and Lactobacillaceae characteristically delayed or absent. In both term and preterm infants, weaning and the introduction of complementary foods trigger a steady increase in microbial diversity, ultimately leading to stable, adult-like communities.

In broad terms, the presence of low numbers of Bifidobacteriaceae and high numbers of Enterobacteriaceae and Clostridiaceae serves as a reasonable starting point to define dysbiosis in the first months of life. This pattern is common in very preterm infants, term infants requiring prolonged hospitalization or antibiotics, and even well-appearing infants in some geographic areas. The term "microbiota immaturity" has been coined for a delay in the patterned progression of the microbiota — a concept first described in children with severe acute malnutrition and now proposed as another useful definition of dysbiosis in infants.

What Causes Intestinal Dysbiosis in Newborns?

Many factors can influence the infant microbiota, and some can cause dysbiosis. Here are the key contributors identified in the article:

Delivery Mode and Feeding

Both mode of delivery (vaginal vs. cesarean) and feeding type (human milk vs. formula vs. a combination) significantly influence the composition of the infant microbiota. Differences in infant microbiota between home and hospital deliveries have also been reported.

Maternal Factors

The mother's diet and the microbes in her milk (which generally resemble the microbiota of maternal skin and feces) influence the infant fecal microbiota, though usually to a modest extent. Maternal smoking is also associated with changes.

Medications

Exposure to intrapartum antibiotics (given to mothers during labor to prevent Group B streptococcal sepsis or because of cesarean section) is extremely common and impacts the neonatal intestinal microbiota. Other medications commonly given to mothers and/or infants that alter the microbiota include:

• Acid-blocking agents (used for reflux)
• Selective serotonin reuptake inhibitors (SSRIs) (antidepressants)
• Metformin (for diabetes)
• Laxatives

Environmental Exposures

Recent studies have demonstrated altered infant microbiota with exposure to environmental toxins, maternal smoking, and proximity to furry animals.

Unique Factors in Very Preterm Infants

Very preterm infants are a unique population. They are "new" from an evolutionary standpoint, have prolonged hospital stays with multiple environmental exposures, are frequently exposed to antibiotics, and have immature immune systems. In these infants, the primary determinants of intestinal microbiota composition are postmenstrual age and age in weeks, but many other factors also play a role, including antenatal corticosteroids, mode of delivery, antibiotic exposure, feeding type, feeding tube dwell time and biofilms, gender, and stress.

Specific Microbiota Changes from Perinatal Exposures

The article's Table 1 details specific alterations in infant fecal microbiota related to various exposures. Here are the highlights:

• Intrapartum antibiotics: Decreased Bacteroides, Parabacteroides, Bifidobacterium, and Actinobacteria; increased Proteobacteria, Veillonella, Enterococcus, Firmicutes, and Clostridia; reduced alpha diversity (overall variety of species); lower fecal acetate; increased antibiotic resistance genes
• Postnatal antibiotics (term infants): Decreased Bacteroidetes, reduced alpha diversity, increased antibiotic resistance genes
• Postnatal antibiotics (preterm infants): Reduced alpha diversity and increased antibiotic resistance genes
• Cesarean delivery: Decreased Actinobacteria and Bacteroidetes; increased Firmicutes
• Home birth: Increased Bifidobacterium, Bacteroides, Streptococcus, and Lactobacillus; decreased Clostridium and Enterobacteriaceae
• Very preterm birth: Increased Proteobacteria; decreased Firmicutes and Bifidobacterium; lower short-chain fatty acids
• Mother's own milk: Increased Bifidobacteriaceae; decreased Staphylococcaceae, Clostridiaceae, and Pasteurellaceae
• Maternal smoking: Increased Ruminococcus, Akkermansia, Bacteroides, and Staphylococcus
• Furry pet in the home: Decreased Streptococcaceae; increased Oscillospira and Ruminococcus
• Disinfectant use: Increased Lachnospiraceae; decreased Haemophilus
• Eco-friendly disinfectant use: Decreased Enterobacteriaceae

Measuring Dysbiosis: The Dysbiosis Index

Researchers have developed a "dysbiosis index" to quantify how far a person's microbiota deviates from a healthy baseline. The first such index was created for new-onset pediatric Crohn's disease, based on the ratio of bacteria increased in patients with the disease (including Enterobacteriaceae, Pasteurellaceae, Veillonellaceae, Fusobacteriaceae, Neisseriaceae, and Gemellaceae) to bacteria decreased in those patients (including Erysipelotrichales, Bacteroidales, Clostridiales, and Bifidobacteriaceae). This index has diagnostic validity and correlates with symptom severity, though it did not predict response to treatment.

A commercially available test called the GA-map™ Dysbiosis Test (Genetic Analysis, Oslo, Norway) compares a patient's microbiota composition with a healthy adult control population and generates a dysbiosis index score. This score correlates with fecal calprotectin, a marker of intestinal inflammation. An elevated dysbiosis index using this product has been demonstrated in adults with ankylosing spondylitis (a type of inflammatory arthritis), irritable bowel syndrome, inflammatory bowel disease, and Sjögren's syndrome (an autoimmune disease affecting moisture-producing glands).

Importantly, no dysbiosis index has yet been developed for term or preterm infants. The authors note that because the infant microbiota develops in a patterned progression, any neonatal dysbiosis index would need to incorporate gestational age and the infant's age at the time of stool collection.

Health Problems Associated with Intestinal Dysbiosis

The list of diseases associated with intestinal dysbiosis is long and diverse. The article's Table 2 divides them into acute/subacute and chronic conditions.

Acute and Subacute Conditions

• Necrotizing enterocolitis (NEC) in preterm infants — a devastating intestinal emergency
• Late-onset neonatal sepsis (LOS) — bloodstream infection occurring after 72 hours of life
• Antibiotic-associated diarrhea
• Clostridium difficile colitis — a severe antibiotic-related intestinal infection
• Infant colic
• Severe acute malnutrition

Chronic Conditions

The chronic conditions associated with dysbiosis are remarkably diverse:

• Type 1 diabetes and type 2 diabetes
• Chronic kidney disease
• Inflammatory bowel disease (Crohn's disease and ulcerative colitis)
• Dyslipidemia (abnormal blood fats)
• Coronary artery disease
• Breast cancer and colon cancer
• Atopic dermatitis (eczema)
• Non-alcoholic fatty liver disease
• Parkinson's disease and Alzheimer's disease
• Obesity
• Depression and schizophrenia

For most of these conditions, a causal link has not been established. However, causality and underlying mechanisms have been demonstrated for some, including type 1 diabetes and atopic disease/asthma. Studies of antibiotic exposure in utero or in the perinatal period and its relationship to childhood obesity, atopic dermatitis, asthma, and allergic rhinitis have produced mixed results.

Necrotizing Enterocolitis (NEC)

NEC is one of the most feared complications in premature infants. Careful studies of the fecal microbiota before disease onset revealed a characteristic pattern: at the phylum level, increased Proteobacteria and decreased Firmicutes and Bacteroidetes. At the family level, there was increased Enterobacteriaceae; at the genus level, increased Klebsiella, as well as increased fimbriae-expressing bacteria.

Several studies have shown that treating preterm infants with antibiotics for more than 4 days increases the risk of later developing NEC. Similarly, giving preterm infants acid-blocking agents is associated with both fecal dysbiosis and an increased risk of NEC. The article also suggests that dysbiosis in hospitalized infants is influenced by microbes on NICU surfaces, which may explain some of the wide variation in NEC rates between hospitals. One recent analysis even demonstrated a NICU "room-specific microbiota" shaped by the infants' gut microbes.

Late-Onset Sepsis (LOS)

The case for dysbiosis in LOS is less clear, as most LOS in the NICU has been attributed to skin microbes and central catheters. However, recent investigation identified identical organisms in the feces and blood cultures of infants with LOS, suggesting that translocation of gut microbes (bacteria crossing the intestinal barrier into the bloodstream) may be a common cause. In rodent models, an abundance of specific intestinal microbes is protective against induced sepsis, while their absence is associated with increased disease severity. In preterm infants, an abundance of Bifidobacterium species appears to be protective — or at least a marker of protection — against LOS.

Infant Colic

Infant colic is common and is associated with an increased risk of long-term learning and behavioral challenges. Several studies have demonstrated an association between intestinal dysbiosis and colic, with specific bacterial types linked to symptom severity.

How Dysbiosis Causes Disease: The Role of Short-Chain Fatty Acids

The article briefly reviews the mechanisms by which dysbiosis triggers local and systemic disease, focusing on well-established pathways and promising new ones.

Well-Established Mechanisms

• Altered intestinal permeability: Gut microbes change how easily substances pass through the intestinal barrier
• Altered local and systemic inflammation: Microbes influence inflammatory responses throughout the body
• Effects on intestinal development: In germ-free conditions or germ-free mice colonized with control feces at weaning, there is a window in early life in which the microbiota can induce a gene called Erdr1 to alter intestinal development and the capacity for regenerative repair
• Serotonin production: Gut microbes stimulate enterochromaffin cells (specialized cells in the intestinal lining) to produce serotonin, the primary neurotransmitter of the enteric (intestinal) nervous system

Short-Chain Fatty Acids (SCFAs)

Short-chain fatty acids — most commonly acetate, propionate, and butyrate — are produced when gut bacteria ferment dietary fiber. They are produced by several key bacterial genera, as outlined in the article's Table 3:

• Bifidobacterium — produces acetate and lactate
• Akkermansia — produces acetate and propionate
• Faecalibacterium — produces butyrate
• Clostridium — produces butyrate
• Eubacterium — produces butyrate
• Roseburia — produces butyrate
• Bacteroides — produces acetate and propionate
• Lactobacillus — produces lactate

SCFAs serve as an important energy source for colonocytes (the cells lining the colon) and modulate insulin sensitivity, glucose and lipid homeostasis, and systemic inflammation.

A recent large-scale analysis of genotype, fecal microbiota, and fecal SCFA levels in adults demonstrated causal associations between:

• Increased fecal butyrate and improved insulin response after oral glucose tolerance testing
• Decreased fecal propionate and an increased risk of type 2 diabetes

SCFAs affect glucose metabolism through induction of intestinal gluconeogenesis (the production of new glucose in the intestine). Their role in energy metabolism may be even broader, with reported effects on appetite regulation and the gut–brain axis. In mice, SCFAs produced by maternal gut microbes influence the differentiation of neural, intestinal, and pancreatic cells in the embryo by activating embryonic G protein-coupled receptors. In rabbits, the cecal microbiota changes early in the transition from suckling to weaning, resulting in increased butyrate production, which impacts intestinal permeability.

Patients with Crohn's disease and ulcerative colitis have low numbers of SCFA-producing bacteria and low levels of fecal SCFAs. Mechanisms by which SCFAs protect against inflammatory bowel disease include:

• Supporting enterocyte (intestinal cell) proliferation
• Inducing tight junction proteins to strengthen the intestinal barrier
• Inducing antimicrobial peptides
• Producing a range of anti-inflammatory effects

SCFAs and lactic acid are produced in abundance when human milk is combined with microbes that can consume human milk oligosaccharides — such as the Bifidobacterium species that have co-evolved with breastfeeding over millions of years.

What This Means for Patients and Families

This research has important implications for how we care for newborns, especially preterm infants:

• Antibiotic stewardship matters: Antibiotics are life-saving in the NICU, but treating preterm infants for more than 4 days increases the risk of NEC. Every antibiotic course should be carefully justified and stopped as soon as possible.
• Acid blockers are not harmless: These medications, commonly prescribed for reflux in infants, are associated with both dysbiosis and increased NEC risk in preterm infants. Parents should ask whether acid blockers are truly necessary.
• Breast milk is powerful medicine: Human milk oligosaccharides selectively feed beneficial Bifidobacterium species, lowering fecal pH and promoting a healthier microbial community. The article describes how mothers shape their infants' microbiota through selective nutrients and antimicrobials in breast milk.
• Delivery mode has consequences: Babies born by cesarean section have a different microbial start than vaginally delivered babies. When C-sections are medically necessary, they are life-saving — but the microbial differences they create are real and may warrant extra attention to other protective factors like breastfeeding.
• Prematurity itself is a risk factor: Very preterm infants have a characteristic dysbiosis pattern with delayed or absent Bifidobacteriaceae. This may contribute to their vulnerability to NEC and LOS.

What This Study Couldn't Prove

The authors are candid about the limitations of the current evidence:

• Association vs. causation: For most diseases listed in Table 2, dysbiosis has not been proven to cause the disease. It may be a result of the disease, or merely coincidental.
• No established "normal": Our understanding of what constitutes a "normal" infant microbiota is incomplete, which limits our ability to define dysbiosis precisely.
• High individual variation: Even healthy infants show a high degree of individual variation in their microbiota, making it difficult to draw universal conclusions.
• No neonatal dysbiosis index: Existing dysbiosis indexes were developed for adults and children with specific diseases; none have been validated for term or preterm infants. A neonatal index would need to account for gestational age and age at stool collection.
• Mixed evidence: Studies linking antibiotic exposure to childhood obesity and allergic diseases have produced conflicting results.

Recommendations for Parents

While research is ongoing, the evidence in this review supports several practical steps for families:

1. Breastfeed when possible. Human milk oligosaccharides selectively feed beneficial bacteria and help establish a healthy microbial community. The difference between breastfed and formula-fed infants' microbiomes is well documented.
2. Ask about antibiotics. If your baby (especially a preterm baby) is prescribed antibiotics, ask your medical team how long the course will be and whether it can be shortened or stopped once tests confirm it is safe. The risk of NEC rises with antibiotic courses lasting more than 4 days.
3. Question acid-blocking medications. If acid blockers are recommended for your infant, ask whether they are truly needed. These medications are associated with dysbiosis and increased NEC risk in preterm infants.
4. Consider the hospital environment. For families of hospitalized infants, it is reassuring to know that NICU rooms develop "room-specific" microbiotas shaped by the infants themselves. Hand hygiene remains crucial, and some evidence suggests that even the type of disinfectant used can influence the infant microbiome.
5. Discuss delivery mode with your obstetric provider. If a C-section is medically necessary, accept it — it can be life-saving. But if you are planning a vaginal delivery, know that it gives your baby a different, potentially beneficial microbial start.
6. Watch for signs of colic and communicate with your pediatrician. Colic is associated with dysbiosis and with an increased risk of long-term learning and behavioral challenges, so it deserves attention beyond simply "waiting it out."

Frequently Asked Questions

What is intestinal dysbiosis in a newborn baby?

Intestinal dysbiosis is an alteration in the intestinal microbiota, the trillions of microbes in the gut, that is associated with disease. In newborns, it often means low numbers of beneficial Bifidobacteria and high numbers of Enterobacteriaceae and Clostridiaceae. This pattern is common in preterm infants and can contribute to health problems.

How does a baby's gut microbiome develop in early life?

The first 3 years of life are the most important for microbiome development. A first wave of bacteria is influenced by delivery mode: vaginally delivered babies are dominated by Enterobacteriaceae, while cesarean-delivered babies have more Staphylococcaceae. A second wave depends on feeding: breastfed infants are dominated by Bifidobacteriaceae, while formula-fed infants have a more diverse population.

What factors cause intestinal dysbiosis in newborns?

Key causes include delivery mode (cesarean vs. vaginal), feeding type (formula vs. breast milk), intrapartum antibiotics given to mothers, postnatal antibiotics in babies, acid-blocking medications, maternal smoking, and exposure to disinfectants. Very preterm infants are especially vulnerable due to prolonged hospital stays, antibiotics, and immature immune systems.

Is there a test to measure dysbiosis in newborns?

Researchers have developed a dysbiosis index that compares a person's microbiota to a healthy baseline, but no dysbiosis index has been validated for term or preterm infants. Existing tests were created for adults with conditions like Crohn's disease. A future newborn index would need to account for gestational age and age at stool collection.

What health problems are associated with newborn gut dysbiosis?

Acute conditions include necrotizing enterocolitis in preterm infants, late-onset sepsis, antibiotic-associated diarrhea, Clostridium difficile colitis, infant colic, and severe acute malnutrition. Chronic conditions linked to dysbiosis include obesity, type 2 diabetes, asthma, inflammatory bowel disease, atopic dermatitis, Parkinson's and Alzheimer's disease, and depression. For most, causation is not proven.

How can parents help promote a healthy gut microbiome in their baby?

Breastfeed when possible, because human milk oligosaccharides selectively feed beneficial Bifidobacteria. Ask about antibiotics—courses over 4 days in preterm infants may increase NEC risk. Question acid-blocking medications, as they are associated with dysbiosis. Discuss delivery mode with your obstetric provider, and practice good hand hygiene, especially in the hospital.

Does newborn gut dysbiosis cause long-term diseases like diabetes or asthma?

For most conditions, a causal link has not been established. However, causality has been demonstrated for type 1 diabetes and allergic disease/asthma. Studies linking antibiotic exposure to childhood obesity and allergies have produced mixed results. Dysbiosis might be a cause, a result, or only a coincidence for many chronic diseases.

Source Information

Original article title: Neonatal intestinal dysbiosis

Authors: Mark A. Underwood, Sagori Mukhopadhyay, Satyan Lakshminrusimha, and Charles L. Bevins

Journal: Journal of Perinatology (2020), Volume 40, pages 1597–1608

DOI: https://doi.org/10.1038/s41372-020-00829-2

Published online: September 23, 2020

Affiliations: Department of Pediatrics, UC Davis School of Medicine, Sacramento, CA; Department of Pediatrics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA; Department of Medical Microbiology and Immunology, UC Davis School of Medicine, Davis, CA.

This patient-friendly article is based on peer-reviewed research. It is intended for educational purposes and does not constitute medical advice. Always consult your child's healthcare provider with questions about your baby's health.