Fed is Best

This is a blog created to inform the public of the dangers of insufficient feeding of exclusively breastfed newborns in the first days of life. Breastfeeding should be achieved with the baby's safety as the top priority. The current guidelines do not sufficiently protect newborns from being underfed and as a results, they are admitted to the hospital for jaundice and dehydration every minute of every day. Please share this with your friends and family.

Saturday, April 18, 2015

Letter to doctors and parents about the dangers of insufficient exclusive breastfeeding

Dear Colleague and Parent:

My name is Christie del Castillo-Hegyi and I am an emergency physician, former NIH scientist, with a background in newborn brain injury research at Brown University, and mother to a 5-year-old child with autism. I am writing you because my child fell victim to newborn jaundice due to insufficient milk intake from delayed milk production in the first days of life. As an expectant mom, I read all the guidelines on breastfeeding my first-born child. Unfortunately, following the guidelines and our pediatrician's advice resulted in my child going 4 days with absolutely no milk intake requiring ICU care. He was subsequently diagnosed with multiple neuro-developmental disabilities.  Being a physician and scientist, I sought out peer-reviewed journals to explain why this happened. I found that there is ample evidence showing the links between neonatal jaundice, dehydration, hypoglycemia and developmental disabilities. I wish to explain to you how I believe this could apply to my son and the many children whose care you are entrusted with.

My son was born 8 pounds and 11 ounces after a healthy pregnancy and normal uneventful vaginal delivery.  He was placed directly on my chest and was nursed immediately.  He was nursed on demand for 20-30 minutes every 3 hours.  Each day of our stay in the hospital, he was seen by the pediatrician as well as the lactation consultant who noted that he had a perfect latch.  He produced the expected number of wet and dirty diapers.  He was noted to be jaundiced by the second day of life and had a transcutaneous bilirubin of 8.9.  We were discharged at 48 hours at 5% weight loss with next-day follow-up.  We were told by the lactation consultant before discharge that he would be hungry and we were instructed to just keep putting him on the breast.  Upon getting home, he became fussy and I nursed him longer and longer into the night.  He cried even after nursing and latched back on immediately.  He did not sleep.  By the next morning, he stopped crying and was quiet.  We saw our pediatrician at around 68 hours of life (end of day 3).  Despite producing the expected number of wet and dirty diapers, he had lost 1 pound 5 ounces, about 15% of his birth weight. At the time, we were not aware of and were not told the percentage lost, and having been up all night long trying to feed a hungry baby, we were too exhausted to figure out that this was an incredible amount of weight loss.  He was jaundiced but no bilirubin was checked.  Our pediatrician told us that we had the option of either feeding formula or waiting for my milk to come in at day 4 or 5 of life.  Wanting badly to succeed in breastfeeding him, we went another day unsuccessfully breastfeeding and went to a lactation consultant the next day who weighed his feeding and discovered that he was getting absolutely no milk.  When I pumped and manually expressed, I realized I produced nothing. I imagined the four days of torture he experienced and how 2 days of near-continuous breastfeeding encouraged by breastfeeding manuals was a sign of this. We fed him formula after that visit and he finally fell asleep. Three hours later, we found him unresponsive. We forced milk into his mouth, which made him more alert, but then he seized. We rushed him to the emergency room. He had a barely normal glucose (50 mg/dL), a severe form of dehydration called hypernatremia (157 mEq/L) and severe jaundice (bilirubin 24 mg/dL).  We were reassured that he would be fine, but having done newborn brain injury research, knowing how little time it takes for brain cells to die due to hypoglycemia and severe dehydration, I did not believe it, although I hoped it. 

At 3 years and 8 months, our son was diagnosed with autism spectrum disorder with severe language impairment. He has also been diagnosed with ADHD, sensory processing disorder, low IQ, fine and gross motor delays and a seizure disorder associated with injury to the language area of the brain. Since my child's diagnosis, I have been researching the scientific literature on breastfeeding insufficiency, newborn starvation, brain injury and developmental disabilities for two years.  In addition, I have collected the breastfeeding stories of over 30,000 women through social media.  

In the September, 2015 issue of Hospital Pediatrics, an article was published describing 11 exclusively breastfed newborn babies who developed profound hypoglycemia between the second and fifth day of life from insufficient breast milk intake.  The child described in the body of the article was a healthy full-term baby who presented just like my son.  He was seen on the third day of life at his pediatrician's office.  Despite that, he was found on the fourth day of life lethargic and unable to feed.  He had lost 10% of his birth weight and had a low glucose of 20 mg/dL (normal > 47 mg/dL).  This child was given IV glucose after which he developed a seizure.  They obtained a brain MRI which showed extensive areas of injury to almost the entire brain.  In addition to this child, 10 other healthy term newborns were identified to have developed hypoglycemia from insufficient breastfeeding as well. They were found lethargic, seizing, hypothermic and/or not breathing.  5 out of the 6 MRIs obtained in these babies showed widespread injury to a third to almost the entire brain in varying patterns.  They subsequently developed long-term neurological disabilities including seizure disorders, motor weakness, visual impairment and feeding difficulties requiring speech therapy.

The answer to the epidemic of developmental disabilities we are seeing may be found in this vulnerable period.  The risk factors for neurological disabilities in children all have to do with brain injury caused by loss of oxygen, circulation and glucose delivery to the brain.  These include pre-eclampsia, intrauterine growth retardation and prematurity, which are caused by poor function of the placenta and decreased circulation to the baby.  Hypoglycemia, umbilical cord prolapse, nuchal cord (cord wrapped around the neck), fetal distress, low Apgar scores, respiratory distress and other labor complications, events that all cause perinatal brain injury also cause long-term neurological disabilities. Although there are many causes of newborn brain injury that we have no control over, we have control over whether or not a child is fed enough for all their neurons to survive.  I believe we may be inducing hypoglycemic brain injury to many newborns by asking mothers who may not be producing sufficient milk for their newborn's physiologic need to exclusively breastfeed.  We are potentially putting ourselves at odds with the protective natural instinct to respond to a baby's cry by telling mothers that their colostrum is enough (which for many it may not be) and by making them fear failure by giving their child supplementation when they need it.

My child's story is not rare.  In a study of 280 mother-baby dyads, 22% of motivated mothers intending to exclusively breastfeed who received close lactation support experienced delayed onset of copious milk production, or lactogenesis II, which put her child at 7-fold increased risk of excessive weight loss greater than 10%.  This means more than 1 in 5 newborns are at risk of starvation-related complications if exclusively breastfed from birth.  In another study, it has been found that 10% of well-monitored exclusively breastfed babies undergoing the Baby-Friendly Hospital Initiative protocol develop hypoglycemia of less the 40 mg/dL within the first 48 hours.  This incidence was even higher in babies born to first-time mothers as 23% developed hypoglycemia.  This level of hypoglycemia has been shown in other studies to result in brain injury on MRI and long-term declines in cognitive function.  One study showed that a glucose of less than 46 mg/dL within the first 24 hours of life was associated with a 3.7-fold increased risk of brain injury on MRI and a 4.8-fold increased odds of lower motor, cognitive and language scores at 1 year of age.  This cognitive impairment persists as evidenced by another study of 1395 newborns showing that newborns who develop transient hypoglycemia of less than 40 mg/dL had a 50% reduction in their fourth-grade achievement test scores in literacy and math.  Even a glucose less than 45 mg/dL resulted in a 38% and 22% reductions in those scores respectively.  The current standard of care tolerates a glucose between 40 and 45 mg/dL within the first 4 hours of life when there is no evidence that neurons have greater tolerance for hypoglycemia in the first hours than they do at any other time.  

I hope you feel the same sense of urgency that I do. Since we received our diagnosis, I have come to know of 40 other mothers, including pediatricians, other doctors, nurses and lactation consultants who experienced the same story of insufficient feeding in the newborn period. All of them have children with long-term neurodevelopmental impairments including autism spectrum disorder, ADHD, sensory processing disorder, severe speech delay, seizure disorders, motor impairments and mental retardation.  While the literature cites poor education in breastfeeding as the cause of these starvation-related complications, in my research of breastfeeding mothers, it is the most educated in breastfeeding that are at highest risks.  The least educated will respond to a baby's cry by offering a bottle.  The mothers that are most educated in breastfeeding are the ones who have been taught that offering just one bottle will ruin her breastfeeding and potentially harm her child.  I have learned that this is a distortion of reality created by breastfeeding education to pressure mothers to exclusively breastfeed that can put her child's life at risk.

I am writing to let you know I believe the current practice guidelines are dangerous. My son suffered an incredible amount of weight loss by the third day, which is often when mothers produce milk. How many newborns are experiencing this same fate?  To date, there are no rigorously done studies on the safety of newborn weight loss and exclusive breastfeeding before lactogenesis II on the newborn brain.  In fact, a study has shown that exclusive breastfeeding at discharge is associated with an 11-fold higher risk of rehospitalization for underfeeding and dehydration.  In addition, the Academy of Breastfeeding Medicine jaundice protocol clearly states that 10-18% of exclusively breastfed baby develop starvation jaundice from insufficient milk intake, a fact disclosed by no breastfeeding manual.

I would like to advocate for a patient safety initiative to increase monitoring and supplementation to prevent adverse neurologic conditions in all exclusively breastfed newborns as described by the following: 

1) Mothers should be instructed on how to manually express to confirm presence of milk, which is available through this link: http://newborns.stanford.edu/Breastfeeding/HandExpression.html. Any baby whose mother has little to no colostrum should be offered supplementation immediately.  

2) Twice daily weighing for exclusively breastfed newborns in the hospital and at home as it has been shown that the least-fed newborns can lose the maximum recommended weight loss of 7% within the first 24 hours.  This practice should be continued at home until breastfeeding meets the child's full metabolic requirement as signaled by the onset of daily weight gain.  The 7% weight loss threshold should be provided to the mother to help signal the need for supplementation in the hospital and at home.  

3) Universal daily transcutaneous bilirubin checks and glucose monitoring while in the hospital for exclusively breastfed newborns before the onset of daily weight gain as the scientific literature has now identified them as a high-risk population for hypoglycemia.  The physical exam is insufficient to rule out hypoglycemia and pathological hyperbilirubinemia.  Any inconsolable child should also have a glucose check as this is an often-missed sign of hypoglycemia.  Supplementation with breast milk or formula as well as IV glucose should be given immediately at a glucose level less than 47 mg/dL as this is the only prospectively validated glucose threshold that if corrected immediately prevents the development of developmental delay.  Supplementation should also be offered for bilirubin levels exceeding 15 mg/dL or any level considered high risk on the bilirubin nomogram. Not only does supplementation for underfed newborns protect a child's brain and stabilize glucose but it also doubles the rates of exclusive breastfeeding at 3 months. 

4) Pre- and post-breastfeeding weights after lactogenesis II to measure the amount of milk transferred to the baby, which should be around 2 ounces per feed.

5)  Next day after discharge follow-up with pediatricians and lactation consultants with universal bilirubin and glucose checks in the office.  Children who are crying inconsolably at home especially before lactogenesis II should be supplemented after nursing UNTIL they reach their health care provider in order to prevent the development of hypoglycemia, dehydration and negative neurological consequences.

6)  I advocate for mothers to be informed of the possibility that her child can become dehydrated, jaundiced and hypoglycemic from insufficient breast milk intake and that these conditions can cause adverse neurologic sequelae.  Signs of this are a child that is not sleeping or crying repeatedly after breastfeeding as well as nursing near-continuously.  Lethargy, poor feeding, seizures, hypothermia (low body temperature) and bradycardia (slow heart rate) are late signs that suggest the presence of profound brain injury from near-complete glucose deprivation to the brain.  Lethargic hypoglycemic babies deserve a brain MRI to provide vital information to parents so that they can closely monitor their development and obtain early intervention as needed.

7)  Every mother should be educated on supplementation after nursing in order to continue the stimulation needed to promote milk production in case the need for supplementation arises, particularly before discharge if lactogenesis II has not occurred.  If a child is hypoglycemic, greater than 7% below the birth weight, hyperbilirubinemic, hypernatremic or crying inconsolably out of hunger, supplementation can be offered 15 mLs at a time as the newborn stomach has been in fact measured to be 20 mL in size at birth, much larger than commonly taught to mothers and health professionals.  Supplementation should be offered until a child's laboratory markers are corrected and the child is no longer in distress. A child's brain will not wait for food.  Once the child is adequately fed, the breastfeeding may then be evaluated to identify the cause of underfeeding.  Supplemented breastfeeding is a valid choice as NO BENEFIT of exclusive breastfeeding justifies the risk of life-long disability caused by hypoglycemic brain injury. Any mother sent home without a supplementation plan is being sent home to potentially starve and disable her child if her milk does not arrive on time. 

Mothers are taught by breastfeeding manuals that they will uniformly be able to produce enough milk for their baby's needs and will feed them near-continuously for weeks without question if their doctors and lactation consultants tell them not to give formula. But as you have witnessed as a matter of routine, breastfeeding jaundice is very common and mothers do not uniformly produce enough milk for their babies' needs.  The learned wisdom of grandparents who know instinctively the sound of a hungry baby is being supplanted by breastfeeding manuals that cannot teach that sound to the new parent.  If you observe non-Western cultures all around the world, babies are given pre-lacteal feeds or milk through wet nurses when mother's milk is not enough in the first days of life because instinctively, we as a species protected our newborns by responding to their hungry cry.  Thousands of years of evolution have wired mothers to respond to this cry and we are interfering with a biologically protective instinct by telling mothers that their child is getting enough when it is apparent to them that they are not.  Babies get admitted to the ICU lethargic, jaundiced and dehydrated every day because their mother did not know it was possible to have insufficient milk.  The scientific literature has shown that 1-6% of breastfed babies all around the world are rehospitalized for complications associated with exclusive breastfeeding in the first days of life. That means millions of babies have been hospitalized since the 1991 publication of the Baby-Friendly Hospital Initiative which codified this protocol. The most recent publication on hospitalizations for newborn jaundice at a Baby-Friendly hospital system showed that out of 104,460 babies born in a 3 year period, 10,583 or 1 in 10 babies were hospitalized for phototherapy, the majority of these cases completely preventable with early supplementation. The Baby-Friendly Hospital Initiative and the WHO breastfeeding protocol protects the breastfeeding more than it protects the baby and countless babies have endured days, weeks and even months of hunger in order to meet its goals.

The time for magical thinking has ended.  Breastfeeding education is based on many premises not consistent with reality.   No time in the history of this planet have we allowed babies to cry out for milk for as long as we tolerate for the purpose of breastfeeding. The first law of nature is and has alway been that Fed is Best. Many parents are led to harm their own babies because of what they have been taught about breastfeeding. As you can see, if such a severe case of jaundice and dehydration can occur to two physicians taking home their first-born son, it can happen to anyone.

To all doctors and parents, my message is simple.  Feed your baby.  Provide your baby its physiologic needs every minute, including the days before milk production. The only person who knows what a newborn needs is that newborn.  The accidental starvation of a newborn child is a tragedy by any definition. We are allowing newborns to receive less than their nutritional requirement and telling parents that they are doing what is best for their children. We must be certain an infant is actually getting fed by every available mean. I hope you join me in informing your colleagues, friends and family of the data and make changes to your practice. Please feel free to share this letter with whomever you wish.

Christie del Castillo-Hegyi, MD
The citations to scientific articles referred to in the letter are available through the links found within the text of the article.
To learn how to prevent newborn feeding complications go to FedisBest.org. There you will find  the following:
To learn more about the Fed is Best Foundation, please go to our About page.
Disclaimer:  This document does not replace in-person physician evaluation and treatment.  This document is meant to inform parents of the most recent data regarding infant feeding and to increase their knowledge on how to protect their newborns from hyperbilirubinemia, dehydration, hypernatremia, hypoglycemia and extended or repeat hospitalizations due to complications from underfeeding.  Earlier supplementation may be needed for babies who are premature or have medical conditions. It is recommended that a parent seeks evaluation by a pediatrician for any concerns regarding the health and safety of her baby if they arise.


Studies supporting the links between insufficient feeding, hyperbilirubinemia, brain injury and other developmental disabilities

HOSPITAL PEDIATRICS Volume 5, Issue 9, September 2015

Late-Onset Hypoglycemia in Term Newborns With Poor Breastfeeding

Laura M. Seske, MD,a,b Stephanie L. Merhar, MD,a,b Beth E. Haberman, MDa,b

Brain injury as a result of significant neonatal hypoglycemia has been recognized for many years. Recently, several case reports from around the world have documented that neonatal hypoglycemia in term infants can result from inadequate intake related to breastfeeding.1 Clinical manifestations can vary from no symptoms, to hypotonia and lethargy, to seizures.2 The blood glucose level and duration of hypoglycemia that lead to neurodevelopmental sequelae have not been established.3 For many years, it was thought that hypoglycemic brain injury was localized to the occipital lobes; however, more recent research has shown that the damage can occur anywhere in the brain.4,5 There have been minimal follow-up data in this patient population to determine long-term prognosis.We report a cohort of 11 term neonates who were admitted to the Cincinnati Children’s Hospital Medical Center(CCHMC) NICU for treatment of hypoglycemia that was not due to endocrinopathies, sepsis, hypoxic-ischemic encephalopathy, or maternal medical problems such as diabetes. All of the infants were discharged from their birth hospitals and within a few days were admitted to the NICU with hypoglycemia.


A retrospective search was conducted to identify all neonates admitted to the CCHMC NICU from January 2010 to December 2013 with the following diagnosis codes: “neonatal convulsions” and/or “neonatal hypoglycemia.” The research was conducted with approval of the CCHMC Institutional Review Board (Protocol 2014-0607). A chart review was performed for all 47 patients identified. Patients were excluded if they had any other diagnosis that could cause hypoglycemia such as: hypoxic-ischemic encephalopathy, meconium aspiration syndrome, sepsis, prematurity,micropenis, ambiguous genitalia, intrauterine growth restriction, small for gestational age, or those who were hypoglycemic immediately after birth. Eleven neonates were included who had isolated hypoglycemia with or without convulsions. All 11 of these infants were admitted to the CCHMC NICU after routine discharge from their birth hospitals. These neonates were born at 6 birthing centers in the greater Cincinnati area.


Case 1: A 39 1/7-week estimated gestational age boy born via vaginal delivery at 2905 g to a G1 P0. Mother was primarily breastfeeding but had reported supplementing with formula intermittently. The amount of formula used, mother’s change in breasts during pregnancy and after delivery, and infant’s ability to feed were not clearly documented and/or reported in the medical record. He presented to his primary medical doctor on day of life 3 for a normal newborn well-child check. On day of life 4, he was seen by a home health nurse and reportedly could not feed with a syringe due to lethargy and was referred to CCHMC emergency department, where his weight was 2600 g, decreased 10.5% from

birth. Glucose was measured to be 20 mg/dL. He was given an intravenous 2-mL/kg bolus of dextrose 10% in water. He had a seizure, which was treated with 1 dose of lorazepam. During his hospital course, he received phenobarbital for seizure prophylaxis. Magnetic resonanceimaging (MRI) showed extensive areas of restricted diffusion involving the bilateral parietal and occipital lobes with subtle restricted diffusion in the right frontal and temporal lobes. He was discharged from the hospital on maintenance phenobarbital.In addition to the case presented in detail,10 other cases were reviewed. The results of all 11 cases can be seen in Table 1. Briefly, 9 of the 11 were first-time mothers. Five of the 11 were exclusively breastfeeding without any expressed milk provided. 

In additional 4 of the 11 were directly breastfeeding and also receiving expressed breast milk via syringe or a bottle, and 2 more were receiving formula in addition to direct breastfeeding. The volume of the supplementation of formula and/or expressed breast milk was not reported inthe medical records. Six patients had an MRI obtained and only 1 was read as normal. Seven patients had follow-up available in their medical charts. Four of those 7 patients continue to have neurologic sequelae as a result of their hypoglycemic event. As of their most recent appointments, two of the patients are still on anti epileptic medication, one completed a phenobarbital wean after discharge but continues to have generalized hypotonia, and one continues to have visual impairment. Of the 2 who remain on medication, 1 continues to have feeding difficulties and is followed by speech therapy.


This case series describes a cohort of11 term neonates with profound hypoglycemia requiring admission to the NICU within a few days of discharge from their birth hospitals. The majority of cases were vaginal deliveries to first-time mothers. Five of the 11 were exclusively breastfeeding without any expressed breastmilk provided. Four of the 11 were breastfeeding and receiving expressed breast milk in the form of a bottle or syringe. Breastfeeding rates in US women continue to increase. The 2014 Centers for Disease Control and Prevention Breastfeeding Report Card stated that 79.2%of women initiate breastfeeding.7 The vast majority of infants do well with exclusive breastfeeding with minimal or no supplementation, but the purpose of our case series is to draw attention to the rare infants who have potentially devastating consequences and discuss how to potentially avoid these consequences in the future.  US Baby-Friendly Hospital guidelines state that before discharge, breastfeeding mothers should have their technique assessed by a health care professional with 2 good-quality feeds documented, should receive education on breastfeeding practices, and should be given referral information for lactation support groups along with adequate timing for the visits after returning home with their newborns.Most birth hospitals now employ lactation consultants, as did all 6 hospitals where the infants in this study were born. However, some hospitals require a physician order for a lactation consult to occur. Although 1 study showed that timing of discharge had no effect on the feeding outcomes of newborns,9 with many hospitals discharging patients at 24 hours of life, not all mothers will receive adequate lactation support before going home. However, all of these mothers should have 2 good-quality feeds observed by a health care professional, inaccordance with US Baby-Friendly Hospital guidelines. The American Academy of Pediatrics policy statement states that infants who are discharged at ∼24 hours of life should have a follow-up with a healthcare provider within 24 to 48 hours.10 We therefore would recommend that with early discharge, a home health visit or primary medical doctor visit occur within 24 to 48 hours of discharge and that a glucose level be obtained at this visit in any infant with feeding difficulty and/or lethargy.  Five patients had seizures reported. One had documented twitching, but the electroencephalogram was negative for seizure activity. Only 6 of the 11 patients had MRIs obtained and 5 of the 6 were abnormal.We would recommend obtaining brain MRIs in all infants who present with profound hypoglycemia and seizures. We would also strongly encourage obtaining a brain MRI in those infants who did not have seizures but had a glucose level ,20 mg/dL with any neurologic symptoms. Abnormalities on MRI would determine which infants warrant closer monitoring for neurologic and developmental sequelae. Knowing the presence and degree of brain injury may allow earlier referral to services, such as early interventions and supportive therapies.  In conclusion, providing mothers with increased education, assessments, and support from a multidisciplinary level on breastfeeding techniques for their newborns will promote success. In addition, the multidisciplinary involvement will allow for identification and diagnosis of inadequate lactation and allow for treatment with alternative feeding plans in those mothers who have inadequate breastfeeding at the time of newborn hospital discharge. This process may help limit these rare but potentially devastating events. Following these patients through school age will be beneficial in tracking their outcomes given that many studies have not gone beyond a few years of life.

Recognizing and Treating Delayed or Failed Lactogenesis II

Nancy M. Hurst, RN, DSN, IBCLC
 | Disclosures
J Midwifery Womens Health. 2007;52(6):588-594. 


Delayed lactogenesis II denotes a longer than usual interval between the colostrum phase and copious milk production, but whereby the mother has the ability to achieve full lactation. Failed lactogenesis II is a condition wherein the mother is either able to achieve full lactation but an extrinsic factor has interfered with the process, or one or more factors results in failure to attain an adequate milk production. Failed lactogenesis can be described further in the context of two types of conditions: a primary inability to produce adequate milk volume, or a secondary condition as a result of improper breastfeeding management and/or infant-related problems.

Although actual rates of failed and delayed lactogenesis are unknown, estimates ranging from 5% to 15%, respectively, have been reported.[24] A variety of situations and conditions have been implicated as potential contributing factors to a delay or failure in the onset of lactogenesis II ( Table 1 ). As previously stated, some hormones indirectly influence mammary gland responsiveness and thus maternal conditions with a hormonal etiology (e.g., diabetes, hypothyroidism, or obesity) may cause a delay in lactogenesis II. Additionally, some delivery modes and conditions that result in a delay in breastfeeding initiation and/or breast stimulation (e.g., preterm, cesarean, or a prolonged second stage of labor [> 1 hour])[4,25] can also delay the onset of copious milk secretion. Examples of primary lactation failure include conditions in the mother such as anatomic breast abnormalities or hormonal aberrations. Insufficient mammary glandular tissue, postpartum hemorrhage with Sheehan syndrome,[26] theca-lutein cyst,[27,28] polycystic ovarian syndrome,[29] and some breast surgeries have been implicated as possible causes of lactation failure. While minor breast surgeries (i.e., lumpectomy) may have little effect on lactation, procedures that require invasive manipulation of the nipple/areolar complex,[30] such as the placement of breast implants, or reduction mammoplasty,[31] may disrupt normal lactation. Possible causes of secondary lactation failure include any condition in the infant that results in an ineffective/weak suck (i.e., prematurity, tongue-tie, palatal anomalies, or congenital heart defects); any condition in the mother that results in incomplete breast emptying (i.e., improper latch-on, timed/scheduled feedings, overuse of pacifiers, the unnecessary use of supplements); and some maternal medications (i.e., pseudoephedrine, progestin-only and/or estrogen containing birth control methods). It should be noted that any of the factors implicated in a delay in lactogenesis II can lead to a secondary failure of lactation if not effectively managed.


Is breastfeeding really favoring early neonatal jaundice?

Bertini G, et al. Pediatrics. 2001.


OBJECTIVE: The purpose of this study was to evaluate the development of significant hyperbilirubinemia in a large unselected newborn population in a metropolitan area with particular attention to the relationship between type of feeding and incidence of neonatal jaundice in the first week of life.
STUDY DESIGN: A population of 2174 infants with gestational age >/=37 weeks was prospectively investigated during the first days of life. Total serum bilirubin determinations were performed on infants with jaundice. The following variables were studied: type of feeding, method of delivery, weight loss after birth in relationship to the type of feeding, and maternal and neonatal risk factors for jaundice. Statistical analyses were performed using the z test for parametric variables and the t test for nonparametric variables. In addition, the multiple logistic regression allows for the estimation of the role of the individual characteristics in the development of hyperbilirubinemia. Data concerning serum bilirubin peak distribution in jaundiced newborns were analyzed using a single and a double Gaussian best fit at least squares. The t test was performed to compare 2 values (high and low) of the serum bilirubin peak in breastfed and supplementary-fed infants with those in bottle-fed infants.
RESULTS: The maximal serum bilirubin concentration exceeded 12.9 mg/dL (221 micromol/L) in 112 infants (5.1%). The study demonstrated a statistically significant positive correlation between patients with a total serum bilirubin concentration >12.9 mg/dL (221 micromol/L) and supplementary feeding; oppositely, breastfed neonates did not present a higher frequency of significant hyperbilirubinemia in the first days of life. However, best Gaussian fitting of our data suggests that a small subpopulation of breastfed infants have a higher serum bilirubin peak than do bottle-fed infants. Newborns with significant hyperbilirubinemia underwent a greater weight loss after birth compared with the overall studied population, and infants given mixed feeding lost more weight than breastfed and formula-fed newborns, indicating that formula has been administered in neonates who had a weight loss beyond a predetermined percentage of birth weight. Significant hyperbilirubinemia was also strongly associated with delivery by vacuum extractor, some perinatal complications (cephalohematoma, positive Coombs' test, and blood group systems of A, AB, B, and O [ABO] incompatibility) and Asian origin. Multiple logistic regression analysis shows that supplementary feeding, weight loss percentage, ABO incompatibility, and vacuum extraction significantly increase the risk of jaundice, while only cesarean section decreases the risk.
CONCLUSION: The present study confirms the important role of fasting in the pathogenesis of neonatal hyperbilirubinemia, although breastfeeding per se does not seem related to the increased frequency of neonatal jaundice but to the higher bilirubin level in a very small subpopulation of infants with jaundice. In fact, in the breastfed infants, there is a small subpopulation with higher serum bilirubin levels. These infants, when starved and/or dehydrated, could probably be at high risk of bilirubin encephalopathy.

Pediatr Clin North Am. 2009 Jun;56(3):671-87, doi: 10.1016/j.pcl.2009.04.005.

Identification of neonates at risk for hazardous hyperbilirubinemia: emerging clinical insights.

Watchko JF1.
Author information


Hyperbilirubinemia is the most common condition requiring evaluation and treatment in neonates. Identifying among all newborns those few at risk to develop marked hyperbilirubinemia is a clinical challenge. Clinical, epidemiologic, and genetic risk factors associated with severe hyperbilirubinemia include late preterm gestational age, exclusive breastfeeding, glucose-6-phosphate dehydrogenase deficiency, ABO hemolytic disease, East Asian ethnicity, jaundice observed in the first 24 hours of life, cephalohematoma or significant bruising, and history of a previous sibling treated with phototherapy. It is increasingly apparent that the etiopathogenesis of severe hyperbilirubinemia is often multifactorial, and emerging evidence suggests that combining risk factor assessment with measurement of predischarge total serum or transcutaneous bilirubin levels will improve hyperbilirubinemia risk prediction.

Bodyweight loss in predicting neonatal hyperbilirubinemia 72 hours after birth in term newborn infants.

Yang WC1, Zhao LL, Li YC, Chen CH, Chang YJ, Fu YC, Wu HP.

• 1Department of Pediatrics, Taichung Tzuchi Hospital, The Buddhist Medical Foundation, Taichung, Taiwan, R,O,C. arthur1226@gmail.com.


Severe dehydration is generally believed to be a cause of significant hyperbilirubinemia in newborn babies. This study aimed to analyze the weight loss of healthy term newborn infants at 24, 48 and 72 hours after birth to predict significant hyperbilirubinemia at 72 hours.

From January 2007 to December 2008, we conducted this retrospective chart review by measuring total bilirubin (transcutaneous and serum) in 343 healthy, term newborns with a birth body weight of more than 2500 g. We then analyzed the association between body weight loss (BWL) and significant hyperbilirubinemia (total bilirubin more than 15 mg/dL) 72 hours after birth. Receiver operating characteristic curves were used to evaluate the appropriate cutoff BWL percentages on the first three days after birth for the prediction of neonatal hyperbilirubinemia 72 hours after birth.

A total of 115 (33.5%) neonates presented with significant hyperbilirubinemia 72 hours after birth, and the percentages of BWL on the first three days were all higher than those in the non-significant hyperbilirubinemia group (all p < 0.05). Breastfeeding was not statistically correlated with significant hyperbilirubinemia (p=0.86). To predict significant hyperbilirubinemia 72 hours after birth, receiver operating characteristic curve analysis showed that the optimum cutoff BWL percentages were 4.48% on the first day of life (sensitivity: 43%, specificity: 70%, positive likelihood ratio [LR+]: 1.43, and negative likelihood ratio [LR-]: 0.82), 7.60% on day 2 (sensitivity: 47%, specificity: 74%, LR+: 1.81, LR-: 0.72), and 8.15% on day 3 (sensitivity: 57%, specificity: 70%, LR+: 1.92, LR-: 0.61) (all p < 0.05). CONCLUSIONS: BWL on the first three days after birth may be a predisposing factor for neonatal hyperbilirubinemia, and may also serve as a helpful clinical factor to prevent significant hyperbilirubinemia 72 hours after birth. The optimal BWL cutoff percentages on the first three days after birth presented in this study may predict hyperbilirubinemia and indicate the need for supplementary feeding.

Pediatr Int. 2008 Feb;50(1):29-34. doi: 10.1111/j.1442-200X.2007.02507.x.
Breast-feeding-associated hypernatremia: retrospective analysis of 169 term newborns.
Unal S1, Arhan E, Kara N, Uncu N, Aliefendioğlu D.

Author information
• 1Neonatal Intensive Care Unit, Turkey Ministry of Health Ankara Diskapi Children's and Research Hospital, Ankara, Turkey. sevimunal2@msn.com

The aim of the present paper was to define the incidence, complications, morbidity and mortality of hypernatremic dehydration due to inadequate breast-feeding in a neonatal intensive care unit.

A retrospective study was carried out between 2002 and 2005, to identify the term breast-fed neonates with serum sodium level > or =150 mEq/L at the Ministry of Health Ankara Diskapi Children's and Research Hospital.

The incidence of hypernatremic dehydration secondary to inadequate breast-feeding was 4.1%, occurring in 169 term infants among 4136 hospitalized term neonates with the following characteristics: mean gestational age, 39.1 weeks (37-42 weeks); birthweight, 3352 g (2200-4500 g); mother's age, 26.1 years (17-38 years); weight loss, 15.9% (5.4-32.7%); proportion of spontaneous vaginal deliveries, 75.7%; and proportion of first-time mothers, 74.6%. Major presenting symptoms were neonatal jaundice (47.3%) and poor infant suck (29.6%). The median sodium; blood urea nitrogen (BUN); and creatinine levels on admission were 155 mmol/L (150-194 mmol/L), 35 mg/dL (7-253 mg/dL), and 0.9 mg/dL (0.2-10 mg/dL), respectively. Major complications were as follows: acute renal failure, 82.8%; elevated liver enzymes, 20.7%; disseminated intravascular coagulation, 6.5%; brain edema, 5.2%; intracranial hemorrhage, 3.6%; cavernous sinus thrombosis, 1.2%; and bilateral iliac artery thrombosis, 0.6%. Ten patients (5.9%) developed seizure within the first 24 h of rehydration therapy with a mean sodium decrease of 11.9 mmol/L per day (4-19 mmol/L per day). Two patients (1.2%) died. There were positive correlation between weight loss and serum sodium, BUN, bilirubin levels (P < 0.01); there was no correlation between weight loss and mothers' age, education level, delivery route, or first-born status (P > 0.05).

Hypernatremic dehydration in neonates due to inadequate breast-feeding is a serious, potentially devastating and life-threatening disorder, and can damage the central nervous system. Follow up of infants for adequate breast-feeding is important. Pediatricians must maintain a high level of suspicion, especially in cases of pathologic infant weight loss after delivery.

Perinatal and background risk factors for childhood autism in central China.

Duan G1, Yao M2, Ma Y3, Zhang W4.

Author information
• 1Center of Children Psychology and Behavior, the Third Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China. Electronic address: hydgq@sina.com.
• 2Center of Children Psychology and Behavior, the Third Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China.
• 3Institute of Child and Adolescent Health, School of Public Health, Peking University Health Science Center, Beijing 100191, China.
• 4Beijing Academy of Education Sciences, Beijing 100045, China.


Perinatal and background risk factors for autism were identified in a cohort of autistic children in Zhengzhou, China, to formulate preventative and treatment strategies for high-risk families. In this case-control study, children were screened for suspected autism using the Autism Behavior Checklist (ABC) and diagnosed according to DSM-IV and the Childhood Autism Rating Scale (CARS). We collected perinatal histories and clinical data of 286 confirmed autistic children treated at the Third Affiliated Hospital Children׳s Psychological Clinic of Zhengzhou University from 2011 to 2013. The control group consisted of 286 healthy children from area kindergartens. Maternal age>30 years, parental introversion as measured by the Eysenck Personality Questionnaire, low level of parental education, smoking, abortion threat, pregnancy complications, maternal illness during pregnancy, maternal mental health, family history of mental illness, neonatal jaundice, birth asphyxia, premature rupture of the fetal membrane, and gestational age<37 weeks were significantly higher in the autism group. These factors were significantly correlated with behavioral symptoms as measured by ABC scores (Kendall rank correlation). Birth asphyxia, neonatal jaundice, maternal age, parental introversion, family history of mental illness, abortion threat, premature delivery, and smoking were identified as independent risk factors by multivariate logistic regression.
Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

J Psychiatr Res. 2014 Jul;54:100-8. doi: 10.1016/j.jpsychires.2014.03.019. Epub 2014 Mar 29.

Prenatal and perinatal risk factors in a twin study of autism spectrum disorders.

Froehlich-Santino W1, Londono Tobon A2, Cleveland S2, Torres A2, Phillips J2, Cohen B3, Torigoe T3, Miller J3, Fedele A3, Collins J4, Smith K5, Lotspeich L2, Croen LA4, Ozonoff S6, Lajonchere C3, Grether JK7, O'Hara R2, Hallmayer J2.
Author information
• 1Department of Psychiatry, Stanford University School of Medicine, Stanford, CA, USA. Electronic address: wendyf@stanford.edu.
• 2Department of Psychiatry, Stanford University School of Medicine, Stanford, CA, USA.
• 3Autism Genetic Resource Exchange, Autism Speaks, Los Angeles, CA, USA.
• 4Division of Research, Kaiser Permanente Northern California, Oakland, CA, USA.
• 5Impact Assessment, Inc, La Jolla, CA, USA.
• 6University of California, Davis, MIND Institute, Sacramento, CA, USA.
• 7Environmental Health Investigations Branch, California Department of Public Health, Richmond, CA, USA.
Multiple studies associate prenatal and perinatal complications with increased risks for autism spectrum disorders (ASDs). The objectives of this study were to utilize a twin study design to 1) Investigate whether shared gestational and perinatal factors increase concordance for ASDs in twins, 2) Determine whether individual neonatal factors are associated with the presence of ASDs in twins, and 3) Explore whether associated factors may influence males and females differently.
Data from medical records and parent response questionnaires from 194 twin pairs, in which at least one twin had an ASD, were analyzed.
Shared factors including parental age, prenatal use of medications, uterine bleeding, and prematurity did not increase concordance risks for ASDs in twins. Among the individual factors, respiratory distress demonstrated the strongest association with increased risk for ASDs in the group as a whole (OR 2.11, 95% CI 1.27-3.51). Furthermore, respiratory distress (OR 2.29, 95% CI 1.12-4.67) and other markers of hypoxia (OR 1.99, 95% CI 1.04-3.80) were associated with increased risks for ASDs in males, while jaundice was associated with an increased risk for ASDs in females (OR 2.94, 95% CI 1.28-6.74).

Perinatal factors associated with respiratory distress and other markers of hypoxia appear to increase risk for autism in a subgroup of twins. Future studies examining potential gender differences and additional prenatal, perinatal and postnatal environmental factors are required for elucidating the etiology of ASDs and suggesting new methods for treatment and prevention.

Prenatal, perinatal and neonatal risk factors of Autism Spectrum Disorder: a comprehensive epidemiological assessment from India.
Mamidala MP1, Polinedi A, P T V PK, Rajesh N, Vallamkonda OR, Udani V, Singhal N, Rajesh V.

Author information
• 1Department of Biological Sciences, BITS, Pilani - Hyderabad Campus, Jawaharnagar, Shamirpet (M), Hyderabad 500078, Andhra Pradesh, India.
Incidence of Autism Spectrum Disorder (ASD) is increasing across the globe and no data is available from India regarding the risk factors of ASD. In this regard a questionnaire based epidemiological assessment was carried out on prenatal, perinatal and neonatal risk factors of ASD across 8 cities in India. A retrospective cohort of 942 children was enrolled for the study. 471 children with ASD, under age of 10, were analyzed for pre-, peri-, and neonatal factors and were compared with the observations from equal number of controls. The quality control of the questionnaire and data collection was done thoroughly and the observations were computed statistically. A total of 25 factors were evaluated by unadjusted and adjusted analysis in this study. Among the prenatal factors considered, advanced maternal age, fetal distress and gestational respiratory infections were found to be associated with ASD and had an odds ratio of 1.8. Evaluation of perinatal and neonatal risk factors showed labor complications, pre-term birth, neonatal jaundice, delayed birth cry and birth asphyxia to be associated with ASD with an odds ratio greater than 1.5. This important study, first of its kind in Indian population gives a firsthand account of the relation of pre-, peri- and neonatal risk factors on ASD from an ethnically and socially diverse country like India, the impact of which was unknown earlier. This advocates additional focused investigations on physiological and genetic changes contributed by these risk factor inducing environments.

Is neonatal jaundice associated with Autism Spectrum Disorders: a systematic review.

Amin SB1, Smith T, Wang H.

Author information
• 1Division of Neonatology, Department of Pediatrics, The University of Rochester School of Medicine and Dentistry, P.O. Box 651, 601 Elmwood Avenue, Rochester, NY 14642, USA. Sanjiv_amin@urmc.rochester.edu
Using guidelines of the Meta-analysis of Observational Studies in Epidemiology Group, we systematically reviewed the literature on neonatal jaundice (unconjugated hyperbilirubinemia) and Autism Spectrum Disorder (ASD) in term and preterm infants. Thirteen studies were included in a meta-analysis. Most used retrospective matched case-control designs. There was significant heterogeneity (Q = 31, p = 0.002) and no evidence of publication bias (p = 0.12). Overall, jaundice, assessed by total serum bilirubin (TSB), was associated with ASD (OR, 1.43, 95% CI 1.22-1.67, random effect model). This association was not found in preterms (OR 0.7, 95% CI 0.38-1.02) but deserves further investigation since other measures of bilirubin such as unbound unconjugated bilirubin may be better predictors of neurotoxicity than TSB in preterms.

See comment in PubMed Commons below
Pediatrics. 2010 Nov;126(5):872-8. doi: 10.1542/peds.2010-0052. Epub 2010 Oct 11.

Neonatal jaundice, autism, and other disorders of psychological development.
Maimburg RD1, Bech BH, Vaeth M, Møller-Madsen B, Olsen J.

Author information
• 1Aarhus University, School of Public Health, Department of Epidemiology, Bartholins Allé 2, 8000 Aarhus C, Denmark. rmai@soci.au.dk


The goals were to study the association between neonatal jaundice and disorders of psychological development in a national, population-based cohort and to study whether gestational age, parity, and season of birth influenced that association.

A population-based, follow-up study of all children born alive in Denmark between 1994 and 2004 (N = 733,826)
was performed, with data collected from 4 national registers. Survival analysis was used to calculate hazard ratios (HRs).

Exposure to jaundice in neonates was associated with increased risk of disorders of psychological development for children born at term. The excess risk of developing a disorder in the spectrum of psychological development disorders after exposure to jaundice as a neonate was between 56% (HR: 1.56 [95% confidence interval [CI]: 1.05-2.30]) and 88% (HR: 1.88 [95% CI: 1.17-3.02]). The excess risk of infantile autism was 67% (HR: 1.67 [95% CI: 1.03-2.71]). This risk for infantile autism was higher if the child was conceived by a parous woman (HR: 2.71 [95% CI: 1.57-4.66]) or was born between October and March (HR: 2.21 [95% CI: 1.24-3.94]). The risk for infantile autism disappeared if the child was conceived by a primiparous woman (HR: 0.58 [95% CI: 0.18-1.83]) or was born between April and September (HR: 1.02 [95% CI: 0.41-2.50]). Similar risk patterns were found for the whole spectrum of autistic disorders.

Neonatal jaundice in children born at term is associated with disorders of psychological development. Parity and season of birth seem to play important roles.

Incidence of pre-, peri-, and post-natal birth and developmental problems of children with sensory processing disorder and children with autism spectrum disorder.
May-Benson TA1, Koomar JA, Teasdale A.

Author information
• 1The Spiral Foundation Watertown, MA, USA.

As the diagnosis of sensory processing disorder (SPD) is advanced, it is important to investigate potential contributing factors to this disorder as well as early diagnostic signs. An exploratory descriptive study, utilizing retrospective chart review, was conducted to investigate the incidence of pre-, peri- and post-natal, birth and developmental problems in a sample of 1000 children with SPD and of 467 children with autism spectrum disorder (ASD), who also had SPD. This study revealed that although no one factor was strongly associated with SPD or ASD, an average of seven events for children with SPD and eight events for children with ASD occurred across categories. These included: one pre-natal/pregnancy problem, delivery complication, assisted delivery, gestational or birth-related injury/illness; one or more early childhood illnesses or injuries; two or more infancy/early childhood developmental problems; and one or more delayed early childhood developmental milestones. When comparing results to national studies of the typical population, most remarkable was the incidence of jaundice, three to four times higher in both the SPD and ASD groups than in typical children. In addition, rates of breech position, cord wrap/ prolapse, assisted delivery methods (particularly forceps and suction deliveries), and high birth-weight were greater in both groups. Incidence of premature birth was higher in the ASD although not significantly different from the SPD group. Also of note was a high frequency of absent or brief crawling phase, and high percentages of problems with ear infections, allergies, and maternal stresses during pregnancy.

Neonatal jaundice: a risk factor for infantile autism?
Maimburg RD1, Vaeth M, Schendel DE, Bech BH, Olsen J, Thorsen P.

Author information
• 1Department of Epidemiology, Institute of Public Health, University of Aarhus, Aarhus, Denmark. rmai@soci.au.dk
In a previous study, we found that infants transferred to a neonatal ward after delivery had an almost twofold increased risk of being diagnosed with infantile autism later in childhood in spite of extensive controlling of obstetric risk factors. We therefore decided to investigate other reasons for transfer to a neonatal ward, in particular hyperbilirubinaemia and neurological abnormalities. We conducted a population-based matched case-control study of 473 children with autism and 473 matched controls born from 1990 to 1999 in Denmark. Cases were children reported with a diagnosis of infantile autism in the Danish Psychiatric Central Register. Conditional logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals [CI] and likelihood ratio tests were used to test for effect modification. We found an almost fourfold risk for infantile autism in infants who had hyperbilirubinaemia after birth (OR 3.7 [95% CI 1.3, 10.5]). In stratified analysis, the association appeared limited to term infants (>or=37 weeks gestation). A strong association was also observed between abnormal neurological signs after birth and infantile autism, especially hypertonicity (OR 6.7 [95% CI 1.5, 29.7]). No associations were found between infantile autism and low Apgar scores, acidosis or hypoglycaemia. Our findings suggest that hyperbilirubinaemia and neurological abnormalities in the neonatal period are important factors to consider when studying causes of infantile autism.

PeerJ. 2014 Mar 4;2:e294. doi: 10.7717/peerj.294. eCollection 2014.

Adult neurobehavioral outcome of hyperbilirubinemia in full term neonates-a 30 year prospective follow-up study.

Hokkanen L1, Launes J1, Michelsson K1.
Author information

Background. Neonatal hyperbilirubinemia (HB) may cause severe neurological damage, but serious consequences are effectively controlled by phototherapy and blood exchange transfusion. HB is still a serious health problem in economically compromised parts of the world. The long term outcome has been regarded favorable based on epidemiological data, but has not been confirmed in prospective follow-up studies extending to adulthood. Methods. We studied the long term consequences of HB in a prospective birth cohort of 128 HB cases and 82 controls. The cases are part of a neonatal at-risk cohort (n = 1196) that has been followed up to 30 years of age. HB cases were newborns ≥ 2500 g birth weight and ≥ 37 weeks of gestation who had bilirubin concentrations > 340 µmol/l or required blood exchange transfusion. Subjects with HB were divided into subgroups based on the presence (affected HB) or absence (unaffected HB) of diagnosed neurobehavioral disorders in childhood, and compared with healthy controls. Subjects were seen at discharge, 5, 9 and 16 years of life and parent's and teacher's assessments were recorded. At 30 years they filled a questionnaire about academic and occupational achievement, life satisfaction, somatic and psychiatric symptoms including a ADHD self-rating score. Cognitive functioning was tested using ITPA, WISC, and reading and writing tests at 9 years of life. Results. Compared to controls, the odds for a child with HB having neurobehavioral symptoms at 9 years was elevated (OR = 4.68). Forty-five per cent of the HB group were affected by cognitive abnormalities in childhood and continued to experience problems in adulthood. This was apparent in academic achievement (p < 0.0001) and the ability to complete secondary (p < 0.0001) and tertiary (p < 0.004) education. Also, the subgroup of affected HB reported persisting cognitive complaints e.g., problems with reading, writing and mathematics. Childhood symptoms of hyperactivity/impulsivity (p < 0.0001) and inattention (p < 0.02) were more common in HB groups, but in adulthood the symptoms were equal. The affected HB had lower scores in parameters reflecting life satisfaction, less controlled drinking, but not increased substance abuse. Discussion. Our results indicate that neonatal HB has negative consequences in adult age. A prospectively collected cohort with strict inclusion criteria enables to control most of the bias factors involved with retrospective data. The control and HB groups were remarkably similar at birth in terms of medical data, and the growth environment of the children, as well as the parents' social groups, education, size of family, type of housing at birth and at 9 years of age. Our findings bear resemblance to disorders of the fronto-striatal network, and also symptoms of the ADHD spectrum were frequent in the HB group suggesting a link of HB to other neurodevelopmental disorders.