Science tells us that when babies cry alone and unattended, they experience panic and anxiety. Their bodies and brains are flooded with adrenaline and cortisol stress hormones. Science has also found that when developing brain tissue is exposed to these hormones for prolonged periods these nerves won’t form connections to other nerves and will degenerate. Is it therefore possible that infants who endure many nights or weeks of crying-it-out alone are actually suffering harmful neurological effects that may have permanent implications on the development of sections of their brain? Here is how science answers this alarming question:
Chemical and hormonal imbalances in the brain
Research has shown that infants who are routinely separated from parents in a stressful way have abnormally high levels of the stress hormone cortisol, as well as lower growth hormone levels. These imbalances inhibit the development of nerve tissue in the brain, suppress growth, and depress the immune system. 5, 9, 11, 16
Researchers at Yale University and Harvard Medical School found that intense stress early in life can alter the brain’s neurotransmitter systems and cause structural and functional changes in regions of the brain similar to those seen in adults with depression. 17
One study showed infants who experienced persistent crying episodes were 10 times more likely to have ADHD as a child, along with poor school performance and antisocial behavior. The researchers concluded these findings may be due to the lack of responsive attitude of the parents toward their babies. 14.
Dr. Bruce Perry’s research at Baylor University may explain this finding. He found when chronic stress over-stimulates an infant’s brain stem (the part of the brain that controls adrenaline release), and the portions of the brain that thrive on physical and emotional input are neglected (such as when a baby is repeatedly left to cry alone), the child will grow up with an over-active adrenaline system. Such a child will display increased aggression, impulsivity, and violence later in life because the brain stem floods the body with adrenaline and other stress hormones at inappropriate and frequent times. 6
Dr. Allan Schore of the UCLA School of Medicine has demonstrated that the stress hormone cortisol (which floods the brain during intense crying and other stressful events) actually destroys nerve connections in critical portions of an infant’s developing brain. In addition, when the portions of the brain responsible for attachment and emotional control are not stimulated during infancy (as may occur when a baby is repeatedly neglected) these sections of the brain will not develop. The result – a violent, impulsive, emotionally unattached child. He concludes that the sensitivity and responsiveness of a parent stimulates and shapes the nerve connections in key sections of the brain responsible for attachment and emotional well-being. 7, 8
Decreased intellectual, emotional, and social development
Infant developmental specialist Dr. Michael Lewis presented research findings at an American Academy of Pediatrics meeting, concluding that “the single most important influence of a child’s intellectual development is the responsiveness of the mother to the cues of her baby.”
Researchers have found babies whose cries are usually ignored will not develop healthy intellectual and social skills. 19
Dr. Rao and colleagues at the National Institutes of Health showed that infants with prolonged crying (but not due to colic) in the first 3 months of life had an average IQ 9 points lower at 5 years of age. They also showed poor fine motor development. (2)
Researchers at Pennsylvania State and Arizona State Universities found that infants with excessive crying during the early months showed more difficulty controlling their emotions and became even fussier when parents tried to consol them at 10 months. 15
Other research has shown that these babies have a more annoying quality to their cry, are more clingy during the day, and take longer to become independent as children 1.
Harmful physiologic changes
Animal and human research has shown when separated from parents, infants and children show unstable temperatures, heart arrhythmias, and decreased REM sleep (the stage of sleep that promotes brain development). 10 12, 13
Dr. Brazy at Duke University and Ludington-Hoe and colleagues at Case Western University showed in 2 separate studies how prolonged crying in infants causes increased blood pressure in the brain, elevates stress hormones, obstructs blood from draining out of the brain, and decreases oxygenation to the brain. They concluded that caregivers should answer cries swiftly, consistently, and comprehensively. (3) and (4)
- P. Heron, “Non-Reactive Cosleeping and Child Behavior: Getting a Good Night’s Sleep All Night, Every Night,” Master’s thesis, Department of Psychology, University of Bristol, 1994.
- M R Rao, et al; Long Term Cognitive Development in Children with Prolonged Crying, National Institutes of Health, Archives of Disease in Childhood 2004; 89:989-992.
- J pediatrics 1988 Brazy, J E. Mar 112 (3): 457-61. Duke University
- Ludington-Hoe SM, Case Western U, Neonatal Network 2002 Mar; 21(2): 29-36
- Butler, S R, et al. Maternal Behavior as a Regulator of Polyamine Biosynthesis in Brain and Heart of Developing Rat Pups. Science 1978, 199:445-447.
- Perry, B. (1997), “Incubated in Terror: Neurodevelopmental Factors in the Cycle of Violence,” Children in a Violent Society, Guilford Press, New York.
- Schore, A.N. (1996), “The Experience-Dependent Maturation of a Regulatory System in the Orbital Prefrontal Cortex and the Origen of Developmental Psychopathology,” Development and Psychopathology 8: 59 – 87.
- Karr-Morse, R, Wiley, M. Interview With Dr. Allan Schore, Ghosts From the Nursery, 1997, pg 200.
- Kuhn, C M, et al. Selective Depression of Serum Growth Hormone During Maternal Deprivation in Rat Pups. Science 1978, 201:1035-1036.
- Hollenbeck, A R, et al. Children with Serious Illness: Behavioral Correlates of Separation and Solution. Child Psychiatry and Human Development 1980, 11:3-11.
- Coe, C L, et al. Endocrine and Immune Responses to Separation and Maternal Loss in Non-Human Primates. The Psychology of Attachment and Separation, ed. M Reite and T Fields, 1985. Pg. 163-199. New York: Academic Press.
- Rosenblum and Moltz, The Mother-Infant Interaction as a Regulator of Infant Physiology and Behavior. In Symbiosis in Parent-Offspring Interactions, New York: Plenum, 1983.
- Hofer, M and H. Shair, Control of Sleep-Wake States in the Infant Rat by Features of the Mother-Infant Relationship. Developmental Psychobiology, 1982, 15:229-243.
- Wolke, D, et al, Persistent Infant Crying and Hyperactivity Problems in Middle Childhood, Pediatrics, 2002; 109:1054-1060.
- Stifter and Spinrad, The Effect of Excessive Crying on the Development of Emotion Regulation, Infancy, 2002; 3(2), 133-152.
- Ahnert L, et al, Transition to Child Care: Associations with Infant-mother Attachment, Infant Negative Emotion, and Cortisol Elevations, Child Development, 2004, May-June; 75(3):649-650.
- Kaufman J, Charney D. Effects of Early Stress on Brain Structure and Function: Implications for Understanding the Relationship Between Child Maltreatment and Depression, Developmental Psychopathology, 2001 Summer; 13(3):451-471.
- Teicher MH et al, The Neurobiological Consequences of Early Stress and Childhood Maltreatment, Neuroscience Biobehavior Review 2003, Jan-Mar; 27(1-2):33-44.
- Leiberman, A. F., & Zeanah, H., Disorders of Attachment in Infancy, Infant Psychiatry 1995, 4:571-587.
Absolutely powerful. An everyday miracle.
My Birth stories – HBA2C (homebirth after two cesareans)
Natural Childbirth of Twins and Triplets!
For all my clients and Doulas. Enjoy! Happy Chanukah.
GBS- The truth
Top 10 things about GBS of the newborn for which there is a lack of research:
1. How many full term babies are permanently injured (not killed) from GBS disease of the newborn? How many experience each of the various types (deafness, learning disabilities, CP) of morbidity?
2. Do prophylactic antibiotics to GBS positive women prevent or decrease long term GBS morbidity in full term newborns (vs. mortality)?
3. The presence of GBS antibodies in the mother has been shown to be protective against Newborn GBS(10). Women with high titers of antibodies to GBS are thought to pass on immunity to GBS to their fetus and thereby have less GBS infected babies. Smokers, drug abusers, obese and immune suppressed women produce less antibodies. Are they more likely to have a baby with GBS disease? Is some/most/all GBS disease of the newborn associated with women with low titers of antibodies to GBS?
4. There is only one published study asking whether pregnant women who culture GBS positive in urine, also culture positive in rectovaginal culture. Of 1036 assymptomatic women who underwent routine urine culture in pregnancy, 10.7% had GBS in their urine, of those 70% of those had <10,000 CFU (colony forming units) and 30% had >10,000 CFU which is considered highly colonized. Of the 111 women who had GBS in their urine (bacteriuria), 40% cultured negative for GBS on rectovaginal swabs. Women who were heavily colonized in urine were no more likely than those lightly colonized in urine to have positive rectovaginal cultures. (16)
Approximately 11% of women colonized positive for GBS in urine and their healthy babies culture positive for GBS than other babies, however no one has ever documented higher rates of GBS DISEASE associated with maternal GBS bacteriuria. GBS in urine has been associated with chorioamnionitis- uterine infections in the mother- which is most closely associated with prolonged labors, as well as frequent vaginal exams, internal monitoring, prolonged ROM, cesareans, and teenage pregnancies, but to date not documented to be associated with GBS disease of the newborn.
There are many claims that antibiotics during pregnancy given to women wiht GBS bacteriuria can prevent preterm birth, but this data is confounded by studying high risk populations. A RCT study contradicts this claim, found that women with GBS bacteriuria, additional exposure to antibiotics is associated with an increased, not decreased, risk of preterm birth. In this study the rate of preterm birth for women with bacteriuria was 16% and without GBS bacteriuria was also 16% and 28% among women with GBS bacteriuria who received antibiotics. (17) All three rates reflect outcomes only seen in extremely high risk populations. Healthy, well fed populations, the preterm rate is 7%. Asymptomatic GBS bacteriuria may not have a role in preterm birth but rather may be a marker for low socioeconomic status which is associated with low birth weight. (18) The quality of even the best studies on asymptomatic bacteriuria in pregnancy is poor. (18)
The unanswered question is: Do heavily colonized full term women have more GBS newborn disease or perhaps less newborn GBS due to higher titers of antibodies against GBS that they pass to the fetus? Are women who heavily colonized with GBS, whether in urine or vagina, more likely or less likely to have babies with GBS disease? We dont know.
Does giving oral antibiotics to pregnant women with asymptomatic GBS bacteriuria decrease or increase the occurrence of GBS disease of newborn?
5. 50% of GBS disease of the newborn occurs to babies of women with the following risk factors: Premature, IUGR, LBW, ROM > 18 hours, and fever. The other 50% occurs to babies of women without those risk factors. Of those women, how many had ROM between 2 and 17.9 hours? Since prolonged ROM is known to increase the risk of GBS disease, how would eliminating AROM affect the occurrence of GBS disease of newborn?
Is there a difference in the GBS disease among women with impressive, flowing ROM which fills up pads quickly and women who have a high leak that is leaks 1 to 2 cc per hour? Is a high leak a risk of newborn GBS at all?
6. On page 11 of the 2002 CDC protocols appears one of several unqualified statement “GBS can cross intact amniotic membranes.” A study of 550 babies born to GBS positive women, by CS without ROM, and without prophylaxis, demonstrated not a single case of GBS disease, where one would expected 5 sick newborn if GBS crossed membranes, supporting the theory that GBS either never crosses membranes. In vitro study has not been able to demonstrate GBS crossing membranes, even at concentrations of 1,000,000,000 CFU. (20) Further investigation into how GBS could cross intact membranes demonstrated that GBS failed to invade amnion cells under a variety of assay conditions (21) and fetal membranes demonstrated an inhibitory effect on GBS. (22). Cases of colonized infants born by CS in the absence of ruptured membranes could be due to any number of other vectors other than the mother that come in contact with the baby.
7. Over 6 vaginal exams significantly increased rates of GBS disease(15). Scalp electrodes double the risk of GBS colonization of amniotic fluid (19)
In my practice, with restricted AROM and Vaginal exams and no scalp electrodes, 3% of births the baby’s head comes out in the sac and never makes direct contact with the uterus, cervix or vaginal walls at all. How would restricted AROM, Vaginal exams and scalp electrodes affect GBS disease rates?.among low risk women? Among high risk women?
8. When does GBS cause disease? 99% of babies colonized with GBS, dont get GBS disease. 99.99% of women colonized with GBS, dont get GBS vaginitis. Why does GBS sometimes attack and sometimes live in ecological balance? Why is GBS present in 2-3 times as many women in the USA than in Ireland, Cambodia, Taiwan, Philippines or Africa? (11) Why is long term (over 6 months duration) Symptomatic GBS Vulvovaginitis becoming more common in the western world? (12)
9. How does GBS inhibit lactobacillus growth?
10. How many newborns will die of GBS disease in 10 years? 20 years? 40 years?
In the presence of so many unknowns, current protocols reflect an bias to take action in the presence of a lack of appreciation or humility for the complex habits of GBS and no consideration of the next generation of newborns.
1. Ohlsson A, Shah VS. Intrapartum antibiotics for known maternal Group B streptococcal colonization. Cochrane Database of Systematic Reviews 2009, Issue 3. Art. No.: CD007467
2. Yancey MK, Schuchat A, Brown LK, Ventura VL, Markenson GR.The accuracy of late antenatal screening cultures in predicting genital group B streptococcal colonization at delivery. Obstet Gynecol 1996;88:811–5.
3. Itakura A.Kurauchi O Morikawaa S, Matsuzawab K Mizutania S, Tomodaa Y. Variability of peripartum vaginal group B streptococcal colonization. International Journal of Gynecology & Obstetrics 55 (1996) 19-22.S
4. Tamerou Asrat, et.al.The accuracy of late third trimester antenatal screening for group B streptococcus in predicting GBS colonization at delivery American Journal of Obstetrics and Gynecology, Volume 195, Issue 6, Supplement 1, December 2006, Page S40
5. Chu YW, Tse C, Tsang GK, So DK, Fung JT, Lo JY. . Invasive group B Streptococcus isolates showing reduced susceptibility to penicillin in Hong Kong. Antimicrob Chemother. 2007 Dec;60(6):1407-9.
6. Joachim A, Matee MI, Massawe FA, Lyamuya EF. Maternal and neonatal colonisation of group B streptococcus at Muhimbili National Hospital in Dar es Salaam, Tanzania: prevalence, risk factors and antimicrobial resistance. BMC Public Health.;2009: 9:437.
7. Klevens RM, Morrison MA, Nadle J, et al.Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA. 2007 Oct 17;298(15):1763-71.
8. Appelbaum, P. C. 1992. Antimicrobial resistance in Streptococcus pneumoniae: an overview. Clin. Infect. Dis. 15:77-83.
9. Jacobs, M. R., S. Bajaksouzian, A. Zilles, G. Lin, et al. 1999. Susceptibilities of Streptococcus pneumoniae and Haemophilus influenzae to 10 oral antimicrobial agents based on pharmacodynamic parameters: 1997 U.S. Surveillance study. Antimicrob. Agents Chemother. 43:1901-1908.
10. Walsh CT Fischbach MA New ways to squash superbugs. Scientific American, 2009. 301:32.
11. Whitney CG. et.al.The International Infections in Pregnancy Study: group B streptococcal colonization in pregnant women. The Journal of Maternal–Fetal and Neonatal Medicine 2004;15:267–274.
12. Cohain, JS. Long term Symptomatic GBS Vulvovaginitis – 8 cases resolved with freshly cut garlic. European Journal of OBGYN Reprod Biology. 2009;146(1):110-1.
14. McKeever TM, Lewis SA, Smith C, Hubbard R. . The importance of prenatal exposures on the development of allergic disease: a birth cohort study using the West Midlands General Practice Database. Am J Respir Crit Care Med. 2002 Sep 15;166(6):827-32.
15. P T Heath,1 G F Balfour,1 H Tighe,1 N Q Verlander,2 T L Lamagni,3 A Efstratiou Group B streptococcal disease in infants: a case control study. Arch Dis Child 2009 94: 674-680.
16. Centelles-Serrano MJ, Pérez-Moreno MO, Llovet-Lombarte MI, Cortell-Ortolá M, Jardí-Baiges AM, Buj-González JI.Effectiveness of systematic investigation for Group B Streptococcus in urine samples to identify colonized pregnant women. Enferm Infecc Microbiol Clin. 2009 Aug-Sep;27(7):394-8.
19. Keski-Nisula L, Kirkinen P, Katila ML, Ollikainen M, Saarikoski S. Cesarean delivery. Microbial colonization in amniotic fluid.J Reprod Med. 1997;42(2):91-8.
20. Kjaergaard N, Helmig RB, Schønheyder HC, Uldbjerg N, Hansen ES, Madsen H. Chorioamniotic membranes constitute a competent barrier to group b streptococcus in vitro. Eur J Obstet Gynecol Reprod Biol. 1999 Apr;83(2):165-9.
23. Centers for Disease Control and Prevention (CDC). Trends in perinatal group B streptococcal disease – United States, 2000-2006. MMWR Morb Mortal Wkly Rep. 2009 Feb 13;58(5):109-12.
COPYRIGHT MIDWIFERY TODAY 2010