“The pain experience is a central aspect of labour [sic], and the psychobiology of labour [sic] pain has been involved in stimulating maternal hormonal, vascular and physiological systems which, in concert, also contribute to postnatal fetal adaptation” (Zanardo, 2001, March, p. 133). Labor naturally releases powerful chemical substances within the maternal and fetal bodies; beta-endorphins are among these influential elements. Too many at the wrong time could create excessive stress and have negative effects. Too few could have the same result. To offer an improved birth experience, better birth outcome, and maximally realized infant potential science must strive to understand these endogenous resources, their impacts, and their triggers, then seek to regulate their production in an effectual manner.
The Role of Beta-Endorphins
Beta-endorphins are natural opiate like substances produced by the body. The pituitary gland produces its precursor, proopiomelanocortin (POMC), as well as adrenocorticotrophic hormone (ACTH) as a response to stress or other stimulus that results in the release of ACTH (Dabo, Nyberg, Zhou, Sunderstorm-Poromaa, & Akerud, 2010). Beta-endorphins affect both the central nervous system (CNS) and peripheral nervous system (PNS) differently. In the CNS, beta-endorphins bind the mu-opioid receptors and thereby prevent the release of the inhibitory neurotransmitter gamma-aminobutyric acid (GAMA). The result is a surplus of dopamine, which creates a pleasure response. In the PNS, an anelgesic effect of reduced pain perception is established by binding mu-opioid recpetors and thus creating a series of interactions that prevent the release of certain protiens responsible for communicating pain (Sprouse-Blum, 2010). Beta-endorphins also hinder the relase of oxytocin, the hormone responsible for establishing contractions. Therefore, during pregnancy one role of these endoprhins may be to prevent premature labor; and during birth to stop labor in the event of stress in order to allow birth to resume under safer or more comfortable circumstances (Douglas, Bicknell, Leng, Russell, & Meddle, 2002). Furthermore, Ombra, Musumeci, Simpore, Palano, & Musumeci (2008) indicate that beta-endorphins also play a role in immune system devleopement.
The fetus/infant is a benefactor of the maternal release of beta-endorphins while in utero, but they also receive beta-enorphins from other sources as well. The placenta serves as a production site for beta-endorphins during pregnancy (Dabo et. al, 2010). Anand and Hickey (1987) established that a fetus also receives beta-endorphins from their own pituitary gland by 20 weeks gestation. Postnatally, the infant receives beta-endorphins through breast milk. Ombra et al. (2008) states that beta-endorphin secretion into breast milk is twice the concentration found in maternal plasma immediately after birth. Release of beta-endorhins during pregnancy and birth is improtant to the mother for pain management and increasing satisfaction with the birth experience. Beta-endorphins also assist in establishing the hypothalamic-ptiuitary-adrenal (HPA) axis which helps establish the fetal neuroendocrine system. Austin, leader, & Reilly (2005) suggest that adverse amounts of beta-enoprphins could increase the propensity to develop depression later in life. For the infant, beta-endorphins are even more important as they not only provide anegelisic benefits, but also aid in the development of the immune system.
Beta-Endorphins and Breast Milk
Colustrum of mothers experiencing a natural birth has been shown by Ombra et al. (2008) and Smith (2007) to be twice the concentration of the mother’s own blood. The only exception appears to be after a cesearean section without labor when Vogl et al. (2006) discovered that “no significant differences in endorphine . . . concentrations between mothers and children was found” (p. 443). Smith (2007) asserts that the beta-endorphin concentration in breast milk remains high for ten days after birth. Ombra et al. (2008) emphasizes that the initial beta-endorphin level does not continue to remain high for the duration of breastfeeding, however, it declines with time. Despite this fact, they argue that the amount of beta-endorphins received by the infant through breast milk each day may actually remain consistent since the quantitiy of milk ingested increases after this period. Mehta &. Petrova (2011) consider that beta-endorphins in breast milk “may be relevant for postnatal adaptation because of its functional activity as an opioid neurotransmitter and immunomodulator” (p. 61). According to Uga and colleagues (2008), beta-endorphins offer pain releif to infants when they are given breast milk either by breastfeeding or bottle/cup during newborn screening test. Zanardo et al. (2001, Feb) came to the conclusion that
Higher levels of B-EP in the colostrum of vaginally delivered lactating women could play a major role in mediating neonatal analgesia, which is probably fundamental in overcoming the painful situation of vaginal delivery and birth, and of importance in the postnatal development of several related biological functions of newborn infants, including the endocrine and the immune response. (p. 133)
Zanardo et. al (2001, Aug) also stated that
Neonates are capable of sustaining high levels during the first days of postnatal life and that milk B-EP supply could play a contributing role early after delivery and in the postnatal development of several related biologic functions of newborn infants, including the endocrine and the immune response, the sleep–wake patterns, imprinting, the learning process, feeding patterns, and behavior. (p. 163)
While release of beta-endorphins are a typical aspect of natural labor and birth, interventions during this period can influence the amount of beta-endorphins available to both the mother and baby (Smith, 2007).
Birth Interventions Impact Beta-Endorphins
Sprouse-Blum (2010) states that production of beneficial endogenous opiates like beta-endorphins is inhibited by providing externally produced opioids to the mother. Smith (2007) makes the similar point that labor anelgesia decreases maternal beta-endorphin levels by decreasing maternal pain. Zanardo et al. (2001, March) discovered that epidural anthesia resulted in a “significant decrease of maternal plasmabeta-endorphin levels” (p.133).
Vogl and colleagues (2006) discovered that infants cord blood concetration of beta-endorphins is also impacted by labor practices. They found that infants born via cesarean section had substainatially lower blood concentrations of beta-endorphins than their vaginally born counterparts. The research on the impact of epidural anethsia on the infant’s beta-endorphin levels is contradicatory, however. Vogl et al. (2006) found beta-endorphin levels to be higher in infants born with epidural anesthesia than those born via cesearean section, natural birth, or even instrumental extraction. On the other hand, Zanardo et al. (2001, March) found that epidural anesthesia had no impact on infant blood levels of beta-endorphins. There are many factors that could attribute to the confounding of these results. Greater care should be taken to identify natural birth mothers who were prepared for birth and able to relax or had support from a trusted person and those who faced their labors with great fear and high pain perceptions. Also, failing to define the point at which mothers received an epidural and the pain level they reported experiencing by the time they received anethesia could impact the results and misconstrue the difference between vaginal birth with and without medication. More research is likely needed to be certain of the impact of maternal pain medications on infant beta-endorphin concetrations.
Smith (2007) also made the point that maternal milk concentrations of beta-endorphins were decreased as a a result of some labor pain medications and ceserean sections perfomed with an absence of labor. Vogl and colleagues (2006) indicate that cesearean section without labor results in substantianly lower maternal blood serum levels of beta-endoprhins than natural, medicated, or instrumentally assisted births. Zanardo et al. (2001, August) also showed that cesarean sections resulted in lower concetration of beta-endorphins in colostrum. In fact, their data indicated that these levels remained substainally higher for mothers experiencing vaginal birth rather than cesarean section until day 10. This fact has lead Smith (2007) to take the stance that “even if the newborn remains with the mother and can suck, the milk of women who have elective cesarean sections is less “pain relieving” than the milk of women who give birth vaginally” (p. 627). Maternal milk may be impacted by immediate postpartum procedures to speed third stage as well. In a study by Ombra et al. (2008) it was revealed that the group of women receiving an “ergot derivative injection” the amount of colostrum produced was smaller and the beta-endorphin concentration was lower (p. 33). It is worth noting that the group of women receiving the injection also experienced childbirth education, birth with a midwife they were familiar with, and higher socio-economic status, which could confound the results. The researchers do note that the quantity of colostrum produced “could be smaller because . . . an ergot derivative is a dopamine receptor agonist that inhibits prolactin secretion, milk production, and the initiation of breast-feeding by 2–3 days” (p. 35).
Though not directly linked to lack of beta-endorphins released in childbirth, cesarean sections without labor are shown to negatively impact the later immune health of the child (Cho & Norman, 2012). Cho and Norman (2012) performed a meta-analysis that demonstrated cesarean sections negatively affect infant immune health by increasing the risk for asthma by 20%, of type 1 diabetes by 23%, of celiac disease, of aseptic necrosis of the head, as well as a greater incidence of allergic rhinitis and hospitalization for gastroenteritis. While other factors, including the greater potential for short term or absence of breastfeeding due to the surgery, may have partial blame for these results, the authors note that these differences between vaginal and cesarean births seem to be driven by immune insufficiencies. Cho and Norman (2012) state, “it is well established that elevated circulating cortisol at birth is an indicator of hypothalamic-pituitary-adrenal axis activation” (p.4). Remembering that beta-endorphins impact the HPA axis may imply a correlation between their lack of increase during cesarean birth and the immune deficiencies listed above.
A reverse implication of beta-endorphin presence during pregnancy can be applied to the use of labor medications. Dabo et al. (2010) researched the impact of beta-endorphins on labor medication use and found a potential correlation. They discovered that women who had higher levels of beta-endorphins before the onset of labor reported less pain during labor. Dabo et al. (2010) noted:
That women within the lowest quartile of b-endorphin levels at gestational week 37 required additional pain medication beyond nitrous oxide to a significantly higher extent, and this finding remained after adjustment for possible confounders such as parity, BMI, duration of labor, cervical opening upon arrival at the delivery unit, and use of oxytocin during labor. (p. 744)
These results seem to indicate that low prenatal beta-endorphins increase the need for analgesia by increasing the amount of labor pain perceived by the mothers and thus their level of stress, which would then increase their beta-endorphin levels drastically during labor, potentially accounting for the increased beta-endorphin concentrations of blood plasma in women experiencing epidural anesthesia or instrumental delivery. Zanardo et al. (2001, Feb) claims that, “substantial maternal emotional distress is associated with abnormal labour [sic], dystocia and higher rates of fetal and maternal morbidity” (p.132). Vogl et al. (2006) indicates that excessive labor stress can delay lactation. Thus, the lack of prenatal beta-endorphin increases may contribute to labor interventions and lack abundant colostrum as well. This information draws the conclusion that maternal beta-endorphin concentration is important before and during labor so that pain might be lessened and interventions avoided, but also so that beta-endorphin levels will be sufficient after labor in colostrum.
Dabo et al. (2010) discovered that exercising during the final two trimesters experienced higher beta-endorphin levels prenatally by the end of the 37th week. This natural prenatal increase would aide in the labor experiencing helping mothers to stay calm and relaxed and reduce the amount of stress experienced in the birth process itself. Ombra et al. (2008) showed a possible correlation to childbirth education during pregnancy and having a familiar midwife to decreasing stress and beta-endorphins during labor. Tiran and Chummun (2004) researched the effects of various therapies on beta-endorphins during pregnancy and birth. They offer an explanation for the value of some stress, to which beta-endorphins are a natural response, while explaining the hazards of excessive stress. They explain the stages of the General Adaptation Syndrome as follows:
The alarm response occurs within seconds of experiencing a stressor, in which headaches, fatigue, nausea, tachycardia and muscle tension are often experienced. The resistance stage causes an increase in production of endocrine hormones such as cortisol and thyroxin, which maintain the adjustment to the continued presence of the stress. The exhaustion or ‘‘burnout’’ stage occurs when these resources are exhausted, eventually weakening several body systems, increasing morbidity and mortality. (p. 163)
They explain that massage and relaxation, including yoga and Qi Gong, reduce stress during pregnancy. During labor, acupuncture and acupressure may increase beta-endorphin release through touch rather than stress and thus decrease pain. Aromatherapy, massage, relaxation and hypnotherapy may be helpful in labor to reduce stress. Reflexology performed regularly during pregnancy also reduces the amount of pain reported by mothers, but the reasons for this are unclear.
The fact that beta-endorphins are powerful components in the process of birth, breastfeeding, and fetal/infant development is clear. They are released due to a variety of reasons and from a variety of sources during pregnancy and especially birth. Understanding the triggers of these endorphins and how to aide in controlling their release can provide better outcomes for mothers and babies. Offering childbirth education, encouraging prenatal exercise, and providing constant labor support that includes hands on relaxation techniques can potentially control beta-endorphins in a manner that yields better birth experiences and development for both mother and baby.
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