Nurturing Starts Before Birth
The lifeway of a child is first shaped in the womb.
Lots of people seem to think that an offspring is a bunch of genes that just have to grow up, that a baby is born with a personality and you just have to put up with the inconvenience of their immaturity till they get big and out of your hair. This is the factory model of understanding babies: everything is determined behind the doors of genetic formation. Parents just have to feed and keep safe the product. Even some researchers have regarded prenatal development only as a matter of rapid physical growth with its age-related related reflexes (Hopkins & Johnson, 2005).
As our ancestors intuited and science confirms, this is a hugely mistaken orientation.
From a speck to a many-pound being, a zygote, then embryo then fetus spends about ten months in a protected chamber inside mother. A moving penthouse, it may seem like a residence isolated from the stresses of life. However, this is not the case. The brain is being shaped in the womb by mother’s experiences.
“When love begins in the womb, the mother is speaking to her baby in “womb-speak,” a language that has no words. Nevertheless, it is a very strong language, perhaps the most critical that will occur in our lives. Every “word” a mother speaks has great impact. In her physiology she is saying to the child, “I am calm. I am normal. And I love you.”” (Janov, 2011, p. 3, emphasis added).
When parents themselves have grown up loved, they will exhibit a calmness that will be communicated to baby. Mother communicates to the womb-baby through her biochemistry, so much so that many aspects of the brain are shaped before birth.
The brain is malleable. It is shaped by experience. During gestation, birth and the early years, the brain is co-constructed by life experience.
The Importance of Womb Experience
One of the most important periods for shaping the functioning of the brain is during gestation. The zygote (until 7 days)-embryo (until 12 weeks)-fetus (thereafter) is learning what life will be like. Nerve cells are rapidly growing throughout this period, so anything the mother does to compromise growth can have lifetime consequences for the child.
In early life, various systems are development rapidly and interactively. Imprints of early experience are distributed in every fiber and cell of our being, from chemical transport mechanisms to hormonal balance in each system to number and function of neurotransmitters (Janov, 2011). Although set-points for various systems are presumed established after birth (e.g., stress response; Lupien et al, 2009), there appear to be various set points established during gestation. With a poor womb environment (maternal stress, smoking, drug use), the functioning of interneurons, controller cells that promote intercellular connections, are impaired (Fishell & Kepecs, 2020).
After the second month of gestation, the fetal brainstem is functioning and the fetus is starting to imprint the mother’s biochemical signals, including stress, anxiety, depression and drug use. Until the fourth month of gestation, trauma is registered at this fundamental level of the brain. After this such imprints may shuttle impressions to higher order systems of the brain. When there are frequent stressful impressions, they impair higher order cortical development. This means they can produce phobias and compulsions if the prefrontal systems are impaired.
Some babies are born more irritable than other babies. Why? Some people just assume it is genetic. But more and more studies are showing that maternal stress during pregnancy correlates with their baby’s irritability.
“Exposure to stress during critical periods in development can have severe long-term consequences, increasing overall risk on psychopathology” (van Bodegom et al., 2017, p. 87).
Stress hormones are transferred to the fetus. Experiments with animals shows that different organs can be affected depending on which one is in rapid development at the time of stress (Gluckman & Hanson, 2005). Stress late in pregnancy can influence physical development. But too much stress anytime during pregnancy is associated with brain changes and, at the very least, a more irritable infant (Davis et al., 2007).
Claudia Buss and colleagues (2012) review the effects of prenatal maternal experiences on the fetus and later child outcomes. Most people are aware that poor maternal nutrition (e.g., Hanswijk et al., 2020) or illicit drug use can affect a fetus’ wellbeing (e.g., Ross et al., 2014). Similarly, most know that exposure to neurotoxins like lead, pesticides and alcohol during sensitive periods of fetal development is associated with long-term deficits in brain structure and function. Exposure to psychosocial stressors also matter, but they have more nuanced effects on developing brains.
Psychosocial stress has various effects on the developing brain, including adverse birth outcomes (Davis et al., 2011), delayed mental and motor development, difficult temperament, and impaired cognitive performance (Davis et al., 2005, 2007; Davis & Sandman, 2010).
Buss et al. (2012) note:
“Elevated psychosocial stress in pregnant women is associated with higher circulating levels of C-reactive protein (CRP), a systemic marker of inflammation, and the proinflammatory cytokines IL-1b, IL-6 and TNFα, and with lower circulating levels of the anti-inflammatory cytokine IL-10.27….Imbalances in pro- and anti-inflammatory cytokines, along with elevated cortisol, can distort fetal brain and body development that results in life-long problems. This occurs in children who are abused and neglected early in life, as documented in the Adverse Childhood Experiences Study. Gestational stress may have similar long-term effects.”
These endocrine and immune markers signal not only maternal stress but also a range of adverse intrauterine conditions such as nutrient and oxygen availability, preeclampsia, and infection, each of which can influence brain development and alter neural outcomes (Entringer et al., 2011; Fowden & Forehead, 2009). Maternal stress reduces permanently the number of corticosterone receptors in the fetal brain (Henry et al., 1994) among other permanent neurological deficits (Fride & Weinstock, 1989; Weinstock, 2001). Exposure to excessive or deficient levels of hormones at inappropriate times of gestation can increase vulnerability to neurodevelopmental disorders and psychopathology (Swanson & Wadhwa, 2008). Timing, intensity, duration and frequency matter for stress effects, as well as social supports for mother.
Chronic stress impairs the neurobiological systems designed to restore balance and homeostasis, instead increasing inflammation and instigating chronic agitation (Hannibal & Bishop, 2014). Too much cortisol in mother will translate as ‘dangerous world ahead.’ The offspring may build up alerting hormones, imprinting his system to be threat reactive after birth, making him irritable and hard to settle. Stress in gestation is associated with all sorts of unhealthy outcomes (e.g., hypertension, insulin deviation) (Gluckman & Hanson, 2005). Most significantly, gestational stress of any kind slows growth, leading to babies small for gestational age and low birthweight, which are associated with a predisposition to later disease (Glover & O’Connor, 2005). Female offspring show impaired maternal behavior (Insel, 1990; Ward, 1972).
The ill effects of maternal stress on the fetus occur through the transfer across the placenta of stress hormones and impaired uterine blood flow from restricted arteries, both upregulating stress hormones in the fetus (Glover & O’Conner, 2005). The body behaves as though constantly under stress, a free-floating anxiety. Prenatal stress is associated with hyperactivity and elevated emotional and behavioral problems when the children are four years old (Glover & O’Connor, 2005).
Anything the mother experiences, the baby experiences even more so. Here are several specific maternal experiences that have been studied.
Maternal Smoking. Smoking transmits nicotine and thousands of other chemicals to the fetus. It also decreases oxygen, affecting biochemistry such as calcium transport across the placenta and physiological development generally—smaller size of the neonate which, again, is associated with a predisposition for disease (Glover & O’Connor, 2005). Smoking has cross-generational effects. Rat females born with limited oxygen were less affectionate with their offspring—less likely to lick or retrieve them (Bonsignore et al., 2003).
Anxiety. Maternal anxiety is associated with a number of poor outcomes such as cognitive, behavioural, and emotional problems in the child (Van den Bergh et al., 2005). When mother is anxious, the fetus gets less oxygen due to a constricted vascular system. When mothers experienced high levels of anxiety in the early second trimester of pregnancy, their children had specific reductions in gray matter volume and impaired executive functioning in middle childhood (Buss et al, 2010; Buss et al., 2011). In a longitudinal study with 7944 participants and multiple controls, maternal prenatal anxiety was predictive of persistently higher behavioral and emotional problems across childhood and into adolescence (O’Donnell et al., 2014).
Maternal anxiety is associated with high hypothalamic-pituitary-adrenal axis (HPA) activation in mother and child whereas post-traumatic-stress-disorder (PTSD) is associated with hyporeactive HPA (Gold & Chrousos, 2002). Neither are healthy as chronic states.
When the expectant mother is calm, eating and ingesting materials responsibly, conveying affection to the fetus, the fetus will grow in a healthy manner. Maternal calm in pregnancy produces a growth-supporting biochemistry.
Maternal Depression. The placenta is a primary source for serotonin in the womb. But if mother is depressed, she has low serotonin levels and doesn’t have much to transmit to the fetus. Serotonin plays a key role in the development of the central nervous system, as neuromodulator influencing neuronal circuitry (Daubert & Condron, 2010). When it is dysregulated in mother, it affects fetal serotonin receptors and function, giving rise to neurodevelopmental and neuropsychiatric disorders. This may be why maternal mood disorder during pregnancy is associated with children’s sleep disturbance in the second and third of life (O’Connor et al., 2007).
When expectant mothers are depressed, fetal growth is delayed though fetal activity is elevated (Field, 2011). Newborns mimic mother’s state: high stress hormones, low dopamine and serotonin, above-normal right frontal brain activity. When children are exposed to both maternal depressed mood and SSRI antidepressants prenatally, they are more sad or withdrawn at age 3 (Oberlander et al., 2010). Babies born with SSRI antidepressants in their systems have lower birth weights and were more likely to experience respiratory distress (Oberlander et al., 2006).
What can be done with a depressed expectant mother? Anti-depressants influence fetal development but so does continued depression. “There is really no great solution, except this: normalizing the system before pregnancy” (Janov, 2011, p. 77)
Painkillers. During pregnancy, the over-the-counter drug acetaminophen/paracetamol can affect child outcomes (Bauer et al., 2021). Its use is associated with genital malformation, childhood attention and behavior problems, lower IQ and language development, and earlier puberty.
Painkillers at birth affects the newborn’s gating system, the brain’s mechanism for dealing with pain (Hollenbeck et al., 1984). The gating system in the brain inhibits feeling when it is too much to bear. However early in gestation, gating chemicals (e.g., serotonin, endorphin) cannot yet be made so the fetus relies on mother’s chemicals, if they are there. If they are not present at the right time, gating systems are not properly established. “Disruption at or before birth often upsets the brain’s organization and is then compounded by more childhood pain until the gaiting system becomes ineffective. So much pain is coming up from the limbic system, in other words, that the mind loses cohesion, it becomes fractured and unable to control the force of lower-level feelings” (Janov, 2011, 252-253). Decrease in cortical activity weakens the prefrontal area. Impaired gating between the amygdala and frontal cortex means that fear and terror get pushed up into impulses, panic and need for immediate resolution that the prefrontal cortex (PFC) cannot control. When feelings well up, they are not integrated into the PFC but travel to other parts of the brain and display as a lack of self-control. The PFC’s organization and connectivity otherwise helps manage anxiety and pain, but cannot when its cells have been assaulted or decreased in the womb.
Drug use in adulthood is associated with drugs used during the individual’s birth. When adult drug users were compared with siblings, three or more doses of drugs given to their mother during childbirth corresponded to five times greater change of drug abuse as an adult (Nyberg et al., 2000).
Remedies
The question is whether once foundational elements are shaped during sensitive periods, are those elements malleable? Since there are millions of interacting elements in layers of development over months, a misdeveloped foundational piece necessarily influences later developments reliant on that piece (Knudsen, 2004). The brain is able to compensate for a while, but then the house of cards may fall apart under developmental surges or stressors.
What kind of remedies are there for children and adults who experienced significant gestational stress? Here are two: the evolved nest and psychotherapy.
The Evolved Nest
Post-birth evolved nest care can compensate for a stressed womb experience. Some of the harms from gestational stressors, such as child fearfulness, can be softened with close nurturance in the first months and years of life (e.g., Bergman et al., 2008). The evolved nest is designed to optimize normal development, providing the buffer for adversity (Tarsha & Narvaez, 2022). Constant loving presence and all the aspects of the nest can rebalance the child’s biopsychology and provide assurance it is safe to grow instead of live in a growth-inhibiting panic and withdrawal.
Here is one example from the nest. Nearly constant positive touch in babyhood is needed for growth and promotes healing.
“Without sufficient touching, however inhibitory neurohormones fire in overdrive, attempting to shut off the pain caused by deprivation. If a lack of love has been imprinted, as we will see later, inhibitory or repressor neurotransmitters may be called upon to do that for a lifetime” (Janov, 2011, p. 6).
A lack of touch leads to various problems, from underdevelopment of the vagus nerve to various set points:
“Eventually, serotonin supplies become depleted. And, in the worst cases, the brain will be compromised: there will be fewer neocortical, top-level neurons to deal with arousal, fewer brain cells to suppress feelings or hold back impulses. The result may be chronic anxiety throughout life—a tendency which beings its life during gestation and infancy.
So what do parents do that is so damaging? Obviously, a tense mother who handles her child roughly is not imparting a feeling of calm in him. Similarly, a mother who desperately needs love may use her baby to fulfill her needs, demanding too much from him so that he cannot be himself.” (Janov, 2011, pp. 6-7).
Therapy. Once sensitive periods pass, it is next to impossible to alter basic neurobiological systems. In adults, a constant state of agitation, indicated by a need to keep busy, is almost always a sign of brainstem reactivity from early stress. Busy, inattentive parents cannot help themselves—they need to discharge excess energy/stress hormones, or else they suffer.
Janov (2011) claims that primal therapy allows us to revamp ourselves, through reliving the moments of biopsychosocial imprint to establish new set points. In primal therapy, one “remembers” with one’s whole physiology and psychological being, not just with the thinking mind. He claims that the full integration of the three brain levels (survival systems, limbic system and cortical) will end free-floating anxiety that manifest in irritable bowels, phobias, and attention problems as well as defensiveness and avoidance of pain. Full consciousness is then possible.
Conclusion
Overall, research is demonstrating that life in the womb programs the neurobiological systems of the fetus, potentially affecting capacities for life. The fetal environment changes when mother experiences extreme stress (e.g., war, death of loved one) or chronic stress (e.g., domestic abuse, drug use). The mother’s stress hormones flood the child, potentially derailing ongoing development, affecting developing physiological systems in unhealthy ways. Unhealed, chronic inflammation from early trauma will eat away at health. Maternal stress during gestation has such extensive effects on the fetus and subsequent development and behavior of the child that Lou and colleagues (1994) suggest the existence of a Fetal Stress Syndrome, a type of fetal programming analogous to Fetal Alcohol Syndrome.
Find out more information about prenatal experience:
For Families and Communities: http://www.prenatalalliance.org/mission.html
Learn more about the science: https://www.prenatalsciencespartnership.org/
References
Bauer, A.Z., Swan, S.H., Kriebel, D., Liew, Z., Taylor, H.S., Bornehag, C.G., Andrade, A.M., Olsen, J., Jensen, R.H., Mitchell, R.T., Skakkebaek, N.E., Jégou, B., & Kristensen, D.M. (2021). Paracetamol use during pregnancy – a call for precautionary action. Nature Reviews Endocrinology, 17(12), 757-766. doi: 10.1038/s41574-021-00553-7.
Bergman, K., Sarkar, P., Glover, V., & O’Connor, T.G. (2008). Quality of child-parent attachment moderates the impact of antenatal stress on child fearfulness. Journal of Child Psychology and Psychiatry, 49, 1089–1098
Bonsignore, G. et al., (2003). Long-term effects of acute perinatal asphyxia on rat maternal behavior. Neurotoxicology Teratology, 25 (5), 571-578.
Buss C, Entringer S, Swanson JM, Wadhwa PD. (2012). The role of stress in brain development: The gestational environment’s long-term effects on the brain. Cerebrum, 4. Available online: https://dana.org/article/the-role-of-stress-in-brain-development/
Buss, C., Davis, E. P., Hobel, C. J., & Sandman, C. A. (2011). Maternal pregnancy-specific anxiety is associated with child executive function at 6-9 years age. Stress, 14(6), 665–676.
Buss, C., Davis, E. P., Muftuler, L. T., Head, K., & Sandman, C. A. (2010). High pregnancy anxiety during mid-gestation is associated with decreased gray matter density in 6-9-year-old children. Psychoneuroendocrinology, 35(1), 141–153.
Daubert, E.A., Condron, B.G. (2010). Serotonin: a regulator of neuronal morphology and circuitry. Trends in Neuroscience, 33(9), 424-34. doi: 10.1016/j.tins.2010.05.005.
Davis, E. P., & Sandman, C. A. (2010). The timing of prenatal exposure to maternal cortisol and psychosocial stress is associated with human infant cognitive development. Child Development, 81(1), 131–148.
Davis, E. P., Glynn, L. M., Dunkel Schetter, C., Hobel, C., Chicz-Demet, A., & Sandman, C. A. (2005). Corticotropin-releasing hormone during pregnancy is associated with infant temperament. Developmental Neuroscience, 27(5), 299–305.
Davis, E. P., Glynn, L. M., Schetter, C. D., Hobel, C., Chicz-Demet, A., & Sandman, C. A. (2007). Prenatal exposure to maternal depression and cortisol influences infant temperament. Journal of the American Academy of Child and Adolescent Psychiatry, 46(6), 737–746.
Davis, E. P., Waffarn, F., & Sandman, C. A. (2011). Prenatal treatment with glucocorticoids sensitizes the hpa axis response to stress among full-term infants. Developmental Psychobiology, 53(2), 175–183.
Entringer, S., Buss, C., & Wadhwa, P. D. (2011). Prenatal stress and developmental programming of human health and disease risk: Concepts and integration of empirical findings. Current Opinion in Endocrinology, Diabetes, and Obesity, 17(6), 507–516.
Field, T. (2011). Prenatal depression effects on early development: A review. Infant Behavior and Development, 34(1), 1–14.
Fishell, G., & Kepecs, A. (2020). Interneuron Types as Attractors and Controllers. Annual Review of Neuroscience, 43, 1-30. doi: 10.1146/annurev-neuro-070918-050421.
Fowden, A. L., & Forhead, A. J. (2009). Endocrine regulation of feto-placental growth. Hormone Research, 72(5), 257–265.
Fride, E., & Weinstock, M. (1989). Alternations in behavioral and striatal dopamine asymmetries induced by prenatal stress. Pharmacology Biochemistry and Behavior, 32, 425-430.
Glover, B., & O’Connor, T.G. (2005). Effects of antenatal maternal stress or anxiety: From Fetus to child. In B. Hopkins & S.P. Johnson (Eds.), Prenatal development of postnatal functions (pp. 221-246). Praeger.
Gluckman, P. D. & Hanson, M. A. (2005). Fetal Matrix: Evolution, development and disease. New York: Cambridge University Press.
Gold, P.W., & Chrousos, G.P. (2002). Organization of the stress system and its dysregulation in melancholic and atypical depression: High versus low CRH/NE states. Molecular Psychiatry, 7, 254-275.
Hannibal, K.E., & Bishop, M.D. (2014). Chronic stress, cortisol dysfunction, and pain: a psychoneuroendocrine rationale for stress management in pain rehabilitation. Physical Therapy, 94(12), 1816-1825. doi: 10.2522/ptj.20130597.
Hanswijk, S.I., Spoelder, M., Shan, L., Verheij, M.M.M., Muilwijk, O.G., Li, W., Liu, C., Kolk, S.M., & Homberg, J.R. (2020). Gestational factors throughout fetal neurodevelopment: The serotonin link. International Journal of Molecular Science, 21(16), 5850. doi: 10.3390/ijms21165850.
Henry, C., Kabbaj, M., Simon, H., Le Moal, M., & Maccari, S. (1994). Prenatal stress increases the hypothalamo-pituitary-adrenal axis response in young and adult rats. Journal of Neuroendocrinology, 6, 341-345.
Hollenbeck, A. R., Gewirtz, J. L., Sebris, S. L., & Scanlon, J. W. (1984). Labor and delivery medication influences parent–infant interaction in the first post-partum month. Infant Behavior & Development, 7(2), 201–210. https://doi.org/10.1016/S0163-6383(84)80058-2
Hopkins, B., & Johnson, S.P. (Eds.) (2005). Prenatal development of postnatal functions. Praeger.
Insel, T. (1990). Prenatal stress has long term effects on brain opiate receptors. Brain Research, 511, 93-97.
Janov, A. (2011). Life before birth: The hidden script that rules our lives. Chicago: NTI Upstream.
Lou, H. C. (1993). Prenatal stressful events of human life affect fetal brain development. Neuropediatrics, 24, 180.
Lou, H.C., Hansen, D., Nordentoft, M., Pryds, O., Jensen, F., Nim, J., & Hemmingsen, R. (1994). Prenatal stressors of human life affect fetal brain development. Developmental Medicine Child Neurology, 36(9), 826-32. doi: 10.1111/j.1469-8749.1994.tb08192.x.
Lou, H.C., Nordentoft, M., Jensen, F., Pryds, 0. Nim. J., & Hemmingsen. R. (1992). Psychosocial stress and severe prematurity. Lancet, 340, 54.
Lupien, S.J., McEwen, B.S., Gunnar, M.R., & Heim, C. (2009). Effects of stress throughout the lifespan on the brain, behaviour and cognition, Nature Reviews Neuroscience, 10(6), 434-445.
Nyberg, K., Buka, S.L., & Lipsitt, L.P. (2000). Perinatal medication as a potential risk factor for adult drug abuse in a North American cohort. Epidemiology, 11(6), 715-716. doi: 10.1097/00001648-200011000-00018.
Oberlander, T.F., et al. (2010). Prenatal effects of selective serotonin reuptake inhibitor antidepressants, serotonin transporter promoter genotype (slc6a4), and maternal mood on child behavior at 3 years of age. Archives of Pediatrics & Adolescent Medicine 164, 444-451.
Oberlander, T.F., Warburton, W., Misri, S., Aghajanian, J., Hertzman, C. (2006). Neonatal outcomes after prenatal exposure to selective serotonin reuptake inhibitor antidepressants and maternal depression using population-based linked health data. Archives of General Psychiatry, 63(8), 898-906. doi: 10.1001/archpsyc.63.8.898.
O’Connor, T.G., Caprariello, P., Blackmore, E.R., Gregory, A.M., Glover, V., Fleming, P. (2007). ALSPAC Study Team. Prenatal mood disturbance predicts sleep problems in infancy and toddlerhood. Early Human Development, 83(7), 451-458.
O’Donnell, K.J., Glover, V., Barker, E.D., & O’Connor, T.G. (2014). The persisting effect of maternal mood in pregnancy on childhood psychopathology. Developmental Psychopathology, 26(2), 393-403. doi: 10.1017/S0954579414000029.
Ross, E.J., Graham, D.L., Money, K.M., & Stanwood, G.D. (2015). Developmental consequences of fetal exposure to drugs: What we know and what we still must learn. Neuropsychopharmacology, 40(1), 61-87.
Swanson, J. M., & Wadhwa, P. D. (2008). Developmental origins of child mental health disorders. Journal of Child Psychology and Psychiatry and Allied Disciplines, 49(10), 1009–1019.
Tarsha, M. S., & Narvaez, D. (2022). Effects of adverse childhood experience on physiological regulation are moderated by evolved developmental niche history. Anxiety, Stress & Coping, 35(4):488-500. DOI: 10.1080/10615806.2021.1989419
van Bodegom, M., Homberg J.R., Henckens, M.J.A.G. (2017). Modulation of the hypothalamic-pituitary-adrenal axis by early life stress exposure. Frontiers Cell Neuroscience, 11, 87. doi: 10.3389/fncel.2017.00087.
Van den Bergh, B.R., Mulder, E.J., Mennes, M., Glover, V. (2005). Antenatal maternal anxiety and stress and the neurobehavioural development of the fetus and child: links and possible mechanisms. A review. Neuroscience Biobehavior Review, 29(2), 237–58.
Ward, I.L. (1972). Prenatal stress feminizes and demasculinizes the behavior of males. Science, 175, 82-84.
Weinstock, M. (2001). Alterations induced by gestational stress in brain morphology and behavior of the offspring. Progress in Neurobiology, 65, 427-451.