How stress and trauma imprints can be transmitted in utero


Pre natal and in utero stress has been found to increase the risk of mental health conditions such as anxiety and depression as well as cardiovascular and metabolic disorders and neuroendocrine imbalances (Harris & Seckl, 2011).


The main mechanism of transmission is through glucocorticoids via the placenta, as a result of altered functioning of the hypothalamus-pituitary-adrenal axis (HPA) which is responsible for modulating the stress and immune response.


Emerging evidence of the effects of epigenetic alteration on neurodevelopment and plasticity (Kundakovic & Jaric, 2017) as well as findings of up to two subsequent generations being affected by stress (Seckl et al, 2000) suggest the need to move beyond the immediate

mother-child dyad and biochemical transmission theories and consider a multifactorial, transgenerational model that encompasses historical and cultural trauma transmitted through ancestral lines.





The consequences of prenatal stress


Prenatal stress is a state of sympathetic overstimulation that a mother experiences during pregnancy. This stress may be present in the system already due to ongoing life events and chronic conditions or can be caused by traumatic events that occur during the pregnancy. Research shows that around 20% of women experience some degree of stress, anxiety or depression during pregnancy (Pampaka et al, 2018).


The biological, psychological and relational changes that occur during pregnancy for both mother and child make it a particularly vulnerable period of time developmentally; embryological tissue divides rapidly and thousands of new synapses form every second (Levitt 2003) in utero. The process of fetal neurological development is highly susceptible to environmental disruptions such as biochemical fluctuations and alterations as a result of stress and also epigenetic programming (Kundakovic & Jaric 2017).


Prenatal stress correlates with alterations in neurological structures but also the innate functioning of the fetal brain and central nervous system (Valsamakis et al, 2019) which can impact physiological health and cognition.


In a world where every third person has multiple chronic health conditions (Hajat & Stein, 2018) and where the burden of chronic disease is rapidly increasing, understanding the root causes is of profound collective and economic value. The emotional dimensions of chronic health conditions including in utero stress are often overlooked (Turner & Kelly, 2000) and this dimension offers much opportunity for effective treatment.



The mechanism of stress transfer in utero



The fetal adrenal system begins to develop as early as the fourth week of gestation (Conklin, 1968) and is highly responsive to environmental and chemical fluctuations. The field of psychoneuroendocrinology which studies how stress is perceived, represented, embodied and transmitted from the neurological system to the endocrine system and back again is of particular importance here as it explains how maternal levels of stress can impact fetal neurological development through stress hormones.


The system that governs the relationship between the neurological and hormonal aspects of the body is called the Hypothalamus-Pituitary-Axis (HPA-Axis). This consists of the hypothalamus at the base of the brain, the pituitary gland located below it and the adrenal glands, which are positioned top of the kidneys. Together, they form a network that strives to maintain balance and modulate stress.

In response to stress or trauma or as a result of being in a state of chronic stress, the mother’s HPA-Axis becomes highly activated; The hypothalamus secretes corticotrophin releasing hormone (CRH) which stimulates the synthesis of Adrenocorticotropic hormone (ACTH) from the pituitary gland. This binds to receptors on the adrenal glands and stimulates the production and secretion of cortisol by the adrenal cortex. Cortisol is the steroid hormone involved in metabolism, blood sugar level regulation and immune response and plays an important role in fetal nervous system development. Whilst surges of cortisol can be regulated, persistent excess cortisol in the bloodstream puts pressure on the mother’s body and the modulation mechanism in the placenta.


Excess cortisol eventually transmits to the fetal system via the placenta. Whilst the placental enzyme 11 β-hydroxysteroid-dehydrogenase type 2 works to modulate cortisol between the mother and fetus and provide a protective barrier by converting it to inactive cortisone, research has found that that persistent exposure to stress eventually inhibits this enzyme (Dy et al, 2008). As a result, the barrier between maternal stress and the fetal system is eroded.


Excess cortisol eventually transmits to the fetal system via the placenta.


The consequences of this are neurotoxicity, modification of the foetal HPA axis structure and function and an excess of glucocorticoids in the fetal system. Furthermore, this is often accompanied by alterations in the epigenetic components of the HPA axis (Valsamakis et al, 2019), (Radtke et al, 2011), (Kundakovic & Jaric, 2017) which means the genetic programming of the child is reflective of the mother’s stress state. As a result of these epigenetic alterations there is evidence that finds up to two subsequent generations are at risk (Seckl et al, 2000). Perinatal stress therefore correlates with disrupted fetal nervous system development which increases the chances of physiological disorders and mental health conditions in childhood and later life (Spencer & Deak, 2017).




Limitations of existing research


As with most human and animal studies these findings are correlational not causational and rely on self reporting from mother as to her stress levels and measurement of stress hormones such as glucocorticoids in the bloodstream.


Whilst glucocorticoids clearly influence neurological development, the endocrine system is extremely complex and studies show that noradrenaline and adrenaline also have an impact on enzyme activity and epigenetics (Sarkar et al, 2001).


Whilst the main mechanism of stress transmission cited by these studies is the maternal-fetal HPA axis, it is also possible to find increased levels of anxiety related behaviours in the absence of HPA axis changes (Holmes et al, 2006) suggestive of other mechanisms of transmission which are not yet fully understood.


Whilst the existing research does well to document the immediate maternal-fetal mechanism of stress transmission, there needs to be more inclusion of the bigger picture including paternal transmission, ancestral inheritance and older transgenerational effects of epigenetic alteration.


There needs to be more inclusion of the bigger picture including paternal transmission, ancestral inheritance and older transgenerational effects of epigenetic alteration.

There is perhaps an over emphasis on the maternal-fetal direction of stress transfer simply because it is more observable and measurable scientifically, which could be a distraction from the root causes of in utero stress and trauma.


Indeed, studies have found that babies who have not been directly exposed to maternal glucocorticoids are also at risk because the impact of stress is such that it can be transmitted to one or two subsequent generations through the epigenetic changes (Harris & Seckl, 2011).


The phenomena of de novo mutations (Guo et al, 2018), i.e gene mutations that cannot be traced back to either parent as well as research around the impact of ancestral stress on subsequent generations (McCreary et al, 2016) leads us into a wider field of discussion of transgenerational stress (Babenko et al, 2015) transmission.


Other factors such as ecological environments and older cultural inheritance (Horsthemke, 2018) are important but much harder to measure. Whilst studies show that grandparents’ environmental and nutritional challenges impact two subsequent generations (Kaati et al, 2007) modelling this and controlling for all other influencing factors over multiple human generations is a great feat. Most epigenetic research to date has been conducted on plants and animals such as rats, guinea pigs, pigs and sheep.




It is more likely that a multifactorial model that supports the complex interplay and co-influence between psychoneuroendocrinology, genetics, history, culture, environmental factors and wider world ecology during gestation rather than immediate womb ecology and biological transmission will offer the depth required to truly address the phenomena of stress transfer in utero.


Furthermore, the research mostly suggest that in utero stress is a biological adaptation designed to help the fetus survive in the environment it finds itself in - however this does not explain why it has the opposite effect, increasing the chances of chronic illness, morbidity or indeed, why if it is a genetic adaptation that is inherited from many previous generations, why there is not an adaptation towards health.


A multifactorial model that supports the complex interplay and co-influence between psychoneuroendocrinology, genetics, history, culture, environmental factors and wider world ecology during gestation rather than immediate womb ecology and biological transmission will offer the depth required to truly address the phenomena of stress transfer in utero.

Critics of a maternal-fetal stress model would point to the fact that many individuals who experience in utero stress in fact do not go on to develop chronic illness or psychopathologies which suggests there are other adaptive mechanisms at play. There is also a potential negative effects bias in the maternal-fetal studies which suggests because researchers are looking for a measurable increase in the stress response and therefore they find it; when in fact some studies have actually found that adversity increases resilience which is a key component of mental health (Seery et al, 2010).


There is a need for a deeper understanding of the purpose of stress transmission, beyond just biological adaptation, belonging and survival. The development of empathy, defined as a mirroring of another’s emotion in neurophysiological, peripheral physiological and behavioral domains (Decety & Ickes, 2009) could be a factor, whereby the development of a stress state is an attempt by the fetus and child to empathise with its ancestral line in order to transmute rather than transmit, trauma.


Could it be that stress transmission is a process of unconscious traumas surfacing, and emerging to be healed? Perhaps then, stress transmission and healing approaches can properly support the unwinding of ancestral trauma by recognising not just the pain it creates but supporting the emergent purpose of it.




Healing considerations


Healing approaches depend on whether stress transmission is seen as a purely biological maternal-fetal dynamic whereby maternal glucocorticoid levels are taken as the sole mediator of foetal programming or whether a broader picture that includes the historical ancestral dynamic and environmental influences can be integrated.


Interventions focused only on the immediate biochemistry ignore epigenetic inheritance from grandparents and great-grandparents, ecological, historical and cultural realities that have been shown to be key drivers of health and wellbeing (Vicary & Westerman, 2004).


Treatment options such as altering level of maternal cortisol during the pregnancy period in order to limit fetal transmission can have detrimental health consequences and carry high risks including lowering birth weight (Ogunyemi, 2005) raising fetal blood pressure and increasing thickness of the myocardial wall (Abbasi et al, 2000) which puts the fetus at higher risk not just during the pregnancy but also after birth.


Antenatal glucocorticoid treatment only began in the 1980’s so the long-term impact and consequences still cannot be determined. Some studies have found that corticosteroid treatments actually have persisting adverse effects and offer no clear additional benefits to the baby (Kay et al, 2000).


Behavioural and cognitive based therapies such as exposure therapy, talking therapy etc can be supportive to help an expectant mother understand and manage her stress to a degree, but there are sociocultural barriers to participation and for marginalised communities in particular, there are often cost inhibitions making these types of therapies inaccessible.


Whilst somatic mother-babies therapies are available the focus yet again is on the immediate mother-child dyad ignoring the wider familial dynamic and the ancestral inheritance and imprint. Transpersonal approaches such as breathwork practices, meditation etc can be supportive to mitigate the stress response and rebalance the body’s sympathetic overstimulation and can also be gently practiced throughout pregnancy, but do not necessarily allow for rapid understanding and resolution of the root cause or underlying trauma.



Indigenous cultures offer a more holistic approach focusing on prevention and community care encompassing physical, nutritional, psychological, spiritual and ecological influences. There is often an inherent emphasis on collective responsibility and ritual, spiritual meaning making, ancestral recognition (Corbett et al, 2017) as healing options rather than disease ontology or symptom elimination. This means there is an inherent understanding of the wider transgenerational effects of stress




Indeed, protective and preventive factors are valuable. Research has found that having strong family and community connections and support networks, feeling connected to cultural roots and a spiritual practice, as well as having a belief in natural healing (Ypinazar et al, 2007) can be supportive of healthy pregnancy.


Furthermore, raising awareness amongst traditional healthcare providers of the importance of maternal mental health and incorporating it as part of routine screening can be supportive, especially if specific cultural sensitivities and spiritual nuances are integrated and supported (McCauley et al, 2019). Whilst empathy and spiritual care has been found to be effective in supporting mothers during their pregnancy and birth experience (Moloney & Gair, 2015) and has long been discussed as a crucial healing ingredient, it remains uncommon in practice.


Raising awareness amongst traditional healthcare providers of the importance of maternal mental health and incorporating it as part of routine screening can be supportive, especially if specific cultural sensitivities and spiritual nuances are integrated

Ultimately, approaches to healing will depend on whether a multifactorial model of mind-body-spirit can be integrated within a sociocultural framework that is relevant to the mother and child and whether the purpose of the stress transmission between mother and child can truly be understood.


If you are reading this and noticing that it resonates or if you are trying to heal from chronic pain or illness or emotional turbulence as a result of your in utero environment, ancestral history or birth experience and would like to speak further about what could support you, please reach out to me.


You might also be interested to join Womb Room, the 10 day rebirthing journey or explore a more indepth 1-1 therapy programme with me. Email safa@kimiyahealing.co.uk

References


Abbasi, S., Hirsch, D., Davis, J., Tolosa, J., Stouffer, N., Debbs, R., & Gerdes, J. S. (2000). Effect of single versus multiple courses of antenatal corticosteroids on maternal and neonatal outcome. American journal of obstetrics and gynecology, 182(5), 1243–1249. https://doi.org/10.1067/mob.2000.104789



Babenko, O., Kovalchuk, I., & Metz, G. A. (2015). Stress-induced perinatal and transgenerational epigenetic programming of brain development and mental health. Neuroscience and biobehavioral reviews, 48, 70–91. https://doi.org/10.1016/j.neubiorev.2014.11.013



Bloomfield, F. H., Knight, D. B., & Harding, J. E. (1998). Side effects of 2 different dexamethasone courses for preterm infants at risk of chronic lung disease: a randomized trial. Journal of pediatrics, 133(3), 395–400. https://doi.org/10.1016/s0022-3476(98)70277-x



Conklin, J. (1968) The development of the human fetal adenohypophysis, The Anatomical Record, 160(1) https://doi.org/10.1002/ar.1091600108



Corbett, C. A., Callister, L. C., Gettys, J. P., & Hickman, J. R. (2017). The Meaning of Giving Birth: Voices of Hmong Women Living in Vietnam. The Journal of perinatal & neonatal nursing, 31(3), 207–215. https://doi.org/10.1097/JPN.0000000000000242



Decety, J., & Ickes, W. (Eds.). (2009). The social neuroscience of empathy. MIT Press. https://doi.org/10.7551/mitpress/9780262012973.001.0001



Dy, J., Guan, H., Sampath-Kumar, R., Richardson, B. S., & Yang, K. (2008). Placental 11beta-hydroxysteroid dehydrogenase type 2 is reduced in pregnancies complicated with idiopathic intrauterine growth Restriction: Placenta, 29(2), 193–200. https://doi.org/10.1016/j.placenta.2007.10.010



Guo, H., Wang, T., Wu, H. et al. (2018). Inherited and multiple de novo mutations in autism/developmental delay risk genes suggest a multifactorial model. Molecular Autism 9(64) https://doi.org/10.1186/s13229-018-0247-z


Hajat, C., & Stein, E. (2018). The global burden of multiple chronic conditions: A narrative review. Preventive medicine reports, 12, 284-293. https://doi.org/10.1016/j.pmedr.2018.10.008


Harris, A., & Seckl, J. (2011). Glucocorticoids, prenatal stress and the programming of disease. Hormones and behavior, 59(3), 279–289. https://doi.org/10.1016/j.yhbeh.2010.06.007



Holmes, M. C., Abrahamsen, C. T., French, K. L., Paterson, J. M., Mullins, J. J., & Seckl, J. R. (2006). The mother or the fetus? 11beta-hydroxysteroid dehydrogenase type 2 null mice provide evidence for direct fetal programming of behavior by endogenous glucocorticoids. The Journal of neuroscience, 26(14), 3840-3844. https://doi.org/10.1523/JNEUROSCI.4464-05.2006



Horsthemke B. (2018). A critical view on transgenerational epigenetic inheritance in humans. Nature communications, 9(1), 2973. https://doi.org/10.1038/s41467-018-05445-5



Kaati, G., Bygren, L. O., Pembrey, M., & Sjöström, M. (2007). Transgenerational response to nutrition, early life circumstances and longevity. European journal of human genetics 15(7), 784-790. https://doi.org/10.1038/sj.ejhg.5201832



Kay, H. H., Bird, I. M., Coe, C. L., & Dudley, D. J. (2000). Antenatal steroid treatment and adverse fetal effects: what is the evidence? Journal of the Society for Gynecologic Investigation, 7(5), 269–278.



Kundakovic, M., & Jaric, I. (2017). The Epigenetic Link between Prenatal Adverse Environments and Neurodevelopmental Disorders. Genes, 8(3), 104. https://doi.org/10.3390/genes8030104



Levitt, P. (2003). Structural and functional maturation of the developing primate brain. The Journal of pediatrics, 143(4), 35–45. https://doi.org/10.1067/s0022-3476(03)00400-1



McCauley, M., Brown, A., Ofosu, B., & van den Broek, N. (2019). "I just wish it becomes part of routine care": Healthcare providers' knowledge, attitudes and perceptions of screening for maternal mental health during and after pregnancy: a qualitative study. BMC psychiatry, 19(1), 279. https://doi.org/10.1186/s12888-019-2261-x



McCreary, J. K., Erickson, Z. T., Hao, Y., Ilnytskyy, Y., Kovalchuk, I., & Metz, G. A. (2016). Environmental Intervention as a Therapy for Adverse Programming by Ancestral Stress. Scientific reports, 6, 37814. https://doi.org/10.1038/srep37814



Moloney, S., & Gair, S. (2015). Empathy and spiritual care in midwifery practice: Contributing to women's enhanced birth experiences. Women and birth : Journal of the Australian College of Midwives, 28(4), 323–328. https://doi.org/10.1016/j.wombi.2015.04.009



Nemoda, Z., & Szyf, M. (2017). Epigenetic Alterations and Prenatal Maternal Depression. Birth defects research,109(12), 888–897. https://doi.org/10.1002/bdr2.1081



Ogunyemi D. (2005). A comparison of the effectiveness of single-dose vs multi-dose antenatal corticosteroids in pre-term neonates. Journal of obstetrics and gynaecology 25(8), 756–760. https://doi.org/10.1080/01443610500314827



Pampaka, D., Papatheodorou, S. I., AlSeaidan, M., Al Wotayan, R., Wright, R. J., Buring, J. E., Dockery, D. W., & Christophi, C. A. (2018). Depressive symptoms and comorbid problems in pregnancy - results from a population based study. Journal of psychosomatic research, 112, 53–58. https://doi.org/10.1016/j.jpsychores.2018.06.01



Radtke, K. M., Ruf, M., Gunter, H. M., Dohrmann, K., Schauer, M., Meyer, A., & Elbert, T. (2011). Transgenerational impact of intimate partner violence on methylation in the promoter of the glucocorticoid receptor. Translational psychiatry, 1(7), 21. https://doi.org/10.1038/tp.2011.21



Seckl, J. R., & Meaney, M. J. (2006). Glucocorticoid "programming" and PTSD risk. Annals of the New York Academy of Sciences, 1071, 351–378. https://doi.org/10.1196/annals.1364.027




Seery, M. D., Holman, E. A., & Silver, R. C. (2010). Whatever does not kill us: cumulative lifetime adversity, vulnerability, and resilience. Journal of personality and social psychology, 99(6), 1025–1041. https://doi.org/10.1037/a0021344



Spencer, R. L., & Deak, T. (2017). A users guide to HPA axis research. Physiology & behavior, 178, 43–65. https://doi.org/10.1016/j.physbeh.2016.11.014



Turner, J., & Kelly, B. (2000). Emotional dimensions of chronic disease. The Western journal of medicine, 172(2), 124-128. https://doi.org/10.1136/ewjm.172.2.124



Valsamakis, G., Chrousos, G., & Mastorakos, G. (2019). Stress, female reproduction and pregnancy. Psychoneuroendocrinology, 100, 48–57 https://doi.org/10.1016/j.psyneuen.2018.09.031



Vicary, David & Westerman, Tracy. (2004). 'That's just the way he is': Some implications of Aboriginal mental health beliefs. Australian e-Journal for the Advancement of Mental Health

3(3) 103-112 https://doi.org/10.5172/jamh.3.3.103



Ypinazar, Valmae A., Margolis, Stephen A., Haswell-Elkins, Melissa and Tsey, Komla (2007) 'Indigenous Australians' understandings regarding mental health and disorders', Australian and New Zealand Journal of Psychiatry,41(6)467-478 10.1080/00048670701332953 URL: http://dx.doi.org/10.1080/00048670701332953