Prenatal stress

Prenatal stress (or prenatal maternal stress) is exposure of an expectant mother to stress, which can be caused by stressful life events or by environmental hardships. The resulting changes to the mother's hormonal and immune system may harm the fetus's (and after birth, the infant's) immune function and brain development.[1][2]

Prenatal stress is shown to have several affects in fetal brain development. In the hippocampus of adult male rats, prenatal stress has shown to decrease the rate of proliferation and cell death in the hypothalamus-pituitary axis.[3] Prenatal stressed animals have prolonged corticosterone response. Removing the adrenal glands of the mother eliminates the effect of the pup's corticosterone response. Supplementing the adrenalectamized mother with corticosterone, rescued the hypothalamic-pituitary-axis response to maternal stress for prenatally stressed offspring. Prenatal stress caused high glucocorticoids, which in turn affects the hypothalamic-pituitary-axis negative feedback.[4] A study by García-Cáceres et al.[5] showed that prenatal stress decreases cell turnover and proliferation in the hypothalamus of adult rats, which reduces structural plasticity and reduces the response to stress in adulthood. This study also showed that when prenatally stressed rats were stressed in adulthood the females showed an increase in corticotropin-releasing hormone suggesting it to be an up-regulation in the hypothalamic-pituitary adrenal axis. Males showed no elevation of corticosterone levels. Increase in adrenocorticotropic hormone with no effect of adult stress and a decrease in the corticotropin-releasing hormone mRNA in the hypothalamus showed a down-regulation. The author concludes that this makes prenatally stressed females less reactive to later life stressors than males.

Prenatal stress and gender differences in hormones

Pups that underwent prenatal stress showed lower plasma testosterone when compared to the control pups. This is caused by the disruption of prenatal development which did not allow the complete masculinization of the prenatally stressed pups’ central nervous system. Particularly in the striatum of the prenatally stressed male pups showed an increase in vanilmandelic acid, dopamine, serotonin, 5-hydroxyindoleacetic acid which all can affect sexual behavior. The prenatally stressed male pups showed a significant latency in mounting behavior when compared to controls.[6] When doing the radial arm maze task prenatally stressed male rats showed a greater increase in dopamine than the prenatally stressed females, which is suggested to facilitate the impairment for the males doing the maze task, but improved the female’s performance. There was also an effect on the corticosterone secretion for prenatally stressed females. Being prenatally stressed increased the anxiety response of the female rats. Yet, it had no effect on the males.[7]

Sexually dimorphic brain regions

Prenatal stress does have an effect on brain sexual differentiation after measuring the volume of the sexually dimorphic nucleus of the preoptic area of both female and males in the control and stressed groups. Prenatal stress inhibits the masculinzation of the male brain by inhibiting the growth of the sexually dimorphic nucleus of the preoptic area. Previous studies found that a decrease in testosterone is seen in pups of prenatally stressed mothers. Authors suggest this may cause the reduced in the sexually dimorphic nucleus of the preoptic area and says it is similar to the effects of neonatal castration. Also, stressed males had larger sexually dimorphic nucleus of the preoptic area at birth, but then at 20 and 60 days are found to only have 50% of the volume of the control males. Whereas control males are two times larger than control females on days 20 and 60, but the stressed males show no statistical difference to control females on respective days. These findings show support that the male brain is not showing the expected sexual dimorphism when prenatally stressed.[8] Another study led by Kerchner et al. investigated the volume of the medial amygdala and the two compartments posterodorsal and the posteroventral in mice that also were prenatally stressed. Posterodorsal is thought to show organizational and activational effects from gonadal steroids. The medial amygdala for the control and stressed males was 85% larger than females with the males (stressed and control) resembling each other. To look for specific regions within the medial amygdala that may have been affected, data showed that both the posterodorsal and posteroventral, all male groups were larger in volume than the females, but male groups did not significantly differ from each other. This study confirmed that the medial amygdala is sexually dimorphic; the males are larger than the females. The posterodorsal and posteroventral were shown to be sexually dimorphic too. The writer suggested that these areas may act similarly to sexually dimorphic nucleus of the preoptic area in response to testosterone, but prenatal stress did not show an effect on the medial amygdala as it does on the sexually dimorphic nucleus of the preoptic area. Also, the posteroventral was 40% larger in control males than females. These results were thought to be caused by the sensitive period of the medial amygdala which is in the first days after birth. The medial amygdala, posterodorsal and posteroventral all show to be resistant against demasculinization from prenatal stress.[9]

Prenatal stress and gender roles

A longitudinal study done on prenatal stress and gender roles showed that prenatal stress only plays a small part in the gender roles the offspring takes on and mentions it has more to do with older siblings, maternal use of alcohol and/or tobacco, maternal education, and the observance or teaching of “traditional sex roles” from the parents.[10]

Prenatal Stress and Mindfulness Based Interventions

Prenatal stress and negative mood during pregnancy has been shown to increase the risk for poor childbirth outcomes and postnatal maternal mood problems. Additionally, prenatal distress can interfere with the mother-infant attachment and child development outcomes.[11][12] Despite the clear association between prenatal stress and child outcomes, frequently women do not receive screening, prevention, or treatment for mood or stress concerns.[13][14]

Given the relationship between prenatal stress and child outcomes, it is essential to examine interventions that aim to reduce anxiety, depression, and stress during pregnancy. Mindfulness based stress reduction has been demonstrated to reduce anxiety and depression for people with stress-related and chronic medical conditions.[15]

One pilot study shows promise for the potential of a mindfulness-based intervention to reduce negative affect and anxiety of women during pregnancy. Based out of the California Pacific Medical Center Research Institute, investigators Dr. Cassandra Vieten and Dr. John Astin conducted a wait-list control pilot study that tested a group-based mindfulness intervention. There were 31 women enrolled in the study: 13 women were assigned to the intervention and 18 women were assigned to the control group. Measures of anxiety, negative affect, positive affect, depression, mindfulness, perceived stress, and affect regulation were taken before intervention or control was assigned and after the intervention or control was completed. Measures were repeated at a follow-up visit 3 months after the intervention or control was completed. The investigators found a significant decrease in anxiety (p<.05) and negative affect (p <.04) in women who completed the mindfulness based intervention, but not a significant decrease in depression, positive affect, mindfulness, affect regulation, and perceived stress. These results suggest that mindfulness intervention during pregnancy reduce anxiety and negative affect of mothers. This study is a promising start to the potential impact that mindfulness based interventions could have on reducing prenatal stress, and thereby improving child outcomes.[16]

References

  1. ↑ Ruiz RJ, Avant KC (2005). "Effects of maternal prenatal stress on infant outcomes: a synthesis of the literature". Adv Nurs Sci. 28 (4): 345–55. PMID 16292020.
  2. ↑ Charil A, Laplante DP, Vaillancourt C, King S (2010). "Prenatal stress and brain development". Brain Res Rev. 65 (1): 56–79. doi:10.1016/j.brainresrev.2010.06.002. PMID 20550950.
  3. ↑ Baquedano E, García-Cáceres C, Diz-Chaves Y, Lagunas N, Calmarza-Font I, Azcoitia I, Garcia-Segura LM, Argente J, Chowen JA, Frago LM (2011). "Prenatal stress induces long-term effects in cell turnover in the hippocampus-hypothalamus-pituitary axis in adult male rats". PLoS ONE. 6 (11): e27549. doi:10.1371/journal.pone.0027549. PMC 3212572Freely accessible. PMID 22096592.
  4. ↑ Barbazanges A, Piazza PV, Le Moal M, Maccari S (June 1996). "Maternal glucocorticoid secretion mediates long-term effects of prenatal stress". J. Neurosci. 16 (12): 3943–9. PMID 8656288.
  5. ↑ García-Cáceres C, Lagunas N, Calmarza-Font I, Azcoitia I, Diz-Chaves Y, García-Segura LM, Baquedano E, Frago LM, Argente J, Chowen JA (November 2010). "Gender differences in the long-term effects of chronic prenatal stress on the HPA axis and hypothalamic structure in rats". Psychoneuroendocrinology. 35 (10): 1525–35. doi:10.1016/j.psyneuen.2010.05.006. PMID 20558007.
  6. ↑ Gerardin DC, Pereira OC, Kempinas WG, Florio JC, Moreira EG, Bernardi MM (January 2005). "Sexual behavior, neuroendocrine, and neurochemical aspects in male rats exposed prenatally to stress". Physiol. Behav. 84 (1): 97–104. doi:10.1016/j.physbeh.2004.10.014. PMID 15642612.
  7. ↑ Bowman RE, MacLusky NJ, Sarmiento Y, Frankfurt M, Gordon M, Luine VN (August 2004). "Sexually dimorphic effects of prenatal stress on cognition, hormonal responses, and central neurotransmitters". Endocrinology. 145 (8): 3778–87. doi:10.1210/en.2003-1759. PMID 15142991.
  8. ↑ Anderson DK, Rhees RW, Fleming DE (April 1985). "Effects of prenatal stress on differentiation of the sexually dimorphic nucleus of the preoptic area (SDN-POA) of the rat brain". Brain Res. 332 (1): 113–8. doi:10.1016/0006-8993(85)90394-4. PMID 3995257.
  9. ↑ Kerchner M, Malsbury CW, Ward OB, Ward IL (February 1995). "Sexually dimorphic areas in the rat medial amygdala: resistance to the demasculinizing effect of prenatal stress". Brain Res. 672 (1-2): 251–60. doi:10.1016/0006-8993(94)01378-U. PMID 7749746.
  10. ↑ Hines M, Johnston KJ, Golombok S, Rust J, Stevens M, Golding J (September 2002). "Prenatal stress and gender role behavior in girls and boys: a longitudinal, population study". Horm Behav. 42 (2): 126–34. doi:10.1006/hbeh.2002.1814. PMID 12367566.
  11. ↑ P.D. Wadha, C.A. Sandman, T.J. Garite (2001). "The neurobiology of stress in human pregnancy: implications for prematurity and development of the fetal central nervous system.". Progress in brain research. 133: 131–142. doi:10.1016/S0079-6123(01)33010-8.
  12. ↑ Bonari, L., Pinto, N., Ahn, E., Einarson, A., Wadha (2004). "The neurobiology of stress in human pregnancy: implications for prematurity and development of the fetal central nervous system.". Canadian Journal of Psychiatry. 49 (11): 726–35. doi:10.1016/S0079-6123(01)33010-8.
  13. ↑ Flynn, H. A., Blow, F. C., & Marcus, S. M. (2006). "). Rates and predictors of depression treatment among pregnant women in hospital-affiliated obstetrics practices.". General hospital psychiatry. 38 (4): 289–295. doi:10.1016/j.genhosppsyych.2006.04.00.
  14. ↑ Marcus, S. M., Flynn, H. A., Blow, F. C., & Barry, K. L. J (2003). "Depressive symptoms among pregnant women screened in obstetrics settings.". Journal of Women's Health. 12 (4): 373–380. doi:10.1089/154099903765448880.
  15. ↑ Astin, J.A., Shapiro S.L., Eisenberg D.M., Forys K.L. (2003). "Mind-body medicine: state of the science, implications for practice.". The Journal of the American Board of Family Practice. 16 (2): 131–147. doi:10.3122/jabfm.16.2.131.
  16. ↑ Veiten, C., & Astin, J. (2008). "Effects of a mindfulness-based intervention during pregnancy on prenatal stress and mood: Results of a pilot study.". Archives Of Women’s Mental Health. 11 (1): 67–74. doi:10.1007/s00737-008-0214-3.
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