Articles Pregnancy and Birth Information

The Origins of Infant Mental Health

Jocelyn and Kai
Jocelyn did much soul searching during the pregnancy to find the right conditions for pregnancy and the birth of Kai and their future lives together
Barker has shown that diet during pregnancy has long term effects, showing a correlation between fetal nourishment and diabetes, hypertension and heart disease in adulthood (1).

Not only can the origins of physical health be traced to fetal wellbeing, but the origins of mental health are increasingly correlated with events that occur in the womb. Optimal maternal nourishment, by laying the foundations of fetal hormonal and neuro-chemical architecture, appears to be associated with the psychological and emotional wellbeing of the fetus, infant, child and adult. Changes in fetal nutrition affect fetal insulin and insulin-like growth factors, which are thought to play a major role in the regulation of fetal growth. (2) Lack of nourishment may retard fetal growth, it may also lead to an increase in the production of cortisol, a hormone produced in response to stress, which in prolonged concentrations may affect brain cell differentiation (3). Effects in the first three months of pregnancy may be harmful to the development of the brain, including memory centres and areas of emotional responsiveness, such as the hippocampus (4).

Research on fetal habituation responses to auditory stimuli suggests that fetal memory is active from about the 22nd week of gestation (5-10). It may serve no function, or it may serve a practice function, similar to the fetal breathing movements that appear from 12 weeks gestation mimicking the breathing movements necessary after birth. Prenatal memory may be important for the development of attachment behaviours, such as preferring the mother’s voice after birth, distinguishing the mother’s speech sounds from other sounds, or recognizing the smell of the mother’s body and/or colostrums, which may have a similar smell to the amniotic fluid (11-14). Prenatal memory may also be important for the establishment of breastfeeding as the amniotic fluid, like the breast milk, is flavoured by the mother’s diet, and the fetus swallows amniotic fluid from about the 12th week of gestation (15-17). The fetus has been shown to differentiate between various speech sounds in the womb, thus suggesting that prenatal memory may also be vital in the acquisition of language (18-21).

Fetal growth, which occurs in the psycho-emotional (neuro-hormonal) maternal matrix, is dependant on the this matrix from conception . When the fertilized zygote cell is multiplying to form an embryo, the cellular structure and fluids are influenced by the surrounding matrix of the mother and the father, and beyond this, their world within the universe. The worst cases and best researched of prenatal influences are those of alcohol and nicotine dependency, because the unborn babies are starved of oxygen and nutrients for growth due to the presence of nicotine and alcohol in the mother’s bloodstream. Babies born to alcohol dependent mothers and/or fathers may be deformed, have specific features of Fetal Alcohol Syndrome, such as eyes set close together, small bridge of the nose and small skull diameter. They show various degrees of developmental delay and in the most detrimental cases are severely mentally retarded. Babies of nicotine dependent parents are often born prematurely, are small at birth and may have developmental delays. Studies have also shown a percentage of lower intelligence quotients. These events are traumatic for the embryo/fetus and, at worst, these babies can never recover from the trauma/injury they have experienced, because the damage is intrinsic to the building blocks of the brain structures. The trauma is embedded in the neuro-chemical systems, and influences growth patterns and levels of intelligence. (22)

The human embryo is particularly impacted by hormones such as insulin, thyroid hormones and glucocorticoids. Glucocorticoids are essential hormones for regulating the bodily processes and play a major role in regulating intra-uterine growth and development. They are produced by the adrenal glands, on top of the kidneys and with the help of the hypothalamus and pituitary gland (HPA axis) help to maintain homeostasis in the body. They also suppress inflammatory responses and immune responses when the whole ‘mind and body’ experiences shock, trauma, or stress. In the short term, this suppression of an inflammatory response is a useful action, as it helps to release glucose in the tissues for energy and keeps the body functioning. However in the long term, that is, if an embryo or fetus cannot recover homeostasis or balanced functioning, persistent glucocorticoid release downgrades receptor cells, which can alter the brain structure, the immune response system and interfere with growth. Glucocorticoids alter cellular function, acting directly on the genes and are closely involved in intra-uterine programming. (23)

In other words, when a mother is functioning under stressful conditions and her body is producing large amounts of stress hormones (glucocorticoids), the embryonic or fetal cells are also bathed in high levels of stress hormones. Prolonged exposure to glucocorticoids result in decreased sensitivity of receptor cells and a downgrading of the HPA axis function, which has long term effects of the immune response system.
Babies in the womb don’t grow well under these conditions and suffer from what is medically termed intra-uterine-growth restriction (IUGR), with a resultant hypoxic effect on the organs and cells. Various factors will influence the extent of the impact, such as the susceptibility of the unborn baby’s genotype to the impact of an adverse prenatal environment. Another factor that will influence the unborn baby’s growth is the interaction between the maternal genotype and risky behaviours such as for example smoking, drug-taking, alcohol, or teenage pregnancy.

Such conditions affect the biological foundations of growth and development, as well as how the unborn baby will respond to stress in the future life. A 2008 study of stress in pregnancy suggests there is a higher risk of psychiatric disease, more specifically, schizophrenia, in offspring, when mothers have experienced extremely stressful events in the first three months of the pregnancy. The researchers conclude: ‘This finding is consistent with ecological evidence from whole populations exposed to severe stressors and suggests that the environment may influence neurodevelopment at the feto-placental-maternal interface’. (24)

Just as the environment for the growth of an unborn baby needs to be nourishing and calm, so does the environment for a pregnant woman need to be stable and loving. Richard Neugebauer describes the retrospective studies of the Dutch (1945) and Chinese Famines (1961). The studies analysed case data from psychiatric institutions and observed an increase in the admission to psychiatric institutions of young adults with symptoms of schizophrenia, 20 years after the famines were documented. Famine is not only associated with lack of food availability, but with higher levels of anxiety and depression. What happens here is that the hypothalamic-pituitary-adrenal gland in the neuro-chemical system of the baby is imprinted in such a way that it is sensitized to stress and this underlies a greater vulnerability to anxiety and depression and other psychiatric symptoms in later life. (25)

When a mother is not supported during her pregnancy by the father of the child, or her friends and family, she is likely to feel abandoned and overwhelmed by the prospect of caring for a baby single handedly, and her baby’s primal health is at stake. She may neither eat correctly nor undertake proper self care, and may be anxious as well as showing signs of fatigue, or depression. A prolonged situation of this nature will lead to a chronic raise in the levels of cortisol in her body, and a suppression of feel good hormones such as dopamine and serotonin. Dopamine is involved in the pleasure and reward system of the body/mind interface and low dopamine levels are linked with depression and sadness. (26) Cortisol inhibits the release of growth hormone, which will therefore affect the growth of the fetus. An event or period of growth restriction during the pregnancy will imprint the baby’s brain, and will be stored in his neuro-chemical structure, lying dormant until the need arises for a particular response to be re-activated by future stressful situations, acute or chronic. To ‘imprint’ means to impress every aspect of our biology with a memory, including our blood vessels, muscles, nerve cells, neurochemicals and hormones.

The Dutch and Chinese Famine studies confirmed an already established link between severe maternal nutritional deficiency in early pregnancy and the increased risk of schizophrenia in the offspring. The lack of micronutrients present in the diet of mothers in early pregnancy elicits changes in the gene expression without disrupting the primary DNA sequence within the genes themselves. This is a ‘traumatic’ imprint which possibly primes the neurochemical structures for aggressive responses to future stressors. National famine is a result of war or global greed, as first world or developing countries adopt harsh economic policies and drive trade with third world countries of intensive agricultural produce, such as GM maize or sugar devoid of micronutrients. War is well known to be associated with wholescale abuse and rape of women, including pregnant women. Modern day economics and global capitalism, while they may be improvement on feudalism, still fail to address the needs of countless women, and thus fail the health of future generations of unborn children.(27)

A report from the Avon Longitudinal Study of Parents and Children (ALSPAC) by Thomas Connor and associates tested the hypothesis that maternal stress and anxiety during pregnancy predicts behavioural problems of the children at the age of 4 years. (28) The conclusions suggest a direct effect of maternal mood on the unborn baby’s brain development. A study by Thomas O’Connor and his colleagues showed that the effects of maternal anxiety lasted till middle childhood or 61/2 years, after controlling for obstetric risks, psychosocial disadvantage and postnatal anxiety and depression. (29)

Preterm labour and low birth weight for gestational age are the outcomes most consistently linked with stress or anxiety in humans. But, in the ALSPAC studies, anxiety at 32 weeks of pregnancy predicted severe behavioural and emotional problems in both boys and girls. Hyperactivity and inattention in boys is significantly associated with anxiety in late pregnancy. Furthermore, evidence strongly suggests a link between antenatal anxiety in early pregnancy and the neurological development of the unborn baby with regard to mixed handedness. If antenatal anxiety is associated with mixed handedness, then it is possible that antenatal anxiety may also play a role in other disorders associated with mixed handedness such as dyslexia and autism.(30) Such are the potential outcomes of stress and trauma incurred by the fetus in the womb in this primal period of life.

An unborn baby is in a critical period for early traumatic imprints. The more a women is nourished and loved before and during pregnancy and childbirth, the better chance an unborn baby has to develop neural architecture that is expanded, thus arming the brain against later adversity in life.

1. Barker, D.J.P., 1998. In Utero programming of chronic disease. Clinical Science 95, 115-128.
2. Oliver, M.H., Harding, J.E., Breier, B.H.,Evans, P.C. and Gluckman, P.D. 1993.Glucose but not a mixed amino acid infusionregulates plama insulin-like growth factor-1 concentrations in fetal sheep. Paeditr Res. 34,62-65.
3. Fowden, A.L. 1989. The role of insulin in prenatal growth. Journal of Developmental Physiology 12, 173-18
4. Weinstock M. in Glover, V & O’Connor, T.G. (2002) Effects of Antenatal Stress and Anxiety. Br J Psychiatry 180: 389-391.
5. Thompson RF. Spencer WA. Habituation: A model for the study of neuronal substrates of behavior. Psycho Rev 1966;73:16-43
6. Hepper PG. Fetal habituation – another pandora’s box? Arch Dis Childhood, in press.
7. 7.Hepper PG. Shadidullah S. Habituation in normal and Down Syndrome fetuses. Quart J Exp Psychol 1992;44:305-17
8. Goldkrand JW, Litvack BL. Demonstration of fetal habituation and patterns of fetal heart response to vibroacoustic stimulation in normal and high risk pregnancies. J Perinatology 1991; 11;25-9
9. Leader LR, Baille P, Martin B, Molteno C. Fetal responses to vibrotactile stimuli: a possible predictor of fetal and neonatal outcome. Aust NZ J Obstet Gynecol 1984;24:251-6
10. Leader LR, Baille P, Martin B, Vermeulen E. The assessment and significance of habituation in normal and high risk pregnancies. J Perinatalogy 1991;11:25-9
11. De Vries JIP, Visser GHA, Prectl IIFR. The emergence of fetal behaviour II. Quantitative aspects. Early Human Devel 1985;12:99-120
12. Kozuma S, Nemoto A, Okai T, Mizuno M. Maturational sequence of fetal breathing movements. Biol Neonate 1991;60;36-40
13. Horimoto N, Hepper PG, Shahidullah S, Koyanagi T. 1993. Fetal eye movements. Ultrasound in Obstet Gynecol 1993;3:362-9
14. Purves D, Riddle DR, White LE, Gutierrez-Ospina G. Neural activity and the development of of the somatic sensory system. Curr Opin Biol 1994;4:120-3
15. Mennella JA, Beauchamp GK. Maternal diet alters the sensory qualities of human milk and the nursling’s behavior. Pediatrics 1991;88:737-744
16. Mennella JA, Beauchamp GK. The transfer of alcohol to human milk: effects on flavor and the infant’s behavior. New Engl J Med 1991;325:981-85
17. Hepper PG. Adaptive fetal learning: prenatal exposure to garlic affects postnatal preference. Animal Behav 1988;36:935-6
18. Hepper PG, Scott D, Shahdullah S. Newborn and fetal response to maternal voice. J Reproduct Infant Psychol. 1993;11:147-53
19. DeCasper AJ, Spence MJ. Prenatal maternal speech influences newborns’ perception of speech sound. Infant Behav Devel 1986;9:133-50
20. Hepper PG, Scott D, Shahdullah S. Newborn and fetal response to maternal voice. J Reproduct Infant Psychol 1993;11:147-53
21. Porter RH. Mutual mother-infant recognition in humans. In: Hepper PG, editor Kin recognition. Cambridge: Cambridge University Press
22. Philip A. May, PhD, J. Phillip Gossage, PhD, Lesley E. Brooke,
BA(Hons), Cudore L. Snell, Dsw, Anna-Susan Marais, RN, Loretta S.
Hendricks, Julie A. Croxford, RN, BA(Hons) and Denis L. Viljoen, MD. 2005. Maternal Risk Factors for Fetal Alcohol Syndrome in the Western Cape Province of South Africa: A Population-Based Study. American Journal of Public Health Vol 95 (7), 1190-1199
23. Fowden, A.L. & Forhead, A.J. 2004. Reproduction 127 515-526, Society for Reproduction and Fertility.
24. Kashan A.S. et al. 2008. Arch Gen Psychiatry. 65(2):146-152.
25. Neugebauer R. 2005. Accumulating Evidence for Prenatal Origins of Mental Disorders. JAMA; 294:621-6239.
26. M. Weinstock. 1988. Prenatal Stress Increases Anxiety-Related Behaviour and alters Cerebral Lateralization of Dopamine Activity. Life Sciences 42: 1059-65.
27. O’Keane, V., Scott, J. 2005. Ed: From ‘obstetric complications’ to a maternal-fetal origin hypothesis of mood disorder. The British Journal of Psychiatry 186: 367-368.
28. O’Connor TG. Heron J. Golding J. Beveridge M. Glover V., 2002. Maternal Antenatal Anxiety and Children’s behavioural/emotional problems at 4 years. Report from the Avon Longitudinal Study of Parents and Children. British Journal of Psychiatry 180: 502-508.
29. O’Connor TG. Heron J. Golding J. Glover V. 2003, Maternal Antenatal Anxiety and behavioural /emotional problems in children: a test of a programming hypothesis. Journal of Child Psychology and Psychiatry 44:7 pp 1025-1036).
30. Glover, V. 2002. Editorial: Effects of antenatal stress and anxiety. British Journal of Psychiatry 180(5): 389.

1 thought on “The Origins of Infant Mental Health”

What do you think?