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We need early interventions or else it is too late

Leading medical groups and charities writing in the Independent in October 2014 welcome ‘the fact that the NHS has risen to the top of the political agenda and some new spending commitments have been made.’ (letter to the editor, The Independent, 5th October 2014).  While new spending commitments are commendable, there is a degree of naivety in how the crisis in healthcare is being understood. More than anything this is because the roots of so many health problems are in very early experiences. They start with psychological stressors, or rather psychobiological insults, which affect which genes are turned on or off, an epigenetic effect that is believed to transmit across generations (Gaydos et al. 2014). An old-fashioned medical model in which current, and purely physical, symptoms are identified and treated can no longer be sufficient. 

In an important letter in the Guardian, Dr Sebastian Kraemer pointed out that ‘the reason that the NHS is getting so expensive is that there are more ill people – obesity and type 2 diabetes are just the tip of an iceberg of preventable disorders. These are not so much lifestyle diseases as life-cycle ones, because the origins of so much chronic illness lie in the earliest stages of life. The best time to reduce it is during pregnancy and the first months of infancy.’  He is arguing for new funding to be spent on a  ‘wraparound physical and mental perinatal service for all…. which will in due course pay for itself in better population health.’ 

Politicians and the medical profession need to grasp fully the profound physical effects of not just poor living conditions but also of poor psychological conditions, in which children are brought up amidst high levels of stress, anxiety, anger, fear, contempt and too often overt abuse and trauma. These all cause serious and often life long psychological and physical health problems. 

A burgeoning body of research shows how exposure early on to stress has a profound physical effect, altering immune functioning, increasing the risk of all manner of diseases later on in life, from diabetes and heart-disease and even cancers. The classic study, a longitudinal one of over 17,000 people, called ACE, measured Adverse Childhood Experiences, and not surprisingly found that the more bad experiences, the worse the outcomes.

For example, one recent paper  (Van Niel et al. 2014) showed that  ‘the major risk factors for causes of death in adults - smoking, alcohol abuse, obesity, physical inactivity, use of illicit drugs, promiscuity, and suicide attempts -  were all increased by ACEs. Compared with persons with an ACE score of 0, those with an ACE score of 4 or more were twice as likely to be smokers, 12 times more likely to have attempted suicide, 7 times more likely to be alcoholic, and 10 times more likely to have injected street drugs’ (2). These are scary statistics. 

In another important recent paper (Romens et al. 2014) we learnt how what we knew about other mammals is also true of humans; the authors found that studies consistently demonstrated that stress or trauma was correlated with higher methylation of a gene, exon 1F of NR3C1, also affected by trauma in animals such as rats. This was shown, for example, by examining brain tissue of deceased human adults who had committed suicide following a history of child abuse (McGowan et al. 2009), the spinal cord blood of infants with depressed mothers (Oberlander et al., 2008), white blood cells of adults with borderline personality disorder or major depressive disorder with a history of child sexual abuse (Perroud et al. 2011) blood of adults with bipolar disorder and a history of child abuse (Perroud et al., 2014), and of adolescents whose mothers were exposed to intimate partner violence during pregnancy  (Radtke et al. 2011) 

As we know from life-course theory (Belsky et al. 2012; Hochberg and Belsky 2013), more stress and anxiety and worse early experiences give rise to speeded up metabolic systems, and increased risk of all kinds of disease. If you are bullied as a child there is more likelihood of higher levels of inflammation, a biomarker for ill-health well into adulthood (Copeland et al. 2014). Similarly social isolation in childhood is linked with higher levels of inflammation and mental and physical problems in adulthood (Lacey et al. 2014). We can try to treat these diseases in mid-life when they manifest themselves, but wouldn’t we be a whole lot better off if we tried to tackle these problems at their core, early on? 

One of the best predictors of illness and early death is shorter telomeres, which are caps on nerve cells. For example, shorter telomere length is hugely associated with family violence (Drury et al. 2014), but also with general life stresses (Epel et al. 2004). There is much other evidence showing how telomeres are profoundly affected by bad experiences. Indeed, telomere length is even affected by exposure to stress in intrauterine life (Entringer et al. 2011), and we also know the profound effects of prenatal stress on the developing infant’s nervous system and other developmental capacities (Glover 2011; Colman et al. 2012; Walder et al. 2014; Howerton and Bale 2012; Michelsen et al. 2007).

This is only the tiniest hint of the mass of evidence that shows how bad emotional experiences literally get under the skin, and that our early experiences “program” our bodies for the future.
As Dr Kraemer urges, we can’t afford not to act in the early years, and then throw money at the end result of problems that were being laid down in very early childhood, infancy and indeed in prenatal life. We need to be arguing instead for social justice alongside more psychological understanding of the impact of bad experiences, and we need interventions, the earlier the better, that build on this new knowledge.

Graham Music
Originally posted in Psychology research and child development blog, September 2014
Adapted for Foundation Years Information and Research, October 2014




Belsky, J., Schlomer, G.L. and Ellis, B.J. 2012. Beyond cumulative risk: Distinguishing harshness and unpredictability as determinants of parenting and early life history strategy. Developmental psychology 48(3), pp. 662–673.

Colman, I., Ataullahjan, A., Naicker, K. and Van Lieshout, R.J. 2012. Birth weight, stress, and symptoms of depression in adolescence: evidence of fetal programming in a national Canadian cohort. Canadian journal of psychiatry. Revue canadienne de psychiatrie 57(7), pp. 422–428.

Copeland, W.E., Wolke, D., Lereya, S.T., Shanahan, L., Worthman, C. and Costello, E.J. 2014. Childhood bullying involvement predicts low-grade systemic inflammation into adulthood. Proceedings of the National Academy of Sciences 111(21), pp. 7570–7575.

Drury, S.S., Mabile, E., Brett, Z.H., Esteves, K., Jones, E., Shirtcliff, E.A. and Theall, K.P. 2014. The association of telomere length with family violence and disruption. Pediatrics 134(1), pp. e128–e137.

Entringer, S., Epel, E.S., Kumsta, R., Lin, J., Hellhammer, D.H., Blackburn, E.H., Wüst, S. and Wadhwa, P.D. 2011. Stress exposure in intrauterine life is associated with shorter telomere length in young adulthood. Proceedings of the National Academy of Sciences 108(33), pp. E513–E518.

Epel, E.S., Blackburn, E.H., Lin, J., Dhabhar, F.S., Adler, N.E., Morrow, J.D. and Cawthon, R.M. 2004. Accelerated telomere shortening in response to life stress. Proceedings of the National Academy of Sciences of the United States of America 101(49), pp. 17312–17315.

L. J. Gaydos, W. Wang, S. Strome. H3K27me and PRC2 transmit a memory of repression across generations and during development. Science, 2014; 345 (6203): 1515 DOI: 10.1126/science.1255023

Glover, V. 2011. Annual Research Review: Prenatal stress and the origins of psychopathology: an evolutionary perspective. Journal of Child Psychology and Psychiatry 52(4), pp. 356–367.

Hochberg, Z. and Belsky, J. 2013. Evo-devo of human adolescence: beyond disease models of early puberty. BMC Medicine 11(1), p. 113.

Howerton, C.L. and Bale, T.L. 2012. Prenatal programing: At the intersection of maternal stress and immune activation. Hormones and Behavior 62(3), pp. 237–242.
Lacey, R.E., Kumari, M. and Bartley, M. 2014. Social isolation in childhood and adult inflammation: Evidence from the National Child Development Study. Psychoneuroendocrinology 50, pp. 85–94.

McGowan, P.O., Sasaki, A., D’Alessio, A.C., Dymov, S., Labonté, B., Szyf, M., Turecki, G. and Meaney, M.J. 2009. Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse. Nature neuroscience 12(3), pp. 342–348.

Michelsen, K.A., van den Hove, D.L.A., Schmitz, C., Segers, O., Prickaerts, J. and Steinbusch, H.W.M. 2007. Prenatal stress and subsequent exposure to chronic mild stress influence dendritic spine density and morphology in the rat medial prefrontal cortex. BMC Neuroscience 8, p. 107.

Van Niel, C., Pachter, L.M., Wade Jr, R., Felitti, V.J. and Stein, M.T. 2014. Adverse Events in Children: Predictors of Adult Physical and Mental Conditions. Journal of developmental and behavioral pediatrics: JDBP.

Perroud, N., Paoloni-Giacobino, A., Prada, P., Olie, E., Salzmann, A., Nicastro, R., Guillaume, S., Mouthon, D., Stouder, C. and Dieben, K. 2011. Increased methylation of glucocorticoid receptor gene (NR3C1) in adults with a history of childhood maltreatment: a link with the severity and type of trauma. Translational psychiatry 1(12), p. e59.

Radtke, K.M., Ruf, M., Gunter, H.M., Dohrmann, K., Schauer, M., Meyer, A. and Elbert, T. 2011. Transgenerational impact of intimate partner violence on methylation in the promoter of the glucocorticoid receptor. Translational Psychiatry 1(7), p. e21.

Romens, S.E., McDonald, J., Svaren, J. and Pollak, S.D. 2014. Associations between early life stress and gene methylation in children. Child development.

Walder, D.J., Laplante, D.P., Sousa-Pires, A., Veru, F., Brunet, A. and King, S. 2014. Prenatal maternal stress predicts autism traits in 6½ year-old children: Project Ice Storm. Psychiatry Research.