Tag Archives: Developmental Plasticity

Orchids or Racehorses


Orchids and Racehorses

In the conference I attended this week in Paris, IACAPAP, I heard many stimulating presentations; I will probably write about some of them in the coming weeks. One that comes immediately to mind was by a researcher named Marius van Ijzendoorn, from Leiden.  

He was talking about how in the age-old Nature-Nurture debate we need to move back to taking Nature more seriously (Belsky & Pluess, 2009).  (In addition to Dr. van Ijzendoorn’s presentation, I derived much of the information in this blog from the important paper of Belsky and Pluess noted above. A wonderful discovery was that many of the papers cited in this paper were available on the internet free of charge.) That is not to say that Nurture is not important – far from it – but that Nature prepares children to respond differentially to the nurture they are given, and that the kind of differential responses we are talking about is not that simple. That was an interesting idea to me. It fit with something I have been telling parents for many years.

I also have noticed an implicit presumption made by much of the research into the environmental influences on early development. The presumption is that all children are affected equally by adverse environmental circumstances – whether poverty, maternal insensitivity, neglect, abuse, etc. This is evident in the studies of children reared in institutions, for example (Bos et al, 2011) (Cicchetti & Rogosh, 1997). 

When attention has been paid to individual child characteristics that contribute to the outcome, it is usually to say either that some children are relatively more constitutionally vulnerable to adverse environmental factors, or that other children – the lucky resilient ones – are less vulnerable. These resilient children are distinguished by – among other things – having a high IQ, a sense of humor, or a mentor to support their healthy development in ways that their parents are unable to do (Garmezy, 1985), (Rutter, 1987), (Werner, 1997). 

Another way of looking at it is to focus on “plasticity”. Children who are “resilient” are less plastic, or malleable, in relation to their experiences with the environment than others (Belsky and Pluess, 2009, p. 345).  What comprises this “plasticity”? In general, it seems that individual children differ in terms of three important markers of differential susceptibility, or plasticity – (1) early temperament; (2) physiological reactivity; and (3) genes. 

What van Izjendoorn and others have proposed is that instead of assuming all children are equally affected by adverse life circumstances, or that some individual children are particularly vulnerable or resilient because of their constitutions, we should consider a new paradigm – that of differential susceptibility (Belsky, 1997) or biological sensitivity to context (Ellis & Boyce, 2008).  This new proposal contends that for temperamental, physiological reasons, some children actually are more susceptible than others to both positive and negative rearing influences (Belsky, Bakermans-K, & van Ijzendoorn, 2007).  Belsky suggest that from an evolutionary point of view it was more advantageous for parents to bear children varying in plasticity, given that our ancestral parents could not have known any more than we know (despite the dogmatic trends in theories of parenting) which child rearing practices would be the most successful in promoting the reproductive fitness of their offspring. That way, if one child rearing technique proved to be problematic, those children who were not strongly affected by parental behaviors would not be adversely affected. 

From the perspective of temperament, two recent studies cited in Belsky & Pluess, found that infants with difficult temperament at 6 months (rated by their mothers)had both more behavior problems in early childhood in conditions of “low quality”, but also display fewer problems and more social skills than other children in conditions of “high quality” caregiving (Belsky & Pluess, 2009, p. 347).

 From the point of view of biological sensibility, children showing high reactivity (blood pressure) during a stress test had higher rates of respiratory illness, while when they were in low stress conditions had a significantly lower incidence of respiratory illness (cited in Boyce & Pluess, 2009, p. 347). In an interesting study by Boyce et al, when 7- year old children scored low in reactivity as indexed by salivary cortisol at the beginning of a stressful evaluation, father involvement in their care failed to predict mental health at age 9, whereas if they were high reactive, low levels of father involvement did predict mental health problems at that age (Boyce et al, 2006). 

As mentioned, genes also feature as a marker of differential susceptibility. In two studies,  Caspi et al, and Taylor et al, found that university students homozygous for short alleles of the serotonin transporter gene polymorphism showed greater depressive symptoms when exposed to early or recent adversity than did individuals with the other allelic variants, but individuals with this apparently vulnerable genotype showed significantly less depressive symptomatology when they experienced a supportive early environment or recent positive experience (cited in Belsky & Pluess, 2009, p. 347). 

What does all this mean to caregivers? Well, what I often tell the parents in my practice is that their children are “race horses” – that they need specialized care but they also have special potential. Then I do my best to help the parents learn how to provide that specialized care. The metaphor van Ijzendoorn used was orchids versus dandelions. He said that orchids (high susceptibility) need specialized care to bloom, but they are prized for their beauty, whereas dandelions (the “resilient” ones) can bloom anywhere but are usually not considered as beautiful. Actually, van Izjendoorn did not devalue dandelions and mentioned some interesting reasons having to with genetic studies that he is partial to them. The real message to my mind, though, is the hopeful one. If you have a child with high susceptibility to environmental influence, it is possible to create a caregiving environment that can support his or her growth in a positive way and produce a racehorse, an orchid. And dandelions are also beautiful, as my French friend, Gisele, explained, they are the first flowers that appear in her French garden as harbingers of Spring.  


Bakermans-Kranenburg & van Ijzendoorn, (2008). Oxytocin receptor (OXTR) and serotonin transporter (5-HTT) genes associated with observed parenting, Soc Cogn Affect Neurosci, 3(2):128-134.

Belsky, J. (1997). Variation in susceptibility to rearing influences: An evolutionary argument. Psychological Inquiry, 8:182-186.

Belsky, J, & Pluess, M, (2009). The nature (and nurture?) of plasticity in human development, Assoc for Psychological Science, 4 (4): 345-351.

Belsky, J., Bakermans-Kranenburg, M. & van Ijzendoorn, M. (2007). For better or worse: Differential susceptibility to environmentalinfluences. Current Directions in Psychological Science, 16(6):300-304.

Bos, K, Zeanah, C, Fox, N, Drury, S, McLaughlin, K, & Nelson, C (2011). Psychiatric outcomes inyoung children with a history of institutionalization, Harvard Review of Psychiatry, 15-24.

Boyce, T., Chesney, M, Alkon, A., Tschann, J, Adams, S, Chesterman, B, Cohen, F, Kaiser, P, Folkman, S, & Wara, D, (1995), Psychobiological reactivity to stress and childhood respiratory illness: Results of two prospective studies, Psychosomatic Medicine 57:411-422.

Boyce, T., Essex, M., Alkon, A., Goldsmith, H., Kramer, H., Kupfer, D. (2006). Early father involvement moderates biobehavioral susceptivility to mental health problems in middle childhood, JAACAP, 45:1510-1520.

Cicchetti, D., & Rogosh, F. A. (1997). The role of self-organization in the promotion of resilience in maltreated children. Development and Psychopathology, 9: 797-815.

Ellis, B. & Boyce, W (2008), Current Directions in Psychological Science, 17(3):183-187. 

Garmezy, N. (1985) Stress resistant children: The search for protective factors. In J.E. Stevenson, ed., Recent research in developmental psychopathology, 220-227.

Rutter, M. (1987). Psychosocial resilience and protective mechanisms, American Journal of Orthopsychiatry 57:51-72. 

Werner, E. (1993) Risk, resilience, and recovery: Perspectives from the Kauai longitudinal study, Development and Psychopathology 5:503-515.


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March Infant Parent Mental Health Meeting: Epigenetics I


Barry Lester taught us about epigenetics. He started with reviewing the background of “fetal origins” and the concept of “fetal programming”. Can the study of genes and environment at the cellular level inform us about molecular influences on behavior? The hypothesis states that susceptibility in cardiovascular disease, non-insulin-dependent diabetes mellitus, and the insulin resistancy syndrome, is programmed in utero as a response to fetal malnutrition. This dates to the German starving of Dutch mothers during World War II. There was a relationship between low birth weight and hypertension, 40 years later. The general concept is that reduced fetal growth leads to altered structure and function in the fetus, leading to increased risk for adult disease. During the famine, the fetuses were starving and they wanted to prepare themselves to survive in a famine environment. Instead, the famine ended and the babies were born into adequately nourishing environments. They had adapted their systems to slowed-down metabolism and couldn’t adapt. 

Developmental plasticity enables the organism to change, reprogram structure and function in response to environmental cues. The adaptive significance is that plasticity enables a range of phenotypes. Many studies have replicated this finding. The idea is that your risk of disease depends on the extent to which you are prepared for, or match with, the external environment. Can these effects be produced by environmental insults other than malnutrition? What might be the underlying mechanisms? Could epigenetics provide the molecular basis for fetal programming? What might be the applicability of this model beyond chronic disease to behavior? 

There is evidence that the fetal origins theory relates to the etiology of neurobehavioral problems and mental illness. Low birth weight is related to schizophrenia, depression, and psychological distress.  What is the molecular basis?

Epigenetics has to do with the heritable and stable control of gene expression beyond DNA sequence. It is heritable – can be passed on to successive cells – yet does not alter the genetic sequence, and inter-generational. It is stable and cannot be altered. It is environmentally sensitive. There are critical periods (a lot of this happens in periods of rapid development) and reversible. Epigenetics controls gene expression and transcription, turning off and on the gene. The gene stays the same, but what the gene makes happen is changed. Conrad Waddington (Professor Genetics, Univ. Edinburgh, 1905-1975) described epigenetics as “cross talk” between the gene and the environment. 

Epigenetic changes happen all the time. The field started in cancer. Epigenetic research has since expanded into behavior. Barry’s “favorite example” is that in which the mother is a drug addict and is loaded with addiction genes. If you could turn them off, the baby will inherit the same DNA but will not inherit the addiction. This is pure fantasy but possible. Epigenetics refers to the changes in gene activity, expression, without changing the gene. It can be silenced, enhanced, and change can be transferred to the next generation some of these changes can be reversed. 

The most common mechanism in which environmental influences can produce stable alterations is DNA methylation. (Histone is another one. The outer layer of the package of DNA is histone.) The metaphor is gum on a light switch. Epigenetic changes occur when genes are being replicated. The DNA is transcribing to RNA and that is producing proteins. The amino acids guanine and cytosine hang out at the gene transcription sites – CPG islands. A protein puts little methyl tags on the gene. That is like gum on a light switch; it turns off the gene. 

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