Childhood adversity and lifespan

 

Here is a study which deserves attention, based on an excellent sample which is dear to me and to many social scientists: the 1958 National Child Development Study (NCDS) which included all live births during 1 week in 1958 (n = 18,555) in Great Britain. If any dataset deserves a monument, this one does. For my generation of psychologists it provided a steady flow of publications on child development, so it is natural to regard it as one of the family, a familiar companion. Their 1972 “From Birth to Seven” had a great impact, serving as a benchmark for the times. Call it the thinking person’s “Seven Up” (a film which tracked a few children).

Now a new team have looked at this old warhorse again, and compared each child’s  documented early childhood “adverse experiences” with their lifespan, finding that real adversity has shortened lifespans. More specifically, a total of 3.2% of all the sample were dead before 50 and for the boys, where the adversity effect was strongest, the low rate of death doubled for those who had two or more adverse events. (The great advantage of a contemporaneous record of these experiences is that we do not have to rely on faulty and possibly biased recall in adulthood). The finding makes sense, from a trauma point of view. The child has been subjected to a dreadful event, the trauma has embedded itself during a sensitive period in development, and as a consequence children’s resources have been diminished,  and it all comes out in the end, by causing a somewhat premature end. An unpleasant finding, but a salutary one, since it shows how vulnerable children are to external events.

The effect is only slightly diminished by controlling for the effects of social class and education. In summary: an impeccable sample, distinguished authors, appropriate statistics, and a clear exposition of the effects in copious tables. It is natural that UCL should choose to mention it in their weekly newsletter, which is where I found out about it. As someone who worked for a long time in trauma, the paper is particularly welcome. Case proven.

http://link.springer.com/article/10.1007%2Fs10654-013-9832-9/fulltext.html

Before turning away, have a look at the list of adverse events.

1. Child in care: child has ever been in public/voluntary care services or foster care at age 7, 11 or 16.

2. Physical neglect: child appears undernourished/dirty aged 7 or 11, information collected from the response from child’s teacher to the Bristol Social Adjustment Guide.

Household dysfunction, as described by Felitti et al. [16], is a dimension of adversity consisting of four categories each contributing to the score:

3. Offenders: The child lived in a household where a family member (person living in the same household as the child) was in prison or on probation (age 11 years) or is in contact with probation service at 7 or 11 years; the child has ever been to prison or been on probation at 16 years.

4. Parental separation: The child has been separated from their father or mother due to death, divorce, or separation at 7, 11 or 16 years.

5. Mental illness: Household has contact with mental health services at 7 or 11 years; Family member has mental illness at 7 and 11 or 16 years.

6. Alcohol abuse: Family member has alcohol abuse problem at 7 years.

About 5% to 7% of the total sample had experienced these events, which put them in what we might call the troubled minority.

Now comes the question: which of these events are truly external? To prompt you, in case you find the question hard: what sort of parents end up with their children in care; physically neglect them; get put in prison; have mental illness; abuse alcohol; and cannot stay together when their children are young and need them? Might they conceivably be parents who are not passing on the very best genes to their offspring? Far from being external, I see these events as arising from bad parenting, and one very vivid possibility is that the offspring have been subjected to a double burden: bad experiences, and genes which make them vulnerable. Even if the authors find it hard to countenance the notion of the heritability of mental illness (see previous post below on “Bad Blood”), one expects some comment.

So, how do the authors deal with this possibility? They do not mention it.

Here is what they say about “prior confounders”: “To examine the relationship between ACE and premature death, prior confounding variables potentially associated with both ACE and mortality were adjusted for in the multivariate models. Among the variables available at baseline, collected from the cohort member’s mothers via a questionnaire at birth, we identified those most likely to be social or biological confounding factors. Household and parental characteristics were included: mother’s age at birth, overcrowding (people-per-room), mother’s partner’s social class (manual/non-manual), and if this was unavailable the mother’s father’s social class was used, mother’s education level (left school before/after minimum leaving age), and maternal smoking during pregnancy (no smoking/sometimes/often/heavy).”

As you will see, there are many things about the parents which they do not know, presumably because they were not asked in the original survey. Social class and education are certainly a help, but they are rather broad categories, and hardly a proxy for biological markers.

What else could these authors have done? Well, they could have looked at intelligence measures, since lower intelligence is associated with shorter lifespans. The children’s intelligence was measured at 11. It does not cover all the possible biological markers, but is associated with it. Finding no association at all would strengthen the trauma explanation.

Gale et al. included intelligence in a study on this sample’s smoking rates, and found “women with lower IQ in childhood were more likely as adults to smoke during pregnancy and to be a smoker currently. Structural equation modelling showed that the effects of childhood IQ on smoking behaviour were indirect, as they were statistically mediated by educational attainment and age at first birth. There was some effect of educational attainment and age at first birth on smoking behaviour over and above the effect of intelligence.”

http://www.ncbi.nlm.nih.gov/pubmed/18812363

If the data are there, why not use them? The authors of the current paper did take measures of education, social class and health at age 23 and they say “in our model, these adult variables at the age of 23 are a proxy for behavioural patterns in early adulthood and controlling for them serves as a first step to understanding possible mechanisms.” Controlling for those did reduce the hazard ratios somewhat.

What could they have done? I assume that in this study the age at death of the parents is known. If the pattern of premature death is as strong in the parents as in their children (for the sample as a whole, not just the adverse event group) that would be germane, and would weaken the trauma-leads-to-death argument.

In summary, I think that a few more checks would potentially strengthen this study. The effect they have found seems noteworthy, but they could at least have mentioned a genetic explanation. In terms of exploring alternative hypotheses,there are so much data in this goldmine of child development that it would be a pity not to complete the picture.

There is one other thing the authors could have done. They could have changed their title to: “Adverse parenting and premature mortality”

Good sample, though.