Mental Ageing Q&A

Form this analysis alone we can only technically claim correlation.  The life course variables (father’s occupation, mother’s education, own cognitive development, education, own occupational complexity, National Adult Reading Test [NART]) may indeed have causal relationships with the ACE-III, but we would need further analyses to be truly confident about this.  However, I think we can be reasonably confident that the associations within cognitive function (childhood cognition to the NART, NART to ACE-III and childhood cognition directly to ACE-III) are indeed causal.

David Winnicott (https://en.wikipedia.org/wiki/Donald_Winnicott), who happens to be a hero of mine.

Among many other things he wrote about childhood daydreaming:

https://www.oxfordclinicalpsych.com/view/10.1093/med:psych/9780190271411.001.0001/med-9780190271411-chapter-46

We can look to see if your performance on the various measures of physical capability (grip strength, walking speed, standing balance) differs from those who did not have a condition that could affect this.  We can do this directly by comparing two groups, e.g. those who did and did not have a stroke.

However, since stroke is still relatively rare in the cohort, more commonly we perform what is called a ‘sensitivity’ analysis, where we look at predictors of physical capability across the whole cohort, then see if results are similar when we repeat the analysis after taking out those with stroke.

We haven’t yet looked at this in NSHD, but studies elsewhere (for example using the Wisconsin Longitudinal Study) suggest that voluntary delayed retirement is associated with higher cognitive function, whereas the opposite tends to be true for early retirement on medical grounds).

We do however plan to look at this carefully in NSHD, where you provided detailed information on timing of, reasons for, and life course predictors of, retirement.

I’m not an expert on this, but from what I can see this is not supported by research: https://www.scientificamerican.com/article/fact-or-fiction-antiperspants-do-more-than-block-sweat/

Ditto for aluminium in pots and pans: https://www.alzheimers.org.uk/about-dementia/risk-factors-and-prevention/metals-and-dementia

To answer the last question first, we cannot obtain new data from participants who have permanently withdrawn from the study, most importantly because we do not have their consent for this. What we do know, however, is that those who have withdrawn tend to be less healthy and less economically and socially advantaged than participants who remain in the study; this is consistent with most longitudinal health studies in the world.

Regarding premature death, my colleague Dan Davis found that this was predicted by cognitive function in early midlife: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6639118/

Some people have argued that education is nothing more than a ‘proxy for IQ’, and by extension that it’s all in our genes and there’s nothing we can do to change our cognitive capability.  At the risk of getting political, this view was revived by Dominic Cummings when he was advisor to Michael Gove at the Department of Education during the coalition government: it’s not education that’s important but the abilities that children already have and bring to the classroom that matter.  I think the evidence from NSHD strongly argues against this, since the path model in my first slide clearly shows that education is associated with later cognitive function even after taking account of cognitive development.  You can look at the paper itself via this link, and see that I refer to this issue in the Discussion: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6502022/

Or if you prefer, here’s a letter I wrote in response to  one of the ‘proxy for IQ’ proponents: https://academic.oup.com/ije/article/40/2/516/731247