Tuesday, 28 October 2014

Intellect and infectiousness

In terms of title deeds to the planet, bugs are the freeholders, and we humans hold a short lease. Bugs got started long before us. We humans arose very recently, as a combination of micro-organisms: a bolted together job, cannibalising tiny biological gadgets useful for survival into one large-headed, improbable, bipedal ape.

The basic reproductive rate of a communicable disease is the number of new cases over the course of infection, in otherwise uninfected person who have not been vaccinated.  When R0 is above 1 the infectious disease spreads, below 1 it dies out. The rate is affected by the duration of infectivity of patients, the infectiousness of the organism, and the number of susceptible people in the population that the affected patients are in contact with.

There is an another factor, not directly mentioned but subsumed into the “susceptible people” calculation, which is whether you can tell whether infected persons are carrying an infection, which then allows you to avoid them. Avoidance may be costly in other ways, but it is usually effective.

The usual R0 calculations show how easily the various bugs can reproduce in human hosts. This is good science, and also makes sense, in that the methods of transmission are comprehensible. No miasmas here. Airborne bugs move from human to human easily,  bugs are conveyed fairly easily in droplets, and in fluids they are transmitted least easily of all.


So, when people say that Ebola is hard to catch, and that measles is more of a problem, they are probably quoting these figures, tabulated by WHO and CDC from various sources. Bugs can be rated for their dangerousness (forgive me for lumping together bacteria, viruses, prions, and all the rest) to the prototypical average human.

That last concept is somewhat fluid. Some humans move around a lot, like truck drivers; interact a lot, like prostitutes and salespeople; or stay at home a lot, like the elderly, the fearful, and bloggers. In other words, the basic reproductive rate is a useful rule of thumb, but not sacrosanct, and subject to revision. For the sexually promiscuous, HIV is dangerous; for the faithful or uninterested, HIV is largely irrelevant. For that reason, the above estimate of 2-5 new HIV cases per infected person reflect behavioural differences between persons and groups, in which intelligence and conscientiousness play a part. For fearful people who act upon their worries about germs, the rate of infection may be lower. For those who never wash their hands the rate may be higher. For parents who do not ask other parents in the class whether their children have been vaccinated, the rates of infection for their own children are probably higher. You cannot have herd immunity unless the herd is willing to cooperate. Cooperative varies from one society to another, depending largely on trust.

Hence, although the bugs themselves vary in virulence, humans vary in their capacity to defend themselves. Not knowing about germ theory (ignorance); not working things out by observation and deduction (lack of intelligence); and not bothering to change habits or protect others (lack of conscientiousness) all affect the infection rate. So, the “pure” reproductive rate needs to be corrected for impure, messy humans, and the main variance seems to lie in conscientiousness and intelligence. The more a society implements the health advice of their brightest researchers, the better their chances of survival. In an evolutionary sense, if people do not quickly change their habits they are at risk of dying. So, the cultural habit of touching and kissing dead bodies, intended to convey respect and love, needs to change fast. Also, people who do not understand contagion, from ignorance, lack of intelligence or lack of conscientiousness, or a combination of all three, will probably die more frequently than those who do.  Denying a disease exists is not clever. So, at the very end, the factors of conscientiousness and intelligence are tested every time an infection gains access to one person. Will it gain access to another, or die out?

Of course, knowledge and good organisation can be imported from outside any community, so good peripatetic teachers can change local behaviours, given time. Some men who would not otherwise have used condoms in Africa will do so if Bill Gates provides them. Some countries organise well, others badly. Knowledge and skills are either home-grown or bought in, and in an open society the best brains, from wherever they can be found, will be applied to the hardest problems, wherever those are found.

The medieval age did not know what caused the great pestilence. One third of the world died as a consequence, or so Froissart thought. Some at that time worked out the bare bones of how it was transmitted from person to person. They imposed quarantine (40 days isolation) and in those cases many lives were saved. The Pope took advice, and sat between two large fires at Avignon, and survived. Some just trusted to luck, dancing, and booze. Not much use, but one way to face likely death. The poor died more than the rich, because they were closer to the disease vectors, rats and fleas; and probably because they had lower defences physiologically.

In some ways the reproductive rate is a typical statistic: it conveys useful information, and leaves out important caveats. Notice I had highlighted that the rates are calculated for unvaccinated persons. Of course, vaccination is the prime example of the application of intelligence to disease control. From a planetary perspective, intelligence aliens will look for civilizations that know how to control diseases. Perhaps, rather than the little green men saying: “Take me to your leader” when they land, they will demand from behind a biohazard barrier “What bugs do you humans carry on this planet?”

The current concern about Ebola is understandable. Ebola is at the stage when it can be almost stamped out, reduced to small recurrent outbreaks over the years which can also be stamped out. If we fail the test and get it wrong then it will spread and be a permanent hazard, rather like AIDS which claims 2.5 million new cases every year. Measles had plenty of time to spread before we could do much about it. That is why it currently infects more people and kills more people in absolute numbers than does Ebola, at present. However, when comparing diseases we need to understand compounding, which changes the statistics rapidly. In military terms we have to stop the invasion before the virus has established a beach head.   We are being tested for our collective intelligence and diligence right now, when a disease known for 40 years (nothing in biological time, but a reasonable period for solving a problem in cultural time) has surged into a larger urbanised population, further from the forests and closer to the airports.

But, apart from intelligent things like vaccination, sterilization, disinfection, epidemiology, and the organisation of public health measures, what does intelligence have to do with disease control? Do diseases really test our intelligence and personality? Questions of that size require a number of answers, so I think we need to step back from the specific issue of infectious disease, and first of all look at the link between intelligence and health more generally.

Modern epidemiology has always understood the impact of class. Social class is easy and cheap to measure, and can even be estimated from afar by looking at people’s occupations, clothing, manners and wealth indicators. Intelligence is harder and more expensive to measure, and casual estimates are likely to be biased towards verbal ability. For all those reasons, IQ as an explanatory cause of variance has taken a back seat. Lastly, genomic analysis has become available only very recently, and is still very expensive, but it is very likely that it will scoop up some of the variance previously ascribed to environmental factors.

How good is the link between intelligence, health and lifespan? Intelligence is associated with better health and longer lifespans, but it is not entirely clear why. The early explanation was that more intelligent people learned quickly how to avoid health hazards. They gave up smoking sooner in life, bothered to read the medicine labels, and followed health advice generally. All this makes sense, and leads to some simple prescriptions: take care, take advice, read the labels, wash your hands and avoid riding motorcycles and putting your fingers in mincing machines.


Currently, it seems possible that both intelligence and health reflect a general underlying bodily system integrity, a fundamental mens sana in corpore sana which, if you are lucky enough to have it, gives you health, intelligence and long life without much exertion on your part. This insight arises from the fact that simple reaction time measures taken in later life (but not the more complex choice reaction time tasks one would have predicted) also show predictive power when it comes to longevity, and partly moderate the effects of childhood IQ. I will come back to that another time.

Always wanting to be on the right side of the very best research, I turned to Stuart Ritchie to suggest the key reference:

Catherine M Calvin, Ian J Deary, Candida Fenton, Beverly A Roberts, Geoff Der, Nicola Leckenby, and G David Batty. Intelligence in youth and all-cause-mortality: systematic review with meta-analysis. Int J Epidemiol. Jun 2011; 40(3): 626–644.


The authors did a systematic review and found 16 independent studies with a combined total of 1,107,022 participants. They checked for publication bias, and were able to exclude it. The bare results are as follows: A 1-standard deviation (SD) advantage in cognitive test scores was associated with a 24% (95% confidence interval 23–25) lower risk of death, during a 17- to 69-year follow-up. There was little evidence of publication bias (Egger’s intercept = 0.10, P = 0.81), and the intelligence–mortality association was similar for men and women. Adjustment for childhood socio-economic status (SES) in the nine studies containing these data had almost no impact on this relationship, suggesting that this is not a confounder of the intelligence–mortality association. Controlling for adult SES in five studies and for education in six studies attenuated the intelligence–mortality hazard ratios by 34 and 54%, respectively.

Before going into any details, it is worth underlining how poorly social class of origin performs in studies which include measures of childhood intelligence. The idea that class, in the sense of family environment and culture, acts as a canon which shoots us out a variable distance into society (small, poor, feeble guns sending their canon balls short distances; large, rich, powerful guns propelling their progeny long distances) appears to be in error. As to adult SES, I think that is more likely to be a creation of prior intelligence than a confounder. Equally, education in societies where it is free is more a measure of intelligence than a fully independent cause of advancement.

Individual differences in intelligence (cognitive ability, mental ability) test scores, as measured by standardized IQ-type tests in childhood, show an inverse association with risk of death from all causes throughout adulthood. That is, higher intelligence appears to confer protection. This finding is replicated in prospective cohorts from several Westernized countries,1 across different ranges of intelligence,2 and in follow-up periods from early through to late adulthood.2–4

Mental ability scores from early life are associated with later adulthood morbidities, and before any somatic symptoms or risk factors of disease are manifest, provide evidence that cognitive abilities may be predictive of later health outcomes.

A second issue yet to be evaluated systematically is the extent to which intelligence as a predictor of mortality is confounded by early-life environmental influences including socio-economic factors. Socio-economic status (SES) is established as an important determinant of public health inequalities,15–18 including risk of mortality, and it can carry influence in childhood, via factors such as family income and parental education, to predict individual differences in childhood intelligence.19,20 In this context, therefore, intelligence may be considered a mediating variable on the pathway between early-life influences and adult health outcomes. If early social factors substantially confound the link between intelligence and longevity, then adjusting for childhood SES would sizeably attenuate the effect size of the association between intelligence and mortality. In their systematic review, Batty et al.1 identified three out of nine studies that adjusted for childhood SES: one of these showed no change from an unadjusted model, and two had modest attenuating effects, suggesting that intelligence has independent effects on .

In a fixed effects model, a 1-SD advantage in intelligence was associated with the lower risk of all-cause mortality (HR 0.76, 95% CI 0.75–0.77) (Figure 3)risk of mortality from those of early socio-economic influences.

Nine studies that included 18,733 deaths, reported effect-size models adjusted for childhood SES, measured either by father’s occupation or income, 2,36,50,51,56,59,61 the highest socio-economic index recorded for either parent,3 or father’s education.53 Heterogeneity was very low in unadjusted (Q =8.56, I2=6.6%, P=0.38) and adjusted models (Q=7.49, I2=0.0%, P=0.48). In a fixed effects basic model the HR for this subgroup of papers did not deviate from the HR for the 16 studies (HR 0.76, 95% CI 0.75–0.77). However, even after adjustment for childhood SES there was a very small attenuation (by 4%) of the effect size (HR 0.77, 95% CI 0.75–0.79) (Figure 5). Excluding the large study of over one million Swedish men had no effect on the aggregate effect size of the childhood SES-adjusted model, except to slightly widen the 95% CI parameters (HR 0.77, 95% CI 0.74–0.80). Compared with the unadjusted model of this smaller group of studies in which there were 4608 deaths (HR 0.77, 95% CI 0.74–0.80), controlling for childhood SES had no effect on the intelligence–mortality gradient when the influence of this largest weighted study was removed.

This is a very important finding, given that some psychologists, when presented with intelligence test results that predict later outcomes, are absolutely sure that intelligence is caused by social class, and thus dismiss the findings out of hand.

The authors go on to “adjust” for later educational attainment, as if it were an externally imposed factor. I think this is incorrect, because in any society which offers free education, attainments will have a very large component of prior intellectual ability. So, to “adjust” in this way is to remove part of the effect of intelligence. However, they may have been indulging in bending over backwards to show exactly how the results would look if this (questionable) procedure were applied, even if they may doubt the fairness of the “correction” themselves. In fact, they reveal the latter point in the discussion: the results to date cannot tell us for certain whether education and adult SES are simply partial mediators of the association between intelligence and mortality, or whether the results reflect over-adjustments if both factors are partial surrogates for intelligence, or if these variables confound intelligence–mortality associations.

Among the six studies that adjusted for educational attainment, there were 16,023 deaths out of 1,026,742 participants.3,51,53,56,63,65 Again, the aggregate effect size for this subgroup of studies in an unadjusted model (HR 0.76, 95% CI 0.74–0.77) was no different from that for all 16 studies. After adjustment for education (HR 0.89, 95% CI 0.86–0.91), the effect of intelligence on mortality was reduced by 54.2% (Figure 5). Exclusion of the large Swedish cohort3 from the model, as expected, widened the CI parameters (HR 0.87, 95% CI 0.81–0.93), but still reduced the intelligence–mortality gradient by 45.8% from the unadjusted model.

In summary, intelligence is a good predictor of later health and lifespan, and is far better than social class of origin. That general pattern has been confirmed in many studies of individual disorders. For example, patients in the UK believe that cardio-vascular problems can be controlled by statins, and they have been led into these beliefs by their doctors. The Deary gang know better.


Does IQ predict cardiovascular disease mortality as strongly as established risk factors? Comparison of effect estimates using the West of Scotland Twenty-07 cohort study are revealing.

When CVD mortality was the outcome of interest, the relative index of inequality (sex-adjusted hazard ratio, 95% confidence interval) for the most disadvantaged relative to the advantaged persons was (in descending order of magnitude for the top five risk factors): 5.58 (2.89, 10.8) for cigarette smoking; 3.76 (2.14, 6.61) for IQ; 3.20 (1.85, 5.54) for income; 2.61 (1.49, 4.57) for systolic blood pressure and 2.06 (1.07, 3.99) for physical activity.

So, after smoking, low IQ is the biggest risk factor in cardiovascular disease, and by prescribing statins doctors are playing about with a pill which may reduce what is only a minor factor.

As we have seen, brighter people tend to live longer, but only partly because they take clever precautions, and partly because of a possible common factor which creates a good brain in a good body.

We can show that childhood IQ predicts later health. We can show that the IQ effect is more powerful than the different environments provided by different social classes in Western countries. Clearly, this raises the obvious corollary, if we can show an IQ effect in UK, USA, Sweden, Australia and Denmark, can we show that the IQ/health relationship holds in other countries across the world?

More of that later.


  1. "Always wanting to be on the right side of the very best research, I turned to Stuart Ritchie to suggest the key reference"

    Since I wrote a whole blog post based on that study, perhaps you should have turned to me? :)

    IQ and Death | JayMan's Blog

    At this point, the connection between IQ and lifespan is firm. There is no doubt that it is not due to privilege or better access to care that afforded by wealth.

    1. How long does the relationship hold (the studies tend to be short in duration, and don't follow the subjects all the way to death)?
    2. To what degree does it emerge from greater self-care, if at all?
    3. To what extent does it emerge from general bodily integrity?
    4. Does better immune function play a role?

    Not wanting to tip my hand, I will say there are studies that make significant headway in answering some of these questions. I'll say that at this point, we definitely need to move past basic correlational studies – even using reaction time. I will also say that it isn't shaping up well for better self-care explaining the association, at least in Western conditions.

  2. Dear Jayman, Reading it again (I remembered the del Sontro case) I should have contacted you! Put it down to fallible recall. 1 Duration need not be tremendously long, in my view. One gets indications after 15-20 years, I think. 2 Self care seems of little relevance within the normal range. 3 is the hot ticket at the moment. 4 Don't know, but Deary thinks that inflamation is a biomarker for physical distress and eventual poor health.
    Agree that Western level self care explanations are looking weaker at the moment, bar smoking.
    Getting past correlational studies will be very hard.

  3. I made this comment in a paper submitted just today:

    Relationships between g and health are ubiquitous and striking. Arden et al. (2009) postulated the existence of a general fitness factor to explain links between these constructs. We suspect that Jensen’s (1998) g nexus, Pesta et al.’s (2010) well-being nexus, and Arden et al.’s (2009) general fitness factor are converging on the same constructs.

    I hope it doesn't get rejected.

    1. I do wish you luck! But correlations between health, well-being, and intelligence are all small. While I have no problem with the idea that the relationships are all held in common and thus reveal an underlying factor of biological functioning, the variance explained by this will necessarily be small.

  4. Excellent. Hope it gets published. Let me know how it goes, so that I can comment on it.

  5. By the way, Dr. Thomson, you write about Ebola a lot; do you have any comments on http://awesomescience.us/disease-modeling ?

  6. Looks interesting. Argues in favour of behaviour change, which is also my view. Quarantine, avoidance of infected persons, changes in hand shaking rituals and funereal rituals should have a big effect. So, the reproduction rate of an infection is partly dependent on changeable human behaviour