The link between tonsil and appendix removal and higher fertility is due to life history strategy

The fast life history strategy is associated with both lower levels of somatic maintenance, which results in worse health, and earlier and more frequent childbearing. As such, it is the underlying factor in the link between appendix and tonsil removal, and more frequent pregnancies and higher birth rate. Inflammation, as a signal and consequence of worse overall health, would also be expected to speed up reproduction in itself, as part of the adaptive response to shorter expected (healthy) lifespan.

There is no evidence in the recent study for a causal effect of appendectomy or tonsillectomy on subsequent fertility. The control group would need to be women with similar rates of inflammation but who didn’t have the procedures, whereas in the recent study it was just women matched for age and practice. It is therefore not possible to conclude, as one study author did, that “More importantly, looking at both the appendix and tonsils together, this study confirms beyond doubt that removal of inflamed organs or organs likely to suffer from repeated inflammation, in women, improves their chances of pregnancy.”

Technically, it doesn’t necessarily mean that appendectomy has no negative effect on fertility, as the cohort who have had the procedure may have otherwise had even higher levels of fertility than the control group.

The Dundee team involved in the research take a behavioural  view of the evidence, with “women enjoying more “liberal sexual activity”, being both more likely to get pregnant and have pelvic inflammatory disease.” More “liberal sexual activity” is another trait of the fast life history strategy, so can be seen both as a proximate cause, and as another component of the coherent suite of biological and behavioural traits which serve to accelerate our life cycle, in order to calibrate it with our life expectancy given our environmental conditions.


By Breck MacGregor

Excess mortality in Glasgow and Scotland – a statistical artefact?

Faster life histories (LHs) underlie the excess mortality in Glasgow and Scotland. They are particularly consistent with premature mortality from risky behaviours, and may also contribute to overall mortality from chronic diseases.

Far from being pathological however, faster LHs evolved as an adaptive response to dangerous and unpredictable circumstances, where long-term survival is uncertain. LH theory simply describes the calibration of someone’s life course to the length of time they can expect to stay alive.

Risk-taking behaviour pays off more in unpredictable environments, where the benefits of long-term investment may not be realised. As a result, we have a tendency to “discount the future” and prefer immediate rewards in such situations. The relevance to drug and alcohol abuse is clear – they are used as a short-term escape from ongoing problems.

Future discounting is also reflected in ways of attaining status – education only leads to higher status in the long term, whereas risk-taking behaviours can lead to immediate social status (especially among males). Excess deaths from road traffic accidents are highest in young males, as driving fast is seen as a way of attaining status. Male competition drives the violence that leads to other excess deaths. Fast LHs, which encourage competition, are triggered by factors like low status and resource scarcity. This is because natural selection acts on reproduction as well as survival – we need to do both for our genes to survive. Low status males have nothing to lose, with dire prospects of reproduction and survival.

Lower investment in long-term health contributes to the excess overall mortality from chronic diseases. This is not just the result of conscious decision-making. At the heart of LHs is a trade-off between growth and reproduction. Curtailed growth means faster maturation and so reproduction, but comes at the cost of lower biological investment in the immune system, tissue repair and maintenance. A lifetime of lower investment in health inevitably leads to the earlier onset of chronic diseases, and higher mortality rates because of them. Unfortunately this is mostly irrelevant in evolutionary terms, as after we stop reproducing, it makes little odds to natural selection whether we die at 65 or 85. (An interesting exception may be due to grandmaternal care, which is a theory why the human menopause evolved, and why women live longer).

Faster LHs explain why poverty and inequality cause worse health and social outcomes. But why are LHs in Glasgow and Scotland even faster than would be expected after accounting for these risk factors? The Glasgow Centre for Population Health recently published a new synthesis of evidence on the excess mortality. The hypotheses in it can be compared to established triggers of faster LHs, to see if they are feasible threats to long-term survival and reproduction. Any potential trigger may not actually threaten survival in modern society, but as a species we evolved largely in small bands of hunter-gatherers, and in this context responses to threats can be understood as more adaptive.

The first factor proposed is historical overcrowding. This was a problem in Glasgow and Scotland from around 1939 until after 2000. The extent was significant – in 1971, overcrowding was more than twice as widespread in Glasgow than in Liverpool or Manchester, across every deprivation decile. In the most deprived decile, more than 60% of households were overcrowded in Glasgow, compared to less than 30% in the English cities.

A time lag would be expected between exposure and a rise in mortality, due to life course effects – early exposure can take a lifetime to manifest itself. The gradual increase of the portion of mortality unexplained by deprivation fits with a mini “epidemic” of people affected by overcrowding growing old and appearing on the mortality statistics. In 1981, most of the higher mortality could still be explained by deprivation, but this declined over the next 20 years according to the previous synthesis of evidence by GCPH.

However, the emergence of unexplained mortality since 1981 may also partly be an artefact of the marked decline of overcrowding during this period. Overcrowding is one of four components of the Carstairs Index, along with car ownership, male unemployment and social class. The index is used to account for area deprivation. In 1981, overcrowding was twice as common in Glasgow as in Liverpool and Manchester, but it is unclear why this should immediately have led to higher mortality (indeed it is likely that all components of the index would show a significant lag effect).

There is no reason to expect mortality to follow immediately as overcrowding declines, as its effects can take a lifetime to show up in mortality statistics. The inverse is that higher levels of mortality from 1981 onwards can be seen as the lagged effect of pre-1981 overcrowding. It just happened to be around 1981 when overcrowding started to decline, creating the illusion of a new phenomenon emerging. The reason for the emerging excess isn’t (just) that mortality decreased more slowly in Glasgow over the past few decades; the decline in overcrowding meant that deprivation accounted for less and less of the mortality.

The natural response is to look for any conditions which worsened around that time, which could have caused the increasing excess mortality. If though it is just an artefact of lagged deprivation, the opposite in fact applies: the rapid improvement in overcrowding created the statistical excess. A more ecologically valid way of accounting for deprivation may be to introduce a lag period in the analysis itself. This could be done by adjusting mortality statistics with the deprivation measure from a certain number of years previous.

The decline in the percentage of mortality in Glasgow which the Carstairs Index can explain between 1981 and 2001 correlates almost perfectly with the decline in overcrowding during the same period. There is no equivalent unexplained excess of poor health, as there is no (or a much shorter) time lag from exposure to outcome. Conversely, people don’t die young solely because of what happens to them in the last year or even decade of their life.

The authors don’t seem to see the excess as the result of the decrease in the deprivation profile: However, the causal pathways are complex, and the relationship [of overcrowding] with excess mortality less clear, given that the excess has increased over a period in which Scotland has become relatively less deprived compared with the rest of Britain.” The two measures are partially confounded however, as the measure of deprivation is used to establish the level of excess mortality. In addition, two of the four components of deprivation (overcrowding and car ownership) have seen Scotland close the gap to England and Wales between 1981-2011.

People born in 1991 would be amongst the first to experience lower levels of overcrowding from birth. In 2011, they would have been 20 – barely old enough to register on premature mortality. As their generation ages though, there would be an expected plateau or decrease in premature mortality, if early years exposure to overcrowding and deprivation more generally is driving the excess mortality. This process of improvement may be slowed by intergenerational effects, including epigenetic effects, which perpetuate the influence of a stressor even after it has been removed. Rats born to depressed or anxious mothers showed increased DNA methylation at the glucocorticoid receptor gene, and increased stress reactivity. Overcrowding is a risk factor for poor mental health, suggesting a potential mechanism for overcrowding to harm health both directly and through intergenerational epigenetic effects.

The lagged effect of overcrowding might predict that premature mortality would show an excess before all age mortality did. If this model is correct, exposure to overcrowding would move through the population as it ages, and premature mortality from overcrowding would be expected to decline before a similar reduction in overall mortality.

Another effect would be that it is the same population exposed to overcrowding that shows up in both premature mortality and all age mortality. This could explain the excess being bigger for premature mortality (around 30% compared to 15%), as exposure shifts mortality towards younger ages. This has a disproportionate effect on premature mortality simply because many fewer people die before the age of 65.

The same process could also contribute to the strong socioeconomic gradient that is shown for premature mortality. Within the exposed cohort, people of low SES face a double disadvantage, and so are much more likely to die before 65. Over-65s in the exposed cohort are therefore disproportionately of higher SES, which cancels out the social gradient in mortality. In overall mortality, this translates into the flat pattern of excess mortality across deprivation deciles. There is still an excess as exposed, high-SES people die younger than non-exposed people of equivalent SES in the comparator areas.

A life course approach may also shed light on low SES groups suffering more early deaths. Early life SES is a strong predictor of SES in early adulthood, and young people experiencing low status both during childhood and currently are at much higher risk. As people age, the correlation between childhood and current SES weakens (although social mobility has declined since the 1980s). People who have moved up or down the social ladder over their life cloud the picture, and flatten the social gradient in all-age mortality. This is consistent with the “health constraint” hypothesis, which posits that socially mobile individuals have health characteristics of both SES groups they move between, minimising health differences between groups.

The other side of the lagged deprivation argument is that it might predict there would be a time period when overcrowding had begun to rise higher in Glasgow, but before it had time to have an impact on mortality. Mortality would then actually be lower than expected given contemporary deprivation as measured by overcrowding.

Early exposure is the core tenet of a cohort effect like this. People who grow up in Scotland and move away still show “Scottish” levels of excess mortality. Conversely, people who grow up elsewhere in the UK and move to Scotland retain lower levels of adult mortality. Both lines of evidence support the theory that early life exposure of some kind is driving the excess mortality in Scotland. Early exposure is also consistent with a “critical period”, during which LHs are calibrated.

The causes of death seem to reflect a cohort process too. The earliest causes, like drug and alcohol abuse and suicide, show a much bigger excess. The lower excess for later-life causes, like cancer and heart disease, may reflect the smaller cohort surviving long enough to contract and die from these diseases.

In terms of the mechanism by which overcrowding harms later health, established disease mechanisms have already been identified. Risk factors of overcrowding like early infections, damp, mould and disturbed sleep, all documented by a report by Shelter into poor housing, could all lead to worse later-life cardiovascular health.

High exposure to infectious diseases is however known to be a vital LH variable. Populations around the world with exceptionally high pathogen loads have independently come to the solution of radically curtailing growth, and become what are commonly known as pygmies. They die much younger on average than other populations, so have to prioritise early maturation and reproduction, at the expense of adult height.

Clearly, Glaswegians aren’t exposed to dangerous levels of tropical diseases. But socioeconomic status (SES) is a strong predictor of both adult height, and of exposure to overcrowding. Height itself correlates with health status. Again, faster LHs can be seen as the overarching factor, reducing height and worsening long-term health.

The effect of infections on LHs may be twofold: firstly, as an indicator of higher general pathogen load in the environment, which predicts more frequent future illnesses. Secondly, early infections can compromise ongoing health status, increasing susceptibility to future insults. Both are important predictors of expected lifespan, and lead to the perhaps counterintuitive outcome that in conditions where health is at risk, the adaptive solution is to sacrifice investment in long-term health.

Another theory put forward in the new synthesis of evidence is that housing policy, especially the building of New Towns and peripheral council estates, increased Glasgow’s vulnerability to poverty and deprivation. The socially selective process of populating the New Towns must have broken up established communities. Slums were cleared, and housing estates and high-rise flats were built on a much larger, and arguably inhuman scale in Glasgow than in Liverpool or Manchester. This suggests the scattering of traditional communities must have been greater. The resulting loss of community described by concepts like social capital and connectedness is thought to be an important social determinant of health.

From a LH perspective, social support is crucial in a social species to long-term survival and reproduction. Any perceived lack of affiliative relationships is likely to affect LHs by speeding them up, as throughout evolutionary history, threats to personal health and safety like victimisation or famine were better resisted with support from kith and kin. Normally, levels of support may be captured by measures of SES, but the fracturing of communities may have decimated support networks, without increasing deprivation per se.

Perhaps significantly, the resettlement was carried out along class lines, with the New Towns “skimming the cream” off Glasgow. The resulting social stratification may have undermined feelings of social solidarity, encouraging a more individualistic, hierarchical outlook, leading to increased status anxiety.

The democratic deficit argument, that Scots and Glaswegians in particular felt a lack of control over their lives from the 1980s onwards, chimes with the psychosocial risk of feeling out of control of one’s life, as the authors point out. LHs may be the mediating factor here, accelerating people’s lives in response to the inherent unpredictability of circumstances at the time.

The huge increase in premature mortality from around 1980 would appear to need a cause that emerged at the same time. Thatcherism is the obvious candidate, but any explanation needs to show why Glasgow and Scotland were particularly disadvantaged. The response of local government is cited as exacerbating UK economic policy in Glasgow, whereas it was mitigated in the other cities. This is linked to the lack of social capital, as lower levels of politicisation meant that there was less opposition to commercial development ahead of social investment in Glasgow.

A final specific risk factor identified was negative physical environment, in particular the amount of vacant and derelict land. This has already been explicitly linked with LHs, with the density of dilapidated structures found to be independently correlated with premature births and low birth weight in the area, two fast LH traits. These are bad health outcomes for infants, but they are also associated with worse lifelong health outcomes, and so increased mortality. The rationale is that dereliction signifies the unpredictability of future outcomes, in turn encouraging riskier reproduction.

Faster LHs are clearly implicated in the biological, cognitive and behavioural strategies which result in the excess mortality in Glasgow and Scotland as a whole. Several of the new hypotheses put forward to account for the excess are feasible triggers of faster strategies, independent of SES. However, just as the overwhelming majority of worse health and social outcomes and inequalities are caused by already understood socioeconomic factors, LHs are also overwhelmingly determined by SES. As the authors note, the definition of deprivation may need to be updated. Factors may need to be added that haven’t been considered part of the concept before, but which predictably lead to faster LHs, and so earlier deaths.

By Breck MacGregor

New voters look a lot like Yes voters

The Scottish independence referendum has produced an amazing engagement with democracy. Since 2011, the majority of eligible voters who weren’t on the electoral register have now registered. They make up over 7% of the electorate. So who are they?

Looking at the groups who are traditionally least likely to be registered gives some clues. According to reports by the Electoral Commission cited here, people renting accommodation from private landlords are much more likely to be unregistered than owner-occupiers. Relatedly, 16-24 year-olds, students and people who have moved recently are less likely to be registered.

This profile looks promising for the Yes campaign. In canvassing returns, home owners are much less likely than private renters to support independence. And poll results consistently show that Yes voters predominate in younger age groups. Lower socioeconomic status (SES) also predicts Yes support, and it can be inferred from the other characteristics of unregistered voters that they are more likely to have low SES. So most newly registered voters fit the mould of typical Yes voters.

The big unknown is whether the polls are taking this new chunk of the electorate into account, let alone people who were already registered but have never or rarely voted before. Criticisms include phone surveys only calling landlines – this would seem to exclude renters, young people and low SES groups who tend to rely more on mobile phones. YouGov’s online panel is a self-selecting group who are presumably already interested in politics, the opposite of people who have never voted.

The polls do of course weight their results to boost the numbers of under-represented groups in their sample. But can this really be accurate when none of a certain social group is present in the sample to begin with?

Support for independence is higher in almost every social group with less power, influence and opportunity – people who are younger, less well off, less well educated, renting. Traditionally they haven’t had a voice, and so have been largely ignored by mainstream politics and media. But the beauty of a referendum is that one vote is worth the same as every other. And the nature of inequality is that advantage is accumulated by a small minority. If turnout is high enough on the 18th, the disadvantaged majority will vote for independence.

By Breck MacGregor

Why older voters are not the key battleground in the independence referendum

The only age group in which a majority say they will vote No is 60+. It’s a heavy majority at that – 59% No to 36% Yes with 5% undecided in the latest YouGov poll – which explains why it tips the balance to give No an overall lead. This generational divide has led some to say the Yes campaign should focus on older voters as the key battleground in the referendum. But there are numerous reasons to believe that this would be the wrong strategy.

Pragmatically, older voters are more likely to use postal votes, and so a disproportionate number of the 60+ vote will already have been cast. 1 in 6 votes are postal in the referendum, a sizeable chunk of the electorate. There are fewer undecided voters too, with the last three You Gov polls having 4-8% of this age group as undecideds, compared to 9-13% of 25-39 year olds.

The polls indicate that the Yes gains are coming both from undecided voters and soft No voters, but there may be less prospect of older soft No voters changing their minds. As Mike Smithson pointed out on Political Betting: “We also know from other polling that the older you are the less likely it is that you will change your mind. That relates to all elections and not just the referendum.”

Is it just an age thing that makes older voters more likely to vote no – a desire to hold on to the status quo? The size of the fall-off in support for independence argues against this. It seems unlikely that so many current 40-59 year-olds will change their minds as they pass 60.

Growing up in the second world war and the ‘golden age’ that followed may have ingrained a sense of Britishness, and more importantly a sense of success and achievement with it. The building of the welfare state including the NHS alongside low unemployment and economic growth defined the early part of today’s pensioners’ lives. Many will have been established in jobs for life by the time the economy faltered.

By contrast, the Thatcher era dominated the early lives of many under 60s, which will inevitably colour their perception of Britishness. Alex Salmond and Nicola Sturgeon recognised this when mentioning Maggie within the first minute of their respective TV debate contributions.

For the reasons above, the 60+ No vote may be more immune to persuasion. It would certainly seem risky to focus on this age group at the expense of others.

By Breck MacGregor Tagged

‘Troubled families’

The term ‘troubled families’ covers a multitude of sins. It refers to both the social problems the families are victim to, and the trouble that the families themselves cause in their communities. The balance of emphasis is presumably down to your own political viewpoint.

The current government has announced that there are more families which fall under their definition of ‘troubled’ than previously thought. The proposed solution is to carry on with the programme of intensive interventions that aim to turn troubled families around. This style of intervention works – families in the programme are twice as likely to stop anti-social behaviour. But there is no attempt to tackle the underlying causes, and prevent families from falling into the category in the first place.

When you look at the government’s criteria, this is surprising. Most of them stem from structural issues, over which families have little control – being on a low income, unable to afford basics, poor housing, and parents with no qualifications. The intervention must then focus on the ‘trouble’ the families cause, rather than that they find themselves in. It’s the usual suspects: antisocial behaviour, domestic violence, and poor health behaviours.

But when they throw things like obesity and chronic disease at an early age into the mix, you blur the line between personal responsibility and the influence of outside factors. This may be just the point; to blame poverty on the poor. Of course both societal and individual factors are important determinants of social problems. But rather than being alternatives, they represent different levels of explanation.

‘Troubled families’ are people who have ended up on a very fast life history strategy. The social problems they experience map perfectly onto the traits identified in the life history theory literature. For instance, the government report aims to get children back into school, reduce youth crime and antisocial behaviour, and ‘put adults on a path back to work’. Domestic violence, and drug and alcohol abuse is also associated with troubled families. Compare these issues with those quoted in a paper on life history theory:

“For example, people who exhibit criminal and delinquent behaviours also tend to abuse legal or illegal substances, experience familial problems, such as familial distress, father absence, unemployment or underemployment, drop out of school, and exhibit social distress, teen pregnancy, and psychopathology.” – Figueredo et al. (2006)

This is in no way surprising – the link between the fast strategy and deprivation is iron-clad – and ‘troubled families’ is just a rebranding of the poorest in society.

The problems which people seem to bring upon themselves make a tragic sense when viewed through the lens of life history theory. Parenting functions to prepare children for adulthood. If all you have experienced in life is harsh conditions and poor relationships, it makes sense (evolutionarily) to prepare your children for the same. This is how we evolved to deal with adversity. It’s just that in modern societies, only some people experience adversity, leaving the rest uncomprehending of the consequences.

The academic literature on life history theory recognises that many social problems fall within its purview. To quote Figueredo et al. (2006):

“The social and behavioural literature indicates that many behavioural traits commonly considered “social problems” in modern industrial society occur in such clusters…[Life History Theory] construes such clusters to be coordinated arrays of contingently adaptive life-history traits.”

The message is that what is considered problem behaviour is in fact our default response to deprivation. Unfortunately, this message hasn’t been communicated to policymakers who could use it as a powerful tool to prevent problems developing. Of course some existing policies are consistent with the implication from life history theory that reducing poverty will have manifold benefits. But their case could be considerably strengthened by a wider understanding of the behavioural syndrome which underlies such a range of social problems.

The strength of the link between the fast life history strategy and social problems, and the variety of separate research fields it has been identified in, suggests that no amount of remedial effort can fully negate it. What actually troubles deprived families, and society in general, is the fast life history strategy.

Why inequality undermines societies – an evolutionary perspective


This article originally appeared on Contributoria, at .

The level of economic inequality within countries has been linked to a range of worse health and social outcomes. Evidence from the evolutionary behavioural sciences of how we have evolved to react to our environment may shed light on why we fail to flourish under extreme inequality.

Five years ago The Spirit Level was published, bringing into the mainstream the evidence on the harms of economic inequality. The two academics behind the book, Richard Wilkinson and Kate Pickett, drew on research in the various social science disciplines involved in their day jobs. They went beyond their own field of social epidemiology to show that more unequal societies are not only less healthy, but have worse outcomes on myriad other measures. It’s worth listing these to emphasise the diversity of inequality’s ill effects: infant mortality, child wellbeing, educational attainment, teenage births, social mobility, obesity, mental health, drug abuse, trust, altruism and cooperation, violence and homicide, imprisonment, foreign aid, and environmental sustainability. In the years since the book was published, inequality has become a major political issue internationally.

The explanations which are put forward to explain the effects of inequality usually focus on our immediate responses. Biologically, our levels of stress hormones rise; behaviourally, we become more prone to compete and be aggressive with others; psychologically, we become anxious and obsessed with our social status. But that’s where most explanations stop asking why – short of asking ‘why do we respond in these ways to inequality?’ On one level, it’s sufficient to know the proximate causes and ignore the ultimate causes, but this misses an opportunity to learn something instructive about human nature.

“Why do we respond in these ways to inequality?”

To go beyond the visible and measurable factors, a more expansive timeframe is needed. As a species we evolved over millions of years – for physical traits, this is uncontested scientifically. There is more vigorous debate over the extent to which mental traits have been subject to natural selection. Evolutionary psychology is often thought to portray traits as genetically determined, innate and fixed. While this is an approach that some academics take, it is clearly inappropriate to apply this to the inequality evidence. However, the responses to inequality appear to be consistent across societies. This indicates that there are adaptive traits which respond to inequality systematically – we have evolved the ability to adjust to our current situation.

This principle of calibration to the environment is well established in the evolutionary field of life history (LH) theory. It characterises a strategy which we take throughout life as a trade-off between growth and reproduction. At any given time, we can invest (unconsciously!) biological resources in growth at the expense of reproduction, or vice-versa. Ideally, we would take time to grow for as long as possible to ensure long-term health, before bringing the next generation into the world. This wasn’t always possible in the ancestral environment we evolved in – famine, war, diseases and other components of ‘environmental harshness’ all reduced life expectancy. With such considerations, it would have been no good taking your time to develop, only to die before you could reproduce. Rather, the onus is on as quickly as possible getting to a state where you can pass on your genes.

What results from the trade-off is a scale of LH strategies from slow to fast. In an uncertain environment, early maturation and reproduction protect against the risk of dying before reproducing. Other traits typical of the fast LH strategy include having more children, as a hedge against high infant mortality, and investing less parental care in them, be it shorter breastfeeding duration or father absence. Babies are born smaller, which leads to lower adult height, but with an increased risk of obesity and certain chronic diseases later in life.

The obvious objection to applying LH theory to modern problems is that thanks to developments of civilisation like modern medicine, sanitation, and the rule of law, we no longer really need to worry about making it to adulthood. But we’ve simply not had enough time to evolve and adapt to our new environment. The result is a mismatch between the environment we are adapted to and the one we find ourselves in. This is why we still respond to cues of environmental harshness.

It appears that inequality is a cue of environmental harshness which accelerates LH strategies. This is understandable in the context of access to resources – food, shelter, social capital – which are essential to survival. But egalitarianism was the norm for our early human ancestors. They lived in bands of hunter-gatherers, where meat was shared equally in the group regardless of who killed it. We can infer this from the archaeological record, as well as anthropological reports of the few remaining tribes of hunter-gatherers. In these groups, counter-dominance strategies like ridicule and ostracism prevent any one individual from gaining too much power.

“Egalitarianism was the norm for our early ancestors”

Groups became unequal with the advent of agriculture and other developments. Again, this may be too recent for evolution to have taken effect. However, we may have adapted to inequality in ancestral groups of hierarchical primates, prior to the emergence of the Homo genus. Either way, inequality seems to elicit faster LH strategies, whether as a functional adaptation or not.

Our response to inequality goes beyond behaviour directly related to reproduction. Natural selection will have acted on aspects of our biology, psychology and behaviour to form a coherent suite of responses to the social environment. For instance, the rational reaction to living with social stratification is to compete for all you can get, as you’re not guaranteed a fair share. Appeasing those above you in the pecking order while exploiting those below you is the usual result –the opposite of the healthy disrespect for authority found in the egalitarian groups. Sycophantic worship of celebrities alongside demonization of people at the lower end of society may be the modern-day version of these social processes.

The cluster of traits associated with the fast LH strategy share the theme of short-termism. This even extends into the choices we make, in the form of a cognitive bias known as future discounting. When offered the choice of a smaller reward now or a larger reward at a certain point in the future, some are better than others at resisting the temptation of instant gratification. But when the long-term future is uncertain, it’s rational to discount it and take what you can get today. This is another trade-off, between taking a hit for a bigger payoff in the long run, or short-term benefits at the expense of long-term costs.

“When the future is uncertain, it’s rational to take what you can today”

LH strategy has a strong social gradient – lower socioeconomic status (SES) tends to mean a faster LH strategy. Returning to the health and social outcomes of The Spirit Level, a recurring theme is that most of them show a social gradient, with worse outcomes at lower SES. What Wilkinson and Pickett demonstrated was that outcomes that are associated with deprivation are also associated with inequality in itself: average outcomes are worse in more unequal societies. It may be that LH traits follow the same pattern, and that the well-established link with SES can be extended to inequality.

Indeed, the effects of inequality seem to reflect the consequences of the fast LH strategy. More babies being born underweight leads to higher infant mortality. Less parental investment in children lowers child wellbeing. An obsession with social status exacerbates depression and anxiety. A bias to discount the future shortens perceived time horizons, leading to lower educational attainment and lower impulse control in drug abuse. Sustainability and climate change are similarly neglected by a short-term perspective. And a general quickening of life stages shortens childhood, increases teenage births and curtails healthy lives.

Excess inequality can be added to deprivation as a scourge that stunts our growth and flourishing. This inevitably follows from our evolved tendency to react to our social environment. What this means for social policy is that outcomes which have been seen as pathological must be reappraised as contingent responses to our circumstances.

This doesn’t mean that they should be accepted of course. But interventions like education campaigns that appeal to reason can’t solve social problems, when social conditions affect our biology, psychology and behaviour through mechanisms which are outside of conscious control. To get to the root cause, society must be made more equal.



Flannery, K. (2012). The creation of inequality: how our prehistoric ancestors set the stage for monarchy, slavery, and empire. Harvard University Press.

Wilkinson, R. G., & Pickett, K. (2011). The spirit level. Penguin, London

Life History Theory

Brumbach, B. H., Figueredo, A. J., & Ellis, B. J. (2009). Effects of Harsh and Unpredictable Environments in Adolescence on Development of Life History Strategies: A Longitudinal Test of an Evolutionary Model. Human Nature (Hawthorne, N.Y.), 20(1), 25–51. doi:10.1007/s12110-009-9059-3


Ellis, B. J., Figueredo, A. J., Brumbach, B. H., & Schlomer, G. L. (2009). Fundamental Dimensions of Environmental Risk. Human Nature (Vol. 20, pp. 204–268). doi:10.1007/s12110-009-9063-7

Figueredo, a, Vasquez, G., Brumbach, B., Schneider, S., Sefcek, J., Tal, I., … Jacobs, W. (2006). Consilience and Life History Theory: From genes to brain to reproductive strategy. Developmental Review, 26(2), 243–275. doi:10.1016/j.dr.2006.02.002

Griskevicius, V., Ackerman, J. M., Cantú, S. M., Delton, A. W., Robertson, T. E., Simpson, J. a, … Tybur, J. M. (2013). When the economy falters, do people spend or save? Responses to resource scarcity depend on childhood environments. Psychological Science, 24(2), 197–205. doi:10.1177/0956797612451471

Kruger, D. J., Munsell, M. A., & French-turner, T. (2011). USING A LIFE HISTORY FRAMEWORK TO UNDERSTAND THE RELATIONSHIP BETWEEN NEIGHBORHOOD STRUCTURAL DETERIORATION AND ADVERSE BIRTH OUTCOMES, 5(4), 260–274. Nettle, D. (2010). Dying young and living fast: variation in life history across English neighborhoods. Behavioral Ecology, 21(2), 387–395. doi:10.1093/beheco/arp202

Future discounting

Daly, M., & Wilson, M. (2005). Carpe diem: Adaptation and devaluing the future. The Quarterly Review of Biology, 80(1), 55-60.

Griskevicius, V., Ackerman, J. M., Cantú, S. M., Delton, A. W., Robertson, T. E., Simpson, J. a, … Tybur, J. M. (2013). When the economy falters, do people spend or save? Responses to resource scarcity depend on childhood environments. Psychological Science, 24(2), 197–205. doi:10.1177/0956797612451471


Scott-samuel, A., Bambra, C., Collins, C., Hunter, D. J., Mccartney, G., & Smith, K. (2013). THE IMPACT OF THATCHERISM ON HEALTH AND WELL-BEING IN BRITAIN, 44(1), 53–71.

Whiten, A., & Erdal, D. (2012). The human socio-cognitive niche and its evolutionary origins. Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences, 367(1599), 2119–29. doi:10.1098/rstb.2012.0114

Image Paul Anderson [CC-BY-SA-2.0 (, via Wikimedia Commons

Evolutionary insights for public policy

The significance of an evolutionary approach to public health is increasingly being recognised. The negative effects of poverty and inequality are also being recognised as a huge burden on health. Occasionally, the two are even combined to acknowledge our evolved responses to inequality.

Overall though the various efforts seem to have stopped short of explicitly proposing an evolutionary explanation to the Spirit Level evidence between countries. Understandably, the focus has been on measures like teenage pregnancy and breastfeeding rates that directly measure life history (LH) strategy (see this post on LH theory). But other outcomes may be the result of a faster LH strategy too: infant mortality may be higher in more unequal countries because of a reduced biological investment in each child, leading to low birthweight and prematurity.

The other outcomes in the Spirit Level can be brought under the life history strategy umbrella too, with its general principle of short-termism. The harsher and more unequal the social environment, the more uncertainty there is over long-term prospects. This would have been true in our ancestral environment too, and with morbidity and mortality rates so much higher, the selection pressure on behavioural strategies would have been extremely strong. The danger of dying before or during reproductive years made early reproduction paramount. As a result, we evolved a comprehensive response to harshness, which speeds up the course and development of key life stages, and prioritises reproduction over growth.

The response is evident in various domains:

Biologically, periods of growth are shortened, and puberty is brought forward. As in Barker’s thrifty phenotype hypothesis, where less important organs like the pancreas get less energetic investment when energy is scarce, physical size is sacrificed to allow reproduction to occur earlier. This under-investment early on in life may lead to the various health problems that develop later. Of course middle-aged health problems wouldn’t have been a major problem evolutionarily, if the early reproduction meant that your genes had been passed on in a difficult environment. They may not even have developed, with an environment of low calorie availability and an active lifestyle avoiding the metabolic disorders seen today. The molecular symptom of quicker development is oxidative stress, which is a measure of the biological stress on an individual. It is linked with chronic low-level inflammation and suppression of the immune system. Heightened cortisol levels, and activation of the hypothalamic-pituitary-adrenal axis which releases adrenaline, are also implicated. The response to stress is complex, but the various measures are consistently related to low socioeconomic status, and so can be argued to be part of the fast LH strategy.

Cognitively, people show a higher rate of a cognitive bias known as future discounting. This involves taking smaller, short-term gains at the expense of larger, long-term ones. Delaying gratification and impulse control require a low rate of future discounting.

Behaviourally, this bias could be argued to underlie almost any of the behavioural problems in the Spirit Level – drop-out rates from high school and low educational attainment, unsustainable environmental practices, addiction of any kind, from gambling to alcohol and drugs. Public goods problems (like climate change) require a long-term assessment of costs and benefits, so a bias to discount the future is disastrous for agreements on action. Hierarchy also encourages conspicuous consumption to signal status – another unsustainable practice. Future discounting may explain why trust is lower in more unequal countries, as a long-term view is needed to help someone today, when you may not be paid back for a while.

Parental investment is another feature which is sacrificed in the fast LH strategy. This is seen in harsher parenting styles. Parental inconsistency has been linked with elevated levels of stress hormones in children. And one of the parents may not even be there – 26% of families in 2011 were single-parent households. Absent fathers account for the vast majority of these. The effect on boys is the development of excessively masculine traits; girls hit puberty earlier. Both genders are more likely than average to repeat their parent’s lifestyle. The UNICEF index of child wellbeing correlates negatively with inequality, as do childhood behavioural problems.

Consequently, mental health suffers in unequal societies – especially anxiety. This can’t be said to be adaptive in modern society, but as with chronic stress, it is possible to theorise how it could have helped in an ancestral environment. In small doses, anxiety and low mood may have been one way of avoiding conflict, by avoiding aggression from others. But as with stress, constant exposure is pathological.

Inequality, by stratifying the social hierarchy, favours competition over cooperation as the way we interact with each other. Status becomes more important, as it has always signalled an ability to access resources, including mates. Excessive inequality means that those at the top can monopolise resources, and those at the bottom have nothing to lose when they try to climb the ladder. This manifests itself in higher rates of violence and homicide. Men may go to greater lengths to keep partners as well as compete for them, using violence and sexual coercion. The violence statistics don’t include sexual violence due to international differences in definitions, but (not unrelatedly) the status of women and gender equality are better in more equal countries.

In order to bring about the policy changes necessary to reduce inequality, disparate interest groups need to be made aware of the wide-ranging effects of inequality and the associated LH traits, in order to campaign with a louder voice together. This means physical and mental health organisations, alcohol and drugs charities, violence reduction schemes and so on could benefit from coming together to work for something that would tackle all of their respective issues at source. It’s not about creating a ‘natural’ environment – there’s no such thing, as we adapt to vastly different societies. It’s recognising that a more equal society brings out the best of our nature.