The Unz Review - Mobile
A Collection of Interesting, Important, and Controversial Perspectives Largely Excluded from the American Mainstream Media
Email This Page to Someone

 Remember My Information

 TeasersJames Thompson Blogview

Bookmark Toggle AllToCAdd to LibraryRemove from Library • BShow CommentNext New CommentNext New Reply
🔊 Listen RSS


Things are moving so fast in genetic research on intelligence that one cannot take a coffee break without missing important announcements. By way of small compensation, even the biggest breakthroughs are based on previous breakthroughs, so most stories in science are about a pattern of results rather than a single paper, and that pattern eventually becomes familiar territory, an increase in understanding which, once digested, may eventually become the new orthodoxy.

Where are we now, in the continuing story of the genetics of intelligence? Usually, one goes to a meta-analysis to discern the pattern of results.

A combined analysis of genetically correlated traits identifies 187 loci and a role for neurogenesis and myelination in intelligence. W. D. Hill, R. E. Marioni, O. Maghzian, S. J. Ritchie, S. P. Hagenaars, A. M. McIntosh, C. R. Gale, G. Davies & I. J. Deary

They say:

Intelligence, or general cognitive function, is phenotypically and genetically correlated with many traits, including a wide range of physical, and mental health variables. Education is strongly genetically correlated with intelligence (r g  = 0.70). We used these findings as foundations for our use of a novel approach—multi-trait analysis of genome-wide association studies (MTAG; Turley et al. 2017)—to combine two large genome-wide association studies (GWASs) of education and intelligence, increasing statistical power and resulting in the largest GWAS of intelligence yet reported. Our study had four goals: first, to facilitate the discovery of new genetic loci associated with intelligence; second, to add to our understanding of the biology of intelligence differences; third, to examine whether combining genetically correlated traits in this way produces results consistent with the primary phenotype of intelligence; and, finally, to test how well this new meta-analytic data sample on intelligence predicts phenotypic intelligence in an independent sample. By combining datasets using MTAG, our functional sample size increased from 199,242 participants to 248,482. We found 187 independent loci associated with intelligence, implicating 538 genes, using both SNP-based and gene-based GWAS. We found evidence that neurogenesis and myelination—as well as genes expressed in the synapse, and those involved in the regulation of the nervous system—may explain some of the biological differences in intelligence. The results of our combined analysis demonstrated the same pattern of genetic correlations as those from previous GWASs of intelligence, providing support for the meta-analysis of these genetically-related phenotypes.

However, the authors not only give us a meta-analysis, they follow the same value-for-money approach traditional for this team: they test their predictions on an independent sample. Keep reading.

Intelligence, also known as general cognitive function or simply g, describes the shared variance that exists between diverse measures of cognitive ability[1]. In a population with a range of cognitive ability, intelligence accounts for around 40% of the variation between individuals in scores on diverse cognitive tests[2]. Intelligence is predictive of health states, including mortality; [3, 4] a lower level of cognitive function in youth is associated with earlier death over the next several decades[5]. Intelligence is a heritable trait, with twin- and family-based estimates of heritability indicating that between 50–80% of differences in intelligence can be explained by genetic factors[6]. These genetic factors make a greater contribution to phenotypic differences as age increases from childhood to adulthood[7]. Heritability estimates derived from molecular genetic data using the GREML-SC [8, 9] method indicate that around 20–30% of variation can be explained by variants in linkage disequilibrium (LD) with genotyped single nucleotide polymorphisms (SNPs)[10]. Some of the association between intelligence and health is due to genetic variants that act across traits [11, 12]. More recent methods to measure heritability, such as GREML-KIN[13], and GREML-MS[14] using imputed SNPs, have found that some of the heritability of intelligence can be found in variants that are in poor LD with genotyped variants; by taking these into consideration, SNP heritability estimates of 0.54 (GREML-KIN) and 0.50 (GREML-MS)[15] have been found.

For those who, like me, don’t take easily to genetic jargon, just think of all this as computer code. If you look through traditional computer code you will find sub-routines and Go To instructions. Some of the code is embedded in sub-routines, some code acts as signposting, and some code does the essential processing work along the way. All these sections of code can develop a flavour: by the time you get to a distant sub-routine your variable names will have drifted further down the alphabet; line numbers will be higher, the types of calculations will have altered, and will involve the products of farprevious sub-routines. Of course, the genetic code is nothing like this, but linkage can be close or , common or unusual, and if a piece of code gets picked out because it is particularly useful, it can carry some neighbouring useless code with it, like fluff on a toffee. New ways of understanding and analyzing the code are being developed fast, so new findings may well arise when analysis moves from exploratory association work to laboratory manipulations of individual genes in Petri dishes.

The authors got their large sample size by using a crafty technique, combining an intelligence test data sample with the proxy phenotype of educational attainment in another sample, and thus getting far more analytic power. The genetic correlation between intelligence and education is 0.7 which is what assists this alignment and pasting-together technique.

Seven novel biological systems associated with intelligence differences were found.

1 Neurogenesis, the process by which neurons are generated from neural stem cells.
2 Genes expressed in the synapse, consistent with previous studies showing a role for synaptic plasticity.
3 Regulation of nervous system development.
4 Neuron projection
5 Neuron differentiation
6 Central nervous system neuron differentiation.
7 Oligodendrocyte differentiation.

In addition to these novel results, the finding that regulation of cell development (gene-set size = 808 genes, P-value 9.71 × 10−7) is enriched for intelligence was replicated.

In summary, if further proof were needed that these bits of the genetic code were associated with brainpower, the list homes in on everything likely to be required for a fast-thinking powerful biological system.

Here is a heat map of the results, which you will find similar to previous studies. (You may need to click on this image to enlarge it).

Hill Deary heat map

Here is a more detailed picture of the tissues involved:

Hill Deary specific tissues

They canter to a conclusion:

• Category: Science • Tags: I.Q. genomics, Intelligence, IQ 
🔊 Listen RSS


Evaluating Hawking’s work is beyond me, so why do I feel so sad about his death? A simple explanation is that a bright and kind media star becomes a friend, in the digital sense, so no wonder so many of us mourn him. I think that for me and many others it was because of his humour, which was inspired and self-mocking, and made me feel I should try to read his famous book. I failed after, ahem, a number of pages. I tried skipping a bit, looking for an easier section, but again it was only the humorous asides that registered. The Chronology Protection Conjecture, for example. Fun. I pretended to understand that black holes could emit something, but that was because a helpful diagram illustrated the point. His approach was friendly, so I did my best to understand some cosmology, although the topic was hardly a major interest of mine.

By comparison, Feynman’s “Six Easy Pieces” were relatively easy until Chapter 4, and then I hit a comprehension ceiling. I had enjoyed the first three chapters sufficiently not to complain that the book had been mis-titled. “Easy” is a relative concept. “Surely you’re joking, Mr Feynman” was even easier, but it was intended to be, yet it introduced interesting concepts. His lectures and interviews are easy as well, mostly. Feynman diagrams are another matter. I only got an inkling of what they were about by understanding a different conjecture based on the analogy of calculating the trajectories of particles as the probability of one of a random collection of passengers in a carriage in the London tube system exiting at a particular distant station. Knowing the London Tube map helped refine the probabilities after every stop, thus simplifying the calculations.

I explain this to make a general point. As items increase in difficulty the personal failure rate increases, until you reach break point, in which the struggle to understand seems a poor investment of effort, and you return to other interesting problems at a manageable level of difficulty. Comprehension ceilings can be breached to some degree by persistence, but perhaps more so by excellent teaching, often using analogies and diagrams. However, to be frank, eventually Maths makes an appearance, and until it does, actual comprehension is sometimes wishful thinking, a veneer for public show. Count wherever possible.

Intellectual life has its challenges. I myself have understood the theory of relativity 7 times. If you put a clock on a train and there is someone with a similar clock watching the train go by……. I have forgotten the details 8 times.

Our individual proficiencies interact with the difficulty of the items until we reach a personal high-water mark. Each test item has a pass rate (this is the sum total of how many people in the population can pass that item), and each person has a personal history of how many of those problems they themselves have solved. If we take a population there is a matrix in which we can plot every person against every test item. The higher a person’s ability relative to the difficulty of an item, the higher the probability of a correct response on that item. Eventually we all reach a point where there is only a 0.5 probability of getting the correct answer. That point will be different for different people, but for all of us that is probably the moment we decide to turn to other pastimes.

So, if most of us did not understand his book, why the adulation of Hawking? For once, people were allowed to value intelligence. He embodied the idea of mind without body, the trapped intellect that might be overlooked by the careless observer. His fortitude in adversity was an inspiration, and also encouraged the view that cerebrally palsied children could be liberated mentally by computer controlled signing devices. Not always, usually in those cases because of other brain injuries.

Hawking was the embodiment of a fictional 1950 series he might have read as a child, Dan Dare and the dastardly Mekon. They had been engineered for high intelligence, had very large brains, atrophied bodies, and moved around on levitating chairs. What fascinated children 70 years ago still has its fascination today. Hawking, like so many of our generation, wanted to be Superman, “because he was everything I am not”. Yet Hawking was someone to stare at, a modern-day Einstein, a Superman of the mind. Millions saw him as the embodiment of intelligence, and permitted themselves to admire him for it.

🔊 Listen RSS

sex diffs cartoon

Will sex differences never end? Sometimes they seem to go one way, sometimes the other, with the gaps closing or staying resolutely the same, but this is the March of Science, as different schools contend, and as new results are added to the old. We should be glad that researchers delve into these matters, particularly in times when sex differences are considered somehow dangerous, and apt to cause offence, public disorder, and a rending of the very fabric of society, as when a diaphanous blouse is torn from a lady’s breast by a brutish leering lout. I digress. I may not have got the hang of current sensibilities.

Anyway, back to “tilt”. I find this a relatively new concept, but perhaps it is more succinct than the former description “verbal-performance discrepancy”. Which way do the fair sex incline: to matters verbal or mathematical? Verbal, it would seem, and all the more so as you go up the ability spectrum.

Sex differences in ability tilt in the right tail of cognitive abilities: A 35-year examination Jonathan Wai, Jaret Hodges, Matthew C. Makel. Intelligence, Volume 67, March–April 2018, Pages 76–83

The authors highlight the following findings:

Sex differences in math-verbal ability tilt in the right tail were examined across 35 years.
Sample included >2 million gifted adolescents across multiple measures in the U.S. and India.
Ability tilt favored males for math > verbal and females for verbal > math.
Sex differences in ability tilt remained fairly stable over time and replicated across measures.
Trends should be monitored given their potential to impact future workforce trends.

Sex differences in cognitive ability level and cognitive ability pattern or tilt (e.g., math > verbal) have been linked to educational and occupational outcomes in STEM and other fields. The present study examines cognitive ability tilt across the last 35 years in 2,053,265 academically talented students in the U.S. (SAT, ACT, EXPLORE) and 7119 students in India (ASSET) who were in the top 5% of cognitive ability, populations that largely feed high level STEM and other occupations. Across all measures and samples, sex differences in ability tilt were uncovered, favoring males for math > verbal and favoring females for verbal > math. As ability tilt increased, sex differences in ability tilt appeared to increase. Additionally, sex differences in tilt increased as ability selectivity increased. Broadly, sex differences in ability tilt remained fairly stable over time, were consistent across most measures, and replicated across the U.S. and India. Such trends should be carefully monitored given their potential to impact future workforce trends.

Before going further, I should digress to sing the praises of Gerd Gigerenzer. Whereas Kahneman and Tversky concentrated on puzzles which many have found contrived, Gigerenzer concentrated on actual, everyday problems with interpreting statistics. Here is an example. We can all guess those people in the top 1% of intelligence are 1 in 100 intellects, but what does 0.01% mean? It “feels like” 1 in a 1000, but is in fact 1 in 10,000. As Gigerenzer says, don’t mix decimals with percentages. They are different tribes. Confusing. Instead, use natural frequencies. In a town of 10,000 people there will be 100 people who are in the top 1% of the population, but only one person who is 1 in 10,000. That is the level that Benbow and Lubinski studied. Eminent minds, Galton called them.

So, skipping a thousand words, here is the pictorial summary, which shows that sex differences increase as ability tilt increases:

sex diff violin plot of tilt Wai

To my eye, starting from the bottom for all students, these violin plots show the following: women are almost perfectly balanced between verbal and mathematical ability, but men incline towards being better at maths than at verbal tasks. Men are more likely to calculate. This relatively slight difference might be the source of contrary imaginations, and some exasperated arguments.

At the higher intellectual level of the top 1 in a 100 of the population both men and women incline more to mathematical thinking, but men predominate more.

At the eminent level of the top 1 in 10,000 of the population, men outnumber women by about 2.5.

The authors caution:

It should be noted it is likely that the magnitude of the selectivity level moderator (top 5%, top 1%, top 0.01%) is underestimated. In the analysis, the ratio of male to females was skewed toward males. This skew increased as selectivity increased. This unbalanced design can lead to the true effect being greater than what is reported. In other words, it is possible that the magnitude of tilt is greater than what is reported.

Of course, the top mathematicians will be even brighter, say 1 in 1,000,000. They will be mostly men.

The paper is rightly restrained in its conclusions, but this stable result is a causal component in the observed sex differences in STEM studies and subsequent occupations. Sex differences in preferences for occupations are mentioned, but are not part of this study. India, which is far less favourable to women’s careers, shows the same trend. Probably, men take to maths more than do women, and at the brightest levels that general trend is accentuated. The current study may under-estimate the male advantage.

• Category: Science • Tags: Gender 
🔊 Listen RSS

Darkest Hour

“History is on every occasion the record of that which one age finds worthy of note in another.”
―Jacob Burckhardt

What is one to make of “Darkest Hour”? Is it only yet another chance to bathe in nostalgia for the Second World War, and to dredge up an old story, out of which the British come out smelling of roses, unlike in some other conflicts? Or is it a story which is too good to be false, and which needs re-working in order to be fully understood?

Rarely have two men been so savagely opposed, and so different in their formative experiences, though each had war experiences . Hitler (1889-1945) rose from nothing to absolute dominion over Europe, and fell like a stick; Churchill (1874-1965) started high, aimed higher, and after years in the wilderness achieved greatness. Within a year of the actual conflict beginning the worst was over, and after Barbarossa in June and Pearl Harbour in December 1941 the balance of power tilted. Even the D-Day invasion might have failed, but the Allies managed to win through. In retrospect it was only a matter of time before the Nazi regime collapsed, though it took millions with it as it did so.

So, the battle of wits between an ascendant 51-year-old Hitler and a last-choice, embattled 66-year-old Churchill is a story always worth telling, perhaps worth telling for ever. Churchill turned the course of history. The very first German biography of Hitler, by Joachim Fest, made the telling point that, for all his oratory, Hitler left little of note in the German language. Art Historian Burckhardt again: “The essence of tyranny is the denial of complexity”. Churchill, on the other hand, lifted English to the sunlit uplands. He was a most quotable man. Does any of this matter, in the cold calculation of war? Yes. Rhetoric is worth many battalions. Language can move hearts because it is the supreme tool of thinking, putting the Olduvai tool set in the shade, though that collection of implements lasted 600,000 years.

Joachim Fest observed that of Hitler it could be said: “Here was a man who changed history”. As biographers of Churchill have noted: “Churchill also”. A truly titanic struggle. The film itself is carried by Gary Oldman, whose performance is a triumph. He becomes the part, from the first strike of a match, and never fails to convince. The rest of the cast is brilliant, a delight, but the star shines through. Lest it seem churlish not to mention it, I liked everything which established the feel of that distant time, known to me mostly from the picture of a relative who left Uruguay to die in the Pathfinders Squadron, and from the guarded recollections of a Spitfire pilot shot down and kept in near starvation in a German prison camp. The film costumes were fine, and so were the hairstyles. Everyone smoked, just like my parents did.

The film itself has to deal with a pressing issue. All this has been done before, and every Second World War film starts with the same shots of London streets, gas masks, bomb shelters and screaming sirens. Director Joe Wright and Director of Photography Bruno Delbonnel shoot the obligatory panning shots of Londoners, but these shots are themselves deliberately panned, as if in stylised slow-motion the director mockingly says: “This is a romantic re-creation, just like in all the other war films, but it really was something like this”. A crafty move, which keeps them in touch with a potentially sceptical war-film-weary audience.

The story is worth telling because to many it is forgotten or was never known. Schoolchildren now struggle to say who fought on which side. Will it be watched in Europe? It will be interesting to see the results. There is much they would wish to forget. The film has taken $131 million so far. It must seem strange to teenagers in Britain that their university studies or working lives could be interrupted by a request to fight a war and possibly die. An inconvenient death, not yet midway through the journey of their lives, all for a distant country of which they knew nothing, and cared less. Almost as much of a shock as being deprived of internet connectivity. Although the war is vicariously quite vivid to me, I still find it difficult to believe that I might have had to serve, and to be tested as that generation were tested.

Overall, this is a good film, worth seeing, and worth thinking about. Joachim Fest again: although Marxist historians have sometimes argued that historical events are inevitable because of major economic forces, and that historical biography is no more than courtly flattery, Hitler proves them wrong. His capture of the German soul and his face-saving explanation for their lost first world war proved all too powerful, with dreadful results. He was the spark in the methane swamp. In my view, if only the bloody, resentful man had been accepted into Art College we might have been spared oceans of misery. We are all allowed counter-factual speculations, are we not?

And on that point, historian Robert Tombs has put forward a good argument that Britain should have ducked out of the war, kept the Empire, and let the Nazi regime fail under its own dreadful contradictions. Conquering with lightening war is one thing, governing for the long term another. Empires are costly. Even subjugated peoples rebel from time to time. Policing them takes time, and saps profits. Ask the English. The audience was not convinced by this championing of prudent self-interest in the face of a barbaric regime, but it was a reasonable position in 1940, as the film, perhaps too vividly, depicts.

As per usual, you will expect me, in the midst of all this praise, to raise a quibble. There is a romantic lapse in the commitment to giving a truthful account, which the team excuse as something which might have happened. Of course, anything might have happened. The truth is that they made it up, in order to convince us about something. They imagined that Churchill would have gone down into the Underground tube system to get an impromptu democratic mandate for his policies from a random carriage-full of passengers. Nope. His mandate came from the House of Commons, where Members had been properly elected to represent their constituents. Britain was democratic, but it was not yet usual to canvas ordinary opinions on matters of foreign policy. Mass Observation was designed to measure morale, not yet to pander to lay opinion. If the ruling class had any interest in what the people thought outside of elections, they consulted their taxi driver. The scene in the Underground is a fiction designed to flatter the audience, and it has dramatic flair. Everyone has a Churchill story, and would like to have met him. The film cleverly caters to that all-too-human wish. In doing so, they try to fiddle a bit with history, but for noble reasons, you may say. It may be a dramatic bridge too far, a contemporary urge to rewrite history in the modern idiom.

• Category: History • Tags: Multiculturalism, World War II 
🔊 Listen RSS

insomnia image

Is sleep the balm of hurt minds? It should be. Happily, sleep usually comes easily to me. There are some exceptions: the night before having to wake early for a long plane flight being one, but these events are few and far between.

Many people complain of insomnia, and this is a private disorder, in that it is rarely on public view. What could be more personal than to be stranded in wakeful isolation while the rest of the world is soundly asleep? However, if you have the great fortune to share a bed with someone else, you can sometimes judge whether the other person slept well, just by noting their regular breathing. You might even try a whispered “Are you awake?” to check whether you are judging their state of somnolence correctly. Then, if in the morning your partner claims not to have slept a wink, you can counter with your own observations about them having slept soundly for at least part of the night.

There are other methods to measure whether people are really awake for hours, or just exaggerating on the basis that any unwanted wakefulness at night can feel as if it lasted for ages. For example, having a bedside timer that has to be responded to every time a little light comes on is one such method used by sleep researchers. If you are wakeful you can do this monitoring task for a long while. Once you fall asleep you can no longer monitor the signals. To some extent, the perception of not having had a full night’s sleep can be measured objectively.

Be all this as it may, to rise from bed in the morning feeling you have not slept properly is a burden. What causes insomnia? A long list of foods and drinks usually follow, plus bad habits about getting too agitated prior to going to bed. “Sleep hygiene” is recommended by psychologists, and often works. You probably know the advice: prepare for sleep by following a sequence. Avoid bright lights and noise and troubling activities. Go through a ritual that calms you down and gently reminds you of comforting topics, and casts away troubling thoughts. If all that doesn’t work, get up and do some of the tasks that are worrying you, or at least write down a to-do list, and then go back to bed and try again.

Now Danielle Posthuma and colleagues have looked at the genetic angle. Are some people more prone to this disorder? So it would seem.

Genome-wide Analysis of Insomnia (N=1,331,010) Identifies Novel Loci and Functional Pathways
Philip R Jansen, Kyoko Watanabe, Sven Stringer, Nathan Skene, Julien Bryois, Anke R Hammerschlag, Chrstiaan A de Leeuw, Jeroen Benjamins, Ana B Munoz-Manchado, Mats Nagel, Jeanne E Savage, Henning Tiemeier, Tonya White, Joyce Y Tung, David A Hinds, Vladimir Vacic, Patrick F Sullivan, Sophie van der Sluis, Tinca JC Polderman, August B Smit, Jens Hjerling-Leffler, Eus JW van Someren, Danielle Posthuma

It is not often that one gets sent a paper with a 1.3 million sample size. I move in refined circles, it would seem.

Insomnia is the second-most prevalent mental disorder, with no sufficient treatment available. Despite a substantial role of genetic factors, only a handful of genes have been implicated and insight into the associated neurobiological pathways remains limited. Here, we use an unprecedented large genetic association sample (N=1,331,010) to allow detection of a substantial number of genetic variants and gain insight into biological functions, cell types and tissues involved in insomnia. We identify 202 genome-wide significant loci implicating 956 genes through positional, eQTL and chromatin interaction mapping. We show involvement of the axonal part of neurons, of specific cortical and subcortical tissues, and of two specific cell-types in insomnia: striatal medium spiny neurons and hypothalamic neurons. These cell-types have been implicated previously in the regulation of reward processing, sleep and arousal in animal studies, but have never been genetically linked to insomnia in humans. We found weak genetic correlations with other sleep-related traits, but strong genetic correlations with psychiatric and metabolic traits. Mendelian randomization identified causal effects of insomnia on specific psychiatric and metabolic traits. Our findings reveal key brain areas and cells implicated in the neurobiology of insomnia and its related disorders, and provide novel targets for treatment.

Well, at first glance these authors are on to something. These are brain areas one might have imagined would be implicated in sleep disorders. Also, the disorder picks up the nexus of psychiatric disorders, long suspected of having some biological roots. Let us read further.

They say:

Insomnia complaints were measured using questionnaire data, and the 36 specific questions were validated to be good proxies of insomnia disorder, using an independent sample (The Netherlands Sleep Register, NSR) in which we had access to 38 similar question data, as well as clinical interviews assessing insomnia disorder.

So, they seem to be measuring insomnia, which increases with age, and is more common among women. They pick up real genetic signals, not spurious associations.

We confirm previously reported genetic correlations between insomnia and neuropsychiatric and metabolic traits, and also identify several GWS SNPs for 249 insomnia that have previously been associated with these traits. The strongest correlations were with depressive symptoms (rg=0.64, SE=0.04 P=1.21×10-71 250 ), followed by anxiety disorder (rg=0.56, SE=0.11 P=1.40×10-7 251 ), subjective well-being (rg=−0.51, SE=0.03 P=4.93×10-52), major depression (rg=0.50, SE=0.07 P=8.08×10-12 252 ) and neuroticism (rg=0.48, SE=0.02 P=8.72×10-80 253 ).

Since a similar high reliability has been reported for both sleep and psychiatric phenotypes, the findings suggest that genetically insomnia more closely resembles neuropsychiatric traits than it resembles other sleep-related traits.

In addition, insomnia was bidirectionally associated with educational attainment, with a stronger effect from insomnia on educational attainment (bxy=−0.32, SE=0.02, P=1.68×10-77 265 ) (i.e. a higher risk for insomnia leads to lower educational attainment) than vice versa (bxy=−0.10, SE=0.01, P=2.27×10-23 266 ), the same pattern was observed for intelligence.

insomnia genetic correlations

This is an extremely detailed paper, and I have only given you the very basic points. Yet, in another way, the results are very familiar. A pattern is beginning to emerge. If you take a behavioural problem, like being unable to get restful sleep, you find a genetic nexus of psychiatric disorders with deleterious effects on intellectual ability.

Dryden, whom I revere, intoned: Great wits are sure to madness near allied, and thin partitions do their bounds divide.

Far from that being the case, wit is diminished by mental disorders. When literary tradition collides with empiricism, woe to tradition.

• Category: Science • Tags: Deep Sleep, Sleep 
🔊 Listen RSS

risky tightrope walker

Do you live life close to the edge? Climb mountains free-style, jump off bridges with small gliding parachutes, have unprotected sex with strangers, or even discuss genetic differences in public meetings? Further, have you been so busy living in the vivid present that you have no savings and no pension, and expect others, who are living boring lives doing dull work, to pay your bills and provide for your old age? If so, and you can bother to pause for a moment to do some reading, here is an interesting study to ponder. Ponder means to think about something carefully, taking your time about it.

Title: Genome-wide study identifies 611 loci associated with risk tolerance and risky behaviors

Linner et al say:

Humans vary substantially in their willingness to take risks. In a combined sample of over one million individuals, we conducted genome-wide association studies (GWAS) of general risk tolerance, adventurousness, and risky behaviors in the driving, drinking, smoking, and sexual domains. We identified 611 approximately independent genetic loci associated with at least one of our phenotypes, including 124 with general risk tolerance. We report evidence of substantial shared genetic influences across general risk tolerance and risky behaviors: 72 of the 124 general risk tolerance loci contain a lead SNP for at least one of our other GWAS, and general risk tolerance is moderately to strongly genetically correlated (r= 0.25 to 0.50) with a range of risky behaviors. Bioinformatics analyses imply that genes near general-risk-tolerance-associated SNPs are highly expressed in brain tissues and point to a role for glutamatergic and GABAergic neurotransmission. We find no evidence of enrichment for genes previously hypothesized to relate to risk tolerance.

They looked at self-assessed risk tolerance, and also risk-taking in automobile speeding, drinking, smoking and number of sexual partners. As per usual, the subjects were European-ancestry subjects. At some stage other ancestries will be studied, I presume, or perhaps not. Once again, these are gigantic sample sizes, and must have taken years and countless meetings and conferences to organize. A bit harder than asking all 60 of your students to fill in a questionnaire.

We also estimated genetic correlations between general risk tolerance and 28 additional phenotypes. These included phenotypes for which we could obtain summary statistics from previous GWAS, as well as five phenotypes for which we conducted new GWAS. The estimated genetic correlations for the personality traits extraversion (r= 0.51), neuroticism (r=0.42), and openness to experience (r=0.33) are substantially larger in magnitude than previously reported phenotypic correlations pointing to substantial shared genetic influences among general risk tolerance and these traits.

Our results provide insights into biological mechanisms that influence general risk tolerance. Our bioinformatics analyses point to the role of gene expression in brain regions that have been identified by neuroscientific studies on decision-making, notably the prefrontal cortex, basal ganglia, and midbrain, thereby providing convergent evidence with that from neuroscience. Yet our analyses failed to find evidence for the main biological pathways that had been previously hypothesized to influence risk tolerance. Instead, our analyses implicate genes involved in glutamatergic and GABAergic neurotransmission, which were heretofore not generally believed to play a role in risk tolerance.

The authors add a cautionary note:

Across the risky behaviors we study, we find that the genetic correlations are considerably higher than the phenotypic correlations (even after the latter are corrected for measurement error) and that many lead SNPs are shared across our phenotypes. These observations suggest that the low phenotypic correlations across domains are due to environmental factors that dilute the effects of a genetically-influenced domain-general factor of risk tolerance.

Risky behaviours genetic correlation

So, what can we conclude from the genetic correlations? Tentatively, that the “genes for” risk taking are associated with the “genes for” having intercourse early in life, having babies while still a teenager, using cannabis and being self-employed (which must cover a wide range of activities); slightly associated to educational attainment and cranial volume, somewhat to ADHD, anxiety disorders, bipolar disorder and schizophrenia, and also to extraversion, openness to experience and to stability, and to household income. This is an interesting constellation of features, and mostly conforms to pattern for “fast life histories” so beloved of evolutionary researchers. It would be interesting to know if these risk-takers have pensions and savings. I assume not. Of course, these are correlations between the genes for one thing (risk-taking) and the genes for other things (attitudes and lifestyles) but in reality the links between the genes for risk-taking and all the other measures are slight in reality. Other factors intervene.

This is a crucial point. Studies like these can point to associations between genes and behaviour. This one has a strong story to tell, one which hangs together and makes sense. Yet, it has low predictive value at the moment. Perhaps risk-taking really does depend on getting into bad company (that is, it requires the amplifying effect of being with other risk-takers for a critical mass of dare-devils to spin into dangerous activities). Could such vulnerable young persons be saved by joining the Boy Scouts? Possibly. Some cultural practices might channel risk-takers into pro-social actions, while other cultural practices let them drift into trouble.

As per usual, the percentage variance accounted for is very small, 1.6% at best. This is the best genetic research ever done on this topic, and yet in future it might be seen as only a starting point, so fast is the genetic field progressing.

Here is a thing, which I could not find directly addressed in the paper. Yes, the subjects of this study are risk takers, but in fact only mildly so. Driving fast, smoking, drinking, and having lots of sex with different people all have their risks, and their pleasures, but they are small beer. The main point is: the real risk takers probably fell out of the gene pool long ago. We are dealing with some of their surviving children, and a vast mass of more cautious survivors.


• Category: Science 
🔊 Listen RSS

calorific meal

I did not expect that my previous post would prove so contentious and would lead to such a wide range of comments. Thank you for those, and for the detailed points made, and the references to published work. I must admit that I sometimes experienced an Alice in Wonderland effect: the discussion has veered away from what I had expected and involves many assumptions which I am trying to understand.

I did not expect that anyone would question the general principle of “calories in/calories out”. I am surprised, and have read the supportive arguments, but do not find them convincing, as I will explain later. I have also been presented with notions about the effects of different types of food, and the balance between protein, fats and carbohydrates. All these are digested down into the working fuel of the body. Eat too much of any or all of these, and your chance of getting fat increases.

Yes, of course these foods could have a different balance point between calories ingested and perceived satiation. If it is possible to choose foods which lead to quick satiation it might be possible to control weight, but only if there is strict control over how much is eaten. My argument, which some found difficult to follow, is that the main cause of obesity is eating too much, and the balance between food types is a secondary consideration to that.

As an obesity clinic at Addenbrook’s Hospital explains:

Obesity is the medical term for having too much fat stored in your body for good health. When people gain weight through a ‘positive energy balance’, that is more energy (food and drink) coming into the body than is being spent through activity and exercise, the surplus energy is stored mainly in fat cells that are present throughout the body. Nothing has to ‘go wrong’ for this process to happen.

I say that if you are over-weight and wish to lose weight, then you should eat less. You should keep eating less until you achieve your desired weight, and then stick to that level of calorific intake. What you eat is up to you, but a good rule of thumb is to reduce your intake of high calorie foods. If you need more guidance, avoid high density calorific foods and eat more low density low calorie foods. There are many published sources of calories for each food type, and some come with helpful pictures so that you can judge calorific intakes by sight.

Increasing your level of activity, by whatever means you choose, is unlikely to have much direct effect. This is because in current times there is so much good food available that you can replace half an hour’s calorie expenditure in about two minutes. A chocolate-coated nut-filled candy bar will do the trick. Short of the high levels of work of our Victorian ancestors, or of frequent treadmill exercise, this is not a viable strategy for losing weight in modern times. The only realistic strategy is to reduce calorie intake. Our metabolisms are very efficient, and food goes a long way. For example, couple a normal dietary intake with using a bicycle and you can achieve many miles per calorie ingested.

Do most over-weight people succeed in losing weight? Apparently not. This does not invalidate the advice that one should eat less. It reveals that people find it very difficult to follow that advice. The spirit is willing, the flesh is weak, all too much of it.

A few words on some familiar topics. You do not disprove a correlation by concentrating on residuals. A good correlation is not a perfect correlation: there will be discrepant instances. There will be individual variations caused by particular foods, digestive upsets, ill-health and other extraneous noise. Some people have a genetic leptin deficiency which denies them feedback about satiation. They eat too much because they still feel hungry. There will always be individual cases, even within the general observation that if you are too fat you should eat less. How much do these variations account for in the general population? Probably not much, in my estimation. However, let us imagine that they accounted for 10% of the variation in converting food calories into fat, such that some people get fat much faster than others on the same calorific intake. This would be a break-through in agriculture and stock rearing, and potentially commercially valuable. Thermodynamics is a general principle, and applies universally.

To attempt to disprove the “calories-in/calories-out” argument with some individual cases or short-term studies will not give you a true picture. Look at large samples over a longer time frame. If you are really in a hurry, look at the results of spending a night in the controlled circumstances of a calorific chamber.

The anorexia clinic at the York Clinic, Guy’s Hospital was not a calorific chamber, but it was a reasonably controlled environment. Some parents helped their children cheat the system, by taking out Complan in flannels in their handbags, fooling us into thinking that the emaciated adolescent was eating as required. However, we could detect the deception at the weekly weigh-ins, and could be sure that something was wrong by the second weigh-in, so close was the correlation between calories-in/calories-out in that controlled circumstance.

Here, as requested, are the summary data on the patients:

Anorexia paper Table 1

As you can see, these were patients who were about to die. They were emaciated, often very frightening to look at. It was painful to see them dying, yet still incapable of taking the steps to save themselves of their own volition. Happily, we never lost a patient in treatment.

Anorexia paper Table 2

Notice that although these patients gained weight, they did not do so at the same rate, an individual variation on a general effect. That said, they had a weekly weight gain which was similar, and predictable.

Another general note of guidance: people are not always reliable reporters about their food intake. Some of the discrepancies are caused by simple forgetting, but much is caused by wishful thinking and selective recall. Typically, people forget snacks between meals, and second helpings. They often ignore calorific drinks, mostly sugary ones.

Processed food is not bad in itself, but it is hard to monitor what is in it, and it is probably best avoided if you wish to lose weight, that is, it should not be a large part of your habitual intake.

In general, all foods are good for you, in moderation. There are circumstances when you may have to eat what is available, even if it is not the best basis for a permanent sustained diet.

Eating less is not a complicated strategy. Yes, at a very detailed level the way the digestive system works can always be investigated further, but enough is known to realise that eating less makes you less likely to get fat.

• Category: Science • Tags: Diet, Weight Loss 
🔊 Listen RSS

calorie balance

At a time when some people may be wishing to set a New Year’s resolution, after some festive eating and drinking, it is apposite to look at a recent very striking headline:

‘I beat type 2 diabetes with 200-calorie drinks’

It describes what is said to be a very promising treatment for the treatment of type 2 diabetes. The breakthrough comes from “200 calories drinks” suggesting that if you have lots of these you can cure an illness. This seems a cheerful suggestion, and a welcome achievement of Science. The article itself, read carefully, has only two mentions of the word “fat”. Here they are:

Body fat building up around the pancreas causes stress to the beta cells in the organ that controls blood sugar levels. They stop producing enough of the hormone insulin, and that causes blood sugar levels to rise out of control. Dieting loses the fat, and then the pancreas works properly again.

This suggests to readers that it is fat round the pancreas which causes the problem, rather than being fat everywhere. In fact, although one can always quibble with epidemiological studies, being fat causes a variety of problems, including in the knees: yet another medical mystery. More widely, arthritis symptoms are worse among fat people.

What is this wonder cure based on?


Complan is what we gave decades ago to women with anorexia nervosa when they came into the York Clinic, Guy’s Hospital, at death’s door when the psychotherapists treating them had fnally realised that inpatient treatment was required. A commercial product, Complan is a vitamin drink with carbohydrates and fat and the full range of nutrients required for a balanced diet. We used a behaviour therapy routine which rewarded patients for weight gain. The total daily calorific intake was 2000-3000 calories, resulting in a mean weight gain of 12.39 kilos over 53 days, a daily gain of 234 grams, or 1.64 kilos (3.6 pounds) a week. That is in fact a reasonable estimate of the weight gains made by a totally sedentary person who eats a 3000 calorie diet. For a higher amount of calories, adjust upwards. Thermodynamics.

Here is the reference to the anorexia paper.

S.Bhanji and J.Thompson. Operant conditioning in the treatment of anorexia nervosa. British Journal of Psychiatry (1974),124,579,166 174.

Enough of that. Here is The Lancet summary of the latest paper on the “treatment” of diabetes 2:

The account does not mention fat at all. They say:

Type 2 diabetes is a chronic disorder that requires lifelong treatment. We aimed to assess whether intensive weight management within routine primary care would achieve remission of type 2 diabetes.

This leads one to ask: How does one catch this illness? Is there some vaccination against this “chronic disorder”? By lifelong, does it really mean that it lasts for ever?

Later in the paper there are a few clues about weight loss after an 850 calorie per day diet. Patients had BMIs of 27 to 45 Kgs per m2 which is from “over-weight” to “morbid obesity”. Patients lost 15 Kg or more.

Patients had been put on Complan, or its equivalent, to break them from the bad habits of their habitual fattening diet. This is good news, and I am in favour of it. What irritates me is the evasion contained in this story, in that it does not mention that the “illness” of type 2 diabetes is merely a consequence of eating too much and becoming fat. What should the headline have been?

Trial shows that fat people who eat less become slimmer and healthier.

I hope this wonder treatment receives lots of publicity. If you wish to avoid hurting anyone’s feelings just don’t mention fatness. In extremis, you may talk about body fat around vital organs, but keep it brief, and generally evasive.

I see little need to update the broad conclusion: if you want to lose weight you should eat less.

However, you do not need to make a New Year’s Resolution about this. Your body is your own temple.

Happy New Year.

Disclosure: I have a wonder diet I have designed and followed since 12th March 2015. Oddly enough, it is simply a way of eating less. It is fully written up, and I am willing to disclose it at the 3 year anniversary next March, or sooner in the case of very generous donations. For all I know, it may boost your IQ.

• Category: Science • Tags: Diet, IQ 
🔊 Listen RSS

Ansty Church in summer

To the 12th Century Church of the Knights Hospitaller of Jerusalem, as is my custom, not for Nine Carols but for the Christmas Day service, on a blowy, very wet warm day, the small stone refuge almost full, the candles lit, and as the plain text service wended its way through the Offices the wind howled in rage outside, as if announcing a numinous new world.

In the pews whole families sat, the children quiet, the clear glass windows engraved with the texts of the waters of life, the carols reproduced on small sheets, the yellow offertory envelopes laid out expectantly. The celebrants were of all ages, though the elderly predominated, the dress code mostly tweeds, country suits, a shooting jacket, sensible shoes, a few brighter sweaters and sneakers.

The service followed the flat tone of motorway English: “And you too, mate”. The faintly remembered sonorous triads of the King James Bible and the Book of Common Prayer were banished to an outbuilding, like a smoky diesel. The improbable story was like an overheard conversation, snatches of incongruous gossip, the extenuating circumstances rehearsed without too much credence: some sort of problem about an unplanned pregnancy.

The requirement, at one point in the service, to Make a Sign of Peace, usually an occasion of deep English embarrassment, as they contemplate fellow humans with whom they have little in common, and much to regret and dispute about, was managed with aplomb. Perhaps the culture is changing, and on one day of the week, or perhaps only one day of the year, the English can tolerate close contact with those of good faith. Tempting to believe that in the eight centuries gone by the villagers loved their fellow Man better than they do now, but that is the deception of history, because, as Dryden observed: “Mankind is ever the same, and nothing is lost out of Nature, although everything is altered”.

Almost all took the sacrament, at first in absolute silence save for the wind, and then when the organist got back to her seat, to respectful accompaniment.

For “Oh Come all ye Faithful” we were permitted a descant on the penultimate verse, to which invitation heroic sopranos soared, dancing on harmonic rooftops of more lowly vocal structures. Unusually, this glorious departure did not unsettle the melodic progress of the congregation. They also serve who hum in lower registers.

In all, a good show, and as we rose at the end to face the wind the farewells were joyous in unfeigned fellowship. A moment of peace.

Reversing my car out of the sodden field, I got stuck in the mud, and in a golden example of Christian charity one neighbour, far more knowledgeable in these matters than most, advised on gear ratios for some minutes and pushed as I tried rocking the car back and forwards, until the other provided a rope and towed me out.

And so endeth the lesson.

Merry Christmas.

🔊 Listen RSS


Michael Shayer says:

As to the sample and whether it was just in one neighbourhood, no, it was 10,000 large, and representative of England and Wales.

To me the other main finding is the push towards Concrete Generalisation, with those at the bottom going up, and those at the top way, way down. I remember years ago Jerry Bruner in the “Man, a Course of Study” created a game that was supposed to push them toward more abstract thinking. All the children did was to juggle around at random.

Yes, our results in the paper would have been better as a Figure would have been better, but there will be more to the story, probably with myself, James Flynn and Michael Woodley doing another paper. I found more information in Woodley’s last paper than he reported, and it agrees with my data.

At my request he send me three of his papers central to his research finding, which I list below.

James Thompson
About James Thompson

James Thompson has lectured in Psychology at the University of London all his working life. His first publication and conference presentation was a critique of Jensen’s 1969 paper, with Arthur Jensen in the audience. He also taught Arthur how to use an English public telephone. Many topics have taken up his attention since then, but mostly he comments on intelligence research.