paternal-age   19

Nasty, brutish, but not that short | West Hunter
Average life span is pretty short for contemporary foragers (30-35 years). For that matter, it was short for agricultural peoples until fairly recently. Most people probably don’t know this. Most of the people who do know fundamentally misunderstand it. Today most people die when they’re old, moderately close to the average age of death. Back in the day, a very large fraction died when young, due to infectious disease and food shortages. And subincision. Most people who know about those short lifespans in the past somehow can’t really believe that infant mortality accounts for most of the difference. If the average lifespan was 30, they figure that hardly anyone made it to 40. I’ve had a doctor explain to me that that hardly anyone lived to be 70 in 1900 in the US (!).

We know that this is not the case in contemporary hunter-gatherers. If you make it to 15, you have a pretty good chance of making it to 60. Life expectancy at 15 was about 48 among the Australian Aborigines and 51 for the !Kung Bushmen. In some other groups, expected lifetime at 15 was lower, in the 30s. Still – even so lots of people made it to 60 or later.

A high average paternal age was only possible if quite a few guys lived well over 50 – but that happened.
west-hunter  scitariat  discussion  rant  knowledge  longevity  farmers-and-foragers  sapiens  demographics  data  regularizer  life-history  paternal-age 
september 2017 by nhaliday
Epidemiology of autism - Wikipedia
This Is How Much of Autism Is Genetic:
Indeed, when Sandin tracked autism diagnoses over time among the sibling pairs, he found that genetics likely accounts for around 83% of the disorder. That compares to nearly 90% reported in previous studies of twins only. Using the new model, environmental factors probably contribute around 17% to the risk of developing autism.
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march 2017 by nhaliday
Social Epistasis Amplifies the Fitness Costs of Deleterious Mutations, Engendering Rapid Fitness Decline Among Modernized Populations | SpringerLink
- Michael A. Woodley

We argue that in social species, interorganismal gene-gene interactions, which in previous literatures have been termed social epistasis, allow genomes carrying deleterious mutations to reduce via group-level pleiotropy the fitness of others, including noncarriers. This fitness reduction occurs by way of degradation of group-level processes that optimize the reproductive ecology of a population for intergroup competition through, among other mechanisms, suppression of free-riding.


Fitness indicators theory (Houle 2000; Miller 2000) predicts that the behavioral and physiological condition of prospective partners strongly influences female mate choice in particular, as these constitute honest indicators of underlying genetic quality. Furthermore, as deleterious mutations are pleiotropic (i.e., they can influence the development of multiple traits simultaneously), they are a source of genetic correlation among diverse behavioral and physiological domains, yielding a latent general fitness factor( f ). This optimizes the efficiency of sexual selection, as selection for quality with respect to one domain will increase the probability of selection for quality “across the board” (Houle 2000; Miller 2000). If purifying selection is primarily cryptic—working by virtue of those lower in f simply being less successful in competition for mates and therefore producing fewer offspring relative to those higher in the factor—then considerably less reproductive failure is needed to solve the mutation load paradox (19% instead of 88% based on simulations in Leseque et al. 2012).


Theoretical work involving humans suggests a loss of intrinsic fitness of around 1% per generation in the populations of modernized countries (Lynch 2016; Muller 1950). Thus, these might yet be undergoing mutational meltdown, albeit very gradually (i.e., over the course of centuries)


An interesting observation is that the fitness of the populations of modernized nations does appear to be rapidly decreasing—although not in a manner consonant with the direct action of deleterious mutations on the fitness of individuals (as per the mutation load paradox).


Increased education has furthermore encouraged individuals to trade fertility against opportunities to enhance their social status and earning power, with the largest fitness losses occurring among those with high status who potentially carry fewer deleterious mutations (i.e., by virtue of possessing higher levels of traits that exhibit some sensitivity to mutation load, such as general intelligence; Spain et al. 2015; Woodley of Menie et al. 2016a). Hitherto not considered is the possibility that the demographic transition represents a potential change in the fitness characteristics of the group-level extended phenotype of modernized populations, indicating that there might exist pathways through which deleterious mutations that accumulate due to ecological mildness could pathologically alter fertility tradeoffs in ways that might account for the maladaptive aspects of the fertility transition (e.g., subreplacement fertility; Basten, Lutz and Scherbov, 2013).


Cooperation, though offering significant fitness benefits to individual organisms and groups, involves some costs for cooperators in order to realize mutual gains for all parties. Free riders are individuals that benefit from cooperation without suffering any of the costs needed to sustain it. Hence, free riders enjoy a fitness advantage relative to cooperators via the former’s parasitism on the latter.


The balance of selection can alternate between the different levels depending on the sorts of selective challenges that a population encounters. For example, group selection may operate on human populations during times of intergroup conflict (i.e., warfare), whereas during times of peace, selection may tend to favor the fitness of individuals instead (Woodley and Figueredo 2013; Wilson 2002). A major factor that seems to permit group-level selection to be viable under certain ecological regimes is the existence of free-rider controls, i.e., features of the group’s social ecology that curb the reproductive fitness of the carriers of “selfish” genetic variants (MacDonald 1994; Wilson 2002).


High-status individuals participate in the generation and vertical cultural transmission of free-rider controls—these take the form of religious and ideological systems which make a virtue out of behaviors that overtly benefit the group, and a vice out of those that only favor individual-level fitness, via the promotion of ethnocentrism, martyrdom, and displays of commitment (MacDonald 1994, 2009, 2010; Wilson 2002). Humans are furthermore equipped with specialized mental adaptations for coordinating as part of a group, such as effortful control—the ability to override implicit behavioral drives via the use of explicit processing systems, which allow them to regulate their behavior based on what is optimal for the group (MacDonald 2008). The interaction between individuals of different degrees of status, i.e., those that generate and maintain cultural norms and those who are merely subject to them, therefore constitutes a form of social epistasis, as the complex patterns of interactions among genomes that characterize human culture have the effect of regulating both individual- and group-level (via the curbing of free-riding) fitness (MacDonald 2009, 2010).

Mutations that push the behavior of high-status individuals away from the promotion of group-selected norms may promote a breakdown of or otherwise alter these social epistatic interactions, causing dysregulation of the group’s reproductive ecology. Behavioral changes are furthermore a highly likely consequence of mutation accumulation, as “behavior” (construed broadly) is a large potential target for new mutations (Miller 2000; Lynch 2016) 1 owing to the fact that approximately 84% of all genes in the human genome are involved in some aspect of brain development and/or maintenance (Hawrylycz et al. 2012).

Consistent with the theorized role of group-level (cultural) regulatory processes in the maintenance of fitness optima, positive correlations exist between religiosity (a major freerider control; MacDonald 1994; Wilson 2002) and fertility, both at the individual differences and cross-cultural levels (Meisenberg 2011). Religiosity has declined in modernized nations—a process that has gone hand-in-hand with the rise of a values system called postmaterialism (Inglehart 1977), which is characterized by the proliferation of individualistic, secular, and antihierarchical values (Welzel 2013). The holding of these values is negatively associated with fertility, both at the individual level (when measured as political liberalism; Goldstone et al. 2011) and across time and cultures (Inglehart and Appel 1989). The rise of postmaterialist values is also associated with increasingly delayed onset of reproduction (Klien 1990) which directly increases the (population) mutation load.

Pathological Altruism

Some of the values embodied in postmaterialism have been linked to the pathological altruism phenomenon, i.e., forms of altruism that damage the intended recipients or givers of largesse (Oakley et al. 2012; Oakley 2013). Virtues associated with altruism such as kindness, fidelity, magnanimity, and heroism, along with quasi-moral traits associated with personality and mental health, may be under sexual selection and might therefore be sensitive, through the f factor, to the deleterious effects of accumulating mutations (Miller 2007).


Another form of pathologically altruistic behavior that Oakley (2013) documents is self-righteousness, which may be increasing, consistent with secular trend data indicating elevated levels of self-regarding behavior among Western populations (sometimes called the narcissism epidemic; Twenge and Campbell 2009). This sort of behavior constitutes a key component of the clever silly phenomenon in which the embrace of counterfactual beliefs is used to leverage social status via virtue signaling (e.g., the conflation of moral equality among individuals, sexes, and populations with biological equality) (Dutton and van der Linden 2015; Charlton 2009; Woodley 2010). There may be a greater number of influential persons inclined to disseminate such beliefs, in that the prevalence of phenotypes disposed toward egoistic behaviors may have increased in Western populations (per Twenge and coworkers’ research), and because egoists, specifically Machiavellians and narcissists, appear advantaged in the acquisition of elite societal stations (Spurk et al. 2015).

[Do Bad Guys Get Ahead or Fall Behind? Relationships of the Dark Triad of Personality With Objective and Subjective Career Success:

After controlling for other relevant variables (i.e., gender, age, job tenure, organization size, education, and work hours), narcissism was positively related to salary, Machiavellianism was positively related to leadership position and career satisfaction, and psychopathy was negatively related to all analyzed outcomes.]


By altering cultural norms, elite egoists may encourage the efflorescence of selfish behaviors against which some older and once highly influential cultural systems acted. For example, Christianity in various forms strongly promoted personal sacrifice for the good of groups and proscribed egoistic behaviors (Rubin 2015), but has declined significantly in terms of cultural power following modernization (Inglehart 1977). Thus, it is possible that a feedback loop exists wherein deleterious mutation accumulation raises population levels of egoism, either directly or indirectly, via the breakdown of developmental constraints on personality canalization; the resultantly greater number of egoists are then able to exploit relevant personality traits to attain positions of sociocultural influence; and through these … [more]
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march 2017 by nhaliday
The Morality of Sperm Donation -
There is a third benefit. Surprisingly, sperm donor-assisted pregnancies result in 1/5th the number of birth defects as pregnancies in general. (The CDC tells me that the defect rate is 1 in 33 or ~3%, and that birth defects in 2006 directly killed 5,819 infants.) Much of this large benefit stems from the paternal age effect - older fathers’ sperm result in more birth defects, lowered IQ, linked to autism, etc. To the extent that a sperm donor donating displaces, at the margin, the conception of future offspring at an elder age, donation directly reduces birth defects and the other mentioned effects.

Indeed, given the mixed data on whether sperm count rates are falling with time and the more reliable data on the striking increases with paternal age of negative effects like birth defects or autism - perhaps due to increased mutations4 - it may be worthwhile even for non-donators to bank their sperm for later use. A quick perusal of one sperm bank’s prices suggests that a 20-year old could store a large sample of his sperm until he is 40 for ~$5000 with the ultimate artificial insemination adding <$4000 to the final cost; if this resulted in cutting the risk of his children being autistic by 30%, would it be worthwhile? Perhaps. It is worth considering.
ratty  gwern  hmm  sex  genetics  genetic-load  paternal-age  parenting  developmental  disease  data  effective-altruism  arbitrage  cost-benefit  analysis  faq  planning 
february 2017 by nhaliday
Neurodiversity | West Hunter
Having an accurate evaluation of a syndrome as a generally bad thing isn’t equivalent to attacking those with that syndrome. Being a leper is a bad thing, not just another wonderful flavor of humanity [insert hot tub joke] , but that doesn’t mean that we have to spend our spare time playing practical jokes on lepers, tempting though that is.. Leper hockey. We can cure leprosy, and we are right to do so. Preventing deafness through rubella vaccination was the right thing too – deafness sucks. And so on. As we get better at treating and preventing, humans are going to get more uniform – and that’s a good thing. Back to normalcy!

interesting discussion of mutational load:
I was thinking again about the consequences of having more small-effect deleterious mutations than average. I don’t think that they would push hard in a particular direction in phenotype space – I don’t believe they would make you look weird, but by definition they would be bad for you, reduce fitness. I remembered a passage in a book by Steve Stirling, in which our heroine felt as if her brain ‘was moving like a mechanism of jewels and steel precisely formed.’ It strikes me that a person with an extra dollop of this kind of genetic load wouldn’t feel like that. And of course that heroine did have low genetic load, being the product of millennia of selective breeding, not to mention an extra boost from the Invisible Crown.
Well, what does the distribution of fitness burden by frequency look like for deleterious mutations of a given fitness penalty?
It’s proportional to the mutation rate for that class. There is reason to believe that there are more ways to moderately or slightly screw up a protein than to really ruin it, which indicates that mild mutations make up most load in protein-coding sequences. More of the genome is made up of conserved regulatory sequences, but mutations there probably have even milder effects, since few mutations in non-coding sequences cause a serious Mendelian disease.
I have wondered if there was some sort of evolutionary tradeoff between muscles and brains over the past hundred thousand years through dystrophin’s dual role. There is some evidence of recent positive selection among proteins that interact with dystrophin, such as DTNBP1 and DTNA.

Any novel environment where higher intelligence can accrue more caloric energy than brute strength alone (see: the invention of the bow) should relax the selection pressure for muscularity. The Neanderthals didn’t fare so well with the brute strength strategy.
Sure: that’s what you might call an inevitable tradeoff, a consequence of the laws of physics. Just as big guys need more food. But because of the way our biochemistry is wired, there can be tradeoffs that exist but are not inevitable consequences of the laws of physics – particularly likely when a gene has two fairly different functions, as they often do.
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february 2017 by nhaliday
Prevalence and architecture of de novo mutations in developmental disorders : Nature
We estimate that 42% of our cohort carry pathogenic DNMs in coding sequences; approximately half of these DNMs disrupt gene function and the remainder result in altered protein function. We estimate that developmental disorders caused by DNMs have an average prevalence of 1 in 213 to 1 in 448 births, depending on parental age. Given current global demographics, this equates to almost 400,000 children born per year.
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february 2017 by nhaliday
Links 2/17: Site Your Sources | Slate Star Codex
The United States not only does poorly on education benchmark PISA, but each decile of wealth also does poorly compared to equivalent deciles in other countries. I find this surprising. Does this torpedo the theory that each US ethnic group does as well as its foreign counterparts, and US underperformance is a Simpson’s Paradox on ethnic distribution?

Twitter: @EveryoneIsDril.

New Study Finds Performance-Enhancing Drugs For Chess. Okay, fine, just modafinil, which we already knew about, but the exact pattern is interesting. Modafinil makes people take longer to make their moves, but the moves are ultimately better. That suggests that its advantage is not increasing IQ per se, but in giving people the increased attention span/concentration to work harder on finding good moves. I think this elegantly ties together a lot of stuff into a good explanation of modafinil’s cognitive-enhancing properties.

New Zealand Wants To Know How Peter Thiel Became A Secret Citizen. Give up, New Zealand; Peter Thiel is a citizen of any country he wants to be a citizen of. Also: Peter Thiel Denies California Governor Run Despite Mysterious Group’s Backing.

I was going to link to the paper Physics Envy May Be Hazardous To Your Wealth, but the part that actually interested me is small enough that I’m just going to include it here as a jpg (h/t Julia Galef).

Nature: Prevalence And Architecture Of De Novo Mutations In Developmental Disorders. There’s been a lot of debate over paternal age effects, and this paper helps clarify that by actually counting people’s de novo mutations and finding that children of older fathers (and to a lesser degree older mothers) have more of them. I am not sure to what degree this answers the objection that fathers with worse genes will tend to get married later; my impression is that it’s circumstantial evidence against (de novo mutations are more specific to paternal age than just bad genes) but not complete disproof.

Psssst, kid, wanna buy a parasitic worm? Key quote: “Those who experience the ‘hookworm bounce’ tend to describe it as ‘feeling as if they are teenagers again'” (h/t pistachi0n).

New paper in Crime And Delinquency: “We find no evidence that the number of fatal police shootings either increased or decreased post-Ferguson. Claims to the contrary are based on weak analyses of short-term trends.” This is especially surprising in light of claims that increased inner-city crime is caused by police withdrawing in order to prevent further fatal shootings; if that’s the police’s plan, it doesn’t seem to be working very well.

Intranasal ghrelin vaccine prevents obesity in mice.

Gene drive testing thwarted when organisms quickly develop resistance. There goes that idea.

New poll: Majority of Europeans support banning Muslim immigration. It’s an Internet-based poll, which is always cause for suspicion, but they seem to be a reputable organization and not the sort of group whose results are 100% due to trolling by 4chan, plus it’s consistent with some other results. Still pretty shocking and an existential-terror-level reminder of partisan bubbles. Also: Rasmussen finds most Americans support Trump’s refugee ban order.

Closely related: M.G. Miles makes the case for banning Muslim immigration. Maybe the first person I have seen make this case in a principled way; everyone else just seems to be screaming about stuff and demanding their readers reinterpret it into argument form. Also, he uses the word “terrorism” zero times, which seems like the correct number of times for a case of this sort. This is what people should be debating and responding to. Rebuttals by Americans would probably want to start with the differences between Muslim immigrants to Europe and Muslim immigrants to the US – Miles discusses the European case, but by my understanding these are very different populations with very different outcomes).

Second Enumerations podcast: Grognor reading interesting essays.

SSRN: Extreme Protest Tactics Reduce Popular Support For Social Movements: “We find across three experiments that extreme protest tactics decreased popular support for a given cause because they reduced feelings of identification with the movement. Though this effect obtained in tests of popular responses to extreme tactics used by animal rights, Black Lives Matter, and anti-Trump protests (Studies 1-3), we found that self-identified political activists were willing to use extreme tactics because they believed them to be effective for recruiting popular support.” Cf. The Toxoplasma Of Rage. (h/t Dain)

The Cagots were an underclass of people in medieval France whom everyone hated, with various purity laws around how decent people weren’t allowed to associate with/marry/touch/go near them. In the 1500s, the Pope personally intervened to tell the French to stop persecuting them, but the French ignored him and persecuted them more than ever. As far as anyone can tell, they looked, spoke, and acted just like everyone else, and exactly how they became so despised is one of the minor mysteries of medieval history.
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february 2017 by nhaliday
Confounder Of The Day: How Sexy Your Parents Were | Slate Star Codex
- "paternal age effect" just a selection effect (men w/ issues end up having kids later due to difficulty finding a mate)
- one other suggested inconsistent explanation: spermatogenic selfish-gene effect
- interesting discussion of sperm freezing
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february 2017 by nhaliday
Judith Rich Harris: Why Do People Believe that Birth Order Has Important Effects on Personality?
Probing Birth-Order Effects on Narrow Traits Using Specification-Curve Analysis:
Although specification-curve analysis clearly confirmed the previously reported birth-order effect on intellect, we found no meaningful effects on life satisfaction, locus of control, interpersonal trust, reciprocity, risk taking, patience, impulsivity, or political orientation. The lack of meaningful birth-order effects on self-reports of personality was not limited to broad traits but also held for more narrowly defined characteristics.
Examining the effects of birth order on personality:
no effect on personality, small effect (-) on IQ
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january 2017 by nhaliday
J. Intell. | Free Full-Text | Zeroing in on the Genetics of Intelligence
Rare variants and mutations of large effect do not appear to play a main role beyond intellectual disability. Common variants can account for about half the heritability of intelligence and show promise that collaborative efforts will identify more causal genetic variants. Gene–gene interactions may explain some of the remainder, but are only starting to be tapped. Evolutionarily, stabilizing selection and selective (near)-neutrality are consistent with the facts known so far.

Idiot Proof:
I was looking at a recent survey of current knowledge in psychological genetics. The gist is that common variants – which can’t have decreased fitness much in the average past, since they’re common – are the main story in the genetic architecture of intelligence. Genetic load doesn’t seem very important, except at the low end. Big-effect deleterious mutations can certainly leave you retarded, but moderate differences in the number of slightly-deleterious mutations don’t have any observable effect – except possibly in the extremely intelligent, but that’s uncertain at this point. Not what I expected, but that’s how things look right now. It would seem that brain development is robust to small tweaks, although there must be some limit. The results with older fathers apparently fit this pattern: they have more kids with something seriously wrong, but although there should be extra mild mutations in their kids as well as the occasional serious one, the kids without obvious serious problems don’t have depressed IQ.
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december 2016 by nhaliday
Talkin’ ’bout their generations | West Hunter
According to the Decode results, mothers contribute 15 mutations, regardless of age, while men contribute 25 + 2*(g-20) mutations, when g is the average paternal age. As I pointed out earlier, if g is the same in both sexes, the average number of mutations is just 2g, which makes for 2 mutations per calendar year. I’ve been checking out average maternal age: it doesn’t vary much. The lowest I’ve seen was 26, the highest 30, so 28 is a reasonable number. So far, in the data we’ve gathered, the population with the highest paternal age was in Gambia, with an average paternal age of 47. If we assume that the average maternal age is 28 (which look about right from the graph: I haven’t digitized it yet) then the average kid would receive 94 new mutations (15 maternal, 79 paternal). With an average generation length of 37.5 years (the average of 28 and 47), that makes for 2.5 mutations per calendar year: about 15% higher than you would see in most populations, where the gap between average maternal and paternal age is not nearly as large.

A Gambia-sized gap would result in a noticeably higher rate of neutral genetic divergence. If it had existed long enough you might be able to notice it, but I think there’s a better chance of seeing this effect in Australian Aborigines, who had high average paternal age and might have had it for a long time. Other than the Australians, I would guess that all the old-dad societies are relatively recent.

The higher mutational load is not just a consequence of the higher per-year mutation rate in these old-dad societies – since generations are longer, there is less selection per calendar year (considering that most selection acts early in life). The number of mutations per generation is probably the most important number. I found some numbers for Polar Eskimos, hunter-gatherers (they gather snow) in a tough environment: average maternal age was 27, average paternal age was 32, for an average generation length of 29.5. They’d have 64 mutations a generation: the per-generation rate in Gambia is 47% higher.

There are also qualitative differences in selection: selection is weaker in childhood and stronger in midlife in an old-dad society, as Henry pointed out. So that situation should select for longer life, except that’s hard to manage in the presence of higher-than-usual genetic load.
According to Jim Crow”s 2006 article, base substitutions are mostly (overwhelmingly) from males and increase with paternal age, but small deletions are contributed about equally by males and females, with no noticeable age effect. Probably the deletions happen during meiosis.

So, with a huge gene like those involved in Duchenne’s muscular dystrophy or neurofibromatosis I, which have many exons (79 for dystrophin), many of the mutations are caused by deletions. The paternal age effect is weaker for those syndromes (since less than half of the causal mutations are base substitutions)
No surprises here save one. While selection for survival should extend male lifespans by 10 to 20 years in the case of old fathers, selection for survival before the age of reproduction is much weaker in the the case of older fathers. A prediction is that adolescent and young male death rates should be higher in old father societies because selection is weaker. I never realized that.

Hamilton’s theory does not describe human life history very well, as Rogers shows in his Figure 16.1 and discusses in the text. Human female fertility ceases long before the theory predicts that it should and humans live much longer. The reconciliation certainly has to do with kin selection or indirect selection. For example Kris Hawkes pushes the “grandmother hypothesis” according to which females cease reproduction and instead work for their daughters’ children. If she is right this grandmother effect selected for the prolonged human lifespan, and the long lifespan of males is a side-effect of selection for long life in females.
west-hunter  objektbuch  genetics  genetic-load  developmental  paternal-age  epidemiology  science-anxiety  scitariat  multi  social-structure  life-history  mutation  🌞  effect-size  data  ideas  speculation  methodology  gender  gender-diff  sex  africa  recent-selection  pop-diff  kinship  selection  population-genetics  electromag  longevity  aging  iq  intelligence  neuro  eden  explanans  age-generation 
november 2016 by nhaliday

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