nhaliday + longevity   77

Heritability of life span in the Old Order Amish | Request PDF
Offspring longevity was correlated with longevity of both parents, and in more or less additive fashion.


We estimated heritability of life span to be 25% +/- 5%, suggesting that the additive effects of genes account for one quarter of the total variability in life span in the OOA. We conclude that longevity is moderately heritable in the OOA, that the genetic effects are additive, and that genetic influences on longevity are likely to be expressed across a broad range of ages.
study  biodet  variance-components  genetics  longevity  time  medicine  health  data  usa  northeast 
september 2018 by nhaliday
Existential Risks: Analyzing Human Extinction Scenarios
Would you endorse choosing policy to max the expected duration of civilization, at least as a good first approximation?
Can anyone suggest a different first approximation that would get more votes?

How useful would it be to agree on a relatively-simple first-approximation observable-after-the-fact metric for what we want from the future universe, such as total life years experienced, or civilization duration?

We're Underestimating the Risk of Human Extinction: https://www.theatlantic.com/technology/archive/2012/03/were-underestimating-the-risk-of-human-extinction/253821/
An Oxford philosopher argues that we are not adequately accounting for technology's risks—but his solution to the problem is not for Luddites.

Anderson: You have argued that we underrate existential risks because of a particular kind of bias called observation selection effect. Can you explain a bit more about that?

Bostrom: The idea of an observation selection effect is maybe best explained by first considering the simpler concept of a selection effect. Let's say you're trying to estimate how large the largest fish in a given pond is, and you use a net to catch a hundred fish and the biggest fish you find is three inches long. You might be tempted to infer that the biggest fish in this pond is not much bigger than three inches, because you've caught a hundred of them and none of them are bigger than three inches. But if it turns out that your net could only catch fish up to a certain length, then the measuring instrument that you used would introduce a selection effect: it would only select from a subset of the domain you were trying to sample.

Now that's a kind of standard fact of statistics, and there are methods for trying to correct for it and you obviously have to take that into account when considering the fish distribution in your pond. An observation selection effect is a selection effect introduced not by limitations in our measurement instrument, but rather by the fact that all observations require the existence of an observer. This becomes important, for instance, in evolutionary biology. For instance, we know that intelligent life evolved on Earth. Naively, one might think that this piece of evidence suggests that life is likely to evolve on most Earth-like planets. But that would be to overlook an observation selection effect. For no matter how small the proportion of all Earth-like planets that evolve intelligent life, we will find ourselves on a planet that did. Our data point-that intelligent life arose on our planet-is predicted equally well by the hypothesis that intelligent life is very improbable even on Earth-like planets as by the hypothesis that intelligent life is highly probable on Earth-like planets. When it comes to human extinction and existential risk, there are certain controversial ways that observation selection effects might be relevant.
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march 2018 by nhaliday
Amish Mutation Protects Against Diabetes and May Extend Life - The New York Times
What Dr. Vaughan and his colleagues discovered was striking. Amish carriers of the mutation live on average to age 85, about 10 years longer than their peers. Among the Amish who did not have the mutation, the rate of Type 2 diabetes was 7 percent. But for carriers of the mutation, the rate was zero, despite leading the same lifestyle and consuming similar diets. Tests showed that carriers of the mutation had 28 percent lower levels of insulin, a hormone whose chronic elevation can lead to Type 2 diabetes.
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november 2017 by nhaliday
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
Alzheimers | West Hunter
Some disease syndromes almost have to be caused by pathogens – for example, any with a fitness impact (prevalence x fitness reduction) > 2% or so, too big to be caused by mutational pressure. I don’t think that this is the case for AD: it hits so late in life that the fitness impact is minimal. However, that hardly means that it can’t be caused by a pathogen or pathogens – a big fraction of all disease syndromes are, including many that strike in old age. That possibility is always worth checking out, not least because infectious diseases are generally easier to prevent and/or treat.

There is new work that strongly suggests that pathogens are the root cause. It appears that the amyloid is an antimicrobial peptide. amyloid-beta binds to invading microbes and then surrounds and entraps them. ‘When researchers injected Salmonella into mice’s hippocampi, a brain area damaged in Alzheimer’s, A-beta quickly sprang into action. It swarmed the bugs and formed aggregates called fibrils and plaques. “Overnight you see the plaques throughout the hippocampus where the bugs were, and then in each single plaque is a single bacterium,” Tanzi says. ‘

obesity and pathogens: https://westhunt.wordpress.com/2016/05/29/alzheimers/#comment-79757
not sure about this guy, but interesting: https://westhunt.wordpress.com/2016/05/29/alzheimers/#comment-79748

All too often we see large, long-lasting research efforts that never produce, never achieve their goal.

For example, the amyloid hypothesis [accumulation of amyloid-beta oligomers is the cause of Alzheimers] has been dominant for more than 20 years, and has driven development of something like 15 drugs. None of them have worked. At the same time the well-known increased risk from APOe4 has been almost entirely ignored, even though it ought to be a clue to the cause.

In general, when a research effort has been spinning its wheels for a generation or more, shouldn’t we try something different? We could at least try putting a fraction of those research dollars into alternative approaches that have not yet failed repeatedly.

Mostly this applies to research efforts that at least wish they were science. ‘educational research’ is in a special class, and I hardly know what to recommend. Most of the remedial actions that occur to me violate one or more of the Geneva conventions.

APOe4 related to lymphatic system: https://en.wikipedia.org/wiki/Apolipoprotein_E

Look,if I could find out the sort of places that I usually misplace my keys – if I did, which I don’t – I could find the keys more easily the next time I lose them. If you find out that practitioners of a given field are not very competent, it marks that field as a likely place to look for relatively easy discovery. Thus medicine is a promising field, because on the whole doctors are not terribly good investigators. For example, none of the drugs developed for Alzheimers have worked at all, which suggests that our ideas on the causation of Alzheimers are likely wrong. Which suggests that it may (repeat may) be possible to make good progress on Alzheimers, either by an entirely empirical approach, which is way underrated nowadays, or by dumping the current explanation, finding a better one, and applying it.

You could start by looking at basic notions of field X and asking yourself: How do we really know that? Is there serious statistical evidence? Does that notion even accord with basic theory? This sort of checking is entirely possible. In most of the social sciences, we don’t, there isn’t, and it doesn’t.

Hygiene and the world distribution of Alzheimer’s disease: Epidemiological evidence for a relationship between microbial environment and age-adjusted disease burden: https://academic.oup.com/emph/article/2013/1/173/1861845/Hygiene-and-the-world-distribution-of-Alzheimer-s

Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer’s disease: http://stm.sciencemag.org/content/8/340/340ra72

Fungus, the bogeyman: http://www.economist.com/news/science-and-technology/21676754-curious-result-hints-possibility-dementia-caused-fungal
Fungus and dementia
paper: http://www.nature.com/articles/srep15015
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july 2017 by nhaliday
Biological Measures of the Standard of Living - American Economic Association
The evidence suggests that the most important proximate source of increasing height was the improving disease environment as reflected by the fall in infant mortality. Rising income and education and falling family size had more modest effects. Improvements in health care are hard to identify, and the effects of welfare state spending seem to have been small.

GROWING TALL BUT UNEQUAL: NEW FINDINGS AND NEW BACKGROUND EVIDENCE ON ANTHROPOMETRIC WELFARE IN 156 COUNTRIES, 18101989: https://pseudoerasmus.files.wordpress.com/2017/03/baten-blum-2012.pdf
This is the first initiative to collate the entire body of anthropometric evidence during the 19th and 20th centuries, on a global scale. By providing a comprehensive dataset on global height developments we are able to emphasise an alternative view of the history of human well-being and a basis for understanding characteristics of well-being in 156 countries, 1810-1989.

Bones of Contention: The Political Economy of Height Inequality: http://piketty.pse.ens.fr/files/BoixRosenbluth2014.pdf
- Carles Boix, et al.

Height in the Dark Ages: https://pseudoerasmus.com/2014/06/12/aside-angus-maddison/
study  economics  growth-econ  broad-econ  history  early-modern  mostly-modern  measurement  methodology  embodied  health  longevity  sapiens  death  wealth  pseudoE  🎩  multi  epidemiology  public-health  roots  europe  policy  wonkish  healthcare  redistribution  welfare-state  disease  parasites-microbiome  wealth-of-nations  education  top-n  data  world  pdf  political-econ  inequality  farmers-and-foragers  leviathan  archaeology  🌞  article  time-series  civilization  iron-age  mediterranean  medieval  gibbon  the-classics  demographics  gender  britain  evidence  traces 
june 2017 by nhaliday
Genetically engineered humans will arrive sooner than you think. And we're not ready. - Vox
lol "epigenetics" makes an appearance ofc


For now, that’s prohibitively expensive, but it won’t always be that way. In 2003, it cost 4 dollars to press one of the keys on Endy’s hypothetical synthesizer. This month, it costs just two cents—a 200-fold decrease in price in just 14 years. In the same time frame, the cost of tuition at Stanford has doubled, and is now around $50,000. Given all of that, the first question that Stanford’s budding bioengineers get is this:

At what point will the cost of printing DNA to create a human equal the cost of teaching a student in Stanford?
And the answer is: 19 years from today.

But the follow-up question is a little more complicated:

If you and your future partner are planning to have kids, would you start saving money for college tuition, or for printing the genome of your offspring?
The question tends to split students down the line, says Endy. About 60 percent say that printing a genome is wrong, and flies against what it means to be a parent. They prize the special nature of education and would opt to save for the tuition. But around 40 percent of the class will say that the value of education may change in the future, and if genetic technology becomes mature, and allows them to secure advantages for them and their lineage, they might as well do that.


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may 2017 by nhaliday
Typos | West Hunter
In a simple model, a given mutant has an equilibrium frequency μ/s, when μ is the mutation rate from good to bad alleles and s is the size of the selective disadvantage. To estimate the total impact of mutation at that locus, you multiply the frequency by the expected harm, s: which means that the fitness decrease (from effects at that locus) is just μ, the mutation rate. If we assume that these fitness effects are multiplicative, the total fitness decrease (also called ‘mutational load’) is approximately 1 – exp(-U), when U is where U=Σ2μ, the total number of new harmful mutations per diploid individual.


interesting, suggestive comment on Africa:
I have reason to believe that few people understand genetic load very well, probably for self-referential reasons, but better explanations are possible.

One key point is that the amount of neutral variation is determined by the long-term mutational rate and population history, while the amount of deleterious variation [genetic load] is set by the selective pressures and the prevailing mutation rate over a much shorter time scale. For example, if you consider the class of mutations that reduce fitness by 1%, what matters is the past few thousand years, not the past few tens or hundreds of of thousands of years.


So, assuming that African populations have more neutral variation than non-African populations (which is well-established), what do we expect to see when we compare the levels of probably-damaging mutations in those two populations? If the Africans and non-Africans had experienced essentially similar mutation rates and selective pressures over the past few thousand years, we would expect to see the same levels of probably-damaging mutations. Bottlenecks that happened at the last glacial maximum or in the expansion out of Africa are irrelevant – too long ago to matter.

But we don’t. The amount of rare synonymous stuff is about 22% higher in Africans. The amount of rare nonsynonymous stuff (usually at least slightly deleterious) is 20.6% higher. The number of rare variants predicted to be more deleterious is ~21.6% higher. The amount of stuff predicted to be even more deleterious is ~27% higher. The number of harmful looking loss-of-function mutations (yet more deleterious) is 25% higher.

It looks as if the excess grows as the severity of the mutations increases. There is a scenario in which this is possible: the mutation rate in Africa has increased recently. Not yesterday, but, say, over the past few thousand years.


What is the most likely cause of such variations in the mutation rate? Right now, I’d say differences in average paternal age. We know that modest differences (~5 years) in average paternal age can easily generate ~20% differences in the mutation rate. Such between-population differences in mutation rates seem quite plausible, particularly since the Neolithic.
more recent: https://westhunt.wordpress.com/2017/06/06/happy-families-are-all-alike-every-unhappy-family-is-unhappy-in-its-own-way/#comment-92491
Probably not, but the question is complex: depends on the shape of the deleterious mutational spectrum [which we don’t know], ancient and recent demography, paternal age, and the extent of truncation selection in the population.
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may 2017 by nhaliday
‘How dare you work on whites’: Professors under fire for research on white mortality - The Washington Post
the paper: http://www.pnas.org/content/112/49/15078

The Nobel laureate Angus Deaton discusses extreme poverty, opioid addiction, Trump voters, robots, and rent-seeking.

co-authored the "dead white people paper" w/ wife

point about expansion of education seems important


Diverging Life Expectancies and Voting Patterns in the 2016 US Presidential Election.: https://www.ncbi.nlm.nih.gov/pubmed/28817322
Changes in county life expectancy from 1980 to 2014 were strongly negatively associated with Trump's vote share, with less support for Trump in counties experiencing greater survival gains. Counties in which life expectancy stagnated or declined saw a 10-percentage-point increase in the Republican vote share between 2008 and 2016.

DESPAIR AND DECADES-LONG DEINDUSTRIALIZATION: https://spottedtoad.wordpress.com/2018/01/10/despair-and-decades-long-deindustrialization/

WE’VE BEEN HERE BEFORE: https://spottedtoad.wordpress.com/2018/01/12/weve-been-here-before/
A concept that seems to me to be missing from the Ruhm vs. Case/Deaton debate on “deaths of despair” is that of social crisis.

This seems to me to be the case for American Indians, who began experiencing what looks like a similar social crisis to non-college educated whites about a decade beforehand: rapidly escalating rates of suicide, drug overdoses, exit from the workforce, and even alcohol-related deaths (which were already very high for American Indians well before 2000, of course):


The common thread here would seem to be replacement of workforce participation with transfer payments, particularly cash transfers (since, my own reservations about Medicaid aside, increases in in-kind payments and SNAP since the 80s haven’t seemed to exert the same disruptive effect.) As I’ve said before, it seems very likely to me that technology will push an ever larger segment of society out of the economy, sooner or later, but how to prevent this from tearing apart our social fabric I don’t know.

Once It Was Overdue Books. Now Librarians Fight Overdoses.: https://www.nytimes.com/2018/02/28/nyregion/librarians-opioid-heroin-overdoses.html
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april 2017 by nhaliday
Interview Greg Cochran by Future Strategist

- IQ enhancement (somewhat apprehensive, wonder why?)
- ~20 years to CRISPR enhancement (very ballpark)
- cloning as an alternative strategy
- environmental effects on IQ, what matters (iodine, getting hit in the head), what doesn't (schools, etc.), and toss-ups (childhood/embryonic near-starvation, disease besides direct CNS-affecting ones [!])
- malnutrition did cause more schizophrenia in Netherlands (WW2) and China (Great Leap Forward) though
- story about New Mexico schools and his children (mostly grad students in physics now)
- clever sillies, weird geniuses, and clueless elites
- life-extension and accidents, half-life ~ a few hundred years for a typical American
- Pinker on Harvard faculty adoptions (always Chinese girls)
- parabiosis, organ harvesting
- Chicago economics talk
- Catholic Church, cousin marriage, and the rise of the West
- Gregory Clark and Farewell to Alms
- retinoblastoma cancer, mutational load, and how to deal w/ it ("something will turn up")
- Tularemia and Stalingrad (ex-Soviet scientist literally mentioned his father doing it)
- germ warfare, nuclear weapons, and testing each
- poison gas, Haber, nerve gas, terrorists, Japan, Syria, and Turkey
- nukes at https://en.wikipedia.org/wiki/Incirlik_Air_Base
- IQ of ancient Greeks
- history of China and the Mongols, cloning Genghis Khan
- Alexander the Great vs. Napoleon, Russian army being late for meetup w/ Austrians
- the reason why to go into Iraq: to find and clone Genghis Khan!
- efficacy of torture
- monogamy, polygamy, and infidelity, the Aboriginal system (reverse aging wives)
- education and twin studies
- errors: passing white, female infanticide, interdisciplinary social science/economic imperialism, the slavery and salt story
- Jewish optimism about environmental interventions, Rabbi didn't want people to know, Israelis don't want people to know about group differences between Ashkenazim and other groups in Israel
- NASA spewing crap on extraterrestrial life (eg, thermodynamic gradient too weak for life in oceans of ice moons)
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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: http://sci-hub.tw/http://journals.sagepub.com/doi/abs/10.1177/1948550615609735

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]
study  speculation  models  biodet  bio  sapiens  evolution  genetic-load  paternal-age  the-monster  slippery-slope  society  social-structure  free-riding  coordination  EGT  dynamical  🌞  fertility  dysgenics  eh  self-control  obesity  altruism  mutation  multi  twitter  social  commentary  perturbation  gnon  new-religion  science-anxiety  population-genetics  biophysical-econ  hmm  discipline  autism  scitariat  clown-world  epidemiology  malaise  sociology  demographic-transition  blowhards  model-organism  nonlinearity  civilization  expression-survival  universalism-particularism  order-disorder  trends  deep-materialism  values  ideology  domestication  cohesion  christopher-lasch  scale  patho-altruism  social-capital  behavioral-gen  madisonian  chart  nihil  aristos  piracy  theos  cultural-dynamics  roots  zeitgeist  rot  the-bones  counter-revolution  pdf  modernity  microfoundations  video  presentation  religion  christianity  health  longevity  ethnocentrism  genetic-correlation  👽  instinct 
march 2017 by nhaliday
A simple offspring-to-mother size ratio predicts post-reproductive lifespan | bioRxiv
Here we show that a candidate proxy of the stress of childbirth explains a large portion of the variance in post-reproductive lifespans across many species. A remarkably simple metric, the offspring ratio (ratio of the size or weight of offspring to that of the mother) explained 77% of the variance of the post-reproductive lifespan in a sample drawn from widely dispersed taxa. Our results suggest that the stress of childbirth is an important and conserved determinant of post-reproductive lifespan. Thus, long post-reproductive lifespan may simply be a byproduct of the somatic health required for reproduction of large progeny, regardless of parental care.
study  preprint  bio  evolution  longevity  nature  sapiens  variance-components  causation  roots  correlation  embodied 
february 2017 by nhaliday
Female Doctors May Be Better Than Male Doctors - The Atlantic
study is linked in article

We examined the association between physician sex and 30-day mortality and readmission rates, adjusted for patient and physician characteristics and hospital fixed effects (effectively comparing female and male physicians within the same hospital). As a sensitivity analysis, we examined only physicians focusing on hospital care (hospitalists), among whom patients are plausibly quasi-randomized to physicians based on the physician’s specific work schedules. We also investigated whether differences in patient outcomes varied by specific condition or by underlying severity of illness.

You'll have to figure this one out for yourselves: http://andrewgelman.com/2016/12/21/youll-figure-one/
news  org:mag  study  summary  medicine  gender  natural-experiment  longevity  healthcare  diversity  intervention  endogenous-exogenous  multi  gelman  replication  critique  scitariat 
december 2016 by nhaliday
The Life-Span of Empires
empires die but don't age

The author examined the distribution of imperial lifetimes using a data set that spans more than three millennia and found that it conforms to a memoryless exponential distribution in which the rate of collapse of an empire is independent of its age.

same is true for species apparently
but it's a power law for larger taxa
pdf  study  history  anthropology  civilization  risk  aphorism  regularizer  objektbuch  distribution  stylized-facts  economics  cliometrics  cycles  red-queen  competition  iron-age  mediterranean  new-religion  the-classics  gibbon  leviathan  nihil  cultural-dynamics  great-powers  time  longevity  conquest-empire  multiplicative  power-law  hari-seldon 
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
The Day Before Forever | West Hunter
Yesterday, I was discussing the possibilities concerning slowing, or reversing aging – why it’s obviously possible, although likely a hard engineering problem. Why partial successes would be valuable, why making use of the evolutionary theory of senescence should help, why we should look at whales and porcupines as well as Jeanne Calment, etc., etc. I talked a long time – it’s a subject that has interested me for many years.

But there’s one big question: why are the powers that be utterly uninterested ?

The Intercollegiate Studies Institute and the Abagail Adams Institute host a debate between Peter Thiel and William Hurlbut. Resolved: Technology Should Treat Death as an Enemy

What if you could buy an extra year of youth for a million bucks (real cost). Clearly this country ( or any country) can’t afford that for everyone. Some people could: and I think it would stick in many people’s craw. Even worse if they do it by harvesting the pineal glands of children and using them to manufacture a waxy nodule that forfends age.

This is something like the days of old, pre-industrial times. Back then, the expensive, effective life-extender was food in a famine year.

Once upon a time, I wrote a long spiel on life extension – before it was cool, apparently. I sent it off to an interested friend [a science fiction editor] who was at that time collaborating on a book with a certain politician. That politician – Speaker of the House, but that could be anyone of thousands of guys, right? – ran into my spiel and read it. His immediate reaction was that greatly extending the healthy human life span would be horrible – it would bankrupt Social Security ! Nice to know that guys running the show always have the big picture in mind.

Reminds me of a sf story [Trouble with Lichens] in which something of that sort is invented and denounced by the British trade unions, as a plot to keep them working forever & never retire.

He’s got the argument backward: sure, natural selection has not favored perfect repair, so says the evolutionary theory of of senescence. If it had, then we could perhaps conclude that perfect repair was very hard to achieve, since we don’t see it, at least not in complex animals.* But since it was not favored, since natural selection never even tried, it may not be that difficult.

Any cost-free longevity gene that made you live to be 120 would have had a small payoff, since various hazards were fairly likely to get you by then anyway… And even if it would have been favored, a similar gene that cost a nickel would not have been. Yet we can afford a nickel.

There are useful natural examples: we don’t have to start from scratch. Bowhead whales live over 200 years: I’m not too proud to learn from them.

Lastly , this would take a lot of work. So what?

*Although we can invent things that evolution can’t – we don’t insist that all the intermediate stages be viable.


doesn't think much of Aubrey de Gray: https://westhunt.wordpress.com/2013/07/21/of-mice-and-men/#comment-15832
I wouldn’t rely on Aubrey de Gray.

It might be easier to fix if we invested more than a millionth of a percent of GNP on longevity research. It’s doable, but hardly anyone is interested. I doubt if most people, including most MDs and biologists, even know that it’s theoretically possible.

I suppose I should do something about it. Some of our recent work ( Henry and me) suggests that people of sub-Saharan African descent might offer some clues – their funny pattern of high paternal age probably causes the late-life mortality crossover, it couldn’t hurt to know the mechanisms involved.

Make Room! Make Room!: https://westhunt.wordpress.com/2015/06/24/make-room-make-room/
There is a recent article in Phys Rev Letters (“Programed Death is Favored by Natural Selection in Spatial Systems”) arguing that aging is an adaptation – natural selection has favored mechanisms that get rid of useless old farts. I can think of other people that have argued for this – some pretty smart cookies (August Weismann, for example, although he later abandoned the idea) and at the other end of the spectrum utter loons like Martin Blaser.


There might could be mutations that significantly extended lifespan but had consequences that were bad for fitness, at least in past environments – but that isn’t too likely if mutational accumulation and antagonistic pleiotropy are the key drivers of senescence in humans. As I said, we’ve never seen any.

more on Martin Blaser:
This is off topic, but I just read Germs Are Us and was struck by the quote from Martin Blaser ““[causing nothing but harm] isn’t how evolution works” […] “H. pylori is an ancestral component of humanity.”
That seems to be the assumption that the inevitable trend is toward symbiosis that I recall from Ewald’s “Plague Time”. My recollection is that it’s false if the pathogen can easily jump to another host. The bulk of the New Yorker article reminded me of Seth Roberts.

I have corresponded at length with Blaser. He’s a damn fool, not just on this. Speaking of, would there be general interest in listing all the damn fools in public life? Of course making the short list would be easier.

I have corresponded at length with Blaser. He’s a damn fool, not just on this. Speaking of, would there be general interest in listing all the damn fools in public life? Of course making the short list would be easier.
enhancement  longevity  aging  discussion  west-hunter  scitariat  multi  thermo  death  money  big-picture  reflection  bounded-cognition  info-dynamics  scifi-fantasy  food  pinker  thinking  evolution  genetics  nature  oceans  inequality  troll  lol  chart  model-organism  shift  smoothness  🌞  🔬  track-record  low-hanging  aphorism  ideas  speculation  complex-systems  volo-avolo  poast  people  paternal-age  life-history  africa  natural-experiment  mutation  genetic-load  questions  study  summary  critique  org:nat  commentary  parasites-microbiome  disease  elite  tradeoffs  homo-hetero  contrarianism  history  medieval  lived-experience  EEA  modernity  malthus  optimization  video  facebook  social  debate  thiel  barons 
november 2016 by nhaliday
Americans Are Dying Faster. Millennials, Too - Bloomberg
is this for static cohort? could be confounded by changing demographics.
news  trends  longevity  usa  data  org:mag  org:biz  age-generation  current-events 
october 2016 by nhaliday
What You Can't Say
E Pur Si Muove:

Sam Altman and the fear of political correctness: http://marginalrevolution.com/marginalrevolution/2017/12/sam-altman-fear-political-correctness.html
Earlier this year, I noticed something in China that really surprised me. I realized I felt more comfortable discussing controversial ideas in Beijing than in San Francisco. I didn’t feel completely comfortable—this was China, after all—just more comfortable than at home.

That showed me just how bad things have become, and how much things have changed since I first got started here in 2005.

It seems easier to accidentally speak heresies in San Francisco every year. Debating a controversial idea, even if you 95% agree with the consensus side, seems ill-advised.
And so it runs with shadow prices for speech, including rights to say things and to ask questions. Whatever you are free to say in America, you have said many times already, and the marginal value of exercising that freedom yet again doesn’t seem so high. But you show up in China, and wow, your pent-up urges are not forbidden topics any more. Just do be careful with your mentions of Uncle Xi, Taiwan, Tibet, Uighur terrorists, and disappearing generals. That said, in downtown Berkeley you can speculate rather freely on whether China will someday end up as a Christian nation, and hardly anybody will be offended.

For this reason, where we live typically seems especially unfree when it comes to speech. And when I am in China, I usually have so, so many new dishes I want to sample, including chestnuts and pumpkin.

replies: http://www.businessinsider.com/sam-altman-ignites-debate-on-whether-silicon-valley-culture-makes-it-tough-to-innovate-2017-12


Baidu's Robin Li is Helping China Win the 21st Century: http://time.com/5107485/baidus-robin-li-helping-china-win-21st-century/
Therein lies the contradiction at the heart of China’s efforts to forge the future: the country has the world’s most severe restrictions on Internet freedom, according to advocacy group Freedom House. China employs a highly sophisticated censorship apparatus, dubbed the Great Firewall, to snuff out any content deemed critical or inappropriate. Google, Facebook and Twitter, as well as news portals like the New York Times, Bloomberg and TIME, are banned. Manned by an army of 2 million online censors, the Great Firewall gives outsiders the impression of deathly silence within.

But in fact, business thrives inside the firewall’s confines–on its guardians’ terms, of course–and the restrictions have not appeared to stymie progress. “It turns out you don’t need to know the truth of what happened in Tiananmen Square to develop a great smartphone app,” says Kaiser Kuo, formerly Baidu’s head of international communications and a co-host of Sinica, an authoritative podcast on China. “There is a deep hubris in the West about this.” The central government in Beijing has a fearsome capacity to get things done and is willing to back its policy priorities with hard cash. The benefits for companies willing or able to go along with its whims are clear. The question for Baidu–and for Li–is how far it is willing to go.

Silicon Valley would be wise to follow China’s lead: https://www.ft.com/content/42daca9e-facc-11e7-9bfc-052cbba03425
The work ethic in Chinese tech companies far outpaces their US rivals

The declaration by Didi, the Chinese ride-hailing company, that delivery business Meituan’s decision to launch a rival service would spark “the war of the century”, throws the intensive competition between the country’s technology companies into stark relief.

The call to arms will certainly act as a spur for Didi employees, although it is difficult to see how they can work even harder. But what it does reveal is the striking contrast between working life in China’s technology companies and their counterparts in the west.

In California, the blogosphere has been full of chatter about the inequity of life. Some of this, especially for women, is true and for certain individuals their day of reckoning has been long overdue. But many of the soul-sapping discussions seem like unwarranted distractions. In recent months, there have been complaints about the political sensibilities of speakers invited to address a corporate audience; debates over the appropriate length of paternity leave or work-life balances; and grumbling about the need for a space for musical jam sessions. These seem like the concerns of a society that is becoming unhinged.


While male chauvinism is still common in the home, women have an easier time gaining recognition and respect in China’s technology workplaces — although they are still seriously under-represented in the senior ranks. Many of these high-flyers only see their children — who are often raised by a grandmother or nanny — for a few minutes a day. There are even examples of husbands, eager to spend time with their wives, who travel with them on business trips as a way to maintain contact.

What I learned from 5 weeks in Beijing + Shanghai:

- startup creation + velocity dwarfs anything in SF
- no one in China I met is remotely worried about U.S. or possibly even cares
- access to capital is crazy
- scale feels about 20x of SF
- endless energy
- not SV jaded


Western values are freeriding on Western innovation.
Comparatively unimpeded pursuit of curiosity into innovation is a Western value that pays the carriage fare.
True. A lot of values are worthwhile in certain contexts but should never have been scaled.

Diversity, "social mobility", iconoclasm
but due to military and technological victory over its competitors
There's something to be said for Western social trust as well, though that's an institution more than an idea
essay  yc  culture  society  philosophy  reflection  contrarianism  meta:rhetoric  thiel  embedded-cognition  paulg  water  🖥  techtariat  barons  info-dynamics  realness  truth  straussian  open-closed  preference-falsification  individualism-collectivism  courage  orwellian  multi  backup  econotariat  marginal-rev  commentary  links  quotes  hard-tech  skunkworks  enhancement  genetics  biotech  sv  tech  trends  civil-liberty  exit-voice  longevity  environment  innovation  frontier  politics  identity-politics  zeitgeist  china  asia  sinosphere  censorship  news  org:lite  org:biz  debate  twitter  social  social-norms  gender  sex  sexuality  org:med  blowhards  drama  google  poll  descriptive  values  rot  humility  tradeoffs  government  the-great-west-whale  internet  occident  org:rec  org:anglo  venture  vitality  gibbon  competition  investing  martial  discussion  albion  journos-pundits  europe  ideology  free-riding  degrees-of-freedom  land  gnon  peace-violence  diversity  mobility  tradition  reason  curiosity  trust  n-factor  institutions  th 
october 2016 by nhaliday
PLOS ONE: Moderate Alcohol Use and Cardiovascular Disease from Mendelian Randomization
Low to moderate alcohol use among men had the expected effects on most CVD risk factors but not fasting glucose. Larger studies are needed to confirm the null associations with IHD, CVD and fasting glucose.
study  methodology  longevity  health  ethanol  cardio  cocktail  habit  long-term  epidemiology  intervention  endo-exo  null-result  public-health  mendel-randomization  endogenous-exogenous 
september 2016 by nhaliday
Physical Activity, Fitness, Glucose Homeostasis, and Brain Morphology in Twins
twin study (N=10) shows exercise increases grey matter, lowers body fat

[Rottensteiner et al, 2016]: http://www.ncbi.nlm.nih.gov.sci-hub.cc/pubmed/27112070
Inactive twins had 31% more intra-abdominal fat than their active co-twins (mean difference 0.52 kg, 95% CI 0.12 to 0.91, P = 0.016), whereas the difference in subcutaneous abdominal fat was only 13% (P = 0.21) and 3% in body mass index (P = 0.28). Intraperitoneal fat mass was 41% higher among inactive twins compared to their active co-twins (mean difference 0.41 kg, 95% CI 0.11 to 0.70, P = 0.012). Dietary intake did not differ between co-twins.

same study: https://twitter.com/timothycbates/status/880326920491106304
Visible changes to body, but zero effect of exercise on mortality (p=.94) in MZ differences lifespan studies... #BGA2017
gwern  pdf  study  fitness  health  genetics  neuro  regularizer  🐸  fitsci  embodied-cognition  variance-components  🌞  twin-study  environmental-effects  c:**  hmm  biodet  virtu  oscillation  brain-scan  intervention  multi  obesity  twitter  social  commentary  scitariat  longevity  null-result  effect-size  piracy  europe  nordic  evidence-based  human-study  solid-study 
september 2016 by nhaliday
Physical activity in adulthood: genes and mortality : Scientific Reports
Observational studies report a strong inverse relationship between leisure-time physical activity and all-cause mortality. Despite suggestive evidence from population-based associations, scientists have not been able to show a beneficial effect of physical activity on the risk of death in controlled intervention studies among individuals who have been healthy at baseline. On the other hand, high cardiorespiratory fitness is known to be a strong predictor of reduced mortality, even more robust than physical activity level itself. Here, in both animals and/or human twins, we show that the same genetic factors influence physical activity levels, cardiorespiratory fitness, and risk of death. Previous observational follow-up studies in humans suggest that increasing fitness through physical activity levels could prolong life; however, our controlled interventional study with laboratory rats bred for low and high intrinsic fitness contrast with these findings. Also, we find no evidence for the suggested association using pairwise analysis among monozygotic twin pairs who are discordant in their physical activity levels. Based on both our animal and human findings, we propose that genetic pleiotropy might partly explain the frequently observed associations between high baseline physical activity and later reduced mortality in humans.

study  longevity  aging  genetics  fitness  idk  fitsci  variance-components  genetic-correlation  twin-study  evidence-based  🌞  org:nat  environmental-effects  c:**  biodet  intervention  cardio  hmm  null-result  human-study  model-organism  solid-study  multi  reddit  social  commentary  ssc  gwern  ratty 
september 2016 by nhaliday
Intermittent Fasting - Gwern.net
Our intuitive mental models are Aristotelian - strength or health are intrinsic qualities which can be developed by certain actions. But the reality is that exercise offers no intrinsic benefit to the body, no more than driving 10,000 miles in a car makes it more fuel-efficient or its tires more robust. Things wear down, in cars and cells. So why is exercise recommended? Because of the biological response to the damage caused by the exercise. Chemical pathways are activated, secretions unleashed, formerly silenced genes suddenly start expressing themselves, and things happen. Chemical cascades can be modified or interrupted by other chemicals, of course. We see proof of this in startling studies, like the consumption of antioxidants destroying the health benefits of exercise; why do antioxidants do that? Because the damage caused by exercise takes, in part, the form of oxidants, and the oxidants trigger some of those chemical pathways; the antioxidants neutralize & eliminate the oxidants, and so those pathways are muted or suppressed.

So much for exercise. Something similar is theorized about the much ballyhooed caloric restriction. It is not the number of calories that has any intrinsic meaning, which finesses any law of physics to enable greater longevity - it is the body’s reactions to the restriction that matters, the changing levels of sirtuin proteins. (Why would evolution not make this reaction the default reaction and would permit the organism to die before it absolutely had to? There are a number of models where aging helps genetic fitness, actually; just another reminder that Nature does not have our best interests at heart.) Presumably some of the pathways could be directly controlled by injecting additional enzymes even as calorie consumption remains intact, and for that reason a number of biotech/pharmacorps have been interested in the sirtuins and other chemicals linked to caloric restriction. All that matters is that the pathways get triggered. A little like a computer - it doesn’t care what a command or file means, it just cares whether the input satisfies whatever entirely arbitrary (from its point of view) criteria the computer holds at that moment.
longevity  health  food  analysis  gwern  aging  ratty  cardio  c:**  nutrition  fitsci  faq  diet  metabolic  chart  guide 
july 2016 by nhaliday
Helpless to Prevent Cancer? Actually, Quite a Bit Is in Your Control - The New York Times
nchelluri on HN:
Interesting article. I don't know that I'd take too much to heart given some of the obvious caveats the author has been nice enough to make explicit, but it sounds like I'd be hard pressed to argue the suggestions contained within.
For the tl;dr crowd:
- written by a physician
- people often think that heart disease is controllable by our actions whereas they feel that cancer is not
- > people can’t change many risk factors of heart disease like age, race and family genetics
- > A more recent study published in Nature argues that there is a lot we can do. [about cancer]
- > Using sophisticated modeling techniques, the researchers argued that less than 30 percent of the lifetime risk of getting cancer was because of intrinsic risk factors, or the “bad luck.”
- > [another study] identified four domains that are often noted to be related to disease prevention: smoking, drinking, obesity and exercise
- if you limit that stuff, and not meaning 0 smoking, but "having quit within the last 5 years", no more than 1 drink a day (women) or 2 drinks a day (men), your BMI is >= 18.5 and <= 27.5 (BMI is such a shit and antiquated metric, IMO, incidentally), and perform 150mins/wk moderate intensity excercise or 75mins/wk vigorous intensity exercise, then you're in the low risk group. so the barrier to entry is not super high.
> No study is perfect, and this is no exception. These cohorts are overwhelmingly white and consist of health professionals, who are not necessarily like the population at large. But the checks against the national data showed that if anything, these results might be underestimating how much cancer is preventable by healthy behaviors.
Optimistic conclusion, for a skeptical cheapskate like myself,
> As we talk about cancer “moonshots” that will most likely cost billions of dollars and might not achieve results, it’s worth considering that — as in many cases — prevention is not only the cheapest course, but also the most effective.
Hard to fault this article. I'm glad you posted it, thank you.
fitness  health  longevity  advice  expert  embodied  aging  cancer  habit  long-term  org:rec  obesity  multi  org:data  epidemiology  fitsci  expert-experience 
july 2016 by nhaliday

bundles : embodiedgrowth

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