nhaliday + candidate-gene   22

1 Genetics and Crime
The broader construct of antisocial behavior – which includes criminal offending, as well as aggression – also shows substantial genetic influence. In a meta-analysis combining effect sizes in 51 twin and adoption studies, Rhee and Waldman (2002) reported a heritability estimate of 41 per cent, with the remaining 59 per cent of variance being due to environmental factors. Interestingly, when comparing results for various definitions of antisocial behavior, only criminal offending appeared to be influenced by both additive genetic effects and non-additive genetic effects – possibly due to genetic dominance and epistatic interactions between genes – based on a pattern of results whereby, on average, identical (monozygotic) twin correlations are more than twice the value of fraternal (dizygotic) twin correlations, and also that biological parent–offspring correlations are less than fraternal twin correlations. Such non-additive genetic effects could arise if one or more high risk alleles act in a recessive fashion, or if certain alleles at one locus affect gene expression at other loci (epistasis).

One intriguing aspect of the literature on genetics and crime is that the strong and consistent genetic influence seen for property offending does not hold true for violent criminal convictions. None of the major adoption studies in Scandinavia or the United States found any elevated risk for violent convictions as a function of either biological or adoptive parent criminal offending, although one early twin study did find greater identical (monozygotic) than fraternal (dizygotic) concordance for violent convictions (see Cloninger and Gottesman, 1987). This pattern of twin, but not parent-offspring, similarity for violent criminal behavior suggests the possibility of non-additive genetic effects due to dominance or epistasis, which would result in increased resemblance for siblings (and twins), but not for parents and offspring. Thus, there may be genetic risk for violent crimes such as murder and rape, which may stem from rare recessive genes, or specific combinations of alleles that do not appear in studies of vertical transmission across generations.

A Swedish national twin study of criminal behavior and its violent, white-collar and property subtypes: https://www.cambridge.org/core/journals/psychological-medicine/article/a-swedish-national-twin-study-of-criminal-behavior-and-its-violent-white-collar-and-property-subtypes/0D9A88185ED0FD5525A5EBD5D2EBA117
For all criminal convictions, heritability was estimated at around 45% in both sexes, with the shared environment accounting for 18% of the variance in liability in females and 27% in males. The correlation of these risk factors across sexes was estimated at +0.63. In men, the magnitudes of genetic and environmental influence were similar in the three criminal conviction subtypes. However, for violent and white-collar convictions, nearly half and one-third of the genetic effects were respectively unique to that criminal subtype. About half of the familial environmental effects were unique to property convictions.

Heritability, Assortative Mating and Gender Differences in Violent Crime: Results from a Total Population Sample Using Twin, Adoption, and Sibling Models: https://link.springer.com/article/10.1007/s10519-011-9483-0
Using 36k twins, violent crime was moderately heritable (~ 55%) w/ 13% shared environment influence. Using 1.5 mil siblings, heritability was higher for males, & family environment higher for females. Moderate assortative mating for violent crime (r = .4).

The impact of neighbourhood deprivation on adolescent violent criminality and substance misuse: A longitudinal, quasi-experimental study of the total Swedish population: https://academic.oup.com/ije/article/42/4/1057/656274/The-impact-of-neighbourhood-deprivation-on
In the crude model, an increase of 1 SD in neighbourhood deprivation was associated with a 57% increase in the odds of being convicted of a violent crime (95% CI 52%–63%). The effect was greatly attenuated when adjustment was made for a number of observed confounders (OR 1.09, 95% CI 1.06–1.11). When we additionally adjusted for unobserved familial confounders, the effect was no longer present (OR 0.96, 95% CI 0.84–1.10). Similar results were observed for substance misuse. The results were not due to poor variability either between neighbourhoods or within families.

Childhood family income, adolescent violent criminality and substance misuse: quasi-experimental total population study: http://bjp.rcpsych.org/content/early/2014/08/14/bjp.bp.113.136200
https://www.economist.com/news/science-and-technology/21613303-disturbing-study-link-between-incomes-and-criminal-behaviour-have-and
What did surprise him was that when he looked at families which had started poor and got richer, the younger children—those born into relative affluence—were just as likely to misbehave when they were teenagers as their elder siblings had been. Family income was not, per se, the determining factor.

Indicators of domestic/intimate partner violence are structured by genetic and nonshared environmental influences: https://www.researchgate.net/publication/233737219_Indicators_of_domesticintimate_partner_violence_are_structured_by_genetic_and_nonshared_environmental_influences
Three indicators of IPV were measured and genetic factors accounted for 24% of the variance in hitting one's partner, 54% of the variance in injuring one's partner, and 51% of the variance in forcing sexual activity on one's partner. The shared environment explained none of the variance across all three indicators and the nonshared environment explained the remainder of the variance.
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october 2017 by nhaliday
The Genetics of Alzheimer Disease
Twin and family studies indicate that genetic factors are estimated to play a role in at least 80% of AD cases. The inheritance of AD exhibits a dichotomous pattern. On one hand, rare mutations in APP, PSEN1, and PSEN2 virtually guarantee early-onset (<60 years) familial AD, which represents ∼5% of AD. On the other hand, common gene polymorphisms, such as the ε4 and ε2 variants of the APOE gene, can influence susceptibility for ∼50% of the common late-onset AD. These four genes account for 30%–50% of the inheritability of AD. Genome-wide association studies have recently led to the identification of 11 additional AD candidate genes.

Role of Genes and Environments for Explaining Alzheimer Disease: http://jamanetwork.com/journals/jamapsychiatry/fullarticle/209307
study  biodet  twin-study  sib-study  variance-components  candidate-gene  GWAS  medicine  neuro  neuro-nitgrit  dementia  disease  🌞  aging  multi  org:nat  genetics  genomics  immune  health 
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
http://perfecthealthdiet.com/2010/06/is-alzheimer%E2%80%99s-caused-by-a-bacterial-infection-of-the-brain/

https://westhunt.wordpress.com/2016/12/13/the-twelfth-battle-of-the-isonzo/
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

https://westhunt.wordpress.com/2012/03/06/spontaneous-generation/#comment-2236
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

Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors: https://advances.sciencemag.org/content/5/1/eaau3333
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july 2017 by nhaliday
Interview: Mostly Sealing Wax | West Hunter
https://soundcloud.com/user-519115521/greg-cochran-part-2
https://medium.com/@houstoneuler/annotating-part-2-of-the-greg-cochran-interview-with-james-miller-678ba33f74fc

- conformity and Google, defense and spying (China knows prob almost all our "secrets")
- in the past you could just find new things faster than people could reverse-engineer. part of the problem is that innovation is slowing down today (part of the reason for convergence by China/developing world).
- introgression from archaics of various kinds
- mutational load and IQ, wrath of khan neanderthal
- trade and antiquity (not that useful besides ideas tbh), Roman empire, disease, smallpox
- spices needed to be grown elsewhere, but besides that...
- analogy: caste system in India (why no Brahmin car repairmen?), slavery in Greco-Roman times, more water mills in medieval times (rivers better in north, but still could have done it), new elite not liking getting hands dirty, low status of engineers, rise of finance
- crookery in finance, hedge fund edge might be substantially insider trading
- long-term wisdom of moving all manufacturing to China...?
- economic myopia: British financialization before WW1 vis-a-vis Germany. North vs. South and cotton/industry, camels in Middle East vs. wagons in Europe
- Western medicine easier to convert to science than Eastern, pseudoscience and wrong theories better than bag of recipes
- Greeks definitely knew some things that were lost (eg, line in Pliny makes reference to combinatorics calculation rediscovered by German dude much later. think he's referring to Catalan numbers?), Lucio Russo book
- Indo-Europeans, Western Europe, Amerindians, India, British Isles, gender, disease, and conquest
- no farming (Dark Age), then why were people still farming on Shetland Islands north of Scotland?
- "symbolic" walls, bodies with arrows
- family stuff, children learning, talking dog, memory and aging
- Chinese/Japanese writing difficulty and children learning to read
- Hatfield-McCoy feud: the McCoy family was actually a case study in a neurological journal. they had anger management issues because of cancers of their adrenal gland (!!).

the Chinese know...: https://macropolo.org/casting-off-real-beijings-cryptic-warnings-finance-taking-economy/
Over the last couple of years, a cryptic idiom has crept into the way China’s top leaders talk about risks in the country’s financial system: tuo shi xiang xu (脱实向虚), which loosely translates as “casting off the real for the empty.” Premier Li Keqiang warned against it at his press conference at the end of the 2016 National People’s Congress (NPC). At this year’s NPC, Li inserted this very expression into his annual work report. And in April, while on an inspection tour of Guangxi, President Xi Jinping used the term, saying that China must “unceasingly promote industrial modernization, raise the level of manufacturing, and not allow the real to be cast off for the empty.”

Such an odd turn of phrase is easy to overlook, but it belies concerns about a significant shift in the way that China’s economy works. What Xi and Li were warning against is typically called financialization in developed economies. It’s when “real” companies—industrial firms, manufacturers, utility companies, property developers, and anyone else that produces a tangible product or service—take their money and, rather than put it back into their businesses, invest it in “empty”, or speculative, assets. It occurs when the returns on financial investments outstrip those in the real economy, leading to a disproportionate amount of money being routed into the financial system.

https://twitter.com/gcochran99/status/1160589827651203073
https://archive.is/Yzjyv
Bad day for Lehman Bros.
--
Good day for everyone else, then.
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may 2017 by nhaliday
Links 5/17: Rip Van Linkle | Slate Star Codex
More on Low-Trust Russia: Do Russian Who Wants To Be A Millionaire contestants avoid asking the audience because they expect audience members to deliberately mislead them?

Xenocrypt on the math of economic geography: “A party’s voters should get more or less seats based on the shape of the monotonic curve with integral one they can be arranged in” might sound like a very silly belief, but it is equivalent to the common mantra that you deserve to lose if your voters are ‘too clustered’”

Okay, look, I went way too long between writing up links posts this time, so you’re getting completely dated obsolete stuff like Actually, Neil Gorsuch Is A Champion Of The Little Guy. But aside from the Gorsuch reference this is actually pretty timeless – basically an argument for strict constructionism on the grounds that “a flexible, living, bendable law will always tend to be bent in the direction of the powerful.”

Otium: Are Adult Developmental Stages Real? Looks at Kohlberg, Kegan, etc.

I mentioned the debate over 5-HTTLPR, a gene supposedly linked to various mental health outcomes, in my review of pharmacogenomics. Now a very complete meta-analysis finds that a lot of the hype around it isn’t true. This is pretty impressive since there are dozens of papers claiming otherwise, and maybe the most striking example yet of how apparently well-replicated a finding can be and still fail to pan out.

Rootclaim describes itself as a crowd-sourced argument mapper. See for example its page on who launched the chemical attack in Syria.

Apparently if you just kill off all the cells that are growing too old, you can partly reverse organisms’ aging (paper, popular article)

The Politics Of The Gene: “Contrary to expectations, however, we find little evidence that it is more common for whites, the socioeconomically advantaged, or political conservatives to believe that genetics are important for health and social outcomes.”

Siberian Fox linked me to two studies that somewhat contradicted my minimalist interpretation of childhood trauma here: Alemany on psychosis and Turkheimer on harsh punishment.

Lyrebird is an AI project which, if fed samples of a person’s voice, can read off any text you want in the same voice. See their demo with Obama, Trump, and Hillary (I find them instantly recognizable but not at all Turing-passing). They say making this available is ethical because it raises awareness of the potential risk, which a Facebook friend compared to “selling nukes to ISIS in order to raise awareness of the risk of someone selling nukes to ISIS.”

Freddie deBoer gives lots of evidence that there is no shortage of qualified STEM workers relative to other fields and the industry is actually pretty saturated. But Wall Street Journal seems to think they have evidence for the opposite? Curious what all of the tech workers here think.

Scott Sumner: How Can There Be A Shortage Of Construction Workers? That is, is it at all plausible that (as help wanted ads would suggest) there are areas where construction companies can’t find unskilled laborers willing to work for $90,000/year? Sumner splits this question in two – first, an economics question of why an efficient market wouldn’t cause salaries to rise to a level that guarantees all jobs get filled. And second, a political question of how this could happen in a country where we’re constantly told that unskilled men are desperate because there are no job opportunities for them anymore. The answers seem to be “there’s a neat but complicated economics reason for the apparent inefficiency” and “the $90,000 number is really misleading but there may still be okay-paying construction jobs going unfilled and that’s still pretty strange”.

Study which is so delightfully contrarian I choose to reblog it before reading it all the way through: mandatory class attendance policies in college decrease grades by preventing students from making rational decisions about when and how to study.
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may 2017 by nhaliday
Missing heritability problem - Wikipedia
The "missing heritability" problem[1][2][3][4][5][6] can be defined as the fact that single genetic variations cannot account for much of the heritability of diseases, behaviors, and other phenotypes. This is a problem that has significant implications for medicine, since a person's susceptibility to disease may depend more on "the combined effect of all the genes in the background than on the disease genes in the foreground", or the role of genes may have been severely overestimated.

The 'missing heritability' problem was named as such in 2008. The Human Genome Project led to optimistic forecasts that the large genetic contributions to many traits and diseases (which were identified by quantitative genetics and behavioral genetics in particular) would soon be mapped and pinned down to specific genes and their genetic variants by methods such as candidate-gene studies which used small samples with limited genetic sequencing to focus on specific genes believed to be involved, examining the SNP kinds of variants. While many hits were found, they often failed to replicate in other studies.

The exponential fall in genome sequencing costs led to the use of GWAS studies which could simultaneously examine all candidate-genes in larger samples than the original finding, where the candidate-gene hits were found to almost always be false positives and only 2-6% replicate;[7][8][9][10][11][12] in the specific case of intelligence candidate-gene hits, only 1 candidate-gene hit replicated,[13] and of 15 neuroimaging hits, none did.[14] The editorial board of Behavior Genetics noted, in setting more stringent requirements for candidate-gene publications, that "the literature on candidate gene associations is full of reports that have not stood up to rigorous replication...it now seems likely that many of the published findings of the last decade are wrong or misleading and have not contributed to real advances in knowledge".[15] Other researchers have characterized the literature as having "yielded an infinitude of publications with very few consistent replications" and called for a phase out of candidate-gene studies in favor of polygenic scores.[16]

This led to a dilemma. Standard genetics methods have long estimated large heritabilities such as 80% for traits such as height or intelligence, yet none of the genes had been found despite sample sizes that, while small, should have been able to detect variants of reasonable effect size such as 1 inch or 5 IQ points. If genes have such strong cumulative effects - where were they? Several resolutions have been proposed, that the missing heritability is some combination of:

...

7. Genetic effects are indeed through common SNPs acting additively, but are highly polygenic: dispersed over hundreds or thousands of variants each of small effect like a fraction of an inch or a fifth of an IQ point and with low prior probability: unexpected enough that a candidate-gene study is unlikely to select the right SNP out of hundreds of thousands of known SNPs, and GWASes up to 2010, with n<20000, would be unable to find hits which reach genome-wide statistical-significance thresholds. Much larger GWAS sample sizes, often n>100k, would be required to find any hits at all, and would steadily increase after that.
This resolution to the missing heritability problem was supported by the introduction of Genome-wide complex trait analysis (GCTA) in 2010, which demonstrated that trait similarity could be predicted by the genetic similarity of unrelated strangers on common SNPs treated additively, and for many traits the SNP heritability was indeed a substantial fraction of the overall heritability. The GCTA results were further buttressed by findings that a small percent of trait variance could be predicted in GWASes without any genome-wide statistically-significant hits by a linear model including all SNPs regardless of p-value; if there were no SNP contribution, this would be unlikely, but it would be what one expected from SNPs whose effects were very imprecisely estimated by a too-small sample. Combined with the upper bound on maximum effect sizes set by the GWASes up to then, this strongly implied that the highly polygenic theory was correct. Examples of complex traits where increasingly large-scale GWASes have yielded the initial hits and then increasing numbers of hits as sample sizes increased from n<20k to n>100k or n>300k include height,[23] intelligence,[24] and schizophrenia.
article  bio  biodet  behavioral-gen  genetics  genomics  GWAS  candidate-gene  methodology  QTL  missing-heritability  twin-study  measurement  epigenetics  nonlinearity  error  history  mostly-modern  reflection  wiki  reference  science  bounded-cognition  replication  being-right  info-dynamics  🌞  linearity  ideas  GCTA  spearhead 
may 2017 by nhaliday
Genetic polymorphisms predict national differences in life history strategy and time orientation
A number of recent studies suggest that some polymorphisms in the androgen receptor gene AR, the dopamine receptor gene DRD4, and the 5-HTTLPR VNTR of the serotonin transporter gene are associated with risk acceptance versus prudence and a short-term versus long-term time orientation, which are important aspects of LHS. We integrated studies from diverse nations reporting the prevalence of these three polymorphisms for many countries. We collected national indices for each of the three polymorphisms and found that they define a strong, single factor, yielding a single LHS-related, national genetic index. As expected, this index is strongly associated with reported national measures of LHS and time orientation, even after controlling for socioeconomic variables. The genetic effect seems especially strong across societies with high socioeconomic inequality.

https://twitter.com/DoctorOcelot/status/836672661736550403
study  biodet  sapiens  time-preference  genetics  attention  long-short-run  uncertainty  correlation  candidate-gene  group-level  regional-scatter-plots  🌞  comparison  world  multi  twitter  social  commentary  neuro-nitgrit  sociology  deep-materialism  behavioral-gen  pdf  piracy  life-history  cultural-dynamics  anthropology  outcome-risk  prudence  broad-econ  wealth-of-nations  speculation  pop-diff  neuro  🎩  n-factor  psychology  cog-psych  microfoundations  hari-seldon 
march 2017 by nhaliday
Association of the Dopamine D4 Receptor (DRD4) Gene and Approach-Related Personality Traits: Meta-Analysis and New Data - Biological Psychiatry
Our initial meta-analysis supported the association of the DRD4 C-521T polymorphism, but not the VNTR polymorphism, with approach-related traits. This conclusion was qualified by evidence of significant publication bias and the failure to detect association in a replication sample comprising individuals at the extremes of the trait distribution. The association of the C-521T polymorphism observed in our initial meta-analysis was robust to the inclusion of these new data, but our revised meta-analysis indicated that the association was present for measures of novelty seeking and impulsivity but not for measures of extraversion.

Meta-analysis of the heterogeneity in association of DRD4 7-repeat allele and AD/HD: stronger association with AD/HD combined type: https://www.ncbi.nlm.nih.gov/pubmed/20468072

Molecular Psychiatry - High prevalence of rare dopamine receptor D4 alleles in children diagnosed with attention-deficit hyperactivity disorder: http://www.nature.com/mp/journal/v8/n5/full/4001350a.html
study  meta-analysis  biodet  psychology  cog-psych  neuro  genetics  replication  QTL  candidate-gene  personality  attention  neuro-nitgrit  behavioral-gen  extra-introversion  multi  disease  psychiatry  epidemiology  GWAS 
february 2017 by nhaliday
European Journal of Human Genetics - A systematic review of cancer GWAS and candidate gene meta-analyses reveals limited overlap but similar effect sizes
Our findings suggest that meta-analyses of well-conducted candidate gene studies may continue to add to our understanding of the genetic associations in the post-GWAS era.
study  org:nat  biodet  methodology  GWAS  meta-analysis  genetics  causation  science  genomics  candidate-gene 
february 2017 by nhaliday
In our genes
The D4 dopamine receptor (DRD4) locus may be a model system for understanding the relationship between genetic variation and human cultural diversity. It has been the subject of intense interest in psychiatry, because bearers of one variant are at increased risk for attention deficit hyperactivity disorder (ADHD) (1). A survey of world frequencies of DRD4 alleles has shown striking differences among populations (2), with population differences greater than those of most neutral markers. In this issue of PNAS Ding et al. (3) provide a detailed molecular portrait of world diversity at the DRD4 locus. They show that the allele associated with ADHD has increased a lot in frequency within the last few thousands to tens of thousands of years, although it has probably been present in our ancestors for hundreds of thousands or even millions of years.

...

Because the prominent phenotypic effects of 7R are in males, we need to ask what is the niche in human societies for males who are energetic, impulsive (i.e., unpredictable), and noncompliant? Whereas tests of hypotheses ought to be careful and conservative, generation of hypotheses ought to be speculative and free-ranging. There is a tradition of caution approaching self-censorship in discussions of human biological diversity, but we will break that tradition in what follows.

https://twitter.com/whyvert/status/827182543594086400
http://ipsr.berkeley.edu/uploads/department_events/1455839539-b80d181fb169f70b4/Dopamine-system%20genes%20and%20cultural%20acquisition.pdf
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february 2017 by nhaliday
The Mass Production of Redundant, Misleading, and Conflicted Systematic Reviews and Meta-analyses - IOANNIDIS - 2016 - The Milbank Quarterly - Wiley Online Library
Currently, _probably more systematic reviews of trials than new randomized trials are published annually_. Most topics addressed by meta-analyses of randomized trials have overlapping, redundant meta-analyses; same-topic meta-analyses may exceed 20 sometimes. Some fields produce massive numbers of meta-analyses; for example, 185 meta-analyses of antidepressants for depression were published between 2007 and 2014. These meta-analyses are often produced either by industry employees or by authors with industry ties and results are aligned with sponsor interests. _China has rapidly become the most prolific producer of English-language, PubMed-indexed meta-analyses_. The most massive presence of Chinese meta-analyses is on genetic associations (63% of global production in 2014), where almost all results are misleading since they combine fragmented information from mostly abandoned era of candidate genes. Furthermore, many contracting companies working on evidence synthesis receive industry contracts to produce meta-analyses, many of which probably remain unpublished. Many other meta-analyses have serious flaws. Of the remaining, most have weak or insufficient evidence to inform decision making. Few systematic reviews and meta-analyses are both non-misleading and useful.
study  ioannidis  science  medicine  replication  methodology  meta:science  critique  evidence-based  meta-analysis  china  asia  genetics  anomie  cochrane  candidate-gene  info-dynamics  sinosphere 
january 2017 by nhaliday
Information Processing: What is medicine’s 5 sigma?
I'm not aware of this history you reference, but I am only a recent entrant into this field. On the other hand Ioannidis is both a long time genomics researcher and someone who does meta-research on science, so he should know. He may have even written a paper on this subject -- I seem to recall he had hard numbers on the rate of replication of candidate gene studies and claimed it was in the low percents. BTW, this result shows that the vaunted intuition of biomedical types about "how things really work" in the human body is worth very little. We are much better off, in my opinion, relying on machine learning methods and brute force statistical power than priors based on, e.g., knowledge of biochemical pathways or cartoon models of cell function. (Even though such things are sometimes deemed sufficient to raise ~$100m in biotech investment!) This situation may change in the future but the record from the first decade of the 21st century is there for any serious scholar of the scientific method to study.

Both Ioannidis and I (through separate and independent analyses) feel that modern genomics is a good example of biomedical science that (now) actually works and produces results that replicate with relatively high confidence. It should be a model for other areas ...
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november 2016 by nhaliday

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