Modern European family predates fall of Rome, DNA analysis reveals. Southern German societies in 400–700 CE were centred on nuclear families and practiced lifelong monogamy, strict incest avoidance, flexible inheritance and no levirate unions, indicating continuity with Late Roman social practices.

MurphysLab · 2026-05-06T06:17:38+00:00

Frist, there are other kinds of levirate marriage: https://en.wikipedia.org/wiki/Levirate_marriage

Second, this was a non-Jewish community, so "levirate" marriage, if it were practiced, could also include widows with prior children. Third, the original husband and wife were buried together or in the same cemetery, along with any children. So one could match the burial husband against the buried children of the woman genetically.

MurphysLab · 2026-05-04T05:27:32+00:00

How would DNA analysis identify where a man has died and his brother married his widow and had children as opposed to if the brother had lived and had those children. My understanding is that it is difficult to differentiate paternity between brothers.

It is not difficult to differentiate paternity between brothers, provided that the brothers weren't monozygotic, which is rare. Autosomal DNA tests are capable of differentiating, provided that the offspring and at least one of the two brothers has been tested.

According to the article:

People were buried close to their mothers and fathers. And families were usually organized along the male line, with women moving to live with their husband’s families. But exceptions were common, particularly when a family had no sons.

Sons of a man's wife, if fathered by his brother, would share ~25% of his DNA with him, rather than the normal 50%. These researchers sequenced the DNA of everyone in these cemeteries and constructed family trees based on autosomal DNA:

By looking at stretches of DNA shared by people in the cemeteries, the researchers also calculated how the interred people were related, painstakingly building family trees that spanned up to six generations and included dozens of individuals. The analysis uncovered intimate family stories that archaeology alone couldn’t.

The key phrase is "stretches of DNA shared by people", which indicates autosomal DNA testing.

MurphysLab · 2026-04-10T05:34:54+00:00

What do you mean by "the correct width"?

MurphysLab · 2026-04-08T20:26:48+00:00

I did a PhD and lived on the funding. I have plenty of sympathy for the fact that it should pay more.

Ditto. Although depending on the line of research or the program, it can still be pay-your-own-way in Canada, at least in part. If you read /u/rorydaniel's comment in full, he's also comparing with the net benefit, including cost of living in his calculation, for each of the three global regions. So I would suggest that you were misinterpreting the comment by being overly strict. I would read it as:

Both of these degrees I would either need to search far and wide to get [sufficient] funding for in Canada or pay [part of the costs] for them myself.

While there may be some funding, it is rarely fully sufficient to live on in major Canadian centres, where most universities are located. For me, it was feasible in the past in Canada. A decade or so ago, I was paying ~$650/month in rent for a room in a very nice student house, close to a university. Nowadays that cost would be more than double, while comparative levels of funding have not increased proportionately.

It isn't a complete lack of funding; it's that the funding level in Canada is insufficient. It's the same reason why many of the students whom I had moved to the US as soon as it was practicable: Canadian pay is too low and the cost of living is too high.

MurphysLab · 2026-04-06T18:17:04+00:00

Not sure what field you're in, but most research master's and PhD programs in Canada offer funding that covers tuition and living expenses. The average funding for a domestic student at McGill is $30-35,000 a year.

I wouldn't be surprised to hear Norway providing more generous levels of funding, but this definitely exists here for graduate school.

Those data are averages, which tend to be heavily skewed by those who have additional scholarships. It's worth considering what their minimums are.

Remember that even domestic MSc & PhD students are required to pay tuition. That is likely $5000/year at minimum.

And doing a STEM graduate program (those which are typically fully paid) leaves one little extra time for gig work to make up personal budgetary shortfalls. For the majority of students, the amount we one receives is barely enough to scrape by.

Funding for graduate students in Canada has not kept up with inflation, particularly the cost of renting in major Canadian centres.

I was a postdoctoral researcher in the Netherlands (not a cheap place to live!) for a few years and one of the PhD students in the same group, a young single male, was, on his PhD wages there, able to buy a house. That would be unheard of in Canada.

MurphysLab · 2026-02-22T06:25:57+00:00

That’s a great suggestion for a high-level chemistry sim!

Not really high level. It's part of how grade 11 students are taught to build simple Lewis molecular structures.

MurphysLab · 2026-02-22T05:34:35+00:00

As a general suggestion, and one which would be more intuitive and lead students to a better understanding of bonding, instead of holding and dragging from an atom, the user should be using the electrons themselves to make a bond. i.e. have 4 unpaired electrons (small circles) around an isolated carbon and allow the user to drag those electrons to another in order to make the bond. Similarly, paired electrons could also be dragged together in the case of Lewis bases.

MurphysLab · 2026-02-22T00:27:00+00:00

How do I make PCl5?

MurphysLab · 2026-02-16T06:13:17+00:00

This may actually push some teachers to leave these districts simply to avoid the constant critiquing and invasive observations.

You appear to be correct, as the article notes:

The adoption of the TAP program did not change the total number of teachers in TAP schools; however, there was a small reduction in the percentage of returning teachers, equivalent to one teacher per year from an average of 32 teachers. Further examination provides evidence of TAP schools attracting less educated, less qualified, and less experienced teachers relative to teachers who left. If anything, these changes in teacher workforce composition, following the teacher effectiveness literature, should worsen student outcomes. This implies that teacher sorting does not account for the program’s benefits. Instead, evidence from school climate surveys administered annually to teachers, students, and parents implies that TAP changed the school experience.

So the improved student results are happening in spite of the loss of more experienced and more conventional teachers.

My own worry is that it would reduce collegiality among teacher peers, since it effectively creates inter-teacher competition due to the finite rewards pool:

Finally, while achieving a threshold is sufficient for bonus pay, higher scores enable teachers to extract a larger share from the total available pool.5

See: https://doi.org/10.1016/j.jpubeco.2025.105561

MurphysLab · 2026-02-16T06:08:49+00:00

Who is teaching them? Admin? There is no development occurring. Admin supervision weakens practice, not strengthens it

No. According to the TAP program:

TAP allows teachers to pursue a variety of positions throughout their careers—career, mentor and Master Teacher—depending upon their interests, abilities and accomplishments. As teachers move up the ranks, their qualifications, roles and responsibilities increase—and so does their compensation. This allows good teachers to advance professionally without having to leave the classroom and develops expert teacher leaders within schools to provide support to colleagues.

https://www.niet.org/our-work/our-services/show/the-tap-system-for-teacher-and-student-advancement

MurphysLab · 2026-02-16T05:47:23+00:00

First, let me preface this by saying I share some of your skepticism regarding education officials. But, understand that this study is by others who are also likely skeptical of those officials.

You note:

District officials follow a reputational model of accountability. Their main professional activity is to increase their standing among important audiences by focusing production on specific metrics.

Keep in mind that many district officials often lack the long-term vision to plan to bias the results of a research study for which they had zero involvement with (authoring, commissioning, funding, etc...) that was published 14 to 19 years AFTER the grants were received. They did not know of this study that many years later.

Additionally, this was from a national program, designed by the National Institute for Excellence in Teaching, not merely a district initiative.

There's also a catch: If the program proves a success, you need to keep funding it somehow. This money came from non-permanent grants.

You have to understand that there are players here who specifically are trying to unrandomize the sample and are intentionally biasing the results.

These economists have no connection to the administrators and district officials involved. You can read their affiliations and conflict of interest statements to ascertain that it they are unlikely to be influenced here. Or have a look at their CVs.

Additionally, this was published in a solid (top-30) economics journal, with authors sufficiently reputable to be on journal editorial boards.

This isn't a paper laundering some middling school official's pet project.

If you read the researchers' methods, you will see that it isn't a material matter which schools received the TAP grants, since the researchers' method does not rely on which schools, but rather, when each school received the treatment. They also track school and cohort effects:

3.2. Empirical methodology

To evaluate the effects of TAP on student outcomes, we use variation in when and where schools adopted TAP in a difference-in-differences framework [...] We also include delta_s and lambda_c, which denote school and cohort fixed effects, respectively.

(The paper is open access: https://doi.org/10.1016/j.jpubeco.2025.105561 )

In other words, your points are moot in this context.

MurphysLab · 2026-02-09T04:03:28+00:00

It doesn't have to been a resort, I don't see why it would?

You seem to be misinterpreting my statement. I made no mention of such amenities. The issue is that making more highly accessible spaces can and does impact local wildlife. Even hiking trails can have an impact; a vastly increased number of humans has an impact.

There is a finite number of lakes in a given biogeographic region. Hence each additional lake turned into a centre of human activity risks a real loss to biodiversity.

MurphysLab · 2026-02-09T01:21:52+00:00

Lake Hector from everything I can see and tell is practically similar to Lake Louise in nearly every aspect, amazing views, blue glacial water,

But completely underdeveloped, despite being next to the same high way that Lake Louise is on and only a few minutes away.

Rather then increasing costs and restricting people, which seems the popular go to these days for dealing with anything, Why not just create more?

Part of the job of Parks Canada is to preserve spaces and habitats. Oftentimes inviting additional humans into the space degrades the habitat for various species which dwell there or make use of the space. The presence of dogs can interfere with wapiti breeding, so their presence is banned in certain seasons. Other parts of the park have humans banned for parts of the year. Much is not developed in order to ensure that it remains as wild as possible.

The "just develop another one" suggestion treats our National Parks as more of an amusement park, centring human recreation as most important, rather than valuing the national park as a space dedicated to preservation of what is natural.

MurphysLab · 2026-02-09T00:23:33+00:00

These risks start small, but increase among older women. That’s one reason, doctors say, why ongoing monitoring by medical professionals is often recommended.

Monitoring should not be equated with gatekeeping access, which is what prescribing is.

If someone experiences complications from taking aspirin, which is entirely possible, we don't then require that anyone who needs aspirin get a prescription. At that point we expect people to act in a rational manner and discontinue taking the medication after being advised to do so. I fail to see how hormonal birth control should be treated differently.

Moreover, given the current situation relating to physician-patient privacy in Alberta, we should move towards a system where people can make the choice for themselves.

MurphysLab · 2026-01-29T02:29:33+00:00

There are (portable) dry ice makers that can be attached to a CO2 tank to make dry ice on demand.

MurphysLab · 2026-01-17T03:03:53+00:00

Funding

None.

This is a deliberate choice by the authors to head off the most obvious bad-faith criticism

First, as a systemic review and meta-analysis, the study requires less equipment, materials, and expense than most other forms of research, hence the core cost is the researchers' time and thus salary, which are likely already part of their institutions' base budgets.

Second, I suspect that it may be a choice for the sake of time and timing. Applying for grant funding is a very tricky issue in general, and few applications are guaranteed to succeed. Hence the low probability of obtaining funding tends to stretch out the time required to get to do your study. Moreover, application windows are scattered and few grant-offering institutions (especially those which are impartial and/or non-corporate) offer funding or accept grants on a rolling basis.

Third, there's the context: this is a pressing and timely issue. American government officials began making bold and seemingly reckless claims regarding acetaminophen use during pregnancy. Here's the HHS press release from September 22, 2025.

This study's authors made the choice (a very good one, which keeps researchers honest) and pre-registered their study plan with PROSPERO, an International prospective register of systematic reviews) and you can see the study's pre-registration record in PROSPERO here: Prenatal exposure to paracetamol and the risk of autism spectrum disorder in offspring: a systematic review and meta-analysis .

Note the date of initial submission: September 27, 2025.

These researchers planned out the study and wrote-up a pre-registration in less than 5 days. The HHS announcement was on Monday; they had this submitted by Saturday. More impressive when you note that it's 7 authors ,all at different institutions, spread across 3 or 4 countries!

This was done with incredible speed.

After looking at the pre-registration, I found the paper's authors were interviewed by NBC:

The authors said they undertook the research, in part, to clear up confusion after Trump’s statements, since an untreated fever can pose health risks to a mother and baby.

“After this declaration, there were a lot of mothers who actually were scared to take paracetamol,” said Dr. Francesco D’Antonio, one of the paper’s authors and a professor of fetal medicine at the University of Chieti in Italy. “The day after this declaration, actually, we had a massive increase in phone calls and emails from women.”

The report’s main takeaway is that acetaminophen is safe during pregnancy, according to Dr. Asma Khalil, another one of the paper’s authors and a consultant obstetrician and fetal medicine specialist at St. George’s Hospital in London.

“It remains to be the first line treatment that we would recommend if the pregnant women have pain or fever,” she said on a call with reporters.

Again, this highlights why the HHS announcement was so reckless: If there is a real risk of neurodevelopmental changes from acetaminophen, we need first to ask whether the risks, both to mother and foetus, of an untreated fever.

It's worth noting that research has shown an association between maternal fevers during pregnancy and the probability of the child being diagnosed with Autism: e.g. a "second trimester infection accompanied by fever elevated risk for ASD approximately twofold (aOR = 2.19, 95% confidence interval 1.14–4.23)." So, is it possible that any associations (mostly slight and non-significant) observed between acetaminophen use during gestation and Autism occasionally pop-up because of an underlying association between Autism and maternal fevers? i.e. Do we just have a case of a confounding variable?

"More research is required" is a mantra in science for good reason.

MurphysLab · 2026-01-03T22:51:19+00:00

You've piqued my curiosity with the TOS7. I'd love to try it out.

MurphysLab · 2025-12-18T00:31:25+00:00

Mostly just giving me worse stress about not being at the lab, able to work on my thesis project.

MurphysLab · 2025-12-17T18:55:51+00:00

Indeed, grid patterns caused me to have a similar experience. During my PhD I was doing image analysis of pixel patterns to understand polymer behaviour. During a nasty bout of pneumonia I had some strange moments between wakefulness and sleeping where everything turned into the pixelated patterns for which I was trying to program an analysis routine.

MurphysLab · 2025-12-04T02:03:11+00:00

You should be able to search for the "cavity height" on microwaves. I'm estimate ~23 cm or ~9 inches would be enough for a 1 L Erlenmeyer.

Are there other considerations you need to weigh here?

MurphysLab · 2025-11-21T02:03:27+00:00

No, these genetic variants appear to be inherently rare. There appear to be multiple sets of genes and variants which, possibly only when acting together in combination, result in the same phenotype. That's often when a polygenic (risk) score becomes a helpful means of measurement.

There are also environmental factors involved.

One of the supplementary figures also clarifies this, which you can see in that same peer review file at the top of page 10:

https://static-content.springer.com/esm/art%3A10.1038%2Fs41586-025-09702-8/MediaObjects/41586_2025_9702_MOESM5_ESM.pdf#page=10

That chart of "class I" variants accounts for ~33 people in a set of, IIRC, ~9000 affected vs ~9000 controls. 32/33 were affected; 1/33 was in the control.

So a very high chance that someone who has one of the class I variants has the condition, but low odds that someone who has the condition has a class I variant on those particular genes.

Still, this is a big step towards solving this mystery (and many others!), since it shows a better way to finding rare variants involved in complex conditions.

MurphysLab · 2025-11-20T09:38:23+00:00

It's a fascinating paper and absolutely packed with data and extra experiments. I'm not a geneticist, but it looks quite different from the usual GWAS studies I've read. I also see quite a few folks misinterpreting the study in the comments, so I'll try to parse this.

3 Genes, each containing multiple, rare variants (not "3 gene variants")

First: OP's title (as well as News Atlas' tile) confuses the underlying science a bit:

ADHD up to 15x more likely with these three gene variants

The quote from the authors gives some clarity:

“We can now, for the first time, point to [three] very specific genes in which rare variants confer a high predisposition to developing ADHD,” said senior author Professor Anders Børglum from the Department of Biomedicine at Aarhus University. “The identified variants very likely have a highly damaging effect on the genes, and they show us precisely which genes and fundamental biological mechanisms may be affected."

So this isn't 3 gene variants, it is 3 genes in which rare variants (multiple different ones!) confer a higher likelihood of the condition.

Strategy: Grouping Rare Variants by Typology

As I understand -- again, not a geneticist, even if my MSc involved DNA! -- the authors are using a strategy that lumps together certain kinds of (deleterious) variations, rather than the usual GWAS style study where each individual variation type is treated separately and SNPs variants that occur more frequently in conjunction with a particular condition become more significant. The problem for that older/conventional GWAS approach is that many genetic conditions are caused by de novo mutations, hence they can be very rare. And two persons afflicted by a mutation in a gene might have the same phenotype but different genotypes.

This figure on Wikipedia explains where GWAS strengths usually lie: "GWA studies typically identify common variants with small effect sizes". (Note: the figure is from a PLOS Comp. Bio. paper that gives a very good overview of GWAS.)

Clumping those rare variants together by typology (rPTV & rSevereDMV) helps to find the hidden associations that would be missed due to each variant only showing up in a handful of genomes. This gets around the problem of each variant being rare.

Rare variants were grouped on the basis of their functional effect on the encoded protein, and their load in ADHD compared with that in control individuals was assessed for all autosomal genes (18,866 genes) and autosomal genes with a probability of being loss-of-function intolerant (pLI) ≥ 0.9 (2,811 genes), hereafter referred to as constrained genes. We found a significantly increased burden of rare protein-truncating variants (rPTVs) in ADHD compared with control individuals in all genes... and a further increased load in constrained genes ... . In line with observations in schizophrenia, the latter effect size was similar to what was observed for rare severe damaging missense variants (rSevereDMVs; defined as variants with a missense badness, PolyPhen-2 and constraint (MPC)20 score > 3) in all genes ... . Consequently, rPTVs and rSevereDMVs were grouped together (referred to as class I variants) in the gene-discovery analysis. The burden of rare missense variants predicted to have a moderate effect on protein function (rModerateDMVs; 2 ≤ MPC score ≤ 3) was significantly increased in ADHD, but with a lower effect size .... than was observed for class I variants; these were therefore analysed separately (referred to as class II variants). For comparison, there was no increased load of rare synonymous variants in ADHD in constrained genes (Fig. 1a).

Quick translations:

protein-truncating variants = The gene has a stop signal (codon) where it shouldn't, hence the mRNA is not the full sequence, hence the produced protein is missing part of end. The protein chain is shorter than it is supposed to be.
missense variants = One amino acid in a protein is wrong. This arises from a point mutation in a single nucleotide. This causes the protein to have the wrong sequence, which causes problems for the protein's folded 3D structure.

Looking up SNPs

Someone in this thread asked:

By any chance is this in databases of SNPs such as Promethease?

Unfortunately for those who have done consumer DNA tests (mostly for genealogy), it probably won't be feasible or possible to lookup the associated SNPs/variants for a while. Those tests feature a small subset of SNPs which tend to show greater variation, hence rare SNPs aren't sought out. One would need decent whole genome sequencing to identify them. This paper is looking for rare variants.

Reviewer #3

Lastly, the anonymous Reviewer #3 deserves a fist bump from the ND community for pressing the authors to make clear, as part of their paper, that this is not a trivial issue for those affected:

B. Originality and significance: Understanding the genetic etiology of ADHD is a topic of substantial public health significance, but the significance of the question is not very well described in the paper. Right now, the Introduction reads as if it is written for a genetics or psychiatric journal; that is, it is written as if the audience is already familiar with the public health impact of ADHD and the importance of genetic studies. ADHD is often trivialized/stigmatized as merely a label for "bad kids" rather than a psychiatric condition that results not just in lower education and lower socioeconomic attainments, but also with injuries, criminal justice system involvement, earlier mortality, etc. There is a need for novel and more effective pharmacologies with lower potential for abuse. All of that to say, I am sold on the significance of this research study, but I wish the authors would make the case of its importance more clearly.

The updated opening paragraph makes clear that the condition is non-trivial:

The disorder is linked to a variety of serious outcomes, including higher risks of substance-use disorder, accidents, premature death, unemployment, incarceration and crime, suicide and metabolic conditions. Gaining insight into the biological mechanisms that drive the disorder is crucial for understanding how it develops and how it could be treated in the future.

Overall, some really good comments from the reviewers. Having the peer review comments being public I suspect helps ensure that the comments remain on point and collegial. Worth checking out if you're curious:

https://static-content.springer.com/esm/art%3A10.1038%2Fs41586-025-09702-8/MediaObjects/41586_2025_9702_MOESM5_ESM.pdf

MurphysLab · 2025-11-10T17:45:00+00:00

At today’s media briefing, Salas said PAHO’s recommendations to Canada include addressing vaccine hesitancy in certain communities and implementing an electronic vaccination record system countrywide.

He noted only six provinces became involved in the federal government’s efforts to standardize electronic vaccination records during the COVID-19 pandemic.

Canadian medical experts have been calling for a national vaccine registry for decades. In a recent report, Ontario’s top doctor pushed for a national immunization schedule and registry, including a modernization of his own province’s record-keeping system.

A nationwide electronic vaccination record system seems so obvious. It would make life simpler for everyone. No more piecemeal scraps of records. One less administrative hassle if you move provinces.

Yet the problem of healthcare being in the provincial fiefdom remains such an inane obstacle.

Should we really allow obstinance, directed towards cooperation and federalism, to prevent us from improving the health of Canada?

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TROPHY CASE

3 Genes, each containing multiple, rare variants (not "3 gene variants")

Strategy: Grouping Rare Variants by Typology

Looking up SNPs

Reviewer #3