Nature journal tries to fix the problem of a scientific literature that's too complex to understand

I recently posted some thoughts on the complexity of the scientific literature noting that many papers are simply too difficult to understand. This includes papers that are well within my areas of interest [How to read the scientific literature? and The scientific literature is becoming more complex].

Nature journal recognizes that there's a problem. A few weeks ago (June 16, 2016) they published a brief comment on Nature distilled.

They begin by describing the problem ...

Any journal that tries to publish the most important results that it is sent, in all fields of science, will run into the same problem. Every bit of our output, we hope, is useful and interesting to somebody somewhere. But even the most optimistic of our editors would concede that the pool of readership for each of these specific advances is only a small subsection of our audience, professional researchers included. To the outside world, science is science. To those who read Nature, science is a multiplicity of specialisms — and specialists.

We know that most of you are specialists, and that you don’t read most of what we present to you. You’re busy people. It is hard enough to follow the literature that you need to read. Even the titles of research papers in an unfamiliar field can look incomprehensible. But if you’re anything like us, one reason you got into science in the first place was curiosity about the world — and not just the tiny piece of it that you now focus on. Wouldn’t it be useful and interesting to keep better track of the rest? Or at least, the rest that is published in Nature, and therefore already judged to be important?

Let's make one thing clear. It's not just the complexity of a paper that's the problem and it's not just that the science isn't explained in easy to understand sentences. There's also the more serious problem of content. Sometimes the papers are hard to understand because the significance of the results is exaggerated and its importance is not placed in proper context.

The ENCODE papers are good examples of this problem. It wasn't easy to understand that they did but, more importantly, it wasn't easy to understand the significance of their results because the authors didn't explain their results very well. They made unsubstantiated claims.

Here's how Nature hopes to fix the problems they identified.

We think so, and this week we begin an experiment to see how many of you agree. We have revisited 15 recently published Nature papers and asked the authors to produce two-page summaries of each. The summaries remain technical — these are not articles suitable for the popular press — but they try to communicate both the research advance and why it matters. The authors of these papers have been enthusiastic — they want the broadest possible readership — and we thank them for their cooperation. Now we want to know what you think. The first three summaries are published online this week (see go.nature.com/1uhcy3x). The rest will be released in the coming weeks. Please take a look. Be brave — pick a topic that you expect to struggle with — and then fill in the online survey to let us know what you think. The rest will be released in the coming weeks. Please take a look. Be brave — pick a topic that you expect to struggle with — and then fill in the online survey to let us know what you think.

I looked at two papers that were about biology and I didn't think the summaries added anything to my understanding. That's partly because the papers weren't that hard to understand in the first place if you were just satisfied with knowing what they did.

Both papers raised lots of questions in my mind about the biological significance of the studies and whether they were accurate and reproducible. The author summaries didn't help much. [Non-coding recurrent mutations in chronic lymphocytic leukaemia and DNA-dependent formation of transcription factor pairs alters their binding specificity].

If the scientific literature is difficult to understand, and it is, then there's a problem with the authors. They aren't able to explain what they did in a reasonable manner and they aren't able to place their work in a proper context so we can evaluate the significance of the result. Asking them to try again (and doubling their citations) is probably not going to help.

The ENCODE authors couldn't do it.

It's a lot like asking the fox to guard the henhouse.

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What is a "gene" and how do genes work according to Siddhartha Mukherjee?

It's difficult to explain fundamental concepts of biology to the average person. That's why I'm so interested in Siddhartha Mukherjee's book "The Gene: an intimate history." It's a #1 bestseller so he must be doing something right.

My working definition of a gene is based on a blog post from several years ago [What Is a Gene?].

A gene is a DNA sequence that is transcribed to produce a functional product.

This covers two types of genes: those that eventually produce proteins (polypeptides); and those that produce functional noncoding RNAs. This distinction is important when discussing what's in our genome.

Paradigm shifting at the Royal Society meeting in November

Suzan Mazur has been making a name for herself by promoting the overthrow of modern evolutionary theory. She began with a lot of hype about the Alternberg 16 back in 2008 and continued with a series of interviews of prominent evolutionary biologists.

Now she's focused on the upcoming meeting in November as another attempt to shift paradigms [see New Trends in Evolutionary Biology: The Program]. She's not entirely wrong. Many of the people involved in those meeting see themselves as paradigm shifters.

TED-Ed misrepresents epigenetics

TED-Ed is the educational arm of TED. Here's what TED says about itself and about TED-Ed ...

TED believes passionately that ideas have the power to change attitudes, lives, and ultimately, the world. This underlying philosophy is the driving force behind all of TED’s endeavors, including the TED Conferences, TEDx, TED Books, the TED Fellows Program, and the TED Open Translation Project. With this philosophy in mind, and with the intention of supporting teachers and sparking the curiosity of learners around the world, TED-Ed was launched in 2012.

TED-Ed is TED’s youth and education initiative. TED-Ed’s mission is to spark and celebrate the ideas of teachers and students around the world. Everything we do supports learning — from producing a growing library of original animated videos , to providing an international platform for teachers to create their own interactive lessons, to helping curious students around the globe bring TED to their schools and gain presentation literacy skills, to celebrating innovative leadership within TED-Ed’s global network of over 250,000 teachers. TED-Ed has grown from an idea worth spreading into an award-winning education platform that serves millions of teachers and students around the world every week.

The scientific literature is becoming more complex

A recent paper by Cordero et al. (2016) looked at the biological scientific literature in 1993, 2003, and 2013. They found that the average publishable unit (APU) almost doubled in twenty years. There were substantial increases in the number of tables & figures and the number of panels per figure. The number of pages increased as did the number of references and the number of authors.

I agree that papers are becoming more complex and more difficult to understand for the average scientist; especially those outside of the specific field of study. The authors of this study point out a number of problems with this increase. I'd like to highlight one of them.

With respect to the number of authors, they say,

Concomitantly, with the increase in information density we note a significant increase in the number of authors per article that also correlated with the average IF of the journal. Since the famous de Solla Price predictions [38], trends toward an increasing number of authors per publication have been widely documented [23,39–44]. Such a trend of increasing collaboration could be explained by the causes suggested above for the growth of information density. The costs associated with the generation of cutting-edge scientific information, the funding restrictions, and the associated risks in scientific publishing in a “winner-take-all” reward system [45] may motivate scientists to team-up, pool resources and fractionate the risks through co-authoring. Also, the increasing complexity of scientific research has resulted in greater specialization of scientists [46], which in turn suggests that the inclusion of additional techniques requires the recruitment of additional investigators to provide that data and thus serve as co-authors. This trend could have both positive and negative consequences. Increased interaction between scientists in diverse fields could translate into greater communication and the possibility for advances at the interfaces of different disciplines. On the other hand, an increase in the number of authors, some of whom bring highly specialized knowledge, could result in reduced supervision of larger groups, and less responsibility per author for the final product and reduced integration of data.

I think the major consequence is the lack of responsibility of individual authors in a multi-author study. With increased specialization, there are fewer and fewer authors who see the big picture and who are capable of integrating the results from several subspecialties. The fact that the studies include work from several highly specialized techniques that only a few people understand also makes it harder for the average reader to evaluate the paper.

It's likely, in my opinion, that many of the authors on the paper don't fully understand the techniques being used by their colleagues. This is a big change from the science I grew up with.

Cordero et al. are worried about the possibility of fraud.

The growth in authors brings with it the concerns about the possibility that as more authors are added, there is an increased likelihood of some individuals with reduced integrity and capable of misconduct joining the group. In this regard, we note that the inclusion of one individual who has been accused of misconduct in numerous studies has led to dozens of retractions of scientific publications.

This is a very real danger but I think that outright fraud is not a significant worry. What concerns me more is the tendency to gloss over the limitations and possible misinterpretations of complex data analyses. The specialist who performs these analyses probably doesn't intend to misrepresent or exaggerate the significance of the result; it's just that they have become so used to using a particular technique (i.e. a software package) that they have forgotten those limitations. They don't communicate them to their colleagues who, because they don't understand the technique, don't realize there's a problem.

Cordero et al. summarize their results ....

In summary, our study documents a change in the literature of the biological sciences toward publications with more data over time. The causes for these trends are complex and probably include increasing experimental options and changes to the culture of science. At first glance, this data could be interpreted as a cultural change opposite to data fragmentation practices. However, it is also possible that an increase in publication density can still occur over a ‘salami slicing’ culture if the publication unit to be segregated is larger to begin with, as the result of technological improvements and increasing numbers of scientific authors. The benefits and debits of this trend for the scientific process are uncertain at this time but it is clear that there have been major changes to the nature of scientific publications in the past two decades that are likely to have major repercussions in all aspects of the scientific enterprise.

I think they're on to something.

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Cordero, R. J., de León-Rodriguez, C. M., Alvarado-Torres, J. K., Rodriguez, A. R., and Casadevall, A. (2016). Life Science’s Average Publishable Unit (APU) Has Increased over the Past Two Decades. PloS one, 11(6), e0156983. [doi: 10.1371/journal.pone.0156983]

How to read the scientific literature?

Science addressed the problem of How to (seriously) read a scientific paper by asking a group of Ph.D. students, post-docs, and scientists how they read the scientific literature. None of the answers will surprise you. The general theme is that you read the abstract to see if the work is relevant then skim the figures and the conclusions before buckling down to slog through the entire paper.

None of the respondents address the most serious problems such as trying to figure out what the researchers actually did while not having a clue how they did it. Nor do they address the serious issue of misleading conclusions and faulty logic.

I asked on Facebook whether we could teach undergraduates to read the primary scientific literature. I'm skeptical since I believe it takes a great deal of experience to be able to profitably read recent scientific papers and it takes a great deal of knowledge of fundamental concepts and principles. We know from experience that many professional scientists can be taken in by papers that are published in the scientific literature. Arseniclife is one example and the ENCODE papers published in September 2012 are another. If professional scientists can be fooled, how are we going to teach undergraduates to be skeptical?

Do Intelligent Design Creationists still think junk DNA refutes ID?

I'm curious about whether Intelligent Design Creationists still think their prediction about junk DNA has been confirmed.

Here's what Stephen Meyer wrote in Darwin's Doubt (p. 400).

The noncoding regions of the genome were assumed to be nonfunctional detritus of the trial-and-error mutational process—the same process that produced the functional code in the genome. As a result, these noncoding regions were deemed "junk DNA," including by no less a scientific luminary than Francis Crick.

Because intelligent design asserts that an intelligent cause produced the genome, design advocates have long predicted that most of the nonprotein-coding sequences in the genome should perform some biological function, even if they do not direct protein synthesis. Design theorists do not deny that mutational processes might have degraded some previously functional DNA, but we have predicted that the functional DNA (the signal) should dwarf the nonfunctional DNA (the noise), and not the reverse. As William Dembski, a leading design proponent, predicted in 1998, "On an evolutionary view we expect a lot of useless DNA. If, on the other hand, organisms are designed, we DNA, as much as possible, to exhibit function."

I'm trying to write about this in my book and I want to be as fair as possible.

Do most ID proponents still believe this is an important prediction from ID theory?

Do most ID proponents still think that most of the human genome is functional?

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New Trends in Evolutionary Biology: The Program

I'm going to London next November to attend The Royal Society conference on New trends in evolutionary biology: biological, philosophical and social science perspectives. This is where all the scientists who want to change evolution will be gathering to spout their claims.

Developments in evolutionary biology and adjacent fields have produced calls for revision of the standard theory of evolution, although the issues involved remain hotly contested. This meeting will present these developments and arguments in a form that will encourage cross-disciplinary discussion and, in particular, involve the humanities and social sciences in order to provide further analytical perspectives and explore the social and philosophical implications.

The program has been published. Here's the list of speakers ...

Gerd B. Müller
The extended evolutionary synthesis

Douglas Futuyma
The evolutionary synthesis today: extend or amend?

Sonia Sultan
Re-conceiving the genotype: developmental plasticity

Russell Lande
Evolution of phenotypic plasticity

Tobias Uller
Heredity and evolutionary theory

John Dupré
The ontology of evolutionary process

Paul Brakefield
Can the way development works bias the path taken by evolution?

Kevin Laland
Niche construction

James Shapiro
Biological action in read-write genome evolution

Paul Griffiths
Genetics/epigenetics in development/evolution

Eva Jablonka
Epigenetic inheritance

Greg Hurst
Symbionts in evolution

Denis Noble
Evolution viewed from medicine and physiology

Andy Gardner
Anthropomorphism in evolutionary biology

Sir Patrick Bateson
The active role of the organism in evolution

Karola Stotz
Developmental niche construction

Tim Lewens
A science of human nature

Agustín Fuentes
Human niche, human behaviour, human nature

Andrew Whiten
The second inheritance system: the extension of biology through culture

Susan Antón
Human evolution, niche construction and plasticity

Melinda Zeder
Domestication as a model system for evolutionary biology

I didn't know that Paul Griffiths and Karola Stotz were going. It's a bit surprising that they would associate with some of these views. I'm glad that Douglas Futuyma will be there to represent the voice of reason. He seems to be one of the few speakers who understands modern evolutionary theory.

There are still a few spots available, according to the organizers. Sign up quickly.

The meeting is at Carlton House Terrace, which is just a few blocks from Trafalger Square and a short walk down The Mall to Buckingham Palace where the Corgis live.

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What does a person's genome reveal about their ethnicity and their appearance?

If you knew the complete genome sequence of someone could you tell where they came from and their ethnic background (race)? The answer is confusing according to Siddhartha Mukherjee writing in his latest book "The Gene: an intimate history." The answer appears to be "yes" but then Mukherjee denies that knowing where someone came from tells us anything about their genome or their phenotype. He writes the following on page 342.

... the genetic diversity within any racial group dominates the diversity between racial groups. This degree of intraracial variability makes "race" a poor surrogate for nearly any feature: in a genetic sense, an African man from Nigeria is so "different" from another man from Namibia that it makes little sense the lump them into the same category.

For race and genetics, then, the genome is strictly a one-way street. You can use the genome to predict where X or Y came from. But knowing where A or B came from, you can predict little about the person's genome. Or: every genome carries a signature of an individual's ancestry—but an individual's racial ancestry predicts little about the person's genome. You can sequence DNA from an African-American man and conclude that his ancestors came from Sierra Leone or Nigeria. But if you encounter a man whose great-grandparents came from Nigeria or Sierra Leone, you can say little about the features of this particular man. The geneticist goes home happy; the racist returns empty-handed.

I find this view very strange. Imagine that you were an anthropologist who was an expert on humans and human evolution. Imagine you were told that there's a woman in the next room whose eight great-grandparents all came from Japan. According to Mukherjee, such a scientist could not predict anything about the features of that woman. Does that make any sense?

I suspect this is just a convoluted way of reconciling science with political correctness.

Steven Monroe Lipkin has a different view. He's a medical geneticist who recently published a book with Jon R. Luoma titled "The Age of Genomes: tales from the front lines of genetic medicine." Here's how they explain it on page 6.

Many ethnic groups carry distinct signatures. For example, from a genome sequence you can usually tell if an individual is African-American, Caucasian, Asian, Satnami, or Ashkenazi Jew, even if you've never laid eyes on the patient. A well-regarded research scientist whom I had never met made his genome sequence publically available as part of a research study. I remember scrolling through his genetic variant files and trying, more successfully than I had expected, to guess what he would look like before I peeked at his webpage photo. The personal genome is more than skin deep.

This makes more sense to me. If you know what you look for—and Simon Monroe certainly does—then many of the features of a particular person can be deduced from their genome sequence. And if you know which variants are more common in certain ethnic groups then you can certainly predict what a person might look like just by knowing where their ancestors came from.

What's wrong with that?

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Can scientists describe what they're doing to a fifth grader?

I'm working on a review of "The Gene" by Siddhartha Mukherjee. It raises a huge number of issues about science writing and the conflict between producing a bestseller and educating the public about science.

As part of the research for that blog post I've been reading all the reviews of his book and I came across an interview with Mukherjee on the Smithsonian website [Siddhartha Mukherjee Follows Up Biography of Cancer With “An Intimate History” of Genetics].

Here's an interesting answer to an important question ...

Evolution according to "New Scientist"

A recent editorial in the magazine New Scientist caught my eye. The title is "Long Live Evolution" and it offers support for "new ideas" about evolution. The online version is titled Darwin’s beautiful theory must itself be allowed to evolve. The author is not identified; I assume it's one of the editors.

Here's the opening paragraph ...
Nothing in evolution makes sense except in the light of population genetics.

Michael Lynch (2007)

Darwin's great theory must itself be allowed to evolve

THE theory of evolution is a splendid thing: an elegant and utterly logical explanation for how natural selection solves the problems of survival and creates the enormous diversity of life we see in the world around us.

There is no such thing as "THE" theory of evolution. Evolutionary theory is complex. It covers several mechanisms (natural selection, random genetic drift) and its core is population genetics—something that was unknown in Darwin's time.

We know that Darwin’s hypothesis of natural selection ... was correct, but we also know that there are more causes of evolution than Darwin realized ...

Douglas Futuyma (2009)
The New Scientists editor is describing the theory of natural selection but he/she even gets that wrong because most of life's diversity is probably NOT due to natural selection.

The irony here is that New Scientist then goes on to say ...

That brings to the fore areas that are not part of the canon of evolutionary theory: epigenetics, for example, which studies how organisms are affected by changes in the ways in which genes are expressed, rather than in the genes themselves.

Attempts to incorporate such elements into evolutionary theory have not always been welcomed, however. That is understandable, given how successful the theory has been without them. Occam’s razor applies: do not add complications unless they are absolutely necessary.

But another motivating factor is undoubtedly the fear that if scientists themselves are seen to suggest that even small details of the theory of evolution could be improved upon, its detractors will seize upon them with avidity. This is a well-founded fear: it happens all the time, with well-funded and highly visible front organisations distorting scientific discussion to create the false impression of disagreement about the basics of evolutionary theory.

It is a fear scientists need to overcome, lest the admirable defence of truth mutates into defensiveness and rigidity. It is one thing to counter reactionaries who reject evolution; it is quite another to be dismissive of or even hostile to scientists who have new ideas to offer.

I recommend that the editors of New Scientist purchase and read any introductory textbook on evolution before they write any more silly editorials. They will learn that "Darwin's great theory" has already been changed beyond anything that Darwin would have recognized. The fact that the editors of a prominent science magazine don't understand evolution is an example of one of the main problems that have led to so much confusion today over recent attempts to extend evolutionary theory.

If science journalists are going to write about whether epigenetics should be part of evolutionary theory then they better do their homework before criticizing prominent evolutionary biologists for being afraid of changing even "small details" of modern evolutionary theory. I suggest they start by reviewing some "small details" like Neutral Theory, random genetic drift, hierarchical theory, species selection, punctuated equilibria, sympatric speciation, group selection, directed mutation, cladistics, kin selection, selfish genes, endosymbiosis, and a host of other aspects of evolution that have been vigorously debated in the scientific literature over the past century.

Maybe after doing their homework they will realize that prominent evolutionary biologists who question epigenetics are not doing it because they fear change ... they're doing it because "epigenetics" has been debated for fifty years and it has little to do with modern evolutionary theory. Maybe the science journalists will realize that proponents of the "extended evolutionary synthesis" are as ignorant of modern evolutionary theory as they were before they did their homework.

The editorial ends with ...

Evolution is true. But it is also a living, breathing idea that must not be allowed to ossify into a dogma of the kind that it has done so much to sweep away.

Ironically, the most common "dogma" is the false idea that evolutionary theory hasn't changed since Darwin's time and the editor of New Scientist is a prime example of this kind of ossification.

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University of Toronto press release distorts conclusions of RNA paper

My colleague, Ben Blencowe, just published a paper ...

Sharma, E., Sterne-Weiler, T., O’Hanlon, D., and Blencowe, B.J. (2016) Global Mapping of Human RNA-RNA Interactions. Molecular Cell, [doi: 10.1016/j.molcel.2016.04.030]

ABSTRACT (Summary)

The majority of the human genome is transcribed into non-coding (nc)RNAs that lack known biological functions or else are only partially characterized. Numerous characterized ncRNAs function via base pairing with target RNA sequences to direct their biological activities, which include critical roles in RNA processing, modification, turnover, and translation. To define roles for ncRNAs, we have developed a method enabling the global-scale mapping of RNA-RNA duplexes crosslinked in vivo, ‘‘LIGation of interacting RNA followed by high-throughput sequencing’’ (LIGR-seq). Applying this method in human cells reveals a remarkable landscape of RNA-RNA interactions involving all major classes of ncRNA and mRNA. LIGR-seq data reveal unexpected interactions between small nucleolar (sno) RNAs and mRNAs, including those involving the orphan C/D box snoRNA, SNORD83B, that control steady-state levels of its target mRNAs. LIGR-seq thus represents a powerful approach for illuminating the functions of the myriad of uncharacterized RNAs that act via base-pairing interactions.

Tim Minchin's "Storm," the animated movie, and another no-so-good Minchin cartoon

I've mentioned this before but it bears repeating. If you haven't listened to "Storm" then you are in for a treat because now you can listen AND watch. If you've heard it before, then hear it again. The message never gets old.


A word of caution. Minchin may be very good at recognizing pseudoscience and quacks but he can be a bit gullible when listening to scientists. He was completely take in by the ENCODE hype back in 2012. This cartoon is also narrated by Tim Minchin but it's not so good.

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Research for a book

I'm on sabbatical this term, working on a possible book whose working title is "What's in Your Genome?: 90% of your genome is junk."

Here's some of the most important books I've read (or re-read) in the past few months.

I've also read a lot of papers and scribbled notes on what's important and what's bullshit not. The most difficult part about keeping up with the scientific literature is organizing it in some meaningful way so you can quickly find it again if you need to—something I do just about every day.

Everyone has their own method. What works for me is to keep an electronic reference with key words and links to a file folder on a particular topic. (I use EndNote.) Here are the folders with all the papers I've been reading in the past few months.

I don't know how other authors behave but for me the most difficult thing about writing a book is organizing my thoughts and planning how to present them in the most effective manner. I tend to write too much on too many topics so the initial drafts usually have to be pared down considerably. Keeping that in mind, what are YOUR favorite topics?

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John Oliver teaches us to be skeptical of scientific publications

We all know that the purpose of education should be to teach students how to think critically. We're not doing a very good job. Take biochemistry, for example. We spend a lot of time transferring information from lecture notes to student notes and then examining students on whether the transfer has worked. We think that teaching students to read the primary literature will make them better scientists when, in fact, teaching them to be skeptical of the primary literature is what's really necessary.

The ENCODE fiasco is just one of many examples where the scientific literature got it wrong. We need to make sure that our students appreciate the important parts of science; namely, the necessity of repeating experiments and the value of scientific consensus. Our students, and many of my colleagues, are prone to hype and promotion just like every one else but that's exactly what critical thinking is supposed to avoid. And it's exactly what proper science—no matter how you define it—is designed to overcome.

If students and scientists are having trouble with these concepts, imagine how difficult it is for the general public. How are they supposed to know that not every "breakthrough" is a real breakthrough and not every new study is correct?

John Oliver did an excellent job of explaining the problem on a recent (May 8, 2016) episode of Last Week Tonight. Watch it. It's worth 20 minutes of your time. The last bit on "Todd Talks" is classic.

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The Encyclopedia of Evolutionary Biology revisits junk DNA

The Enclyopedia of Evolutionary Biology is a four volume set of articles by leading evolutionary biologists. An online version is available at ScienceDirect. Many universities will have free access.

I was interested in what they had to say about junk DNA and the evolution of large complex genomes. The only article that directly addressed the topic was "Noncoding DNA Evolution: Junk DNA Revisited" by Michael Z. Ludwig of the Department of Ecology and Evolution at the University of Chicago. Ludwig is a Research Associate (Assistant Professor) who works with Martin Kreitman on "Developmental regulation of gene expression and the genetic basis for evolution of regulatory DNA."

As you could guess from the title of the article, Michael Ludwig divides the genome into two fractions; protein-coding genes and noncoding DNA. The fact that organismal complexity doesn't correlate with the number of genes (protein-coding) is a problem that requires an explanation, according to Ludwig. He assumes that the term "junk DNA" was used in the past to account for our lack of knowledge about noncoding DNA.

Eukaryotic genomes mostly consist of DNA that is not translated into protein sequence. However, noncoding DNA (ncDNA) has been little studied relative to proteins. The lack of knowledge about its functional significance has led to hypotheses that much nongenic DNA is useless "junk" (Ohno, 1972) or that it exists only to replicate itself (Doolittle and Sapienza, 1980; Orgel and Crick, 1980).

Ludwig says that we now know some of the functions of non-coding DNA and one of them is regulation of gene expression.

These regulatory sequences are distributed among selfish transposons and middle or short repetitive DNAs. The genome is an extremely complex machine; functionally as well as structurally it is generally not possible to disentangle the regulatory function from the junk selfish activity. The idea of junk DNA needs to be revisited.

Of course we all know about regulatory sequences. We've known about this function of non-coding DNA for half a century. The question that interests us is not whether non-coding DNA has a function but whether a large proportion of noncoding DNA is junk.

Ludwig seems to be arguing that a significant fraction of the mammalian genome is devoted to regulation. He doesn't ever specify what this fraction is but apparently it's large enough to "revisit" junk DNA.

The biggest obstacle to his thesis is the fact that only 8% of the human genome is conserved (Rands et al., 2014). Ludwig says that 1% of the genome is coding DNA and 7% "has a functional regulatory gene expression role" according to the Rands et al. study. This is somewhat misleading since Rands et al. specifically mention that not all of this conserved DNA will be regulatory.

All of this is consistent with a definition of function specifying that it must be under negative selection (i.e. conserved). It leads to the conclusion that about 90% of the human genome is junk. That doesn't require a re-evaluation of junk.

In order to "revisit" junk DNA, the proponents of the "complex machine" view of evolution must come up with plausible reasons why lack of sequence conservation does not rule out function. Ludwig offers up the standard rationales ...

1. Some ultra-conserved sequences don't seem to have a function and this "shows that the extent of sequence conservation is not a good predictor of the functional importance of a sequence."
2. The amount of conserved sequence depends on the alignment and alignment is difficult.
3. About 40%-70% of the noncoding DNA in Drosophila melanogaster is under functional constraint within the species but not between D. melanogaster and D. simulans. Therefore, some large fraction of functional regulatory sequences might only be conserved in the human lineage and it won't show up in comparisons between species. (Does this explain onions?)

The idea here is that there is rapid turnover of functional DNA binding sites required for regulation but the overall fraction of DNA devoted to regulation remains large. This explains why there doesn't seem to be a correlation between the amount of conserved DNA and the amount that can possibly be devoted to regulating gene expression. The argument implies that much more than 7% of the genome is required for regulation. The amount has to be >50% or so in order to justify overthrowing the concept of junk DNA.

That's a ridiculous number, but so is 7%. Imagine that "only" 7% of the genome is functionally involved in regulating expression of the protein-coding genes. That's 224 million base pairs of DNA or approximately 10 thousand base pairs of cis-regulatory elements (CREs) for every protein-coding gene.

There is no evidence whatsoever that even this amount (7%) of DNA is required for regulation but Ludwig would like to think that the actual amount is much greater. The lack of conservation is dismissed by assuming rapid turnover while conserving function and/or stabilizing selection on polymorphic sequences.

The problem here is that Ludwig is constructing a just-so evolutionary story to explain something that doesn't require an explanation. If there's no evidence that a large fraction of the genome is required for regulation then there's no problem that needs explaining. Ludwig does not tell us why he believes that most of our genome is required for regulation. Maybe it's because of ENCODE?

Since this is published in the Encyclopedia of Evolutionary Biolgoy, I assume that this sort of evolutionary argument resonates with many evolutionary biologists. That's sad.

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Rands, C. M., Meader, S., Ponting, C. P., and Lunter, G. (2014) 8.2% of the Human Genome Is Constrained: Variation in Rates of Turnover across Functional Element Classes in the Human Lineage. PLoS Genetics, 10(7), e1004525. [doi: 10.1371/journal.pgen.1004525]

Fun and games with Otangelo Grasso about photosynthesis

Otangelo Grasso just posted another one of his screeds. This time it's on photosynthesis. All of his "essays' conform to the same pattern. He looks for some complex set of biochemical reactions, usually in complex animals, then claims that it couldn't possibly have evolved because the whole thing is irreducibly complex according to his understanding of biochemistry and evolution.

It's a classic argument from ignorance.

In this case it's photosynthesis in flowering plants. He posted this figure from the Kegg database ....

Then he says,

In photosynthesis , 26 protein complexes and enzymes are required to go through the light and light independent reactions, a chemical process that transforms sunlight into chemical energy, to get glucose as end product , a metabolic intermediate for cell respiration. A good part of the protein complexes are uniquely used in photosynthesis. The pathway must go all the way through, and all steps are required, otherwise glucose is not produced. Also, in the oxygen evolving complex, which splits water into electrons, protons, and CO2, if the light-induced electron transfer reactions do not go all the five steps through, no oxygen, no protons and electrons are produced, no advanced life would be possible on earth. So, photosynthesis is a interdependent system, that could not have evolved, since all parts had to be in place right from the beginning. It contains many interdependent systems composed of parts that would be useless without the presence of all the other necessary parts. In these systems, nothing works until all the necessary components are present and working. So how could someone rationally say, the individual parts, proteins and enzymes, co-factors and assembly proteins not present in the final assemblage, all happened by a series of natural events that we can call ad hoc mistake "formed in one particular moment without ability to consider any application." , to then somehow interlink in a meaningful way, to form electron transport chains, proton gradients to " feed " ATP synthase nano motors to produce ATP , and so on ? Such independent structures would have not aided survival. Consider the light harvesting complex, and the electron transport chain, that did not exist at exactly the same moment--would they ever "get together" since they would neither have any correlation to each other nor help survival separately? Repair of PSII via turnover of the damaged protein subunits is a complex process involving highly regulated reversible phosphorylation of several PSII core subunits. If this mechanism would not work starting right from the beginning, various radicals and active oxygen species with harmful effects on photosystem II (PSII) would make it cease to function. So it seems that photosynthesis falsifies the theory of evolution, where all small steps need to provide a survival advantage.

I responded on Facebook, pointing out that the cytochrome bc complex and ATP synthase pre-date photosynthesis [Facebook: Photosynthesis]. I also pointed out that there are many living species that use only simpler versions of photsystem I or only photosystem II to carry out photosynthesis [e.g. A Simple Version of Photosynthesis]. Those nasty little facts don't seem to fit with his claim that, "In these systems, nothing works until all the necessary components are present and working."

I probably should have known better. Otangelo Grasso's standard response to such criticism is to avoid dealing directly with his false statements and shift the goalposts on to some other topic. He then posts all kinds of links to websites that seem to back up his claims even if they have nothing to do with the criticisms. You can see him at work on the Facebook thread.

It's pretty frustrating. I probably shouldn't respond to kooks, especially those who think they are experts in biochemistry.

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Theme: Genealogy

Monday, April 11, 2016
My DNA ancestry

I sent a DNA sample off to ancestry.com a few weeks ago and here are the results.

Monday, November 30, 2015
Celebrating Lucy Maud Montgomery

Today Google celebrates the birthday of Lucy Maud Montgomery (November 30, 1874 – April 24, 1942). She is the author of Anne of Green Gables. ...

Lucy Maud Montgomery is a distant cousin of mine. I descend from James Cole and his wife Mary (maiden name unknown) who came to North America from Bletchley, England. Their son, Benjamin Cole, is my great⁴-grandfather. James Cole died sometime around 1765 and Mary married George Penman. The history is confusing, they may have lived in New England and fled to P.E.I. after the American Revolution. They self-identify as United Empire Loyalists.

Friday, November 27, 2015
Hawker Hurricanes and Typhoons in World War II

My father, F/L Laurence Victor "Vic" Kirsch,¹ was a fighter pilot in World War II and he flew Hurricanes and, later, rocket-firing Hawker Typhoons with the RAF 164 Squadron known as the Argentine British Squadron because of the volunteers from Argentina. (My father was seconded from the RCAF (Canada)).

Here's a picture of him in the cockpit of one of his planes.

Wednesday, August 19, 2015
The Burghers of Calais at the Metropolitan Museum of Art in New York

The burghers thought they were sacrificing their lives to save the inhabitants of Calais, which was being starved into submission by Edward III of England in 1347. Their lives were spared after Queen Philippa convinced her husband to be lenient.

One of my ancestors is Paon de Roet. He was a knight in Queen Phillippa's retinue and was one of two knights assigned to protect the burghers of Calais. I descend from Paon de Roet's daughter, Katherine. Her sister, Philippa (named after the Queen), married a poet named Geoffrey Chaucer [My Connection to Geoffrey Chaucer and Medieval Science].

Thursday, May 14, 2015
James Hutton and John Playfair and a genealogical connection

Hutton's work would not have been widely known if it hadn't been promoted by an Edinburgh professor named John Playfair (left). He published Illustrations of the Huttonian Theory of the Earth in 1802.

John Playfair's brother was William Playfair who was a friend of James Watt and Erasmus Darwin and the inventor of the bar graph and the pie chart [see Bar Graphs, Pie Charts, and Darwin and Bastille Day]. William Playfair is Ms Sandwalk's great⁵ grandfather and my childrens' great⁶ grandfather. William's son founded Playfairville in Eastern Ontario.

Tuesday, November 3, 2015
We are all Irish according to Ancestry.com

One of my wife's relatives just had her DNA tested by Ancestry.com and the results show that she is 61% Irish.¹ She was (pleasantly) surprised so she shared the information with her relatives, including Ms. Sandwalk.

I was also surprised because I have a pretty extensive genealogy of my wife's side of the family and there's no ancestor from Ireland. Her grandparents—the aunt's parents—have typically Scottish surnames and they are the product of several generations of Scottish ancestors from a small community in Eastern Ontario.

Sunday, November 10, 2013
I'm Related to a Philosopher! Edwin Proctor Robins (1872-1899)

This was intriguing. I know I am related to all the Robins (Robbins) descendants from Prince Edward Island but I'd never heard of Edwin Proctor Robins. His great-grandfather, Robert Robbins, is a United Empire Loyalist who came to PEI from New Jersey when the American Revolution ended. Edwin Proctor Robins and I are fourth cousins, three times removed. Why did he die at Cornell University?

Sunday, October 6, 2013
Dr. Azor Betts vs Smallpox and George Washington

Dr. Azor Betts (1740-1809) is a distant cousin of mine. His mother was Mary Beldon and I descend from another Mary Beldon who is a cousin of Dr. Azor Betts' mother. Our common ancestor is Daniel Belden (1648-1732) of Deerfield, Massachusetts.

Dr. Betts' father was Nathan Betts and I'm also related to him through my ancestor Tama Betts (1754 - ).

Wednesday, September 4, 2013
James Hood (1776-1859)

James Hood is my wife's great, great, great, great, grandfather (and the great⁵ grandfather of Gordon and Jane). He is also the great, great, great grandfather of Mitt Romney.

Sunday, July 28, 2013
My Connection to Geoffrey Chaucer and Medieval Science

Katherine's sister, also called Philippa (1346-1387) [Philippa Roet] was a prominent member of Queen Philippa's court in England. At first, she was a child companion of the children of Elizabeth of Ulster and the Queen but later on she was a lady-in-waiting. Geoffrey Chaucer became a page in the household of Elizabeth of Ulster in 1357 when he was 14 and Phillipa was 11.


Sunday, March 23, 2013
Happy Saint Patrick's Day!

One of the cool things about studying your genealogy is that you can find connections to almost everyone. This means you can celebrate dozens of special days. In my case it was easy to find ancestors from England, Scotland, Netherlands, Germany, France, Spain, Poland, Lithuania, Belgium, Ukraine, Russia, United States, and, of course, Ireland.

We will be celebrating St. Patrick's Day today. It's rather hectic keeping up with all the national holidays but somebody has to keep the traditions alive!

Here's my Irish connection.¹ The shortest connection is to the parents of my grandmother. My great-grandfather was Thomas (Keys) Foster, born in County Tyrone on September 5, 1852. He immigrated to Canada in 1876. Thomas married Eliza Ann Job, born in Fintona, County Tyrone on August 18, 1852. She immigrated to Canada in 1877.

My wife and our children are cousins of Mitt Romney. This is the story of their common ancestor James Hood and his Mormon descendants.Thursday, February 2, 2012
A Mormon Tale: The Romney Connection

Hannah Hood Hill arrived in Salt Lake City when she was eight years old. She lived there with her father Archibald Newell Hill and his four wives. (Hannah’s mother, Isabella Hood, died at Winters Quarters in 1847.)

On May 10, 1862 Hannah Hood Hill married Miles Park Romney. Miles was born on August 18, 1843 in Nauvoo. His parents had been converted to the Church of the Latter Day Saints while living in England.

Wednesday, February 1, 2012
A Mormon Tale: Navoo to Utah

Archibald Hill returned to Nauvoo and brought his family out to Winter Quarters. They arrived in early autumn. Presumably the advance party had already built houses and planted crops in preparation for winter.

Isabella Hood Hill was 25 years old. Samuel Hood Hill was six, Hannah Hood Hill was four, and Rebeccah Hood Hill was only one year old.

About 1000 settlers died that winter of illness or starvation. One of them was Isabella Hood Hill. She died on March 20, 1847 and she is buried in the Mormon Cemetery in Florence, Nebraska [grave #109].

Tuesday, January 31, 2012
A Mormon Tale: Ontario to Nauvoo

By the time of Smith’s murder, the population of Nauvoo and its suburbs was over 20,000. Vigilante gangs from other parts of the state harassed the outlying settlements forcing the Mormon inhabitants to move into Nauvoo. The Illinois militia shelled the city in September 1846 ("Battle of Nauvoo").3 The Saints had already decided that they needed to move west. Once Brigham Young became leader (after considerable infighting), preparations began in earnest for the trek westward and the Hill family was very involved in that effort. The future Mormon "Kingdom" would be in Utah.

Rebecca Hood Hill was born in Nauvoo on April 2, 1845 and the following year the entire ill family left Nauvoo for Utah. Hannah Hood Hill was four years old. In her autobiography she remembers her stay in Nauvoo ...

Thursday, November 24, 2011
What William the Conqueror's Companions Teach Us about Effective Population Size
My mother has been working on genealogy for several decades. She recently gave me a little book called My Ancestors Came with the Conqueror by Anthony J. Camp, first published in 1988. Camp is a professional genealogist. Before discussing this book, I should let you know that the relationship between professional genealogists and the amateur genealogy found on ancestry.com is similar to the relationship between scientists and Intelligent Design Creationism.

It's estimated that half the population of Great Britain claims to have descended from William the Conqueror who defeated King Harold at the Battle of Hastings in 1066. Not all claims meet the rigorous standards of professional genealogists but it's quite reasonable that there are millions of direct descendants of William.

Sunday, October 22, 2011
Daniel Belden and the Deerfield Massacre

William Beldon (1609-1655) was born in Heptonstall Parish, Yorkshire, England. He settled in Wethersfield in the Colony of Connecticut in 1641. (Wethersfield is just south of Hartford.)

William Beldon married Thomasine Sherwood (1615-1655) and they had the following children.

1. Samuel Beldon (1647-1737)
2. Daniel Belden (Belding) (1648-1732)
3. John Belden (1650-1713)
4. Susannah Beldon (1651-1706)
5. Mary Beldon (1653-1724)
6. Nathaniel Beldon (1654- )

I descend from John Beldon (1659-1713) and his wife Ruth Hale Hayes (1646-1700). But this is story about his brother, Daniel Beldon (sometimes known as Daniel Belding).

Friday, August 5, 2011
Cousin Lucy

We've been at the Chautauqua Institution in upstate New York for the past few days learning about Iran. On Wednesday afternoon we took a short trip to nearby Jamestown and visited the cemetery where Lucille Ball is buried.

Lucille Désirée Ball was born in Jamestown, New York, in 1911 and she died in Los Angeles in 1989. Her ancestors moved to Chautauqua County in the early 1800's from Connecticut. Lucy and her mother, Désirée Evelyn Hunt, are descendants of Thomas Sherwood (~1586 - 1655) and his second wife Mary Onge (?).

I descend on my mother's side from Thomas Sherwood and his first wife Alice Tiler (1585 - 1635).

Wednesday, June 29, 2011
Losing Charlemagne
Back in October 2009 I published my genealogical connection to Emperor Charlemagne [My Family and Other Emperors]. It is wrong. I relied too much on the information found in Ancestry.com and much of that information is unreliable.

In my case the connection was through Ruhamah Hill (b ~1708) who married John Belden (1728 - ). They were British citizens who lived in Norwalk, Fairfield Country, Connecticut (a colony of Great Britain). The parents of Ruhamah Hill are often listed as William Hill and Abigail Barlow of Greenfield Connecticut but there's no evidence to support this connection. On the other hand, historical records say that Ruhamah Hill is the daughter of Captain John Hill (1669 - 1768?) of Westerley, Rhode Island and this seems much more reasonable since Captain John Hill married Ruhamah Wyer (1670 - ).


Saturday, October 24, 2010
The Pillars of the Earth

Matilda married Henry V, Holy Roman Emperor, when she was 13 years old and she became known as Empress Matilda at that point. She returned to England when her husband, Henry V, died in 1125. In the movie she is depicted as a young girl who is present when the King learns of his son's death on the White Ship. In fact, she was already 18 years old and married to the Holy Roman Emperor when the ship went down.

Empress Matilda, known as Maud in the movie, married Geoffrey Plantagenet, Count of Anjou in 1128. They had a son who eventually becomes Henry II of England and founds the Plantagenet dynasty. (Oops, I just gave away the ending!

I descend from Geoffrey and Matilda through my Scottish Stewart ancestors.

Friday, September 24, 2010
Our Ancestor Charlemagne: Taller than Average?

John Hawks found a paper analyzing the height of Charlemagne (742-814). Rühli et al. (2010) looked at measurements of Charlemagne's left tibia in order to determine his total height and robustness. The result indicates that he was 1.84 m tall (6' 0"). This is considerably taller than the average height of his male contemporaries at 1.69 m (5' 6"). Thus Charlemagne was taller than 99% of the men around him and qualifies as "great" in more ways than one.

The average height of Germans today is 1.78 m (5' 10") and Belgians are a bit taller at 1.795 (5' 10½"). (Charlemagne comes from the area around Liege in Belgium and Aachen in Germany.) Charlemagne would be taller than average in today's society but not notably taller.

Thursday, July 22, 2010
Bouillon
Godfrey was the son of Eustace II, Count of Boulogne and Ida of Lorraine. Eustace II fought with William the Conqueror at the Battle of Hastings. His father was Eustace I, Count of Boulogne who married Matilda of Leuven (Louvain). (She was the daughter of Lambert I, Count of Leuven (~950-1015). We have many Belgian ancestors.)

Eustace I and Matilda are Zoë's direct ancestors via their other son Lambert II, Count of Lens (1025-1054). We descend from his daughter Judith of Lens whose mother (wife of Lambert II) was Adelaide of Normandy, sister of William the Conqueror.

The majority of people reading this blog are also descendants of these people. You just don't know it.

Monday, April 12, 2010
Lance Corporal Robert Alexander Hood (1895 - 1917)

Robert Alexander Hood was born in 1895 in a small village north-west of Waterloo, Ontario, Canada. He went to France in 1916 when he was only 21 years old. Robert fought with the 73rd Battalion and he was killed in action at Vimy Ridge on this day, April 12, in 1917. He was a cousin of Ms. Sandwalk's grandfather.

Canadians "celebrate" the battle of Vimy Ridge as a great Canadian victory. It was part of the larger Battle of Arras, which in turn was a diversionary attack in support of the larger Nivelle Offensive carried out by the French Army. About 3,600 young Canadian men were killed during the four day battle and 7,000 more were wounded. This is just a small fraction of the casualties on both sides during World War I.

Thursday, October 15, 2009
Are You a Descendant of Charlemagne?
Thousands of amateur genealogists have contributed to a huge database of family relationships, including genetic analyses. What does this teach us about human populations and evolution?

It may seem like a ridiculous question to ask whether you are a descendant of Charlemagne, who was crowned Emperor on December 25, 800. If you live in Asia or Africa, or your ancestors are from Asia or Africa, then you are probably not a descendant of Charlemagne.

Tuesday, September 22, 2009
The Hanging of Goodwife Knapp in 1653

The remarkable thing about the Goodwife Knapp execution is not the trial itself but the aftermath. Roger Ludlow, the Deputy Governor of Connecticut, had been fighting on and off for several years with his neighbor Mary Staples (wife of Thomas Staples, also known as Staplies). In 1651 Ludlow won a suit against Mary Staples for slander but this did not put and end to their dispute.

The reason for my interest in this trial is that many of my ancestors lived in Fairfield at the time and their names are mentioned in the account. Some of my ancestors were friends of the Staples and defended Mary Staples while others sided with Roger Ludlow. Ludlow lost the case and he left Fairfield the following year (1654), making his way eventually back to England and then to Ireland where he remained for the rest of his life.

By an extraordinary coincidence, my good friend and former best man at my wedding, Charles Beach, is a descendant of Mary Staples and Thomas Staples. Their daughter, Mary Nicol Staples (1630-1677) married John Beach (1623-1677).


Saturday, January 31, 2009
My New York Ancestors

Arbraham Rycken and his wife owned a lot of property on Long Island, including a small island off the coast near their farms. Their children adopted several names including "van Lent" and "Riker." The small island remained in the family for several hundred years and it is still known as Rikers Island—now the site of a large prison.

Their daughter, Aeltje, married Captain Jan Harmse, a descendant of German/Dutch immigrants. Captain Harmse was born in New Amsterdam (New York) in 1657. Their son, Harmen Harmse (1684-1720), married Margaret Montras (1691-1739) thus uniting my French and Dutch ancestors. Harmen took his wife's last name. They moved to Tarrytown New York and joined the congregation of the Dutch Reformed Church of Sleepy Hollow.

The son of Harman and Margaret Montras is Peter Montras (1715-1790). He was my great⁶ grandfather.

Thursday, October 23, 2008
Niall Nóigiallach - Niall of the Nine Hostages

Niall is also famous for another reason. DNA studies indicate that one in twelve Irish men carry a Y chromosome haplotype that traces back to Niall. The haplotype is also common in Scotland and England, and on the continent. This makes Niall one of only a handful of men who have millions of direct male descendants. (Genghis Khan was another [Genghis Khan a Prolific Lover, DNA Data Implies].)

Families that trace their ancestry back to Niall of the Nine Hostages include: (O')Neill, (O')Gallagher, (O')Boyle, (O')Doherty, O'Donnell, Connor, Cannon, Bradley, O'Reilly, Flynn, (Mc)Kee, Campbell, Devlin, Donnelly, Egan, Gormley, Hynes, McCaul, McGovern, McLoughlin, McManus, McMenamin, Molloy, O'Kane, O'Rourke and Quinn.

My mother's maiden name is Doherty. We are descendants of the O'Dochartaigh's of Donegal in the north-west part Ireland.

Thursday, October 23, 2008
Bar Graphs, Pie Charts, and Darwin

One of Ms. Sandwalk's ancestors is William Playfair (1789 - 1823). Her great grandfather—the great-great-grandfather of my children—was John Playfair Leslie. John's mother is a direct descendant of William Playfair.

William Playfair was an interesting man for many reasons. He is most famous for inventing statistical graphs; especially pie charts and bar graphs. These were printed in his famous book, Commercial and Political Atlas, published in 1786. Two examples of figures from that book are shown here.


Sunday, September 28, 2008
Sleepy Hollow

This is a view of the cemetery of the Old Dutch Church of Sleepy Hollow. It was taken by a visitor who posted it on the Friends of the Old Dutch Burying Gorund website.

When Harman married Margaret Montras he took her name as his surname and became known as Harmen Montras. Their fourth child, Peter (Petrus) Montras, was baptized on March 6, 1715 in the Dutch Church of Sleepy Hollow. He is my great- great- great- great- great- great-grandfather. Peter's descendants changed their last name to Montrose or Montross.

Harmen Montras and his wife Margaret Montras are almost certainly buried in the Old Dutch Church of Sleepy Hollow cemetery in unmarked graves and so are Harmen's parents Jan Harmse and Aeltje. That's four direct ancestors of mine. Part of the house built by Jan Harmse is still standing in Irvington, New York.

Monday, August 11, 2008
Horse Thieves, Skeletons and Black Sheep in the Family
After serving his eight years as an indentured servant, Daniel Robins married Hope Potter in New Haven Conn. in 1641. Now here's the interesting part. Hope Potter's father was William Potter (b. 1608) who first came to New England in 1635. When searching for information about William Potter, my mother came across this opening paragraph on a listserve.

Every amateur genealogist has in the back of his or her mind that someday an ancestral skeleton will appear, perhaps the legendary "horse thief". For those who are descendants of William Potter, the skeleton has appeared, but he did not steal the horses.

Hmmm ....

Saturday, December 8, 2007
The DNA Genealogy Scam

CBC News has a show on television called Marketplace. It often covers scams and commercial frauds that Canadians need to be wary of. Last week they ran a segment on home DNA testing kits and the claims of those who sell them to the general public. You can watch the entire segment on their website [Who's Your Grand Daddy?].

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I Think We Have the Same Eyes

Ancestry.com (ancestry.ca) has this neat feature where they combine all their family trees into a big "One World" tree. If you know your ancestors, you can access the "one world" tree and check to see who you're related to. It's especially fun to see which famous people are your distance cousins.

There's only one problem. You really have to know something about your ancestors before you trust the results. Most of the relationships are wrong because someone has entered the wrong data and it gets propagated to the "one world" tree. This is a problem with all such databases—including scientific ones.

Here's one of the reliable hits. It shows how Bette Davis is a distant cousin. She descends from my great¹⁰ grandparents Captain Richard Norman and his wife Margaret Alford. They were born in Orchard Portman, Somerset, England (midway between Exeter and Bristol) and came to Massachusetts Colony in 1626.

UPDATE: This is wrong. There's a mistake on the internet! I am NOT a descendant of Richard Norman and Margaret Alford.

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