Saturday, October 24, 2009

Chicago

 
I'm in Chicago with Ms. Sandwalk and another couple who we hang out with. We have a wonderful time at the art gallery, took the architectural boat tour and ate delicious deep dish pizza.










Are You Sexually Attracted to Male Musk Deer?

 
The other day I had to get up and move to new seat on the subway. The cause of my discomfort was a young woman who reeked of musk—the scent that male musk deer (Moschus moschiferus) use to attract females. I don't know why this woman wanted attention from female musk deer but I was pretty sure she wasn't going to find any on the subway.

The main scent is due to muscone [see Monday's Molecule #127] and nowadays the muscone used in perfumes is completely artificial. But that wasn't always the case. Musk originally came from the scent glands of Asian musk deer [MUSK An Essay].
Only the mature male Moschus produces musk. The substance occurs in only one location on the deer's body: on its abdomen, just in front of its penis, is a hairy pouch known as the musk gland. This sac is about the size of a golf ball. It is composed of several layers of skin, with two openings immediately above the animal's urethra.

In the early summer, unripe liquid musk drains into the gland from the surrounding tissues, and is stored there for some weeks or months. During the course of this time, the musk - 30 grams of it or so - "matures" into a granular, waxy, reddish-brown substance with an extremely potent and familiar smell.

When the musk has ripened - shortly before the autumn rutting season - the deer begin to discharge it mixed with their urine, apparently to mark their territory and attract females. (This behavior is familiar to anyone who has come in contact with a tomcat that "sprays.") Even in winter, male musk deer have been reported to leave behind fragrant red snow, rather than yellow.
I'm told that humans of both sexes get turned on by this smell. If so, the woman on the subway is not only going to attract female musk deer but she's also going to get a lot of attention from both men and women of a different species. I guess it's a good thing that I freed up the seat next to her.

There ought to be rules about perfume, When a man or a woman is wearing too much, they should be told to go home and take a shower—with lots of unscented soap.


Friday, October 23, 2009

Picking a Religion

 
What if you are truly confused about what you believe and which group you should belong to? Here's a handy-dandy algorithm to help you decide. I got it from Friendly Atheist.



Thursday, October 22, 2009

Richard Dawkins' View of Random Genetic Drift

The Greatest Show on Earth is Richard Dawkins' latest book. It's his eighth book on evolution: the others are The Selfish Gene (1976), The Extended Phenotype (1982), The Blind Watchmaker (1986), River Out of Eden (1995), Climbing Mount Improbable (1996), Unweaving the Rainbow (1998) and The Ancestors Tale (2004).

I'm interested in the evolution of Richard Dawkins' ideas about evolution; in particular, his ideas about random genetic drift and mechanisms of evolution other than natural selection.

In Chapter 1 Dawkins says, "All reputable biologists go on to agree that natural selection is one of its most important driving forces, although—as some biologists insist more than others—not the only one."

This looks promising. Dawkins is saying— in chapter 1—that there are two mechanisms (driving forces) of evolution. He implies that he accepts random genetic drift as a "driving force" of evolution. (Assuming that random genetic drift is what he has in mind.) It's clear that "some biologists" have influenced him, although it's not clear from the sentence whether those biologists are "reputable"!

Since this is a book about the evidence for evolution, I eagerly anticipated his explanation of random genetic drift. Would it be as good as Jerry Coyne's?1 In fact, I was so eager that I couldn't wait. I jumped to the index to look under "random."

Nothing. Not to worry. The other important mechanism must be here somewhere. Is it indexed under "genetic"? No. What about "drift"? No, not there either.

What gives? How can you write a book about evolution in the 21st century without mentioning random genetic drift as an important mechanism of evolution? Even the other adaptationist, Jerry Coyne, has it in the index to Why Evolution Is True.

Maybe Dawkins uses another term for the second mechanism of evolution. I recalled that he often gets mixed up about the difference between neutral theory and random genetic drift. Let's see if "Neutral Theory" is in the index. Nope.

What about "Kimura"? Success at last! Check out page 332.

Page 332 is in the middle of a section on The Molecular Clock in Chapter 10. It seems a bit late to begin discussing the second mechanism of evolution, but, as I said before, it's promising that Dawkins even concedes that there is one.

Dawkins explains that the reason why there's a molecular clock is because the majority of changes at the genetic level are neutral and these changes are fixed in a regular, clock-like, albeit stochastic, process. He then goes on to say...
When the neutral theory of molecular evolution was first proposed by, among others, the great Japanese geneticist Motoo Kimura, it was controversial. Some version of it is now widely accepted and, without going into the detailed evidence here, I am going to accept it in this book. Since I have a reputation as an arch-"adaptationist" (allegedly obsessed with natural selection as the major or even only driving force of evolution) you can have some confidence that if even I support the neutral theory it is unlikely that many other biologists will oppose it!
I can't think of any serious biologists who would deny that neutral mutations exist. The essence of Neutral Theory, or Nearly Neutral Theory as it is currently called, is undoubtedly correct. The fact that Richard Dawkins accepts it in this book is not remarkable. What's remarkable is that he has to tell us that he accepts it, especially in a book about the evidence for evolution.

Meanwhile, we are still waiting for the explanation of the "other" mechanism of evolution. The one that was mentioned in Chapter 1 when he said that natural selection does not account for all of evolution. He can't have been thinking about "Neutral Theory" since that's not a mechanism of evolution. And he can't just have been thinking about a mechanism for fixing neutral mutations since he surely knows that the "other" mechanism can result in the loss of beneficial alleles and the fixation of detrimental ones.

Still waiting. What we see in Chapter 10 is an explanation of neutral mutations but no mention of random genetic drift—the mechanism responsible for fixing neutral mutations in a population. He does briefly mention on page 335 that neutral mutations can "go to fixation by chance." I get the impression that he goes out of his way to not name the other mechanism of evolution. You know what I'm referring to, it's the mechanism that gets a whole chapter to itself in all the evolutionary biology textbooks [Evolution: Table of Contents].

Dawkins concedes that the vast majority of the human genome consists of sequences that aren't genes. Here's how he puts it ...
It is a remarkable fact that the greater part (95% in the case of humans) of the genome might as well not be there, for all the difference it makes. The neutral theory applies even to many of the genes in the remaining 5%—the genes that are read and used. It applies even to genes that are totally vital for survival. I must be clear here. We are not saying that a gene to which the neutral theory applies has no effect on the body. What we are saying is that a mutant version of the gene has exactly the same effect as the unmutated version.
In other words, the vast majority of the DNA in our genome is junk. Mutations that occur in junk DNA will become fixed in spite of the fact that they are not seen by natural selection. This is what he means when he says that most mutations are neutral and it's equivalent to saying that the dominant mechanism of evolution, in terms of overall frequency, is random genetic drift and not natural selection. I just wish he'd come right out and say it.

It's a shame that Dawkins does not actually mention the mechanism by which those neutral mutations become fixed but instead continuously refers to neutral theory as the alternate mode of evolution. The general public needs to hear about random genetic drift and Dawkins is—like it or not—the most prominent evolutionist on the planet.

Dawkins has not changed his mind about the existence of these neutral mutations and he has not changed his mind about their importance. While they may exist, they are not important as far as evolution is concerned. He makes this very clear—once again—in this book.
As it happens, it is probably true to say that most mutations are neutral. They are undetectable by natural selection, but detectable by molecular geneticists; and that is an ideal combination for an evolutionary clock.

None of this is to downgrade the all-important tip of the iceberg—the minority of mutations that are not neutral. It is they that are selected, positively or negatively, in the evolution of improvements. They are the ones whose effects we actually see—and natural selection "sees" too. They are the ones whose selection gives living things their breathtaking illusion of design. But it is the rest of the iceberg—the neutral mutations which are in the majority—that concerns us when we are talking about the molecular clock.

As geological time goes by, the genome is subjected to a rain of attrition in the form of mutations. In that small portion of the genome where the mutations really matter for survival, natural selection soon gets rid of the bad ones and favors the good ones. The neutral mutations, on the other hand, simply pile up, unpunished and unnoticed—except by molecular geneticists.
This is the way the adaptationist dismisses non-adaptive evolution. It's not really of interest to real biologists. It's only interesting to molecular geneticists. And we all know that those people are not real evolutionary biologists!

Now we come to one of the most interesting sentences in the entire book; at least as far as I'm concerned. As most Sandwalk readers know, we have long debated whether or not visible mutations can be neutral. Once you have an observed phenotype, can you ever attribute it to neutrality? Many adaptationists argue that you can't.

Here's what Richard Dawkins says in his latest book.
It is also possible (although "ultra-Darwinists" like me incline against the idea) that some mutations really do change the body, but in such a way as to have no effect on survival, one way or the other.
This is progress. Back when he wrote The Extended Phenotype, in 1982, Richard Dawkins said.
The adaptationism controversy is quite different. It is concerned with whether, given that we're dealing with a phenotypic effect big enough to see and ask questions about, we should assume that it is the product of natural selection. The biochemist's "neutral mutations" are more than neutral. As far as those of us who look at gross morphology, physiology and behavior are concerned, they are not mutations at all. It was in this spirit that Maynard Smith (1976) wrote: "I interpret 'rate of evolution' as a rate of adaptive change. In this sense, the substitution of a neutral allele would not constitute evolution ..." If a whole organism biologist sees a genetically determined differences among phenotypes, he already knows he cannot be dealing with neutrality in the sense of the modern controversy among biochemical geneticists.
Finally, in 2009, Richard Dawkins admits that it is "possible" that visible mutations could be neutral. Hallelujah!

I'm looking forward to book #9.


1. Jerry Coyne's View of Random Genetic Drift

Evolution in Action and Michael Behe's Reaction

Of the many scientists who are trying to understand evolution, Richard Lenski stands out for his experimental approach. He has maintained stocks of E. coli growing under stressful conditions for over 40,000 generations.

During that time, the cells have been forced to adapt to conditions of low carbon source (glucose) and Lenski's group has been tracking the mutations that arise. In the past, they have done a heroic job of identifying new mutations but that job has become much easier with new technology. Now that rapid genome sequencing is possible it becomes feasible to sequence the genomes of bacteria that were preserved from earlier generations and determine every single mutation that arose.

Barrick et al. (2009) have published the result from just such an experiment. They sequenced the genomes of the original, ancestral, strain and samples of a single lineage from 2,000, 5,000, 10,000, 15,000 20,000 and 40,000 generations.

This information can address a number if issues as they explain in the introduction to their paper.
Genomic changes underlie evolutionary adaptation, but mutations—even those substituted (fixed) in evolving populations—are not necessarily beneficial.Variation in the rate of genomic evolution is also subject to many influences and complications.On the one hand, theory predicts that neutral mutations should accumulate by drift at a uniform rate, albeit stochastically, provided the mutation rate is constant. On the other hand, rates of substitution of beneficial and deleterious mutations depend on selection, and hence the environment, as well as on population size and structure. Moreover, the relative proportions of substitutions that are neutral, deleterious and beneficial are usually difficult to infer given imperfect knowledge of any organism’s genetics and ecology, in the past as well as in the present.

Experiments with tractable model organisms evolving in controlled laboratory environments minimize many of these complications and uncertainties15,16. Moreover, new methods have made it feasible to sequence complete genomes from evolution experiments with bacteria. To date, such analyses have focused on finding the mutations responsible for particular adaptations. However, the application of comparative genome sequencing to experimental evolution studies also offers the opportunity to address major conceptual issues, including whether the dynamics of genomic and adaptive evolution are coupled very tightly or only loosely.
At 20K generations, there were 29 single nucleotide polymorphisms (SNP) and 16 deletions, insertions, and chromosomal rearrangements (DIP) for a total of 45 different events (see figure). Not all of these contributed to adaptation and the rapid growth phenotype but many of them did. Some were mutations that inactivated a gene and some were amino acid substitutions that change activity of an enzyme.

The authors do not report the distribution of beneficial vs neutral mutations but the data suggests that most of the 45 mutations were beneficial. The authors do not tell us how many of these beneficial mutations destroyed the activity of a gene and how many just changed the activity of a gene product but it looks like there were about equal numbers of both kinds of mutations.

Much of the paper is about adaptive vs. non-adaptive mutations. At 40,000 generations there were 627 SNP and 26 DIP mutations. The increase was due, in part, to an increase in mutation rate because of a mutation in the mutT gene. One might expect that the initial adaptation would result in selection for beneficial alleles and that neutral alleles would accumulate by random genetic drift in subsequent generations (i.e. from 20K generations to 40K generations). This is probably what happened from 20K generations to 40K generations

In the first 20K generations the strain adapted rapidly to the low glucose concentration and from then on its rate of growth under these conditions increased more slowly. This could also be explained by the initial fixation of adaptive mutations followed by fixation of non-adaptive, neutral, alleles. The authors argue convincingly that this didn't happen. Instead, almost all of the first 45 mutations were probably adaptive. Presumably, the mutations that arose later on (between 10K and 20K generations) were much less beneficial (lower selection coefficient) than the ones that first appeared in the population. This is the interesting, and controversial, part of the paper.

This is a paper that the IDiots can't ignore because it's all about evidence for evolution. It doesn't come as a big surprise that Michael Behe already has a poting on the DISCO website: New Work by Richard Lenski.

There was a time a few years ago when you could predict that the IDiots would try to discredit such a paper. The new strategy seems to be the opposite. They agree with the conclusions and offer them as support for Intelligent Design Creationism.

Here's the latest example from Behe's posting.
Despite his understandable desire to spin the results his way, Lenski’s decades-long work lines up wonderfully with what an ID person would expect — in a huge number of tries, one sees minor changes, mostly degradative, and no new complex systems. So much for the power of random mutation and natural selection. For his work in this area we should be very grateful. It gives us solid results to point to, rather than having to debate speculative scenarios.
I don't think I need to comment on such stupidity.


Barrick, J.E., Yu, D.S., Yoon, S.H., Jeong, H., Oh, T,K., Schneider, D., Lenski, R.E., and Kim, J.F. (2009) Genome evolution and adaptation in a long-term experiment with Escherichia coli. Nature Oct 18. [Epub ahead of print] [PubMed] [doi: 10.1038/nature08480]

What Does a Skeptic Believe?

 
Jim Lippard has posted some controversial opinions about skepticism: Skepticism, belief revision, and science.

I don't have time to debate him but I know there are skeptics out there who will want to take him on. They may read Sandwalk but may not be aware of The Lippard Blog. I'm quoting part of Jim's beliefs here but I'm going to shut off comments in order to encourage you to comment on Jim's blog.
Is everything a skeptic believes something which is a conclusion reached by scientific methods?

No. Much of what we believe, we believe on the basis of testimony from other people who we trust, including our knowledge of our own names and date and place of birth, parts of our childhood history, the history of our communities and culture, and knowledge of places we haven't visited. We also have various beliefs that are not scientifically testable, such as that there is an external world that persists independently of our experience of it, that there are other minds having experiences, that certain experiences and outcomes are intrinsically or instrumentally valuable, that the future will continue to resemble the past in various predictable ways, etc. If you did believe that skeptics should only believe conclusions which are reached by scientific methods, that would be a belief that is not reached by scientific methods.



David Sloan Wilson on ScienceBlogs

 
David Sloan Wilson has joined ScienceBlogs of the SEED consortium. You can read the new version at: Evolution for Everyone.

This is going to be fun since Wilson is a strong advocate of group selection and, in addition, he is a firm opponent of the co-called "New Atheists."

Here's his opening salvo in Goodbye HuffPost, Hello ScienceBlogs: Science as a Religion that Worships Truth as its God.
Thinking of science as a religion that worships truth as it god enables me to praise its virtues and criticize its shortcomings at the same time. In my previous blogs, I have played the role of scientific reformer for two major issues. The first is the "new atheism" movement spearheaded by the so-called four horsemen: Richard Dawkins, Daniel Dennett, Samuel Harris, and Christopher Hitchens. Isn't it wonderful how scientists and rationalists reflexively adopt religious imagery? I am an atheist in the sense that I regard religion as 100% a human construction, but I'm here to testify that the "new atheists" depart from factual reality in their own way. So did Ayn Rand, the "new atheist" of her day, as we are learning to our sorrow from the collapse of the free market belief system that she helped to create. If we worry about religions for their departures from factual reality, then we should really worry about "stealth religions" that do the same thing without invoking the gods, because they do a better job of masquerading as reality. As someone who is seriously committed to studying religion from a scientific and evolutionary perspective, I'm here to say that the new atheists can't bring themselves to accept the facts about religion as a human construction. Read my six-part series on "Atheism as a Stealth Religion", now archived on my ScienceBlog site, for more. Even better, start acquainting yourself with the emerging field of evolutionary religious studies, whose members are more serious about holding each other accountable for what they say about religion.
Hmmmm ... my sympathies lie with Dawkins et al so I guess this is aimed at me. I was completely unaware of the possibility he mentions; namely, that I don't accept the facts about religion as a human construction. I'll have to think carefully about that one. Is it possible that, as an atheist, I was secretly thinking that religion might actually have been constructed by supernatural beings? Nope, I don't think so.

I was also under the impression that I was "acquainted" with the emerging field of evolutionary religious studies. After all, didn't I just post an article about Michael Persinger [Religion Makes Women Stupid?]? Perhaps David Sloan Wilson is confused about the difference between "getting acquainted" and "recognizing scientific nonsense"?
The second major issue that requires scientific reform is group selection, a theory that explains how groups can become well adapted to their environments in the same sense that individuals do. The theory of group selection began with Darwin and involves a simple set of issues that anyone can understand. Yet, it remains endlessly controversial. Next year marks the 35th anniversary of my first publication on group selection and I'm confident that the controversy will continue for decades more unless something is done. That "something" is a truth and reconciliation process, similar to the resolution of political conflicts that otherwise might continue forever. The idea that a scientific controversy might require a truth and reconciliation process similar to a political controversy speaks volumes about science as a fallible and culturally influenced process.
I don't have a dog in this fight. It will be interesting to watch and learn.


Wednesday, October 21, 2009

Evolution Makes Women Stupid

 
I've been a vocal critic of evolutionary psychology and just-so stories but from time to time they might be right.

This article by Lauren Sandler combines all the right scientific arguments for why women are more stupid religious than men [Why Do More Women Than Men Still Believe in God?].

It even quotes that famous Canadian scientist, Michael Persinger, who not only built a cool helmet, but also won an award for being Ontario's best university teacher. Here's what Lauren Sandler writes.
Researchers have offered many theories about why women are religious in greater numbers than men. Most are inconclusive; all are fascinating. Some investigators locate the engine of belief in our very brain chemistry, and find the female brain far more apt to sense the divine. Canadian cognitive neuroscientist Michael Persinger, the reigning cleric of the neurology of belief, has asserted that the “experience” of God, or feeling the presence of the divine, is literally built into the brain, specifically in the limbic system or the temporal lobe. When Persinger applied magnetic fields over the temporal lobe to mimic the reaction he found in electromagnetic studies, the gender difference was “quite impressive”—that women sensed the presence of a “sentient being” in greater numbers than men.

“Belief,” Persinger told me, “relates more to how the person relates, interprets, and reconstructs the experience.” In other words, even when men and women had the same response in the brain, women were more apt to attribute it to something divine, “out of body.” Other scientists have found these limbic tendencies particularly pronounced in adolescent girls, concurrent with the final stages of brain development. As Barry Kosmin, a coauthor of the new Trinity College study says, “That's why when anybody sees the Virgin Mary, it's a couple of young girls on a mountainside in Southern Europe.” ....

Some researchers hypothesize that women are hardwired to believe because of evolutionary imperatives. Belief in God—or the Mount Olympus ensemble cast, or a phalanx of wood spirits, and so on—has long been connected with tribal ritual, and formed the center of communities. Women relied on these communities for the survival of their children, while men were off spearing buffalo, pillaging neighboring settlements—or whatever the caveman business trip furnished. The relationship between belonging and belief is an ancient one. It may have resulted in the development of certain alleles connected to a sense of God, or at least a commitment to religion.
It's not their fault that women fall for superstitious nonsense. Their brains are built differently and evolution is to blame.


[Hat Tip: Friendly Atheist: Science or Sexism?]

Does Evolution Explain Why Some People Are Mean to Strangers?

 
Does Evolution Explain Why Some People Are Mean to Strangers? Yes, according to some researchers in an article published on the Smithsonian website. If it's published by Smithsonian, it must be right? Right?

Rob Dunn writes in: The Culture of Being Rude.
Recently a group of biologists has offered a theory that they say explains, if not tube socks, then nearly everything else. In a series of high-profile papers, Corey Fincher and Randy Thornhill, both at the University of New Mexico, and Mark Schaller and Damian Murray of the University of British Columbia argue that one factor, disease, ultimately determines much of who we are and how we behave.

Their theory is simple. Where diseases are common, individuals are mean to strangers. Strangers may carry new diseases and so one would do best to avoid them. When people avoid strangers—those outside the tribe—communication among tribes breaks down. That breakdown allows peoples, through time, to become more different.

Differences accumulate until in places with more diseases, for example Nigeria or Brazil, there are more cultures and languages. Sweden, for example, has few diseases and only 15 languages; Ghana, which is a similar size, has many diseases and 89 languages. Cultural diversity is, in this view, a consequence of disease.

Then Fincher and colleagues go even further. Where people are more xenophobic and cultures more differentiated from one another, wars are more likely. Democratic governments are less likely because the tribe or group comes first; the nation and individuals in other tribes within the nation come second. And finally, poverty becomes nearly inevitable as a consequence of poor governance, hostility between groups, and the factor that triggered this cascade in the first place—disease.
Dunn expresses some skepticism using appropriate language but he goes on to describe "data" (correlations, actually) that supports the idea. The tone of the article is quite supportive of the idea that evolution is behind this behavior.

Evolution absolutely requires genes and alleles. There no evidence to suggest that we have an allele that encourages us to avoid diseased strangers. It could be entirely cultural based on the fact that we have a large brain that's capable of reasoning.

Keep this in mind next time I'm mean to you. It may not be my genes that are making me do it. It may just be my brain and my life experience telling me that I should behave that way!


[Hat Tip: a skeptical John Hawks]

Tuesday, October 20, 2009

Ode to Peter Mitchell

Everyone knows about Watson & Crick and Albert Einstein and a few other famous scientists who have discovered something new.

But few people know Peter Mitchell and why he is more important than most other scientists.

Mitchell is one of a handful of scientists who really have changed the way we think about a subject—in this case how energy is produced in living cells [see PETER MITCHELL
AND CHEMIOSMOTIC THEORY
]

Nick Lane has just published an article in New Scientist that highlights Mitchell's contribution to biochemistry. Not only did Peter Mitchell show us how chemical energy is produced in living cells, he also provided tremendous insight into how it must have worked when life first began [Was our oldest ancestor a proton-powered rock? ].

Here's the opening paragraphs of Nick Lane's excellent article. You really should read the whole thing—buy the magazine if you have to.
PETER MITCHELL was an eccentric figure. For much of his career he worked in his own lab in a restored manor house in Cornwall in the UK, his research funded in part by a herd of dairy cows. His ideas about the most basic process of life - how it gets energy - seemed ridiculous to his fellow biologists.

"I remember thinking to myself that I would bet anything that [it] didn't work that way," biochemist Leslie Orgel wrote of his meeting with Mitchell half a century ago. "Not since Darwin and Wallace has biology come up with an idea as counter-intuitive as those of, say, Einstein, Heisenberg and Schrödinger."

Over the following decades, however, it became clear that Mitchell was right. His vindication was complete when he won a Nobel prize in 1978. Even today, though, most biologists have yet to grasp the full implications of his revolutionary ideas - especially for the origin of life.
I wish this weren't so but I'm afraid the last statement is correct. It's not only biologists who fail to grasp the implications, there are even biochemists who don't understand chemiosmotic theory and don't teach it correctly in undergraduate courses.

Some of the most popular biochemistry textbooks didn't explain it properly until their most recent editions in 2006 and 2007. That's shocking.

Peter Mitchell deserves a lot more credit than he gets.

The molecule shown above is ubiquinone:cytochrome c oxidoreductase, also known as complex III [PDB 1PP9]. It is one of the most important enzymes in all of biology. It's structure provided the ultimate proof of chemiosmotic theory since it catalyzes the Q cycle, the key step in creating a proton gradient across a membrane [see Ubiquinone and the Proton Pump].

Every student who takes an introductory biochemistry course should be intimately familiar with this enzyme and how it works. In fact, if they're not, you can be sure that the biochemistry course was not taught properly.


Monday's Molecule #141: Winner

 
The molecule is cholic acid, which usually exists as sodium cholate. It's one of the major bile acids in mammals. The bile acids help solubilize lipids during digestion.

The Nobel Laureate is Heinrich Otto Wieland who received the prize for his work on the structure and function of bile acids.

This week's winner is Alex Ling of the University of Toronto. There were quite a few people who got the right answer and this was a surprise to me. Lipids are not the kind of molecules that excite me and I was not expecting that so many of you would recognize cholic acid.

There were winners from four continents. I think that's a first. Readers in Africa and South America are going to have to get try harder if we're ever going to set a six continent record. (As far as I know, there are no Sandwalk readers in Antarctica.




Identify this molecule. Be as specific as possible. Briefly describe what it does.

There's a Nobel Prize connected to this molecule. The prize was for identifying it and working out its structure, and the structure of many derivatives.

The first person to identify the molecule and name the Nobel Laureate(s) wins a free lunch. Previous winners are ineligible for six weeks from the time they first won the prize.

There are only six ineligible candidates for this week's reward: Ben Morgan of the University of North Carolina at Chapel Hill, Frank Schmidt of the University of Missouri, Joshua Johnson of Victoria University in Australia, Markus-Frederik Bohn of the Lehrstuhl für Biotechnik in Erlangen, Germany, Jason Oakley a biochemistry student at the University of Toronto, and Dima Klenchin of the University of Wisconsin, Madison.

Joshua and Dima have agreed to donate their free lunch to an undergraduate. Consequently, I have two extra free lunches for deserving undergraduates so I'm going to award an additional prize to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch. If you can't make it for lunch then please consider donating it to someone who can in the next round.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule(s) and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours. Comments are now open.


Monday, October 19, 2009

Monday's Molecule #141


 
Identify this molecule. Be as specific as possible. Briefly describe what it does.

There's a Nobel Prize connected to this molecule. The prize was for identifying it and working out its structure, and the structure of many derivatives.

The first person to identify the molecule and name the Nobel Laureate(s) wins a free lunch. Previous winners are ineligible for six weeks from the time they first won the prize.

There are only six ineligible candidates for this week's reward: Ben Morgan of the University of North Carolina at Chapel Hill, Frank Schmidt of the University of Missouri, Joshua Johnson of Victoria University in Australia, Markus-Frederik Bohn of the Lehrstuhl für Biotechnik in Erlangen, Germany, Jason Oakley a biochemistry student at the University of Toronto, and Dima Klenchin of the University of Wisconsin, Madison.

Joshua and Dima have agreed to donate their free lunch to an undergraduate. Consequently, I have two extra free lunches for deserving undergraduates so I'm going to award an additional prize to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch. If you can't make it for lunch then please consider donating it to someone who can in the next round.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule(s) and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours. Comments are now open.



What's the Connection between Hpa II and CpG Islands?

 
Epigenetics is all the rage today but the idea that gene expression could be regulated by modifying DNA and/or chromatin has been around for three decades.

Methylation is one of the ways that DNA can be modified and methylation at specific sites can be heritable. This observation grew out of studies on restriction/modification systems where DNA is protected from the action of restriction endonucleases by methylating the bases.

I didn't realize that the study of restriction enzymes led to the discovery of methylated regions of eukaryotic DNA. Find out how by reading an interview with Adrian Bird in PLoS Genetics: On the Track of DNA Methylation: An Interview with Adrian Bird.

This is also a good example of chance and serendipity in science. You can't plan for this stuff to happen—but that doesn't prevent politicians and administrators from trying.


Howler Monkeys in New York

 
Here's a photo of some Howler Monkeys in New York City. I've met some of them. I'm not sure I want to meet the others ... just kidding. :-)

How many can you recognize? (Check here for their identities.)



An Exposé of the Evolution Industry?

Susan Mazur is a science writer. A few years ago she got wind of a conference that was planed for Altenberg in Austria. This was going to be a small meeting for 16 biologists who were promoting some unusual perspectives on evolution.

She started to write about this meeting, promoting the idea that there was some sort of conspiracy to overthrow modern evolutionary theory. She managed to raise enough of a stink that the odor reached Science and Nature. [See The Altenberg 16 Make It into Nature.]

Of course, by the time Nature got on to the story it was easy to debunk the conspiracy theory and demonstrate that some of the Altenberg 16 were, how shall I put it? ... not in the mainstream of biological thinking [Biological theory: Postmodern evolution?].

Susan Mazur contacted me at the beginning of this episode and I tried to help her understand the difference between legitimate controversies in science and pseudo-controversies promoted by kooks. For a while I thought she was making progress but this turned out to be an illusion. She soon discovered that there was more fame and glory to be had by associating with the kooks than by siding with good science.

But here's the problem. There really are some important issues in evolutionary biology that need to be worked out. I think the so-called "Modern Synthesis" (hardened version) has to be extended in order to incorporate a more pluralist ic view [We Need to Soften the Modern Synthesis]. In that sense, I agree with some of the participants at the Alternberg meeting. However, they made a big mistake by including other, not-so-legitmate, controversies. That allows many evolutionary biologists to dismiss the entire exercise; as reported by Elizabeth Pennisi, in Science [Modernizing the Modern Synthesis].
That hyperbole has reverberated throughout the evolutionary biology community, putting Pigliucci and the 15 other participants at the forefront of a debate over whether ideas about evolution need updating. The mere mention of the "Altenberg 16," as Mazur dubbed the group, causes some evolutionary biologists to roll their eyes. It's a joke, says Jerry Coyne of the University of Chicago in Illinois. "I don't think there's anything that needs fixing." Mazur's attention, Pigliucci admits, "frankly caused me embarrassment."
Jerry Coyne was wrong. There are some things that need fixing. Anyone who has read Stephen Jay Gould's The Structure of Evolutionary Theory should know that.

Susan Mazur has now published the book that we all expected. As you can see from the title, the theme is still conspiracy, plus the idea that evolution is in trouble. It would have been great if Mazur had focused on the real problems in evolutionary theory and helped the general public understand that some of the "controversies" are not legitimate.

Alas, that lofty goal is too difficult for her. We'll have to wait until a better science writer picks up the baton.


Saturday, October 17, 2009

Alternative Medicine at the University of Toronto

 
Several readers and bloggers have noted that there's an AutismOne conference being held on the University of Toronto campus in a few weeks. The conference is loaded with anti-science speakers and quacks so this is an embarrassment. It's being held in the auditorium of the Medical Sciences Building where I work.

The original publicity for this conference implied that it was being sponsored by the Faculty of Pharmacy but that turns out to be untrue as explained on the blog Science-Based Pharmacy: When universities sell their name and let the pseudoscience in.
Well it seems our feedback to the University of Toronto about the upcoming Autism One conference has had an effect. As I noted earlier, Autism One is hosting a conference on autism in Toronto in October. The original brochure listed boldly that the conference was being presented with the Dalla Lana School of Public Health. Understandably concerned, I, along with many of you, contacted the university to register our concerns. Why would a school of public health support a program that touts dubious biomedical treatments for autism, and the ultimate quackery, homeopathy?

Well it turns out the school has acted – quickly and decisively. I’ve heard directly from the school, and have been assured that they were never an official supporter of the program. The brochure and website suggested that the school was actually co-hosting. The school has asked for its name to be removed – and the organizers have complied, as Orac noted earlier this week. The online version of the brochure no longer lists the school’s name.

But what about the SickKids Foundation? Well, this event has brought to light that the SickKids Foundation “takes a neutral stance on complementary and alternative health care” and seems satisfied to remain a sponsor of antivaccination pseudoscience. Their name is still on the brochure.

Which brings me to the topic of the post. Universities never have the funding that they think they need, and do whatever they can to bring in other types of revenue. So the Univeristy of Toronto has rented its space to AutismOne for the conference, and the brochure correctly notes that the address is the Medical Sciences Building on campus. Has a nice ring, doesn’t it? Despite the agenda clearly lacking both valid medicine or science, the conference has bought an air of legitimacy by locating itself on campus. It’s clearly a problem that needs to be addressed, as there’s stuff happening elsewhere on campus…
I don't excuse the SickKids Foundation for their stupid attitude and support for this kind of quackery but the situation with respect to the University of Toronto is a bit different.

I'm all for freedom of expression on the university campus [see Censorship at McGill] so if the event were sponsored by a university group that would be fine with me. I would love to see pickets and signs outside of the auditorium explaining to the press, and everyone else, that this ain't science.

I have a problem with renting out space to non-university groups since it's so difficult to make the public understand that not all events on a university campus are sponsored by the university. This is the sort of thing that got some American museums in trouble when the Intelligent Design Creationists rented their facilities.

Okay, that's one issue, and it's more complicated than people first realized.

Now, along comes a more serious issue. There's a Natural Health Products Symposium being held at the University of Toronto and this one really is being sponsored by the Leslie Dan Faculty of Pharmacy. Some of the other sponsors include for-profit companies that supply medical products to the alternative medicine community. (Keep in mind that "alternative" medicine is, by definition, medicine that is not evidence based.)

Science-Based Pharmacy is on top of the story [What’s Happening to Pharmacy Continuing Education at the University of Toronto?].
If a homeopathy manufacturer is providing sponsorship dollars for this symposium, the likelihood of the content being science-based is, well, probably homeopathic.

It pains me to point this out, as U of T is my pharmacy alma mater, and the school is filled with superb faculty, students, and researchers. So why is the Leslie Dan Faculty of Pharmacy willing to tarnish its good name by offering a continuing education program containing pseudoscience, sponsored by a company that makes homeopathy? Do they really need the money? Or have they run out of science-based topics to teach?

If this is the state of pharmacy continuing education, we should all be dismayed. Because when academic institutions that should know better are facilitating pseuodoscience like homeopathy, and accepting sponsorship from homeopathic manufacturers, what chance does pharmacy really have to be a science-based profession? And what does it mean for patient care, when pharmacists are learning how to use elaborate placebo systems to treat chronic pain?
There's no excuse for this. The Faculty of Pharmacy should be ashamed. All members of the University of Toronto community should be embarrassed. I know I am.

This isn't the worst of it. We actually teach a course on alternative medicine in our undergraduate life science programs [HMB434H]. The lecturers promote alternative medicine, including homeopathy, as real science.
HMB434H1
Complementary and Alternative Medicine [20L, 4S]


Integrative health care is a phenomenon that is developing in health care systems in North America, China, India, and Vietnam, among others. It involves the coordination of multi-disciplinary and culturally-specific health services in the treatment of illness and disease, and an expanded concept of health, illness, and wellness.
I've spoken to the person who runs the Human Biology Program (Valorie Watt). She helped organize this course and she hired the lecturers. She doesn't see a problem.

Do you see a problem? Maybe you'd like to let the Human Biology Program know about your concerns? Their email address is easy to find on the website.


[Photo Credit: Peter Macdiarmid/Getty: A kind of magic?]

Friday, October 16, 2009

Jerry Coyne's View of Random Genetic Drift

Why Evolution Is True by Jerry Coyne is one of the best popular books on evolution. If you can only buy one book this year then this is the one to buy. It contains an excellent explanation of all the basic facts about evolution.

I'm not going to review this book, instead, I'm going to comment on just two things that interest me: how Jerry Coyne treats the mechanisms of evolution (natural selection and random genetic drift); and how he treats speciation—his area of expertise. I'll also discuss Richard Dawkins' treatment of these two topic in his book. (That's four separate postings.)

The first chapter in Why Evolution Is True is "What Is Evolution?" This is an appropriate way to begin and Jerry Coyne starts off nicely by saying that "Darwinism" is the theory of evolution by natural selection. He then proceeds to describe the main tenets of the modern theory of evolution, taking the time to point out that, "the mechanism of most (but not all) of evolutionary change is natural selection."

The sixth tenet of modern evolutionary theory is, "processes other than natural selection can cause evolutionary change." He's talking about random genetic drift although, like most adaptationists, he feels compelled to add a qualifier.
The influence of this process on important evolutionary change, though, is probably minor, because it does not have the moulding power of natural selection. Natural selection remains the only process that can produce adaptation. Nevertheless, we'll see in chapter 5 that genetic drift may play some evolutionary role in small populations and probably accounts for some non-adaptive features of DNA.
Okay, so it's not perfect, but at least he isn't confused about the difference between "evolutionary theory" and "Darwinism". Right?

Wrong. Before the chapter is finished he's talking about the six tenets of "Darwinism" and freely using "Darwinism" and "evolutionary theory" as symptoms. [See Jerry Coyne on Darwinism]

I don't get it. If Darwinism is evolution by natural selection and modern evolutionary theory includes the idea that not all evolution is caused by natural selection, then how can Darwinism be used as a synonym for evolutionary theory? I checked the index for "Darwinism" to see if there was a discussion about this elsewhere in the book. It wasn't much help since the index entry was: "Darwinism, see evolution."

Jerry Coyne is an adaptationist in the sense that he focuses most of his attention on natural selection and gives other mechanisms of evolution short shrift. This does not mean that he ignores them completely as I just showed. He knows about random genetic drift and he described it accurately (see below). The problem is that he tends to forget his lessons when his mind isn't focused on the differences between evolution and natural selection, and Darwinism vs random genetic drift.

In spite of the title of chapter 1, it doesn't really explain what evolution is. It concentrates more on describing evolutionary theory than on actually defining evolution. However, when we get to chapter 5 we to find an adequate definition of evolution. Jerry Coyne says, "Most biologists define evolution as a change in the porportion of alleles (different forms of a gene) in a population."

He then describes how the frequencies of alleles can change in a population by random stochastic means. Using ABO blood types as an example, he describes the typical behavior of alleles in a population of sexually producing organisms. He then says, ...
Such random change in the frequency of genes over time is called genetic drift. It is a legitimate type of evolution, since it involves changes in the frequencies of alleles over time, but it doesn't arise from natural selection. One example of evolution by drift may be the unusual frequencies of blood types (as in the ABO system) in the Old Order Amish and Dunker religious communities in America. These are small, isolated, religious groups whose members intermarry—just the right circumstances for rapid evolution by genetic drift.1

Accidents of sampling can also happen when a population is founded by just a few immigrants, as occurs when individuals colonize an island or a new area. The almost complete absence of genes producing the B blood type in Native American populations, for example, may reflect the loss of this gene in a small population of humans that colonized North America from Asia around twelve thousand years ago.2

Both drift and natural selection produce genetic change that we recognize as evolution. But there's an important difference. Drift is a random process, while selection is the anti-thesis of randomness. Genetic drift can change the frequencies of alleles regardless of how useful they are to their carrier. Selection, on the other hand, always gets part of harmful alleles and raises the frequencies of beneficial ones.

As a purely random process, genetic drift can't cause the evolution of adaptations. It could never build a wing or an eye. That takes nonrandom natural selection. What drift can do is cause the evolution of features that are neither useful nor harmful to the organism.
This sounds like a typical adaptationist speaking. As a general rule, adaptationists admit to random genetic drift but confine it to small populations. They also make sure you understand that drift can't cause adaptation. Finally they state their opinion that drift only affects neutral alleles.

This is exactly the sort of thing Gould and Lewontin were complaining about in the "Spandrels" paper of 1978.
At this point, some evolutionists will protest that we are caricaturing their view of adaptation. After all, do they not admit genetic drift, allometry, and a variety of reasons for non-adaptive evolution? They do, to be sure, but we make a different point. In natural history, all possible things happen sometimes; you generally do not support your favorite phenomenon by declaring rivals impossible in theory. Rather, you acknowledge the rival, but circumscribe its domain of action so narrowly that it cannot have any importance in the affairs of nature. Then you often congratulate yourself for being such an undogmatic and ecumenical chap. We maintain that alternatives to selection for best overall design have generally been relegated to unimportance by this mode of argument.
This describes the views of many adaptationists but Jerry Coyne does not exactly fall into that mode of thinking—at least not when his attention is focused on the issue.
In fact, genetic drift is not only powerless to create adaptation, but can actually overpower natural selection. Especially in small populations, the sampling effect can be so large that it raises the frequency of harmful genes even though selection is working in the opposite direction. This is almost certainly why we see a high incidence of genetically based diseases in isolated human communities, including Gaucher's disease in northern Swedes, Tay-Sachs in the Cajuns of Louisiana, and in retinitis pigmentosa in the inhabitants in the inhabitants of the island of Tristan da Cunha.
This is very important and Jerry Coyne is one of the few adaptationists who get it. Random genetic drift doesn't just work on neutral alleles. It can also lead to high levels of deleterious alleles. Even their eventual fixation.

It would have been great if he had pointed out that random genetic drift can also lead to the loss of beneficial alleles making natural selection a stochastic process.
Because certain variations in DNA or protein sequence may be, as Darwin puts it "neither useful nor injurious" (or "neutral" as we now call them), such variants are especially liable to evolution by drift. For example, some mutations in a gene don't affect the sequence of the protein that it produces, and so don't change the fitness of its carrier. The same goes for mutations in non-functioning pseudogenes—old wrecks of genes still kicking around in the genome. Any mutations in these genes have no effect on the organism, and therefore can evolve only by genetic drift.

Many aspects of molecular evolution, then, such as certain changes in DNA sequence, may reflect drift rather than selection. It's also possible that many externally visible features of organisms could evolve via drift, especially if they don't affect reproduction. The diverse shapes of leaves of different tree species—like the differences between oaks and maple trees -- were once suggested to be "neutral" traits that evolved by genetic drift. But it's hard to prove that a trait has absolutely no selective advantage. Even a tiny advantage, so small as to be unmeasurable or unobservable by biologists in real time, can lead to important evolutionary changes over eons.

The relative importance of genetic drift versus selection in evolution remains a topic of hot debate among biologists.
It's impressive that Coyne admits to the possibility that externally visible features could be neutral and could evolve by random genetic drift. However, he immediately qualifies the statement by pointing out that it's very difficult to prove whether a trait has absolutely no selective advantage. This is true, but adaptationists usually forget to mention two things about natural selection that weaken this argument. First, they forget to mention that it's often just as difficult to prove that a trait has a selective advantage. Second, traits with small advantages are most often lost before they are fixed. Natural selection is not random but neither is it as much of a sure thing as most people believe.

To my way of thinking, Jerry Coyne clearly falls into the adaptationist camp. But on the continuum from pluralist to adaptationist he lies somewhere close to the middle, albeit still on the adaptationist side.

The fact that he's close to the middle is among the reasons why I think this book is so good.

Hear Coyne talk about his book: Phrasing a Coyne: Jerry Coyne on Why Evolution Is True.


1. This is technically correct. Individual alleles will be fixed much faster in small populations than in large populations ... if they are fixed. But this does not mean that random genetic drift only fixes genes in small populations.

2. The founder effect is an important feature of evolution by accident.

IDiots, Evolution, and False Dichotomies

 
Casey Luskin is one of the DISCO defenders of Intelligent Design Creationism. He's all upset these days because their movie Darwin's Dilemma, isn't getting any Oscar nominations.

Maybe it's because they're only showing it in a few "scientific" venues—such as museums—that can be booked by the general public. The idea is to rent the space then promote the movie as though it's actually sponsored by the museum.

When this false representation gets them in trouble, they can always claim censorship [Darwin’s Dilemma: Evolutionary Elite Choose Censorship over Scientific Debate].

That's only one part of the IDiot strategy. The other is to set up false dichotomies in order to strengthen their case. Luskin writes,
There are two ways that modern evolutionists approach the Cambrian explosion, or what has been called “Darwin’s dilemma”:

A. Some freely acknowledge that the Cambrian fossil evidence essentially shows the opposite of what was expected under neo-Darwinian evolution.

B. Others deal with the Cambrian explosion by sweeping its problems under the rug and trying to change the subject.
Here's another option.

There's nothing about the Cambrian explosion that directly conflicts with the proper understanding of evolution and evolutionary theory. However, there are some lessons that could be important in understanding the way life evolved. In particular, the Cambrian explosion should make us appreciate contingency and diversity.

The multicellular animals that appear during the Cambrian explosion have an earlier history as documented in the fossil record and confirmed by molecular studies. That's a prediction by evolutionary biologists that turned out to be correct. We still don't know why these relatively complex animals arose from more simple animals over the period of about 50 million years, but there are several interesting scientific explanations that are being tested.

Call that option C. There are others. All of them are scientific.

So far, the IDiots have not offered their own explanation of this phenomenon as you can see by Casey Luskin's own admission. (He would have included it in his article if it existed.) This is just another case where the only "evidence" for Intelligent Design Creationism is in attacking science. Another example of a false dichotomy.


Calling All Science Writers!

 
The pathway of information flow runs from DNA to RNA to proteins. There are a bunch of fundamentally important steps in this pathway including transcription, RNA processing, and translation.

Translation, or protein synthesis, is the process that utilizes the information in Messenger RNA (mRNA) to build a polypeptide (protein). Over the past few decades this process has been worked out in hundreds of labs all around the world but recent progress has been quite remarkable.

One of the key players in translation is the ribosome. (The others are mRNA, tRNAs and translation factors.) The ribosome and the other translation components form a complex molecular machine. The ribosome itself is complex, consisting of several RNA molecules (ribosomal RNAs) and several dozen proteins.

Thanks to the work of Harry Noller, we now know that one of these ribosomal RNAs is the molecule that actually catalyzes the formation of a peptide bond. The basic activity in proteins synthesis doesn't require a protein enzyme, it's an RNA molecule that does the job.

Thanks to this year's Nobel Laureates, and Harry Noller, we now know the structure of the ribosome at the molecular level and we know where the tRNAs and the translation factors bind.

We've known about these sites—the P and A sites are the most important—for some time but now we have a real picture of what they look like in the actual molecule. And it's led to some significant advances in our understanding of this important biological process.

This is basic science. It's not some speculative discovery that may or may not be a breakthrough and may or may not cure cancer (probably not). This is the stuff that goes into the textbooks. This is what science is all about.

The 2009 Nobel Prizes provide science writers with an excellent opportunity to highlight some discoveries that are really important in biology. You'd think that science writers would be all over this.

Where are they when the work is worth writing about? Are they going to be as silent about this as they were about the Nobel Prize for transcription in 2006?

See also: All Your Ribosomes Belong to Us.


Joe Thornton vs Michael Behe

A few weeks ago I blogged about an important series of papers on the evolution of the glucocorticoid receptor gene [see You Can't Go Home Again]. This is work from the Thornton lab and it shows the effect of accumulating neutral mutations over millions of years. I like the papers because it demonstrates clearly where Michael Behe goes wrong in his latest book The Edge of Evolution.

Carl Zimmer liked the papers as well and he wrote about them in a great big blog called The New York Times [see Can Evolution Run in Reverse? A Study Says It’s a One-Way Street]. I hate it when he does that. It makes me look bad.

Not surprisingly, Michael Behe read the papers. Surprisingly, he actually thought they helped his case rather that hurt it [see Nature Publishes Paper on the Edge of Evolution]. I was going to follow up on this since it was the reason I brought the papers to your attention in the first place. Now I'm glad I didn't because Carl Zimmer has done a much better job.

Carl asked Joe Thornton to comment on what Michael Behe said on the DISCO website. Thorton replied with a devastating put down of Behe that Carl has posted on The Loom: The Blind Locksmith Continued: An Update from Joe Thornton.

This is a really important article for a variety of reasons. You must read it if you want to learn about modern concepts in evolution.

Here's an excerpt from Thornton's letter that should induce you to visit the rest of the article.
Thanks for asking for my reaction to Behe’s post on our recent paper in Nature. His interpretation of our work is incorrect. He confuses “contingent” or “unlikely” with “impossible.” He ignores the key role of genetic drift in evolution. And he erroneously concludes that because the probability is low that some specific biological form will evolve, it must be impossible for ANY form to evolve.

Behe contends that our findings support his argument that adaptations requiring more than one mutation cannot evolve by Darwinian processes. The many errors in Behe’s Edge of Evolution — the book in which he makes this argument — have been discussed in numerous publications.

In his posts about our paper, Behe’s first error is to ignore the fact that adaptive combinations of mutations can and do evolve by pathways involving neutral intermediates. Behe says that if it takes more than one mutation to produce even a crude version of the new protein function, then selection cannot drive acquisition of the adaptive combination.


[Photo Credit: Joe Thornton by Jack Liu Photographer]

Thursday, October 15, 2009

My Family and Other Emperors


Here's how my family descends from Charlemagne. The last people on the list are my maternal grandparents. I think the data is accurate but I look forward to any corrections or comments.



UPDATE: I'm almost certainly NOT related to Charlemagne in the lineage shown below. Link #34 is wrong. The father of Ruhama Hill is NOT William Hill of Fairfield, Connecticut but Captain John Hill of Westerley, Rhode Island.



1-Charlemagne (Charles) King of the Franks,
Emperor (2 April 742-28 January 814)
+Hildegarde of Vinzgouw (758-April 783)

2-Louis I (Ludwig) "The Pious" King of France
(16 April 778-20 June 840)
+Ermengarde Princess of Hesbaye (778-3 October 818)

3-Lothair I King of Italy (795-29 September 855)
+Ermengarde of Orleans and Tours
   (about 805-20 March 856)

4-Ermengarde (Helletrude) de Lorraine (about 830-about 864)
+Giselbert II von Maasgau (about 815-after 877

5-Reginier (Rainer, Reginar) I de Hainault (about 850-916)
+Hersent de France? (about 865-after 919)

6-Regnier (Rainier, Reginar) II de Hainault Count of Hainault (about 890-after 932)
+Adelaide of Burgundy (about 903-)

7-Amaury de Hainault (about 925-about 983)
+Judith de Camrai (about 931-about 983)

8-William de Bastinbourg (about 965-about 1002)
+Albreda de Nogent Montfort de Esperon (-about 1022)

9-Amauri (Amalric) I de Montfort (993-about 1053)
+Bertrude "d’epernon" de Gometz (about 1001-after 1051)

10-Simon de Montfort (about 1026-1087)
+Angus d'Evereux (about 1030-about 1087)

11-Bertrade de Montfort (about 1070-February 1117)
+Foulques (Fulk) IV "le Réchin" Count of Anjou (1043-1109)

12-Foulques (Fulk) of Jerusulem Count of Anjou, King o Jerusalem (1089/92-13 November 1143)
+Ermengarde de la Flèche Erembourg of Maine Countess of Maine (-1126)

13-Geoffrey Plantagenet Count of Anjou (24 August 1113-7 September 1151)
+Empress Matilda (Maud) of England (7 February 1102-10 September 1167)

14-Henry II Plantagenet King of England (25 March 1133-8 July 1189)
+Ida de Tosny (about 1158-)

15-William de Longespée Earl of Salisbury (17 August 1152-April 1206)
+Ella of Salisbury Countess (-)

16-Stephen de Longespée Earl of Ulster, Justiciar of Ireland (1216-)
+Emeline Riddlesford (about 1223-1276)

17-Emmeline de Longespee (1250-)
+Baron Offaly Maurice Fitzmaurice (about 1242-1286)

18-Juliane Fitzmaurice of Offaly (between 1249 and 1266-between 1300 and 1309)
+Lord Thomond Thomas de Clare (about 1246-29 August 1287)

19-Matilda (Maude) de Clare (1280-1365)
+Lord Robert de Clifford (de Clare) (1 April 1274-24 June 1314 (Battle of Bannockburn))

20-Idoine (Idonea) de Clifford (de Clare) (about 1303-24 August 1365)
+Baron Henry de Percy (Feb. 6, 1300/01-about Feb. 26, 1351.52)

21-Maud de Percy (about 1335-Feb. 18, 1378/79)
+Baron John de Neville 3rd Lord Neville of Raby (1328-17 October 1388)

22-Eleanor de Neville (1360-1441)
+Ralph de Lumley (1360-)

23-Catherine de Lumley (1400-before 1461)
+John Chideocke (Chidlock) (1393-1450)

24-Catherine Chideocke (Chidlock) (1423-10 April 1479)
+John de Arundel VII (7 January 1421-22 November 1473)

25-Margaret de Arundel (about 1464-December 1519)
+Sir William Capel (1428-6 September 1515)
Lord Mayor of London

26-Sir Giles Capel (about 1486 May 1556)
[Tournament Helm]
+Isabel Newton (-)

27-Margaret Capel (about 1486-)
+Robert Ward (about 1484-)

28-Thomas Ward (-)
+? Hare (-)

29-Sir Richard Ward (about 1540-January 1615)
+Ann Gunville (Guiville?) (about 1540-after 1552)

30-Andrew Ward (about 1572-23 January 1615)
+? ? (-)

31-Andrew Ward (1597-1659)
+Hesther Sherman (1 April 1606-28 February 1665/6)

32-Ens. William Ward (1631-December 1675)
+Deborah Lockwood (12 October 1636-UNKNOWN)

33-Esther (Hester?) Ward (18 April 1664-18 April 1732)
+Eliphalet Hill (about 1663-before 30 January 1695)

34-William Hill (17 November 1692-25 April 1775)
+Abigail Barlow (30 June 1697-16 April 1743)

35-Ruhama (Ruhamah) Hill (-)
+John Belden (-)

36-Mary Belden (22 March 1747/8-5 April 1830)
+Joseph Treen Sr. (16 November 1744-July 1830)

37-William Treen (25 July 1774-26 April 1826)
+Catherine Montross (Montrose) (about 1785-)

38-Ester Treen (1807-~1891)
+Richard Cole (1789-1847)

39-Mary Cole (18 October 1837-9 May 1874)
+John Burns (1818-13 May 1875)

40-Isabelle (Bella) Hooper Burns (18 October 1862-15 August 1923)
+William Findley Docherty (9 March 1852-3 June 1920)

41-William Alvin Doherty (26 December 1878-9 June 1941)
+Ella Jane Foster (7 April 1887-7 February 1961)



[Image Credits:
Charlemange Empire map
Emperor Charlemagne]

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.

But if any of your ancestors lived in Europe, especially western Europe, then it's almost certain that Charlemagne is one of your ancestors. No matter where your ancestors are from they probably share a common ancestor with everyone else from that region. What's surprising is that many of those common ancestors lived only 1200 years ago.

I'm talking about big regions here, like most of Europe or Asia, or Africa. There's a remarkable amount of inbreeding among human populations at that scale. It's a good example of how evolution works. It's populations that evolve.

With only a few exceptions, species are subdivided into numerous populations with restricted gene flow between them. The sub divisions range from very large group called races, or subspecies, to progressively smaller populations down to local demes or extended families. In small populations, alleles can become rapidly fixed by random genetic drift but the existence of these populations means that it is much more difficult for these alleles to spread to the rest of the species. What we expect to see under those conditions is races or demes that differ substantially in their allele frequencies.

The explosion in amateur genealogy in recent years has highlighted these kinds of population structures in our own species. More and more people are putting their genealogical research on publicly accessible databases such as ancestry.com and many others. The collective result of these, mostly amateur, investigations is remarkable. It means that every one of us can make a family tree.

Well, perhaps not everyone. There's a huge bias towards Caucasians in the genealogy databases. There are many reasons for this bias but we won't go into them in this posting. The important result is that we can all learn something about human populations from this data even if it doesn't include your own ancestors.

The other recent development is the increasing number of people who are having their DNA analyzed and posting the results online. This is much more important since people all over the world are participating and we will soon have a good picture of the genetic structure of today's populations. This complements the family tree data in the same way that gene phylogenies complement the fossil record.

What about Charlemagne? Amateur European genealogists have to do a lot of work to document their ancestors back four or five generations. This takes them to the 1800s (30 years per generation).1 At that point in time they have 16 or 32 direct ancestors and chances are they'll be able to hook up with others who share these ancestors. The farther back you go on your own, the greater the chances that someone will have researched your ancestor.

The idea that many of us are related to Charlemagne is not new. Here's what they say on the Genealogy of Presidents website.

Genealogists have mathematically demonstrated how all Americans of European descent must be related to Charlemagne. In this regard, genealogists have established the exact lines of descent from Charlemagne for 14 U.S. Presidents. Two of these are President George W. Bush and his father President George H.W. Bush. Other Presidents whose descent from Charlemagne have been traced include: George Washington, Ulysses Grant, Franklin Roosevelt, Teddy Roosevelt, and Gerald Ford. To demonstrate how we are all related, the New England Historical Society has researched the genealogy of Barack Obama and determined that on his mother's side he is related to six other previous presidents: George W. Bush, George H. W. Bush, Lyndon Johnson, Harry Truman, Gerald Ford, and James Madison. Presumably, if Barack Obama's ancestry on his mother's side could be traced far enough back, he also would be shown to be descended from Charlemagne. Meanwhile, on his father's side, we are all related to President Barack Obama since anthropologists have determined that all modern humans are descended from a common African ancestor.

If you examine the List of United States Presidents by genealogical relationship you'll see that 19 US Presidents are descendants of British royalty and therefore, almost certainly, descendants of Charlemagne. Note that US Presidents are not royalty, they are, to all intents and purposes, ordinary citizens, just like you and me.

It's almost trivial to find connections to the US Presidents if you have ancestors who settled in the British colonies in the 1600s. I'm related to George Bush, for example, through the Shermans of Rhode Island and Connecticut. The good news is that I'm also related to Winston Churchill though the same family.

The amazing thing about genealogy is how closely related everyone is once you start looking. This isn't so amazing to population geneticists.

It's not so hard for North Americans to find European ancestors but many lineages terminate because parish records have not been preserved and because there are no other sources for the ancestors of average citizens. But every now and then you'll stumble upon lineages that have been well researched. Among my own ancestors for example there are half a dozen lineages that reach back to the 1400s and beyond. All I did was find the connections to those lineages.

The history of European nobility is well known. Chances are, you have at least one ancestor who connects to the various Dukes, barons, Counts, and Knights and their spouses in medieval times . A large percentage of the nobility of the European nobility can claim descent from Charlemagne. He had 20 children.

With a little effort, almost everyone of European descent can find the path to Charlemagne. If your ancestors are from England or Scotland your connection often runs through William of Normandy and a bunch of other tourists from France who visited England in 1066. Be careful, though, because there are many incorrect genealogies on the web and you'll need to do some fact checking. I found three different connections to nobility but two of them were figments of someone's overactive imagination. [See My Family and Other Emperors for my relationship to Charelmeange.]

Expert genealogists, as opposed to amateurs, are very frustrated by these errors on the internet. Because of the nature of the databases, it's very hard to remove errors once they start being incorporated into various genealogies. [See An Open Letter from Michael Wood for one example of this problem.]

The fact that all Europeans have several recent common ancestors tells us a lot about the genetic makeup of this population. It is quite homogeneous and there's a lot of inbreeding. It seems to be extremely rare to discover a non-European ancestor once one goes back a few hundred years. (It's much more common in recent times.) I presume this lack of outbreeding also applies to Asians, Africans, and all other groups.

Given that the average generation is 30 years2, if you go back to 800 that's about 40 generations. Potentially you have 240 ancestors. That's more than 1 trillion ancestors alive in 800. I don't know what the population of Europe was in 800 but I strongly suspect it wasn't even close to one trillion people. I suspect it was only about 25 million. It's not surprising that you are related to many of them.

It would be interesting to know how many people who were alive in 800 have direct descendants who are alive today. Maybe there's a way of calculating this?


1. In my case it was my mother who did/does all the work. I just surfed the internet using her data.

2. The actual calculated value for my ancestors is 29 years per generation.