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.)

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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.

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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.

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

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.

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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.

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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.

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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.

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[Photo Credit: Joe Thornton by Jack Liu Photographer]

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.

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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.

UPDATE (Jan. 2015): An informed read has pointed out that Julianne FiztMaurice (#18) is the daughter of Maurice FitzMaurice and his first wife, Matilda de Predergast, and not his second wife Emmiline de Longspree (#17) as I've shown.

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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)

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[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.

Remember that it's populations that evolve, not individuals. 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 post. 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.

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?

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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.

Nobel Laureates: Erwin Neher and Bert Sakmann

 

The Nobel Prize in Physiology or Medicine 1991

"for their discoveries concerning the function of single ion channels in cells"

Erwin Neher (1944 - ) and Bert Sakmann (1942 - ) won the Nobel Prize for developing a technique to measure the voltage changes produced by single ion channels in cell membranes.

This is a remarkable achievement. The ion channel is in it's natural environment and the voltage change it produces is minuscule. The technique, called the "patch clamp", could not have been discovered without sensitive instruments developed in other disciplines.

1991 is part of the modern era on the Nobel Prize website so there's an excellent press release available to explain the award and describe the science. Here's the Press Release.
THEME:
Nobel Laureates

Summary

Each living cell is surrounded by a membrane which separates the world within the cell from its exterior. In this membrane there are channels, through which the cell communicates with its surroundings. These channels consist of single molecules or complexes of molecules and have the ability to allow passage of charged atoms, that is ions. The regulation of ion channels influences the life of the cell and its functions under normal and pathological conditions. The Nobel Prize in Physiology or Medicine for 1991 is awarded for the discoveries of the function of ion channels. The two German cell physiologists Erwin Neher and Bert Sakmann have together developed a technique that allows the registration of the incredibly small electrical currents (amounting to a picoampere - 10-12A) that passes through a single ion channel. The technique is unique in that it records how a single channel molecule alters its shape and in that way controls the flow of current within a time frame of a few millionths of a second.

Neher and Sakmann conclusively established with their technique that ion channels do exist and how they function. They have demonstrated what happens during the opening or closure of an ion channel with a diameter corresponding to that of a single sodium or chloride ion. Several ion channels are regulated by a receptor localized to one part of the channel molecule which upon activation alters its shape. Neher and Sakmann have shown which parts of the molecule that constitute the "sensor" and the interior wall of the channel. They also showed how the channel regulates the passage of positively or negatively charged ions. This new knowledge and this new analytical tool has during the past ten years revolutionized modern biology, facilitated research, and contributed to the understanding of the cellular mechanisms underlying several diseases, including diabetes and cystic fibrosis.

What Happens Inside the Cell?

Inside the cell membrane there is a well-defined environment, in which many complex biochemical processes take place. The interior of the cell differs in important respects from its outside. For example the contents of positive sodium and potassium ions and negatively charged chloride ions are quite different. This leads to a difference in electrical potential over the cell membrane, amounting to 0.03 to 0.1 volts. This is usually referred to as the membrane potential.

The cell uses the membrane potential in several ways. By rapidly opening channels for sodium ions the membrane potential is altered radically within a thousandth of a second. Cells in the nervous system communicate with each other by means of such electrical signals of around a tenth of a volt that rapidly travel along the nerve processes. When they reach the point of contact between two cells - the synapse - they induce the release of a transmitter substance. This substance affects receptors on the target cell, often by opening ion channels. The membrane potential is hereby altered so that the cell is stimulated or inhibited. The nervous system consists of a series of networks each comprised of nerve cells connected by synapses with different functions. New memory traces in the brain are for example created by altering the number of available ion channels in the synapses of a given network.

All cells function in a similar way. In fact, life itself begins with a change in membrane potential. As the sperm merges with the egg cell at the instant of fertilization ion channels are activated. The resultant change in membrane potential prevents the access of other sperm cells. All cells - for instance nerve cells, gland cells, and blood cells - have a characteristic set of ion channels that enable them to carry out their specific functions. The ion channels consist of single molecules or complexes of molecules, that forms the wall of the channel - or pore - that traverses the cell membrane and connects the exterior to the interior of the cell (Figure 1B and 1D). The diameter of the pore is so small that it corresponds to that of a single ion (0.5-0.6 millionths of a millimetre). An immediate change in the shape of the molecule leads to either an opening or a closure of the ion channel. This can occur upon activation of the receptor part of the molecule (Figure 1D) by a specific signal molecule. Alternatively a specific part of the molecule that senses changes in membrane potential can open or close the ion channel.

Figure 1. Registration of the flow of current through single ion channels using the recording technique of Neher and Sakmann. A schematically shows how a glass micropipette is brought in contact with the cell, and B, using a higher magnification, a part of the cell membrane, with ion channels, in close contact with the tip of the pipette. The interior of the pipette is connected to an electronic amplifier. C shows a channel in greater magnification with its receptor facing the exterior of the cell and its ion filter. D shows the current passing through the ion channel as it opens.

Neher and Sakmann Record the Electric Current Flowing Through a Single Ion Channel

It has long been known that there is a rapid ion exchange over the cell membrane, but Neher and Sakmann were the first to show that specific ion channels actually exist. To elucidate how an ion channel operates it is necessary to be able to record how the channel opens and closes. This appeared elusive since the ionic current through a single ion channel is extraordinarily small. In addition, the small ion channel molecules are embedded in the cell membrane. Neher and Sakmann succeeded in solving these difficulties. They developed a thin glass micropipette (a thousandths of a millimeter in diameter) as a recording electrode. When it is brought in contact with the cell membrane, it will form a tight seal with the periphery of the pipette orifice (Figure 1A, B). As a consequence the exchange of ions between the inside of the pipette and the outside can only occur through the ion channel in the membrane fragment (Figure 1B). When a single ion channel opens, ions will move through the channel as an electric current, since they are charged. Through a refinement of the electronic equipment and the experimental conditions they succeeded in measuring this "microscopical" current by laborious methodological developments during the seventies (Figure 1C).

How Does an Ion Channel Operate?

Ion channels are of different types. Some only permit the flow of positively charged sodium, potassium or calcium ions, others only negatively charged chloride ions. Neher and Sakmann discovered how this specificity is accomplished. One reason is the diameter of the ion channel, which is adapted to the diameter of a particular ion. In one class of ion channels, there are also two rings of positively or negatively charged amino acids. They form an ionic filter (see Figure 1D), which only permits ions with an opposite charge to pass through the filter. In particular Sakmann through a creative interaction with different molecular biologists elucidated how the different parts of the ion channel molecule(s) operate. Neher and Sakmann's scientific achievements have radically changed our views on the function of the cell and the contents of text books of cell biology. Their methods are now used by thousands of scientists all over the world.

The Study of Secretory Processes

Nerve cells, as well as hormone-producing cells and cells engaged in the host defence (like mast cells) secrete different agents. They are stored in vesicles enclosed by a membrane. When the cell is stimulated the vesicles move to the cell surface. The cell and vesicle membranes fuse and the agent is liberated. The mast cell secretes histamine and other agents that give rise to local inflammatory reactions. The cells of the adrenal medulla liberate the stress hormone adrenaline, and the beta cells in the pancreas insulin. Neher elucidated the secretory processes in these cell types through the development of a new technique which records the fusion of the vesicle(s) with the cell membrane. Neher realized that the electric properties of a cell would change if its surface area increased making it possible to record the actual secretory process. Through further developments of their sophisticated equipment the resolution finally permitted recording of each little vesicle fusing with the cell membrane.

Regulation of Ion Channel Function

Neher and Sakmann also used the electrode pipette to inject different agents into the cell, and they could thereby investigate the different steps in the secretory process within the cell itself (see above). In this way a number of cellular secretory mechanisms have been clarified such as the role of cyclic AMP (see Nobel Prize to Sutherland 1971) or calcium ions. For instance, we now have a better understanding of how the hormone levels in the blood are maintained at a certain level.

Also the basal mechanisms underlying the secretion of insulin have been identified. The level of blood glucose controls the level of glucose within the insulin-forming cell, which in turn regulates the level of the energy rich substance ATP. ATP acts directly on a particular type of ion channel which controls the electric membrane potential of the cell. The change of membrane potential then indirectly influences other ion channels, which permit calcium ions to pass into the cell. The calcium ions subsequently trigger the insulin secretion. In diabetes the insulin secretion is out of order. Certain drugs commonly used to stimulate insulin secretion in diabetes act directly on the ATP-controlled ion channels.

Many other diseases depend entirely, or partially, on a defect regulation of ion channels, and a number of drugs act directly on ion channels. Many pathological mechanisms have been clarified during the eighties through ion channel studies, for instance cystic fibrosis (cloride ion channels), epilepsy (sodium and potassium ion channels), several cardio-vascular diseases (calcium ion channels), and neuro-muscular disorders like Lambert-Eatons disease (calcium ion channels). With the help of the technique of Neher and Sakmann it is now possible to tailormake drugs, to achieve an optimal effect on particular ion channels of importance in a given disease. Drugs against anxiety act for instance on certain inhibitory ionic channels in the brain. Alcohol, nicotine and other poisons act on yet other sets of ion channels.

In summary, Neher and Sakmann's contributions have meant a revolution for the field of cell biology, for the understanding of different disease mechanisms, and opened a way to develop new and more specific drugs.

References

Alberts et al.: The Molecular Biology of the Cell. Garland Press, 1990, 2nd edition, pp. 156, 312-326, 1065-1084.

Grillner, S. I: N. Calder (ed.). Scientific Europe. Foundation Scientific Europe, 1990.

Grillner, S. & Hökfelt, T.: Svindlande snabb utveckling präglar neurovetenskapen. Läkartidningen 1990, 87, 2777-2786.

Rorsman, P. & Fredholm, B.B.: Jonkanaler - molekylär bakgrund till nervtransmission. Läkartidningen 1991, 88, 2868-2877.

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The images of the Nobel Prize medals are registered trademarks of the Nobel Foundation (© The Nobel Foundation). They are used here, with permission, for educational purposes only.

The McNeil Medal for the Public Awareness of Science Goes to Brian Alters

 
The Royal Society of Canada regularly presents the McNeil Medal for the Public Awareness of Science to deserving educators. This year the award was given to Brian Alters of McGill University for his contributions to the teaching of evolution in public schools and universities.

Professor Alters is a member of the board of directors of the National Center for Science Education [see Brian Alters honored by Royal Society of Canada]. He has some wise words about teaching evolution.

The following excerpts are from Brian Alters' book Teaching Biological Evolution in Higher Education: Methodological, Religious, and Nonreligious issues.

Critical thinking—most faculty want students to be critical thinkers. Many students, however, are epistemological duelists, viewing the academic world in terms of true or false, right or wrong, credit or no credit. Instead of analyzing evidence that contradicts their erroneous conceptions, students often just passively receive knowledge from authorities—professors. To become active learners, students need professors to use methods that involve them in grasping the important concepts; but, only 10%-30% of professors use methods other than traditional lectures as their primary pedagogy.

Do these sound like motherhood statements? If you answered "yes" then you aren't paying attention.

Alters is saying that students will readily cope with "information" in a course even if it contradicts their misconceptions. They'll simply make it part of their worldview or, even worse, ignore the fact that it conflicts and spew it back on the exam.

Whether or not students have taken courses in biology or evolution, they come to the science classroom with a variety of memories, knowledge, experience, and evolution conceptions. Often, some of those conceptions are different from scientific concepts. Students develop these conceptions from what they read in the popular press, find on the Web, and see on television and from their interactions with "nature," their peers, and their parents and other authority figures. Instructors at all levels have a complex task: to tap into what students know to assist them in building on their scientific knowledge, to help them replace their misconceptions with scientifically useful conceptions, and to help them construct meaning from their learning experiences.

Helping students construct meaning from their learning experiences is a daunting task. Only the students can do it; instructors cannot "fill" them with knowledge. All instructors can do is to provide learning experiences that facilitates students' generating links between relevant information they already know and new information. From such a constructivist perspective, learning is a social process in which students make sense of experience in terms of what they already know. But how does the professor engineer lessons to help students link the new information with the old in useful, accurate, and appropriate ways? And what happens when the "old" information consists of one or more scientific misconceptions?

What many instructors know from their own classroom experience is that student misconceptions (also called native conceptions, alternate conceptions, intuitive use, prior conceptions, preconceptions, or undesired understandings) are not easily changed. What many people do not realize, however, is that the process of conceptual change takes a long time, perhaps years, depending on the concept, and appears to be an incremental process. In learning evolutionary concepts in particular, students appear to need an extended exposure to and interaction with these concepts for growth in their understanding to occur. Instructors, therefore, may think of the learning experiences they provide for students is only one stepping stone towards the goal of more complete under standing.

To facilitate a constructivist approach in the classroom, an instructor should provide situations in which students examine the adequacy of their prior conceptions, allowing them to argue about and test them. The contradictions students may face during this testing process can provide the opportunity for them to acquire more scientifically appropriate concepts.

What this means is that students carry a lot of baggage into the university classroom. You're not going to change their conceptual understanding of evolution by just presenting the facts are you see them. You're also not going to be successful if you think that just giving them the right concepts—such as the importance of random genetic drift—is all it takes.

In order to start down the path toward changing their misconceptions, you need to directly challenge those misconceptions and bring the conflict out into the open. You need to do this even if you think the misconceptions are based on non-scientific issues.

In other words, teach the controversy.

I agree with Brian Alters on all these points. I disagree with him about some other things and, in one case, I think he makes a big mistake. In all his writings he assumes that student misconceptions need to be addressed and university instructors only need to learn which methods are most effective. In my opinion, he doesn't pay enough attention to the fact the instructors also have misconceptions that need to be corrected.

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[Image Credit: Project X]

Monday's Molecule #140: Winner

 
The molecule is the potassium ion channel from rat brain cells. Roderick MacKinnon solved this structure and he got the Nobel Prize in 2003 for his work on the structure and function of the potassiunm ion channel [see Nobel Laureat: Roderick MacKinnon]

The Nobel Laureates for this week are Erwin Neher and Bert Sakmann for working out a technique to measure the voltage changes during ion transport.

The winner is Dima Klenchin of the University of Wisconsin, Madison.

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

There's a Nobel Prize indirectly connected to this molecule. The prize was for developing a technique that could be used to study the function of molecules like this one.

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 five 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, and Jason Oakley a biochemistry student at the University of Toronto.

Frank and Joshua have agreed to donate their free lunch to an undergraduate. Consequently, I have an extra free lunch for a deserving undergraduate 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.

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[Image Credit: Brookhaven National Laboratory]

The Adaptive Value of Menopause

One of the problems with adaptationist just-so stories is that they often sound so plausible that everyone just assumes they must be true and stops thinking critically. One of the classic examples is the adaptationist explanation of menopause.

The "Grandmother Hypothesis" says that menopause arose in primitive hominids because it prevented pregnancies in older women thereby freeing them to assist in the care of their grandchildren. This extra care had a significant effect on the survivability of the grandchildren thereby increasing the probability that the frequency of the menopause allele would increase in the population.

Over the course of thousands of generations, the allele for menopause became fixed in our ancestral populations because it conferred a significant adaptive advantage.

Razib Khan believes in this adaptationist explanation for menopause. He quotes from a recent study that seems. on the surface, to lend support to the idea. See the recent posting on Gene Expression: Menopause as an adaptation.

The study by Virpi Lummaa looked at the presumed benefit of grandmothers among Finnish families. She reports that children with the support of a grandmother are 12% more likely to survive than children without such support.

The prompts Razib to write.

12% is a very big effect and would lead to rapid evolutionary change (on the order of thousands of years in the most simple population genetic model of a single locus of dominant effect).

I posted a comment on his blog. I'm reproducing it here in order to get more feedback.

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12% is, indeed, a very large effect but what does it have to do with evolution?

We're looking at a study where every single woman underwent menopause so one of the things we certainly aren't doing is testing to see whether menopause has an effect on the survivability of grandchildren.

Let's think about reasons why some families have grandmothers to help out and some don't. First, there's the relative proximity of living grandmothers. Then there's the question of the relationship between parents and grandparents. Let's not forget possible financial help that has nothing to do with direct caregiving. Finally, there's the issue of whether a family even has a surviving grandmother.

None of theses things are affected in any way by the fertility or non-fertility of the grandmother, right? The 12% difference has nothing to do with menopause.

Now let's think about a time in the past when menopause was presumably evolving. You had two kinds of females in the population, those who underwent menopause and those who didn't. There will still be all kinds of families who experience the help of a grandmother irrespective of whether she can still have kids or not. That's the background that a presumed adaptation has to deal with.

If there are non-menopausal women who live into their fifties, are close to their grandchildren, and whose husband is dead, then they will presumably help raise thier grandchildren. Same thing applies to non-menopausal women who simply don't risk getting pregnant any more even though their spouse is alive. (Just say "no." It's probably more common than you think. Women are not stupid.)

In fact, the adaptationist just-so story only really applies to that small subset of women who have the following characteristics.

1. They live past 50 years old.
2. They have grandchildren who are young and still need care.
3. They don't have too many grandchildren in different families so their caregiving can be effective.
4. They live near their grandchildren and can help out.
5. They have a good relationship with their children and their spouses.
6. Their husbands are still living.
7. They choose to get pregnant.

That's the only group that menopause affects. It eliminates #7 but has no effect on any of the other factors. It certainly doesn't have any effect on whether the grandmother was dead or alive at 50 years old.

Given that there were many families that received no help from grandmothers, whether they had the menopause allele or not, and given that there were many families who received help even if the grandmothers did not have the menopause allele, the question is "what is the adaptive value of menopause under those circumstances."

What does the Lummaa study have to say about that?

Since you are a supporter of this adaptationist explanation can you describe for me the kind of society where you think this allele became fixed in the population? Was it a hunter-gather society of small bands or a large agricultural society of small towns? Or something else?

I'd like to hear more details about how this grandmother hypothesis actually worked in Australopithicus or Homo erectus societies. Please include your estimate of how many grandmothers survived past the age where menopause could make a difference as you estimate the fitness coefficient.

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[Image Credit: "Rudyard Kipling’s illustration for The Elephant’s Child from Just So Stories (1902)." From Encyclopedia Britannica

Pee Zed Myers Teaches Mr. Deity About Evolution

 

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