Lawyers and Scientists

There’s been a skirmish between Larry Moran and Barry Arrington about whether Barry understands the Theory of Evolution, and the latest salvo is a piece at UD, entitled, Can a Lowly Lawyer Make a Useful Contribution? Maybe.

Well, in a sense, Barry makes a useful contribution in that post, as he gives a very nice illustration of a common misunderstanding about the process of hypothesis testing, in this case, basic model-fitting and null hypothesis testing, the workhorse (with all its faults) of scientific research.  Barry writes:

[Philip]Johnson is saying that attorneys are trained to detect baloney.  And that training is very helpful in the evolution debate, because that debate is chock-full of faulty logic (especially circular reasoning), abuse of language (especially equivocations), assumptions masquerading as facts, unexamined premises, etc. etc.

Consider, to take one example of many, cladistics.  It does not take a genius to know that cladistic techniques do not establish common descent; rather they assume it.  But I bet if one asked, 9 out of 10 materialist evolutionists, even the trained scientists among them, would tell you that cladistics is powerful evidence for common descent.  As Johnson argues, a lawyer’s training may help him understand when faulty arguments are being made, sometimes even better than those with a far superior grasp of the technical aspects of the field.  This is not to say that common descent is necessarily false; only cladistics does not establish the matter one way or the other.

In summary, I am trained to evaluate arguments by stripping them down to examine the meaning of the terms used, exposing the underlying assumptions, and following the logic (or, as is often the case, exposing the lack of logic).  And I think I do a pretty fair job of that, both in my legal practice and here at UD.

Barry has made two common errors here.  First he has confused the assumption of common descent with the conclusion of common descent, and thus detected circular reasoning where there is none.  Secondly he has confused the process of fitting a model with the broader concept of a hypothesised model.

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Alzheimer’s and Evolution

I have to say, while the UD “newsdesk” is terrible source for comment on scientific news, the links themselves are often interesting.  Today, the UD “newsdesk” reports on a pretty interesting study, reported in Nature, here, and a preprint of which seems to be open access here

It’s been apparent for a while from Genome-Wide Association Studies (GWAS) that “risk” alleles for various mental disorders, despite being statistically significant, have extremely small effect sizes.  In other words, while the studies show that many mental disorders are indeed associated with specific alleles (and we already know that many are highly heritable, including schizophrenia, ADHD and Alzheimer’s), there aren’t just a few rogue alleles of large effect (well, there are, but they are far rarer than these disorders), but instead, a whole cocktail of alleles with very slightly raised Odds Ratios for certain disorders (and some are shared between multiple disorders).  This means that the vast majority of people carrying these “risk alleles” are perfectly fine. That would help explain why they have not been weeded out by selection.

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The Twilight of Intelligent Design (Open thread)

Sunset

It just dawned on me that ID is dead.

Dembski is off all radar. He doesn’t even show up in the search box at South Carolina bible college or whatever. The last post on the Design Inference is a year old.

Meyer’s book went up like a firework and came down with the stick.

Most of the static websites are moribund. UD has banned virtually all dissenters. The few brave enough to wander over to TSZ bail out after a couple of rounds. The biologic institute inflates its “selected publications” with publications that have nothing to do with the biologic institute and seems to be doing no more than pretending to produce output.

Bio-Complexity is moribund.

Behe doesn’t seem to have much to say.

The big guys won’t come out to debate. The small ones mostly won’t leave heavily censored sites. Even the UD newsdesk peddles 6 year old stories as “news”.

And all the threads are about religion. Or tossing coins.

I don’t know why I hadn’t seen it before.

It’s dead.

Posted at “After the Bar Closes on Jan. 05 2014,16:37 by Febble (Elizabeth Liddle) Continue reading

The Double-Blind Newcombian Placebo Paradox

Here’s something I slopped together recently. I’m not really familiar with the literature on any of this, so maybe it’s all pretty well known (or well known to be confused).  Anyhow, comments are welcome, and I apologize in advance for my usual pile of typos, grammatical  errors, and other miscellaneous blunders.

W

 

Johnny Woulda, 45, has had chronic tendonitis in both of his elbows since he was about 30.  He’s always been told that there’s no help for it except rest and steroid injections, but the rest hasn’t worked, and he’s afraid the injections will be worse for him than the elbow pain.  He takes a bus to work every day and one day he sees a poster that says “Do you have tendonitis? We are testing a new non-steroidal oral drug, and if you are an otherwise healthy male between the ages of 18 and 48 you could earn $100 by taking part in our clinical trial.”  The drug company, Montrezl, is interested in testing the effectiveness of their experimental product, Elbowftra©.  Based on their tests on chimpanzees, which have no belief one way or the other whether they are being given a real drug, they believe that Elbowftra© drug would have at least a 50% effectiveness rate on humans people—higher if the person is credulous (the sort of person now spending a ton of money on herbal remedies).  The FDA has assured Montrezl that if they can confirm that at least 30% more human volunteers are cured by Elbowftra© than are cured by a sugar pill placebo, as determined by blind reviewers, they should have no problem getting their drug approved.  On the other hand, if there’s not much difference between Ebowftra’s effectiveness and that of a placebo, there isn’t much hope.

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Neuroimaging

I’ve been meaning to write a post in this for a while, but as usual, Barry Arrington has prompted me into action (I’m really very grateful to Barry sometimes :))  (Golly, just checked – it’s already half way down the UD page!  Does Barry really want his posts buried quite so rapidly?  We are going to see fossilisation at this rate!)

Anyhoo….  Neuroimaging is one of the things I do.  Here is one of my favorite images (probably the most reproduced fMRI image of all time), by Fox et al, 2005:

Although it may not have the form that some readers might be more familiar with, as it’s plotted on a “flat[ish] map” of the cortical surface.

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Protein Space and Hoyle’s Fallacy – a response to vjtorley

‘vjtorley’ has honoured me with my very own OP at Uncommon Descent in response to my piece on Protein Space. I cannot, of course, respond over there (being so darned uncivil and all!), so I will put my response in this here bottle and hope that a favourable wind will drive it to vjt’s shores. It’s a bit long (and I’m sure not any the better for it…but I’m responding to vjt and his several sources … ! ;)).


“Build me a protein – no guidance allowed!”

The title is an apparent demand for a ‘proof of concept’, but it is beyond intelligence too at the moment, despite a working system we can reverse engineer (a luxury not available to Ye Olde Designer). Of course I haven’t solved the problem, which is why I haven’t dusted off a space on my piano for that Nobel Prize. But endless repetition of Hoyle’s Fallacy from multiple sources does not stop it being a fallacious argument.

Dr Torley bookends his post with a bit of misdirection. We get pictures of, respectively, a modern protein and a modern ribozyme. It has never been disputed that modern proteins and ribozymes are complex, and almost certainly not achievable in a single step. But

1) Is modern complexity relevant to abiogenesis?

2) Is modern complexity relevant to evolution?


Here are three more complex objects:

DESCRIPTION HERE

Circuit Board

DESCRIPTION HERE

Panda playing the flute

DESCRIPTION HERE

er … not yet in service!

 

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Journal club – Protein Space. Big, isn’t it?

Simplistic combinatorial analyses are an honoured tradition in anti-evolutionary circles. Hoyle’s is the archetype of the combinatorial approach, and he gets a whole fallacy named after him for his trouble. The approach will be familiar – a string of length n composed of v different kinds of subunit is one point in a permutation space containing vn points in total. The chance of hitting any given sequence in one step, such as the one you have selected as ‘target’, is the reciprocal of that number. Exponentiation being the powerful tool it is, it takes only a little work with a calculator to assess the permutations available to the biological polymers DNA and protein and come up with some implausibly large numbers and conclude that Life – and, if you are feeling bold, evolution – is impossible.

Dryden, Thomson and White of Edinburgh University’s Chemistry department argue in this 2008 paper that not only is the combinatorial space of the canonical 20 L-acids much smaller than simplistically assumed, but more surprisingly, that it is sufficiently small to have been explored completely during the history of life on earth. Continue reading