The host of the Cross Examined radio show Dr. Frank Turek talks with Stephen C. Meyer and Doug Axe about a recent conference of Royal Society scientists discussing the problems with the theory of macro-evolution.
the main topic was whether naturalistic mechanisms can produce new body plans and new organ types
no one disputes micro-evolution: beaks changing size, antibiotic resistance
many of the naturalistic scientists admitted the problems with current naturalistic theories, but they don’t want to embrace the need for a designer
none of the proposals that were debated solved the real problems with macro-evolution
Problem #1: the sudden origin of body plans in the fossil record
Problem #2: the origin of information (e.g. – in protein molecule)
Problem #3: need for favorable early mutations (for body plans)
Problem #4: the problem of epigenetics
Problem #5: the universality of the design intuition
Some of these problems have actually gotten worse for naturalistic evolution as our scientific knowledge has grown.
If you want the two best books on intelligent design, get Dr. Meyer’s “Signature in the Cell” and “Darwin’s Doubt”. I should note that Dr. Meyer is not a young Earth creationist, and has defended the Big Bang cosmology as a solid evidence for a Creator of the universe. Being in favor of an old universe and an old Earth is compatible with being opposed to evolution – because of scientific reasons.
Evolution News reported on a 27-minute debate featuring Dr. Stephen C. Meyer – probably the best proponent of intelligent design there is.
We often say that Darwinists are reluctant to debate advocates of intelligent design, but here are two who deserve a tip of the hat. Keith Pannell is a chemist at the University of Texas at El Paso who hosts a program, Science Studio, on the NPR station there. He invited Stephen Meyer on to talk about the science of ID, pegged to the Dover anniversary.
Clearly Pannell is an ID critic so he gets kudos for being willing to have a civil and informative conversation. Perhaps feeling insecure about facing the author of Darwin’s Doubt by himself, Dr. Pannell invited a biologist colleague, Ricardo Bernal, to serve as “co-host.”
So it was two against one, but no worries. Meyer is, as always, superb, and the discussion sounds like it was an education for the two Texas scientists. Listen and enjoy.
Critic: but we used the scientific method to disprove the Darwinian predictions, you don’t like the scientific method
intelligent design proponents love science, and the scientific method, and they do work in labs to confirm their hypotheses, (WK:for example, the probability of generating a protein by chance)
Critic: what about the Dover court case that you lost?
the Discovery Institute objected to actions taken by the Dover school board
Critic: what about the molecular machines, how are they related to intelligent design?
even in the simplest living organisms, there are tiny machines that are tightly integrated, and cannot be built up in a stepwise fashion
Critic: I’ve worked with the ATP-synthase and other molecular machines, but “you can kind of begin to tease how some of these molecular machines have come about” – pieces have multiple functions, and they are co-opted into larger systems
the problem with the co-option argument breaks down when you look at the specific details of different machines
for example – the type III secretory system cannot be an precursor to the bacterial flagellum, it is younger, not older than the bacterial flagellum
Critic: what would it take for your view to be falsified?
demonstrable undirected processes that are capable of creating functional information in DNA, or processes that can build up an irreducibly complex molecular machine within the time available with a decent probability
If you like this debate, check out Stephen C. Meyer’s two books: “Signature in the Cell” and “Darwin’s Doubt”. They are now out as audio books, too.
I have read and listened and watched a lot of material on intelligent design, but I have never seen so much value packed into such a short lecture. I really hope you’ll watch this and that it’s helpful to you.
the big question when discussing the origin of life: where did the information in living systems come from?
Until 530 million years ago, the oceans were largely devoid of life
In a 10 million year period, many new forms of animal life emerged
New biological forms of life require new information
the discovery of DNA shows that living systems work because cells have information that allows them to build the components of molecular machines: cell types, proteins, etc.
can random mutation and natural selection create new functional information?
normally, random mutations tend to degrade the functionality of information, e.g. – randomly changing symbols in an applications code does not usually introduce useful new functions, it usually renders what is there non-functional
the majority of possible sequences will NOT have functions, so random mutations will more likely give you non-functional code, rather than functional code
example: a bicycle lock with 4 numbers has many possible sequences for the 4 numbers, and only one of them has unlock functionality, the rest have no functionality
if you have lots of time, then you might be able to guess the combination, but if the lock as has 10 billion numbers, and only one combination that unlocks, you can spend your whole life trying to unlock it and won’t succeed
how likely is it to arrive at a functional protein or gene by chance? Is it more like the 4-dial lock (can be done with lots of time) or the 10 billion dial lock (amount of time required exceeds the time available)?
the probability is LOW because there is only one sequence of numbers that has unlock function
consider a short protein of 150 amino acids has 10 to the 195th power possible sequences
if many of these sequences of amino acides had biological function, then it might be easier to get to one by random mutation and selection than it is with a lock that only unlocks for ONE sequence
how many of the possible sequences have biological function?
Thanks to research done by Douglas Axe, we now know that the number of functional amino acid sequences for even a short protein is incredibly small…
Axe found that the odds of getting a functional sequence of amino acids that will fold and have biological function is 1 in 10 to the 77th power
Is that number too improbable to reach by chance? well, there are 10 to 65th atoms in the entire Milky Way galaxy… so yes, this is a very improbable outcome
can random genetic mutations search through all the sequences in order to find the one in 10 to the 77th power one that has biological function? It depends on how much guessers we have and how many guesses we get in the time available
even with the entire 3.5 billion year history of life on Earth, only about 10 to the 40th organisms have ever lived, which far smaller fraction of the 10 to the 77th total sequences
even with a very fast mutation rate, you would not be able to reach a functional protein even with all that time, and even with all those organisms
I was once having a discussion with a woman about the research that Axe did at the Cambridge University lab. He published four articles in the Journal of Molecular Biology. I held out one of the papers to her and showed her the numbers. She said over and over “I hate the Discovery Institute! I hate the Discovery Institute!” Well, yeah, but you can’t make the Journal of Molecular Biology go away with hating the Discovery Institute. JMB is peer-reviewed, and this was experimental evidence – not a theory, not a hypothesis.
We have been blessed by the Creator and Designer of the universe in this time and place with overwhelming evidence – an abundance of riches. For those who have an open mind, this is what you’ve been waiting for to make your decision. For the naturalists who struggle so mightily to block out the progress of experimental science, they’ll need to shout louder and shut their eyes tighter and push harder to block their ears. Maybe if they keep screaming “Star Trek” and “Star Wars” over and over to themselves, they will be able to ignore the real science a little longer.
It’s often argued that when two or more organisms share viral genes in the same place, it is evidence those organisms evolved from a common ancestor. Wikipedia’s Evidence for Common Descent page frames it as follows:
Endogenous retroviruses (or ERVs) are remnant sequences in the genome left from ancient viral infections in an organism. The retroviruses (or virogenes) are always passed on to the next generation of that organism that received the infection. This leaves the virogene left in the genome. Because this event is rare and random, finding identical chromosomal positions of a virogene in two different species suggests common ancestry.
This argument presupposes that the viruses inserted themselves into genomes randomly and stick around as junk DNA baggage, rather than genomes originally being designed with viral-like genes that perform useful functions. However this argument has unraveled as we’ve discovered useful functions for many viral-like genes, including functions that specifically require a viral-like sequence. Some examples among many:
ERV sequences protect against viral infection through interference–a matching-but-opposite strand of RNA is created to bind to and disable RNA from a virus.
Likewise, ERV’s seem to function “during embryo implantation to help prevent immune recognition by the mother’s immune system”
In worms, an ERV has been observed to create actual viruses that transfer DNA from somatic cells (skin/brain/heart/etc.) to germline (sperm/egg) cells whenever the worm is exposed to too much heat, allowing them to rewrite their own DNA for future generations.
Viral envelopes from ERV transcripts attach to cell membranes in the placenta and causes them to fuse as a normal part of development: “The HERV-W [a human ERV] envelope glycoprotein named syncytin 1 is expressed in all trophoblastic [part of the placenta] cells and directly involved in human trophoblast fusion and differentiation [cells taking on specialized roles]”
These aren’t isolated cases of function. Phys.org interviewed one researcher: “When we investigated public data from embryonic cells, we found that many RNAs originated from regions in the human genome that are ERVs. We did not only observe isolated events, but systematic activation of these ERVs. Every cell type showed transcription of specific classes, something that is very unlikely to occur by chance”.
Those cases all involve RNA viruses and that’s old news. But two weeks ago, a single-celled eukaryote called Cafeteria roenbergensis was found to harbor maviruses within its own DNA that remain dormant until it is attacked by a large virus known as CroV. When this happens the maviruses activate to form an attack fleet, as NewScientist reports:
A voracious marine predator plagued by a giant virus has a defence system we’ve never seen before – it fights back by making its very own virus… Rather than waiting for maviruses to arrive by chance when CroVs attack, it actually carries the genes that code for mavirus inside its own genome. These genes are usually dormant, but they get turned on when Cafeteria is invaded by CroV. “It acts as an inducible antiviral defence system,” write Fischer and his colleague Thomas Hackl in a new preprint paper.
This process kills the Cafeteria roenbergensis cell, but is useful in defending other members of its own species. In this experiment maviruses were deliberately inserted into the Cafeteria roenbergensis genome (see the original paper), but more interestingly, sequences similar to the Cafeteria roenbergensis viral genes have been found in a wide range of animals:
A wide range of animals, from sea anemones to crocodiles, harbour genetic elements called Maverick transposons that closely resemble the mavirus genes. It’s possible that some of these organisms can also unleash viruses that attack giant viruses.
In spite of this, New Scientist still argues “our genomes are littered with the mutant remains of viruses and genetic parasites.” But these discoveries reveal this as a rapidly-shrinking argument of the gaps.
Save this for the next time someone insists that viral genes are useless junk DNA and therefore evidence of common descent.
I highly recommend watching the lecture, and looking at the slides. The quality of the video and the content is first class. There is some Q&A (9 minutes) at the end of the lecture.
intelligent design is concerned with measuring the information-creating capabilities of natural forces like mutation and selection
Darwinists think that random mutations and natural selection can explain the origin and diversification of living systems
Darwinian mechanisms are capable of explaining small-scale adaptive changes within types of organisms
but there is skepticism, even among naturalists, that Darwinian mechanisms can explain the origin of animal designs
even if you concede that Darwinism can account for all of the basic animal body plans, there is still the problem of life’s origin
can Darwinian mechanisms explain the origin of the first life? Is there a good naturalistic hypothesis to explain it?
there are at least two places in the history of life where new information is needed: origin of life, and Cambrian explosion
overview of the structure of DNA and protein synthesis (he has helpful pictures and he uses the snap lock blocks, too)
the DNA molecule is composed of a sequence of bases that code for proteins, and the sequence is carefully selected to have biological function
meaningful sequences of things like computer code, English sentences, etc. require an adequate cause
it is very hard to arrive at a meaningful sequence of a non-trivial length by randomly picking symbols/letters
although any random sequence of letters is improbable, the vast majority of sequences are gibberish/non-compiling code
similarly, most random sequences of amino acids are lab-proven (Doug Axe’s work) to be non-functional gibberish
the research showing this was conducted at Cambridge University and published in the Journal of Molecular Biology
so, random mutation cannot explain the origin of the first living cell
however, even natural selection coupled with random mutation cannot explain the first living cell
there must already be replication in order for mutation and selection to work, so they can’t explain the first replicator
but the origin of life is the origin of the first replicator – there is no replication prior to the first replicator
the information in the first replicator cannot be explained by law, such as by chemical bonding affinities
the amino acids are attached like magnetic letters on a refrigerator
the magnetic force sticks the letters ON the fridge, but they don’t determine the specific sequence of the letters
if laws did determine the sequence of letters, then the sequences would be repetitive
the three materialist explanations – chance alone, chance and law, law alone – are not adequate to explain the effect
the best explanation is that an intelligent cause is responsible for the biological explanation in the first replicator
we know that intelligent causes can produce functional sequences of information, e.g. – English, Java code
the structure and design of DNA matches up nicely with the design patterns used by software engineers (like WK!)
There are some very good tips in this lecture so that you will be able to explain intelligent design to others in simple ways, using everyday household items and children’s toys to symbolize the amino acids, proteins, sugar phosphate backbones, etc.
Proteins are constructed from a sequence of amino acids:
Proteins sticking onto the double helix structure of DNA:
I highly, highly recommend this lecture. You will be delighted and you will learn something.
Here is an article that gives a general overview of how intelligent design challenges. If you want to read something more detailed about the material that he is covering in the lecture above related to the origin of life, there is a pretty good article here.
There is a good breakdown of some of the slides with helpful flow charts here on Uncommon Descent.