Feature Article - November 2015
by Do-While Jones

A “Nobel” Argument Against Evolution

This year’s Nobel Prize for chemistry spells trouble for evolution.

Tomas Lindahl, Paul Modrich, and Aziz Sancar won this year’s Chemistry Nobel Prize in recognition of their mechanistic studies of DNA repair. Their discoveries raise issues about some of the fundamental assumptions of the theory of evolution.

There are two fundamental assumptions at the base of the theory of evolution. One has to do with the origin of the genetic code. The other has to do with genetic mutation. The fallacies in both of these assumptions are evident in light of the research that won this year’s Nobel Prize in chemistry.

Origin of DNA

Since evolutionists always complain when we talk about the impossibility of the spontaneous origin of life, let’s give them the first living cell. We generously grant the assumption that Frankencell somehow came to life all by itself (without the aid of a mad scientist and deformed lab assistant), and allow that Frankencell had some DNA. Would the DNA in a primitive cell last long enough to keep the cell alive all by itself? This year’s Nobel Prize makes it doubtful.

Life has survived through the ages because enzymes inside every cell ensure that DNA remains in proper working order. This year's Nobel Prize in chemistry, announced 7 October [2015], recognizes three scientists who discovered key mechanisms for fixing the damage. “These are classic studies and a great prize for DNA repair,” says Jacqueline Barton, a chemist at California Institute of Technology in Pasadena.

The discoveries were made in the 1970s and 1980s by Paul Modrich of Duke University School of Medicine in Durham, North Carolina; Aziz Sancar of the University of North Carolina, Chapel Hill—the first Turkish scientist to receive a Nobel—and Tomas Lindahl of the Francis Crick Institute at Clare Hall Laboratory in Hertfordshire, U.K. 1

These discoveries were made 41 years ago, and are just being recognized now. What took so long?

Biologists have long known that DNA wasn't rock solid. Blasts of xrays [sic], for example, could cause mutations in cells. Yet most researchers believed that the molecule was inherently stable. After all, cancer and other genetic malfunctions are the exception, not the rule.

As a postdoc in the late 1960s, however, Lindahl began to have doubts. Samples of RNA in his experiments rapidly degraded when heated. Further experiments showed that even under normal conditions, DNA quickly suffered enough damage to make life impossible. 2

In other words, inside a cell, DNA is stable; but outside the cell, DNA and RNA degrade quickly. There has to be something inside the cell that protects the DNA from falling apart.

Lindahl began to search for enzymes that might repair this unseen damage. … Lindahl discovered a process, now called base excision repair, in which enzymes continually spot and replace such interloper bases. He and colleagues described the mechanism in 1974.

At about this time, Sancar, … uncovered another repair mechanism, nucleotide excision repair, which allows cells to fix a different kind of damage from the one Lindahl studied, using different enzymes.

Modrich tackled a third source of error: mistakes that happen during replication, when the two strands of DNA unzip and are copied. … Enzymes efficiently fix these errors—and Modrich helped figure out how it happens. In the late 1970s …

Many other mechanisms also fix faulty DNA, and many other researchers have made key contributions to their study. That fact has raised the inevitable question of who should have won the Nobel for DNA repair. 3

DNA is so fragile that it needs more than three different enzyme processes to keep it from falling apart. Therefore, when Frankencell miraculously came into existence, it not only had to have functional DNA, it also needed several kinds of enzymes working to hold the DNA together long enough to survive.

The indisputable, observational evidence is that a living cell needs several complex processes operating simultaneously to keep it alive. It is hard enough to believe that these processes could come about by chance sequentially over a long period of time. It is even harder to believe that all the necessary processes happened simultaneously by chance at exactly the right time. There is no simple step-by-step way in which primitive life could have evolved. Several enzymes had to be there, fully functional, in order to hold the DNA together long enough for the simplest life to continue to live.

This has been known for decades. Not only that, it has been known by so many scientists that it was hard to decide who should get the credit for discovering it.

Genetic Mutation

The theory of evolution depends upon genetic change filtered by natural selection to produce organisms more capable of survival. Darwin believed that diet, exercise, and climate caused adaptations that could be inherited. Scientists now know acquired characteristics are not inheritable. Working out at the gym might make my muscles bigger and my tummy tighter, but it won’t affect the physique of my children. That’s why Darwinian evolution was replaced by Neo-Darwinian evolution.

In Neo-Darwinian evolution, random mutations to the DNA are assumed to produce the variations which are filtered by natural selection to produce organisms more capable of survival. But what scientists have known for decades (which has now finally been acknowledged by the award of the Chemistry Nobel Prize) is that most mutations are fatal, and cells need several complex enzyme mechanisms which repair most mutations as soon as they occur.

The Neo-Darwinian Theory depends upon lots of random mutations for evolution to occur. Why would cells have evolved methods to prevent DNA changes? Why would cells evolve a defense against evolution? That doesn’t make much sense!

Quick links to
Science Against Evolution
Home Page
Back issues of
(our newsletter)
Web Site
of the Month
Topical Index


1 Stokstad, Science, 16 October 2015, “DNA's repair tricks win chemistry's top prize”, https://www.science.org/doi/10.1126/science.350.6258.266
2 ibid.
3 ibid.