How to Overcome Extinction: Darwin and Genetics
How to Overcome Extinction: Darwin and Genetics

How to Overcome Extinction: Darwin and Genetics

“On the Origin of Species” by Charles Darwin in 1859 is considered to be the foundation of evolutionary biology. It postulates that complex life forms began from primitive life forms due to mutation. This theory is deeply entrenched in modern academia and is even proclaimed as fact on Wikipedia and elsewhere. However modern research in genetics, and a bit of common sense, make it clear that this theory is flawed. Instead of developing new species, small populations of inbred species move toward extinction due to mutation.

Consider Real World Genetics

While marrying a relative will not inevitably cause deformities, since we all are related to varying degrees, marrying close relatives does cause problems today. This is a biological fact of genetics. The DNA code copies genes from one generation to the next, and like a photocopy process introduces some mutations or mistakes with each copy of a copy. Usually these mistakes are not a problem because the other parent has the normal gene which functions like a backup copy to correct the defective gene. Diseases like cystic fibrosis, hemophilia, and sickle cell anemia occur when both parents have a defective gene. This is why there are laws today that prohibit marrying a close relative. Hemophilia is sometimes referred to as “the royal disease,” because it affected the royal families of England, Germany, Russia and Spain in the 19th and 20th centuries due to intermarriage in a small population of royals.

Charles Darwin’s family was affected by this too, having a history of marrying close relatives. The reproductive relationships in the Darwin family are enough to make your head spin. Charles Darwin married his first cousin, Emma Wedgewood. His sister also married one of her Wedgewood cousins and two other Wedgewood cousins married their Darwin first cousins. Among the 62 uncles, cousins and aunts 38 had no (zero) progeny surviving to adulthood. Charles and Emma had 10 children, 3 of whom died in infancy, 3 more were likely infertile, only 3 had children. Darwin’s children had a relatively high coefficient of inbreeding, so their risk of negative traits and child mortality was higher.

This greatly concerned Darwin, but he didn’t see the obvious contradiction this posed to his theory of origins. Mutations are not helpful but harmful, time only exacerbates the problem. Once Darwin even wrote to a friend, “We are a wretched family & ought to be exterminated.” Darwin’s five surviving sons became actively involved in the eugenics movement. His son George compiled statistics on the offspring of first-cousin marriages and also checked lunatic asylums for traits of inferior human beings. His youngest son Horace, the sickliest of the lot, started an engineering company to make anthropometric instruments used in measuring body parts to assess genetic quality. And both sons worked closely with Francis Galton, cousin of Charles Darwin and founder of the eugenics movement in the 1880s, which was hailed as “a new basis of moral obligation.”

These concerns were very valid, the impact of mutations on genetics has been detailed in the book “Genetic Entropy” by Geneticist Dr. John Sanford. He begins by examining how random mutation and natural selection actually operate, and shows that simple logic demands that genomes must degenerate. In collaboration with other scientists, he shows that real biological populations clearly manifest genetic degeneration. Their findings invalidate classic neo-Darwinian theory, showing that mutations are incapable of creating our genomes, but instead erode them. This occurs despite the benefits of natural selection, regardless of whether the time frame is 100 years or 100 million.

Genetic Erosion has been defined as the deteriorating genetic health of a small inbred population contributing to a higher probability of extinction. Whether you call it Genetic Entropy, Genetic Load, or Genetic Drift, conservationists agree that this is a danger to the extinction of a species. When endangered wildlife, such as the lowland gorilla, gets inbred, it loses genetic diversity. Evolutionary theory argues that mutations can be beneficial and produce genetic diversity, but all the evidence shows otherwise. Genetic diversity seems to be inherent and variations are simply revealed over time to adapt to the local context.

This same principle, that mutations lead to extinction, is visible at the level of an individual organism. Since our cells are constantly reproducing we are also introducing mutations into our bodies. Mutations have long been known to be at the root of cancer, but whether they were important for ageing has been debated for decades. Recent studies show that how long animals live is linked to how quickly their genetic code mutates. There is a strong correlation between ageing and mutations. This all should cause us to ask questions like:

  • What causes aging? Why does every living thing die?
  • Aren’t mutations what drive evolution? Why then is inbreeding bad?
  • Were not the first frogs, dogs, birds a small population size? How did they survive inbreeding?
  • Why do the few proposed transitionary fossils not hold up to close scrutiny? (Archaeopteryx)
  • How many species became extinct in the last 500 years? How many new ones evolved?
  • Why do species when crossed always produce infertile offspring (mules), but varieties of species are unimpaired?
  • Do you see the contradiction between real world genetics and evolutionary theory?

The number of intermediate varieties, which have formerly existed on the earth, (must) be truly enormous. Why then is not every geological formation and every stratum full of such intermediate links? Geology assuredly does not reveal any such finely graduated organic chain; and this, perhaps, is the most obvious and gravest objection which can be urged against my theory.

Darwin, C. (1859)
The Origin of Species (Reprint of the first edition)
Avenel Books, Crown Publishers, New York, 1979, p. 292

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