How likely is human extinction?

Every species seems to come and go. Some last longer than others, but nothing lasts forever. Humans are a relatively recent phenomenon, jumping out of trees and striding across the land around 200 000 years ago. Will we persist for many millions of years to come, or are we headed for an evolutionary makeover, or even extinction?

According to Reinhard Stindl, of the Institute of Medical Biology in Vienna, the answer to this question could lie at the tips of our chromosomes. In a controversial new theory he suggests that all eukaryotic species (everything except bacteria and algae) have an evolutionary "clock" that ticks through generations, counting down to an eventual extinction date. This clock might help to explain some of the more puzzling aspects of evolution, but it also overturns current thinking and even questions the orthodoxy of Darwin's natural selection.

For over 100 years, scientists have grappled with the cause of "background" extinction. Mass extinction events, like the wiping out of dinosaurs 65m years ago, are impressive and dramatic, but account for only around 4% of now extinct species. The majority slip away quietly and without any fanfare. Over 99% of all the species that ever lived on Earth have already passed on, so what happened to the species that weren't annihilated during mass extinction events?

Charles Darwin proposed that evolution is controlled by "survival of the fittest". Current natural selection models imply that evolution is a slow and steady process, with continuous genetic mutations leading to new species that find a niche to live in, or die. But digging through the layers of rock, palaeontologists have found that evolution seems to go in fits and starts. Most species seem to have long stable periods followed by a burst of change: not the slow, steady process predicted by natural selection. Originally scientists attributed this jagged pattern to the imperfections of the fossil record. But in recent years more detailed studies have backed up the idea that evolution proceeds in fits and starts.

The quiet periods in the fossil record where evolution seems to stagnate are a big problem for natural selection: evolution can't just switch on and off. Over 20 years ago the late Stephen Jay Gould suggested internal genetic mechanisms could regulate these quiet evolutionary periods but until now no-one could explain how it would work.

Stindl argues that the protective caps on the end of chromosomes, called telomeres, provide the answer. Like plastic tips on the end of shoelaces, all eukaryotic species have telomeres on the end of their chromosomes to prevent instability. However, cells seem to struggle to copy telomeres properly when they divide, and very gradually the telomeres become shorter.

Stindl's idea is that there is also a tiny loss of telomere length between each generations, mirroring the individual ageing process.

Once a telomere becomes critically short it causes diseases related to chromosomal instability, or limited tissue regeneration, such as cancer and immunodeficiency. "The shortening of telomeres between generations means that eventually the telomeres become critically short for a particular species, causing outbreaks of disease and finally a population crash," says Stindl. "It could explain the disappearance of a seemingly successful species, like Neanderthal man, with no need for external factors such as climate change."

After a population crash there are likely to be isolated groups remaining. Stindl postulates that inbreeding within these groups could "reset" the species clock, elongating telomeres and potentially starting a new species. Studies on mice provide strong evidence to support this. "Established strains of lab mice have exceptionally long telomeres compared to those in wild mice, their ancestors," says Stindl. "Those strains of lab mice were inbred intensively from a small population."

Current estimates suggest telomeres shorten only a tiny amount between each generation, taking thousands of generations to erode to a critical level. Many species can remain stable for tens to hundreds of thousands of years, creating long flat periods in evolution, when nothing much seems to happen.

Telomere erosion is a compelling theory, helping to explain some of the more mysterious patterns in evolution and extinction. There are few data - partly because telomeres are tiny and difficult to measure - but new DNA sequencing techniques could soon change that. Studies have already shown a huge variation in telomere length between different species.

Other scientists are going to take some convincing. David Jablonski, a palaeontologist from the University of Chicago, says: "The telomere hypothesis is interesting, but must be tested against factors like geographic extent, or population size and variability, that have already been proven effective in predicting extinction risk."

Stindl accepts that more experiments need to be done to test his ideas. "We need to compare average telomere lengths between endangered species and current successful species," he says. "I don't expect all endangered species to have short telomeres, since there are clearly other extinction mechanisms resulting from human threats to ecosystems, but I would expect some correlation between extinction risk and telomere length."

If Stindl is correct it will have interesting implications for mankind. Although inbreeding seems to have been the traditional way of lengthening telomeres, there could be a less drastic alternative. Stindl believes that it may be possible to elongate telomeres by increasing the activity of the enzyme telomerase in the embryo. So humans could perhaps boost biodiversity and save endangered species simply by elongating their telomeres. We may even be able to save ourselves when our own telomeres become critically short, making humans the first species to take hold of destiny and prevent their own extinction.

Indicators for human extinction Human telomeres are already relatively short. Are we likely to become extinct soon?

Cancer: Cancer incidence does seem to have increased, but it is hard to say whether this is due to longer lifespans, more pollution, or telomere erosion. The shortest telomere in humans occurs on the short arm of chromosome 17; most human cancers are affected by the loss of a tumour suppressor gene on this chromosome.

Immunodeficiency: Symptoms of an impaired immune system (like those seen in the Aids patients or the elderly) are related to telomere erosion through immune cells being unable to regenerate. Young people starting to suffer more from diseases caused by an impaired immune system might be a result of telomere shortening between generations.

Heart attacks and strokes: Vascular disease could be caused by cells lining blood vessels being unable to replace themselves - a potential symptom of telomere erosion.

Sperm counts: Reduction in male sperm count (the jury is still out on whether this is the case) may indicate severe telomere erosion, but other causes are possible.

It seems whenever people start to lose interest some "scientist" comes up with another wacky idea that can't be tested, can't be observed and can't be proven as a way of explaining the inadequacy of their original theories ~ sheltonmac
How convenient that you skipped over this test the author proposed:
"Stindl accepts that more experiments need to be done to test his ideas. "We need to compare average telomere lengths between endangered species and current successful species," he says. "I don't expect all endangered species to have short telomeres, since there are clearly other extinction mechanisms resulting from human threats to ecosystems, but I would expect some correlation between extinction risk and telomere length."

And that's not the only prediction he makes or test he proposes. Here's his paper which spawned the press release. It includes these proposed tests:

The publication of an unusual phenomenon observed on a small island off the coast of Great Britain might give us a hint of the species clock at work. In 1987, Parker and Wilby conducted chromosome analyses of 227 plants of the dioecious species (Rumex acetosa) collected on Skomer Island and detected extreme chromosomal heterogeneity. They found fourteen different chromosomal polymorphisms; the great majority of these were detected in 67 plants found in a small area (Parker and Wilby, ’89), that had experienced a population crash in 1977. This is in stark contrast to the three common chromosomal rearrangements seen on the mainland, although it has to be mentioned that Rumex acetosa is known for its cytological heterogeneity, typically involving the Y-chromosome. Fourteen years after the publication of their paper, it would be very interesting to do a chromosomal reanalysis and to measure telomere length in these plants. It might well be that one of these chromosomal variants has taken over and is now dominating on Skomer Island.
When it comes to chromosomal polymorphisms, one of the best studied animals is the house mouse, M. m. domesticus. The ancestral karyotype consists of 40 acrocentric chromosomes. Over the last several thousand years, it has undergone major chromosomal changes resulting in over 40 distinct chromosomal races (Nachman and Searle, ’95). The new races are mainly a result of robertsonian fusion of two acrocentrics forming a metacentric chromosome. Intriguingly, telomeres on the p-arms (getting lost during fusion) appear shorter than telomeres on the long arms of mouse chromosomes (Slijepcevic, 98). Numerous chromosomal analyses in a large number of individuals would be required to study the degree of chromosomal polymorphisms and the occurrence of chromosomal instability in many species. Unfortunately, cytogeneticists are a dying species (not related to telomeres, of course), since current science has entirely focused on DNA sequence and genes.
Indeed, the species clock model can explain the punctuated patterns of speciation seen in the fossil record of higher organisms, but it would be fatal to disregard the gradualistic model of speciation. Certain microfossil groups (unicellular eukaryotes like radiolaria, diatoms, and foraminifera) frequently show gradualistic patterns of speciation (Benton and Pearson, 2001), yet, future research may show that most of these organisms have circular chromosomes, without telomeres.

I'm sure I missed a few.

When I read this article at first I dismissed this hypothesis as wild speculation, because the article only vaguely alludes to evidence that inbred populations had their telomeres lengthened over time. But apparently there is some indirect evidence for that:

Nevertheless, in addition to the healing process, is there any evidence for extensive telomere elongation? The existence of extremely long telomeres (up to 1 Mega base pairs in some birds [Lejnine et al., ’95; Delany et al., 2000]) implies that there must be a mechanism which can produce them. Although it is a common feature of plant tissue culture (Osborne and Boubriak, 2002), extensive telomere elongation has not been observed in vivo yet (this is compatible with the rarity of telomere elongation). Indirect evidence for extensive telomere elongation in vivo comes from lab mice. In 1990, when hypervariable ultralong telomeres were discovered in established strains of lab mice, it was assumed that this is a general feature of Mus musculus (Kipling and Cooke, ’90). Ten years later, it was shown that inbred strains recently derived from wild mice have short telomeres (Hemann and Greider, 2000). To be specific, established inbred and outbred strains of lab mice have exceptionally long telomeres in the range of 30–150 kbp, in contrast to short telomeres of 8–10 kbp seen in wild mice (Hemann and Greider, 2000). Hence, despite their progenitors’ (Mus m. musculus and Mus m. domesticus) short telomeres, laboratory mice somehow multiplied telomere length (Hemann and Greider, 2000). Since mean telomere length differs greatly between closely related strains (subspecies), those differences must have originated after the split of two species. Hemann and Greider suggested that telomere elongation in established strains of lab mice might have resulted from extensive breeding of an isolated colony. In a more recent paper, Manning and colleagues go even further by claiming that inbreeding, through unknown mechanisms, results in the elongation of telomeres (Manning et al., 2002).

I don't know if this intriguing hypothesis will pan out, but he sure does provide some avenues for investigation. I predict we'll be hearing a lot more about this hypothesis in the future.

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