Are Humans Still Evolving?

Evolution may be defined with or with out the requirements of selective pressure, but in terms of discussing the possibility of current human evolution it is only sensible to accept a definition that is selection inclusive. Accepting this, fact based arguments which suggest the absence of current human evolution may seems valid, but can be easily refuted on the basis of 4 common misperceptions of evolution that lie as hidden assumptions behind such claims. These four classes of error will be outlined below and the relevance to the types of arguments raised that claim humans are no longer evolving will be made apparent.

Originally, evolution meant ‘unfolding’ [1] and was most often used to refer to the process of development – the unfolding of a series of specific events leading to a final product. For instance, an acorn would evolve into an oak tree, a fetus into a baby. As the world view gradually changed during the enlightenment period of the 18th century – from that of a stationary world created by God into a world which gradually shaped by geological change over a considerable period of time – it was natural that this term should be applied to the ‘evolution’ of the world. The association to biology quickly followed as the idea that species may not be immutable gained favour and several possible theories emerged, including Lamarck’s and eventually Darwin’s. Since this time Evolution came to be particularly strongly associated with biology and the ‘unfolding’ of species over time. Although Ernst Haeckel’s famous claim that ‘Ontogeny recapitulates phylogeny’ may no longer be accepted, the word once used to describe ontogeny was quickly adapted so that phylogeny could be described in exactly the same way: Evolution. From our modern standpoint though evolution is much more explicit than just the unfolding of species – it has come into a much more meaningful and exact description, commonly defined as ‘the change in the gene pool of a population over time.’ [2]

Using this definition, the possibility of questioning whether humans are still evolving is not even worth asking. The simple fact is that change in the gene pool over time in any species is completely unavoidable. Eyre-Walker and Keightley claimed in 1999 that humans have had on average 4.2 amino acid altering mutations every generation since humans separated from chimpanzees [3]. This measurement ignores the synonymous substitution of base pairs, and all of the mutations which occur in the non-translated regions of Genome DNA. Since only about 1.5% of the human genome is translated [4], this number is quite incredible. With this introduction of change every generation, the ‘change in the gene pool over time’ is assured. Genetic drift is another mechanism through which gene frequencies are changed overtime, and its occurrence is an undeniable phenomenon. Chance events lead to the increase or decrease of numbers of a particular gene in a population, occasionally leading to fixation of a gene (no other variants exist) or extinction of that gene.

These two prime examples of random changes in the genetic makeup of populations are accepted biological phenomena which apply to humans as much as any other species. To say that these two phenomena are classified as evolution means to say that Humans evolve. Of this there can simply be no question.

It is therefore clear that another more specific definition of evolution must be used in order for any sort of productive inquiry into this subject to take place. To account for the affect of random changes alone being considered evolutionary a definition that requires a selective pressure can be used. By defining evolution as ‘the change in a gene pool over time due to a selective pressure’ we no longer have the random changes problem, and the people claiming that humans are no longer evolving actually have something that they can use: The possible lack of selective pressures. From now on this will be the meaning of evolution for the rest of this paper.

Evolution may be directed by a number of selective pressures, one being sexual selection, and most of the others falling under the general title of natural selection. Natural selection affects the evolution of species in every aspect of their life, from their developmental rate, to their ability to survive to reproductive maturity, their ability to find and copulate with a mate, the viability of those offspring, and how much longer after sexual maturity/copulation that organism may continue living. Natural Selection is the true driving force behind any sort of adaptive evolution.

With selection included we can now describe evolution according to a theory described by Dennett in 1995 based on the earlier work of Lewontin and Brandon [5]. In this definition evolution is said to occur whenever there is variation, heredity and a differential ‘fitness’ (i.e.: allowing a point of action for a selection pressure). In the case of all biological creatures heredity is an absolute standard which goes without saying. The fact that there is replication of the genetic makeup from one organism into the next generation is the backbone of the process of evolution. It is upon this backbone of heredity that variation may build up, brought about by mutations, and that differential fitnesses may arise and in turn be selected. So the question now becomes, “Do humans have variety in their gene pool, and is there a differential fitness to these variants?”

Those who believe that humans are no longer evolving accept that we have variety. As pointed out above with the previous definition of evolution, we have 4.2 Amino Acid altering mutations every generation, and then we have genetic drift; it is entirely unreasonable to claim that we do not have variety between humans. What they do doubt though, is that there is any selective pressure left. They claim that due to the advent of modern medicine, technology, farming techniques, food distribution, heating and cooling systems etc, there are no longer any selective pressures in our lives to separate the fit from the unfit. The fitness differential is irrelevant in the environment that we have made for ourselves because we do everything we can to make sure ‘everyone’ survives. Additionally, even if some people die to unforseen virus or bacterial outbreaks etc, then although they may die, the reaction of medical intervention will be infinitely quicker than that of the evolutionary adaptation to the new selective pressure, and so no net evolution will actually occur. The capabilities within our modern society and the speed with which our culture adapts to change has completely overruled the process of natural selection and so stopped evolution.

There are several problems with these claims. These problems can be placed into several classes of error including;

1. Misunderstanding the nature and power of Natural Selection,
2. Forgetting other forms of selection, such as sexual selection,
3. Assumptions about the entire world from the specific first world lifestyles of the very people claiming this, and
4. Mistakenly taking the term ‘current evolution’ to mean that evolution must happen before our eyes.

Class 1

The first class of error may actually be the most subtle. It comes from the assumption that selection only works on the more obvious phenotypic traits and little else. In its worst form this error is manifest in the claims that humans are de-evolving (an oxymoron in itself) because we are creating easier lives for ourselves, resulting in future generations who have evolved weak skeletons, fat bodies and slow reactions etc. While an easier life may allow for these phenotypic changes to exist, to say that we would evolve in that direction is to either revert to the previous definition of evolution, or misunderstand how evolution due to natural selection works. Evolution due to natural selection occurs only in such a way that better adapted creatures become more prevalent than less adapted creatures. If bodies with weaker skeletons (for example birds), more fat (for example seals), and slower reactions (for example sloths) were advantageous to humans, then that is how we would evolve. If that happened to be the case, then the irony would then be that these phenotypes would be advantageous (direct inference from how evolution works), and the claims of ‘de-evolutionists’ would be shown for exactly what they are, oxymoronic.

The more subtle side of this can be made clear though, in realising that this altering of what is and what is not advantageous from era to era is entirely unpredictable to us. We perceive certain things as ‘good’ attributes (commonly: Sharp teeth, strong muscles, fast runner, intelligence) and other things as ‘bad’ attributes (commonly: obesity, skin prone to sunburn, unco-ordination) and we decide that anything which departs from the good and/or acquires more bad attributes is losing its selective advantage. While this may often be true, the fact of the matter is that our own judgement has been crafted by evolution and we are biased in our judgements towards the things which were adaptive in the past. We have no idea what is going to happen next and so we can’t be sure that our crafted judgements are any longer valid. As well as that we have no way of knowing what hidden benefits may lay under some superficial phenotype. Combine these two consideration and you are faced with a situation in which you may have superficially ‘bad’ (according to our current judgement) phenotypes with underlying attributes which may in the next few hundred generations come to be so advantageous that they create a selective pressure in themselves. Darwin himself observed that “the struggle will generally be more severe between species of the same genus, when they come into competition with each other, than between species of distinct genera,” [6] and so it is with humans already, and probably will continue to become more and more as we reach the limits of our extended niche. What variation it is that holds the key to the adaptive advantage is surely unknown to us, but it seems incredibly unlikely that the advantage will be with those able to outrun or successfully hunt a lion.

On a less subtle level though there is one more element within this class of error that is ignored by people who claim that humans are no longer evolving. Natural Selection is thorough. Amongst all of the variation which we can and cannot discriminate superficially, Natural Selection screens everything. Natural Selection, unlike our ability to pass judgement, is an unrelenting eternal force sifting through every single probabilistic relation within an organism, between members of a community, between organisms in a species, and between an organism and its environment; all at once. To say that modern humans are no longer under a selective pressure is to claim two things: It is claiming that we know what Natural Selection works on; and it claims that we have used this knowledge to control every single instance of potential selective pressure. We certainly do not know this, and we most certainly have not controlled it. Humans are just as subject to selective pressures as every other organism, even if we can’t see them.

Class 2

The second category of error is simply a case of forgetting that there is more to selective pressures than mere survival. The need to procreate is just as important in evolution, and to procreate humans need to find mates. Sexual selection is present throughout nature and is undoubtedly present in Homo sapiens too. One theory even claims that our enlarged brains, our paedomorphic ape appearance, the size difference between males and females, and various other factors are all consequences of sexual selection [7]. Medicines, technology and abundant shelter will never affect the role sexual selection plays in the evolution process, but culture itself may. It is almost impossible to guarantee that our sexual desires, choices and behaviours are guided by our own and our potential mate’s genetic make up, rather than being guided by the culture we live in. To make it a little more complicated, its not even easy to figure out whether our culture is largely guided by our genetic make up, and therefore only an intermediate between our genes telling us what we want and what we actually choose. Whatever the case one fact remains: Sexual selection – on whatever level – occurs. As long as it continues to occur there will be a selective pressure present, and evolution will occur.

Class 3

The third category of error is the belief that the entire world is like the society we are lucky enough to live in. A society where medicine is provided for everyone, where housing is plentiful, where there is available electricity, running water etc. The fact of the matter is that this isn’t the case at all, but instead around 80% of the world’s population lives in developing countries [6]. If we are to talk about the evolution of Humans and we want to focus on one lifestyle, it would in fact make much more sense to focus on developing countries and talk about their way of life. Of course though, if we were to do this, then most of the points raised about medicines, technology, distribution of food, and general ease/comfort of life would no longer apply, and there would be no case. Obviously when the claim ‘Humans are no longer evolving’ is made, the claim is actually meant to be ‘Humans in developed countries are no longer evolving.’

Class 4

The fourth class of error actually intermingles with every other class on some level. Evolution takes many thousands of years to occur and must be discussed accordingly. To talk only about the way things are now and then to try to infer facts about evolution from that flash of existence, is to fall into this error.

This particular error is all encompassing in its nature and is the sort of error that humans are very prone to make. Being organisms that deal with time in units like seconds, minutes, hours, years, and even up to decades, the concept of hundreds of years or several hundred years turns into ‘A long time’ and nothing else. To think of a hundred years, is to think of something only just graspable. To think of a thousand years though, is really something beyond our grasp and we tend to resort to ‘a really long time’ and that is as far as our imagination goes. We may be able to grasp some sort of awe over the length of it, but we do not comprehend it. Tens of thousands of years, millions of years, billions of years all meld into this one conception of ‘a really long time’ and nothing else. There is little meaning in any of it. To then speak of evolution, something which takes thousands of years for any real changes to start being apparent, is to talk of something which we can’t grasp the timeframe of. Falling into this class of error when talking about Evolution is almost inevitable for anyone not consciously aware of this problem.

Understanding now that evolution only works over the course of many thousands of years means that the claim that ‘humans are no longer evolving’ translates into ‘humans will not evolve at all over the next few thousand years’. Realising this, to maintain the claim that humans are no longer evolving is to claim that our control over our environment is so all encompassing and so certain that nothing that happens will break our control. It is a claim that we will never run out of food, that our population growth will never reach maximum capacity, that rising waters will never cause massive loss of farmland or living space, and that no virus or bacterial pathogens will ever break out into a pandemic. It is to claim that humankind has already completely conquered nature in all of its forms.

Whether we accept evolution as something that occurs with or without a selective pressure, the arguments presented to show that humans are no longer evolving tend to become meaningless in light of how evolution actually works. The points may seem valid in some regard, but they all miss a vital point somewhere and so can be easily shown as the empty claim they are. Humans are varied, humans are being selected, and a time will come not so far off in the future when massive selection may be applied as a consequence of our own actions. Humans are still evolving.

References

1. Webster’s 1828 dictionary, http://www.christiantech.com/
2. Chris Colby. Introduction to Evolutionary Biology, Version 2. 1996. http://talkorigins.org/faqs/faq-intro-to-biology.html
3. A. Eyre-Walker, P.D. Keightley. 1999. High genomic deleterious mutation rates in hominids. Nature 397:344-347
4. B Alberts, A Johnson, J Lewis, M Raff, K Roberts, P Walter. 2002. Molecular Biology of the Cell 4th Edition, Chapter 4, p 202, table 4-1.
5. D Dennett. 1995. Darwin’s Dangerous Idea: evolution and the meaning of life. New York. p 343
6. C Darwin. 1859. The Origin of Species, first edition, reprinted in penguin classics 1985, chapter 3:p127.
7. D Brin. 1996. Neoteny and Two-Way Sexual Selection in Human Evolution. Journal of Social and Evolutionary Systems 18(3):257-276
8. http://www.unfpa.org/sustainable/demographics.htm

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Evolution as a Scientific Theory

Evolutionary theory is the current Paradigm of biologists. Evolution provides the framework for our biological belief structure and allows scientists working in Molecular Biology, Microbiology, Botany, Zoology, Ecology, Marine Biology and Archaeology to put all of their observations and experiments into a theoretical framework. It is from the theory of evolution that scientists feel free to assume that a gene found in Saccharomyces cerevisiae may have a related gene in mice and humans and have a similar role to play in all three organisms. It is from the theory of evolution that scientists tend to classify relatedness between species, and work within the assumption of those relationships. It is from the theory of evolution that archaeologists are able to make assumptions about extinct animals and their bone structure and skeletal organisations based on extant species. It is from the theory of evolution that medical researchers are able to understand the recurrence of bacterial infection and viral infection year after year of the same organism that has been inoculated against time and time again.

The theory of evolution undoubtedly plays an active role in our approach to biological science and affects every medical and scientific advancement made under its paradigm.

And more importantly than acting like a scientific paradigm as described by Kuhn, Evolution acts like an Ideal science as described by Karl Popper. It has a number of tenants that if shown to be wrong, would clearly disprove much of the theory if not the whole thing.

A number of these points of falsification are listed:
1. There was a static fossil record
2. True chimeras, that is, organisms that combined parts from several different and diverse lineages (such as mermaids and centaurs) and which are not explained by lateral gene transfer, which transfers relatively small amounts of DNA between lineages, or symbiosis, where two whole organisms come together
3. a mechanism that would prevent mutations from occurring or accumulating
4. observations of organisms being created
5. Fossils found out of sequence
6. Demonstrating similar species have less genetic similarity than dissimilar species; i.e. showing Chicken DNA is closer to human DNA than Chimpanzee DNA
7. Demonstrating that the Earth is not Billions of years old

Some of these points would falsify that evolution could possibly occur (3 for instance) while others would simply falsify that evolution is the cause of the variety of life we now witness on Earth (7 for instance). But if any one of those points of falsification were clearly demonstrated to be true, the theory of evolution would require drastic rethinking or complete dismissal. A brand new theory would need to be formulated which explains all of the existing information as well as the new information which expelled Evolutionary theory from common scientific acceptance.

There is no doubt about the scientific nature of evolutionary theory, and there are plenty of principles of falsification, upon which evolution has stubbornly refused to be falsified by,

Shane

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The Scientific Method – First draft of section one

The goal of this first section is to dispell a bit of myth about Science and ‘The Scientific Method’. Science has manged to attain a mythical status for itself: The purveyor of truth, the only avenue to real practical knowledge, “Scientists show that…”, and for a day to day purpose perhaps it is appropriate. But from a purely philosophical point of view it is far from an accurate representation.

A naieve point of view of science has it that the Scientific method is all about observing, hypothesising, testing and proving. It is unlikley that any science is ever really done that way. A more sophisticated view was presented by Karl Popper: Hypothesis, try to falsify. Karl popper revolutionised the way the world viewed science; suddenly there was a criteria for whether something was Scientific or not. If it was falsifiable, it was scientific. All scientists were supposed to have a theory on how things worked, and they were then supposed to spend all of their time trying to prove the theory wrong so that an improved theory could be stated. This is of course too idealistic for reality. Scientists rarely set their goal as “Prove general relativity wrong” “Prove the atomic model wrong” “Prove evolution wrong”. While the concept surrounding Poppers philosophy of science is logically sound, specifically, no theory can ever be proven correct but a theory can certainly be proven wrong, most scientists actually do neither in their work. Most scientists work to discover new concepts within a theory.

This is where Thomas Kuhn’s theory of Scientific Revolutions comes in as a descriptive philosophy of science. Popper seemed to hit on something of a prescriptive ideal for science: Science should forever strive to prove itself wrong so that it may reliably move on whenever it is wrong. It must not cling to theories for the sake of tradition or sentimental sake. Kuhn’s theory of science however much more accurately described what scientists do: They use the prevailing theory of the day (the Paradigm) to guide their actions in their research. The Paradigm (for instance Newtonian Physics, General relativity, quantum mechanics or evolution) creates a system of beliefs for the scientists and provides them with a ‘Tool Kit’ for how to go about studying their field. They use these beleifs so that their observations make sense, then their observations are made to fit with the paradigm, and the combination of their paradigm tool kit logic and paradigm inspired observations are intwined to make predictions and generate new research avenues.

Scientific revolution occurs when anomolies arise from the research which no amount of effort will force into the paradigm belief system. A few anomalies are allowed to exist for a while, rationalised as bad data, bad technique, specific case or simply ignored until a later time, but when numerous anomalies come to the surface it is inevitable that one or more scientists will be forced to acknowledge these anomolies. Contrary to Poppers theory of falsification the paradigm is not discarded at the first sign of trouble. With mounting anomalous results some (certainly not all) scientists will start to question the paradigm, but ultimately will be ignored because a paradigm is required for science to continue. Without a paradigm, how will the data be interpretted? It isn’t until someone manages to put the peices of the puzzle together to formulate a new hypothesis which actually manages to cover all of the previous data as well as the new anomolous data in one fancy new theory that some people will start to consider discarding the old paradigm. Even then many scientists will cling to all they know and not accept the new paradigm.

With this quick introduction to the Philosophy of Science it is clear to see that Evolutionary Theory is the paradigm under which Biology currently operates. It is used as a toolbox to make predictions about molecular biology, morphology of organisms, paleantology, even medicine. Evolution came to be the accepted scientific paradigm more than 50 years after Origin of The Species was written after the particulate inheritence of genetic material was rediscovered. Until that was rediscovered it was assumed that all offspring blended the characteristics of their parents and so would reduce diversity rather than increase it as predicted by Darwins theory. Evolution replaced the previous paradigm: Creationism. until the Evolution was set up as the Paradigm, no theory adequately described life on earth sufficiently well at all (Lamarkianism was a contender, but never fully accepted) and in general people assumed “God made it” in whatever form they wanted to believe God did it.

As a scientific theory, creationism is a non-paradigm, it makes no active tool kit and no method of interpretting the data. Everything you see can be explained with “And thats how God wants it”. Everything is equally perfect in its own way, and everything has its perfect purpose. The theory is functionally useless from a scientific point of view, and this can be argued on both counts of Kuhnian philosophy as well as Poopperian philosophy. “God made it” is impossible to falsify. Evolutionary theory, from a scientific point of view was far superior to its predessesor.

Clearly no year can ever be placed on the implementation of a paradigm, but a time frame may be indicated from when it started to be taught in educational institutions. Evolution really started to be accepted inthe early 1900’s. Since then, the increase in biological knowledge has been staggering. From accepting that genetic inheritence was particulate (that is there is a peice of genetic material which is inherited in its entirety that determines a trait: a gene for blue eyes, a gene for black hair etc) to discovering the double helix structure of DNA and showing that it was the genetic material, to then mapping the entire genomes of over 180 organisms in the last 10 years!!! For a paradigm to encounter that amount of NEW, BRAND NEW information integration and stay as the only contended paradigm is a true indication of the strength of the theory of evolution.

Also interesting to find out: How many paradigms ahve come into phsyics since evolution was proposed? General relativity, special relativity, quantum mechanics… and physics has not advanced nearly as fast or as far as Biology.

Interesting links:
Synopsis of Kuhns Scientific Revolutions
Wikipedia entry on Kuhn
Wikipedia entry on Popper

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Proving Evolution Format: First Draft

This entry should virtually be point form, but i haven’t bothered with the actual points. This is really just an attempt to colelct my thoughts, form a logical sequence to the argument and form points where I need to do more research. I would appreciate any feedback or additional thoughts which you think I should add.

The Scientific Method and Paradigms
Under both of the prevailing philosophies of science, Evolutionary theory resides as a strong Science. Under Popperian philosophy, Evolution has many falsification principles and has been tested on many of those principles and never yet ultimately falsified. By Kuhn’s theory of Scientific revolutions, Evolution is the current biological Paradigm and it will remain so until formally trained biological scientists continually find fault and error with the predictions made by the theory and it becomes obvious that another theory is required. The new theory must explain all of the previous data better than evolutionary theory plus the new anomalies which evolutionary theory doesn’t explain before a revolution will occur.

Examples of previous scientific revolutions include Copernicus et al gradually convincing Europe that the Earth was not the center of our solar system. This took several generations. The second famous example of a scientific revolution is the gradual acceptance of Evolutionary Theory in replace of the previous theory: Creationism.

Falsification Of Evolution

What principles in the theory of evolution are falsifiable? There are many falsifiable principles in evolutionary theory that would either falsify evolutionary theory outright, or cause a major reshaping of the theory. Usually multiple falsifcation principles will be touched upon before a ‘revolution’ will occur according to Kuhn.

1. a static fossil record;
2. true chimeras, that is, organisms that combined parts from several different and diverse lineages (such as mermaids and centaurs) and which are not explained by lateral gene transfer, which transfers relatively small amounts of DNA between lineages, or symbiosis, where two whole organisms come together;
3. a mechanism that would prevent mutations from occurring or accumulating;
4. observations of organisms being created.
5. Fossils found out of sequence
6. Demonstrating similar species have less genetic similarity than dis-similar species; i.e. showing Chicken DNA is closer to human DNA than Chimpanzee DNA
7. Demonstrating that the Earth is not Billions of years old

Every new fossil that is dug up, could potentially falsify evolutionary theory. Every new genome sequenced could falsify evolutionary theory. Every new organism found could falsify evolutionary theory.

Evolutionary theory has survived over 150 years of this constant bombardment of falsification pressure without any major strikes of falsification. It has been revised a few times in light of Mendels laws of particulate inheritence, then updating to include Genetic theory and many other advances in scientific knowledge, but the core theory remains unchallenged by observations.

The Principles of Evolutionary Theory
The core tennant of evolutionary theory has a beautifully simplistic expression. Wheresoever there is something which:
1. Replicates itself (produces offspring with hereditary information)
2. Encounters small variations in that replication (mutations)
3. There is a differential fitness (Some will replicate more than others, some will not)
there will be evolution.

*This concept has been verified many times since the creation of computers which run evolutionary models.
*Evolutionary algorithms have been used to design things
*Programs have been designed to show proof of principle

There can’t be any denying this concept, so the question of the truth of Evolutionary theory as it applies to our Natural world is whether the organisms we see around us are actually the consequence of this process or not.

Darwin argued that our short history of animal husbandry was evidence enough of the existence of the three principles above (Although he didn’t ever expresss evolution in those terms). Clearly anyone can see that animals pass down hereditary information with variation, and if we actively select them than we could affect their form. We had done this as a civilisation for a few thousand years and acheived amazing diversity within the species with which we have practiced it. Based on that information, if life has existed for billions of years, that could be enough time for the huge variety in life we witness today to have arisen.

From such a simple central premise 150 years ago, so much more has been discovered which has come to support evolutionary theory. Not only the peripheral information:
Discovering the Sun burns by Fission, hence billions of years old.
Discovery of Radiometric dating techniques.
(others?)

but also core biological information which Darwin had no knowledge about. All of which creates a much stronger case for evolution than that originall posed by Darwin.

For a start, we discovered that Hereditary information is carried in genetic code, a system very amiable to the Descent with modification theory. The modifications could now be substantively measured. This was a HUGE leap for evolution. If evolution was wrong, then being able to quantify and exactly measure the variation in descent should surely indicate the error. But instead it has done nothing but verify it.
Sequenced genomes and found relatedness in them.
Discovered many new species in our explorations of the globe.

This will probably be expanded more, but I need to figure out the bounds between this section and the next section…


Accumulating Evidence For Evolutionary Theory
Before publishing Origin of the Species, Darwin spent 20 years collecting data to support his theory. He understood the ramifications of his theory and wanted to present the strongest case he could.

He presented much evidence for his theory including:
*collect data*

Since his time we have added much to the list..
Relatedness phenotypically AND genetically.
http://www.talkorigins.org/faqs/comdesc/
Junk DNA consistency
…more to come.

I’ll revise this again soon and start working on the first section. I’ll hopefully be able to fill that out pretty easily. It is the later chapters which will be data intensive and require some solid foundational research.

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Challenge to Intelligent Design Believers

I have spent a lot of time looking around YouTube.com at the Intelligent Design films, and even looking around a lot of ID and Creationism websites and reading the junk that they make. And it has given me cause to set up this challenge. It is rather simple and I sincerely hope to get at least a couple of people succesful in it.

Show me an argument or a claim or a critical questions proposed by an advocate of Intelligent Design against evolutionary theory or in support of Intelligent Design which is not based on:
1. An appeal to ignorance or incredulity
2. An appeal to Emotion (Also explained here)
3. Begging the Question
4. Any other form of logically fallaciouos argument
which has not previously been raised by a supporter of Evolutionary theory.

Then I will pay you US$50 for bringing this argument to my attention. This is a genuine offer. And one I promise to pay out. Simply post the argument/claim etc as a comment (or a link to the argument) and I will then edit this post to show that argument and explain either that I will not pay it because the argument falls victim to one of these fallacies, or I will post it and pay the $50 and explain why it is a good argument and then do my best to provide an adequate argument against it.

Of course, I reserve the right to change any aspect of this challenge as we proceed, but if you get in before I change anything, then I will stay true to my word as it stands when you post the comment.

————————————————————–
First Argument:
*waiting*

————————————-
After one attempted challenge which actually was an attempt on the non-existence of God, rather than an attempt on evolution, I feel compelled to cease this challenge because it seems I have a winner: www.talkorigins.org, the most thorough evolutionist website online has won the challenge by listing every single argument ever presented against evolution or for ID.

WOW.

If talkorigins actually submitted this list to my challenge, I would owe them like a million dollars! Check this out: http://www.talkorigins.org/indexcc/list.html

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Proving Evolution – Rationale

The reason I want to write a paper called “Proving Evolutionary Theory” is for a number of reasons. It is to firstly explain how scientific theories are never really “Proven” they simply reach a stage of acceptance and use for a period of time until they are replaced by a better theory. I will go into a bit of scientific theory on this topic in an attempt to show people how scientific revolutions occur and how Paradigms are used as a tool kit according to Thomas Kuhn’s theories.

With a decent understanding of how scientific paradigms work it should be easy to show how “Intelligent Design” is not a contending theory, nor is it ever going to be the end of Evolutionary Theory. Ironically, Intelligent Design is the very theory that Evolution replaced. It is the theory which was unhinged and replaced by the far superior theory of evolution. The only reason any debate continues to this date is because unlike the earth being the centre of the universe, this is much harder to prove conclusively with a simple observation. If people were still stuck to the ground without Telescopes, I guarantee the Religious majorities of the earth would still be claiming that Earth was the centre of the universe just as vehemently as they claim that Evolution isn’t possible.

As such, the second goal of my paper will then be to proceed to show conclusively that Evolutionary Theory can’t be denied through inductive logic. That is, case after case after case of evidence which supports the theory where it would otherwise be expected not to.

How I intend on doing this will rely on the fact that Darwin wrote Origin of the Species 150 years ago. Only in the last 50 years have we come to know that the genetic material was DNA, and only in the last few years have we come to know what our genetic code actually is. So with this new data at hand, surely this 150 year old theory would be clearly disproved by now. Surely our understanding of genetic inheritance based on genome analysis would CLEARLY show that evolution was wrong! Right? Well, I plan on analysing some genomes comparatively to show relatedness between species and find some clear evidence which will either show clearly that evolution is wrong, or that it may still yet be right.

Based on the opening sections of the paper, it will be clear that no amount of supporting evidence will ever prove evolutionary theory, and thus I will never claim that any piece of evidence does prove it. Unlike the exponents of ID who regularly refuse to maintain intellectual dignity, I will not take cheap shots and cheap victories at the expense of intellectual honesty. I will not refer to a good argument or superb peace of evidence as absolute proof of evolution, no matter how much it may seem to be so, because I know that the truth of the matter is that Science never actually can know the truth. And in that is Sciences strength. Only believers in God believe they know “absolute truth” and that is why they are so regularly wrong.

Anyway, the culmination of the paper should be to show how Science works, to show why Evolutionary theory is assisting science greatly and justify its use as a tool. In the end my main hope is to simply explain adequately well that evolutionary theory is true enough to be accepted and followed as a theory so that people I know will actually accept it. The debate in the USA is a non-event made public by the media abusing religious. The scientists refuse to ‘debate’ the matter because they know that there is no debate. In the end, I only right this for the individuals who have been swayed by the circular logic of these religious media manipulators. The people who never actually make a rational argument, but instead appeal to ignorance. Appeal to emotions. Appeal to incredulity. They constantly create straw man arguments against evolutionary theory and the media, and uninformed individuals who know no better feel compelled to accept them. It IS absurd that a monkey should ever give birth to a human. That’s right… but that is not evolutionary theory… And it distresses me greatly that supposedly “educated” full grown men will willingly say that on television in an attempt to “WIN” people over to their side. It fills me with anger to be completely honest. These people who say this thing spend their lives “debating” this topic, and they either do so without having any idea what they are talking about, OR they blatantly LIE. Either of those options is a betrayal of the “faith” of their followers.

I think I will also make a few posts addressing some of these people over time in this blog. Maybe one day I will even inspire one of them to come here and defend their actions.

Shane

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Proving Evolution – Rationale

The reason I want to write a paper called “Proving Evolutionary Theory” is for a number of reasons. It is to firstly explain how scientific theories are never really “Proven” they simply reach a stage of acceptance and use for a period of time until they are replaced by a better theory. I will go into a bit of scientific theory on this topic in an attempt to show people how scientific revolutions occur and how Paradigms are used as a tool kit according to Thomas Kuhn’s theories.

With a decent understanding of how scientific paradigms work it should be easy to show how “Intelligent Design” is not a contending theory, nor is it ever going to be the end of Evolutionary Theory. Ironically, Intelligent Design is the very theory that Evolution replaced. It is the theory which was unhinged and replaced by the far superior theory of evolution. The only reason any debate continues to this date is because unlike the earth being the centre of the universe, this is much harder to prove conclusively with a simple observation. If people were still stuck to the ground without Telescopes, I guarantee the Religious majorities of the earth would still be claiming that Earth was the centre of the universe just as vehemently as they claim that Evolution isn’t possible.

As such, the second goal of my paper will then be to proceed to show conclusively that Evolutionary Theory can’t be denied through inductive logic. That is, case after case after case of evidence which supports the theory where it would otherwise be expected not to.

How I intend on doing this will rely on the fact that Darwin wrote Origin of the Species 150 years ago. Only in the last 50 years have we come to know that the genetic material was DNA, and only in the last few years have we come to know what our genetic code actually is. So with this new data at hand, surely this 150 year old theory would be clearly disproved by now. Surely our understanding of genetic inheritance based on genome analysis would CLEARLY show that evolution was wrong! Right? Well, I plan on analysing some genomes comparatively to show relatedness between species and find some clear evidence which will either show clearly that evolution is wrong, or that it may still yet be right.

Based on the opening sections of the paper, it will be clear that no amount of supporting evidence will ever prove evolutionary theory, and thus I will never claim that any piece of evidence does prove it. Unlike the exponents of ID who regularly refuse to maintain intellectual dignity, I will not take cheap shots and cheap victories at the expense of intellectual honesty. I will not refer to a good argument or superb peace of evidence as absolute proof of evolution, no matter how much it may seem to be so, because I know that the truth of the matter is that Science never actually can know the truth. And in that is Sciences strength. Only believers in God believe they know “absolute truth” and that is why they are so regularly wrong.

Anyway, the culmination of the paper should be to show how Science works, to show why Evolutionary theory is assisting science greatly and justify its use as a tool. In the end my main hope is to simply explain adequately well that evolutionary theory is true enough to be accepted and followed as a theory so that people I know will actually accept it. The debate in the USA is a non-event made public by the media abusing religious. The scientists refuse to ‘debate’ the matter because they know that there is no debate. In the end, I only right this for the individuals who have been swayed by the circular logic of these religious media manipulators. The people who never actually make a rational argument, but instead appeal to ignorance. Appeal to emotions. Appeal to incredulity. They constantly create straw man arguments against evolutionary theory and the media, and uninformed individuals who know no better feel compelled to accept them. It IS absurd that a monkey should ever give birth to a human. That’s right… but that is not evolutionary theory… And it distresses me greatly that supposedly “educated” full grown men will willingly say that on television in an attempt to “WIN” people over to their side. It fills me with anger to be completely honest. These people who say this thing spend their lives “debating” this topic, and they either do so without having any idea what they are talking about, OR they blatantly LIE. Either of those options is a betrayal of the “faith” of their followers.

I think I will also make a few posts addressing some of these people over time in this blog. Maybe one day I will even inspire one of them to come here and defend their actions.

Shane

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Why Do We Age?

The Evolutionary Context of Senescence

People have rationalised aging and the inevitability of death throughout the past as ‘only natural’, ‘For the good of the species’ or as ‘Making way for the next generation’. Taking a closer look at the evidence though quickly makes it plainly clear that these explanations are simply wrong. In a typical natural environment organisms die through predation, accident, starvation, infection and other such events long before aging becomes a factor [20]. Aging, as a general rule, has virtually no influence in the natural world, and it this fact precisely that explains how it is that aging arose in the first place.

In 1957 Williams wrote a paper called “Pleiotropy, Natural Selection, and the Evolution of Senescence” which built on the idea introduced in 1952 by Medawar [14] that evolution would not be able to exert any real selective pressure on genes which act after the reproductive age. Williams proposed a more practical idea, that genes which produce an advantage early in life but have a later acting negative effect would still be selected regardless of the later effect. He claimed that “natural selection may be said to be biased in favour of youth over old age whenever a conflict of interest arises [20].” This theory, known as ‘Antagonistic Pleiotropy’ has since been expanded once more by Kirkwood in 1977 with the addition of the ‘Disposable Soma Theory’ [10]. This latest addition picks up on the bias natural selection has for youth and suggests that organisms evolve in a way which puts as many resources into ensuring youthful vigour and reproductive success as is required, and only after these two facets are assured do any resources get distributed into maintaining the somatic cells. In other words, evolution cannot select long living individuals if they are going to die before reproduction anyway. Evolution recognises that the body is disposable and so allocates resources appropriately.

These theories are important because they form a basis from which investigations into the mechanisms of aging can be approached from. These theories imply that it is unlikely for there to be any genes ‘for’ aging as such, but instead there will actually be genes ‘against’ aging. They imply that the causes of aging will actually be side effects of otherwise beneficial genes. They also imply that the genes associated with longevity will actually be genes which affect the durability and maintenance of the somatic cells [11].

The Free Radical Theory of Aging

The Free Radical Theory of aging has become one of the main focuses of aging research today. The theory proposes that reactive oxygen species (ROS – The ‘Free Radicals’), largely produced as a side effect of normal mitochondrial metabolism, cause progressive damage resulting in the functional decline that defines aging [4]. A lot of evidence for the theory is apparent in the fact that most lab organisms which have had an increased life span, have also been shown to have an increased oxidative stress response [2][13][19].

The overwhelming correlation between increased stress response and increased lifespan has an incredibly strong implication that ROS may cause some aspect of aging. The stress response which combats the ROS, extending lifespan, happens to be a perfect example of the expected type of relationship to form under the Antagonistic Pleiotropy theory. Aerobic metabolism undoubtedly evolved shortly after the mass extinction of most obligate anaerobes was caused by the flooding of Earth in O2 from Cyanobacteria photosynthesis. The surviving bacteria must have had some sort of oxidation resistance already, but those which utilised their existing photosynthetic electron transport chains to extract energy from the newly abundant energy source of O2 would have had a much larger advantage over its anaerobic competitors [3].

The evolution of aerobic respiration was undoubtedly beneficial in its context and the basic control of oxidative damage was already set up, while the accumulation of damage from the occasional escaped superoxide particle was unlikely to have any noticeable deleterious effect on the quickly replicating bacteria. It isn’t until evolutionary history proceeds, conditions change, life expectancies change as complexity increases, and the small amounts of damage become increasingly important. The evolution of increasingly efficient antioxidants is the only method available to counteract this side effect of an otherwise incredibly beneficial gene.

This hypothetical story may not be completely accurate, but the evidence does support something at least similar. Overexpression of the genes for superoxide dismutase (SOD) and catalase in Drosophila, the two primary ROS scavenging enzymes, increases lifespan by around 34% [9], demonstrating both the effect ROS may have on lifespan, as well as the importance of controlling the ROS. More interestingly, overexpression of just the human SOD1 gene increased its lifespan by 40% [9], implying the more effective scavenging ability of the human SOD enzyme which would be expected in a longer living organism. age-1 mutants in C. elegans live twice as long as the controls and were found to also increase SOD and catalse activity [9], while the Methuselah mutant Drosophila also demonstrated increased resistance to oxidative stress, high temperature and starvation, and lived 35% longer than their parent strain [13]. Both of these examples also show how counteracting the ROS may be incredibly influential in longevity.

Having said that, an important criticism raised recently by Spencer et al [19] about the quality of specimens used for longevity comparisons may just undermine exactly how meaningful an ‘extension’ of 30-50% in lifespan may be. The breeding techniques employed in labs to maintain their stocks of Drosophila, results in a selection pressure for rapid reproduction and large litters [15]. The Disposable Soma Theory states that this would create an evolutionary pressure to direct resources to those areas at the expense of soma durability and maintenance. Spencer et al demonstrated that the extension in life from overexpression of SOD was in fact dependent on the genetic background the specimen was taken from, showing some results which had a noticeable increase in longevity, and occasional results which actually decreased longevity. Perhaps naturally living Drosophila naturally ‘overexpress’ SOD and catalase already?

Whatever the case may be, it seems reasonable enough to accept that ROS plays a key role in aging, and Antioxidant enzymes like SOD play a key role in controlling ROS. Whether this information can be used to actually extend lifespan or improve the average quality of life in older age is far from certain, but at least we have something to work with.

Other Theories on Aging

Far from being the only theory on aging though, the Free Radical Theory is only one of many theories. There is the alternative version of the Free Radical Theory, the Mitochondrial Theory of aging, which uses the ROS idea in a vicious circle where damage to the Mitochondrion causes more ROS to be created, resulting in an exponential increase in oxidative damage [7]. This theory has lost favour in more recent times, though still attracts interest [7][16][8]. Genome Instability, the accumulation of mutations, rearrangements and changes in chromosome number have been proposed as another cause of aging [9], while an offshoot of this theory is based on the accumulation of ribosomal DNA loops which bud out of the genome then proceed to replicate themselves, growing in number and eventually causing fragmentation of the nucleolus [18]. This has only been observed in S. Cerevisiae though so has little following as a general theory of aging. Research into the WRN gene, the gene responsible for the human progeria disease Werner Syndrome, has implicated the function of DNA Helicases and their actions in suppressing DNA recombination in aging [9]. Genetic programs for aging based on genes found in C. elegans [9], accumulation of potentially harmful abnormal proteins [12], and the cell death theory which claims that gradual loss of cells in postmitotic organs eventually leads to degeneration, are all offered as aging theories. A theory of Systemic Control of aging in the body by something such as the endocrine system has been suggested with evidence from C. elegans. Apfeld and Kenyon (1998) demonstrated that a small number of mutant cells could confer increased lifespan to the entire animal [9], believing that this meant that the gene in question produced a secreted factor which dictated the pace of aging.

An important implication from all these theories and all of the research done on these theories over the years is becoming more and more clear: It is unlikely that we are going to find ‘The’ cause of aging. Even if a systemic control factor of aging is discovered, it is unlikely to provide a simple way out of aging. Assuming we could just trick the body into behaving like it was 18 years old, we would still have to deal with the accumulation of oxidative damage, the loss of postmitotic cells, the risks of cancer, heart disease and other diseases of accumulation/degeneration.

Telomeres

Now implicit in the cell death theory of aging, Telomeres have gained particular notoriety as the biological clock of aging. In 1961 Hayflick and Moorhead reported the limited number of replication events human fibroblasts could go through before entering a quiescent, viable state, unable to enter further rounds of replication [6]. This number of replications was called the ‘Hayflick Limit’ and was explained in 1990 when Harley claimed that Telomeres act as the counting mechanism which limit the replication of the fibroblasts [5].

Telomeres serve several functions in the genome, some of which include solving the “end-replication problem” [1], preventing end-to-end fusions of chromosomes, and preventing exonucleolytic degradation. Telomerase is an enzyme produced by cells which lengthens telomeres, counteracting the shortening of the end-replication problem, but it is not active in somatic cells in humans. Why not? It is most likely not active because it gives too much freedom for rogue cells to turn cancerous and threaten the entire body. The control over every individual cell by the body is incredibly important, and if a cell breaks free of that control, then the inevitable death of that cell is important.

These functions of telomeres are all now unavoidable. As long as we have linear DNA, replicate our DNA through DNA polymerase and exist as a multicellular organism, we need telomeres. The apparent link to aging is unfortunate and stands once again as an example of Antagonistic Pleiotropy.

Interestingly, evidence has shown oxidative damage itself may directly cause telomere shortening [17]. This fact reiterates the confusing intermingling of aging mechanisms faced by researchers, further highlighting the unlikelihood of ever finding a single ‘cause of aging’.

Conclusion

Understanding aging will be a matter of understanding Cell Biology as a whole. The evidence so far seems to be loud and clear that there is no such thing as a single cause of aging let a lone a single solution to it. Instead the evidence implies that aging is just an accumulation of complex side effects piled on top of each other in a somewhat random uncontrolled way, resulting in all sorts of nasty phenotypes that most just wish to avoid. Perhaps when our understanding of Cell Biology reaches a high enough level we will be able to design novel solutions for the issues which cause aging, but until that time all you can do is restrict your calorie intake and avoid standing in the middle of major roads in peak hour.

References

  1. Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P. 2002. Molecular Biology of the Cell – 4th ed. Garland Science, New York, Ch. 5, Pp. 263
  2. Cabo R, Furer-Galban S, Anson RM, Gilman C, Gorospe M, Lane MA. 2003. An in Vitro Model of Caloric Restriction. Experimental Gerontology 38:631-639
  3. Campbell N, Reece J, Mitchell L. 1999. Biology (Fifth Edition) Benjamin Cummings, California. Chapter 27:511-512
  4. Golden TR, Hinerfeld DA, Melov S. 2002. Oxidative Stress and Aging: Beyond Correlation. Aging Cell 1:117-123
  5. Harley CB, Futcher AB, Greider CW. 1990. Telomeres Shorten During Ageing of Human Fibroblasts. Nature 345:458-60
  6. Hayflick L, Moorhead P. 1961. The Serial Cultivation of Human Diploid Cell Strains. Experimental Cell Research 25:585-621
  7. Jacobs HT. 2003. The Mitochondrial Theory of Aging: Dead or Alive? Aging Cell 2:11-17
  8. Jacobs HT. 2003. Rebuttal to Pak et al.: New Data, Old Chestnuts. Aging Cell 2:19-20
  9. Johnson FB, Sinclair DA, Guarente L. 1999. Molecular Biology of Aging. CELL 96 (2): 291-302
  10. Kirkwood TBL. 1977. Evolution of Aging. Nature 270:301-304
  11. Kirkwood TBL. 2002. Evolution of Ageing. Mechanisms of Ageing and Development 123:737-745
  12. Koubova J, Guarente L. 2003. How does calorie restriction work? Genes and Development 17(2):313-321
  13. Lin YJ, Seroude L, Benzer S. 1998. Extended Life-Span and Stress Resistance in the Drosophila Mutant Methuselah. Science 282:943-946
  14. Medawar PB. 1952. An Unsolved Problem of Biology. Lewis, London
  15. Miller RA, Austad S, Burke D, Chrisp C, Dysko R, Galecki A, Jackson A, Monnier V. 1999. Exotic Mice as Models for Ageing Research:Polemic and Prospectus. Neurobiol. Aging 20:217-231
  16. Pak JW, Herbst A, Bua E, Gokey N, McKenzie D, Aiken JM. 2003. Rebuttal to Jacobs: The Mitochondrial Theory of Aging: Alive and Well. Aging Cell 2:9-10
  17. Ren JG, Xia HL, Just T, Dai YR. 2001. Hydroxyl Radical-Induced Apoptosis in Human Tumor Cells is Associated With Telomere Shortening But Not Telomerase Inhibition And Caspase Activation. FEBS Letters 488:123-132
  18. Sinclair D, Mills K, Guarente L. 1998. Aging in Saccharomyces Cerevisiae. Annual Review of Microbiology 52:533-560
  19. Spencer CC, Howell CE, Wright AR, Promislow DEL. 2003. Testing an ‘aging gene’ in long-lived Drosophila strains: increased longevity depends on sex and genetic background. Aging Cell 2: 123-130
  20. Williams GC. 1957. Pleiotropy, Natural Selection, and the Evolution of Senescence. Evolution 11:398-411

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The Purpose Of This Blog

Welcome everyone to my first post in this blog.

This blog is not original. Not for the internet in general, or even for me. I have made websites before when I was younger to express my Ideas and my philosophies. I have even had an online diary which I maintained well for over 3 years. I wrote many many ideas thoughts ruminations and philosophies in that. So this is not original at all.

But it is different

In this blog I will attempt to work towards actual ‘academic style’ papers on topics of interest to myself. Primarily I have an interest in ageing research, but I also have a lot of other interests which I will explore. Namely: Evolution, Morality and philosophy of the mind. How I will work this blog is by seperating daily weekly and monthly ruminations and data collection from the end products. The regular posts will be my haphazzard thoughts. The tid bits of interesting information I have found. Reveiws of articles which I found relevent to the end goal. Drafts of the final works and so forth.

And then, after perhaps many months of considerations and self-discussion (and hopefully lots of public feedback) I will convert numerous drafts into a final “article” and post that in the “Article” section.

I make no promises of timeline for the completion of articles. i have no idea how complex I will take them until I get there. Knowing me, I may never finish. But hopefully the journey there will be just as interesting. But as a guide, here are a few topics I hope to complete my first articles on:

Proving Evolutionary Theory
Morality: What it is, where it comes from, and why we have it.
The Evolutionary Context Of Ageing (A more thorough version)
What Causes Ageing?

My plan is to tackle the Evolutionary Theory first, because it is my pet interest, and because the rest of my topics all assume evolution is true. While I have confidence that it is, I know too many people question it as if it is madeup. I feel a need to show how solid a theory it is before I proceed to assume it in my following papers.

Once these papers have been completed (which could take a decade for all I know) then i willprobably have plenty of other papers which I am interested in writing.

I look forward to plenty of good discussions to come with everyone who disagrees with me, and everyone with interesting insight into my topics!

Shane

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Why Do We Age?

The Evolutionary Context of Senescence

People have rationalised aging and the inevitability of death throughout the past as ‘only natural’, ‘For the good of the species’ or as ‘Making way for the next generation’. Taking a closer look at the evidence though quickly makes it plainly clear that these explanations are simply wrong. In a typical natural environment organisms die through predation, accident, starvation, infection and other such events long before aging becomes a factor [20]. Aging, as a general rule, has virtually no influence in the natural world, and it this fact precisely that explains how it is that aging arose in the first place.

In 1957 Williams wrote a paper called “Pleiotropy, Natural Selection, and the Evolution of Senescence” which built on the idea introduced in 1952 by Medawar [14] that evolution would not be able to exert any real selective pressure on genes which act after the reproductive age. Williams proposed a more practical idea, that genes which produce an advantage early in life but have a later acting negative effect would still be selected regardless of the later effect. He claimed that “natural selection may be said to be biased in favour of youth over old age whenever a conflict of interest arises [20].” This theory, known as ‘Antagonistic Pleiotropy’ has since been expanded once more by Kirkwood in 1977 with the addition of the ‘Disposable Soma Theory’ [10]. This latest addition picks up on the bias natural selection has for youth and suggests that organisms evolve in a way which puts as many resources into ensuring youthful vigour and reproductive success as is required, and only after these two facets are assured do any resources get distributed into maintaining the somatic cells. In other words, evolution cannot select long living individuals if they are going to die before reproduction anyway. Evolution recognises that the body is disposable and so allocates resources appropriately.

These theories are important because they form a basis from which investigations into the mechanisms of aging can be approached from. These theories imply that it is unlikely for there to be any genes ‘for’ aging as such, but instead there will actually be genes ‘against’ aging. They imply that the causes of aging will actually be side effects of otherwise beneficial genes. They also imply that the genes associated with longevity will actually be genes which affect the durability and maintenance of the somatic cells [11].

The Free Radical Theory of Aging

The Free Radical Theory of aging has become one of the main focuses of aging research today. The theory proposes that reactive oxygen species (ROS – The ‘Free Radicals’), largely produced as a side effect of normal mitochondrial metabolism, cause progressive damage resulting in the functional decline that defines aging [4]. A lot of evidence for the theory is apparent in the fact that most lab organisms which have had an increased life span, have also been shown to have an increased oxidative stress response [2][13][19].
The overwhelming correlation between increased stress response and increased lifespan has an incredibly strong implication that ROS may cause some aspect of aging. The stress response which combats the ROS, extending lifespan, happens to be a perfect example of the expected type of relationship to form under the Antagonistic Pleiotropy theory. Aerobic metabolism undoubtedly evolved shortly after the mass extinction of most obligate anaerobes was caused by the flooding of Earth in O2 from Cyanobacteria photosynthesis. The surviving bacteria must have had some sort of oxidation resistance already, but those which utilised their existing photosynthetic electron transport chains to extract energy from the newly abundant energy source of O2 would have had a much larger advantage over its anaerobic competitors [3].
The evolution of aerobic respiration was undoubtedly beneficial in its context and the basic control of oxidative damage was already set up, while the accumulation of damage from the occasional escaped superoxide particle was unlikely to have any noticeable deleterious effect on the quickly replicating bacteria. It isn’t until evolutionary history proceeds, conditions change, life expectancies change as complexity increases, and the small amounts of damage become increasingly important. The evolution of increasingly efficient antioxidants is the only method available to counteract this side effect of an otherwise incredibly beneficial gene.
This hypothetical story may not be completely accurate, but the evidence does support something at least similar. Overexpression of the genes for superoxide dismutase (SOD) and catalase in Drosophila, the two primary ROS scavenging enzymes, increases lifespan by around 34% [9], demonstrating both the effect ROS may have on lifespan, as well as the importance of controlling the ROS. More interestingly, overexpression of just the human SOD1 gene increased its lifespan by 40% [9], implying the more effective scavenging ability of the human SOD enzyme which would be expected in a longer living organism. age-1 mutants in C. elegans live twice as long as the controls and were found to also increase SOD and catalse activity [9], while the Methuselah mutant Drosophila also demonstrated increased resistance to oxidative stress, high temperature and starvation, and lived 35% longer than their parent strain [13]. Both of these examples also show how counteracting the ROS may be incredibly influential in longevity.

Having said that, an important criticism raised recently by Spencer et al [19] about the quality of specimens used for longevity comparisons may just undermine exactly how meaningful an ‘extension’ of 30-50% in lifespan may be. The breeding techniques employed in labs to maintain their stocks of Drosophila, results in a selection pressure for rapid reproduction and large litters [15]. The Disposable Soma Theory states that this would create an evolutionary pressure to direct resources to those areas at the expense of soma durability and maintenance. Spencer et al demonstrated that the extension in life from overexpression of SOD was in fact dependent on the genetic background the specimen was taken from, showing some results which had a noticeable increase in longevity, and occasional results which actually decreased longevity. Perhaps naturally living Drosophila naturally ‘overexpress’ SOD and catalase already?

Whatever the case may be, it seems reasonable enough to accept that ROS plays a key role in aging, and Antioxidant enzymes like SOD play a key role in controlling ROS. Whether this information can be used to actually extend lifespan or improve the average quality of life in older age is far from certain, but at least we have something to work with.

Other Theories on Aging

Far from being the only theory on aging though, the Free Radical Theory is only one of many theories. There is the alternative version of the Free Radical Theory, the Mitochondrial Theory of aging, which uses the ROS idea in a vicious circle where damage to the Mitochondrion causes more ROS to be created, resulting in an exponential increase in oxidative damage [7]. This theory has lost favour in more recent times, though still attracts interest [7][16][8]. Genome Instability, the accumulation of mutations, rearrangements and changes in chromosome number have been proposed as another cause of aging [9], while an offshoot of this theory is based on the accumulation of ribosomal DNA loops which bud out of the genome then proceed to replicate themselves, growing in number and eventually causing fragmentation of the nucleolus [18]. This has only been observed in S. Cerevisiae though so has little following as a general theory of aging. Research into the WRN gene, the gene responsible for the human progeria disease Werner Syndrome, has implicated the function of DNA Helicases and their actions in suppressing DNA recombination in aging [9]. Genetic programs for aging based on genes found in C. elegans [9], accumulation of potentially harmful abnormal proteins [12], and the cell death theory which claims that gradual loss of cells in postmitotic organs eventually leads to degeneration, are all offered as aging theories. A theory of Systemic Control of aging in the body by something such as the endocrine system has been suggested with evidence from C. elegans. Apfeld and Kenyon (1998) demonstrated that a small number of mutant cells could confer increased lifespan to the entire animal [9], believing that this meant that the gene in question produced a secreted factor which dictated the pace of aging.

An important implication from all these theories and all of the research done on these theories over the years is becoming more and more clear: It is unlikely that we are going to find ‘The’ cause of aging. Even if a systemic control factor of aging is discovered, it is unlikely to provide a simple way out of aging. Assuming we could just trick the body into behaving like it was 18 years old, we would still have to deal with the accumulation of oxidative damage, the loss of postmitotic cells, the risks of cancer, heart disease and other diseases of accumulation/degeneration.

Telomeres

Now implicit in the cell death theory of aging, Telomeres have gained particular notoriety as the biological clock of aging. In 1961 Hayflick and Moorhead reported the limited number of replication events human fibroblasts could go through before entering a quiescent, viable state, unable to enter further rounds of replication [6]. This number of replications was called the ‘Hayflick Limit’ and was explained in 1990 when Harley claimed that Telomeres act as the counting mechanism which limit the replication of the fibroblasts [5].

Telomeres serve several functions in the genome, some of which include solving the “end-replication problem” [1], preventing end-to-end fusions of chromosomes, and preventing exonucleolytic degradation. Telomerase is an enzyme produced by cells which lengthens telomeres, counteracting the shortening of the end-replication problem, but it is not active in somatic cells in humans. Why not? It is most likely not active because it gives too much freedom for rogue cells to turn cancerous and threaten the entire body. The control over every individual cell by the body is incredibly important, and if a cell breaks free of that control, then the inevitable death of that cell is important.

These functions of telomeres are all now unavoidable. As long as we have linear DNA, replicate our DNA through DNA polymerase and exist as a multicellular organism, we need telomeres. The apparent link to aging is unfortunate and stands once again as an example of Antagonistic Pleiotropy.

Interestingly, evidence has shown oxidative damage itself may directly cause telomere shortening [17]. This fact reiterates the confusing intermingling of aging mechanisms faced by researchers, further highlighting the unlikelihood of ever finding a single ‘cause of aging’.

Conclusion

Understanding aging will be a matter of understanding Cell Biology as a whole. The evidence so far seems to be loud and clear that there is no such thing as a single cause of aging let a lone a single solution to it. Instead the evidence implies that aging is just an accumulation of complex side effects piled on top of each other in a somewhat random uncontrolled way, resulting in all sorts of nasty phenotypes that most just wish to avoid. Perhaps when our understanding of Cell Biology reaches a high enough level we will be able to design novel solutions for the issues which cause aging, but until that time all you can do is restrict your calorie intake and avoid standing in the middle of major roads in peak hour.

References

  1. Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P. 2002. Molecular Biology of the Cell – 4th ed. Garland Science, New York, Ch. 5, Pp. 263
  2. Cabo R, Furer-Galban S, Anson RM, Gilman C, Gorospe M, Lane MA. 2003. An in Vitro Model of Caloric Restriction. Experimental Gerontology 38:631-639
  3. Campbell N, Reece J, Mitchell L. 1999. Biology (Fifth Edition) Benjamin Cummings, California. Chapter 27:511-512
  4. Golden TR, Hinerfeld DA, Melov S. 2002. Oxidative Stress and Aging: Beyond Correlation. Aging Cell 1:117-123
  5. Harley CB, Futcher AB, Greider CW. 1990. Telomeres Shorten During Ageing of Human Fibroblasts. Nature 345:458-60
  6. Hayflick L, Moorhead P. 1961. The Serial Cultivation of Human Diploid Cell Strains. Experimental Cell Research 25:585-621
  7. Jacobs HT. 2003. The Mitochondrial Theory of Aging: Dead or Alive? Aging Cell 2:11-17
  8. Jacobs HT. 2003. Rebuttal to Pak et al.: New Data, Old Chestnuts. Aging Cell 2:19-20
  9. Johnson FB, Sinclair DA, Guarente L. 1999. Molecular Biology of Aging. CELL 96 (2): 291-302
  10. Kirkwood TBL. 1977. Evolution of Aging. Nature 270:301-304
  11. Kirkwood TBL. 2002. Evolution of Ageing. Mechanisms of Ageing and Development 123:737-745
  12. Koubova J, Guarente L. 2003. How does calorie restriction work? Genes and Development 17(2):313-321
  13. Lin YJ, Seroude L, Benzer S. 1998. Extended Life-Span and Stress Resistance in the Drosophila Mutant Methuselah. Science 282:943-946
  14. Medawar PB. 1952. An Unsolved Problem of Biology. Lewis, London
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