Friday 31 October 2014

Chance, form and natural selection in the origins of life

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Biology is the science of living things, therefore the definition of life is a matter outside biology.

Indeed, the definition of life is, properly speaking, outside of science; despite that the mainstream current definition is derived from chemistry - based on the replication of molecules with the possibility for variation and selection. But that this really constitutes 'life', does not come from science but is a non-scientific assertion or assumption.

The other mainstream definition of life refers 'metabolism' - but the 'real' nature of life is just a matter of choosing a definition - there is no right answer; and furthermore replication and metabolism may have evolved separately and using different molecular types.

(For example, Freeman Dyson has argued that metabolic life may have evolved firstly among proteins, and this metabolism was parasitised by replicating RNA molecules - and later protein and nucleic acids co-evolved to join in that symbiosis we observe as 'the cell'.)

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Natural selection must have something to work on - and that something must be sufficiently stable to allow for some reasonably large number of generations to do the work of natural selection.

(In a deeper, metaphysical sense; natural selection presupposes an understanding and identification of 'form'; because form dictates what it is that evolves, and when that form stays the same or when it changes to another and different form. Unless form, its constancy and change are already known, in a definition originating outwith biology, then the workings of natural selection could never be observed.)    

Therefore, life must have been initiated by chance; then this spontaneous life must have 'fallen-into' some natural form, pre-existent order, stereotypical pattern, auto-catalytic system,  or 'strange attractor' which kept it going for a while - because only then could natural selection do its work.

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Even with natural forms - when it comes to life: what chance has given, chance also can take away. And any form of life will have a tendency towards extinction from what has been termed 'error catastrophe' (unless it has evolved methods for preventing this).

Error catastrophe is what happens in a metabolising or replicating system due to the spontaneous occurrence of errors to processes and copying. Such errors will naturally accumulate over time, unless there is some means to prevent them accumulating.

(Mutation accumulation is a special type of error catastrophe:
http://iqpersonalitygenius.blogspot.co.uk/search?q=mutation+accumulation )

And the vast majority of errors will damage functionality (because only a tiny proportion of undirected changes will improve functionality), and each new accumulating error will tend further to damage functioning - tending towards a catastrophic loss of function with death of the individual and/or extinction of the lineage.

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But however life is defined, the principles apply that life must form and have some degree of stability by some combination of chance and natural forms; and then the first job of natural selection is to stabilise life.

Put it another way - life may form spontaneously - but it will not last without the help of natural selection.

Natural selection must primarily be about sustaining life, because only when life is being sustained, is there a possibility of the of life being improved.

Because it is statistically improbable for an error to be an improvement; and therefore it typically requires considerable time (in terms of generations), and or a considerable population (because numbers amplify the number of generations) before the undirected ('random') occurrence of a beneficial error.

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So, life happens by chance but life is also is doomed by chance to be short-lasting; therefore the first 'job' of natural selection is to keep life going just as it is - just as it has arisen by chance.

And only after life has evolved such as to have been kept going just as it is by chance, is there any possibility of natural selection to produce adaptation of organisms.

Natural selection and the origins of life: First sustaining, then later (perhaps) improvement.

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Saturday 11 October 2014

A common misunderstanding of r/K selection - if you LOSE K adaptations, that does NOT make you r-selected

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The idea of r/K selection theory applied to humans is that a population could be r-selected for fast Life History - such as rapid sexual maturation and high fertility, with relatively low levels of parental investment into each offspring;

or else K-selected, for a slower and more long-termist Life History - fewer offspring with more gradual and delayed development, and investing more resources per child (with the aim of generating more cognitively specialized adults).

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(In a nutshell, and approximately - r selection is for quantity, K selection is for quality. In some environments only 'high quality' offspring - making which requires longer development and more resources - are able to compete successfully with other members by aiming for narrow niches requiring particular qualities.)

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But r and K are not opposites. Nor are they reciprocal: to reduce one does NOT mean to increase the other. 

Because 'selected-for' means 'specialized-for'.

And specialization implies adaptation.

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Therefore to be r-selected is to be specialized-for r - this means that an r-selected population has evolved a suite of adaptations which together enable it to become better at rapid and fecund reproduction.

And to be K-selected is to be specialized in producing offspring who have a better chance of themselves reproducing in a context of more long-termist Life History.

And to lose long-termist adaptations of K-selection is NOT thereby to gain short-termist adaptations; and to lose short-termist adaptations is NOT thereby to gain long termist adaptations.

So, in the modern world, the selective regime in the West has resulted in sub-replacement fertility for K-selected populations, and this will indeed destroy-K selected adaptations; but the resulting population will NOT thereby have r-selected adaptations by default - the population will just lose adaptiveness!

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(Loss of adaptiveness is - more or less - disease. Mutation accumulation is disease. On average, disease does not benefit adaptation in any way.)

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And a selective regime (such as the modern world) which reduces child mortality from approximately 60 percent to about 1 percent, allows mutation accumulation in r-selected populations.

Mutation accumulation will NOT increase r-selected abilities, it will NOT improve short-termist adaptations - but the opposite: these r-selected populations will lose their Fast Life History adaptations, as these specialized attributes enabling a fast Life History will be damaged by accumulating deleterious mutations.

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So the modern world is NOT becoming more r-selected - it is become less K-selected AND less r-selected: the modern world is becoming less adapted all round. 

This is concealed (temporarily) by the expansion in numbers of the previously r-selected populations- which is enabled by the massive reduction in child mortality rates and an increase in longevity - and an illusion of r-adaptedness - but in fact these populations are LESS r-adapted now than they were before their populations began to expand.

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If r-selection is summarized as specializing for quantity and K-selection as specializing for quality - then both high quantity and high quality are adaptive products of evolution. And, destroying quantity does not improve quality - also destroying quality does not improve quantity.

So modernity does NOT increase r at the expense of K - instead, modernity destroys BOTH r and K adaptations by means of mutation accumulation.

What results is that humans as a whole have lost adaptations, both short-term adaptations and long-term adaptations: the human genome has been damaged.

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Note: The above idea comes from Michael A Woodley - to whom credit should be attributed; but any errors or inaccuracies in expression are my responsibility.
http://psycnet.apa.org/?&fa=main.doiLanding&doi=10.1037/a0024348
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Monday 6 October 2014

An objective and biologically-valid definition of dysgenics - mutation accumulation is the real dysgenics

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It has been pointed out that in its common usage the term 'dysgenics' lacks biological validity.

For example, the decline of average intelligence in a population is often described as a dysgenic change, on the basis that a decline in intelligence is (it can be argued) a bad thing on the whole for human society.

However, it could be argued that insofar as a decline in intelligence was due to a differential selection against higher intelligence people (for example, by a chosen reduction in fertility) and in favour of lower intelligence people (who perhaps cannot or will not use contraception) - then this is just 'natural selection as usual' - and indeed the fitness of the population is being enhanced under conditions where fertility rates are either very low, sometimes at sub-replacement/ long-term extinction levels.

Insofar as this is what is happening with the decline of intelligence then it is indeed just natural -selection-as-usual in that genetic mutations leading to adaptations are being handed-on from parents to their offspring.

Better adapted parents - i.e. those parents resistant to the fertility-suppressing effects of modernity - are producing a higher proportion of offspring (in the next generation) than are parents who are susceptible to fertility suppression. 

Fitter parents (fitter in terms of the actual environment) have fitter children.

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But insofar as the decline in intelligence is due to an accumulation of deleterious mutations (and the vast majority of new mutations will be more-or-less deleterious), then this is real dysgenics: objectively measurable, and biologically distinct from natural-selection-as-usual.

This is because with mutation accumulation, the parent is not transmitting adaptations to the offspring, but newly-occurred genetic damage. The parent does not share the mutational damage which is suffered by the offspring - since that genetic damage has occurred during the process of reproduction.

Since the new genetic mutations have not been inherited from a parent, and parents are not handing-on adaptations - then mutation accumulation is not a consequence of natural selection.

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So in principle mutation accumulation is a biologically-objective dysgenic process (while differential selection of heritable traits is not) - and mutation accumulation could be measured phenotypically in terms of damage to adaptations, or genetically in terms of mutational damage to those suites of genes which underlie phenotypic adaptations.

For example, objectively and biologically dysgenic change from mutation accumulation, would include new (not inherited) mutations which led to infertility, or blindness, or fatal genetic diseases of childhood - since these phenotypic changes are objective; or else (if known) detectable as the genetic changes which underlie adaptations such as sexual attraction mate selection, fertility, child care, vision, or the functionality of any major essential organ system such as blood, cardiovascular or respiratory.

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With mutation accumulation children are less fit than parents.

Or, offspring are less fit than parents with reference to the parental environment.

(It is necessary to add this rider, because in modern conditions the less fit offspring have experienced a different, and more favourable, environment than their parents. So, the functional impairment of several generations of offspring has been concealed by a 'softer' and more supportive environment, as society became richer per capita, and mortality rates fell. )

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In conclusion, dysgenics can be used in a non-biological and subjective way - to refer to any disapproved-of genetic change in a population; or in a rigorous, objective and biologically-valid way - to describe a non-hereditary generational reduction in fitness in a population: the incremental loss of functional adaptations in a population.

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Reference: The essence of this idea came from, and should be attributed to, Michael A Woodley.