söndag 18 november 2012

Nature, nurture and natural selection. Epigenetic memory.

Nowhere has the debate about nature and nurture been so controversial as in the study of mental ability in humans. IQ is a phenotypic measurement of relative performance on a series of mental ability tests. Our immune system is a sort of loose brain, in that most immune cells float free in our body, while our brain's neurons function within a highly interconnected web. Both systems are functionally similar.

As Jean Piaget used to say, intelligence is what you use when you don’t know what to do, when all the standard answers are inadequate.  To be smart is another thing. It is about making the right choises. We can subconsciously try out variations, using many brain regions. Eventually, as quality improves, we become conscious of our new invention. 

This is when we become aware of our intentions and thoughts? As examle mathematics? The Libet readiness potential?

 

Brain developement and nature - nurture effect.
Heritability patterns of IQ for young, preschool individuals are generally more to the nurture factors than for elder humans. How is this tested when we know that the developement of the nerves and theit net formations in the brain is very much depending on the nurture effects? Twins have been used in the majority of studies to estimate the heritability of IQ, both monozygote and dizygote twins.  MZ twins are substantially more similar in IQ than DZ twins, whether they are raised together or apart. Reported estimates of heritability for IQ from twin studies are remarkably consistent in the range of 0.5–0.8, across many age groups. Studies with adults show that they have a higher heritability of IQ than children do and that heritability could be as high as 0.8. Here can you also test your IQ.

Gerald Edelman won the Nobel Prize in 1972 for his discovery that the immune system doesn't operate through an instruction/memory model, as had been thought, but rather through evolutionary natural selection procedures. He found, rather, that through natural selection processes occurring over eons of time, we are born with a vast number of specific antibodies that each recognize and respond to a specific type of harmful invader that shares our environment. If we lack such a natural immunity to a specific invader (such as the AIDS virus), we may die if infected. Our immune system can't learn how to destroy the invader; it simply has or hasn't the capacity at birth. Edelman then studied our functionally similar brain to see whether it also operates principally on natural selection, rather than on instruction and learning. His controversial theory, Neural Darwinism, (here a review) argues that our brain does operate on the basis of natural selection—or at least that natural selection is the process that explains instruction and learning. Neuronal selection is another term with good results.

The powerful role that emotion plays in regulating brain activity, and the preponderance of parallel (rather than linear) processing in our brain, points to a biological model, not technological.

Edelmann proposes that the electrochemical dynamics of our brain's development and operation resemble the rich, layered ecology of a jungle environment. A jungle has no external developer, no predetermined goals. Indeed, it's a messy place characterized more by organic excess than by goal-directed economy and efficiency. No one organism or group runs the jungle. All plants and animals participate in the process, each carrying out a variety of ecological functions. The jungle environment doesn't instruct organisms how to behave, for example, by teaching trees how to position their limbs and roots to get sunlight and soil nutrients. Evolution works by selection, not instruction. The environment selects from among the built-in options available—it doesn't modify (instruct) the competing organisms. (No homunculus is there?) An infant brain doesn't have to learn how to recognize specific sounds and line segments; such basic neural networks are operational at birth. We don't teach a child to walk or talk; we simply provide opportunities for adaptations to an already operational process. Gazzaniga (1992) argues that all we do in life is discover what's already built into our brain. What we see as learning is actually a search through our brain's existing library of operating networks for the combinations of those that best allow us to respond to the immediate challenge; our DNA couldn't possibly encode our brain's networks for every possible combination of sights/sounds/smells/textures/tastes/movements that our brain can process. Instead, it encodes a basic developmental program that regulates how neurons will differentiate and interconnect.

The homunculus-theory has been a big obstacle in biology.He has unconscious thoughts, here discussed by Fracis Crich and Christof Koch, 2000.

Many has thought of the nurture side as being dominant, but these new theories argue that nature plays a  more important role than previously believed. They also suggest that many current beliefs about instruction, learning, and memory are wrong. The theories will become culturally controversial because they will require reconceptualizations of such concepts as parenting, teaching, learning, identity, free will, and human potential. Further, some people may misuse the theories to support racist, sexist, and elitist beliefs. Certainly those who reject Darwinian evolution will be disturbed by the evolutionary base of the new theories.

Fernando et al. suggests a neuronal basis for causal inference, function copying, and natural selection within the human brain. To date, no model of neuronal topology copying exists. We present three increasingly sophisticated mechanisms to demonstrate how topographic map formation coupled with Spike-Time Dependent Plasticity (STDP) can copy neuronal topology motifs.  A unit of selection is an entity that can replicate, and have hereditary variation. If these units have differential fitness they can evolve by natural selection.
Both Edelman and Changeux's groups have produced an impressive range of detailed models of hill-climbing type (exploration and exploitation) algorithms that can explain a wide range of behavioural and cognitive phenomena at various levels of abstraction [16]; such as category formation [12], reinforcement learning using spike-time dependent plasticity modulated by dopamine reward [17], visual-motor control in a robotic brain-based device [18], temporal sequence learning [19], effortful cognition in the Stroop task [20], and planning [21]. Importantly, both these research programs avoid the need for replication of neuronal groups, i.e. none of their algorithms require units of selection. The algorithms of Edelman and Changeux fundamentally consist of a population of stochastic hill-climbers [25]. Each neuronal group is randomly initialized, and those groups that are closest to a good solution obtain a greater quantity of synaptic resources allowing them to ‘grow’ and/or ‘change’. 

The heritability of IQ , (here wikipedia), investigates the relative importance of genetics and environment for phenotypic variation in intelligence quotient (IQ) in a population. If there is biological inheritance, heredity, of IQ, then the relatives of a person with a high IQ should exhibit a comparably high IQ with a much higher probability than the general population.

In biology, and specifically genetics, epigenetics is the study of heritable changes in gene expression or cellular phenotype caused by mechanisms other than changes in the underlying DNA sequence.
This is why the differentiated cells in a multi-cellular organism express only the genes that are necessary for their own activity. Epigenetic changes are preserved when cells divide, but usually (?) not into the germline, which is conserved, sheltered, and divide very slowly (in off-state).

Several neurophysiological factors have been correlated with intelligence in humans, including the ratio of brain weight to body weight and the size, shape and activity level of different parts of the brain. Specific features that may affect IQ include the size and shape of the frontal lobes, the amount of blood and chemical activity in the frontal lobes, the total amount of gray matter in the brain, the overall thickness of the cortex and the glucose metabolic rate.

IQ is a polygenic trait (50 genes?) under normal circumstances according to recent research. However, certain single gene genetic disorders can severely affect intelligence, with phenylketonuria as an example. The example of phenylketonuria (PKU) is informative. Untreated, this is a completely penetrant genetic disorder causing brain damage and progressive mental retardation. PKU can be treated by the elimination of phenylalanine from the diet. Hence, a character (PKU) that used to have a virtually perfect heritability is not heritable any more if modern medicine is available (the actual allele causing PKU would still be inherited, but the phenotype PKU would not be expressed anymore).

Various studies have as instance found the heritability of IQ to be between 0.7 and 0.8 in adults and 0.45 in childhood in US.

Governments have implemented several health policies regarding nutrients and toxins known to influence cognitive function, as laws requiring fortification of certain food products and laws establishing safe levels of pollutants (e.g. lead, mercury, and organochlorides). Improvements in nutrition, and in public policy in general, have been implicated in worldwide IQ increases.

This new field of epigenetics means that a lot of the traditional assumptions in the field of genetic engineering are dangerously wrong. For example, the assumption that it is only the sequence of codons that create certain behaviours or attributes. It is not only the sequence but how that sequence interacts with other sequences which determines it's function - that means that a lot of the richness of expression is being completely stultified when they simply worry about the basic sequence, as they do in genetic modification.

Matt Ridley blog: In other words, hygienic, well-fed life enables people to maximize their genetic potential so that the only variation left is innate. Intelligence becomes significantly more heritable when environmental hurdles to a child's development have been dismantled. 
An objection to this is that in the well-fed conditions there are lots of diseases, so stress is obviously also a shelter for us. This is seen as instance in the cancer research on chaperones, or stress-proteins, also on kinases and regulation.

The American Psychological Association's report "Intelligence: Knowns and Unknowns" (1995) states that "there is no doubt that normal child development requires a certain minimum level of responsible care. Here, environment is playing a role in what is believed to be fully genetic (intelligence) but it was found that severely deprived, neglectful, or abusive environments have highly negative effects on many aspects of children's intellect development.  Regarding sex differences so have most standard tests of intelligence been constructed to show equal results, but some studies show small differences. Males do better on visual-spatial tasks, with a particularly large difference on mental rotation (nearly 1 SD), which is significant for their generally better performance in tasks that involve aiming and throwing. Males also do relatively better on on tests of proportional and mechanical reasoning as well as on mathematics. Females do better on verbal tests and some memory tests. They do relatively better in tests of literature, English composition, Spanish, reading, and spelling. More males have dyslexia and stuttering. Possible causes include gender roles and differences in brain structure which in turn may be due genetics and/or environment. Differences in sex hormones may be another explanation. Female exposure to high levels of male hormones in utero is associated with higher spatial abilities as well as more spatial ability as well as more play with "boys' toys" and less with 'girls' toys". Males with higher testosterone levels do better on visuo-spatial abilities and worse on verbal abilities. Older males given testosterone score better on visuo-spatial tests."

I almost never played with dolls nor 'girl toys'. More about gender differencies here.
  • HEREDITY refers to traits passing on from parent to offspring.
  • HERITABILITY refers to the proportion/percentage of VARIABILITY that can be attributed to genetic differences. Please note that this does not mean that that same proportion of the trait is attributed to Genetics. 
Note: Cognition, thinking, will, intention, consciousness are still open fundamental questions. Correlation studies are also just that, correlations. This maybe also shed some light also on the question what exactly is natural selection? Natural selection acts on the phenotypePhenotype is determined by an organism's genetic make-up (genotype) and the environment in which the organism lives.
A prerequisite for natural selection to result in adaptive evolution, novel traits and speciation, is the presence of heritable genetic variation that results in fitness differences. In the past, most changes in the genetic material were considered neutral or close to neutral because they occurred in noncoding DNA or resulted in a synonymous substitution. However, recent research suggests that many mutations in non-coding DNA do have slight deleterious effects.
But they can also give advantages! An example is intelligence and learning abilities?
 
Epigenetics is underlying the nurture effect. An example is how plants "remember" the length of the cold winter period in order to exquisitely time flowering so that pollination, development, seed dispersal and germination can all happen at the appropriate time. This requires an epigenetic longlasting 'memory', which explains how an organism can create a biological memory of some variable condition, such as quality of nutrition or temperature.They found that a key gene called 'Flowering Locus C' is either completely off or completely on in any one cell and also later in its progeny. They found that the longer the cold period, the higher the proportion of cells that have FLC stably flipped to the off position. This delays flowering and is down to a phenomenon known as epigenetic memory.
To provide experimental evidence to back up the model, the group used a technique where any cell that had the FLC gene switched on, showed up blue under a microscope. From  observations, it was clear that cells were either completely switched or not switched at all, in agreement with the theory.
They also showed that the histone proteins near the FLC gene were modified during the cold period, in such a way that would account for the switching off of the gene.
  • Andrew Angel, Jie Song, Caroline Dean, Martin Howard. A Polycomb-based switch underlying quantitative epigenetic memory. Nature, 2011; DOI: 10.1038/nature10241
The FTL gene was found in Arabidopsis research, one of the most extensively studied herbs. As instance here, Regulation of flowering in A. by an FTL homologue.
Reward sensory value-labelling, sleep connected to future expectations, etc. also requires some memory modulation.
 
Also stochastic resonance of different non-chemical forms? Stochastic resonance is a phenomenon that occurs in a threshold measurement system. This requires signals, and for plants light and carbon are signalling systems, also for animals the carbon signalling systems are real energetic entities, underlying the choise for the different molecular motors. See also the Negentropy Maximation Principle NMP in TGD.
The energy problem with too little available energy in biological ATP is maybe also partly solved?
See the short intro in earlier post.

3 kommentarer:

  1. http://www.mskcc.org/sites/www.mskcc.org/files/node/1522/documents/transcription.pdf

    Yeast growing for a considerable time in glucose ‘remember’ a previous exposure to galactose, the inducer of its galactose-utilization (GAL) genes. This memory is conveyed by a cytoplasmically transmitted
    galactokinase working as a signal transducer.
    The picture that emerges, then, is that growth in galactose causes expression to a high level of Gal1. Enough of this protein is then distributed to some six or seven generations’ worth of progeny cells produced in glucose so that, thanks to the Gal3-like activity of Gal1, those progeny cells induce quickly in response to galactose. Gal3 cannot confer memory simply because it is produced at a much lower level than Gal1, and so is quickly diluted out as the cells begin to divide.

    In the example of Zacharioudakis et al. [3], we see an example of a cytoplasmically transmitted protein that does not self-perpetuate itself, and so the life span of the memory, though considerable, is necessarily limited. The authors point out that the effect they analyze had previously been ascribed to ‘chromatin effects’. Perhaps this is not surprising: epigenetic changes are often defined as changes in chromatin modifications.

    ‘‘The following could be a unifying definition of epigenetic events: the structural adaptation of chromosomal regions so as to register, signal or perpetuate altered activity states’’ [12]. Such definitions would exclude all cytoplasmically
    transmitted epigenetic changes, including the lambda and prion cases, as well as the yeast example analyzed here.

    SvaraRadera
  2. http://www.eurekalert.org/pub_releases/2012-12/nifm-sfe120612.php sex-specific epi-marks, which normally do not pass between generations and are thus "erased," can lead to homosexuality when they escape erasure and are transmitted from father to daughter or mother to son.

    SvaraRadera
  3. http://www.biomedcentral.com/1741-7015/11/29/abstract
    the possible impact on the reprogramming of methylation profiles at imprinted genes at a much earlier time point, such as during spermatogenesis or oogenesis, has not previously been considered. In this study, our aim was to determine associations between preconceptional obesity and DNA methylation profiles in the offspring, particularly at the differentially methylated regions (DMRs) of the imprinted Insulin-like Growth Factor 2 (IGF2) gene.

    SvaraRadera