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Genetics “Central Dogma” Is Dead
09/12/2007
“The gene is dead... long live the gene,” announced subtitles to an article in Science News this week.1 Geneticists have come to a striking conclusion over the last few years: genes are not the most important things in DNA, if they even exist as a concept.
http://www.sciencenews.org/articles/20070908/bob9.asp
The “central dogma” of genetics, since Watson and Crick determined the structure of DNA, is that genetic information flows one-way – from the gene to the protein. In the textbooks, a gene was supposed to be a finite stretch of DNA that, when read by the translation process, produced a messenger RNA, which recruited transfer RNAs to assemble the amino acids for one protein.
As Patrick Barry described in his article “Genome 2.0,”1 the situation in real cells is much messier. “Mountains of new data are challenging old views,” his subtitle announced, including the “modern orthodoxy” that only genes are important.
Researchers slowly realized, however, that genes occupy only about 1.5 percent of the genome. The other 98.5 percent, dubbed “junk DNA,“ was regarded as useless scraps left over from billions of years of random genetic mutations. As geneticists’ knowledge progressed, this basic picture remained largely unquestioned....
Closer examination of the full human genome is now causing scientists to return to some questions they thought they had settled. For one, they’re revisiting the very notion of what a gene is.
Some of the findings in the genomic era include:
-- The human genome has far fewer genes than expected.
-- Some lower animals have as many genes as humans (e.g., 05/01/2007).
-- Most of the human genome does not code for genes.
-- The code for proteins can be split between distant parts of the genome – even on different chromosomes.2
-- The non-coding DNA, once considered evolutionary junk (06/15/2007), is actually heavily involved in gene regulation (04/24/2007).
-- Genetic information processing acts more like a network than a static library of genes.
-- RNA transcripts vastly outnumber gene transcripts: some 74 to 93% of the genome.
-- RNA is much more than a messenger in the cell. Numerous small and micro RNA transcripts are heavily involved in “fine tuning” the production of protein.
-- Gene regulation appears more important than the genes themselves.
-- Scientists “are finding disease-associated mutations in regions of the genome formerly regarded as junk.”
-- Some genes overlap with codes for micro-RNAs or regulatory elements.
-- Genes can be read in multiple ways that can yield far more than one protein (alternative splicing; see 05/20/2007)).
-- Messenger-RNA transcripts undergo significant modification and regulation in the nucleus.
-- The translation process can even yield transcripts from the opposing strand.3
It remains indisputable that DNA codes for proteins via messenger RNA, and that proteins perform the major structural and functional operations of the cell. But as Hui Ge of the Whitehead Institute in Cambridge, Massachusetts said, “What we thought was important before was really just the tip of the iceberg.” Barry used a homey analogy to illustrate how gene regulation can be more important than genes themselves:
Consider the difference between a one-bedroom bungalow and an ornate, three-story McMansion. Both are made from roughly the same materials—lumber, drywall, wiring, plumbing—and are put together with the same tools—hammers, saws, nails, and screws. What makes the mansion more complex is the way that its construction is orchestrated by rules that specify when and where each tool and material must be used.
In cells, regulation controls when and where proteins spring into action. If the traditional genome is a set of blueprints for an organism, RNA regulatory networks are the assembly instructions. In fact, some scientists think that these additional layers of complexity in genome regulation could be the answer to a long-standing puzzle...
...that puzzle being the unexpected low number of genes in the human genome. It might explain the physical differences between humans and roundworms, which both have similar numbers of protein-coding genes.
Barry’s article provides a good summary of numerous papers that have been casting serious doubt on the Central Dogma, and even the concept of a gene itself:
More fundamentally, it muddies scientists’ conception of just what constitutes a gene. In the established definition, a gene is a discrete region of DNA that produces a single, identifiable protein in a cell. But the functioning of a protein often depends on a host of RNAs that control its activity. If a stretch of DNA known to be a protein-coding gene also produces regulatory RNAs essential for several other genes, is it somehow a part of all those other genes as well?
Some scientists are advocating changing our focus from genes to “functional RNA transcripts.” But that seems to just relocate the problem. If DNA is a passive code, what codes for its activity? If gene regulation by a network of transcripts is now more important than genes, what regulates the regulators? Come back for Genome 3.0.
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1Patrick Barry, “Genome 2.0,” Science News, Week of Sept. 8, 2007; Vol. 172, No. 10 , p. 154.
2“The ENCODE project revealed that about 90 percent of protein-coding genes possessed previously unknown coding fragments that were located far from the main gene, sometimes on other chromosomes.”
3“According to the ENCODE project results, up to 72 percent of known genes have transcripts on the facing DNA strand as well as the main strand.”
Many previous entries have dealt with these subjects (e.g., 06/15/2007, 12/29/2006 bullet 2, 11/09/2006, 07/06/2006). This is a classic case of a paradigm change in science occurring before our eyes. Even what we mean by an intuitively-obvious word like gene is being questioned: is there such a thing? Does it have physical reality, or is it a mental picture humans have imposed on a much more subtle reality? The new buzzword is network, but is that an accurate characterization? Networking is concerned more with the interactions of entities than with the entities themselves; this means that the rules of the game are more important than the nodes of the network. How could that fit within a materialistic world view?
Whatever comes in the days ahead, it appears that there is far more information processing occurring in the cell than even Watson and Crick imagined – and that was startling and elegant enough. Barry states that the raw genetic information transcribed in DNA now appears to be 62 times what genes alone would produce. The fundamental operational unit of life may, therefore, be nonphysical: information, not molecules. These are exciting times for science – troubling times for Darwinists. Don’t expect them to have any remorse over leading mankind into a “modern orthodoxy” that was mistaken.
I myself have already anticipated the fall of reductionist genetic determinism of Dawkinsian school:
http://www.thephora.net/forum/showthread.php?t=6114
Gene Expression: the slow death of the "one gene-one enzyme" hypothesis
http://www.thephora.net/forum/showthread.php?t=7720
http://www.thephora.net/forum/showthread.php?t=8066
http://www.thephora.net/forum/showthread.php?t=7153
http://www.thephora.net/forum/showthread.php?t=26756
Potyondi (who actually has scientific training on this topic) asserted back in early 2006:
"Once the contradictions start piling up, 'DNA fetishists' (Lewontin's term) and eugenic fanatics must either eat crow or bluster; as you pointed out, their arrogance prompts them to choose the latter."
http://www.thephora.net/forum/showthread.php?t=6366&page=2&highlight=mccabe
Potty's prediction might be coming true.
Petr
Kodos
09-13-2007, 11:09 PM
I myself have already anticipated the fall of reductionist genetic determinism of Dawkinsian school:
Ill be getting detailed instructions (I have an embryonic tech startup to which this question is very relevant, though MY backround is in Electrical Engineering) on Sunday the 22.
Professor John Frink
09-14-2007, 12:14 AM
Geneticist don't use words like "dogma", Pekka.
Geneticist don't use words like "dogma", Pekka.
Oh yes they do. You don't seem to know that much about these things after all, professor my ass.
http://en.wikipedia.org/wiki/Central_dogma
Petr
Ahknaton
09-14-2007, 01:13 AM
Barry states that the raw genetic information transcribed in DNA now appears to be 62 times what genes alone would produce. The fundamental operational unit of life may, therefore, be nonphysical: information, not molecules.
This is certainly an interesting development but I don't see how it has the metaphysical implications that are being attributed to it. Regardless of exactly HOW information is encoded into DNA, be it in some kind of distributed "network" fashion or a simple one-gene-one-enzyme fashion, it's still a case of information being encoded into a physical medium. I personally think that the information is the important thing and the material substrate is incidental, but you can take that view regardless of the particularities of how DNA works, it's not a position that suddenly becomes suggested by these latest discoveries.
Kodos
09-14-2007, 01:16 AM
We only use the 'one gene - one enzyme' for finding the basics as finding two genes for one enzyme is far too hard. The reality is that most enzymes are made up by multiple proteins, which makes tracking down the source of the proteins extremely hard (hence why very little research has been done on it).
And they can't make a computer network powerful enough to crunch the numbers in protein folding problems yet...
http://www.nytimes.com/2008/09/16/science/16prof.html?_r=1&oref=slogin
A Dissenting Voice as the Genome Is Sifted to Fight Disease
By NICHOLAS WADE
Published: September 15, 2008
The principal rationale for the $3 billion spent to decode the human genome was that it would enable the discovery of the variant genes that predispose people to common diseases like cancer and Alzheimer’s. A major expectation was that these variants had not been eliminated by natural selection because they harm people only later in life after their reproductive years are over, and hence that they would be common.
This idea, called the common disease/common variant hypothesis, drove major developments in biology over the last five years. Washington financed the HapMap, a catalog of common genetic variation in the human population. Companies like Affymetrix and Illumina developed powerful gene chips for scanning the human genome. Medical statisticians designed the genomewide association study, a robust methodology for discovering true disease genes and sidestepping the many false positives that have plagued the field.
But David B. Goldstein of Duke University, a leading young population geneticist known partly for his research into the genetic roots of Jewish ancestry, says the effort to nail down the genetics of most common diseases is not working. “There is absolutely no question,” he said, “that for the whole hope of personalized medicine, the news has been just about as bleak as it could be.”
Of the HapMap and other techniques developed to make sense of the human genome, Dr. Goldstein said, “Technically, it was a tour de force.” But in his view, this prodigious labor has produced just a handful of genes that account for very little of the overall genetic risk.
“After doing comprehensive studies for common diseases, we can explain only a few percent of the genetic component of most of these traits,” he said. “For schizophrenia and bipolar disorder, we get almost nothing; for Type 2 diabetes, 20 variants, but they explain only 2 to 3 percent of familial clustering, and so on.”
The reason for this disappointing outcome, in his view, is that natural selection has been far more efficient than many researchers expected at screening out disease-causing variants. The common disease/common variant idea is largely wrong. What has happened is that a multitude of rare variants lie at the root of most common diseases, being rigorously pruned away as soon as any starts to become widespread.
It takes large, expensive trials with hundreds of patients in different countries to find even common variants behind a disease. Rare variants lie beyond present reach. “It’s an astounding thing,” Dr. Goldstein said, “that we have cracked open the human genome and can look at the entire complement of common genetic variants, and what do we find? Almost nothing. That is absolutely beyond belief.”
If rare variants account for most of the genetic burden of disease, then the idea of decoding everyone’s genome to see to what diseases they are vulnerable to will not work, at least not in the form envisaged. “I don’t believe we should do more and more genomewide association studies for common diseases,” Dr. Goldstein said. Instead, he suggested, the “missing heritability” might be tracked by thoroughly studying the genome of specific patients.
...
http://www.arn.org/blogs/index.php/2/2008/11/15/farewell_fat_gene_goodbye_gay_gene_so_lo
11/15/08
Farewell, fat gene ... goodbye gay gene ... so long, sloppiness gene ...
by Denyse O'Leary
ARN correspondent
When someone tells you it (whatever it is) is in their genes, show them this article:
http://www.nytimes.com/2008/11/11/science/11gene.html?_r=2&oref=slogin&oref=slogin
... new large-scale studies of DNA are causing her and many of her colleagues to rethink the very nature of genes. They no longer conceive of a typical gene as a single chunk of DNA encoding a single protein. "It cannot work that way," Dr. Prohaska said. There are simply too many exceptions to the conventional rules for genes.
It turns out, for example, that several different proteins may be produced from a single stretch of DNA. Most of the molecules produced from DNA may not even be proteins, but another chemical known as RNA. The familiar double helix of DNA no longer has a monopoly on heredity. Other molecules clinging to DNA can produce striking differences between two organisms with the same genes. And those molecules can be inherited along with DNA.
The gene, in other words, is in an identity crisis.
- "Now the Rest of the Genome" by Carl Zimmer (November 10, 2008)
Now, can someone please text Lamarck and tell him, come back, all is forgiven?
...
http://www.arn.org/blogs/index.php/2/2008/11/15/farewell_fat_gene_goodbye_gay_gene_so_lo
11/15/08
Farewell, fat gene ... goodbye gay gene ... so long, sloppiness gene ...
by Denyse O'Leary
ARN correspondent
When someone tells you it (whatever it is) is in their genes, show them this article:
http://www.nytimes.com/2008/11/11/science/11gene.html?_r=2&oref=slogin&oref=slogin
Now, can someone please text Lamarck and tell him, come back, all is forgiven?
...
Lamarck thought that acquired traits are heritable. This has not been shown to be true, so why bring him back? As for the claims that "the central dogma is dead.." -- some biologists, like some other people, like to be sensationalist. This sensationalism got you to post their work here, and that was probably their motive. I studied biology in the last 9 years, and I can tell you that no reasonable biologist would say that they know for sure that gay = one gene, or that fat = one gene. One gene might encode for a specific enzyme in a metabolic pathway, but even in such a case you can't rule out other functions.
In our lab, some people are studying a protein that is believed to have a function in translation, in signaling, and in cell growth, and is located either in the membrane or in the cytoplasm. We can't rule out other functions, and we can't rule out being wrong about some of the functions we think it has. We recently found out that the gene itself might have additional functions besides encoding the protein. This is the nature of biological research (and indeed, any research), and always has been. You discover new things, and modify your old ideas.
Personal genomes: The case of the missing heritability
When scientists opened up the human genome, they expected to find the genetic components of common traits and diseases. But they were nowhere to be seen. Brendan Maher shines a light on six places where the missing loot could be stashed away.
http://www.nature.com/news/2008/081105/full/456018a.html
If you want to predict how tall your children might one day be, a good bet would be to look in the mirror, and at your mate. Studies going back almost a century have estimated that height is 80-90% heritable. So if 29 centimetres separate the tallest 5% of a population from the shortest, then genetics would account for as many as 27 of them1.
This year, three groups of researchers2,3,4 scoured the genomes of huge populations (the largest study4 looked at more than 30,000 people) for genetic variants associated with the height differences. More than 40 turned up.
But there was a problem: the variants had tiny effects. Altogether, they accounted for little more than 5% of height's heritability - just 6 centimetres by the calculations above. Even though these genome-wide association studies (GWAS) turned up dozens of variants, they did "very little of the prediction that you would do just by asking people how tall their parents are", says Joel Hirschhorn at the Broad Institute in Cambridge, Massachusetts, who led one of the studies3.
[ ... ]
There could be scarier and more intractable reasons for unaccounted-for heritability that are not even being discussed. "It's a possibility that there's something we just don't fundamentally understand," Kruglyak says. "That it's so different from what we're thinking about that we're not thinking about it yet."
Still the mystery continues to draw its sleuths, for Kruglyak as for many other basic-research scientists. "You have this clear, tangible phenomenon in which children resemble their parents," he says. "Despite what students get told in elementary-school science, we just don't know how that works."
They call it research for a reason. If we knew everything, we'd call it refound, and scientists would be drinking pina coladas on a white sandy beach instead of going to cold, dusky labs every day.
We know that there are simple genetic traits, and more complex genetic traits. We know that by changing a single nucleotide in a gene that encodes for, say, an enzyme that is needed in the histidine synthesis pathway in bacteria, we can alter the gene in a way that will result in a defective enzyme. We can run proteins on a gel, and see that the functional enzyme is not there, we can see that the bacteria don't grow without histidine, and we can rescue the bacteria by adding histidine or by adding a plasmid (DNA) that encodes for a functional enzyme to the bacteria.
These experiments can be repeated in any lab, and nobody has yet to come up with a reasonable alternative explanation for what we see. This is an example of a simple genetic trait. We also know that there are more complex genetic traits, like human intelligence, which are likely the result of interactions between many genes (+ the environment). So maybe height is a complex trait. Maybe geneticists need to work a bit harder to figure out the heritable properties of this trait in humans. Maybe the researchers missed something here. It would hardly be the first time. The only way we will find out is by doing the research. I don't think that is a particularly "scary" notion. If the alternative is to base your hypothesis on texts written 2,000 years ago, without conducting a single experiment, then I'd say that it's a pretty soothing thought, actually.
It isn't that we cannot compute it, it is that we do not know how it folds and why it folds like it does and not in the millions of other ways that you could think of. Once we can do this then we should be able to reverse-engineer enzymes into their DNA code and then insert it into the DNA of a specific organism that lacks that enzyme. This would be a possible future cure for a lot of genetic diseases that humanity suffers from.
BTW, this is not exactly true, Delos. :) You don't need to understand how enzymes fold in order to reverse-engineer them into DNA. All you need to know is their amino acid sequence, and there are ways to figure that out today (e.g. mass spectrometry). We can already insert the DNA of any enzyme that we can purify into cells (e.g. in a petri dish). The problem is how to efficiently insert it into the correct cells in fully developed humans, and to have it expressed properly in these cells.
Below is documentation on Darwin's latent Lamarckianism and antipathy to Mendelism. This is a big skeleton in the closet of orthodox neo-Darwinism:
http://creationsafaris.com/crev200903.htm#20090304a
Darwin Had Genetic Blinders
03/04/2009
March 4, 2009 — Darwin was a contemporary of Mendel, so why did he get inheritance wrong? That question was addressed on Science Daily by Jonathan Howard of the University of Cologne, Germany. His thesis is that Darwin had philosophical blinders on that prevented him from recognizing the significance of evidence before him.
http://www.sciencedaily.com/releases/2009/02/090227072739.htm
“Why Didn’t Darwin Discover Mendel’s Laws?” reads the title of the article. “Darwin’s commitment to quantitative variation as the raw material of evolution meant he could not see the logic of inheritance, argues Jonathan Howard of the University of Cologne, Germany.” Quantitative variation forms the core of Darwin’s theory, he said, but that is the last place to see Mendel’s laws, which are based on discreet (discontinuous) inheritance. For instance, Darwin could have seen discontinuous variation in his own breeding experiments with plants. In his book The Different Forms of Flowers on Plants of the Same Species, Darwin even noticed a well-defined unit character, but dismissed its significance. Why? Because he “insisted, because of his belief that only quantitative variation contributed to evolution, that the rules of inheritance were too complex and not ready for definitive analysis.” He left it “unremarked,” therefore, while Mendel, with different assumptions, found this observation a key to a major discovery. “Darwin boxed himself in, unable to see the laws of inheritance in continuous variation, unable to see the real importance of discontinuous variation where the laws of inheritance could be discerned.”
Where did the blinders come from? Howard thinks Lyell provided them. “Darwin’s view of biology was greatly influenced by geologist Charles Lyell during and after the 1831-1836 Beagle voyage, leading to Darwin’s focus on infinitely tiny differences between individuals giving infinitesimal advantages or disadvantages in survival,” the article explains. Janet Browne, in her biography of Darwin, portrayed him as obsessed with the idea that small changes could accumulate over time (see 03/05/2004). This theme colored his entire view of the natural world – geology and biology. That’s not all it did. Darwin “never freed himself from the incorrect belief that environmentally determined changes could also be inherited,” Science Daily said. This error was “another victim of his focus on quantitative characters, height, weight and so on, which are strongly influenced by environmental effects.”
The article also praised Mendel over Darwin. “Mendel had a good understanding of biology, but his understanding of physics, statistics and probability theory were far superior to Darwin’s.” The article includes the reference to Jonathan Howard’s paper in the Journal of Biology.1
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1. Howard et al., “Why didn’t Darwin discover Mendel’s laws?” Journal of Biology, 2009; 8 (2): 15 DOI: 10.1186/jbiol123.
This is a remarkable article. It’s a case study on how a scientist can be blinded to facts right before his nose when the data are filtered by his world view. Darwin took image-distorting glasses out of Lyell’s book and wore them all his life. It made him see everything in terms of slow, gradual accumulation of tiny variations. Look what that did. It influenced generations of followers. Darwin Glasses became the new fad, and millions put them on. Evolutionary biologists continue to mistakenly assume that environmental changes can be inherited, and that this creates adaptation. (It may filter out the ones who are not pre-adapted, but no one has demonstrated this neo-Lamarckian hypothesis can originate new genetic information.)
Modern evolutionists will harrumph and declare that all this has been solved. They will admit that Darwin made some mistakes. The few and minor mistakes of this greatest and most perfect scientist who ever walked this planet were all thoroughly corrected in the neo-Darwinian synthesis of the 1940s, so it is evil to disparage the reputation of the King Charles, the Bearded Buddha. “Now we KNOW that we evolutionary biologists wear NO blinders. We have 20-20 vision, 20-20 hindsight, and 20-20 foresight. All is clear. Now we KNOW that creationists look funny. Blinders? We don’t see no blinders. We’re scientists. We don’t put on blinders any more.” (They don’t need to. They’ve become fused to their eyeballs.)
http://post-darwinist.blogspot.com/2008/08/darwins-odd-musings-on-circumcision.html
Tuesday, August 26, 2008
Darwin's odd musings on circumcision: Believe whatever you like ... he certainly did
Friend Malcolm Chisholm, who is "finding that the Darwin we have been taught about is not the same as Darwin in his own words" has been reading Darwin's odd musings on circumcision, from the second edition (1875) of Darwin's The Variation of Animals and Plants under Domestication, which he is "wading through." Of this book, he notes,
It was first published in 1868, but the second edition has the chapter on Pangenesis largely rewritten. Since Darwin died in 1882, this is pretty much as close as we get to the synthesis of his life of thought and final positions.
And what were these? Well, certainly not what the Darwin cult will tell you ...
First, he found, Darwin confirms himself as definitely Lamarckian. That is,
He absolutely believes that if a part of the body falls into disuse - or is removed - an inherited effect will reduce the appearance of this part of the body in subsequent generations. The mechanism he proposes for this is "Pangenesis" whereby every bit of the organism is responsible for getting itself inherited into the next generation.
He sees this being achieved via "gemmules" - units of inheritance that each cell (or maybe part of the body) passes on to succeeding generations, where they cause the same character to be expressed. If a bit of the body is removed, it cannot send its signal via the gemmules to the next generation, and so disappears. If a bit of the body falls into disuse, it produces fewer gemmules, so is less well expressed in succeeding generations.
Now, why does this matter? Because the Darwin fanatics attribute magical powers to natural selection (survival of the fittest) to produce major changes - and typically denounce Lamarckism (inheritance of acquired characteristics).
Now, Lamarck (the early French biologist who gave his name to Lamarckism) and Darwin might be right about the inheritance of acquired characteristics. Generations of environmentalists have worried that they are - that eggs and sperm may be damaged by environmental effects, for example, thus introducing acquired characteristics to inheritance. But Lamarckism is nonetheless Bad Thought, Wrong Thought, as you doubtless learned from your Darwinist biology texts.
From what Chisholm has discovered, Darwin himself wouldn't have agreed with those texts. But with the Founder safely dead, the cult carries on regardless.
...
Read the whole thing...
Petr
New Scientist
03-16-2009, 08:03 AM
This is an old debate thats being going on since dawkins wrote "the selfish gene". That there is no book of life in the genome, its just a database which responds to top down group selection. Thats a politically loaded statement, because this means our instincts to form groups and select the best genes for that group are operating all the way through our biological systems.
Its a hot debate so look up "systems biology"
Denis Noble is a proponent of systems biology.
http://en.wikipedia.org/wiki/Denis_Noble
Principles of Systems Biology
Noble offers 10 Principles of Systems Biology[4]:
Biological functionality is multi-level
Transmission of information is not one way.
DNA is not the sole transmitter of inheritance.
The theory of biological relativity: there is no privileged level of causality
Gene ontology will fail without higher-level insight
There is no genetic program
There are no programs at any other level
There are no programs in the brain
The self is not an object
There are many more to be discovered; a genuine ‘theory of biology’ does not yet exist
Then for the flipside of this debate Syndey Brenner tells us why he doesnt like systems biology, but hes coming out swinging from the crick and watson camp.
http://thesciencenetwork.org/programs/reading-the-human-genome-with-sydney-brenner/much-ado-about-nothing-systems-biology-and-inverse-problems
I notice these people like to misrepresent each others work in lectures. Well they are competing for the same grant money. One thing they are all agreed in is that computational biology is the only means by which genomics can be reconstructed to make sense. At the most you can links genes through linear regression and cluster analysis, then try and figure out their assembly mechanism. The hot debate is at what level you begin running the integration programs. Molecules (proteins), biological pathways, organs, the individual or the group. If they pick the wrong level it could set progress back by decades. Its likely each level will get farmed out to competing groups.
New Scientist
03-16-2009, 08:15 AM
Below is documentation on Darwin's latent Lamarckianism and antipathy to Mendelism. This is a big skeleton in the closet of orthodox neo-Darwinism:
http://creationsafaris.com/crev200903.htm#20090304a
http://post-darwinist.blogspot.com/2008/08/darwins-odd-musings-on-circumcision.html
Read the whole thing...
Petr
There is a shitload of evidence coming out for lamarckism. Hormonal modulation vastly affects genetic expression. (andrew Lehman)
Noble cites experiments on altered gene expression through emotional modulation that is the altered genes gets passed on.
Identical twins have different brain folding patterns (brain structures) ..its not genetic and brain folding affect cognition.
Then there is parental age of conception itself affecting whether children develop creative talents from schizoid/aspergers spectrum genes. If any of these kids develop a sparkling talent, or times call for a load of the creative genes, those genes will themselves be under high selective pressure.
There is a shitload of evidence coming out for lamarckism.
Are you a Lamarckian yourself?
Petr
New Scientist
03-16-2009, 06:15 PM
Are you a Lamarckian yourself?
Petr
Well if i am ..then we all must be
Anarch
03-18-2009, 10:09 AM
If Lamarck was correct, Jews would be born without foreskins.
They aren't. Go figure.
New Scientist
03-18-2009, 01:22 PM
If Lamarck was correct, Jews would be born without foreskins.
They aren't. Go figure.
There is no way for selection to reduce foreskin size. If somebody is born with a shorter foreskin it causes problems and has to be cut anyway.
Most of the lamarckian mechanisms being discovered affect things like temprament, immunity strength and behaviour.
There is a shitload of evidence coming out for lamarckism. Hormonal modulation vastly affects genetic expression. (andrew Lehman)
Noble cites experiments on altered gene expression through emotional modulation that is the altered genes gets passed on.
Identical twins have different brain folding patterns (brain structures) ..its not genetic and brain folding affect cognition.
Then there is parental age of conception itself affecting whether children develop creative talents from schizoid/aspergers spectrum genes. If any of these kids develop a sparkling talent, or times call for a load of the creative genes, those genes will themselves be under high selective pressure.
Can you explain the molecular mechanism by which Lamarckism works? Can you give a specific, detailed example?
Ahknaton
03-19-2009, 01:43 AM
Can you explain the molecular mechanism by which Lamarckism works? Can you give a specific, detailed example?
http://www.newsweek.com/id/180103/output/print
The lab mice, of course, came first. Since 1999 scientists in several labs have shown that an experience a mouse mother has while she is pregnant can leave a physical mark on the DNA in her eggs. Just to emphasize, this is not a mutation, the only way new traits are supposedly transmitted to children. Instead, if mother mouse eats a diet rich in vitamin B12, folic acid or genistein (found in soy), her offspring are slim, healthy and brown—even though they carry a gene that makes them fat, at risk of diabetes and cancer, and yellow. It turns out that the vitamins slap a molecular "off" switch on the obesity/diabetes/yellow-fur gene. (Don't try this at home: no one knows which human genes soy, B12 and folic acid might silence.) This was the first evidence, now confirmed multiple times, that an experience of the mother (what she eats) can reach into the DNA in her eggs and alter the genes her pups inherit. "There can be a molecular memory of the parent's experience, in this case diet," says Emma Whitelaw of Queensland Institute of Medical Research, who did the first of these mouse studies. "It fits with Lamarck because it's the inheritance of a trait the parent acquired. There is even some evidence that the diet of a pregnant mouse can affect not only her offspring's coat color, but that of later generations."
New Scientist
03-19-2009, 02:16 AM
Can you explain the molecular mechanism by which Lamarckism works? Can you give a specific, detailed example?
this article is referring to
http://www.guardian.co.uk/education/2008/dec/16/denis-noble
"Neither is it just a matter of argument or interpretation, as research on epigenetic marking in rats, published last year, showed that the stroking behaviour of adult rats changed the protein levels in a particular gene to alter the behaviour of their young. In other words, genetic determinism was not an absolute truth; rather, genes were as much a part of the system as they were its cause. "This doesn't invalidate our understanding of genetics," Noble is quick to point out. "It just shows that things aren't quite as straightforward as some people thought they might be, and that there is room for a variety of scientific approaches."
this study
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0J-4RM7MYJ-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=dfd71342c3c946412a3e82ca8132fd25
The long-term consequences of early environmental experiences for development have been explored extensively in animal models to better understand the mechanisms mediating risk of psychopathology in individuals exposed to childhood adversity. One common feature of these models is disruption of the mother–infant relationship which is associated with impairments in stress responsivity and maternal behavior in adult offspring. These behavioral and physiological characteristics are associated with stable changes in gene expression which emerge in infancy and are sustained into adulthood. Recent evidence suggests that these long-term effects may be mediated by epigenetic modification to the promoter regions of steroid receptor genes. In particular, DNA methylation may be critical to maternal effects on gene expression and thus generate phenotypic differentiation of offspring and, through effects on maternal behavior of offspring, mediate the transmission of these effects across generations. In this review we explore evidence for the influence of mother–infant interactions on the epigenome and consider evidence for and the implications of such epigenetic effects for human mental health.
The above research is important because its taking the lamarckism modulators out of the womb, and into further generations.
Andrew Lehman has done a ton of research summarizing lamarckism in pregnancy as modulating brain types, and this is mostly hormonal. He relies heavily on Annets, Right shift theory.
http://www.sexualselection.org/
I had a thread here on him previously. I had known him for a number of years, but had a dispute with him recently. He is basically spinning what might be good theories with a pro-jewish political slant. That is he is proposing we mess about with these lamarckism mechanisms to increase feminism as men are destroying the world. I got really pissed of at this, as his ideas basically propose to destablize gene lines and increases mental disorders so that we might have added creativity.
More recently a truckload of studies, mostly from israel showing that fathering children later increases genes associated with Schizoid and autism spectrum. So thats mutations to DNA occuring withing a parents lifetime inducing long term genetic changes. If those behavioural changes prove beneficial to a society such as increasing geeks when we need technology, there will be selections bias within groups on them.
New Scientist
03-19-2009, 02:21 AM
I can get full access to the paper
"Epigenetic mechanisms mediating the long-term effects of maternal care on development"
If anybody is that interested.
Below is documentation on Darwin's latent Lamarckianism and antipathy to Mendelism. This is a big skeleton in the closet of orthodox neo-Darwinism:
Darwin's theory of inheritance, Pangenesis, did have Lamarkian aspects. I fail to see how this presents a problem to "neo-Darwinists," unless you believe that evolutions should regard him as a saint whose word is infallible and unquestionable. He was wrong on heredity, just as Einstein was wrong on some things too.
http://www.newsweek.com/id/180103/output/print
Well, this kind of "Lamarckian evolution" has been known for many years. In bacteria. But if the DNA doesn't change, then these changes are probably not as permanent as regular run-of-the-mill evolution.
New Scientist
03-21-2009, 02:38 PM
Well, this kind of "Lamarckian evolution" has been known for many years. In bacteria. But if the DNA doesn't change, then these changes are probably not as permanent as regular run-of-the-mill evolution.
from the previous study
DNA methylation may be critical to maternal effects on gene expression and thus generate phenotypic differentiation of offspring and, through effects on maternal behavior of offspring, mediate the transmission of these effects across generations
from the previous study
DNA methylation may be critical to maternal effects on gene expression and thus generate phenotypic differentiation of offspring and, through effects on maternal behavior of offspring, mediate the transmission of these effects across generations
I am aware of this. But it's still not exactly as permanent as a change in the DNA. Of course, changes in the DNA aren't permanent either, but some protein sequences have stayed basically the same for millions of years. I doubt DNA methylation levels stay constant for that long. BTW, the ability to methylate DNA is itself encoded in our DNA. Without methylases there is no methylation, and without DNA there are no methylases. So Lamarck still needs a bit of Darwin in him.
New Scientist
03-22-2009, 02:34 AM
I am aware of this. But it's still not exactly as permanent as a change in the DNA. Of course, changes in the DNA aren't permanent either, but some protein sequences have stayed basically the same for millions of years. I doubt DNA methylation levels stay constant for that long. BTW, the ability to methylate DNA is itself encoded in our DNA. Without methylases there is no methylation, and without DNA there are no methylases. So Lamarck still needs a bit of Darwin in him.
I dont think anybody is throwing out darwin, the systems biologists are just saying that there is a lamarck/darwin interaction. And they have a problem just getting lamarck in the picture at all. Because science is a get stuck in the groove kind of thing.
Mutation is clustered within social behaviour, and operates at the group level. Its not this one gene at a time idea. Female instincts lead them to mutate more variations on a succesfull theme. Having observed female behaviour there seems to be a tendency for many to flock and synchronise to whatever male attracts the wealth of crowds, and if they cant get that, then the next most similiar male will do. They will gossip amongst themselves as to how similiar a man is to the guy with the greatest social status.
Women will prefer to mate with an older involved man with social status than a younger single man without. You would think this goes against healthy selection for strong DNA. As a man ages the DNA degrades and his offspring are more likely to be mutated, especially in regards to genes which affect mental functions. (Many new studies show this.) This desire to mutate variations on a proven theme is the mechanism behind most cheating in relationships.
I dont think anybody is throwing out darwin, the systems biologists are just saying that there is a lamarck/darwin interaction. And they have a problem just getting lamarck in the picture at all. Because science is a get stuck in the groove kind of thing.
Well, the philosophy of science can get stuck in grooves just as easily as science can, and today their groove king is Thomas Kuhn (a nice Jewish guy from Cincinnati). Of course some scientists (especially older ones, who are more likely to have "science power") can get boxed, too, but I don't think there is much objection in the scientific community to the claims that methylation has an multi-generational effect.
The way I look at it, it's not that Lamarck is vindicated by these studies, but rather that as we accumulate more knowledge, we discover many details about evolution that were not obvious 150 years ago (and sometimes even 5 years ago). Over all, evolution is probably mostly a result of mutations in the DNA, and those are (for the most part) non-Lamarckian. The gills in fish, the wings on birds, and our very own opposable thumbs are likely the result of mutations in the DNA.
New Scientist
03-22-2009, 03:45 AM
Well, the philosophy of science can get stuck in grooves just as easily as science can, and today their groove king is Thomas Kuhn (a nice Jewish guy from Cincinnati). Of course some scientists (especially older ones, who are more likely to have "science power") can get boxed, too, but I don't think there is much objection in the scientific community to the claims that methylation has an multi-generational effect.
The way I look at it, it's not that Lamarck is vindicated by these studies, but rather that as we accumulate more knowledge, we discover many details about evolution that were not obvious 150 years ago (and sometimes even 5 years ago). Over all, evolution is probably mostly a result of mutations in the DNA, and those are (for the most part) non-Lamarckian. The gills in fish, the wings on birds, and our very own opposable thumbs are likely the result of mutations in the DNA.
that was then. Just because evolution worked in that way on species physical shapes and tools, does not mean it works this way now. I wasnt going to think of Kuhn but glad you brought it up. humans are now the de-facto complex system, with the interaction of systems we create new means of evolution are occuring. We arent waiting about for 500 years to mutate a new kind of nose.
If anything most of the mutations are now focussed on changes in human behaviour. Ive citied a few examples where these can be rapidly altered for by lamarkism. As humans groups we are self selecting for alterations in behaviour that operate now.
that was then. Just because evolution worked in that way on species physical shapes and tools, does not mean it works this way now. I wasnt going to think of Kuhn but glad you brought it up. humans are now the de-facto complex system, with the interaction of systems we create new means of evolution are occuring. We arent waiting about for 500 years to mutate a new kind of nose.
If anything most of the mutations are now focussed on changes in human behaviour. Ive citied a few examples where these can be rapidly altered for by lamarkism. As humans groups we are self selecting for alterations in behaviour that operate now.
Well for the sake of a slow learner, can you explain specifically how Lamarckism works in these human societies? I'm not saying that it doesn't work. Maybe it does. I don't know. I just don't see the connection between women preferring older men (sometimes), and Lamarckism.
New Scientist
03-24-2009, 07:39 PM
Well for the sake of a slow learner, can you explain specifically how Lamarckism works in these human societies? I'm not saying that it doesn't work. Maybe it does. I don't know. I just don't see the connection between women preferring older men (sometimes), and Lamarckism.
DNA in sperm is altered as men age, not always to detriment. The alterations increase chances of schizoid/aspergers spectrum. Those genes can then become under selective pressure for various kinds of creativity.
Heterochronic shift. This really is a quiet breakthrough of sorts
http://serpentfd.org/graphics/transmodel.gif
http://serpentfd.org/3-neuropsychology.html
This model (andrew Lehmans) describes how the balance of hormones affects the genetically expressed structure of cognition. Environment has a now effect on hormones - Heterochronic shift. If a woman is stressed while pregnant she produces more tesosterone and this affects offspring brain structure.
This model does not give a genetic alteration like the previous example. Its still a post conception altering of entire patterns of behavioural genetic expression very strongly. If these altered offspring are under selective pressure, then the genetic mechanisms whereby they became altered will also be enhanced, although that depends on whether you buy into newer genetic theories of focussed mutations. (Lynn Caporale)
I buy into focussed mutations in type r populations. Shift theory ties into what i remember of an older project, which is aside for a rainy day at the moment. (so do not have access to the references, and some of its foggy) There may be race differences in the mutation rates and genetic convergence for annets model. That is that those on the acceleration spectrum of the annet heterochronic model (african or type r) have higher penetration mutations (prone to high linkage disequilibrium, autosomal dominant) and those on the delayed end the reverse (linkage equilibrium, autosomal recessive) jews, orientals etc. (type K).
Guide on the concept here
http://scienceblogs.com/gnxp/2007/01/basic_concepts_linkage_disequi.php
So basically even though the annet model does not directly imply genetic alterations- if its linked to the sensitivity to different types of genetic alterations which may be peculiar to type K and r populations, then yes you also have another lamarck model, as these two kinds of human populations (K and r) are on an axis with each other. The model should predict types of genetic change such as higher drift in a type r population and higher mutation focus in a type K population. Annets work ought to be taken up a step, but of course most of us are too busy grant grazing to get into this stuff, so strangely guys like lehman do it in their spare time for free.
.
DNA in sperm is altered as men age, not always to detriment. The alterations increase chances of schizoid/aspergers spectrum. Those genes can then become under selective pressure for various kinds of creativity.
Heterochronic shift. This really is a quiet breakthrough of sorts
http://serpentfd.org/graphics/transmodel.gif
http://serpentfd.org/3-neuropsychology.html
This model (andrew Lehmans) describes how the balance of hormones affects the genetically expressed structure of cognition. Environment has a now effect on hormones - Heterochronic shift. If a woman is stressed while pregnant she produces more tesosterone and this affects offspring brain structure.
We all know that hormones can have an effect on the child, and that the environment can have an effect on the child, but that's not Lamarckism.
Lamarck spoke about a giraffe stretching its neck to reach food, and passing this trait to its offspring. That would be true Lamarckism. The fact that the hormonal level in a pregnant female affects the fetus is not Lamarckism. In other words, the key concept behind Lamarckism (i.e. traits are generated in an adult and are then transferred to its progeny) is missing here. [see edit below..]
Furthermore, like I said, these non-Lamarckian changes are also not as permanent as mutations in the DNA, which can last for millions of years if they are advantageous. Lastly, as I mentioned earlier -- hormones (and the factors regulating their expression) are themselves a product of Darwinian evolution. I still don't see how Lamarck fits into any of this.
This model does not give a genetic alteration like the previous example. Its still a post conception altering of entire patterns of behavioural genetic expression very strongly. If these altered offspring are under selective pressure, then the genetic mechanisms whereby they became altered will also be enhanced, although that depends on whether you buy into newer genetic theories of focussed mutations. (Lynn Caporale)
I buy into focussed mutations in type r populations. Shift theory ties into what i remember of an older project, which is aside for a rainy day at the moment. (so do not have access to the references, and some of its foggy) There may be race differences in the mutation rates and genetic convergence for annets model. That is that those on the acceleration spectrum of the annet heterochronic model (african or type r) have higher penetration mutations (prone to high linkage disequilibrium, autosomal dominant) and those on the delayed end the reverse (linkage equilibrium, autosomal recessive) jews, orientals etc. (type K).
Guide on the concept here
http://scienceblogs.com/gnxp/2007/01/basic_concepts_linkage_disequi.php
So basically even though the annet model does not directly imply genetic alterations- if its linked to the sensitivity to different types of genetic alterations which may be peculiar to type K and r populations, then yes you also have another lamarck model, as these two kinds of human populations (K and r) are on an axis with each other. The model should predict types of genetic change such as higher drift in a type r population and higher mutation focus in a type K population. Annets work ought to be taken up a step, but of course most of us are too busy grant grazing to get into this stuff, so strangely guys like lehman do it in their spare time for free.
.
I appreciate the time you spent on this reply, but I'm not sure that this level of complexity is needed to answer the simple question of whether or not this mechanism is Lamarckian in its essence. Like I said, a classic example of Lamarckism would be a trait that is generated in an adult and is then transferred to its progeny.
EDIT: Are you suggesting that these hormones have the same effect on the mother as they do on the child? If so, then that might be semi-Lamarckian (it still probably won't be a very long-term change, though). But I'm not sure if this is the case here. One would have to prove that these changes have the same effect in the mother and in the child, and that might not be trivial to prove. Anyway, even if this were the case, this still isn't exactly what Lamarck was talking about.
New Scientist
03-25-2009, 01:30 AM
[B][QUOTE=guy]We all know that hormones can have an effect on the child, and that the environment can have an effect on the child, but that's not Lamarckism.
Lamarck spoke about a giraffe stretching its neck to reach food, and passing this trait to its offspring. That would be true Lamarckism. The fact that the hormonal level in a pregnant female affects the fetus is not Lamarckism. In other words, the key concept behind Lamarckism (i.e. traits are generated in an adult and are then transferred to its progeny) is missing here. [see edit below..]
Furthermore, like I said, these non-Lamarckian changes are also not as permanent as mutations in the DNA, which can last for millions of years if they are advantageous. Lastly, as I mentioned earlier --
hormones (and the factors regulating their expression) are themselves a product of Darwinian evolution. I still don't see how Lamarck fits into any of this.
They are permanent. If hormones or ageing cause changes, and the people with these changes are under selection pressure, then how is that not permanent ?
According to my friend who is doing this at uni whats happened since darwin is that genetics has focussed heavily on genetic recombination at conception and this is what graduates think of. Hence any process which effects genetic structures outside of the zygote and is passed onto future genes, is put into the lamarck camp even if neither interpration is strictly true to the originators. Thats why i guess the authors of these theories are then calling it lamarckism.
a review here might explain this better than me. Note on page 2 again they are reffering to stressed mothers.
http://www.technologyreview.com/biomedicine/22061/page1/
Wednesday, February 04, 2009
A Comeback for Lamarckian Evolution?
Two new studies show that the effects of a mother's early environment can be passed on to the next generation.
==================
You could if you wanted say everything in nature converges back to darwinian evolution. One physicist can say make a case that every mechanism converges to time, while another can make a case that time does not exist. This is all semantics. Whats important is to at least agree on the playing field. In humans would you agree that the playing field is operating at the level of group selection ? or that there are type K and r populations ?
New Scientist
03-25-2009, 01:37 AM
also of interest how germ line mutations occur within the father and affect the behaviour of their offspring.
http://www.schizophreniaforum.org/for/curr/Malaspina/default.asp
Schizophrenia Risk and the Paternal Germ Line
By Dolores Malaspina
Paternal age at conception is a robust risk factor for schizophrenia. Possible mechanisms include de novo point mutations or defective epigenetic regulation of paternal genes. The predisposing genetic events appear to occur probabilistically (stochastically) in proportion to advancing paternal age, but might also be induced by toxic exposures, nutritional deficiencies, suboptimal DNA repair enzymes, or other factors that influence the
fidelity of genetic information in the constantly replicating male germ line. We propose that de novo genetic alterations in the paternal germ line cause an independent and common variant of schizophrenia.
They are permanent. If hormones or ageing cause changes, and the people with these changes are under selection pressure, then how is that not permanent ?
I meant permanent from an evolutionary POV.
When there is a mutation in the DNA, it is "permanent" (not really, but it can last millions of years), becuase the change is recorded in a very simple manner (a change in the DNA sequence).
But how is a change in the hormone level recorded? There are so many factors involved. You said it yourself -- the environment changes the hormone levels. So they are not permanent. They can change every generation.
According to my friend who is doing this at uni whats happened since darwin is that genetics has focussed heavily on genetic recombination at conception and this is what graduates think of. Hence any process which effects genetic structures outside of the zygote and is passed onto future genes, is put into the lamarck camp even if neither interpration is strictly true to the originators. Thats why i guess the authors of these theories are then calling it lamarckism.
I think it just sounds cool, really. People are more likely to pay attention to a paper if the paper states something sensational like "Lamarck was right!", but these sort of things are not, IMO, what Lamarck was talking about.
a review here might explain this better than me. Note on page 2 again they are reffering to stressed mothers.
http://www.technologyreview.com/biomedicine/22061/page1/
Wednesday, February 04, 2009
A Comeback for Lamarckian Evolution?
I'll read this if I'll have some time to spare.
Two new studies show that the effects of a mother's early environment can be passed on to the next generation.
Perfectly fine, but probably not really Lamarckian.
You could if you wanted say everything in nature converges back to darwinian evolution. One physicist can say make a case that every mechanism converges to time, while another can make a case that time does not exist. This is all semantics. Whats important is to at least agree on the playing field. In humans would you agree that the playing field is operating at the level of group selection ? or that there are type K and r populations ?
I don't think the playing field in humans is at the level of group selection. I think there is selection at various levels (gene level, organism level, and group level), but I'm not sure that the group level is particulalry important in humans (or indeed in other species). Of course there are K and r populations, but that doesn't mean that the selection of individual traits occurs at the group level.
New Scientist
03-25-2009, 02:47 PM
[QUOTE=guy]I meant permanent from an evolutionary POV.
When there is a mutation in the DNA, it is "permanent" (not really, but it can last millions of years), becuase the change is recorded in a very simple manner (a change in the DNA sequence).
But how is a change in the hormone level recorded? There are so many factors involved. You said it yourself -- the environment changes the hormone levels. So they are not permanent. They can change every generation.
Depends on how you look at it. If hormone levels change the post uterine zygote, then the behaviour of those offspring will be altered, and so will their future selection behaviours, if these changes are concerted at the group level. thats the idea behind shift theory, although its not my theory so i really dont want to spend much time trying to defend it.
I don't think the playing field in humans is at the level of group selection. I think there is selection at various levels (gene level, organism level, and group level), but I'm not sure that the group level is particulalry important in humans (or indeed in other species). Of course there are K and r populations, but that doesn't mean that the selection of individual traits occurs at the group level.
thats the big question in biology. What levels is the current action at. Cluster analysis would answer it, but they at least need to program the computers to look for group selection in the first place. It has to be group selection that is the biggest factor. Religions, nations, races all have human hierarchies where decisions are being made as to whether you thrive or not.
Even if it were just genes for resistance to specific diseases that were clustering the recent research in neuropsychology is showing that the parts of our brains involved in forming races, tribes, nations etc are extentions of the basic disgust instinct which form to keep others with disease at bay. As there are major differences in group selection between type r and K i would think that the search algorithmns should be programmed to look for mutation clusters at that level.
It depends on how you look at biosystems. the trend has been growth towards larger groups, who can co-operate and subdivide tasks. i.e. Humans. The most recent clustering for brain development, is mostly in executive function which is there to deal with faciliating the large complex social structures we have today.
It has to be group selection, such as religion or nation..what else could it be ?
Depends on how you look at it. If hormone levels change the post uterine zygote, then the behaviour of those offspring will be altered, and so will their future selection behaviours, if these changes are concerted at the group level. thats the idea behind shift theory, although its not my theory so i really dont want to spend much time trying to defend it.
thats the big question in biology. What levels is the current action at. Cluster analysis would answer it, but they at least need to program the computers to look for group selection in the first place. It has to be group selection that is the biggest factor. Religions, nations, races all have human hierarchies where decisions are being made as to whether you thrive or not.
Even if it were just genes for resistance to specific diseases that were clustering the recent research in neuropsychology is showing that the parts of our brains involved in forming races, tribes, nations etc are extentions of the basic disgust instinct which form to keep others with disease at bay. As there are major differences in group selection between type r and K i would think that the search algorithmns should be programmed to look for mutation clusters at that level.
It depends on how you look at biosystems. the trend has been growth towards larger groups, who can co-operate and subdivide tasks. i.e. Humans. The most recent clustering for brain development, is mostly in executive function which is there to deal with faciliating the large complex social structures we have today.
It has to be group selection, such as religion or nation..what else could it be ?
I don't have time to answer this right now, but I must say that we seem to have very different approaches. I'm a linear thinker, and like to answer simple questions with simple answers, and complex questions by chopping them into simple questions whenever I can. I don't jump from one subject to another without explaining the connection. The connection is key for me. LOL.
The most recent clustering for brain development could be considered an evolutionary trend, or it could be considered a transient social trend, depending on your POV. I agree that today, human evolution is not what it used to be. When I spoke of gene/organism/group selection, I was thinking in historic (or prehistoric) terms, not in present-day terms. The topic of this thread is the central dogma of genetics, not recent changes in human evolution.
BTW, what exactly does "the most recent clustering for brain development" mean? How is this determined? And what do you mean by "recent"? How do you know how brain development looked like 10 years ago (let alone 10,000 years ago)?
New Scientist
03-25-2009, 06:42 PM
BTW, what exactly does "the most recent clustering for brain development" mean? How is this determined? And what do you mean by "recent"? How do you know how brain development looked like 10 years ago (let alone 10,000 years ago)?
There was a good science documentry on this, i'll try and dig it out. They were looking at the whole issue of recent genetic changes for intelligence which marked out the difference between central europeans, asians etc. When they went to pakistan to trace some deficient variants of the older intelligence genes.. where there had been a lot of inbreeding for countless generations, they were finding these village idiot types who also posessed skulls that were quite Australopithecus afarensis looking.
So basically you can broadly trace some major aspects of intelligence according to skull type. The more modern human has a more rounded skull, which gives more prominence to frontal lobe processing. The evolution of homo sapiens shows this progression, although there are variations.
Most fronal lobe processing concentrates completely on social interactions, and co-ordination of other brain regions. Having a bit more space up front in the brain, faciliates higher degrees of frontal lobe executive function, and gives more room for various offshoots of brain development up there. The frontal lobes make groups more efficient, as when they operate properly they supress individuality. Not completely. People just take their cues when to be individuals from the group. Having a larger and evolved group orientated mind, allows for more complex group interactions, and more complex human systems to grow such as a religion or nation. As these groups become more powerfull they are obviously going to exert selection pressure in a top down manner.
So yes that gives a traditional break it down to fragments scientist a big problem. evolution is heading towards the growth of abilities to deal with people who can thrive in the management of more complex human societies, then how can you break it down. You need to step outside and have a top down view just to see what you are dealing with.
New Scientist
03-25-2009, 06:55 PM
[QUOTE=guy]I don't have time to answer this right now, but I must say that we seem to have very different approaches. I'm a linear thinker, and like to answer simple questions with simple answers, and complex questions by chopping them into simple questions whenever I can. I don't jump from one subject to another without explaining the connection. The connection is key for me. LOL.
but when i'm trying to feel my way around in a new area, (like human systems/genetics is for me) i jump around to try and determine the overall structure of the system then when i think i can see the entire picture, will try to look for connections later.
Then you look for simplifications. The simple answer is normally right, but not always possible to get too simple. In complex systems science (not creationism) they talk a lot lately about irreducability. That is there is a point where you cannot simplify and when you figure where that is, then you have the correct view of the system. Good summary of complex systems here, most of the top people are in this
http://videolectures.net/eccs08_kondor_srcics/
The most recent clustering for brain development could be considered an evolutionary trend, or it could be considered a transient social trend, depending on your POV. I agree that today, human evolution is not what it used to be. When I spoke of gene/organism/group selection, I was thinking in historic (or prehistoric) terms, not in present-day terms. The topic of this thread is the central dogma of genetics, not recent changes in human evolution.
Its the same thing. Biosystems of which humans lead the way. From the lectures i have seen the geneticists who are discussing these matters are debating where to begin. On one camp you have denis noble who plays a big role in systems biology, who is saying forget the genetic approach, start top down from the human brain or higher. Then his rival on the other side, who you would probably prefer Sydney Brenner attacking the top down approach.
http://thesciencenetwork.org/programs/reading-the-human-genome-with-sydney-brenner
There was a good science documentry on this, i'll try and dig it out. They were looking at the whole issue of recent genetic changes for intelligence which marked out the difference between central europeans, asians etc. When they went to pakistan to trace some deficient variants of the older intelligence genes.. where there had been a lot of inbreeding for countless generations, they were finding these village idiot types who also posessed skulls that were quite Australopithecus afarensis looking.
So basically you can broadly trace some major aspects of intelligence according to skull type. The more modern human has a more rounded skull, which gives more prominence to frontal lobe processing. The evolution of homo sapiens shows this progression, although there are variations.
Most fronal lobe processing concentrates completely on social interactions, and co-ordination of other brain regions. Having a bit more space up front in the brain, faciliates higher degrees of frontal lobe executive function, and gives more room for various offshoots of brain development up there. The frontal lobes make groups more efficient, as when they operate properly they supress individuality. Not completely. People just take their cues when to be individuals from the group. Having a larger and evolved group orientated mind, allows for more complex group interactions, and more complex human systems to grow such as a religion or nation. As these groups become more powerfull they are obviously going to exert selection pressure in a top down manner.
So yes that gives a traditional break it down to fragments scientist a big problem. evolution is heading towards the growth of abilities to deal with people who can thrive in the management of more complex human societies, then how can you break it down. You need to step outside and have a top down view just to see what you are dealing with.
1. Is there any evidence supporting the hypothesis that these changes are not the result of mutations in the DNA?
2. What do you mean when you say "As these groups become more powerfull they are obviously going to exert selection pressure in a top down manner."? It's not at all obvious to me. I don't know what you mean by "top down manner".
but when i'm trying to feel my way around in a new area, (like human systems/genetics is for me) i jump around to try and determine the overall structure of the system then when i think i can see the entire picture, will try to look for connections later.
Then you look for simplifications. The simple answer is normally right, but not always possible to get too simple. In complex systems science (not creationism) they talk a lot lately about irreducability. That is there is a point where you cannot simplify and when you figure where that is, then you have the correct view of the system. Good summary of complex systems here, most of the top people are in this
http://videolectures.net/eccs08_kondor_srcics/
The most recent clustering for brain development could be considered an evolutionary trend, or it could be considered a transient social trend, depending on your POV. I agree that today, human evolution is not what it used to be. When I spoke of gene/organism/group selection, I was thinking in historic (or prehistoric) terms, not in present-day terms. The topic of this thread is the central dogma of genetics, not recent changes in human evolution.
Its the same thing. Biosystems of which humans lead the way. From the lectures i have seen the geneticists who are discussing these matters are debating where to begin. On one camp you have denis noble who plays a big role in systems biology, who is saying forget the genetic approach, start top down from the human brain or higher. Then his rival on the other side, who you would probably prefer Sydney Brenner attacking the top down approach.
http://thesciencenetwork.org/programs/reading-the-human-genome-with-sydney-brenner
You aren't going to be able to communicate with other people (that have no idea what you are talking about) if you don't simplify things.
New Scientist
03-25-2009, 07:51 PM
[QUOTE=guy]1. Is there any evidence supporting the hypothesis that these changes are not the result of mutations in the DNA?
I wasnt making the point that these were not the result of mutations. Not my area to say what caused them.
2. What do you mean when you say "As these groups become more powerfull they are obviously going to exert selection pressure in a top down manner."? It's not at all obvious to me. I don't know what you mean by "top down manner".
Most human groups have hierarchies, otherwise they would fragment. I often point out the jewish group as an example of a non-hiearchical group that fragments easily, and you can see this from the political system in israel, (nowhere near a majority party, at most 20% of vote)
The larger a group the stronger the hierarchy has to be. Hierarchies subdivide tasks and allot them to people within the group. Status is defined by those tasks, so if you are say a muslim, then they might have more need to grant high status to the most stubborn religious figures, but if you are in china the higher group status can be given to the best industrialists.
The high status decides reproductive success. Women want to copy variants of the higher status males within their groups, as higher status males afford most protection. They want the highest status male, and if they cannot have that will make do with a similiar type of male lower down the pecking order. (the phenomena where working class males copy the hairstyle and postures of leading sportsmen to get a girlfriend) So sexual selection criteria and the reproduction of genes is defined by the group. this is top down sexual selection because the definition of status is occuring from the highest levels of the group.
New Scientist
03-25-2009, 07:53 PM
You aren't going to be able to communicate with other people (that have no idea what you are talking about) if you don't simplify things.
i know, i just got a paper back from trial review with 30 points that need properly explained.
I wasnt making the point that these were not the result of mutations. Not my area to say what caused them.
I thought you brought this up as an example for Lamarckism. I thought we were talking about Lamarckism. Guess I was wrong. So why did you bring this up again?
i know, i just got a paper back from trial review with 30 points that need properly explained.
I can find more than that in an average post here. :/
New Scientist
03-26-2009, 12:19 AM
[QUOTE=guy]I thought you brought this up as an example for Lamarckism. I thought we were talking about Lamarckism. Guess I was wrong. So why did you bring this up again?
Well it was just a sidetrack to discuss that the human/primate evolution itself was becoming focussed on our frontal lobes, to make the point that our evolution is gearing itself towards our brains being capable of complex social lives and structures. So this can be connected to the concept that fast group selection, such as lamarckism type mechanisms rather than 300 year messing around with sexual recombination is more important for humans, as our complex societies often need to change structure quickly.
Look at other species. Do they change their group structure much ? Look at humans, you can hardly recognise the world of 50 years ago to the one we have now. Human societies are nothing like anything you see in other species, yet the brain structure is only markedly different from other species at the frontal lobes, and size of course.
Well it was just a sidetrack to discuss that the human/primate evolution itself was becoming focussed on our frontal lobes, to make the point that our evolution is gearing itself towards our brains being capable of complex social lives and structures. So this can be connected to the concept that fast group selection, such as lamarckism type mechanisms rather than 300 year messing around with sexual recombination is more important for humans, as our complex societies often need to change structure quickly.
Look at other species. Do they change their group structure much ? Look at humans, you can hardly recognise the world of 50 years ago to the one we have now. Human societies are nothing like anything you see in other species, yet the brain structure is only markedly different from other species at the frontal lobes, and size of course.
But are the changes in the last 50 years heritable, or are they environmental (and non-heritable)?
BTW, I don't think evolution is gearing itself up towards anything (hopefully that was just a figure of speech). The question is who has more children. If people that are capable of complex social lives have more children, and this quality is heritable, then the result would be evolution in that direction. But that doesn't really seem to be the case today.
EDIT: oops looks like I reverted back to Darwinism.
http://www.nytimes.com/2009/04/16/health/research/16gene.html?_r=2
Genes Show Limited Value in Predicting Diseases
By NICHOLAS WADE
Published: April 15, 2009
The era of personal genomic medicine may have to wait. The genetic analysis of common disease is turning out to be a lot more complex than expected.
Since the human genome was decoded in 2003, researchers have been developing a powerful method for comparing the genomes of patients and healthy people, with the hope of pinpointing the DNA changes responsible for common diseases.
This method, called a genomewide association study, has proved technically successful despite many skeptics’ initial doubts. But it has been disappointing in that the kind of genetic variation it detects has turned out to explain surprisingly little of the genetic links to most diseases.
A set of commentaries in this week’s issue of The New England Journal of Medicine appears to be the first public attempt by scientists to make sense of this puzzling result.
One issue of debate among researchers is whether, despite the prospect of diminishing returns, to continue with the genomewide studies, which cost many millions of dollars apiece, or switch to a new approach like decoding the entire genomes of individual patients.
The unexpected impasse also affects companies that offer personal genomic information and that had assumed they could inform customers of their genetic risk for common diseases, based on researchers’ discoveries.
These companies are probably not performing any useful service at present, said David B. Goldstein, a Duke University geneticist who wrote one of the commentaries appearing in the journal.
“With only a few exceptions, what the genomics companies are doing right now is recreational genomics,” Dr. Goldstein said in an interview. “The information has little or in many cases no clinical relevance.”
Unlike the rare diseases caused by a change affecting only one gene, common diseases like cancer and diabetes are caused by a set of several genetic variations in each person. Since these common diseases generally strike later in life, after people have had children, the theory has been that natural selection is powerless to weed them out.
The problem addressed in the commentaries is that these diseases were expected to be promoted by genetic variations that are common in the population. More than 100 genomewide association studies, often involving thousands of patients in several countries, have now been completed for many diseases, and some common variants have been found. But in almost all cases they carry only a modest risk for the disease. Most of the genetic link to disease remains unexplained.
Dr. Goldstein argues that the genetic burden of common diseases must be mostly carried by large numbers of rare variants. In this theory, schizophrenia, say, would be caused by combinations of 1,000 rare genetic variants, not of 10 common genetic variants.
This would be bleak news for those who argue that the common variants detected so far, even if they explain only a small percentage of the risk, will nonetheless identify the biological pathways through which a disease emerges, and hence point to drugs that may correct the errant pathways. If hundreds of rare variants are involved in a disease, they may implicate too much of the body’s biochemistry to be useful.
“In pointing at everything,” Dr. Goldstein writes in the journal, “genetics would point at nothing.”
Two other geneticists, Peter Kraft and David J. Hunter of the Harvard School of Public Health, also writing in the journal, largely agree with Dr. Goldstein in concluding that probably many genetic variants, rather than few, “are responsible for the majority of the inherited risk of each common disease.”
But they disagree with his belief that there will be diminishing returns from more genomewide association studies.
“There will be more common variants to find,” Dr. Hunter said. “It would be unfortunate if we gave up now.”
Dr. Goldstein, however, said it was “beyond the grasp of the genomewide association studies” to find rare variants with small effects, even by recruiting enormous numbers of patients. He said resources should be switched away from these highly expensive studies, which in his view have now done their job.
“If you ask what is the fastest way for us to make progress in genetics that is clinically helpful,” he said, “I am absolutely certain it is to marshal our resources to interrogate full genomes, not in fine-tuning our analyses of common variations.”
He advocates decoding the full DNA of carefully selected patients.
Dr. Kraft and Dr. Hunter say that a person’s genetic risk of common diseases can be estimated only roughly at present but that estimates will improve as more variants are found. But that means any risk estimate offered by personal genomics companies today is unstable, Dr. Kraft said, and subject to upward or downward revision in the future.
Further, people who obtain a genomic risk profile are likely to focus with horror on the disease for which they are told they are at highest risk. Yet this is almost certain to be an overestimate, Dr. Kraft said.
The reason is that the many risk estimates derived from a person’s genomic data will include some that are too high and some that are too low. So any estimate of high risk is likely to be too high. The phenomenon is called the “winner’s curse,” by analogy to auctions in which the true value of an item is probably the average of all bids; the winner by definition has bid higher than that, and so has overpaid.
Dr. Kari Stefansson, chief executive of deCODE Genetics, an Icelandic gene-hunting company that also offers a personal genome testing service, said deCODE alerted clients to pay attention to diseases for which testing shows their risk is three times as great as average, not to trivial increases in risk.
Dr. Stefansson said his company had discovered 60 percent of the disease variants known so far.
“We have beaten them in every aspect of the game,” he said of rival gene hunters at American and British universities.
The undiscovered share of genetic risk for common diseases, he said, probably lies not with rare variants, as suggested by Dr. Goldstein, but in unexpected biological mechanisms. DeCODE has found, for instance, that the same genetic variant carries risks that differ depending on whether it is inherited from the mother or the father.
Intellectual
04-19-2009, 06:37 AM
These companies are probably not performing any useful service at present, said David B. Goldstein, a Duke University geneticist who wrote one of the commentaries appearing in the journal.
“With only a few exceptions, what the genomics companies are doing right now is recreational genomics,” Dr. Goldstein said in an interview. “The information has little or in many cases no clinical relevance.”
Except for jews, according to Goldstein.
Jacob's Legacy: A Genetic View of Jewish History (Hardcover)
by David B. Goldstein
From Publishers Weekly
Duke University geneticist Goldstein was part of a team that did groundbreaking, headline-making research on Jewish genetic history. Goldstein clearly and succinctly explains such concepts as haplotypes and genetic drift as he reviews such findings as that more than half of contemporary Cohanim, or priests—traditionally believed to descend from the biblical Aaron—actually share a genetic marker called the Cohen Modal Haplotype. Among other subjects, he also explores evidence consistent with the claim of the obscure Lemba tribe of southern Africa to be descendants of ancient Israel.
http://www.amazon.ca/Jacobs-Legacy-Genetic-Jewish-History/dp/0300125836
David B. Goldstein only thinks Jews are genetically different. While the other races are cattle or goyim.
Gregz
05-02-2009, 01:51 PM
Jews are obsessed with there own blood lines. Goldstein like all biologists is a Jerk off!
Now that Bush is gone and the flat earth lobby are out the way. The US has restarted embryological research. :222:
Jews are obsessed with there own blood lines. Goldstein like all biologists is a Jerk off!
Sounds like you're a genetic-determinist who does not like to hear the information presented on this thread - you are wrong if you think you can overturn it all with ad hominem attack at one researcher.
Now that Bush is gone and the flat earth lobby are out the way. The US has restarted embryological research. :222:
Was that supposed to be a slam at principled people who oppose massively-overhyped ESC vampirism?
Petr
Except for jews, according to Goldstein.
Well, besides Goldstein I can now cite Craig Venter, the current big hero of genetics for his creation of "synthetic genome", on the limits of genetic medicine:
http://www.spiegel.de/international/world/0,1518,709174,00.html
07/29/2010
SPIEGEL Interview with Craig Venter
'We Have Learned Nothing from the Genome'
...
SPIEGEL: The genome project hasn't just raised hopes -- but also worries. Do you understand those concerns?
Venter: Yes. There are two groups of people. People either want to know the information or they prefer to live like an ostrich with their head in the sand, not knowing anything. The fear is based on the ill-founded belief that those who know the DNA sequence also know every aspect of life. This nonsense has been spread by the same geneticists who were afraid of the commercialization of this stuff. From the time of the first few discoveries of gene defects -- Huntington's disease, for example, everybody thought that if you knew your genome, you would know when you would die and what you would die from. That is nonsense.
SPIEGEL: So the significance of the genome isn't so great after all?
Venter: Not at all. I can tell you from my own experience. I put my own genome on the Internet. People had the notion this was the scariest thing out there. But what happened? Nothing.
SPIEGEL: Nevertheless, Jim Watson, the co-discoverer of the DNA double helix, has said he doesn't want to know which variant of the so-called ApoE gene he has -- it could say something about his risk for developing Alzheimer's, and he's afraid of that …
Venter: That was silliness. At that age? Watson is over 80.
SPIEGEL: Are you interested in finding out what ApoE variant you have?
Venter: I know it. And according to it, I have a slightly increased risk for Alzheimer's disease. But it impresses me little because I could have dozens of other genes that counteract it. Because we do not know that, this information is meaningless.
SPIEGEL: And what about the fears about the abuse of gene data through insurers or employers, for example? Do you see that as sheer hysteria?
Venter: Abuse is not a question of whether the data is available. It is an issue of laws. You can't do anything to change the availability of genetic data. Look at this bottle that you have touched -- that's all I need to obtain your entire genetic information.
SPIEGEL: How much would you be able to learn about us by doing so?
Venter: If anything, we don't really know how to read the genome and it can't tell us very much right now. So what's the ethical debate about?
SPIEGEL: The decoding of your personal genome has so far revealed little more than the fact that your ear wax tends to be moist.
Venter: That's what you say. And what else have I learned from my genome? Very little. We couldn't even be certain from my genome what my eye color was. Isn't that sad? Everyone was looking for miracle 'yes/no' answers in the genome. "Yes, you'll have cancer." Or "No, you won't have cancer." But that's just not the way it is.
SPIEGEL: So the Human Genome Project has had very little medical benefits so far?
Venter: Close to zero to put it precisely.
SPIEGEL: Did it at least provide us with some new knowledge?
Venter: It certainly has. Eleven years ago, we didn't even know how many genes humans have. Many estimated that number at 100,000, and some went as high as 300,000. We made a lot of enemies when we claimed that there appeared to be considerably fewer -- probably closer to the neighborhood of 40,000! And then we found out that there are only half as many. I was just in Stockholm for the 200th anniversary of the Karolinska Institute. The first presentation was about the many achievements the decoding of the genome has brought. Then I spoke and said that this century will be remembered for how little, and not how much, happened in this field.
SPIEGEL: Why is it taking so long for the results of genome research to be applied in medicine?
Venter: Because we have, in truth, learned nothing from the genome other than probabilities. How does a 1 or 3 percent increased risk for something translate into the clinic? It is useless information.
SPIEGEL: There are hundreds of hereditary diseases that can be traced to defects in individual genes. You can determine a lot more than just probabilities through them. But that still hasn't led to a flood of new treatments.
Venter: There were false expectations. Take Ataxia telangiectasia, for example, a horrible disease. The nervous system degenerates, and people who have it often die in their early teens. The cause is a defect in a single gene, but it is a developmental gene. If your body is built in the wrong way, then you can't just take a magic pill to rebuild it. If your brain is wired wrong, then it is wired wrong.
SPIEGEL: Who is to blame for those false expectations?
Venter: We were simply always looking at single genes because they were the only genes we had. When people lose their keys at night, they look under the lamp post. Why? Because that's where you can still see something.
SPIEGEL: But the keys are really located in the dark?
Venter: Exactly. Why did people think there were so many human genes? It's because they thought there was going to be one gene for each human trait. And if you want to cure greed, you change the greed gene, right? Or the envy gene, which is probably far more dangerous. But it turns out that we're pretty complex. If you want to find out why someone gets Alzheimer's or cancer, then it is not enough to look at one gene. To do so, we have to have the whole picture. It's like saying you want to explore Valencia and the only thing you can see is this table. You see a little rust, but that tells you nothing about Valencia other than that the air is maybe salty. That's where we are with the genome. We know nothing.
SPIEGEL: Do you think there will be a time when you can extract all this information to yield real medical results?
Venter: For that to happen we need a lot more information: Information about your body's chemistry, your physiology, your complete medical history, your brain and your entire life. We would need to do that a million times on different people and correlate that data with their genetic information.
SPIEGEL: Will that lead in the end to the kind of personalized medicine that genetic researchers have always touted? Each person would get his or her own personal treatment that is tailored precisely to that person's genetic make-up?
Venter: That was another one of these silly naïve notions that was out there. It's not, 'Oh, we know your genome, we're going to make this drug for you.' That will never happen. It is more important that you use the information in the genome about your personal risks and reduce them through intelligent behavior.
Brechun
08-04-2010, 05:36 AM
What became of the claim in the OP of revising the entire concept of the gene and questioning it even exists?
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