Register | Sign In


Understanding through Discussion


EvC Forum active members: 64 (9164 total)
6 online now:
Newest Member: ChatGPT
Post Volume: Total: 916,844 Year: 4,101/9,624 Month: 972/974 Week: 299/286 Day: 20/40 Hour: 1/3


Thread  Details

Email This Thread
Newer Topic | Older Topic
  
Author Topic:   Bill Nye vs. Ken Ham
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


Message 257 of 824 (718998)
02-10-2014 5:56 AM
Reply to: Message 256 by Faith
02-10-2014 5:01 AM


I call it ordinary microevolution, there's nothing "super" about it.
What is to prevent microevolution from becoming macroevolution?

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 256 by Faith, posted 02-10-2014 5:01 AM Faith has replied

Replies to this message:
 Message 266 by arachnophilia, posted 02-10-2014 6:46 PM DevilsAdvocate has not replied
 Message 275 by Faith, posted 02-11-2014 2:36 AM DevilsAdvocate has replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


(1)
Message 282 of 824 (719085)
02-11-2014 8:43 AM
Reply to: Message 275 by Faith
02-11-2014 2:36 AM


Re: Why microevolution doesn't become macroevolution
I think the processes that bring about evolution or the development of varieties or races, etc., require the reduction of genetic diversity because alleles for traits other than those of the identifiable variety or race have to be eliminated from the gene pool.
That is completely not true. Where do you get that evolution (whether micro or macro) REQUIRES a reduction in genetic diversity? There is no requirement for traits to be eliminated from the gene pool. Evolution itself is based on the introduction of new traits (heterozygous alleles) through mutation, gene flow, genetic shuffling and other factors to create new species. If you mean that species are subject to a genetic reduction of diversity that is partly true only in the fact that once a new species comes into existance, natural selection and other factors winnow out the outlier species population to create a more genetically similar population. However, this is a balancing act between forces which narrow down genetic diversity (i.e. natural selection, genetic drift, etc) and those that increase genetic diversity (introduce new genetic traits).
For a trait to "breed true" requires homozygosity for that trait, that is, NO other alleles than those that determine that trait.
Yes, but organisms do not need to be homozygous to be a species. In fact humans as well as many other animals are both homozygous and heterozygous for many of their traits (alleles). Pure bred (homozygous) is not required for the evolution of species.
What this means is that as any particular variety develops the GENETIC ability to keep on varying becomes less and less, which is the opposite of what the ToE requires.
Word salad. For a 'variety' or trait (allele) to perpetuate, that is somewhat true only in the fact that if the trait changed it would no longer be that trait. This may or may not have an effect (either beneficial or detrimental or neutral to the survival of that species) on the evolution of an organism. However, this in no way contradicts the TOE.
So you reach a point through evolution where evolution is simply no longer possible.
Which is completely opposite of what YEC teach. They require super-evolution to create the diversity of life from 'kinds' that existed after the flood.
You are self-contradictory and have a poor understanding of the TOE.
Edited by DevilsAdvocate, : No reason given.
Edited by DevilsAdvocate, : No reason given.
Edited by DevilsAdvocate, : No reason given.

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 275 by Faith, posted 02-11-2014 2:36 AM Faith has replied

Replies to this message:
 Message 290 by Faith, posted 02-11-2014 12:53 PM DevilsAdvocate has replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


(1)
Message 295 of 824 (719126)
02-11-2014 3:58 PM
Reply to: Message 290 by Faith
02-11-2014 12:53 PM


Re: Why microevolution doesn't become macroevolution
It's clearer if you think about what happens in domestic breeding, where the main method of getting a breed is to eliminate unwanted traits, which means eliminating the genetic stuff for those traits, meaning the alleles for those other traits. In the wild the culling may not be so drastic.
Which is an event which is intentionally directed by human intelligence not a natural process. So your point is void.
Or if you get a bottleneck as happened with the cheetah, it may. and of course it will be random unless there is a strong natural selection involved.
Again, one case of genetic uniformity and bottlenecking in an existing species does not descredit the entire TOE. All this shows is that genetic uniformity and bottlenecking caused by various natural factors may occur in geographically, socially, and genetically isolated populations of organisms.
So in essense you are only showing once side of the genetic equation so to speak. The other side which causes genetic diversity are genetic mutations, gene flow, and natural selection.
Gene flow and genetic shuffling add nothing new to the gene pool
Evolution itself is based on the introduction of new traits (heterozygous alleles) through mutation, gene flow, genetic shuffling and other factors to create new species.
It depends on what you are defining as the "gene pool". Are you talking about the entire genetic makeup of a species. If so you correct. Gene flow by itself does not introduce new traits. However in relation to subgroupings of individual organisms of a species aka populations may have new traits introduced through these mechanisms from one population to the next.
Genetic shuffling also increases the genetic diversity of a population by intermixing alleles (traits) within that species population and a result help to decrease (but not eliminate) the amount of speciation that occurs.
As far as mutations being useless or deleterious that is a seperate subject. Most mutations which are know to occur are neutral not beneficial or harmful, in that they provide minimal impact on an organism. Of course the only ones that make a difference in speciation are those that occur in an organisms gametes.
What you gloss over is that natural selection favors mutations that benefit a species effictively weeding out the deleterious ones. This is the main driver of evolution and you have shown no evidence which contradicts this.
If you do have gene flow it can be a healthy factor in a population by keeping up the genetic variability, and yes a species can have high genetic variability, but I'm trying to keep in focus how new variations develop from former populations and, especially if we're thinking of the situation right after the Flood, that would most likely be from the formation of many daughter populations in reproductive isolation from the parent population.
Again which begs the question of what prevents your in-species evolution from producing enough genetic variation to create new species of organisms that can interbreed. That is these new "daughter" populations are new species that evolved from parent populations just as you suggest. You are making the case for the TOE.
It's really only after many population splits that you should start to see appreciable reduction in genetic variability, but that is the normal trend.
What is the mechanism for this reduction in genetic variability?
You have not provided one. Obviously it is not mutation as it continuously adds diversity to the "gene pool". Gene flow causes more genetic diversity between isolated populations of a species. Genetic shuffling (aka sex) also increases genetic variability within a species.
Two factors that can cause a reduction in genetic variability in a species are natural selection and genetic drift. However, at the same time as reducing genetic variability, these forces are counteracted by the forces of mutation, genertic flow, and shuffling. Occassionally genetic unformity wins out in a species and it becomes extinct or may bottleneck (i.e. the cheetah). Or in other cases genetic isolation of a population may increase to the point that a new species may occur.
The only possible new genetic material would have to come from mutations, and since it is usually understood to take a very long time to produce any kind of beneficial mutation that can be passed on in the population, it's as good as useless anyway.
Mutations do not take a long time to occur. They occur an incalculable number of times every day in organisms around the world.
This is true, but the point is that this is the DIRECTION of variation. You may only see it at the drastic ends of the processes involved. But I think this trend is probably growing for many species.
Provide the evidence.
But in actual fact, the processes that most predictably bring about evolution or variation involve the reduction of genetic diversity.
Again you are unfavorably weighing one side of the equation. Mutations, genetic shuffling and genetic drift cause genetic diversity.
But is this really evolution and where does the population go from there?
If there is enough of a change that this new population cannot interbreed from the original population of organisms it is now a new species aka TOE. What keeps this from happening?
Not required to BE a species, but reduction of genetic diversity IS required for the formation of NEW varieties/"species." Homozygosity is the extreme but I mention it to illustrate the direction.
You are muddying the water metaphorically here. Speciation only requires that one population of a species becomes genetically divergent enough that it can't breed with the original species. So in that respect, genetic diversity must increase between the original population and the new population not the opposite. I think you are possibly confusing this with the fact that genetic drift reintroduces genes between populations of a species and may produce a breaking effect so to speak on speciation (but not eliminating it). Again it is all a balancing act by nature, which can tip one way or another at times depending on the environmental (climate, ecosystem, etc) and other forces involved.
Well, if what you want is actually evolution, which is change in traits, it DOES contradict the ToE.
This may or may not have an effect (either beneficial or detrimental or neutral to the survival of that species) on the evolution of an organism. However, this in no way contradicts the TOE.
How?
To get new phenotypes you reduce the GENETIC variability.
What? That does not even make sense. Do you know what phenotypes are? They are the obserbable traits of an organism. How does a reduction of genetic variability cause new phenotypes. Again word salad.
The creation of daughter populations of necessity is going to lead to reduction of genetic diversity especially over many such splits into further daughter populations
You have not shown any mechanism of how or why this is done.
but each time that happens you'll get new variations or new phenotypes that come to expression because the competition from other traits that characterized the former populations has been suppressed or eliminated
A reduction in genetic diversity is going to cause new variations? What?!? this does not even make sense. That is like saying that as you remove more and more Beetles of other colors from a Volkswagon car lot except for red Beetles you are going to see more and more Beetles of other colors than red appear. This makes no sense. Please read up on Mendelian genetics.
Edited by DevilsAdvocate, : No reason given.
Edited by DevilsAdvocate, : No reason given.

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 290 by Faith, posted 02-11-2014 12:53 PM Faith has not replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


(2)
Message 297 of 824 (719128)
02-11-2014 4:11 PM
Reply to: Message 296 by mike the wiz
02-11-2014 4:05 PM


Re: One Simple Question for Faith
I won't be coming back to EvC, but I just wanted to let you know I think you've made some good points, I know it won't be acknowledged but don't worry, because I am cleverer than most people at this forum, and my opinion is that you've made some good, cogent points. Not to say that to boast, but that you should listen to the person that is perhaps in the best position to judge.
No inflated sense of yourself I see. Why not just stand on a pedstal and say "Nah, nah, nah nah nah, You are all wrong and I am smarter than you." You brought nothing to this debate but arrogance and ignorance.
This is what many would categorize as Humble Bragging.

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 296 by mike the wiz, posted 02-11-2014 4:05 PM mike the wiz has replied

Replies to this message:
 Message 298 by mike the wiz, posted 02-11-2014 4:44 PM DevilsAdvocate has replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


(1)
Message 303 of 824 (719142)
02-11-2014 6:37 PM
Reply to: Message 298 by mike the wiz
02-11-2014 4:44 PM


Re: One Simple Question for Faith
Calm down dear, I was only trying to encourage her, it can be hard being one soldier against the many. Nobody is going to encourage me, that's for sure, so I can at least state some positives about myself.
Encouraging Faith by boasting about yourself. That is a new one.
Those two particular emotive terms, are called epithets. Epithets are usually used IN PLACE of arguments, as with this empty assertion.
That may have applied if you had provided an argument, which you did not. Even so these are not epithets. I did not say 'Mike the Arrogant Buffoon and Ignoramus' which would be an epithet. Instead, these are assessments of your post attempting to "encourage" Faith.
ut I don't feel the need to insult you back, as that would be ad hominem.
Ad hominem only applies if you provided an argument, which you did not. I do not even know what your argument in this debate is. I was ridiculing your ridiculous post defending Faith not a post by you defending YEC.
And largely that's why I urge clever creationists like Faith to not hang around these parts too long, because if they do, they will soon realize that they are expending exponential energy fighting against an angry mob.
I would have thought that was obvious if you had read my posts, it's because I prefer to provide a syllogistic and sound argument to back up my claims, as I so did, without refutation.
What argument!?! What are you talking about. You only posted twice in this thread. Both have nothing to do with the subject of this thread.

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 298 by mike the wiz, posted 02-11-2014 4:44 PM mike the wiz has not replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


Message 328 of 824 (719171)
02-11-2014 10:05 PM
Reply to: Message 325 by Faith
02-11-2014 9:35 PM


Re: genetics
But mutations mostly just change an existing sequence of the DNA into another sequence, they do not change the structure of the genome
These two thing are synonymous. Changing the "sequence of DNA" is changing the genome or genetic information of an organism. It is the same thing. Mutations create new genetic information from existing DNA by modifying the sequence of already existing nucleotides and/or by changing one nucleotide into another (point mutations, insertions and deletions).
, even if mutations did provide viable genetic possibilities, they would only be subject to the same processes of reduction in the formation of new phenotypes anyway. .
How do new phenotypes reduce the effects of mutation on gamete DNA?
Edited by DevilsAdvocate, : No reason given.

This message is a reply to:
 Message 325 by Faith, posted 02-11-2014 9:35 PM Faith has replied

Replies to this message:
 Message 331 by Faith, posted 02-11-2014 11:53 PM DevilsAdvocate has replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


(2)
Message 356 of 824 (719217)
02-12-2014 8:41 AM
Reply to: Message 331 by Faith
02-11-2014 11:53 PM


Re: genetics
Changing the sequence theoretically substitutes one allele for the other at a particular gene locus, so all it changes is what that allele does to that gene, it varies that trait.
Changing the sequence of DNA can create an entirely new allele (trait) that did not previously exist. That is this new sequence of DNA will, in turn, construct new sequences of amino acids which, in turn, combine to form new protiens which, in turn, can alter the morphological characteristics of that type of organism. All that evolution needs to move forward is enough variation in a population to genetically isolate it from other populations of the same species enough to not be able to interbreed with the previous population and thus make a new species.
If it's a gene for eye color, then the mutation may replace an allele for blue eyes with an allele for gray eyes.
Or create an allele for a new trait not previously existing in that type of organism.
But in reality all that usually happens is that nothing changes anyway, OR it simply destroys the allele altogether.
Most mutations are neutral not destructive. That is because many multicellular organisms are diploid and have duplicate chromosomes which can correct or mitigate the effects caused by mutations that may occur on the other chromosome. However, sometimes the effects of mutations (point, insert, deletion, frameshift, etc) overcome this mitigating factor to the point that new traits can come into existence. Since natural selection and other factors weed out the organisms with mutations that are potentially harmful to a species, mutations which cause new traits to be introduced are inherently 'favored' by nature to perpetuate.
In any case this doesn't change anything in the structure of the genome. If it's a cat genome it remains a cat genome.
It changes the sequence of the genome which by definition changes the genome just like changing the amount of ingredients or the procedural steps of a recipe for a cake can change the outcome of that cake (or even create something different from a cake).
Yeah, right, usually either producing no change at all or producing something destructive.
See my explanation above.
Mutations have probably contributed more to junk DNA than anything else.
Junk DNA is a misnomer. Much of this 'junk' DNA actually serves a purpose and is a carry over of mutations from previous generations. The very existence of junk DNA, much carried over from the evolving of one species to another, is evidence for the TOE.
In any case if they did produce something viable it would only be a change in a particular trait, not a change in the formula for the Species itself
Changes in traits combine to change the "formula" for that species.
The point I've been trying to make is that all that changes is within the existing DNA strand, you aren't getting brand new genes for instance, you are only getting one form of a gene in the place of another
A change in the sequence of nucleotides in DNA can produce new traits. Even in single cell organisms such as E-coli bacteria there may be over 4 million base pairs (nucleotides), yet this bacteria only has about 3000 genes. Are you saying that any mutations of this DNA will ONLY result in one of the 3000 pre-defined genes being changed of another, and never creating a new gene with a different sequence of base pairs? If so what is keeping new sequences of gene base pairs other than the already exhibited genes from being created?
The processes that bring out new phenotypes reduce genetic diversity, whether that genetic diversity was built in, which I as a creationist believe it was, or produced by mutations.
No evidence to back up this claim.
Either way the allele is either selected or rejected.
Correct, but this allele (gene sequence) can be a newly introduced one as opposed to one that existed previously in a population so your point it moot.
Below is an example of the evolution of hindwings of fruit flys and beetles caried over by mutations in the regulatory genes of ancestral four wing insects as an example of how mutations in DNA can cause new traits to arise. This is but one of many examples of how mutations can cause new genetic traits to be introduced.
For more in depth analysis of this, here is the link: From DNA to Diversity: Molecular Genetics and the Evolution of Animal Design - Sean B. Carroll, Jennifer K. Grenier, Scott D. Weatherbee - Google Books
Edited by DevilsAdvocate, : No reason given.
Edited by DevilsAdvocate, : No reason given.
Edited by DevilsAdvocate, : No reason given.
Edited by DevilsAdvocate, : No reason given.

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 331 by Faith, posted 02-11-2014 11:53 PM Faith has replied

Replies to this message:
 Message 395 by Faith, posted 02-13-2014 2:49 PM DevilsAdvocate has replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


(2)
Message 373 of 824 (719287)
02-12-2014 6:44 PM
Reply to: Message 371 by Faith
02-12-2014 5:23 PM


Re: One Simple Question for Faith
I don't know how hydraulic sorting would work and neither do you so why are you speculating about it?
Herebedragons is discussing it because you brought it up. Why mention it in the first place if you know nothing about it.
As I said I don't know how it all happened and I don't think it's necessary to explain everything.
Than you know nothing about science. Science is man's attempt to explain the world around him.
But what I do know is that the strata look like they had to have been laid down in a huge deluge. that WOULD have involved transportation in water, and the usual interpretation of them as time periods is ridiculous, I mean insanely ridiculous.
Why would anyone want to engage you on this since you don't even care to back up your claims with any shred of evidence.
I will leave off with these quotes about evidence for you to ponder.
John Adams writes:
Facts are stubborn things; and whatever may be our wishes, our inclinations, or the dictates of our passion, they cannot alter the state of facts and evidence.
John Adams
Isaac Asimov writes:
Don't you believe in flying saucers, they ask me? Don't you believe in telepathy? in ancient astronauts? in the Bermuda triangle? in life after death?
No, I reply. No, no, no, no, and again no.
One person recently, goaded into desperation by the litany of unrelieved negation, burst out "Don't you believe in anything?"
Yes", I said. "I believe in evidence. I believe in observation, measurement, and reasoning, confirmed by independent observers. I'll believe anything, no matter how wild and ridiculous, if there is evidence for it. The wilder and more ridiculous something is, however, the firmer and more solid the evidence will have to be.
Isaac Asimov
Edited by DevilsAdvocate, : No reason given.

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 371 by Faith, posted 02-12-2014 5:23 PM Faith has not replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


(1)
Message 376 of 824 (719294)
02-12-2014 8:43 PM
Reply to: Message 375 by Coyote
02-12-2014 8:33 PM


Re: One Simple Question for Faith
For Faith, the bible trumps any and all evidence no matter what.
I am a church goer and Bible believer, but I accept the reality of evolution. There are many other Bible believers who do not hold the YEC worldview and are able to reconcile the TOE to their world view. The problem is when you hold an interpretation of the Bible which is inconsistent with science and historical evidence. I am probably one of the few admirers of both Carl Sagan, Isaac Asimov and Jesus Christ.

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 375 by Coyote, posted 02-12-2014 8:33 PM Coyote has seen this message but not replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


(1)
Message 411 of 824 (719423)
02-14-2014 12:05 AM
Reply to: Message 395 by Faith
02-13-2014 2:49 PM


Re: genetics
Yes, this is the theory, that it "can create an entirely new allele (trait),".
Actually any mutation or change in the DNA is a "new" allele since an allele is defined as an alternate form of a gene (a sequence of DNA on a chromosome that code for the production of one or more proteins). In other words a mutation causes a change in the DNA sequence through insertion, deletion, frameshift or by point mutation, which in turn changes that gene/allele. So bottom line is, all mutations create new alleles. However, not all changes in alleles cause phenotypic trait (exhibited) changes to that organism or its offspring (depending on whether the mutation was germinal or somatic).
Now, whether these changes cause by mutations are beneficial, harmful or neutral to the organism and its offspring is another matter.
but in actual fact what usually happens is that it makes no difference at all in the trait, OR it changes in the direction of a genetic disease, OR it simply kills the gene altogether
True, in the fact that most mutations are neutral, but what prevents traits from being created which benefit the species. Again you are missing the whole point of natural selection weeding out the organisms with harmful mutations and favoring those with mutations that benefit the species. At the molecular level there is no difference from a beneficial mutation and a deleterious one. A mutation is a mutation in DNA world. It is only at the macroscopic scale of the organism and ultimately a population of genetically similar organisms aka species that it makes a difference.
That's another statement of the theory but the reality is something different.
Please provide evidence for your assertion.
To get that variation in phenotypes through reproductive isolation involves a trend to reduction of genetic variability as I keep arguing.
And which you provide no evidence for.
Again how does variation in phenotypes (aka traits) come about by a reduction in genetic variability (aka traits). Makes no sense and has no evidence to back it up.
You have to get the change in gene frequencies brought about by the formation of a new daughter population to bring out the new phenotypes
Ok, new daughter populations may bring out new phenotypes through the reinforcement of already existing alleles or the creation of new alleles through mutations, which may be either beneficial, neutral or harmful to that population. So yes, this may change the gene frequency of certain alleles (new or existing) in that population.
But if you DO get complete isolation and the inability to interbreed its only a definitional trick to call that a new "species"
Why is this a definitional "trick"? Scientists have been defining species as organisms that have the inability (or near inability, some can breed but produce infertile offspring) to interbreed, for nearly 200 years. So what is your definition of a species? Obviously you are smarter than the millions of biological scientists in the world.
but in fact you've got a reduced genetic variability in that new population now
I think you mean genetic diversity not genetic variation correct? That is you are trying to say that that amount of traits reduces in a new population not that the genetic difference between these traits reduces, correct? Either way, what specifically is causing this. I need to understand what you are trying to say, to see if it is valid or not.
la. It's always assumed you can just go on getting more variability, through mutations or whatever, but in fact you don't.
There are several ways of getting more genetic variation (wider variation between genetic traits of a population): mutations, gene flow and sex (genetic reshuffling of traits). That is a population with a higher mutational rate and/or gene flow and/or sexual activity (especially between those with differing alleles) will create a wider range of genetic variation. Those with the opposite will create a more narrow range of genetic variation. For example, human populations which interbreed more with each other instead of those outside their group will create less genetic variation not more since dominant genes will be reinforced and the recessive genes may eventually be removed from the gene pool hence why you see very few red heads in oriental cultures.
Of course the trend to reduction of genetic variability is really only noticeable if the daughter population is formed from appreciably smaller numbers, but one thing you never get is an increase, which is what the ToE implies and assumes and needs.
You fundamentally misunderstand this process and oversimplify it. Enough genetic variation is needed to make a daughter population of an organism genetically different than its parent to a degree that it can no longer effectively breed with that original population. This can be cause by physical dislocation of the two populations which cause each population to drift apart genetically and/or by a reduction of gene flow caused by numerous reasons between these two populations to the degree that they differ enough genetically to not produce fertile offspring.
Not if the gene is the recipe for eye color. A viable allele for that particular gene is only going to affect eye color. You are not going to get a new trait. For that you need a whole different gene.
You missed my point, mutations can create a new allele from an existing one merely by changing DNA sequence of the existing allele. A change in the structure of the gene i.e. mutations which change the nucleotides will change the gene.
Yes, as to their effect on the organism, but if the process of mutation is in reality a mistake, a disease process, then even if there is no recognizable effect from a particular change, the process is nevertheless destructive to the DNA itself and further mutations would only increase that destructive effect.
Destructive to DNA does not make sense in reference to mutations. Mutations typically don't destroy DNA, destroy usually means eliminating it. We have so many mutations (aka changes) in our DNA that we don't know where previous mutations begin or end. Our DNA is built up over eons of changes aka mutations. Again, it does not make sense to call mutations at the molecular level harmful, beneficial or even neutral. Mutations are mutations. It is only at the organism level and above that these terms make sense.
If you mean harmful to the survival of that particular species than yes the cumulative effect of mutations to an organism's gamete DNA can possibly be destructive to that organism's offspring. But again, natural selection and other factors will weed these individual organisms out of the gene pool or that species may possibly die out because of the cumulative results of the deleterious changes to the DNA.
This is pure theory, an article of faith, in reality it does not happen.
Hand waving away a logical and sound explanation does not help your case. If you don't like it, provide solid reasons why besides just saying it can't or doesn't happen.
Fortunately the effects can be mitigated to some extent but if mutations are basically a disease process, which I believe but the ToE denies and obscures, this is really more theory taken on faith, not reality. A recital of the ToE Creed.
Mutations are not a disease process per se since mutations can be benefit as well as harm the survivability of that species. Mutations are a natural process. Your body, cells, and DNA are in a constant barrage of background (radiation from the Earth, other organisms, and man-made sources) and cosmic radiation which produce a number of mutations in the DNA of your body. However, our DNA is very good at correcting and counteracting these mutations. Basically we have a self-correcting DNA repair system in place. The number I found was that approximately 175 mutations (those that are not corrected) occur in one humans genome during his or her lifetime. And a very small amount of any of these for one individual occur in the gametes and passed down to future generations. However, more primitive organisms have a lower ability to correct these mutations.
Yes, but the gene determines WHAT that sequence is going to do.
No, the gene IS the sequence. A gene is a sequence of DNA which allows the manufacture of amino acids which link up to form proteins.
You are not changing the gene sequence by substituting another allele,
If you change the sequence of nucleotides you ARE creating new alleles than what existed previously.
you are only varying the expression of what that gene is designed to do.
There are typically 88 keys on a modern piano. By changing the sequence of keys played you change the music that is heard. In a similar way changing the sequence of base pairs in a gene may produce a new allele to be introduced. There are over 3 billion base pairs in the human genome and a little over 20,000 protein-coding genes. In fact only a tiny percent, 1.5%, of the entire human genome are protein-coding genes. Therefore if the sequence in even one of these 20,000 genes which an extremely small portion of the genome changes, this can create an entirely new gene/allele and may or may not produce a new phenotypic trait depending on its effect on that organism.
Maybe this illustration will help. It shows a point mutation of a specific nucleotide. This creates a new sequence which in turn depending on its location can create a new variation of a gene aka an allele.
If it makes cat whiskers all the alleles for that gene are going to make cat whiskers of some kind or another, long or short, black or green, curly or straight, thick or thin. They are not going to make something OTHER than cat whiskers.
If a mutation changes the nucleotides in that specific gene than it is possible to vary that cat whisker enough to make it change morphologically.
It can only do what the gene sequence itself is designed to do, make a particular trait,
The modification or "making" of traits over time is what evolution is all about. You are proving the case for the TOE.
Green whiskers instead of yellow etc.
Or lengthening or shortening that whisker until it becomes something other than a whisker.
Maybe it will be so destructive it will eliminate the whiskers altogether
True. I wouldn't call this "destructive" unless it is harmful to the survival of that organism and its offspring.
or make scraggly droopy whiskers or something like that.
You prove my case above.
But it isn't going to affect anything other than the whiskers.
No one mutation typically doesn't affect more than one gene. However, changes in traits over time can cause more morphological changes for the species.
but I don't know what makes a gene a gene. The sequence can change, that's what the different alleles are, changes in that sequence, but still change only the expression of that gene, it isn't going to change what that gene does,
Of course it changes what the gene does. A gene is nothing more than the a protein-coding portion of DNA. So by changing the sequence of nucleotides in a gene you are changing the amino acids that the gene codes for which in turn changes the protein(s) produced. By changing the proteins produced you effectively change the function of the gene. Bottom line is that mutations change the coding of the gene which in turn change what the gene "does".
Something in the design of the DNA, whatever that is. If it were as malleable as you seem to think it is there would never be a recognizable species at all.
I gave you the reason above concerning the human genome in that the higher-level organisms such as humans has an error-correcting mechanism which helps reduce the amount of changes that occur in the genome from one generation to the next. But it is not fool proof. Changes do occur. With lower-level organisms this error-correcting process is much less full proof if it exists at all. Thus the level of mutational changes are higher in these organisms.
There, I argued your own case. You are welcome. Now go do some reading on genetics and microbiology.
phenotypic variation is usually accompanied by a trend to reduction in variability.
Repeating it over and over does not make it true.
Theoretically and only theoretically. All you are stating here is theory.
Theory is the bread and butter to a scientist. Heliocentrism (the idea that the Earth revolves around the Sun) is a "theory" (quotes are for emphasis). Newtons laws (a fancy word for a mathematical explanation of something) of motion are derived from his "theories" on gravitation and other forces, Quantum mechanics is a "theory". General relativity is a "theory". Plate tectonics is a "theory". All of these "theories" have been proven over and over from observation and repeated experimentation by peers to be correct. So to call this a theory is a complement to a scientist, who actually knows what the word "theory" means.
[ABE: In this post I'm mostly countering your theory with my own theory, but all you have posted IS theory and you don't seem to know that. ]
It is not MY theory. It is the Theory of Evolution by Natural Selection which has been peer-review for over 100 years by millions of scientists. And yours is not a theory it is a discombobulated attempt at a hypothesis for why "macroevolution" can not occur brought about by a poor understanding of the subject area.
Edited by DevilsAdvocate, : No reason given.
Edited by DevilsAdvocate, : No reason given.

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 395 by Faith, posted 02-13-2014 2:49 PM Faith has replied

Replies to this message:
 Message 421 by Faith, posted 02-14-2014 1:06 AM DevilsAdvocate has replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


(2)
Message 433 of 824 (719454)
02-14-2014 6:03 AM
Reply to: Message 421 by Faith
02-14-2014 1:06 AM


Re: genetics
This is kind of like saying that you can substitute rat poison for the beef in a recipe for beef stew and it's still beef stew.
Yes, this is the theory, that it "can create an entirely new allele (trait),".
Actually any mutation or change in the DNA is a "new" allele since an allele is defined as an alternate form of a gene (a sequence of DNA on a chromosome that code for the production of one or more proteins). In other words a mutation causes a change in the DNA sequence through insertion, deletion, frameshift or by point mutation, which in turn changes that gene/allele. So bottom line is, all mutations create new alleles. However, not all changes in alleles cause phenotypic trait (exhibited) changes to that organism or its offspring (depending on whether the mutation was germinal or somatic).
That is precisely the opposite of what I am saying. I am saying that the recipe for beef stew will change into something else, i.e. a recipe for beef stroganoff for example. However this would require many changes to the recipe and thus an evolution between these two recipes occur with many beef stew/beef stroganoff intermediates. In short order the beef stew recipe can be adapted and changed just like in your kitchen.
Edited by DevilsAdvocate, : No reason given.

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 421 by Faith, posted 02-14-2014 1:06 AM Faith has replied

Replies to this message:
 Message 443 by Faith, posted 02-14-2014 2:43 PM DevilsAdvocate has replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


(1)
Message 451 of 824 (719550)
02-15-2014 4:10 AM
Reply to: Message 443 by Faith
02-14-2014 2:43 PM


Re: genetics
What you think is just a new tasty recipe is really rat poison.
Not always. Here is one of several examples of a mutation of an existing DNA sequence for a protein of which the mutation provides a beneficial effect to humans. Specifically having to do with a mutation in gene called Apolipoprotein AI used for lipid (fat) metabolism.
This mutation called ApoA-1 Milano manifests itself in the AP AI gene and was discovered to exist in a small group of people of an town in northern Italy called Limone sul Garda. The mutation of this gene is traced back to Giovanni Pomarelli who lived in the late 1700s and early 1800s. This group of people have extremely low amounts of HDL cholesterol, which is the good kind that helps reduce the "bad" LDL cholesterol. However, even though this small group of people had very low amounts of HDL, had poor diets, and many smoked, they have negligible amounts of heart disease. The reason is because they had a mutated form of the AP AI gene which modified the HDL cholesterol to be even more aggressive in getting rid LDL than it would with non-mutated AP AI genes. Here is some more information on this beneficial mutation.
BigThink.com writes:
All humans have a gene for a protein called Apolipoprotein AI, which is part of the system that transports cholesterol through the bloodstream. Apo-AI is one of the HDLs, already known to be beneficial because they remove cholesterol from artery walls. But a small community in Italy is known to have a mutant version of this protein, named Apolipoprotein AI-Milano, or Apo-AIM for short. Apo-AIM is even more effective than Apo-AI at removing cholesterol from cells and dissolving arterial plaques, and additionally functions as an antioxidant, preventing some of the damage from inflammation that normally occurs in arteriosclerosis. People with the Apo-AIM gene have significantly lower levels of risk than the general population for heart attack and stroke, and pharmaceutical companies are looking into marketing an artificial version of the protein as a cardioprotective drug.
Wikipedia writes:
Apolipoprotein A-I is a protein that in humans is encoded by the APOA1 gene.[1][2] It has a specific role in lipid metabolism.
Apolipoprotein A-I is the major protein component of high density lipoprotein (HDL) in plasma...
As a major component of the high-density lipoprotein complex (protective "fat removal" particles), apo A-I helps to clear fats, including cholesterol, from white blood cells within artery walls, making the WBCs less likely to become fat overloaded, transform into foam cells, die and contribute to progressive atheroma. Five of nine men found to carry a mutation (E164X) who were at least 35 years of age had developed premature coronary artery disease. One of four mutants of apo A-I is present in roughly 0.3% of the Japanese population, but is found 6% of those with low HDL cholesterol levels.
ApoA-1 Milano is a naturally occurring mutant of apo A-I, found in a few families in Limone sul Garda, Italy, and, by genetic + church record family tree detective work, traced to a single individual in the 14th century. Described in 1980, it was the first known molecular abnormality of apolipoproteins.[8] Paradoxically, carriers of this mutation have very low HDL-C (HDL-Cholesterol) levels, but no increase in the risk of heart disease, often living to age 100 or older. This unusual observation was what lead Italian investigators to track down what was going on and lead to the discovery of apo A-I Milano (the city, Milano, ~160 KM away, in which the researcher's lab was located). Biochemically, apo A-I contains an extra cysteine bridge, causing it to exist as a homodimer or as a heterodimer with apo A-II. However, the enhanced cardioprotective activity of this mutant (which likely depends on fat & cholesterol efflux) cannot easily be replicated by other cysteine mutants.
Recombinant apo A-I Milano dimers formulated into liposomes can reduce atheromas in animal models by up to 30%.[10] Apo A-I Milano has also been shown in small clinical trials to have a statistically significant effect in reducing (reversing) plaque build-up on arterial walls.
Also
"AIMilano apoprotein identification of the complete kindred and evidence of a dominant genetic transmission" Research Report writes:
The AlMilano apoprotein variant is associated with a marked reduction of high density lipoprotein (HDL) cholesterol levels and with increased triglyceridemia. In spite of the low HDL-cholesterol (HDLCh), carriers do not generally show clinical signs of atherosclerosis. The biochemical disorder is linked to a molecular change in apoprotein Al, that is, an arg -- cys substitution in the 173 position, thus allowing the formation of AIMilano-AIMilano dimers and AIMilano-AII complexes. The origin of the variant gene has been located in Limone sul Garda, a small community in Northern Italy (about 1,000 individuals). This community has a genetic, biochemical, and clinical individuality,
consequent to its isolation up to a few years ago; the citizens show highly uniform alimentary habits and elevated consanguinity.
The complete population of the small village was sampled, and, by the use of an analytical isoelectric focusing technique for the detection of the mutant, a total of 33 living carriers, ranging in age from 2 to 81 yrs, were identified. Analysis of the genealogic tree of the complete family groups showed that the apoprotein (apo) AIMilano is transmitted as an autosomal dominant trait, all carriers coming from a single mating couple, living in the eighteenth century. The carriers are heterozygous for the apoprotein variant.
Research Papers on this beneficial mutation:
Bielicki and Oda (2002) "Apolipoprotein A-IMilano and apolipoprotein A-IParis exhibit an antioxidant activity distinct from that of wild-type apolipoprotein A-I." Biochemistry 41, 2089-2096. [PubMed]
Calabresi L, et al. (1999) "Cell cholesterol efflux to reconstituted high-density lipoproteins containing the apolipoprotein A-IMilano dimer." Biochemistry 38, 16307-14. [PubMed]
Franceschini G, Sirtori M, Gianfranceschi G, Sirtori CR (May 1981). "Relation between the HDL apoproteins and A-I isoproteins in subjects with the AIMilano abnormality". Metab. Clin. Exp. 30 (5): 502—9. doi:10.1016/0026-0495(81)90188-8. PMID 6785551.
Franceschini G, Sirtori CR, Capurso A, Weisgraber KH, Mahley RW (1980). "A-IMilano apoprotein. Decreased high density lipoprotein cholesterol levels with significant lipoprotein modifications and without clinical atherosclerosis in an Italian family" (PDF). J. Clin. Invest. 66 (5): 892—900. doi:10.1172/JCI109956. PMC 371523. PMID 7430351.
Franceschini G, Calabresi L, Chiesa G, Parolini C, Sirtori CR, Canavesi M, Bernini F. (1999) "Increased Cholesterol Efflux Potential of Sera From ApoA-IMilano Carriers and Transgenic Mice." Arterioscler Thromb Vasc Biol. 19, 1257-62. Increased Cholesterol Efflux Potential of Sera From ApoA-IMilano Carriers and Transgenic Mice | Arteriosclerosis, Thrombosis, and Vascular Biology
Gualandri V, Franceschini G, Sirtori CR, Gianfranceschi G, Orsini GB, Cerrone A, Menotti A (1985) "AIMilano apoprotein identification of the complete kindred and evidence of a dominant genetic transmission." Am J Hum Genet. 37, 1083-97
Weisgraber KH, Rall SC, Bersot TP, Mahley RW, Franceschini G, Sirtori CR (25 February 1983). "Apolipoprotein A-IMilano. Detection of normal A-I in affected subjects and evidence for a cysteine for arginine substitution in the variant A-I" (PDF). J. Biol. Chem. 258 (4): 2508—13. PMID 6401735.
Zhu X, Wu G, Zeng W, Xue H, Chen B (2005). "Cysteine mutants of human apolipoprotein A-I: a study of secondary structural and functional properties". J. Lipid Res. 46 (6): 1303—11. doi:10.1194/jlr.M400401-JLR200. PMID 15805548.
Edited by DevilsAdvocate, : No reason given.
Edited by DevilsAdvocate, : No reason given.

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 443 by Faith, posted 02-14-2014 2:43 PM Faith has replied

Replies to this message:
 Message 452 by Faith, posted 02-15-2014 4:16 AM DevilsAdvocate has replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


Message 453 of 824 (719553)
02-15-2014 4:23 AM
Reply to: Message 452 by Faith
02-15-2014 4:16 AM


Re: genetics
How do you know it was a mutation and not simply a normally occurring but rare allele that happens to be possessed by the people identified?
Because it does not exist anywhere else in the human population and can be traced back to one person.
Besides a mutation to a gene is an allele. An allele is just an alternate form of a gene.
Edited by DevilsAdvocate, : No reason given.

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 452 by Faith, posted 02-15-2014 4:16 AM Faith has not replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


(1)
Message 454 of 824 (719554)
02-15-2014 4:30 AM
Reply to: Message 452 by Faith
02-15-2014 4:16 AM


Re: genetics
How do you know it was a mutation and not simply a normally occurring but rare allele that happens to be possessed by the people identified?
I assume your real question is, how do we know this mutation is not a preexisting allele which was original part of the human genome not a mutation that occurred later on, correct? My answer in the previous post explains this. The fact is that all the people with this mutated gene can all trace their lineage back to this one person. No one else has been discovered to have this gene mutation.
There are only 35 people in this small Italian village to have this mutated gene.
Here is the down and dirty on this from a news journalist aspect for those who have a hard time deciphering science journals:
"Why Mutants Might Save My Life" ABC News 13 Oct 2013 http://abcnews.go.com/Health/mutants-save-life/story?id=20720645 writes:
His name is Giovanni Pomarelli from the small Italian Mountain village of Limone sur Garda. He and his descendants have something you and I don't havea specific set of mutant genes...
Giovanni's descendants (about 35) have a much different destiny. They have a rare, unknown until recently, genetic protection against clogged arteries. Many of his family, I hear, eat whatever they want. Some smoke and I'll bet don't even know the recommendations of the American Heart Association. To make it all the more amazing they have bad numbers.hardly any "good" cholesterol or HDL. What they do have is something scientists call the ApoA-Milano protein. It's not normal. There's a spot in that wonderful protein DNA double helix (spot 173) that should be occupied by something called cysteine. Arginine is there instead. It's a mutant.
I've had several conversations with the experts hoping to be able to explain how this all works. I'll save you. They don't know exactly how it all works. The best explanation is the Pomarelli family has their own kind of good cholesterol. It prevents the bad stuff from hanging out in the blood vessels.
Scientists have figured out how to create the ApoA Milano protein. It was tried out in animals, folks in Italy and finally here in the United States. It's as close as they come to an arterial rotor-rooter--Drano for the Heart, to borrow a Time Magazine headline. Forty seven lucky patients finished the U.S. study in just six weeks. In that short amount of time this relentless disease went into reverse. Their arteries were measurably cleaner. The normally conservative scientific community described the results as "dramatic" and "surprising." "We were pretty stunned that in a six-week period of time we could see a significant reduction in the burden of plaque," says study leader Dr. Stephen Nissen. "It showed us the disease was far more malleable, more amenable to very rapid changes than we would have ever guessed."
Edited by DevilsAdvocate, : No reason given.
Edited by DevilsAdvocate, : No reason given.

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 452 by Faith, posted 02-15-2014 4:16 AM Faith has replied

Replies to this message:
 Message 455 by DevilsAdvocate, posted 02-15-2014 4:46 AM DevilsAdvocate has not replied
 Message 456 by Faith, posted 02-15-2014 4:50 AM DevilsAdvocate has replied

  
DevilsAdvocate
Member (Idle past 3129 days)
Posts: 1548
Joined: 06-05-2008


(1)
Message 455 of 824 (719556)
02-15-2014 4:46 AM
Reply to: Message 454 by DevilsAdvocate
02-15-2014 4:30 AM


Re: genetics
BTW, I just noticed the news article is wrong where it says
"Why Mutants Might Save My Life" ABC News 13 Oct 2013 http://abcnews.go.com/Health/mutants-save-life/story?id=20720645 writes:
There's a spot in that wonderful protein DNA double helix (spot 173) that should be occupied by something called cysteine. Arginine is there instead.
This is totally BS in that DNA is not a protein, and cysteine and arginine are the amino acids coded by DNA, they do not exist in the DNA. This is what happens when idiot reporters try to report on science.
Here is a better news article:
"Drug removes arterial plaque in surprising clinical trial" Baltimore Sun writes:
A small clinical trial has shown for the first time that it is possible to use drugs to remove plaque from clogged arteries, a finding that could lead to radically new ways to treat heart disease, the No. 1 killer in the United States.
Infusions of a genetically engineered mutant form of high-density lipoprotein, the so-called good cholesterol, over a five-week period were shown to reduce plaque volume in patients suffering from chest pain.
"This is an extraordinary and unprecedented finding," said Dr. Steven E. Nissen of the Cleveland Clinic Foundation, who led the study reported in today's issue of The Journal of the American Medical Association.
Current therapies targeting cholesterol use a family of drugs called statins to reduce levels of low-density lipoproteins, the "bad cholesterol."
Increasing good cholesterol, or HDL, is not only substantially more effective at reducing plaque, but also appears to change its composition, stabilizing it so that chunks are less likely to break off and cause heart attacks or strokes.
Surgical alternatives for eliminating blockages include angioplasty (in which a balloon is used to smash the plaque flat) and coronary artery bypass surgery. Both treat only small blockages, however, while the new approach works throughout the body.
"The results of this study are surprising to even the most optimistic supporters of the concept of targeting HDL as a therapy for atherosclerosis," wrote Dr. Daniel J. Rader of the University of Pennsylvania School of Medicine in an editorial in the same issue. He suggested that HDL-targeted therapies could be one of the most important clinical developments of the next two decades.
And researchers owe it all to a young man named Giovanni Pomarelli, who was born in the small northern Italian village of Limone sur Garda in 1780. Although he didn't know it, he was born with a genetic mutation that proved highly beneficial.
Two centuries later, a team led by Dr. Cesare Sirtori of the University of Milan discovered that about 40 residents of Limone had unusually low levels of HDL but were nonetheless exceptionally healthy. Even though they ate poor diets and most of them smoked, their arteries were largely free of cholesterol deposits. Their one common ancestor was Pomarelli.
Sirtori found that they carried a mutant gene that served as the blueprint for a protein called apolipoprotein A-1, or ApoA-1, a key component of HDL. Those with this mutant form, called ApoA-1 Milano, have HDL that is apparently unusually aggressive at removing LDL from the circulation. In essence, the mutant HDL seemed to protect its bearer from heart disease.
This speculation was confirmed during the 1990s in an elegant set of animal experiments by Dr. P.K. Shah of the Cedars-Sinai Medical Center in Los Angeles. Shah found that infusions of a synthetically produced ApoA-1 Milano in a complex with phospholipids could block the buildup of plaque in the arteries of mice and rabbits with high cholesterol and could even repair damage that had already been done, actually causing plaque to shrink.
The mutant HDL also changed the composition of the remaining plaque, removing triglycerides and inflammatory cytokines, thereby making the plaque more stable and less likely to fragment.
Nissen and his colleagues decided to test this approach in humans, even though they were skeptical that it would work.
"It seemed improbable, but it appeared the drug had the potential to cull plaque out of arteries in weeks, not years," he said. "We thought it was a long shot, not even a 1-in-10,000 chance, but it did work. We were rather pleased, but very surprised."
They enrolled 57 patients with acute coronary syndrome, all of whom suffered chest pains, had high levels of cholesterol and suffered partial artery blockages that were not yet severe enough to require angioplasty or bypasses; 47 completed the study.
Thirty-six of the patients received weekly infusions of the synthetic mutant HDL - produced by Esperion Therapeutics Inc. of Ann Arbor, Mich. - for five weeks and 11 received a placebo. The size of their atherosclerotic plaques was measured before and after the treatment using an ultrasound probe that fit inside the artery.
They reported that the volume of plaque was reduced by an average of 4.2 percent in those receiving the treatment, while the volume increased slightly in those receiving the placebo. Although that seems a small decrease, it is actually much larger than that achieved with any other technique, Nissen said.
With the statin drugs, "reversal of plaque is rare and, even when it occurs, it takes many months to years to see regression," Shah said. The new results "provide proof of the concept that HDL-based therapy has the potential to rapidly and favorably change human atherosclerotic plaques."
Nissen said the speed with which results were observed "tells us something very important about the biology of heart disease: that it is a dynamic process that can be reversed rapidly."
Researchers already knew that lowering LDL was an important way of fighting heart disease.
"Now we know that raising HDL is a really important therapeutic target," Nissen said. "If we can find a way to both lower LDL and raise HDL, we have a real chance to make a huge impact on millions of patients with coronary heart disease."
The next step is a much larger trial to determine whether the therapy reduces the incidence of heart attacks and strokes. Nissen and others have begun planning such a trial, but it is not clear who will pay for it, he said.
Now that his group has proved that HDL manipulation can be clinically useful, Nissen said, "There is going to be a frenzy of activity to understand what happened, why it worked, and how we can do this for the most patients at the least cost."
Edited by DevilsAdvocate, : No reason given.

"It is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring." - Carl Sagan, The Demon-Haunted World

This message is a reply to:
 Message 454 by DevilsAdvocate, posted 02-15-2014 4:30 AM DevilsAdvocate has not replied

  
Newer Topic | Older Topic
Jump to:


Copyright 2001-2023 by EvC Forum, All Rights Reserved

™ Version 4.2
Innovative software from Qwixotic © 2024