The Theory of Evolution

[ForThePeople]

Originally posted by: rahvin

Originally posted by: ForThePeople
Your numbers are wrong. It is 80-140x more likely for DVT as a homo and 8-10x as a hetero. It is beneficial because it overclots where other disorders underclot, it persists in those same populations.

It's bad that you need warfarin but if you had Factor VIII deficiency you would love your Leiden, I promise you.

And yes, I am a medical student. If you want much more info on it you can see my earlier post on the other evolution thread.

As far as the numbers, they change them every year, my numbers were accurate for 2001.

It persists because (before medical intradiction) the condition often doesn't have symptoms until well after puberty is reached often allowing a person to have offspring before it kills them. It also doesn't propagate further (beyond the 2% that have it) because it causes blood clots in the placenta of women with the condition often making it nearly impossible for them to have children. (It's a standard test in infertility exams). I'm well aware that other blood mutations are far more dangerous but to use that as an excuse to call Factor V beneficial is just inconcievable. As opposed to other mutations it may be less bad, but as opposed to normal clotting, Factor V is a dissadvantage in most cases and as a result a bad mutation. And myself and the thousands of other people that are on warfarin as a result of the mutation are testament to that.

I'm doing a study right now to really nail down that number. We're testing everyone who comes to our service with a DVT for Leiden.

And when I say "persist" I don't mean that it concerns one person - I mean it persists in the gene pool, that it is a heritable variation that had been passed down. It is very unusual for single point mutations to persist in a gene pool, basically because there is an extra copy of a perfectly correct one right next door. The easiest types of mutations to correct are single point mutations. So if one sticks around there is a reason.

It is about 5% of the US population that is either heterozygous or homozygous, the vast majority are hetero and have no symptoms for any of their life. It is in the homozygous, the rare minority, that we find lots of problems.

Factor V most decidedly is a good mutation. The carriers (heterozygotes) suffer no ill effects and only the homozygous bear the brunt of it's bad effects. For populations that have clotting problems a heterozygous condition will likely compensate for their other problems, making it very beneficial.

So it sucks to be one of the rare minority homozygous for a defect. But if 1 / 10,000 people suffer so that 500 / 10,000 benefit it is clearly beneficial.

That's evolution for you - it's about survival of the fittest and life sucks if you happen to not be one of the fittest.

 

[rahvin]

And when I say "persist" I don't mean that it concerns one person - I mean it persists in the gene pool, that it is a heritable variation that had been passed down.

As was I. I believe it presists in the population because the people that have it reproduce before they die.

It is about 5% of the US population that is either heterozygous or homozygous, the vast majority are hetero and have no symptoms for any of their life. It is in the homozygous, the rare minority, that we find lots of problems.

I'm heterozygous, and I've met quite a few people that are as well, while waiting for my blood tests at the anti-coagulation clinic. It's dishonest to say that heterozygous don't have problems. Personally I'm quite convinced that a lot of people that die of blood clots in their 20's are Factor V and untested.

You act as if Factor V is equivalent to the anemia mutation which is beneficial in a malaria prone area, but it isn't. It has no proven benefit and only documented negatives. DVT's are not a good thing. You need to be carefull in your statements that we know all about such things like Factor V. It's an incredibly new detection (on the timescale of medicine) and it's NOT fully understood. The simple fact that you can make the statement that no heterozygous have problems when in fact they do is a perfect example of that.

I stand by my statement that Factor V is NOT a beneficial mutation, and I stand by that posistion as someone who nearly went blind because of an SVT directly attributed to my Factor V mutation.

 

[ForThePeople]

Originally posted by: rahvin

And when I say "persist" I don't mean that it concerns one person - I mean it persists in the gene pool, that it is a heritable variation that had been passed down.

As was I. I believe it presists in the population because the people that have it reproduce before they die.

It is about 5% of the US population that is either heterozygous or homozygous, the vast majority are hetero and have no symptoms for any of their life. It is in the homozygous, the rare minority, that we find lots of problems.

I'm heterozygous, and I've met quite a few people that are as well, while waiting for my blood tests at the anti-coagulation clinic. It's dishonest to say that heterozygous don't have problems. Personally I'm quite convinced that a lot of people that die of blood clots in their 20's are Factor V and untested.

You act as if Factor V is equivalent to the anemia mutation which is beneficial in a malaria prone area, but it isn't. It has no proven benefit and only documented negatives. DVT's are not a good thing. You need to be carefull in your statements that we know all about such things like Factor V. It's an incredibly new detection (on the timescale of medicine) and it's NOT fully understood. The simple fact that you can make the statement that no heterozygous have problems when in fact they do is a perfect example of that.

I stand by my statement that Factor V is NOT a beneficial mutation, and I stand by that posistion as someone who nearly went blind because of an SVT directly attributed to my Factor V mutation.

You'll note my "vast majority" part. I didn't say all, I said "vast majority."

So you are in the thin minority of heterozygous people with actual problems.

But let's do some math... Let's say the US has 300 million people and that Factor V prevalence is 5%. So about 15,000,000 people have at least 1 bad gene. Do you think that we see anywhere near that number? Do you think that 1 out of 20 of my patients have clotting problems? That's absurd.

You are in the tiny minority of people that are heterozygous and develop real problems.

Let me give you an analogy. If you look at people who have gallstones (about 20% of the population), then about 80% of them will never have any problems at all. But that other 20% - the ones who do have problems - will have recurring, constant problems. So about 4% of the population gets the bad end of the deal and has problematic gallstones while 96% escape with no problem, including 80% of people with gallstones.

So it sucks to be the 4% but not in the 96% - and here you are in the 4% type role. I feel bad for you, trust me I do, but that mutation has helped people with serious hemophilia not bleed to death. It most certainly is beneficial.

Medicine and evolution are full of these kinds of trade offs where one group suffers while the majority gets away scott free.

 

[cquark]

Originally posted by: Fox5

Originally posted by: cquark

Originally posted by: Tommunist
another reason to continue funding PBS....

True, especially as the anti-evolution Discovery Institute is one of the main political movers behind the threat of defunding PBS.

Discovery Institute doesn't equal the Discovery channel right? Cause that's a pretty kick ass channel.

No, the Discovery channel is a product of Discovery Communications Inc., which is a private corporation not owned by the Discovery Institute.

 

[rahvin]

Originally posted by: ForThePeople
So it sucks to be the 4% but not in the 96% - and here you are in the 4% type role. I feel bad for you, trust me I do, but that mutation has helped people with serious hemophilia not bleed to death. It most certainly is beneficial.

So the (most common blood coagulation disorder) mutation that can kill you is a good mutation because it can help someone else that has a different (and much more rare) mutation that is worse? :roll:

You will pardon me if I don't agree with your assertians.

Factor V Leiden is the most common hereditary blood coagualtion disorder in the United States. It is present 5% of the in the Caucasian population and 1.2% of the African American population.

Factor V Leiden increases the risk of venous thrombosis 3-8 fold for heterozygous (one bad gene inherited) and substantially more, 30-140 fold, for homozygous (two bad gene inherited) individuals.

The prothrombin 20210 mutation is the second most common inherited clotting abnormality. It is more common than protein S and C deficiency and Antithrombin deficiency combined; 2% of the general population is heterozygous. It is only a mild risk factor for clots, but together with other risk factors (such as oral contraceptives, surgery, trauma, high blood pressure, obesity, smoking, etc) or combined with other clotting disorders (like Factor V Leiden), the risk of clotting increases dramatically.

 

[ForThePeople]

Originally posted by: rahvin

Originally posted by: ForThePeople
So it sucks to be the 4% but not in the 96% - and here you are in the 4% type role. I feel bad for you, trust me I do, but that mutation has helped people with serious hemophilia not bleed to death. It most certainly is beneficial.

So the (most common blood coagulation disorder) mutation that can kill you is a good mutation because it can help someone else that has a different (and much more rare) mutation that is worse?

You will pardon me if I don't agree with your assertians.

Absolutely. That's exactly what I am describing. Sickle cell carrier is a bad thing in America - but if we suddenly had an outbreak of malaria it would be a very good thing to have. Evolutions concerns both the organism and the environment.

Clotting disorders tend to run together because they are probably near each other on a chromosome. In reality there is not perfectly random assortment.

Factor V Leiden amplification (going from rare to common) is a result of many already completed evolutionary forces, including probably the founder effect. It is a pain in the butt today because we don't have the same problems that it solved - just like how we lack malaria - but it is beneficial.

It is the most common in the US because the US was settled by white Europeans, who, in turn, used to be the population affected. When you settle a new land you bring your genetic problems with you, and because you have cut yourself off from the main population you will amplify any problems that you do have. Add some time and you'll have what we see in Factor V today.

As to my assertions you don't have to agree with them but that doesn't make them wrong.

You got the raw end of the stick, I feel for you, but such is life.

 

[dannybin1742]

this may be a little OT at this stage of the thread, but for prebiotic life conditions, there are two good articles in may 13 2005 journal science

the first one is an article showing evolution of complex hydrocarbons in titan's atmosphere (moon of saturn), with direct comparison's to what earth's early atmosphere was p975

the first paragraph of the article talks about similarities between titan's atmosphere and earth's early atmosphere

high N2 and CH4 concentrations, compounds detected so far are

C2H6, C2H2, C3H8, HCN, C2H4, CO2, C3H4, C4H2, HC3N

for anyone interested in prebiotic conditions


the second article is about hydrogen escape in early earth atmosphere that has a direct impact on formation of biological molecules, in an ANOXIC (no free oxygen) environment, with high levels of CO2

both are interesting reads, if you know a library that has a subscription


also, rip: science has changed immensly in the last 20 years, even biochem has changed alot in the last 5 years, the knowledge back then is nothing compared to what is known now, a simple indicator is to look at the number of deposited structures in the protein databank, and look at the rate increases of the last 5 years, it follows the rise of computers, also look athe number of papers published, it parralells growth of computer speed, simple because in many areas of science the technology wasn't there to test theory yet, now for the most part it is

 

[cquark]

As most of you know, new features typically arise in a population through duplication of genes, followed by adaptation of the duplicates to perform new functions. This mechanism works because the organism doesn't need the duplicate genes to perform their original task, as the original version of the gene is already doing that job adequately. We can see the effects of this mechanism in the nine different globin genes on two different chromosomes in humans, all of which can be traced back to a single ancestor.

Ignoring this well-known mechanism and claiming as a result that genes can't adapt because organisms need them to do their original job is a standard argument of ID propagandists, as we have seen many times. That's boring. What's interesting is a new exploration of the details of this mechanism published in Nat. Genet. this month.

Science and Sensibility blog offers a popular explanation of the model at
http://science_boy.blogspot.com/2005/06/how-do-old-genomes-learn-new-tricks.html

Breaking it down to the bare essentials Francino's model involves four stages:

1. A new biochemical niche appears - perhaps a new signalling chemical or DNA sequence that would be advantageous for an organism to recognise
2. This niche is then filled by the duplication of an existing gene that currently performs a chemically related but distinct role.
3. Mutations will then crop up in the duplicates that make some of the duplicate genes better at performing the new biochemical trick
4. Selection will fix the best of the duplicates while others fall by the wayside

What's more exciting is that research to be published next month should offer evidence of whether her extended model is correct or not, so we should know soon which version of the model works in nature.

 

[NeenerNeener]

Can someone point me to a good website that has a breakdown of the human genome (the entire code) with all the regions we know about and possibly what they do?

 

[ForThePeople]

Originally posted by: NeenerNeener
Can someone point me to a good website that has a breakdown of the human genome (the entire code) with all the regions we know about and possibly what they do?

Google is your friend.

http://www.ncbi.nlm.nih.gov/entrez/quer...=Retrieve&dopt=Overview&list_uids=9558

You aren't likely to see an entire reprinting as it is 3+ billion base pairs long. But here it is chromosome by chromosome.

 

[rahvin]

Originally posted by: NeenerNeener
Can someone point me to a good website that has a breakdown of the human genome (the entire code) with all the regions we know about and possibly what they do?

Could you point me to a good website that has detailed trade secrets of every US corporation or provides new cars for $1?

 

[dannybin1742]

what?

 

[NeenerNeener]

Originally posted by: ForThePeople

Originally posted by: NeenerNeener
Can someone point me to a good website that has a breakdown of the human genome (the entire code) with all the regions we know about and possibly what they do?

Google is your friend.

http://www.ncbi.nlm.nih.gov/entrez/quer...=Retrieve&dopt=Overview&list_uids=9558

You aren't likely to see an entire reprinting as it is 3+ billion base pairs long. But here it is chromosome by chromosome.

Sweet! Thanks.

 

[Riprorin]

Originally posted by: ForThePeople

Originally posted by: rahvin

Originally posted by: ForThePeople
So it sucks to be the 4% but not in the 96% - and here you are in the 4% type role. I feel bad for you, trust me I do, but that mutation has helped people with serious hemophilia not bleed to death. It most certainly is beneficial.

So the (most common blood coagulation disorder) mutation that can kill you is a good mutation because it can help someone else that has a different (and much more rare) mutation that is worse?

You will pardon me if I don't agree with your assertians.

Absolutely. That's exactly what I am describing. Sickle cell carrier is a bad thing in America - but if we suddenly had an outbreak of malaria it would be a very good thing to have. Evolutions concerns both the organism and the environment.

Clotting disorders tend to run together because they are probably near each other on a chromosome. In reality there is not perfectly random assortment.

Factor V Leiden amplification (going from rare to common) is a result of many already completed evolutionary forces, including probably the founder effect. It is a pain in the butt today because we don't have the same problems that it solved - just like how we lack malaria - but it is beneficial.

It is the most common in the US because the US was settled by white Europeans, who, in turn, used to be the population affected. When you settle a new land you bring your genetic problems with you, and because you have cut yourself off from the main population you will amplify any problems that you do have. Add some time and you'll have what we see in Factor V today.

As to my assertions you don't have to agree with them but that doesn't make them wrong.

You got the raw end of the stick, I feel for you, but such is life.

You cite sicke-sell as a "beneficial" mutation since people who have sickle-cell anemia are less likely to contract malaria.

Yet, sickle-cell produce anemia prevents the proper absorbtion of food and oxygen.

If I became a qudraplegic, I would be less likely to killed in a bicycle accident since I'd be in a wheel chair and not likely riding a bike.

Is having a 25% less chance of contracting malaria advantageous versus suffering premature death as a result of having sickle cell?

 

[shira]

Originally posted by: Riprorin
Is having a 25% less chance of contracting malaria advantageous versus suffering premature death as a result of having sickle cell?

You've got your numbers confused.

Assume that a person how has two copies of the sickle-cell gene will not survive to sexual maturity (and won't reproduce).

Now, if two adults, each with one copy of the gene produce offspring:

1 in 4 will get two copies of the gene, and will die.

2 in 4 will get one copy of the gene, and will live (and be immune to malaria).

1 in 4 will get no copies of the gene, and will live, but will be susceptible to malaria (and may die young because of it).

Now assume two adults without gene produce four children:

4 out of 4 children will get no copies of the gene, and will live, but will be suseptible to malaria (and may die young because of it).

So we end up with 2 children with the gene, immune to malaria.

And we end up with 5 children without the gene, susceptible to malaria.

Sooooo,

If the early mortality rate from malaria is at least 60% (so that at least 3 of the 5 children without the gene will die), more offspring WITH the gene will survive to reproduce than will children without the gene.

Thus, if extremely virulent strains of malaria occur (strains with high death rates), the incidence of the sickle cell gene will tend to increase in the population.

End of lesson.

 

[Riprorin]

Sickle-cell clearly impairs the function of the hemogloblin molecule.

It is NOT an impovement in humans even though it's preservation is enhanced in malaria-endemic regions of Africa by natural selection.

Genetic Disease Profile: Sickle Cell Anemia

 

[shoegazer]

what about people of different skin colors?

darker skin is beneficial in areas that receive a lot of sunlight because it protects against uv radiation. lighter skin is beneficial in areas that get less sunlight because it allows for more production of vitamin D3.

 

[Bitek]

Originally posted by: Riprorin

Originally posted by: ForThePeople

Originally posted by: rahvin

Originally posted by: ForThePeople
...yada yada yada...

You cite sicke-sell as a "beneficial" mutation since people who have sickle-cell anemia are less likely to contract malaria.

Yet, sickle-cell produce anemia prevents the proper absorbtion of food and oxygen.

If I became a qudraplegic, I would be less likely to killed in a bicycle accident since I'd be in a wheel chair and not likely riding a bike.

Is having a 25% less chance of contracting malaria advantageous versus suffering premature death as a result of having sickle cell?

Yes, could be. Depends on the on the prevalence of malaria in the local environment. If death rates from malaria are higher than the death rates of sickle cell, than possession of the gene in the local gene pool will be favored, and the prevalence of the sickle cell gene will increase until it reaches an equalibrium.

Another example is albinism. Albinism ("Albinos") is not entirely uncommon, even in humans and eg, can easily arise by breaking or removing an enzyme (protein) in a pigment synthesis pathway. Normally this is deleterious, as you are blind & light-sensitive.
However, under certain condits albinism is evolutionarily favored b/c is is metabolismically less expensive than pigment synthesis.

Ex. Albino Cave fish/rats/ etc. Sight and pigment is useless to them, so then do not require as much food and rare minerals in a nutrient-poor environment, so will have a higher fitness than their pigmented counter-parts and will be evolutionarily favored.

It is easy to imagine this situation occuring. Say and earthquake/ erosion or rising seas flood a once dry cave of sufficient size. A local minnow population spreads into the cave populating it. It is probable a mutation will eventually occur that will create an albino fish. The mutation is not harmful in this enviro & fish reproduces. A small population of albino fish is established with a now higher fitness and fecundity rate. If five albino fish survive for every 3 "wild/normal" fish, albinism will eventually dominate the population.
Other factors, such as body size/shape etc may further differentiate the cave fish from their wild ancestors until the two populations do not readily interchange genetic information, ie, a new species is born. As time passes the genetic simularity between the two populations can only become dissimilar because there is not free-flow of information occuring between them.

In a non-biological way, this can be thought of as in terms of language. English speakers founded this country, and as the population of english speakers spread, local variations in pronunciation/ slang/ terminology develop. Without sufficient interaction/interchange between two populations, their language diverges, creating accents, then dialects, and given enough time and seperation, divergent languages.

Evolution is inevitable. Not because it is a principality of biology, but because it is a inherent property of information systems. Biology is subject to evolution because at its root it is an information system. DNA is merely coded information, and in no way immune to the laws and mechanisms governing such a system.

 

[Bitek]

Originally posted by: Riprorin
Sickle-cell clearly impairs the function of the hemogloblin molecule.

It is NOT an impovement in humans even though it's preservation is enhanced in malaria-endemic regions of Africa by natural selection.

Genetic Disease Profile: Sickle Cell Anemia

Evolution does not seek perfection. There is no perfect. It is not concious, and not predictive. Therefore it cannot work towards "advancement". It only works towards what is better given a set of conditions.

Sickle-cell IS an improvement, under specific conditions. In other conditions it is not, so is not favored.


Its like trying to say "What is the best tool? A screwdriver, a hammer or a saw?" None are better. Some are more effective depending on the situation. And sometimes a less-useful tool can work well enough. I can still pound things with a screwdriver if I don't have a hammer.
Such is Evolution

 

[Riprorin]

Sickle-cell anaemia does not prove evolution!

Dr Felix Konotey-Ahulu, M.D. (Lond.), FRCP, DTMH, is a world authority on sickle-cell disease, with 25 years? experience as a physician, clinical geneticist and consultant physician in Ghana and subsequently in London. He is a visiting professor at Howard University College of Medicine in Washington, and honorary consultant to its Center for Sickle Cell Disease. He is the author of a major 643-page text, The Sickle Cell Disease Patient (Macmillan, 1991, ISBN 0333­39239-6).

This article is abstracted with Dr Konotey-Ahulu's permission from pages 106-108 of his book.

 

[dannybin1742]

nice website, go figure, you found one phd that agrees with you, but you seem to disregard the the other 99% that don't

you still didn't answer my question or comment on my post heere you go again

How old is the earth?

how long have humans been on earth?

did dinosaurs exist and when did they walk the earth?

this may be a little OT at this stage of the thread, but for prebiotic life conditions, there are two good articles in may 13 2005 journal science

the first one is an article showing evolution of complex hydrocarbons in titan's atmosphere (moon of saturn), with direct comparison's to what earth's early atmosphere was p975

the first paragraph of the article talks about similarities between titan's atmosphere and earth's early atmosphere

high N2 and CH4 concentrations, compounds detected so far are

C2H6, C2H2, C3H8, HCN, C2H4, CO2, C3H4, C4H2, HC3N

for anyone interested in prebiotic conditions


the second article is about hydrogen escape in early earth atmosphere that has a direct impact on formation of biological molecules, in an ANOXIC (no free oxygen) environment, with high levels of CO2

both are interesting reads, if you know a library that has a subscription


also, rip: science has changed immensly in the last 20 years, even biochem has changed alot in the last 5 years, the knowledge back then is nothing compared to what is known now, a simple indicator is to look at the number of deposited structures in the protein databank, and look at the rate increases of the last 5 years, it follows the rise of computers, also look athe number of papers published, it parralells growth of computer speed, simple because in many areas of science the technology wasn't there to test theory yet, now for the most part it is

 

[Riprorin]

Originally posted by: dannybin1742
nice website, go figure, you found one phd that agrees with you, but you seem to disregard the the other 99% that don't

you still didn't answer my question or comment on my post heere you go again

How old is the earth?

how long have humans been on earth?

did dinosaurs exist and when did they walk the earth?

this may be a little OT at this stage of the thread, but for prebiotic life conditions, there are two good articles in may 13 2005 journal science

the first one is an article showing evolution of complex hydrocarbons in titan's atmosphere (moon of saturn), with direct comparison's to what earth's early atmosphere was p975

the first paragraph of the article talks about similarities between titan's atmosphere and earth's early atmosphere

high N2 and CH4 concentrations, compounds detected so far are

C2H6, C2H2, C3H8, HCN, C2H4, CO2, C3H4, C4H2, HC3N

for anyone interested in prebiotic conditions


the second article is about hydrogen escape in early earth atmosphere that has a direct impact on formation of biological molecules, in an ANOXIC (no free oxygen) environment, with high levels of CO2

both are interesting reads, if you know a library that has a subscription


also, rip: science has changed immensly in the last 20 years, even biochem has changed alot in the last 5 years, the knowledge back then is nothing compared to what is known now, a simple indicator is to look at the number of deposited structures in the protein databank, and look at the rate increases of the last 5 years, it follows the rise of computers, also look athe number of papers published, it parralells growth of computer speed, simple because in many areas of science the technology wasn't there to test theory yet, now for the most part it is

Dr Felix Konotey-Ahulu, M.D. (Lond.), FRCP, DTMH, is a world authority on sickle-cell disease, with 25 years? experience as a physician, clinical geneticist and consultant physician in Ghana and subsequently in London. He is a visiting professor at Howard University College of Medicine in Washington, and honorary consultant to its Center for Sickle Cell Disease. He is the author of a major 643-page text, The Sickle Cell Disease Patient (Macmillan, 1991, ISBN 0333­39239-6).

This article is abstracted with Dr Konotey-Ahulu's permission from pages 106-108 of his book.

Care to discuss the content?

Topic Title: The Theory of Evolution
Topic Summary: Whaddya think?

I think that the notion that we are products of a "?big bang?, leading to single-celled organisms, multicelled organisms, invertebrates, vertebrates, and on up to man" is absurd.

 

[imported_tss4]

Originally posted by: Riprorin

I think that the notion that we are products of a "?big bang?, leading to single-celled organisms, multicelled organisms, invertebrates, vertebrates, and on up to man" is absurd.

And that says it all. This discussion with you is a waste of time for everyone involved.

 

[Riprorin]

One PhD? Hardly.

Creation Scientists

 

[imported_tss4]

Originally posted by: Riprorin
One PhD? Hardly.

Creation Scientists

Wow, you guys have got to check out the research papers on this site. I remember laughing at some muslim universities that conducted resarch "How far Away From the Earth was Heaven". They have nothing on these guys. Some example papers:

HYPERCANES FOLLOWING THE GENESIS FLOOD

CATASTROPHIC PLATE TECTONICS: THE PHYSICS BEHIND THE GENESIS FLOOD

Patterns of Ocean Circulation Over the Continents During Noah's Flood

The Sands of Time: A Biblical Model of Deep Sea-Floor Sedimentation

The Cooling of Thick Igneous Bodies on A Young Earth

Toward the Development of an Instrument for Measuring a Christian Creationist Worldview

Earthquakes and the End Times: A Geological and Biblical Perspective

Newton's Approach to Science: Honoring Scripture