Question 2: Natural Selection

Simon · Post by **Simon** » Thu Dec 02, 2004 4:23 pm

According to Richard Dawkins, the "evidence of evolution reveals a universe without design." Yet he also states, "Biology is the study of complicated things that give the appearance of having been designed for a purpose." How does Dawkins know that living things only appear to be designed but are not actually designed?

2 and 92 · Post by **2 and 92** » Fri Dec 03, 2004 7:25 am

Natural selection is a design process, just not intelligent design.

If our DNA looked like a computer program then you could imply intelligent design. However, it does not; it looks more like what you would expect from a non-intelligent design process.

jwu · Post by **jwu** » Fri Dec 03, 2004 7:40 am

Even technical layouts can evolve, e.g. as this one:
http://www.genetic-programming.com/hc/v ... rence.html

There are plenty more examples on that website. Some results of genetic programming even outperform human designs:
http://www.genetic-programming.com/huma ... itive.html

Genetic programming meanwhile has become a very serious and interesting field of study.

jwu

potwalloper. · Post by **potwalloper.** » Fri Dec 03, 2004 7:57 am

If our DNA looked like a computer program then you could imply intelligent design. However, it does not; it looks more like what you would expect from a non-intelligent design process.

Which is why alterations in DNA, DNA damage and erroneous DNA replication can result in some cases in cancers etc.

I would have difficulty in believing that anything that could be described as "intelligent" could design a system that, whilst complex, contains so many inherent flaws.

Perhaps the proposal should be for Idiotic Design...this would explain the existence of the appendix, genetic predisposition for disease, epilepsy...the list of flaws in human function is endless.

So - perhaps there is a God but he is simply stupid

Post by **otseng** » Fri Dec 03, 2004 9:04 am

potwalloper. wrote: So - perhaps there is a God but he is simply stupid

Some comments about this statement.

First off, your argument to lead to your conclusion does not follow.

potwalloper. wrote: Perhaps the proposal should be for Idiotic Design...this would explain the existence of the appendix, genetic predisposition for disease, epilepsy...the list of flaws in human function is endless.

Because we do not fully understand the appendix, that does not mean it is of idiotic design. There are several theories on the purpose of the human vermiform appendix:

1. Embryological

During the fifth foetal week it is the appendix which develops from a bud at the junction of the small and large bowel and undergoes rapid growth into a pouch. In the sixth week there is a transient nubbin surmounting the pouch indicative of being involved in the rapid development of the pouch which is very strategically placed near the apex of the highly significant mid-gut loop. It is only after the fifth foetal month that the proximal end of this pouch, which has appeared to be a very insignificant structure up until this stage, starts growing differentially to give rise to the true caecum which continues to develop into infancy.

The embryonic appendix has finger-like projections (villi) on its inside surface and it is only around birth that the long ribbons (taeniae) causing the sacculation of the large bowel start to develop. These ribbons, of course, converge on the base of the appendix.

2. Physiological

The goblet cells lining the appendix and adjacent caecum and colon secrete a special type of mucus which can be regarded as an antibacterial paint controlling the organisms which develop in the bowel in the region. The paint contains a high concentration of IgA type immunoglobulins, secretory antibodies produced for mucosal or surface immunity and part of the bowel-blood barrier.

3. Bacteriological

Through the cells within and overlying the lymphoid follicles and their production of secretory and humoral antibodies the appendix would be involved in the control of which essential bacteria come to reside in the caecum and colon in neonatal life. As well it would be involved in the development of systemic tolerance to certain antigenic agents within the alimentary tract whether they are derived from bacteria, foodstuffs or even the body’s own proteolytic enzymes.

4. Biochemical

One in three hundred or so appendectomy specimens contains a carcinoid tumour composed of a highly specialised type of cell rich in vaso-active peptides such as serotonin. The exact function of such agents in the entire bowel is still being elucidated, but the fact that the majority4 of such tumours occur within the appendix is indicative that the appendix could well be involved in some way with such substances.

5. Immunological

This is the area where the appendix would seem to have its predominant functions due to its content of lymphoid follicles, which are highly specialised structures. Although it was thought the appendix itself could be the site for B-lymphocyte induction (a Bursa of Fabricius equivalent)26 the latest opinions favour this programming being more centralised in the bone marrow. The appendix may still have a role in this highly significant function, but not alone, and its lymphoid tissue is known for certain to be involved in antibody production (the function of B- type lymphocytes). These antibodies are of two types:

1. IgA type immunoglobulins for secretory or mucosal surface immunity, and
2. IgM and IgG immunoglobulins for humoral or bloodstream immunity.

The above type functions have proven the appendix to be part of the G.A.L.T.2,4,23,25 (Gut Associated Lymphoid Tissue), but it has also been shown that the appendix after the neonatal period is dispensable, meaning that normal G.A.L.T. functions remain after appendectomy. This result is not unexpected as similar lymphoid tissue is distributed up and down the alimentary tract, there being a considerable reserve potential. Experiments in rabbits have shown that the appendix alone can provide normal humoral antibody levels if necessary27 and also replenish depleted lymphocyte populations secondary to neonatal thymectomy.28

These results have been in rabbits, and the rabbit appendix is not exactly the same as the human. Studies of the functions of the human appendix, however, have tended to concentrate on extrapolating across from animal models where it is difficult to escape evolutionary overtones and possibly repeating the errors Darwin made when using homology.

Other studies on the human appendix have tended to concentrate on tissue from young adults when the appendix has probably completed its major role. Recently the topography14 of immune cells and their products in the appendix have been described both in the presence and absence of acute inflammation, as well as it becoming evident that lymphocytes individually move into the appendix between the tenth and twentieth foetal week.14 Such studies have also highlighted the mode of immune cell reactions both with each other and other cells in the area in a detail not known before and quite significant advances have been made. Of course, lymphoid follicles do not actually appear as such in the appendix until two weeks after birth4 at the same time that colonisation of the large bowel with bacteria which are safe to their host begins. The follicles increase steadily in number to a maximum of two hundred at about fifteen to twenty years of age and decline back to about one hundred by thirty years of age and decline further, even to disappearance, throughout the rest of life. The peak incidence of acute appendicitis coincides very well with the peak number of lymphoid follicles and their enlargement with infection, whether it be initially viral or bacterial, probably contributes significantly to the luminal obstruction29 so important in the initiation of acute appendicitis.

In the past decade we have increased our knowledge considerably of the cells lining the gastrointestinal tract, especially in the small bowel and ileocaecal region, where new hormones and their functions have been discovered and so have received a lot of attention in appropriate journals. Clarification of B-lymphocyte induction9,13,26 and topography of the cells in foetal and neonatal appendiceal tissues is awaited with interest.

In summary therefore, the human vermiform appendix appears to be a complex and organised structure both in its development and maturation, and almost certainly has corresponding complexity in its functions which, like most gastrointestinal functions, are still awaiting further clarification. It would appear that the functions of the appendix would be most important when the organ itself has most prominence, and this is in the developing foetus and early existence after birth. The inside of the bowel is outside the body and the area where substances foreign to it have their greatest chance of attack. The appendix appears to be strategically placed and structurally composed of tissues which are vital in establishing and maintaining the various types of body defences or immunity necessary in recognition of such assaults and having a part to play in their repulsion. The appendix is thus one of the guardians of the internal environment of the body from the hostile external environment.

potwalloper. wrote: genetic predisposition for disease, epilepsy...the list of flaws in human function is endless.

Humans were not created with a genetic predisposition for disease. Please support your case for this.

If your argument is to be used as a flaw against God, then it can also be equally applied as a flaw in the theory of evolution. Evolution is supposed to create better suited organisms, not organisms with greater flaws over time.

Lastly, the statement "perhaps there is a God but he is simply stupid" does not follow the standards of a civil and respectful debate. There is no need to call anyone stupid, not even for an entity that you do not believe to exist. On this forum, many people believe that God exists and such statements do not respect their beliefs.

Lotan · Post by **Lotan** » Fri Dec 03, 2004 9:33 am

Please be aware that the argument put forth on this thread belongs to William Dembski.

jwu · Post by **jwu** » Fri Dec 03, 2004 9:34 am

First off, i agree that the appendix is not useless. If that benefit outweighs the risk of an appendicitis remains to be seen though.

If your argument is to be used as a flaw against God, then it can also be equally applied as a flaw in the theory of evolution. Evolution is supposed to create better suited organisms, not organisms with greater flaws over time.

In evolutionary theory not every improvement that is possible *has to* happen.

On the other hand, massive design flaws which would get any human engineer fired are not what one would expect to see if everything was created by a perfect creator.

E.g. the coccyx - it makes perfect sense as the remainder of a previous tail, but it's of no use to humans anymore (except perhaps to remind us not to sit down too fast, the painful way). There are even still muscles which seem to be supposed to move bones that are fused together.

jwu

potwalloper. · Post by **potwalloper.** » Fri Dec 03, 2004 9:37 am

Because we do not fully understand the appendix, that does not mean it is of idiotic design.

Are you really trying to say that the appendix is not a vestigial organ even though it appears in other mammals with the primary purpose of digesting vegetable tissue but does not do so in humans? And why on earth would you add an organ that has no clearly determined function but has resulted in the agonizing deaths of so many prior to the development of modern surgical intervention? Not something that would make it into the Design Museum methinks...

Theories do not equal reality. Now it is easy to invent functions for an organ that is patently useless - perhaps it was put there to test our faith, just like fossils?

Humans were not created with a genetic predisposition for disease. Please support your case for this.

perhaps this will do to start: http://www.ncbi.nlm.nih.gov/books/bv.fc ... ection.216:

Rett syndrome

Rett syndrome (RTT) is a progressive neurodevelopmental disorder that almost exclusively affects females. It has an incidence of about 1 in 10,000 births, making it one of the most common causes of profound mental retardation in girls. Individuals with RTT develop normally until the age of 6 to 18 months, when they begin to lose purposeful use of their hands and speech. Affected individuals also show reduced muscle tone, wringing hand movements, autistic-like behavior and seizures.

A gene which causes RTT, MeCP2, has been found on the long arm of chromosome X (Xq28). Normally, females have two X chromosomes and males have an X and a Y. Since males do not have an additional copy of X to offset a defect, most X-linked diseases affect males. Then, why are males not affected by RTT? One possible explanation is that the absence of a functional copy of MeCP2 is lethal to the male fetus before birth. Researchers have shown this to be the case in a mouse model. Another question is why females are affected by RTT, even though one of their X chromosomes is normal. This is likely due to X inactivation, a normal process whereby one X chromosome is randomly inactivated in every cell. This partial deficiency - where the normal copy of MeCP2 is active in some cells and inactive in others - allows girls with RTT to survive and develop normally during early infancy.

MeCP2 is believed to code for a protein which controls gene expression in the cell. Although it is not clear what the mechanism is, partial loss of this protein may lead to over expression of certain genes, leading to the RTT phenotype. With the discovery of MeCP2, investigators hope to develop a test for RTT which will allow for early diagnosis, prenatal detection and, ultimately, presymptomatic therapy.

Or this?

FRAGILE X SYNDROME is the most common inherited form of mental retardation currently known. Fragile X syndrome is a defect in the X chromosome and its effects are seen more frequently, and with greater severity, in males than females.
In normal individuals, the FMR1 gene is transmitted stably from parent to child. However, in Fragile X individuals, there is a mutation in one end of the gene (the 5' untranslated region), consisting of an amplification of a CGG repeat. Patients with fragile X syndrome have 200 or more copies of the CGG motif. The huge expansion of this repeat means that the FMR1 gene is not expressed, so no FMR1 protein is made. Although the exact function of FMR1 protein in the cell is unclear, it is known that it binds RNA.
A similar nucleotide repeat expansion is seen in other diseases, such as Huntington disease. Research in mice has proven helpful in elucidating some of the mechanisms that cause the instability of this gene. Our methods for identifying carriers of Fragile X syndrome have also improved, and further research will help people carrying 'premutations' to avoid having children who have a larger expansion (ie more CGG repeats) in FMR1, and therefore suffer from fragile X syndrome.

or

Ataxia telangiectasia

The first signs of ataxia telangiectasia (A-T) usually appear in the second year of life as a lack of balance and slurred speech. It is a progressive, degenerative disease characterized by cerebellar degeneration, immunodeficiency, radiosensitivity (sensitivity to radiant energy, such as x-ray), and a predisposition to cancer.

Back in 1988 the gene responsible for A-T was mapped to chromosome 11. The subsequent identification of the gene proved difficult; it was 7 more years until the human ATM gene was cloned. The diverse symptoms seen in A-T reflect the main role of ATM, which is to induce several cellular responses to DNA damage. When the ATM gene is mutated, these signaling networks are impaired, and so the cell does not respond correctly to minimize the damage.

Some of the ATM-dependent signaling pathways are found in yeast. Because these pathways appear to be conserved throughout evolution, they are likely to be central to the DNA damage response. Research into finding an effective therapy for A-T sufferers is likely to be helped by harnessing the power of yeast genetics, which allows more rapid and systematic study of the pathways affected by an ATM mutation.

or

Atherosclerosis

Atherosclerosis is a disease that can affect people at any age, although it usually doesn't pose a threat until people reach their forties or fifties. It is characterized by a narrowing of the arteries caused by cholesterol-rich plaques of immune system cells. Key risk factors for atherosclerosis, which can be genetic and/or environmental, include: elevated levels of cholesterol and triglyceride in the blood, high blood pressure, and cigarette smoke.

A protein called apolipoprotein E, which can exist in several different forms, is coded for by a gene found on chromosome 19. It is important for removing excess cholesterol from the blood, and does so by carrying cholesterol to receptors on the surface of liver cells. Defects in apolipoprotein E sometimes result in its inability to bind to the receptors, which leads to an increase a person's blood cholesterol and consequently their risk of atherosclerosis.

Currently, a debate is raging over how the various mutated forms of apolipoprotein E effect the body. As a result, many of the treatments proposed remain in their experimental phase. While mice are proving useful for modeling the human disease, a great deal of research is still required before we can fully understand the mechanisms that regulate the levels of lipoproteinslike apolipoprotein Ein the blood.

or

Von Hippel-Lindau syndrome

Von Hippel-Lindau syndrome is an inherited multi-system disorder characterized by abnormal growth of blood vessels. While blood vessels normally grow like trees, in people with VHL little knots of blood capillaries sometimes occur. These knots are called angiomas or hemangioblastomas. Growths may develop in the retina, certain areas of the brain, the spinal cord, the adrenal glands and other parts of the body.

The gene for Von-Hippel Lindau disease (VHL) is found on chromosome 3, and is inherited in a dominant fashion. If one parent has a dominant gene, each child has a 50-50 chance of inheriting that gene. The VHL gene is a tumor suppressor gene. This means that its role in a normal cell is to stop uncontrolled growth and proliferation. If the gene is lost or mutated, then its inhibitory effect on cell growth is lost or diminished, which, in combination with defects in other regulatory proteins, can lead to cancerous growth. LIke the Rb tumor suppressor gene, VHL seems to act as a 'gatekeeper' to the multistep process of tumorigenesis.

Although unrelated to any other known family of human proteins, homologs to human VHL are found in mice and rats. Experiments using these animals as model organisms for the human disease are helping researchers discover the normal physiological role of VHL, which will shed light on its mechanism of pathogenesis. Initial results suggest that VHL may play a role in regulating exit form the cell cycle.

I could go on...

If your argument is to be used as a flaw against God, then it can also be equally applied as a flaw in the theory of evolution. Evolution is supposed to create better suited organisms, not organisms with greater flaws over time.

The two arguments are not the same. The concept of intelligent design infers the intervention by some divine being in the creation of life. If the Christian view of God's omniscience is applied how could this divine being have made so many mistakes? Humans are a bag of faults just waiting to go wrong...

The alteration of genetic material over time will, by definition, result in some positive and some less positive effects. Sickle cell anaemia is a good example where the condition offers a degree of protection against maleria - some advantages, some disadvantages.

http://en.wikipedia.org/wiki/Malaria

Sickle cell anemia and other genetic effects
Carriers of the sickle cell anaemia gene are protected against malaria because of their particular hemoglobin mutation; this explains why sickle cell anemia is particularly common among people of African origin. There is a theory that another hemoglobin mutation, which causes the genetic disease thalassemia, may also give its carriers an enhanced immunity to malaria.

Another disease that gives protection against malaria is glucose-6-phosphate dehydrogenase deficiency (G6PD). It protects against malaria caused by Plasmodium falciparum as the presence of this enzyme is critical to survival of these parasites within red blood cells.

It is thought that humans have been afflicted by malaria for about 50,000 years, and several human genes responsible for blood cell proteins and the immune system have been shaped by the struggle against the parasite.

Lastly, the statement "perhaps there is a God but he is simply stupid" does not follow the standards of a civil and respectful debate. There is no need to call anyone stupid, not even for an entity that you do not believe to exist. On this forum, many people believe that God exists and such statements do not respect their beliefs.

I do appreciate this and, however it may appear, do respect the beliefs of others. However the discussion concerned "intelligent" - if something is not intelligent then what is it?

Jose · Post by **Jose** » Fri Dec 03, 2004 10:53 am

otseng wrote:Humans were not created with a genetic predisposition for disease. Please support your case for this.

If your argument is to be used as a flaw against God, then it can also be equally applied as a flaw in the theory of evolution. Evolution is supposed to create better suited organisms, not organisms with greater flaws over time.

Potwalloper has addressed the genetic predispositions adequately, so I won't add more. Apparently, many of us do have genetic predispositions for disease. And, of course, being humans, we have a genetic predisposition for those infectious diseases that are specialized in infecting humans.

What is more important is to discuss the idea that evolution is supposed to create better-suited organisms. This is a concept that seems to be pretty common, but is actually not true. Evolution works by simply modifying existing structures by mutation, with some of the resulting organisms faring well, and some faring poorly. There is no way to "target" a mutation to a particular gene, and thereby create something that is well-adapted to a particular environment. Over time, the individuals with mutations that happen to be helpful are the ones that have the most offspring, and therefore take over the population--like the humans in Europe, most of whom carry the lactose-tolerance mutation, which is advantageous in cultures that rely upon milk as a source of protein.

What happens with an appendix, or a tail, that is no longer able to perform its earlier function because other changes have occurred? It depends on what mutations happen to occur. If a mutation occurs that blocks its development altogether, then it disappears. If no such mutations occur, then it is still there. If its original form is actually a disadvantage, then any mutations that happen to make the structure smaller are likely to be selected for, if they occur. This seems to be the case with our appendix and our tail/coccyx.

But, of course, to be perfectly adapted to an environment requires fine-tuning of many structures and many enzyme systems. The mutations that would produce such fine-tuning don't all happen at once, and cannot be caused on purpose. Some may happen, some may not. There may also be counter-selection, wherein a particular structure cannot become fully adapted for purpose A because that makes it maladapted for purpose B. As much as we'd like to imagine that we are fine-tuned to be "the best," close inspection reveals that we are not. This sloppiness of evolution explains the hodge-podge of adaptations much better than does design.

The Idiot Designer idea has been kicked around a lot, although usually under the term of Sloppy Designer. It does come across sounding a bit rude, especially for those who really believe they are products of a designer who has an important purpose for them. Still, it is necessary to understand the origins of these features that we have that are just not very good. Who would actually try to design a prostate so that it wraps around the urethra, and enlarges with age, so that it gets harder and harder to pee? Who would try to design eyes so that they become progressively worse at seeing things? Why design us so that we cannot produce lysine (or the other essential amino acids), and therefore must rely on animal products for an adequate source of protein? Are these kinds of things punishments, or purposeful flaws that test our faith, or design flaws, or just the result of an uncaring, unthinking evolutionary process? I find the latter much easier to understand.

Lotan · Post by **Lotan** » Fri Dec 03, 2004 11:11 am

somebody wrote:How does Dawkins know that living things only appear to be designed but are not actually designed?

Isn't this argument a non-starter anyway?
Obviously a structure that performs its function well will be selected for. A fish's fin resembles a paddle because they both perform the same function. I fail to see the mystery.

ST88 · Post by **ST88** » Fri Dec 03, 2004 12:51 pm

Jose wrote:The Idiot Designer idea has been kicked around a lot, although usually under the term of Sloppy Designer. It does come across sounding a bit rude, especially for those who really believe they are products of a designer who has an important purpose for them. Still, it is necessary to understand the origins of these features that we have that are just not very good. Who would actually try to design a prostate so that it wraps around the urethra, and enlarges with age, so that it gets harder and harder to pee? Who would try to design eyes so that they become progressively worse at seeing things? Why design us so that we cannot produce lysine (or the other essential amino acids), and therefore must rely on animal products for an adequate source of protein? Are these kinds of things punishments, or purposeful flaws that test our faith, or design flaws, or just the result of an uncaring, unthinking evolutionary process? I find the latter much easier to understand.

But doesn't this idea imply that God wouldn't have a reason for making us deteriorate as we get older? I don't find any logical problems with this. Maybe God wanted children to respect and take care of their elders because their bodies deteriorate. Maybe it is a final test of faith to gradually take away one's capacity for living in a physical world. Maybe it is a final preparation for living without one's body in s spiritual realm.

I have to return to my admonition about anthropomorphizing God. If I were God, this is what I'd do. I don't see the God as described as thinking that He should make lives easier for his children as time goes on. At the time of the Old Testament, people rarely lived past 50, and the diseases we are faced with today most often show up in people over this age. I think it has only been since 1950 that life expectancy reached above 70. Perhaps our scientific findings about nutrition leading to longer lives has been a double-edged sword precisely because of this.

My point here is not to show that natural selection isn't true, only that this part of the argument, the poor-design argument doesn't necessarily go anywhere. I would suggest that the arguments for this fall victim to the lack-of-imagination fallacy. Naturally, we would not know exactly why God did this to us, but for those who believe, they would also believe that this has a purpose, and their lack of ability to articulate what that purpose might be is not evidence that the poor-design argument has credibility.