how does sickle cell anemia provide evidence for evolution?

Question

how does sickle cell anemia provide evidence for evolution?

Answer 1

Evolution Of Sickle Cell Anemia

Answer 2

Having sickle cell anemia is very obviously a disadvantage if there is no malaria around. But it is an advantage if malaria is around.



Consequently if evolution does happen we would not expect to find a population of humans where sickle anemia is common unless there is a reasonably high incidence of malaria in that area. We don't.



In addition it's a point mutation where only one amino acid is changed in the hemoglobin and only a single nucleobase is different.



BTW, this is not a loss of information at all. the information of that particular codon changed from GAG to GTG, Count the letters. Same number. No loss of information. A change of information leads to a change of phenotype. It also confers malaria resistance. A new trait. Saying it doesn't have any advantage would be ignoring the obvious.

Answer 3

There is plenty of evidence for evolution in modern times. See below for an example. When you study evolution you are looking at a history, some parts have remained in the history books, others are lost - just the same as any other history. We have no idea, what if anything that happens in 2009 will be recorded and still of interest to historians in 200 years time that is only a tiny timeframe compared to evolutionary time. What we see as 'normal' genetic variation in one species today might be 6 new species in a million years time. If you are a serious student of evolution, then there is no excuse for not having encountered the forerunner of the zebra in your searches. The equine fossil record is the most complete one there is and I've attached a link to a picture, just one of many that exist. As equines evolved in the Americas, all specimens pre Equus were found there and I'm sure all the best fossils are in American museums, but there are some in the UK. Earthworms and bees are not as well preserved, but nonetheless there are enough fossils to be able to study the evolution of annelids and insects. Onto modern day evolution. Here is a human example. In parts of Africa and India in particular, populations are exposed to Plasmodium falciparum, a malaria parasite which frequently causes death, especially in young children. In the same populations sickle cell anaemia also exists. Why? The sickle cell anaemia protects against malaria in people who carry one sickle cell allele and one 'normal' allele, to the extent that in some cases there may be up to a 30% better chance of surviving to adulthood - this is a huge effect - natural selection in action. Also, the sickle cell alleles in Central and West Africa and India have evolved independently of one another. The terrible downside of course is that people who carry two sickle alleles are ill and have reduced life expectancy. But, guess what there is another newer variant of that gene, that is also malaria protective, but has fewer negative consequences in homozygous sufferers - we would expect this allele to start to increase in frequency because of the benefits it has - this is evolution, but we'll have to wait a bit longer to find out what will happen in the future, unless we can solve the malaria problem first.

Answer 4

Sickle-cell anemia is often used as an example to support evolution, but the mutation is a defect and causes a loss of normal function with no new ability or increase in complexity. The protection against malaria comes at the high cost of a less functional hemoglobin molecule. That's not onward and upward evolution, it's actually de-evolution.



It's like people trying to use wingless beetles and blind cave fish as evidence. Wingless beetles on a windy island and blind cave fish have a survival advantage, but it comes from a loss of information. These are "going the wrong way" as far as evolution is concerned.



As Dr. Michael Behe (who has a Ph.D. in Biochemistry) said, “...most evolutionary changes are ones which either break or degrade genes—and these are the helpful mutations! But you can't build new molecular machinery by breaking genes” (A Conversation with Dr. Michael Behe).



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Dr. Mike Behe spends quite a bit of time on this in his book: “Let's pause here for a moment to consider several simple points about the sickle and HbC mutations. The first point is that both sickle and HbC are quintessentially hurtful mutations because they diminish the functioning of the human body. Both induce anemia and other detrimental effects. In happier times they would never gain a foothold in human populations. But in desperate times, when an invasion threatens the city, it can be better in the short run to burn a bridge to keep the enemy out. A second point is that the mutations are not in the process of joining to build a more complex, interactive biochemical system. The sickle and C mutations are mutually exclusive, vying for the same site on hemoglobin—the sixth position of the beta chain. They do not fit together to do something. A related point is that neither hemoglobin mutation occurs in the immune system, the system that is generally responsible for defending the body from microscopic predators. So the mutations are neither making a new system nor even adding to an established one. In this book we are concerned with how machinery can be built. To build a complex machine many different pieces have to be brought together and fitted to one another” (The Edge of Evolution).

Answer 5

".... Were the presence of the SCA (heterozygous) allele to confer only negative traits, its allele frequency would be expected to decrease generation after generation, until its presence were completely eliminated by selection and by chance.



However, convincing evidence indicates, in areas with persistent malaria outbreaks, individuals with the heterozygous state have a distinct advantage (and this is why individuals with heterozygous alleles are far more common in these areas).[2] Those with the benign sickle trait possess a resistance to malarial infection. The pathogen that causes the disease spends part of its cycle in the red blood cells, and those with sickle cells effectively stop the pathogen in its tracks, until the immune system destroys the foreign bodies. These individuals have a great immunity to infection and have a greater chance of surviving outbreaks. However, those with two alleles for SCA may survive malaria, but will typically die from their genetic disease unless they have access to advanced medical care. Those of the homozygous "normal" or wild-type case will have a greater chance of passing on their genes successfully, in that there is no chance of their offspring's suffering from SCA; yet, they are more susceptible to dying from malarial infection before they have a chance to pass on their genes.



This resistance to infection is the main reason the SCA allele and SCA disease still exist. It is found in greatest frequency in populations where malaria was and often still is a serious problem."

Answer 6

HbAA hemoglobins in RBCs have no problem with O2 stress but have no protection from the plasmodium. These people are infected and die from malaria.



HbSS proteins cause sickling RBCs and these people die from their genetic condition.



HbSA is the heterozygote individual with a tendency towards RBC sickling with O2 stress BUT HbS proteins inhibit the malarial plasmodium's growth. Plasmodium infected cells are likeliest to sickle and this kills the parasite but not the host.



Heterozygotes however have positive selection with reproductive success so the HbS & HbA allele frequency is stabilized between the opposing selective pressures. 50% of the children born to two carriers will die from being homozygotic but half will have reproductive success from being heterozygotes. This mixed phenotype was fit enough to keep the HbS allele in the population's gene pool so such a detrimental allele established due to the greater selective pressure from the parasite.



The reality is actually more complex as these people have an African horticultural complex of plants that provides cyanates, metabolites that prevent or reduce RBC sickling with HbS in plasmodium free cells. The metabolites reduce the cost of the alleles. Cyanate metabolites, such as thiocyanate, further inhibit the growth cycle of plasmodium in the RBC. Infected cells are much more likely to sickle or be removed by the immune system so the malarial load is reduced.



The heterozygotes have more severe symptoms when not eating the plants.

http://webcache.googleusercontent.com/search?q=cache:kbG-R86IN0EJ:www2.ku.edu/~lba/courses/articles/Crawford%2520Carib.pdf+&cd=6&hl=en&ct=clnk&gl=us&client=firefox-a

Answer 7

The sickle cell gene is most prevalent in regions where malaria is endemic. The heterozygote advantage drives the prevalence up where there is malaria and down where sickle cell is only a disadvantage. The Hardy-Weinberg model approximates the distributions.

Answer 8

The fact that it's advantageous affects the percentage of people in a certain region who have it, because they survive and pass the trait onto their offspring. Those who didn't have that advantage tended to die off and not pass their genes on.

Answer 9

It doesn't. It demonstrates DEvolution.



Sickle-cell anaemia is caused by an inherited defect in the instructions which code for the production of haemoglobin, the oxygen-carrying pigment in red blood cells. You will only develop the full-blown, serious disease if both of your parents have the defective gene. If you inherit the defect from only one parent, the healthy gene from the other one will largely enable you to escape the effects of this serious condition.



However, this means you are capable of transmitting the defective gene to your offspring, and it also happens that such carriers are less likely to develop malaria, which is often fatal. Being a carrier of sickle-cell disease without suffering it (heterozygosity is the technical term) is far more common in those areas of the world which are high-risk malaria areas, especially Africa.



This is good evidence that natural selection plays a part in maintaining a higher frequency of this carrier state. If you are resistant to malaria, you are more likely to survive to pass on your genes. Nevertheless, it is a defect, not an increase in complexity or an improvement in function which is being selected for, and having more carriers in the population means that there will be more people suffering from this terrible disease. Demonstrating natural selection does not demonstrate that ‘upward evolution’ is a fact, yet many schoolchildren are taught this as a ‘proof’ of evolution.

Answer 10

This is evolution. The affected populations have evolved partial resistance to malaria through the spread of the HbS allele through the population, which is positively selected in the heterozygous condition. Without this allele, nearly all children infected with the parasite would die and the populations would face extinction. As it is the death rate is huge. Being heterozygous gives as much as a 30% increased survival chance.

Answer 11

It only provides evidence for evolution if your definition of evolution is 'change in allele frequency' which is the common definition. If your definition would include the creation of new genetic code then sickle cell anemia is not evidence at all. It’s the equivalent of having a life threatening infection on your arm, and then having an accident and your arm comes off. You wouldn’t exactly call that evolving, would you? And the reason you wouldn’t call it evolving is not because it’s happening to a single person as apposed to a population. Or maybe you would call that evolution.