Moalem tells on pages 14-15 about Hemochromatosis most likely originated from Vikings who spread the gene for the disease across Northern Europe. He says that because Hemochromatosis creates iron deficient macrophages, the organism is more likely to resist disease, like the plague that spread across Europe. He then says that people with Hemochromatosis may have been more likely to survive the plague and, in turn, pass on their genes to the next generation. This is what has caused Hemochromatosis to remain prevalent in European populations.
Similarly, sickle cell anemia is more commonly found in African populations. This may be due to the fact that the African environment houses many diseases, one of them being malaria. It is believed that those with the gene for sickle cell anemia are more likely to survive malaria than those who do not have it. This means that those with the sickle cell anemia gene in Africa are more likely to pass on their genes to the next generation.
These two examples relate to Big Idea 1; the process of evolution drives the diversity and unity of life. Those ethnic groups mentioned above were better able to survive and reproduce in their corresponding environments because of the diseases these groups are more likely to have.
Research another disease that is more prevalent in a certain ethnic or religious group and explain possible reasons for why this disease is in that particular group of people. Also, explain possible selective advantages the people of that population may have because of their particular disease.
(Aaron Chai, achai4@students.d125.org)
Thalassemia, a recessive genetic disorder, is more common in those of Mediterranean descent. Thalassemia is more prevalent in these people because Malaria is more common in these tropical regions. Thalassemia has been shown to give increased immunity to malaria and thus people in the Mediterranean with Thalassemia were able to survive and reproduce more frequently.
ReplyDeleteMalaria is an infectious disease spread by mosquitoes. Malaria develops in two stages, beginning by attacking the liver, then the red blood cells. Symptoms usually develop in 8-25 days which include fever, vomiting, headaches, and jaundice amongst other symptoms. On page 583 of the Campbell text, the book describes how the Malaria parasites usually escape detection by the immune system by wrapping itself in the cell membrane of the infected liver or red blood cell. The characteristic waves of fever brought on by Malaria are caused by the parasites escaping and infecting more red blood cells. These infected cells may breach the blood brain barrier causing cerebral malaria.
According to the “α +-Thalassemia and Protection from Malaria” article of PLOS Medicine, the Thalassemia trait is a selective advantage for those in Malaria-ridden areas as people with Thalassemia have misshapen α or β globin chain of the hemoglobin. Although there is no hard evidence, a study conducted by PLOS shows that people with α +-Thalassemia had significantly reduced hospital admittance rates for malaria. This study suggests that there is a strong possibility of Thalassemia providing people with a degree of Malaria resistance.
This relates to Big Idea 1: the process of evolution drives the diversity and unity of life. People with the Thalassemia trait living in the Mediterranean area were selected for and were more likely to survive malaria outbreaks and survive and reproduce.
(Christopher Yao, chyao4@students.d125.org)
One such disease is Tay-Sachs, most commonly found in Ashkenazi Jews. Tay-Sachs Disease (TSD) is an autosomal recessive genetic disorder caused by a mutation of the HEXA gene on human chromosome 15. In Ashkenazi Jews, it is caused by a four base pair insertion of TATC at exon 4. The infantile form manifests itself at about six months of age with neurodegeneration which causes blindness, deafness, dysphagia (inability to swallow), and paralysis, leading to deaf before the age of five. A characteristic symptom is a red spot in the fovea (a part of the retina).
ReplyDeleteAccording to Kelly, et. al, one possible reason for the high prevalence of TSD is the idea of the founder effect. This hypothesis states that a small colony of Ashkenazi Jews, when founded, contained people who were carriers of the disease. Because a disproportionally large part of the founding group was a carrier, the prevalence for the disease would increase. Today, according to the Centre for Genetics Education, TSD prevalence in Ashkenazi Jews is 1 in 30 versus 1 in 280 for the general population. In other words, the high prevalence of TSD in Ashkenazi Jews is due simply to chance.
However, there are dissenters. Myrianthopoulos et. al. claim that the approximate date of a founding population of about 1333 – 1370 in Poland under Casmir the Great, who offered protection to Jews who wanted to immigrate, is unlikely due to statistical improbabilities that would result from such a theory, such as an overly large portion of the founding population would have be a carrier for the disease. Instead, he and his peers pose an argument of heterozygote advantage. It is possible for a carrier of TSD to have a greater resistance to pulmonary tuberculosis (PTB), and would thus help Ashkenazi Jews survive the sometimes harsh conditions of Central and Eastern Europe. He claims this through the fact that PTB is virtually absent among populations which contained large numbers of TSD grandparents, and that PTB is most common where TSD grandparents were few. This theory is also supported by Chakravarti and Chakraborty.
This is most closely related to Big Idea 1, which states that “the process of evolution drives the diversity and unity of life.” The idea of TSD prevalence, and especially the disease’s possible heterozygote advantage, would make sense as a selective advantage to carriers in preventing tuberculosis. Science, though, is still dived in the matter.
Kelly, et. al
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1762873/
Myrianthopoulos, et. al
http://www.researchgate.net/publication/18139787_Founder_effect_in_Tay-Sachs_disease_unlikely
Chakravarti and Chakraborty
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1685578/