“Recent copious and regional evolution” = current events

read for comprehension and not for a knee jerk reaction and you may get a clue! As is usual for beneficial adaptations, the gain in fitness came at a cost of functional information. Moreover, the mutation appears to arise by an epigenetic process, i.e. a 'directed' mutation, not by a 'random' process.bornagain77

May 13, 2014

May

05

May

13

13

2014

04:11 PM

4

04

11

PM

PDT

Copy Comment Link

"Adult Lactose Tolerance Is Not an Advantageous Evolutionary Trait". How do you figure this? Maintaining the lactase enzyme into adulthood opens up a new nutrient source for those smart enough to learn how to milk a cow or a goat. Natural selection would certainly favour those that can metabolize milk over those who can't.Acartia_bogart

May 13, 2014

May

05

May

13

13

2014

03:05 PM

3

03

05

PM

PDT

Copy Comment Link

lactose intolerance and the ability to live at high altitudes are examples of loss, not gain, in functional information: Recently new rare 'beneficial' mutations were found in Tibetans that have allowed them to survive in extremely high altitudes, with less oxygen. Yet once again the new 'beneficial mutations' are actually found to be 'slightly detrimnetal' because they in fact result in a limit on the red cell blood count for Tibetans: Tibetans Developed Genes to Help Them Adapt to Life at High Elevations - May 2010 Excerpt: "What's unique about Tibetans is they don't develop high red blood cells counts," http://www.sciencedaily.com/releases/2010/05/100513143453.htm Yet high red blood cell counts are found to be good,, Extremely fit individuals may have higher values—significantly more red cells in their bodies and significantly more oxygen-carrying capacity—but still maintain normal hematocrit values. http://wiki.medpedia.com/Red_Blood_Cells#How_It_Works ,,,Thus they were actually incorrect to imply that all high red blood cell counts found in humans are detrimental,,, This following article goes into more detail and points out many other inconsistencies with the Tibetan mutations that evaporate any claim for evidence of a 'truly' beneficial mutation: Tibetans Evolved Altitude Tolerance in 3,000 Years? - July 2010 http://www.creationsafaris.com/crev201007.htm#20100703a , lactase persistence is actually a loss of a instruction in the genome to turn the lactase enzyme off, so the mutation clearly does not violate Genetic Entropy (nor Dr. Michael Behe's 'Edge Of Evolution'). Got milk? Research finds evidence of dairy farming 7,000 years ago in Sahara Excerpt: In premature babies, the gene coding for lactase is sometimes not yet active. And in much of the world’s population, the gene is downregulated after weaning, eventually producing some degree of lactose intolerance. Those whose genes are not downregulated are said to have “lactase persistence.” However, even lactose-intolerant people still have genes coding for lactase enzyme; they are just switched off. In an adult with lactase persistence, one or both alleles of the lactase gene remain switched on. http://www.answersingenesis.org/articles/2012/07/07/news-to-note-07072012 Moreover lactase persistence clearly appears to be a 'designed mutation',, Adult Lactose Tolerance Is Not an Advantageous Evolutionary Trait - Juan Brines, MD Excerpt: In short, evidence does not support the evolutionary hypothesis of lactase persistence in human adults as a consequence of selection. A founder effect could be a more suitable explanation to justify this trait, and this mechanism does not need the cooperation of natural selection. http://pediatrics.aappublications.org/content/114/5/1372.1.full a 'designed mutation' that has 'serendipitously' originated independently three different times: Convergent adaptation of human lactase persistence in Africa and Europe Excerpt: We conducted a genotype-phenotype association study in 470 Tanzanians, Kenyans and Sudanese and identified three SNPs (G/C-14010, T/G-13915 and C/G-13907) that are associated with lactase persistence and that have derived alleles that significantly enhance transcription from the LCT promoter in vitro. These SNPs originated on different haplotype backgrounds from the European C/T-13910 SNP and from each other. http://www.nature.com/ng/journal/v39/n1/full/ng1946.html Of related note: Daily thought: blue eyes and other gene mutations, April 25, 2013 Excerpt: "Research on blue-eyes has led many scientist to further affirm that humans are truly mere variations of the same origin. About 8% of the world's total population has blue eyes so blue eyes are fairly rare. In fact, blue eyes are actually a gene mutation that scientist have researched and found to have happened when the OCA2 gene "turned off the ability to produce brown eyes." http://www.examiner.com/article/daily-thought-blue-eyes-and-other-gene-mutations Critic ignores reality of Genetic Entropy - Dr John Sanford - 7 March 2013 Excerpt: Where are the beneficial mutations in man? It is very well documented that there are thousands of deleterious Mendelian mutations accumulating in the human gene pool, even though there is strong selection against such mutations. Yet such easily recognized deleterious mutations are just the tip of the iceberg. The vast majority of deleterious mutations will not display any clear phenotype at all. There is a very high rate of visible birth defects, all of which appear deleterious. Again, this is just the tip of the iceberg. Why are no beneficial birth anomalies being seen? This is not just a matter of identifying positive changes. If there are so many beneficial mutations happening in the human population, selection should very effectively amplify them. They should be popping up virtually everywhere. They should be much more common than genetic pathologies. Where are they? European adult lactose tolerance appears to be due to a broken lactase promoter [see Can’t drink milk? You’re ‘normal’! Ed.]. African resistance to malaria is due to a broken hemoglobin protein [see Sickle-cell disease. Also, immunity of an estimated 20% of western Europeans to HIV infection is due to a broken chemokine receptor—see CCR5-delta32: a very beneficial mutation. Ed.] Beneficials happen, but generally they are loss-of-function mutations, and even then they are very rare! http://creation.com/genetic-entropy Human Genetic Variation Recent, Varies Among Populations - (Nov. 28, 2012) Excerpt: Nearly three-quarters of mutations in genes that code for proteins -- the workhorses of the cell -- occurred within the past 5,000 to 10,000 years,,, "One of the most interesting points is that Europeans have more new deleterious (potentially disease-causing) mutations than Africans,",,, "Having so many of these new variants can be partially explained by the population explosion in the European population. However, variation that occur in genes that are involved in Mendelian traits and in those that affect genes essential to the proper functioning of the cell tend to be much older." (A Mendelian trait is controlled by a single gene. Mutations in that gene can have devastating effects.) The amount variation or mutation identified in protein-coding genes (the exome) in this study is very different from what would have been seen 5,000 years ago,,, The report shows that "recent" events have a potent effect on the human genome. Eighty-six percent of the genetic variation or mutations that are expected to be harmful arose in European-Americans in the last five thousand years, said the researchers. The researchers used established bioinformatics techniques to calculate the age of more than a million changes in single base pairs (the A-T, C-G of the genetic code) that are part of the exome or protein-coding portion of the genomes (human genetic blueprint) of 6,515 people of both European-American and African-American decent.,,, http://www.sciencedaily.com/releases/2012/11/121128132259.htmbornagain77

May 13, 2014

May

05

May

13

13

2014

09:24 AM

9

09

24

AM

PDT

Copy Comment Link