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Thread: Genetic Basis of Cold Tolerance?

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    Post Genetic Basis of Cold Tolerance?

    Hey folks--Here are a couple articles I found that report on a recent study out of U Cal Irvine that suggest a genetic basis for cold tolerance amongst certain populations--including Nordeuropids. I also was able to procure the actual study as well. If anyone wants this, email me and I'd be happy to send you the PDF file...

    All of this though assumes the Out of Africa model though which is of course another debate for another day.

    cheerio!

    From the New York Times:

    By NICHOLAS WADE

    Published: January 9, 2004

    "A team of California geneticists has found that many of the world's peoples are genetically adapted to the cold because their ancestors lived in northern climates during the Ice Age. The genetic change affects basic body metabolism and may influence susceptibility to disease and to the risks of the calorie-laden modern diet.

    The finding also breaks ground in showing that the human population has continued to adapt to forces of natural selection since the dispersal from its ancestral homeland in Africa some 50,000 years ago.

    The genetic adaptation to cold is still carried by many Northern Europeans, East Asians and American Indians, most of whose ancestors once lived in Siberia. But it is absent from peoples native to Africa, a difference that the California team, led by Dr. Douglas C. Wallace of the University of California, Irvine, suggest could contribute to the greater burden of certain diseases in the African-American population.

    Other experts praised the findings about adaptation to cold but said the role of mitochondria, relics of captured bacteria that serve as the batteries of living cells, in these diseases was less certain.

    The genetic change affects the mitochondria, which break down glucose and convert it into the chemical energy that drives the muscles and other body processes. But the mitochondria will generate heat as well, and less chemical energy, if certain mutations occur in their DNA that make the process less efficient. Just such a change would have been very helpful to early humans trying to survive in cold climates.

    Dr. Wallace and his colleagues have now decoded the full mitochondrial DNA from more than 1,000 people around the world and found signs of natural selection. By analyzing the changes in the DNA, they have been able to distinguish positive mutations, those selected because they are good or adaptive, from negative or harmful mutations. In today's issue of the journal Science, they report that several lineages of mitochondrial DNA show signs of positive selection.

    These lineages are not found at all in Africans but occur in 14 percent of people in temperate zones and in 75 percent of those inhabiting Arctic zones. Dr. Wallace and his colleagues say this correlation is evidence that the lineages were positively selected because they help the body generate more heat.

    Until now, most genetic change in the human population since it left Africa has been thought to be either random or just the elimination of harmful mutations. The evidence of the new analysis is that positive or adaptive selection "played an increasingly important role as people migrated out of Africa into temperate and Arctic Eurasia," the California team writes.

    One implication is that everyone is adapted to a particular climate zone, and that moving to different zones may cause certain stresses. Mitochondria of the lineages found in Africa, Dr. Wallace suggests, may contribute the extra burden of certain diseases found among African-Americans, like diabetes and prostate cancer.

    His reasoning is that African lineage mitochondria have never had to develop a mechanism for generating extra heat. So when an African-American and a European-American eat the same high calorie diet, the European's mitochondria burn some calories off as heat but the more efficient African mitochondria are liable to generate more fat deposition and oxidative damage, two results that could underlie the higher disease rates, Dr. Wallace said.

    Separately, some of the European mitochondrial lineages appear to protect against Alzheimer's and Parkinson diseases and to be associated with greater longevity.

    "Therefore," the California team writes, "to understand individual predisposition to modern diseases, we must also understand our genetic past, the goal of the new discipline of evolutionary medicine."

    While many scientists study the genes of the human cell's nucleus, Dr. Wallace has focused on the tiny mitochondrial genome for 33 years. Along with the late Dr. Allan Wilson, he has pioneered the tracing of the 20 or so mitochondrial lineages found in the human population, all of which link back to a single individual known as the mitochondrial Eve.

    Several other experts said that Dr. Wallace's ideas were promising but that the role of mitochondria in degenerative diseases had yet to be established. "It's a very attractive idea and may well turn out to be right, although the biochemical evidence of uncoupling differences between the mitochondrial lineages has yet to be nailed down," said Dr. Lawrence Grossman, a mitochondria expert at Wayne State University.

    Dr. Mark Seielstad, a population geneticist at the Genome Institute of Singapore, said the positive selection was likely to have been a "major architect" in shaping mitochondria and that Dr. Wallace's work should throw open discussion of the subject.

    Two experts on mitochondrial disease, Dr. Michael Brown of the Mercer University School of Medicine in Macon, Ga., and Dr. Gino Cortopassi of the University of California, Davis, said Dr. Wallace's ideas about African mitochondria made sense but had yet to reach practical significance. "We've not yet got to the stage of being able to give advice to African Americans," Dr. Brown said.

    Dr. Wallace says that climatic selection may have operated on the human population from the moment it moved north of the African tropics. Most such pioneers died but two lineages, known as M and N, arose in northeast Africa some 65,000 years ago and might have been adapted to temperate climates. Almost everyone outside of sub-Saharan Africa has mitochondria descended from the M and N lineages."


    Another article that I ripped-off but can't remember from where...


    "Ancient DNA mutations permitted humans to adapt to colder climates, UCI researchers find

    Changes in cells' mitochondria may explain current predispositions to common diseases

    Irvine, Calif., January 12, 2004
    How did early humans who migrated from Africa survive in the colder climates of Europe, Asia and the New World? According to a new UC Irvine study, it may be the same reason some people today are more prone to obesity, Alzheimer's disease and the effects of aging.

    In the Jan. 9, 2004, issue of Science, a UCI research team reports that key mutations in the mitochondrial DNA (mtDNA) of human cells may have helped our migrating ancestors adapt to more northerly climates, and ultimately link people with this ancestral history to specific diseases.

    Found outside the cell's nucleus, mitochondria are the power plants of cells that are responsible for burning the calories in our diet. The cellular energy is used for two purposes: to generate heat to maintain our body temperature and to synthesize ATP (adenosine triphosphate), a chemical form of energy that permits us to do work such as exercise, think, write, and make and repair cells and tissues. The mtDNAs are the blue prints for our mitochondrial power plants and determine the proportion of the calories in our diet that are allocated to generate body heat versus work.

    According to Douglas C. Wallace, the Donald Bren Professor of Biological Sciences and Molecular Medicine at UCI and one of the co-authors of the report, after early humans migrated to colder climates, their chances of survival increased when mutations in their mtDNA resulted in greater body heat production during the extreme cold of the northern winters.

    "In the warm tropical and subtropical environments of Africa it was most optimal for more of the dietary calories to be allocated to ATP to do work and less to heat, thus permitting individuals to run longer, faster and to function better in hot climates," Wallace said. "In Eurasia and Siberia, however, such an allocation would have resulted in more people being killed by the cold of winter. The mtDNA mutations made it possible for individuals to survive the winter, reproduce and colonize the higher latitudes.

    "This explains the striking correlation between mtDNA lineage and geographic location that we still see today in indigenous populations around the world."

    It also explains why people with a certain ancestral history may be more susceptible to some diseases.

    "When heat and cold are managed by technology, not metabolism, and people from warmer climates are eating the high fat and calorie diets of northern climates, there is a rise in obesity and the age-related degenerative diseases," Wallace said. "The caloric intake and local climate of many individuals are out of balance with their genetic history. Thus, our genetic history is linked to our current diseases, resulting in the new field of evolutionary medicine."

    One link would be the production of oxygen radicals in cells. Created when mitochondria burn our dietary fuel, this by-product can be responsible for damaging and killing cells, leading to several age-related diseases. "When calories are unutilized for producing heat or ATP, they are redirected to generate oxygen radicals," Wallace said. "Since the mutated DNA of cold-adapted people allocates more calories to heat, there are fewer left over to generate oxygen radicals. Hence these people are less prone to aging and age-related degenerative diseases." (For more details on oxygen radicals, see below.)

    In the study, Wallace and his UCI colleagues Eduardo Ruiz-Pesini, Dan Mishmar, Martin Brandon and Vincent Procaccio analyzed 1,125 human mtDNA sequences from around the world to reconstruct the mutational history of the human mtDNA back to the original mtDNA, known as the mitochondrial Eve.

    Wallace is the director of the Center for Molecular and Mitochondrial Medicine and Genetics at UCI and is a faculty member in the Departments of Ecology and Evolutionary Biology, Biological Chemistry and Pediatrics. This study was funded by the National Institutes of Health and the Ellison Medical Foundation.

    How mtDNA control the production of oxygen radicals
    When mitochondria burn our dietary fuel, they generate a toxic by-product called oxygen radicals, the mitochondrial equivalent to the smoke generated by coal-burning power plants. Oxygen radicals damage the mitochondria, mtDNA and the surrounding cell. Eventually oxygen radicals can cause the cell to die when sufficient oxidative damage accumulates in the mitochondria and the cell.

    Since many of the tissues of our bodies have a finite number of cells, when sufficient cells die organs malfunction, resulting in the symptoms of age-related degenerative diseases and aging. As a result, the chronic level of mitochondrial oxidative stress will determine an individual's aging rate and susceptibility to a variety of diseases such as diabetes, memory loss, forms of deafness and vision loss, cardiovascular disease, etc.

    If all the calories that an individual consumes are used in generating carbon dioxide, water and energy, little fuel is left over to generate the oxygen radicals; however, if more calories are consumed than are needed to make energy, then these excess calories are stored as fat and drive a chronic increase in mitochondrial oxygen radical production.

    Consider two individuals that eat the same number of calories and get the same amount of exercise. The individual with a mtDNA mutant that increases heat production will require more calories for energy production and thus will have fewer calories left over to produce oxygen radicals. This individual will be partially protected from age-related diseases and will live longer. By contrast, the individual with mitochondria that make more ATP per calorie burned will store fat and generate more oxygen radicals if he or she eats the same level of calories as the individual with the cold-adapted mitochondria."

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    Post Re: genetic basis of cold tolerance?

    Really interesting theory.

    There are many adaptions to temperated and cold climate of course.
    One of many reasons for saying that it is more rational to let races optimal adapted to a specific climate in the region for what they are made for.

    Especially Negrid which are just made for a very specific climate and culture.
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    Post Re: genetic basis of cold tolerance?

    How about a real life example and a question. I live in the mountains. This winter my dog, a Malamute, has persuaded me to let him sleep inside, out of the snow. Since I have done this he has gained a great deal of weight. This bulk might have otherwise been converted into heat. He now weighs over 130 lbs. This must be a mitrochondrial-heat transformation. Should I kick him back outside?

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    Post Re: genetic basis of cold tolerance?

    I have another example. This was a study conducted on Norwegian submarine mates about 60 years ago before our adventure into DNA. I can't site the reference because I can't find it, but I can give a summary.

    The men on the submarine that had the least and fewest occurrences of frostbite were blonde-haired and blue-eyed. The most frequent sufferers of frostbite were the dark-haired with dark eyes followed by dark-haired with light eyes. Even amongst full brothers, one having light hair & eyes and the other having dark hair & light eyes, the dark-haired were more susceptible to frostbite and other cold injuries.

    I wish I could find this study. Grrrr.

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    Post Re: genetic basis of cold tolerance?

    I believe lighter skin is has a greater adaption to the cold because there is less melinonin is the skin and I am pretty sure that protects you from sunburn and cannot get hot as easily. Nords can be sunburnt extemely easily and must wear sun block at all time on hot days. I know freckles are melinonin and maybe that is why blacks have "clamier skin" I do not wear sun tan lotion because I do not need it. I had sun poisioning last summer(in the South),but I really only need sun block in the southern states. The North's hottest weather will not do anything to my skin. I never really answered the question though" Is it genetic"?, I would say yes and no. If your mother is very nordic and your father is med, the child could take all the mother's skin features. No, because if you are darker skinned you will get colder.

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