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Ancient DNA Mutations Permitted Humans To Adapt To Colder Climates,
Researchers Find
Irvine, Calif., Jan. 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.
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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.
About the University of California, Irvine: The University of
California, Irvine is a top-ranked public university dedicated to
research, scholarship and community. Founded in 1965, UCI is among the
fastest-growing University of California campuses, with more than 23,000
undergraduate and graduate students and about 1,300 faculty members. The
third-largest employer in dynamic Orange County, UCI contributes an
annual economic impact of $3 billion.
------------------------------------------------------------------------
/This story has been adapted from a news release issued by University Of
California - Irvine./
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