Atherosclerosis
is contributed to a healthy diet and adequate exercise, but family genetics can
be the X factor. The concern for this
disease should not be secluded to only people that lack exercise or a healthy
diet. A proper healthy diet low on fats and complimented with adequate exercise
can reduce the probability of heart disease, but it does not eliminate the
chances.
Currently
the London Olympics of 2012 is under the spotlight, but a great swimmer is not
among them due to atherosclerosis. Certainly, everyone understands the strict
diets and daily exercise routines that Olympic athletes undergo during
training. The death of a Norwegian athlete swimmer, by the name of Alexander
Dale Oen, came at almost a complete surprise.
Alexander
Dale Oen, born on May 21st 1985, was only age 26 on April 30th 2012 when he was
found unconscious in this hotel room in
Arizona during his training camp in the USA. After being brought to the hospital in
Flagstaff Medical Center he was pronounced dead. A later autopsy found that he
had suffered from a heart attack due to a chronic, coronary heart disease. A more detailed autopsy reported that his
left descending artery was blocked by
atherosclerotic plaque.
Alexander
is Norway's first Olympic medalist. He won silver during the 2008 Beijing
Olympics by coming second in the 100 meter breaststroke finals. Alexander is
also had some notable achievements over his swimming career including gold at
the 2008 European Championships and setting a new Nordic record for the 100 meter
breaststroke.
A picture of Alexander Dale Oen:
Unfortunately,
he will not be participating in this year's Olympics. This goes to show that atherosclerosis
genuinely is not discriminatory towards healthy individuals with top physical
fitness compared to individuals of less physical fitness. Although a healthy
diet and adequate exercise may help reduce the risks of a heart disease, the
genes passed down by past generations can play a major factor.
A tribute to Alexander by his admirers:
Genetics
help map out our bodies are constructed from within. Scientists have found that
there is a major gene that contributes to how our body stores certain fats. A
proposed mechanism of lipid peroxides being stored is thought to be related to
how genes recognize, oxidize, and produce an inflammatory response to lipids.
A
recent study published online on July 3, 2012 in the journal Cell Metabolism
commented that they have identified a signaling pathway that may control both
atherosclerosis and obesity. Scientist
from the Singapore Bioimaging Consortium and institute of Molecular and Cell
Biology determined that mice deficient in the Wip1 gene were resilient against
weight gain and atherosclerosis. This gene can potentially affect how lipids
are stored and recognized in the body and help prevent many disease, including
heart disease. The mice in this study were found that through the regulation of
the Ataxia telangiectasia mutated gene and the signaling molecule mTor, the
mice was able to resistant to weight gain and atherosclerosis. Whether, or not,
this gene is applicable to humans yet is still unclear, but nevertheless, this
is a leap forward in finding a potential treatment in the genetic aspect of
atherosclerosis.
References:
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http://in.news.yahoo.com/mechanism-controls-both-obesity-atherosclerosis-identified-121155576.html
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