Epigenetics: Understanding Gene Expression

Posted: February 27, 2013 in Uncategorized
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As a strength coach and nutritionist I hear one excuse more then others.  People tend to blame their issues on their genetic makeup.  There are some things that we cannot control such as: eye color, sex, and height.  However, that does not mean we are destined for a life of being sick and overweight.

Our genetic code is wrapped up in our DNA and then bundled into 23 pairs of chromosomes.  The DNA is wrapped around proteins that are called histones. On the outside of these histones are chemicals that listen for cues from inside our body and from our outside environment.  This whole piece is referred to as the epigenome.

The epigenome is responsible for the shape and structure of our genome.  It tightly wraps up inactive genes so that they are not able to be read by other cells.  On the contrary it relaxes its grip around active genes so that cells can easily access them.  The DNA code is fixed for a lifetime, but the epigenome can be altered by environmental changes and this is referred to as epigenetics.

The chemicals that surround the outside of the epigenome react to cues from our environment.  Some of these cues include diet and stress.  This is an amazing piece of the human body.  It allows us to thrive in changing environments.  A good example of how this process works is using exercise.  If we lift weights the chemical tags on the outside of the epigenome pick up on that cue.  To counter the changes in the outside environment they signal the production of new muscle tissue.  If it were not for that mechanism I would probably still be wearing children’s clothes!

Understanding this concept is important when looking at genetic disorders.  A disease such as Huntington’s Disease (HD) usually comes on post-reproductive age.  Huntington’s Disease is a trinucleotide repeat disorder.  This is referred to as the CAG repeat.  A non-HD person will typically have 10-28 of these CAG repeats while a HD positive person will have 36-120.  This can cause the cells to act abnormally.

The CAG repeats form what is known as polyglutamine tracts.  These polyglutamine tracts cause abnormal cell architecture and the longer they are the more damage they do (http://www.ncbi.nlm.nih.gov/pubmed/9462744).  We need to look at the epigenetic factors that are causing this gene to express itself.  One of these issues is gluten in which we will get to in much greater detail at a later time.

The range in which people start showing symptoms of the disease is usually between 35-50 years old.  Tends to be that the longer the CAG repeats the earlier it begins, but this is not always the case.  Why does one person with a 36 CAG repeat get a disease much later then a similar person with the same CAG repeat?  Having this observational data would make a starting point much easier.

Just because you have a specific genetic disorder it does not mean that that gene needs to express itself.  We need to figure out the environmental triggers that are causing that to occur.  This may prove to be a much simpler test then attempting to develop a drug or proceedure to fix it.  However, there is a group of drugs called antisense oligonucleotides (AS0) that show great promise in blocking the Huntington protein message in monkeys and mice.  This was published in the journal Neuron in June (http://www.dailymail.co.uk/health/article-2162132/Huntingdons-disease-cure-step-closer-scientists-slow-disorder-mice.html).  We will discuss the mechanisms of those drugs to further understand the disease and how to prevent it in the next blog post.

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