Genes-R-Us DNA, environment slow dancing since conception

Genes-R-Us DNA, environment slow dancing since conception

Posted: Wednesday, December 14, 2011 5:03 pm

By NANCY LATIMER
Special to The Messenger
Last week you were formally introduced to epigenetics. However, you and your epigenome are hardly strangers. Since conception, your DNA and your environment have been slow dancing. And if your family’s medical history has you feeling as if you drew the “short DNA straw,” epigenetics is good news for you, indeed. Genes, as it turns out, are only part of your story.
Your epigenetic environment includes so many things like your diet, exercise level,  management of stress at home and at work, quality of friendship network, childhood exposure to second hand smoke, mom’s prenatal physical and mental health, dad’s drinking history prior to your conception, quality and quantity of sleep and so on. 
Even the diet of grandparents, who were exposed to severe food shortages at certain times in their physical development, can impact the way genes are expressed two generations later. 
So how do scientists disentangle genetic and environmental effects? 
One way to order the importance of genetics versus the environment is by examining the difference in traits between very large numbers of identical twins and fraternal twins.
Identical twins have the exact same genome (i.e., DNA). Fraternal twins share the same amount of DNA as any other set of full siblings. On average, full siblings share around 50 percent but it can vary down to 0 percent. 
Clearly identical twins are genetically more similar than fraternal twins. But any set of twins, identical or fraternal, are scientifically valuable compared to full non-twin siblings in that twins shared the same in utero environment. Even without DNA analysis, scientists can study differences between identical and fraternal twins to learn about genetic versus environmental effects.
How? Scientists study which traits and diseases are more common in identical twins as compared to fraternal twins. In general, higher rates in identical twins will imply a greater genetic influence. However, the differences between rates for the identical versus. fraternal twins groups must also be considered. 
Such studies have been used to infer the relative order of genes versus environment for various traits and diseases (i.e. phenotypes). The effect of environment increases relative to the effect of genetics as one moves down this list of traits: height, reading disability, autism, Alzheimer’s disease, schizophrenia, alcoholism, bipolar disorder, hypertension, diabetes, multiple sclerosis, breast cancer, Crohn’s disease, stroke, rheumatoid arthritis. 
Height is at the top of the list above. Ninety percent of identical twins are the same height compared to less than 60 percent of fraternal twins. Compare this to stroke, near the bottom, where less than 20 percent of identical twins share this trait compared to around 5 percent for fraternal twins.
Loosely speaking, epigenetics is the study of the “choke-hold” that environment puts onto the genome that somehow silences (as is usually the case) or activates genes. And, yes, there are cases where the “choke-hold” can be transmitted to subsequent generations. How does this “choke-hold” happen, biochemically speaking?
There is no simple answer, as the various biochemical processes are rather complex. Just consider one process called methylation. Methyl groups (one carbon plus three hydrogen atoms — the stuff of organic chemists’ dreams) attach themselves to DNA and, thereby, can change how much protein a gene is able to manufacture.  
A certain breed of laboratory rats provides an amazing illustration of methylation. The anxiety level of these rats is completely controlled by how much licking the baby rats receive in the first week after birth. Pups without the licking are more anxious than those getting the maternal licks. 
The baby rats’ blood level of cortisol, a stress hormone (or protein), is a biomarker for the pups level of anxiety. Ignored pups have higher baseline levels of cortisol. 
Here is what is happening. The “molecular mop” for the stress hormone cortisol is made by a gene called the glucocorticoid receptor (Gr). When the pup is born, the Gr gene has a whole bunch of methyl groups attached to it. The Gr gene is thus turned off  and, consequently, there are very few mops around to suck up the excess cortisol.
When momma licks her pup, the methyl groups are released from the DNA on and around the GR gene. This allows the cortisol mopping-up protein to be manufactured by the GR gene.
Once the mopping proteins are in the bloodstream, they start soaking up the excessive cortisol, binding it up, so it not free to induce stress in the pups. 
Amazingly, it is only in the first week or so where these methyl groups can be dislodged from the GR gene. So once the pup is anxious, it tends to stay anxious as an adult.
Please don’t blame any General Anxiety Disorder on your mother because she did not cuddle you enough as a baby. One must be very careful in extrapolating rat models for anxiety to humans.  
Editor’s note: Nancy Miller Latimer has worked in scientific research and development for 27 years. She blogs at neuronalbeauty.blogspot.com.
Published in The Messenger 12.14.11

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