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    Home»Lifestyle»Wellness»Rewriting Your Genetic Blueprint
    Wellness

    Rewriting Your Genetic Blueprint

    Marnie Blount-GowanBy Marnie Blount-GowanSeptember 11, 2013Updated:October 29, 2013No Comments5 Mins Read0 Views
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    Do we make genes our scapegoats? How often have you heard someone say, “I’ll probably get (fill in the blank disease) because it’s in my genes.” This thinking is understandable, but there is more to the story.

    Research shows that genes, which carry traits from one generation to another and were once considered unchangeable elements in our biological blueprint, can be altered during a person’s lifetime.

    Emerging research in genetics and epigenetics indicates that everything we do and experience can affect our genes, our health and the health of future generations. It’s all about gene expression. In humans, to express oneself is to communicate. At a cellular level, a similar “expression” happens with genes.

    The medical community has long suggested that a healthy lifestyle—including exercise, good nutrition and stress reduction practices—can strengthen our resistance to disease. Yet we may have discounted the need to change our behavior by thinking our genetic makeup would doom us to suffer certain diseases anyway.

    Today, the science of epigenetics shows that a genetic code predisposed to a specific disease or disorder doesn’t necessarily determine how it will manifest itself in the body. Epigenetics is a hopeful field that blends psychiatry, chemistry and physiology to benefit the whole person.

    “It is hoped that epigenetic research will help us understand more clearly the causes of human diseases and also how we are different from one another,” explains Dr. Stephen Faraone, professor of psychiatry and behavioral sciences, director of medical genetics research and head of child and adolescent psychiatry research at SUNY Upstate Medical University.

    Genes may be modified by environmental factors, pharmaceuticals and behaviors. Faraone adds, “Current research into epigenetics makes the old conversation about nature vs. nurture irrelevant. Epigenetics studies the modification of the effect of genes, the activity of genes, and the amount and type of protein that the gene expresses. . . all of which may make us more or less susceptible to disease.”

    The hope is that treatments designed with an understanding of epigenetics would reduce someone’s susceptibility to diseases. Local researchers at SUNY Upstate Medical University attempt to identify what could be called “switches” that turn on or off and how these switches change the type of protein and expression of protein in the cells. For example, Faraone’s studies focus on ADHD (attention deficit hyperactivity disorder), identifying protein transporters that affect neurotransmission and ADHD symptoms.

    There may be up to 1,000 genes involved in ADHD, about 30 percent of them have been identified. These genes have accumulative predisposition to ADHD, so the more you have, the more likely you are to have ADHD. Faraone suggests that, “Like blood pressure {which everyone has, but some of us have high or low blood pressure}, many people can have the same genes but they can be expressed in many different ways.” Those different gene expressions may have different impact on an individual’s well-being.

    In the research at SUNY Upstate, they discovered genes with multiple variants. The message is, “It’s not just one bad gene but many, many variations, which once identified, could potentially be targets for epigenetic modification.”

    Faraone explains that because there can be overlay in disorders, such as ADHD and autism, genetic and epigenetic research may be applied to a wide spectrum of symptoms. While this research offers promise for medical treatment and preventative interventions, Faraone emphasizes the need for current interventions. “We have good pharmacological and cognitive behavior treatments, and those with symptoms should seek help.”

    Another area of study is the epigenetics of stress. Recently, researchers at the National Institutes of Health found that chronic exposure to stress hormones causes modifications to DNA in the brains of mice, prompting changes in gene expression. When rats were subjected to neglectful mothering, the normal number of glucocorticoid receptors (positive gene expressions) were prevented from being transcribed in the baby rat’s brain, causing them to grow up to be nervous wrecks. But after receiving a drug to remove the methyl group (negative gene expressions), the animals showed none of the behavior problems.

    Other research shows an epigenetic link between maternal behaviors and stress. In rats, licking shows love. Rats reared by high-licking mothers grew up to be less stressed as adults than those raised by low-licking mothers. Scientists saw that if they exchanged babies born to high- and low-stress mothers, the baby rats took on the characteristics expressed by the mother rearing it, not their biological mother. These findings suggest that the expression of genes that regulate stress activity can be transmitted from one generation to the next through behavior because that behavior causes an epigenetic change.

    Faraone suggests that stress-reduction practices—such as meditation and other healthy behaviors, which are supported by strong clinical evidence—can be useful to people.

    Whether or not, or how, a healthy lifestyle changes gene expression and susceptibility to disease, the positive effects of exercise, nutrition and stress management are well documented. We can’t just blame our genes when our behavior, environment and proven drug interventions can send good signals to our cells and benefit our lives.

    “There is a very important argument to be made that anything we do or any environmental event has the potential to cause changes in gene expression,” concludes Faraone.

    For information: Genetics Home Reference (National Institutes of Health) ghr.nlm.nih.gov.

    Marnie Blount-Gowan is a member of the Crouse Hospital Integrated Health Alliance.

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    Marnie Blount-Gowan

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