Anxiety
Anxiety disorders are incredibly debilitating due to their effect of manifesting worry and avoidance that greatly impairs the individual at school, work, home, etc.. Those at highest risk of developing an anxiety disorder are children and young adults. Panic and social anxiety disorders have been used to study epigenetic mechanisms that could potentially influence this expression. Treatment for anxiety disorders are rooted in methods such as therapy, but it appears that this technique only helps with short-term treatment. Since much isn't known about the development of anxiety disorders, prescribing medication to treat anxiety can cause serious complications due to the eleven types of anxiety disorders that have been classified. Therefore, it is through illuminating the biological processes involved epigenetically that it can be determined what mechanisms are responsible for the regulation of genes involved in anxiety expression.
There is a 30-50% range in which genetic variance contributes to the development of an anxiety disorder. So, this leaves a 50-70% variance range that could potentially have environmental influence. This development could be due to epigenetic mechanisms that could begin in utero, due to mother's influence regarding DNA methylation of the gene NR3C1 at the promoter region. Implementing candidate genes for further study could potentially highlight how a person is susceptible to develop an anxiety disorder epigenetically.
As seen previously in the post regarding eating disorders, neural development is comprised when maternal stress occurs during pregnancy. This essentially has a negative impact on development, for there is decreased methylation in the CpG sites on the Crh promoter found in the hypothalamus of the brain, which leads to elevated stress in offspring. Maternal stress also influences epigenetic changes in the cortex. Rln helps to regulate brain development, therefore when increase DNA methylation is found on the promoter region, this may be a contributing factor to how anxiety disorders become developed. The effect of the environment on the fetus during pregnancy plays a significant role in gene expression in regards to development of anxiousness.
Changes in environment during early life can also influence epigenetic changes that contribute to the expression in genes that result in anxiety behaviors. Maternal separation impacts the genes found within the hippocampus. There is an increase in DNA methylation within many of these genes at the promoter, which suggests the potential for offspring to respond negative to stress. The amygdala is also affected by maternal separation, where increased methylation is also found at the promoter regions of many genes responsible for the activity of neurotransmitters. Therefore, early life experiences contribute to epigenetic changes in many genes found within these regions of the brain.
In human studies, DNA methylation is found in patients with anxiety disorders, such as, panic and social anxiety. Understanding where the sites of methylation occur could be critical in the designing of treatment strategies for the specific disorders being studied. Drugs can also be a factor used to treat individuals suffering from anxiety disorders, but these can also cause epigenetic changes. Greater understanding of methylation in associatiion with pharmacological treatment could be incredibly helpful in alleviating anxiousness and panic.
Furthermore, understanding the epigenetic and genetic interactions are important to consider as well. Exposure to stress early in life in relation to family experiences can leave lasting effects on anxiety behaviors and epigenetic changes. The effect of stress on a female can result in influencing their epigenome due to the care that they give their offspring, which could lead to epigenetic changes in the child. Therefore, familial association is significant in their ability to influence inherited epigenetic effects regarding maternal behavior to their offspring.
Each individual is unique in their own way. Even when it comes to anxiety disorders and the scale we fall on in association to how extreme these behaviors are expressed. When implementing and designing treatment strategies, making personal connections to an individual's genotype, methylation status, and personal experience all need to be considered when administering the right care. The more time and energy we give towards researching the epigenetic influence on each of the unique anxiety disorders could be monumental in its ability to provide specific treatment options for individuals. Many great discoveries have been presented in connecting what it is the epigenetic changes are targeting to result in the expression of anxiety behaviors. Genes that regulate the HPA axis (in relation to stress), neurotransmitter systems, and neuroplasticity have been discussed. What deserves more focus is the epigenetic influence on different time spans in an individual's life: differences in development, childhood, and adulthood. How the changes in environment over the span of our lifetime could contribute to greater expression of behavioral disorders in association with anxiety.
Some tips and tools to utilize if you find yourself struggling during an anxiety or panic attack:
References:
1. Nieto, S. J., Patriquin, M. A., Nielsen, D. A., & Kosten, T. A. (2016). Don’t worry; be informed about the epigenetics of anxiety. Pharmacology, Biochemistry, and Behavior, 146-147, 60–72. http://doi.org/10.1016/j.pbb.2016.05.006
There is a 30-50% range in which genetic variance contributes to the development of an anxiety disorder. So, this leaves a 50-70% variance range that could potentially have environmental influence. This development could be due to epigenetic mechanisms that could begin in utero, due to mother's influence regarding DNA methylation of the gene NR3C1 at the promoter region. Implementing candidate genes for further study could potentially highlight how a person is susceptible to develop an anxiety disorder epigenetically.
As seen previously in the post regarding eating disorders, neural development is comprised when maternal stress occurs during pregnancy. This essentially has a negative impact on development, for there is decreased methylation in the CpG sites on the Crh promoter found in the hypothalamus of the brain, which leads to elevated stress in offspring. Maternal stress also influences epigenetic changes in the cortex. Rln helps to regulate brain development, therefore when increase DNA methylation is found on the promoter region, this may be a contributing factor to how anxiety disorders become developed. The effect of the environment on the fetus during pregnancy plays a significant role in gene expression in regards to development of anxiousness.
Changes in environment during early life can also influence epigenetic changes that contribute to the expression in genes that result in anxiety behaviors. Maternal separation impacts the genes found within the hippocampus. There is an increase in DNA methylation within many of these genes at the promoter, which suggests the potential for offspring to respond negative to stress. The amygdala is also affected by maternal separation, where increased methylation is also found at the promoter regions of many genes responsible for the activity of neurotransmitters. Therefore, early life experiences contribute to epigenetic changes in many genes found within these regions of the brain.
In human studies, DNA methylation is found in patients with anxiety disorders, such as, panic and social anxiety. Understanding where the sites of methylation occur could be critical in the designing of treatment strategies for the specific disorders being studied. Drugs can also be a factor used to treat individuals suffering from anxiety disorders, but these can also cause epigenetic changes. Greater understanding of methylation in associatiion with pharmacological treatment could be incredibly helpful in alleviating anxiousness and panic.
Furthermore, understanding the epigenetic and genetic interactions are important to consider as well. Exposure to stress early in life in relation to family experiences can leave lasting effects on anxiety behaviors and epigenetic changes. The effect of stress on a female can result in influencing their epigenome due to the care that they give their offspring, which could lead to epigenetic changes in the child. Therefore, familial association is significant in their ability to influence inherited epigenetic effects regarding maternal behavior to their offspring.
Each individual is unique in their own way. Even when it comes to anxiety disorders and the scale we fall on in association to how extreme these behaviors are expressed. When implementing and designing treatment strategies, making personal connections to an individual's genotype, methylation status, and personal experience all need to be considered when administering the right care. The more time and energy we give towards researching the epigenetic influence on each of the unique anxiety disorders could be monumental in its ability to provide specific treatment options for individuals. Many great discoveries have been presented in connecting what it is the epigenetic changes are targeting to result in the expression of anxiety behaviors. Genes that regulate the HPA axis (in relation to stress), neurotransmitter systems, and neuroplasticity have been discussed. What deserves more focus is the epigenetic influence on different time spans in an individual's life: differences in development, childhood, and adulthood. How the changes in environment over the span of our lifetime could contribute to greater expression of behavioral disorders in association with anxiety.
Some tips and tools to utilize if you find yourself struggling during an anxiety or panic attack:
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References:
1. Nieto, S. J., Patriquin, M. A., Nielsen, D. A., & Kosten, T. A. (2016). Don’t worry; be informed about the epigenetics of anxiety. Pharmacology, Biochemistry, and Behavior, 146-147, 60–72. http://doi.org/10.1016/j.pbb.2016.05.006
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