Is General Anxiety Disorder Genetic?

 Anxiety disorders, which include generalized anxiety disorder, panic disorder, and phobias, are among the most prevalent forms of mental illness, with a lifetime incidence of over twenty percent. Both obsessive-compulsive disorder and post-traumatic stress disorder were removed from the DSM's diagnostic category because of the unique neurobiological and etiological components of each condition. Anxiety disorders have a high rate of co-occurring conditions and are recognized as one of the leading contributors to disability on a global scale. They are extremely chronic and rank sixth among mental and somatic disorders in terms of "years lived with disability" and "disability-adjusted life years" per 100,000 persons. They also have a high prevalence rate. Genes and environmental stressors are the most commonly cited contributors to the development of anxiety disorders, and both are known to play a significant role in the disorder's etiology. The present body of research has a primary emphasis on the hereditary, acquired, and epigenetic factors that contribute to the development of anxiety disorders.

The evidence supporting the heritability of anxiety disorders is investigated in this paper. Particular attention is paid to the results of large-scale, unbiased GWAS studies as well as EWAS efforts to detect differential DNA methylation patterns. On the other hand, the majority of findings are not able to be reliably duplicated, and the majority of research does not have the power to decipher the intricate genetic architecture of anxiety disorders. To improve illness prognosis, disease course, and response to treatment therapies, the focus of future research should shift toward large samples that have been thoroughly defined as well as meta-analyses. To treat anxiety, it is vital to take advantage of the genetic covariance that exists with other illnesses, and it is essential to take into account both environmental and biological risk factors while attempting to prevent or cure anxiety disorders.

https://link.springer.com/article/10.1007/s11920-019-1002-7

https://www.sciencedirect.com/science/article/pii/S0306452209010616?casa_token=rkomevOg5MQAAAAA:ojCnHeu6kYtHWJw67993KYSnIGUbGcyJXxJdR3ntvTOY0oMRpjq7PS-jKJ7rZsVUhU8WI8Peebls

FKBP5 Befriends Chronic Pain

              Recently published in the United Kingdom’s Science Translational Medicine Journal, researchers suggested that a new protein blocking mechanism may be the key to treating chronic pain. Chronic pain is defined as pain that begins over a twelve week period, and lasts for weeks to years. This condition is normally found in the lower back region, but in some cases it can affect the neck and face. Chronic pain is associated with post-traumatic stress disorder and depression which is caused by certain variations of a gene called FKBP5. Researchers pursue to gain better knowledge on how FKBP5 adds to chronic pain.

              During their research, genetically modified mice were altered to lack FKBP51, a variation of FKBP5, which plays a role in stress regulation. There were no negative side effects and mice were more mobile with normal pain responses. In the second half of the experiment, researchers blocked FKBP51 in the spinal cord with a protein gene called SAFit2. This protein is normally used to reduce anxiety by blocking brain activity, but by using SAFit2 to block FKBP1, mice showed that it significantly reduced chronic pain. Although this is a new study, researchers may have found the answer they were looking for to cure chronic pain.

               In my opinion, I believe this research has potential to solve chronic pain in humans. Even though this research is fairly new, SAFit2 has shown significant results in reducing chronic pain within mice spinal cords. Mice have been model icons for research and have lead many of diseases and conditions to multiple cures. The only disadvantage to using mice for chronic pain research is that the gene that regulates stress in humans is different than the gene that regulates mice stress. Although the variation of FKBP1 can be blocked by SAFit2 , the P5 variation may require different proteins to block it in humans. Researchers have definitely moved closer to solving the mystery of chronic pain, but without developing a drug that can be used within humans, researchers will find them further exploring this unusual condition.

Inherited Stress

On March 7, 2014, New York Times posted an article called “Inheriting Stress.” This article explains how they believe that the stress experienced in a person’s lifetime is correlated with the stress-related problems in that person’s offspring. Scientist tried to prove this by studying the children and grandchildren of the Holocaust survivors. Research showed that the survivors’ children had greater chances of having stress related illnesses. An example of an illness is post traumatic disorder. Researchers also found similar correlations in other populations like in Rwanda, Nigeria, Cambodia, and Armenia. Scientists did a study on female rats. The female rats went through a mild stress procedure for seven days and then mated with non-stressed male rats. The study showed that there were behavioral differences between the adult progeny of the stressed and non-stressed females. The researchers questioned how the stress was transmitted and focused on a gene that encodes a molecule involved in the body’s response to stress. They found larger amounts of the molecular product of this gene in the brains of the previously stressed female rats and also found this gene present in their ova. The researchers believed that the gene was transferred by the ova. Stress can play a major role in a person’s life. This article was very interesting. I have never thought about stress as a molecular product of a gene that can be inherited. Hopefully there will be more research and a result to prove if this is true or not. 

Gene Linked to PTSD

When referring to Post-traumatic Stress Disorder, it is often said that not all wounds are visible.  PTSD is a debilitating disorder that quite literally destroys lives.  Trauma that initiates PTSD becomes so embedded in the mind of the person suffering from the disorder that it can lead to major depression, anxiety, insomnia, difficulty forming relationships, and even suicide.  But now, it has been discovered that there is indeed a genetic component to this disorder, which may eventually lead scientists to a cure.

According to Medical News Today, Ya-Ping Tang, MD, PhD, of New Orleans has found that a specific gene is critical to the adult-onset PTSD.  In particular, the action of this specific gene occurs during adolescent exposure to trauma.  This specific transgene has been identified as CCKR-2.

Not only is the original trauma significant to PTSD, but in most cases, a second stressor or "re-victimization" is essential to the development of this disorder.  In studies done with mice, original trauma and a second stressor were not enough on their own to cause PTSD.  However, with the introduction of CCKR-2, PTSD-like behavior was finally observed.

This identification of CCKR-2 and its significance in the development of Post-traumatic Stress Disorder have finally provided fresh hope for treatment of those who suffer from this life-altering condition.  Now that CCKR-2 is a known cofactor in the brain that coincides with adolescent trauma, it is possible for scientists to prevent and even cure PTSD by developing a way to block the reception of the neurotransmitter CCKR-2.  By doing so, generations could be spared the intense agony that is known as PTSD.

Study Identifies PTSD Genes

A study done by UCLA scientists have linked two genes to the cause of post traumatic stress disorder. Some people will be affected by this disorder, and others who undergo the same experiences will not be affected by PTSD. These genes are in serotonin production, and lead to a higher risk of developing PTSD. The findings suggest that PTSD is inherited, and there may be new ways to screen for it and treat the disorder. Dr. Armen Goenjian, a research professor of psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA, says that people can develop post-traumatic stress disorder after surviving a life-threatening ordeal like war, rape or a natural disaster. He says, "If confirmed, our findings could eventually lead to new ways to screen people at risk for PTSD and target specific medicines for preventing and treating the disorder." PTSD can arise following child abuse, terrorist attacks, sexual or physical assault, major accidents, natural disasters or exposure to war or combat. Symptoms include flashbacks, feeling emotionally numb, and avoiding situations that remind the individual of the original trauma.

Goenjian and his team took the DNA of 200 adults from several generations of 12 extended families who suffered PTSD symptoms after surviving the devastating 1988 earthquake in Armenia. In this study of the families' genes, researchers found that those who possessed specific variants of two genes were more likely to develop PTSD symptoms. These genes are TPH1 and TPH2, and they control the production of serotonin, a brain chemical that regulates mood, sleep and alertness. These symptoms are all disrupted in PTSD. Geonjian suggests that the gene variants produce less serotonin, and predisposes these family members to PTSD after exposure to violence or disaster. He wants to try and replicate the findings in a larger, more heterogeneous population as a next step for the study.  "A diagnostic tool based upon TPH1 and TPH2 could enable military leaders to identify soldiers who are at higher risk of developing PTSD, and reassign their combat duties accordingly," says Goenjian. "Our findings may also help scientists uncover alternative treatments for the disorder, such as gene therapy or new drugs that regulate the chemicals responsible for PTSD symptoms."

[caption id="attachment_4365" align="aligncenter" width="220" caption="Regions of the brain associated with stress and post traumatic stress disorder"][/caption]