Need a complete rewrite.
Genetics and Depression:
Born to Be Unhappy
Dec. 3, 2020
Honors Biology; Genetics and Society
Abstract
No matter what degree, major, or career we want to pursue for settling down in the society, to live a happy and fulfilling life is the ultimately goal for all of us. Unfortunately, happiness is not as rational as math equation or chemical reaction, it requires subjective judgements to be enjoyfully configured. Therefore the ability for human beings to feel happy is very important. It may sound incensivable, but we do have people who feels happy in a poor condition and rich people constantly being depressed live an ideal life that most people in modern soceity could only see it in daydreams. The key point turned out to be how the individual thinks about what they deserved to gain from their limited lifetime and their own definition of a satisfied life quality. Therefore, the concept of depression as a disorder had built to construct the world of those people who get lost due to their disability to dig hapiness out from their clutered situation.
But depression as a mental illness is not easy to define and treat, smetimes the individual refuse to get help, and sometimes the medcine mistaken them into a worse situation due to severe side effects. Obvisely, the lack of scientific approved diagnose leads to many trageties related to depression and the treatments of depression. So the idea of using genetic technologies looks like the light covers the end of turnel as it could not only detect the posibilities for an individual to fell dow the well of depression, but also helps with figuring out more efficent way to treat it based on certain medicine and gene editing. Both treatments for depression and technologies have a huge unknown space for us to explore.
In this review of literature, I try to picture how genetics could contribute to depression and what an exicting challenge is waiting us to go further as accurate as possible.
The earliest written accounts of what is now known as depression appeared in the second millennium B.C.E. in Mesopotamia. In these writings, depression was discussed as a spiritual rather than a physical condition. Like other mental illnesses, it was believed to be caused by demonic possession. As such, it was dealt with by priests rather than physicians.[1] The understanding of depression being caused by devild or evil spirits has existed in many cultures in the world, not limited to the ancient Greeks, Romans, Babylonians, Chinese, and Egyptians…… Due to this belief, it was often treated with methods like physical restraint, and sometimes beatings and starvation in order to drive the demons out. And it is not just the history, those rituals to make mental illed person better are still practiced nowadays somewhere untouched by to much modern technologies.
Clinical depression, also known as major depressive disorder, is the most common form of depression. The Stanford School of Medicine estimates that 10 percent of Americans will experience this type of depression at some point in their lives. This type is also more likely to be shared by siblings and children. A person with a relative who suffers from depression is almost five times as likely to develop it. A British research team recently isolated a gene that appears to be prevalent in multiple family members with depression. The chromosome 3p25-26 was found in more than 800 families with recurrent depression. Scientists believe that as many as 40 percent of those with depression can trace it to a genetic link. Environmental and other factors make up the other 60 percent.
Research has also shown that people with parents or siblings who have depression are up to three times more likely to have the condition. This can be due to heredity or environmental factors that have a strong influence.[2] It clearly show that genes and depression are associated, but the environment also plays a strong key for someone to develop the symptoms. “Anxiety was at the forefront of medical and psychiatric attention in the United States during the 1950s and 1960s. Yet since that time, depression—considered a rare disease in the post–World War II period—has become the focus of mental health concern. One of the most puzzling phenomena in the recent history of psychiatric diagnosis is why depression replaced anxiety as the most commonly treated and researched mental health condition associated with the stress tradition.[3]” It is already very difficult when we see the big environment could dramatically infleunce what the main mental illness in the society that people need to cope with, but it gets to be more coloful when consider with other factors in personal and daily life. Some research already showed that an individual who grows up with someone with depression may be more susceptible to depression as well; A child who observed a depressed parent or sibling may adapt that person’s behavior under some conditions. It is not hard to understand because if a child sees a parent spend days in bed as always, they may not think it should be considered as something unusual. And Gender may also be a factor: There is one study found that women had a 42 percent chance of hereditary depression, but men had only a 29 percent chance.
Depression is just like diabetes when we talk about the outcome from treatments, it is incurable, and the best we can expect from the best treatments are avoiding the symptoms as much as possible to make life easier. But it does not mean that any new research is powerless, there still a lot of spaces about this disease we need to explore to understand it better. Since we learned that there are many genes related to depression, scientists never stoped trying to dig deeper to find a better way to diagnose depression based on scientific evidence instead of psychological evaluation based on interviews. “In 2006, Dr. Lobo and her colleagues found that the Slc6a15 gene was more common among specific neurons in the brain. They recently demonstrated that these neurons were important in depression. Since this gene was recently implicated in depression by other researchers, her lab decided to investigate its role in these specific neurons. In this latest study, she and her team focused on a part of the brain called the nucleus accumbens. This region plays a central role in the brain’s “reward circuit.” When you eat a delicious meal, have sex, drink alcohol, or have any other kind of enjoyable experience, neurons in the nucleus accumbens are activated, letting you know that the experience is pushing the proper buttons. In depression, any kind of enjoyment becomes difficult or impossible; this symptom is known as anhedonia, which in Latin means the inability to experience pleasure. The researchers focused on a subset of neurons in the nucleus accumbens called D2 neurons. These neurons respond to the neurotransmitter dopamine, which plays a central role in the reward circuit. They studied mice susceptible to depression; when subjected to social stress — exposure to larger, more aggressive mice — they tend to withdraw and exhibit behavior that indicates depression, such as social withdrawal and lack of interest in food that they normally enjoy. Dr. Lobo found that when these animals were subjected to chronic social stress, levels of the Slc6a15 gene in the D2 neurons of the nucleus accumbens was markedly reduced. The researchers also studied mice in which the gene had been reduced in D2 neurons. When those mice were subjected to stress, they also exhibited signs of depression. Conversely, when the researchers enhanced Slc6a15 levels in D2 neurons, the mice showed a resilient response to stress. Next, Dr. Lobo looked at the brains of humans who had a history of major depression and who had committed suicide. In the nucleus accumbens of these brains, the gene was reduced. This indicates that the link between gene and behavior extends from mice to humans. It is not clear exactly how Slc6a15 works in the brain. Dr. Lobo says it may work by altering neurotransmitter levels in the brain, a theory that has some evidence from other studies. She says her research could eventually lead to targeted therapies focused on Slc6a15 as a new way to treat depression.[4]” Although it is good to see the genetic factors linked to depression from experiences, depression is still not just caused by a simple mutation. Another research done by a team at the University of Edinburgh showed genome-wide meta-analysis of genetic data from more than two million individuals has showed that there are 102 genetic variants and 269 genes linked with depression, and found associations between the mental disorder and a lot of behavioral traits. The researchers believe their results gained from studies offer new insights into the genetic basis of depression, therefore, helps with inventing new treatments. “Subsequent evaluation of the 269 depression-linked genes for interactions with prescribed drugs in the Drug Gene Interaction Database identified hundreds of interactions between 57 genes and 514 drugs. The researchers pointed out that the drug interaction findings suggest that there are many already available drugs that could target the genetic component of depression, or which may provide unpredicted benefits or have adverse effects in people with the disorder. ‘Further, our work highlights other potential druggable genes associated with depression that are not, to our knowledge, currently associated with antidepressant treatment or mood-associated adverse effects,’ they noted.[5]” The pharmacogenetic testing so far brings up questions and sructures on the future treatments. “More than ten antidepressants (including tricyclics, selective serotonin reuptake inhibitors and venlafaxine) have already genetic biomarkers of response/side effects in clinical guidelines and drug labels. These are represented by functional genetic variants in genes coding for cytochrome enzymes (CYP2D6 and CYP2C19). Depending on the predicted metabolic activity, guidelines provide recommendations on drug choice and dosing. Despite not conclusive, the current evidence suggests that testing can be useful in patients who did not respond or tolerate at least one previous pharmacotherapy. However, the current recommendations are based on pharmacokinetic genes only (CYP450 enzymes), while pharmacodynamic genes (modulating antidepressant mechanisms of action in the brain) are still being studied because of their greater complexity. This may be captured by polygenic risk scores, which reflect the cumulative contribution of many genetic variants to a trait, and they may provide future clinical applications of pharmacogenetics. A more extensive use of genotyping in clinical practice may lead to improvement in treatment outcomes thanks to personalized treatments, but possible ethical issues and disparities should be taken into account and prevented.[6]”
Scientists define “environment factors” for everything under the unbrella of mental illness could go as far as everything that is not an inherited gene.
Although there are studies clearly showed us the linkage between genetics and depression, there are still other strong voices out there point out to environmental factors. Even if there is no sepecific questions on depression genes, mental illness should also be treated as same as physical illness which means that environmental factors definitely are way more important than genetics under certain conditions. Dr. Don Mordecai from Kaiser Permanente said, “It’s a complicated picture. When we say an illness is ‘genetic,’ really we’re saying that there’s some component of it that is genetic. Of the [conditions] that have been studied so far for genetic markers, there aren’t any where if you have the gene, you have the illness.” “What we can definitely see is that there is a genetic predisposition. Genetics can increase your risk, but it’s not a guarantee,” added Dr. Mordecai.[7] A study from the April 2007 issue of Pediatrics as the largest known data shows that children who have at least one depressed parent are more likely to use expensive health services than others. From nearly 25,000 of the children had at least one parent who had been diagnosed as having depression, although teenagers of depressed parents had 5% fewer routine visits, they were more likely to visit emergency departments and specialties like mental health, optometry, orthopedic, ophthalmology, dermatology, and allergy. And infants with depressed parents had 14% more sick visits and 18% more emergency department visits than other infants whose parents are not diagnosed with depression. More screening and treatment of parental depression would result in fewer emergency department visits and other expensive health care practices, and maternal screening during well child visits has already proven successful. [8] From this study, we could see that depression itself could act as an environmental factor to cause a lot of health issues which may not be heritaged as depression to the next generation because more screening and treatment of parental depression works on reducing the frequency of emergency department and other specialtiest visits.
Any teribble experiences- for example, sexual abuse, being victim to crime, lost loved ones, all can produce psychosocial stress. “Feelings of pure loss might lead to depressive disorders, while feelings of pure danger might lead to anxiety disorders,” explains Ronald Kessler, a professor of health care policy at Harvard Medical School. “And feelings of loss and danger might lead to both simultaneously.” Either alone or in combination, psychosocial and physiological stressors can interact with genetic vulnerability to alter brain chemistry and thus alter the individual’s mental health.[9] It brings us back to the time when we just defined depression as a mental disorder and still had no idea about depression genes. Maybe we will just keep rolling around this cycle infinitely since depression is for sure an incurable condition.
To sum up, there is no research was done by no reason, the only way for human beings to survive the depression should be the benefits from a holistic treatments include healthy diet[10] and lifestyle change. The genetics technologies still represet the hope since it is still growing and even if it still cannot accurately point out what cause the depresson, it still help us understand genetic diseases better than before.
Reference:
2 Medically reviewed by Timothy J. Legg, Ph.D., CRNP — Written by Stephanie Faris. Is Depression Genetic? — Updated on July 25, 2017 https://www.healthline.com/health/depression/genetic
[1] Reynolds EH, Wilson JV. Depression and anxiety in Babylon. J R Soc Med. 2013;106(12):478-481. doi:10.1177/0141076813486262
[2] Medically reviewed by Timothy J. Legg, Ph.D., CRNP — Written by Stephanie Faris. Is Depression Genetic? — Updated on July 25, 2017 https://www.healthline.com/health/depression/genetic
[3] Allan V Horwitz, How an Age of Anxiety Became an Age of Depression. Milbank Q. 2010 Mar; 88(1): 112–138. doi: 10.1111/j.1468-0009.2010.00591.x
[4] Ramesh Chandra, T. Chase Francis, Hyungwoo Nam, Lace M. Riggs, Michel Engeln, Sarah Rudzinskas, Prasad Konkalmatt, Scott J. Russo, Gustavo Turecki, Sergio D. Iniguez, Mary Kay Lobo. Reduced Slc6a15 in Nucleus Accumbens D2-Neurons Underlies Stress Susceptibility. The Journal of Neuroscience, 2017; 37 (27): 6527 DOI: 10.1523/JNEUROSCI.3250-16.2017
[5] Genetic Engineering & Biotechnology News, https://www.genengnews.com/news/genetics-of-depression-linked-with-hundreds-of-genes-and-different-behavioural-traits/
[6] Chiara Fabbri1 and Alessandro Serretti, Genetics of Treatment Outcomes in Major Depressive Disorder: Present and Future. Clin Psychopharmacol Neurosci. 2020 Feb; 18(1): 1–9. Published online 2020 Feb 29. doi: 10.9758/cpn.2020.18.1.1
[7]Scott Bloomer, Is Mental Health Illness Hereditary? Are There Any Genetic Roots? https://www.myhealthyclick.com/is-mental-health-illness-hereditary-are-there-any-genetic-roots/
[8] Sills MR, Shetterly S, Xu S, Magid D, Kempe A. 2007. Association between parental depression and children’s health care use. Pediatrics 119(4):e829–e836.
[10] Ellen Greenlaw, A Holistic Approach to Treating Depression. https://www.webmd.com/depression/features/holistic-medicine#1
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