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Lucky Man, by Michael J. Fox, is an autobiography documenting the story of his personal  life and career before and after being diagnosed with Parkinson’s. The book covers his life before Parkinson’s, including his childhood growing up on various military bases across Canada, his relationship with his family, and his initial interest in acting. He writes about his explosive rise and success in the television and film industry, perhaps most notably his roles in Family Ties and the Back to the Future films, which made him a worldwide celebrity. His discovery of Parkinson’s symptoms began when he noticed a twitching in his pinkie. Parkinson’s most commonly occurs in patients between fifty and sixty years of age, and Fox had just turned thirty at the time, so the doctors said it was unlikely that somebody his age would have such a disorder. However, he was officially diagnosed with Young Onset Parkinson’s disease. For some time, understably, Fox was in denial, hoping that the diagnosis was a mistake. Parkinson’s is a murky disease since there is no definitive cause, but a combination of genetic and environmental factors may have contributed to his development of it. As time went on, he struggled with dealing with the news. In the early days he felt exasperation, fear, frustration, and anger, and often questioned who to blame. He started out taking the prescribed medications, and did not go to see a neurologist until years later. Fox writes with honesty about his denial and how he dealt with the news of the disease with alcohol abuse. For a long time, Fox turned to alcohol as an ally to help him cope with his struggle with Parkinson’s. He finally recognized his drinking problem and that alcohol was an adversary that threatened to ruin his life and the things and people he cared about. He finally made the decision to quit, and succeeded with the support of his family and friends. He describes that this decision to quit drinking was one of the first things he is grateful to Parkinson’s for. Throughout the novel, Fox refers to the disease as a “gift”, and that living since being diagnosed with it has made him lucky. One of the “gifts” of the disease is a clarity about other aspects of his life, and appreciation for the areas one actually has control over. Fox also discusses his struggle in keeping his disease a secret from the public and trying to hide his tremors in order to keep his career going. At the height of his career he kept his disease a secret for seven years since diagnosis, and finally in September of 1998 he announced that he had Parkinson’s. After this point he retired from the television show Spin City and started his career as a spokesperson for Parkinson’s disease and other neurological disorders. He started the Michael J. Fox Foundation, dedicated to finding a cure for PD through aggressive funding and research into developing therapies for those battling Parkinson’s. The book is written with honesty, self-deprecation, and humor, and has an overall positive note. Michael J. Fox recounts his experiences as a chance to appreciate his life and career, and the opportunity to help look for a cure and spread awareness of the disease; he considers the ten years since his diagnosis to be a gift, making him a lucky man. Inside the O’Briens Summary Inside the O’Briens, by Lisa Genova, is a fictional book about a middle-aged man who is diagnosed with Huntington’s disease. The book documents his personal life: he is a dedicated police officer in his mid-forties, who lives with his family in an Irish Catholic neighborhood in Charlestown, Massachusetts. The book explores his life which is occupied by the typical issues surrounding marriage, career, and children. When he is finally diagnosed with Huntington’s disease, this drastically changes his and his family’s life, and the standard issues that most people face pale in comparison. He begins to notice the signs of the diseases when he starts having atypical outbursts of hot temper, becomes disorganized, especially related to his job, and experiences random, involuntary movements, as well as the loss of voluntary motor control. At first, he thinks these things are caused by the excessive stress of his job, but it soon becomes evident that there is something much more serious at hand. He finally sees a neurologist and is diagnosed with Huntington’s disease. The book documents how this diagnosis affects him and his family. He very easily loses his temper, gets extreme and uncontrollable bouts of anger, is unable to do his job, and eventually loses the ability to even hold things. The author delves deep into the emotions of Joe and his family, exploring the family dynamic and the prevalence of desperation, depression, anger, and frustration throughout. The book explores the struggles of his wife, Rosie, to maintain patience as her husband slowly loses his mind. He drops things, breaks things, and punches holes in walls in his fits of anger. Along with exploring the struggle of Joe and his wife, the book also explores the struggle of his children after finding out that they are at such high risk of developing the disease as well. The story focuses on his twenty-one year old daughter Katie who, along with his other three children, are torn about whether or not they should get genetically tested to find out if they have the mutated gene. Is it better to live without knowing and only find out if and when symptoms arise? Or is it better to get tested so that they do not risk passing it on to their own children in the future? Not knowing fills their life with fear and uncertainty, but on the other hand, living with knowledge that they will develop symptoms like their father and most likely die an extremely slow and painful death, is a huge burden. The book is extremely raw and delves into the effects of the merciless disease on a fairly normal family. The author educates readers on the disorder, while also maintaining a compelling and dynamic story. Parkinson’s DiseaseIntroduction and Symptoms. Parkinson’s disease is a long-term neurodegenerative disorder of the central nervous system, that mainly affects the motor system, primarily neurons that produce dopamine in the substantia nigra of the brain. Parkinson’s tends to develop gradually, often starting with a slight tremor just in one hand, transitioning to stiffness and slowing of movement (Mayo Clinic Staff, 2015). Although the progression of symptoms is different from one person to another, symptoms generally progress to more severe tremors, bradykinesia (slowed movement), limb and muscle rigidity, gait, posture, and balance issues, and slurred and soft speech. Besides these direct symptoms, Parkinson’s is also accompanied by additional complications including depression or other emotional shifts, difficulties in cognitive ability and thinking, problems swallowing, sleep disorders, bladder and constipation issues, blood pressure alterations, a flawed sense of smell, and sexual dysfunction (Elkouzi, 2017). Parkinson’s generally develops in middle or later life, and the risk increases with age. Most commonly, people around the age of sixty or older develop the disease. Other risk factors include heredity, age, and sex. Having a relative with Parkinson’s increases the chances of someone getting the disease, and if many people in a family have it, the chances increase even more. Men are also around 1.5 times more likely than women to develop Parkinson’s (Mayo Clinic Staff, 2015). There is not yet a cure for Parkinson’s, but certain medications and treatments can improve symptoms. The reason there is no cure and proven prevention is unknown is because the direct cause is unknown, however there are several known factors that play a role. Disease Causes. Parkinson’s is described as idiopathic, in which the exact cause is unknown. With Parkinson’s, neurons in the brain gradually break down or die. Most of the neurons are ones that produce dopamine, and as the dopamine levels decrease, abnormal brain activity increases, leading to manifestation of Parkinson’s symptoms. The cause of this neuron death is unexplained, but the main factors that play a role are a person’s genetics and environmental triggers. Certain research has identified specific genetic mutations that may cause Parkinson’s, however they are fairly uncommon – less than ten percent of cases are primarily due to genetic causes. This rare case is most commonly marked by a mutation in a gene called LRRK2, a member of the leucine-rich repeat kinase family. The defect in LRRK2 is especially frequent in families of North African or Jewish descent (“Causes of Parkinson’s”, 2017). Some research shows that mutations in the alpha-synuclein protein of the brain have been found to trigger the disease, although this is rather rare. In most cases, about ninety percent, no primary genetic cause has been found. Another potential factor that may contribute to the development of Parkinson’s is environmental. Ongoing exposure to certain toxins, like herbicides, pesticides, or heavy metals, may put one at a slightly increased risk of Parkinson’s. The connection, however, is difficult to formulate because a very long time can pass between an exposure to toxins and the appearance of disease symptoms. Another environmental factor, besides exposure to toxins, may include repeated head injuries (Mayo Clinic Staff, 2015). Although it is difficult to confirm the connection between specific environmental factors and the disease, it does seem likely that they do influence the development of the disease especially in people who have a genetic susceptibility as well. Treatments. Currently there exists no cure for Parkinson’s, but certain measures can be taken to control symptoms. Treatments include various medications, lifestyle changes, surgical procedures, pathology etc. Medications manage problems associated with movement and tremors because most increase and/or substitute for dopamine. Medications include carbidopa-levodopa, carbidopa-levodopa infusion, dopamine agonists, MAO-B inhibitors, COMT inhibitors, and anticholinergics. Carbidopa-levodopa is currently the most effective medication: levodopa is a chemical that once passed through the brain converts to dopamine. It is combined with carbidopa which defends the levodopa from converting to dopamine outside of the brain, lessening nausea. Although this medication is effective, after many years as Parkinson’s progresses, the benefits may become unstable and wear off. Carbidopa-levodopa infusion is administered through a drug called Duopa which is delivered through a feeding tube in a gel straight from the small intestine. This is given to patients at an advanced stage of the disease. Dopamine agonists are not as effective as levodopa but they do last longer and may be used in tandem with levodopa to stabilize levodopa’s on-and-off effect. These drugs mimic the dopamine effect in your brain, they do not change into dopamine. MAO-B inhibitors are drugs that prevent the breakdown of dopamine in the brain by inhibiting the enzyme that metabolizes dopamine. Often these drugs are added to carbidopa-levodopa. COMT inhibitors prolong the effect of levodopa therapy by blocking enzymes that break down dopamine. Anticholinergics help control tremors, however the small benefits are counteracted by bad side effects (Mayo Clinic Staff, 2015). In the later stages of Parkinson’s, surgical procedures may also be done. Deep Brain Stimulation (DBS) is a surgical procedure done for Parkinson’s patients because it does not destroy brain tissue, it is adjustable as the disease progresses, is reversible, and bilateral procedures are able to be done without negative effects. DBS is performed by surgeons who implant electrodes into a specific area of the brain. These electrodes are connected to a generator implanted in the chest area near the collarbone. This generator sends electrical impulses to the brain and reduces some symptoms of the disease. This is most commonly offered to people with an advanced stage of Parkinson’s who have unstable responses to medication like levodopa. What DBS can do is stabilize the responses to medication, diminish involuntary movements and tremors, and improve the slowing of movement that often comes with the disease. DBS often provides a continuous aid for symptoms, however, it does not keep the disease from progressing (Hauser et. al., 2017). Lifestyle adjustments including changes to diet, exercise, and daily routine, may also help make living with Parkinson’s a bit easier. A combination of medications, possible DBS surgery, and lifestyle changes help control the symptoms of Parkinson’s disease, although no cure currently exists. Genetic Testing and Ethical Issues Surrounding. Genetic testing is an option for some Parkinson’s disease patients: it should by no means be conducted in every patient, but there are genetic factors that should be considered when dealing with a patient. Most cases of Parkinson’s are sporadic, only ten to fifteen percent have genetic ties. The three most common gene mutations are in the PARK2 (parkin), LRRK2, and glucocerebrosidase (GBA) genes. Parkin testing is difficult because it is a large gene, and testing is only likely to provide a meaningful result for an early onset of the disease. It is mostly worthwhile for juvenile (before the age of twenty), or sometimes before the age of thirty, onset. LRRK2 testing may be worthwhile in North African Arabs because about thirty to forty percent have the LRRK2 gene with a thirty to forty percent penetrance. Since many mutations may not cause the disease and have low rates of penetrance, genetic testing is primarily used for research purposes, and may help find the rare families with an autosomal dominant or recessive form of parkinsonism (“Learning About Parkinson’s Disease”, 2014). Some of the ethical issues surrounding genetic testing are related to test access, informed consent, return of results, policies to prevent discrimination, and risk estimation. Presymptomatic testing is performed on an individual who has no symptoms of the disease at the time of testing, but wants to see whether or not they have a mutant gene and identify their risk of developing the disease (Watson Thus, the main ethical issue with this is, is a person better off knowing? This question is very personal and it is important to allow for personal autonomy, so if a person does or does not want to know, they should have the right to make that choice. The psychological cost that comes with knowing one’s fate is an ethical concern which makes this decision very difficult. There does not currently exist one standard, singular process of completing genetic testing, so the fact that people must go through the process differently raises some ethical and practice issues. It is important to make sure that everybody has equal access to tests, test results are returned, communicated and dealt with adequately, and there exist certain policies to prevent genetic discrimination. Equality, access and adequacy of the process may mean different things to different people, which is why this is a hazy subject to approach, raising many questions surrounding the fairness of genetic testing (Roberts, 2013). The ethics of genetic testing applies to all diseases that have a hereditary aspect, like Parkinson’s, Alzheimer’s, Huntington’s etc., however, as discussed previously, Parkinson’s disease has a fairly small genetic connection. Therefore the ethical concerns surrounding genetic testing are not as prevalent as they are for extremely hereditary diseases such as Huntington’s. Huntington’s Disease Introduction and Symptoms. Huntington’s Disease is a fatal, genetic, progressive disorder that causes the breakdown of nerve cells in the brain. The disease has no cure and severely deteriorates the individual’s physical and mental abilities. Symptoms of the disease most commonly appear between the ages of thirty and fifty, and gradually get worse over the course of ten to twenty-five years. The disease is fatal because ultimately, the individual gives in to a complication such as pneumonia or heart failure. Symptoms of the disease include movement disorders such as involuntary jerking and writhing, abnormal eye movement, muscle rigidity known as dystonia, impaired posture and balance, and difficulty with speaking and swallowing. Cognitive disorders associated with Huntington’s include difficulty in organization and prioritization of tasks, lack of impulse control and flexibility of thought, absence of awareness of one’s behaviors and abilities, difficulty in processing thoughts, finding words, and learning new information. Psychiatric disorders that often come with the disease include OCD, mania, and bipolar disorder (Mayo Clinic Staff, 2017). In the early stage of HD, the individual develops subtle changes in coordination and mood, becoming more depressed and irritable. These changes make a person less functional in regular activities and their work. In the middle stage, the movement disorder develops further and poses more problems. Diminished speech and complications in swallowing accompany the movement complications. In the late stage, the person with HD is almost entirely dependant on others to take care of them. The individual may no longer be able to walk or talk, but can generally comprehend language and retains awareness. Death is not directly from the disease, but from complications that come with it such as choking, or infection (“What Is Huntington’s Disease?”, 2017). Disease Cause and Treatments.  Huntington’s Disease is hereditary, caused by an inherited defect in a gene. It is an autosomal dominant disorder, meaning that the mutated gene is a dominant gene located on a nonsex chromosome. This means that if a child has a parent with the disease, the child has a fifty percent chance of inheriting the gene that causes the disease. If the gene is not inherited by the child, they do not risk ever developing or passing the disease. The pattern of inheritance is such that the altered HTT gene is passed from one generation to the next, and the size of the CAG repeat increases. A phenomenon known as anticipation takes place, meaning that a larger number of repeats is associated with the early onset of the disorder. People with a juvenile-onset form of HD have more CAG repeats in the HTT gene than people with adult-onset of the disorder (“Huntington’s disease – Genetics Home Reference”, 2013). There is no treatment for the disease but some medications can help a person deal with many of the symptoms associated with movement and psychiatric disorders. A drug called Tetrabenazine suppresses involuntary jerking and writhing, also known as chorea. Antipsychotic drugs have side effects of suppressing movement, so may be helpful in lessening chorea. Other medications can help lessen cognitive effects. Medications to treat psychiatric disorders depend on the person, because everyone has different psychiatric responses to the disease. Medications may include antidepressants, antipsychotic drugs, and mood-stabilizing drugs. Psychotherapy, speech therapy, physical therapy, and occupational therapy may also be helpful in dealing with the symptoms of the disease. The lifestyle of people with HD will need to change because as the disease progresses, they will need to depend more on caregivers to help them handle everyday tasks such as eating, dressing, prioritizing and initiating tasks, avoiding stressors, and maintaining social interactions  (Mayo Clinic Staff, 2017).Genetic Testing and Ethical Issues Surrounding. Since Huntington’s is an autosomal dominant disorder, an individual has a fifty percent chance of passing the mutated gene to their child, therefore, the decision to have predictive testing done is one many have to struggle with. The test works by taking a blood sample from the individual and the genetic test analyzes the DNA for the mutation by counting the number of CAG repeats found in the huntingtin gene. Those who have fewer than twenty eight repeats do not have the disease, and individuals who do have it generally have forty or more repeats (“Learning About Huntington’s Disease”, 2011).  Testing leads to ethical debates regarding the decision to know one’s fate, reproductive rights, third party disclosure and genetic discrimination. The first question is whether or not it is ethical to provide individuals with information regarding their future when no cure for the disease is available. Ultimately, it is the individual’s choice, and they have the right to know their future health. However, it is important to discuss how to conduct the disclosure of results and support the patient after they receive the results, since this news drastically changes an individual’s life. Some argue that the knowledge of having the disease may do more harm than good because it will be a huge psychological burden on the individual and their loved ones, making living with that knowledge, even before the symptoms arise, extremely difficult. Others argue that it is very important for a person to know, so that they are able to plan their lives effectively with the time they have remaining. Either way, the decision is extremely personal and critical, so pre-testing psychiatric evaluation must be performed to establish the person’s ability to handle results. Another ethical issue that comes with genetic testing for HD is the right to reproduce. Many with HD and those at-risk for HD struggle with the decision to reproduce, since the offspring would be at such a high risk of developing HD. Is it ethical to have a child knowing that the child might develop the fatal disease? A related dilemma is whether a parent has the right to know health information about their children. If a parent who is at-risk of HD has a child and wants to find out if the child has the gene mutation, they currently cannot. Genetic testing for children or adolescents is prohibited unless the child shows symptoms, as the child might not understand the implications of testing. It may seem unreasonable for a mother not to know the health future of her child, but when the child becomes an autonomous adult they can get tested, and symptoms can only arise when the child will be an autonomous adult. Another ethical concern for those at risk of carrying the gene is genetic discrimination, a denial of rights or opportunities based on genetic information. There is the possibility of stigma and discrimination in fields like insurance, employment, and relationships. The ethical dilemma of third-party disclosure is a large issue because the information could be used by these third parties, like insurers or employers, to deny individuals opportunities they would have received otherwise. There are certain regulations in place to prevent genetic discrimination, but issues do still arise (Kromberg et. al., 2013). Genetic testing is a highly individual and drastic choice that an at-risk person struggles with, and many ethical issues surrounding autonomy, reproductive rights, and genetic discrimination, must be taken into consideration by individuals and medical professionals when considering and evaluating genetic testing.