This research paper is a proposal for an epidemiological survey that examines some of the gaps and deficiencies to overcome and the necessary interventions to reduce or completely cure Huntington’s disease. The paper will identify and discuss the population at risk of getting Huntington’s disease, an analysis of the background of the illness and its genetic epidemiological effect. In addition to this, an analysis will be carried out that hypothesizes the elements that contribute to or expand the gap that exists between the progression of the disease’s cure and its status. It is at this point, where the research paper will propose a solution that seeks to minimize this gap. Furthermore, a discussion of the methodology of the research will be provided, in addition to, identification of useful statistics, and applicable legal and ethical ramifications. Finally the paper will draw a summary that examines the future opportunities and the current ones for how the study could be essential in addressing these gaps to come up with applicable solutions to Huntington’s disease.
There is currently a gap that exists between the new research on Huntington’s disease and the fading guidelines developed by the EHDN, the European Huntington’s Disease Network, for the utilization of genetic testing to predict the presence of the disease, information about the cure and ways to prevent the disease and familiarity on ways to eradicate or reduce the disease. Such a gap could result to numerous challenges. If not dealt with, the gap and absence of knowledge and information will keep on growing and could limit genetic testing, treatment, and management of the disease as the number of symptomatic individuals, especially from the Baby Boomer generation, and soon their offspring, increases in the coming years. This could in turn lead to the development of a roadblock in the management or treatment of Huntington’s disease that would rattle clinical labs and hospitals in the globe, potentially hurting the patient treatment outcomes(Nuffield Council on Bioethics, 2006).
A number of organizations, for instance European Huntington’s Disease network, seems to have identified the issue and appears to be willing to solve the problem. In one of its studies, the organization observed that the reactions, comments and suggestions from the participants in the coming congress are critical in filling this void. EHDN came up with numerous guidelines for predictive testing based on genes in 1994, a year later after scientist cloned with the first Huntingtin gene, which was mapped in 1983 to chromosome 4. Since then, the scientists have made some considerable advancement, as medical centers and other management centers offering prenatal tests and care gained significant amount of experience on how to deal with the disease(Nuffield Council on Bioethics, 2006).
However, 15 years later, little has been done in terms of updating guidelines, tests, management techniques, cures and other ways to restore body functions and to reduce the implications of Huntington’s disease. In the past few years, scientists in numerous, different institutions have made great improvements in understanding the underlying causes of Huntington’s disease and other neurogenerative disease(Nuffield Council on Bioethics, 2006). As they come up with more details of such diseases and disorders, it is becoming likely that they will be competent to avoid and care for these diseases with time. Nevertheless, as for most key projects, the greater resources are brought together, the more likely the discovery of cures and the faster the progress. As it follows, despite the fact that scientists are doing a remarkable job at research aimed at coming up with a cure and decreasing symptoms of the disease, more encompassing studies and research is required to comprehend the impacts of the illness on the individuals, the role of professionals in providing care, appropriate environments and setting to care for the patients, and better treatment options for the disease(Prainsack &Siegal, 2006).
The purpose of this research proposal, therefore, is to point out to some gaps in information and knowledge that can be useful in eliminating or reducing Huntington’s disease. The proposal seeks to point out where these gaps exist, why they exist and ways in which scientists can close these gaps to result to palliative care of patients of Huntington’s disease that is more comprehensive, improved and that, which leads to better patient outcomes.
The mean age at Huntington’s disease onset is about 37 years of age, but not necessary that age as it might range between individuals aged two years old and 85, several cases occurring outside this range. In individual cases, Huntington’s disease onset may be hard to identify, especially when psychiatric and behavioral changes are out to consideration, in those patients who are followed closely, a zone of onset of symptoms manifests itself across 3 to 5 years, the occurring symptoms also are distinct. A survey carried out to discover out the nature of onset of Huntington’s disease, the researchers found that neurological symptoms showed the onset of the disease in around 59 percent of the participants, while psychiatric or psychological symptoms were noted first in 23 percent of the participants, and 18 percent of the participants displayed both at disease onset(Haddad& Cummings, 1997).
Studies carried out on a population with frequent Huntington’s disease endemic indicated that patients first develop subtle changes in clumsiness and volitional eye movement before they display frank changes in motor abilities due to the disease. At first, individuals affected by the disease show, spasmodic, involuntary movements of facial and limb muscles. Over a period, such individuals lose normal motor abilities and functions and they eventually are not able to move at all. This is indicative of patients affected by the disease. Juvenile Huntington’s disease, which has significantly noticeable, different phenotype starts with rigidity, akinesia and dystonia and is usually accompanied by myoclonic tremors in the muscles and seizures or twitches. The progression of the disease takes place independent of any healthcare interventions. One evident gap in this case is that scientists have not yet determined whether or not the speed of progress of the disease is reliant on the repeats of CAG length, therefore, limiting the prognostic genetic testing value of the severity of the disease and progression or not (Haddad& Cummings, 1997).
Studies estimate that the prevalence of Huntington’s disease is between 3 and 10 individuals in every 100, 000 people in Europe. Most HD patients are identified because of the presence of a suggestive issue with the neurological system with a positive HD family history. Although a certain study found out that more than 25 percent of the HD patients did not have any family history with the disease. Although in most cases, the disease family history of the patient is obscured by competitive mortality, misdiagnosis or obfuscation, scientist show that not less than 8 percent of Huntington’s disease patients with negative disease family history may show new mutations in their genes resulting from borderline permutations(Harper& Morris, 1991). In addition to this, it is likely that the study of Huntington’s disease suffers immensely from lack of information and poor reporting of patients, studies carried out on mutational flow show that appropriate and accurate disease diagnosis is poor with Huntington’s disease that occurs later in life. Current epidemiological data indicates that there are between 25 and 30 thousand Huntington’s disease patients in the US alone. On average, five first level relatives are at risk of developing Huntington’s disease from each affected person. As it follows, this study is dealing with about 75 to 150 thousand individuals in the United States alone who might be at risk of developing Huntington’s disease (Harper& Morris, 1991).
Huntington’s disease occurs, as a result, of degeneration of brain cells known as neurons, a process that is genetically programmed in particular parts of the brain. The degeneration in turn leads to uncontrolled movements, emotional disturbance and loss of faculties for intellectual reasoning. Huntington’s disease is a familial disease, and it is passed from parent to offspring though the mutation of a functional, normal gene. As it follows, each child of a parent with Huntington’s disease has a significant chance of inheriting the mutated Huntington’s disease gene. However, if the offspring does not inherit the disease, he or she will not have the ability to pass it to the next generation and will most likely not develop the disease. An individual who receives the mutated gene will, in most cases, suffer from the disorder and has a likelihood of passing it to the next generation. Whether one offspring inherits a Huntington’s disease gene or not does not determine whether the other off springswill not or will inherit the mutated gene (Harper& Morris, 1991).
The disease manifests itself in numerous ways. Some of the early symptoms indicating the presence of the Huntington’s disease causing gene include mood swings, irritability, depression or trouble driving, remembering things, learning new things or making choices and decisions. As the disorder develops and progresses, concentration on intellectual activities become difficult and the patient experiences difficulties in doing certain activities like feeding themselves or swallowing. The age of onset and the speed of development of the illnessare different in different individuals, a genetic test combined with a complete family medical history and laboratory and neurological tests are used to determine whether an individual has Huntington’s disease or not (Harper& Morris, 1991).
The genetic mutation that leads to the development of Huntington’s disease is a trinucleotide repeat that is both unstable and expanded found in the short arm of the chromosome 4. In this region of the genome, the affected gene usually has less than 30 repeats of CAG. In cases where there are about 40 or more repeats of CAG, Huntington’s disease is usually completely penetrant. A gene becomes fully penetrant when all carriers of the gene show or develop the disease. When penetrance is low or reduced, some carriers never develop the symptoms for the disease (Haddad& Cummings, 1997). In cases where there are between 36 and 40 repeats of CAG in the causative gene, Huntingtin gene, Huntington’s disease is usually less than completely penetrant, butbecause of the instability resulting from the mutation, a mutation that is full length may be passed to ones off springs where the disease develops. When there are between 30 and 35 repeats, the carrier of the gene usually develops the disease, even though a longer repeat of CAG length may be transferred to the subsequentage group. The instability in the trinucleotide repeat is usually more prominent in genes of male carriers, which results to the rare development of juvenile symptoms onset in some children of men with Huntington’s disease (and in some cases women). Because of this persistent instability, the mutation may develop de novo in a certain family (Haddad& Cummings, 1997).
Since information, knowledge and resources for health interventions are limited and few, high priority has to be placed on the need to establish which interventions are most useful and beneficial to the population in treating and managing Huntington’s disease (Haddad& Cummings, 1997). However, despite this fact, efforts to come up with interventions to cure and manage Huntington’s disease have been slowed down and limited by the gap that exists between theprogression of Huntington’s disease cure and the current status of the disease. There are different factors contributing to the progression of this gap. Before identifying these factors, the paper has to point out to the current status of the disease.
Scientists argue that to improve the outcomes of a screening program for Huntington’s disease, one option is to target individuals who at a higher risk of developing HD, usually the families of the affected individuals. In this case, the approach limits the amount of resources required for screening and increases the outcomes of screening. It is, however, unfortunately limited by the fact that numerous, new cases of Huntington’s disease and other genetic diseases occur in people without any family history who would not be pointed out by screening based on families. In other case, ethnic groups are at times targeted for screening programs, especially, when the incidence of the disease is exceedingly high in that certain group(Green, 2006).
Genetic screening and testing have come part of public health and modern medicine initiatives. While these terms are at times utilized interchangeably, they both mean different things. Testing indicates a genetic test done on a voluntary individual and screening indicates large- scale testing usually associated with initiatives in public health. The impetus to identify the genetic cause of a disease such as Huntington’s disease or susceptibility indicates the ability to act on the knowledge: providing treatment in a timely manner, avoiding exposure to risks and influencing choices in reproduction(Doukas&Berg, 2001).
With the current advances in the disease, there are various options that science has pointed out as key ways to prevent Huntington’s disease. For instance, one option is resorting to prenatal testing, however, with the only option of prevention in case of an affected baby being abortion. This option is in cases where one is already pregnant with a baby with Huntington’s disease. There are available options, which are done before one becomes married to an individual carrying a mutated gene. One way to avoid complications is by carrying out a premarital genetic testing to find out the genetic status of prospective partners, allowing carriers of a defective gene the choice of not to reproduce or marry (Doukas&Berg, 2001).
As it was mentioned in the previous paragraphs, advances in the search for cure and prevention for the development of Huntington’s disease are still few despite such developments as genetic testing and screening. There are numerous reasons as to why these advances in science for prevention of Huntington’s disease have not been practiced, leading to more gaps. Most of these reasons have to do with the social, ethical and legal implications of the health interventions(Burris,Gostin& Tress, 2000).
Most westerners do not participate in matchmaking and developing a system for safe predating scrutiny of genes would seem inappropriate and unacceptable, and, generally, not feasible. This has been one of the most crucial causes of the expansion of the gap in intervention solutions available to Huntington’s disease patients. Another problem that has furthered the gap between available interventions and the progress of Huntington’s cure is the strict limits to access and confidentiality to test results most institutions implement even from the tested individual, which is exceedingly different from the ethical paradigms practiced and provided for the west (Davis, 2000). Most institutions feel like this is the best approach to handling such information to avoid unnecessary life- long possession of the knowledge in case a recessive carrier does not end up producing a baby with someone with the similar mutated gene. However, hiding this information makes it difficult for individuals to avoid reproduction, which can result to the birth of a child affected by Huntington’s disease(Committee on Bioethics & American Academy of Pediatrics, 2001).
More importantly, social cohesion is usually tighter in certain societies, a critical element to the implementation of a successful premarital genetic testing program. Institutions implementing such programs depend on a powerful trusting relationship between the governance of the project, something missing in the American context, and the constituents. As programs of premarital genetic testing become accepted practices, the individual appears to have lost the ability and freedom to make a choice whether or not to be tested. Such ostensible curtailments to personal freedom are difficult to sell in most developed countries, especially in the US (Davis, 2000).
Indeed, premarital genetic testing might establish a new ideology of genetic identity. With premarital genetic testing, individual responsibility in regards to genetic identity may show itself in different ways some that might contribute to the widening of the gap between intervention and available treatment options. Individual carriers bear the burden of knowing the genetic risk they have and are expected to either have an abortion if required or avoid marriage (which does not take place in most cases)(Motulsky& Beutler, 2000). Individuals tested only assume the responsibility to make decisions that are genetically responsible in relation to their future spouses. They do not receive information of their certain carrier statuses, as it lacks any importance unless matched with a spouse who is also a career. This establishes some form of genetic couplehood. This in turn is a representation of a notion that in not individualistic of an individual’s genetic make- up. This could act as a significant development for American and western cultures, where heightened individualism is common(Davis, 2000).
In summary, it would be true for one to argue that in some western countries and especially the United States, widespread premarital genetic testing is not anywhere near to be realized or practiced. However, one can imagine a future inquiry in people’s genomes that is based on evidence and focused on diseases that affect specific populations such as Huntington’s disease. The transformation to initiatives that are large scale or the development of an initiative of public health, could lead to the realization and development of significant resistance to the disease. To this end, solutions and more knowledge and information in regards to the health and genetic education of the public, data protection, management, genetic screening, and testing are needed if the available interventions are to be implemented successfully (Committee on Bioethics & American Academy of Pediatrics, 2001).
To this effect, this paper proposes the need for interventions that will lead to effective approaches to address and minimize this gap. Genetic tests and screening are quickly being established and marketed for clinical treatment, diagnosis and prevention of genetic disease such as Huntington’s disease and are available for numerous chromosomal and inherited diseases, disorders and predispositions of genes. However, for these genetic tests and screens to be successful in diagnosing, screening and treating diseases like Huntington’s disease, solutions have to be created to deal with some of the factors that limit the practice of new advances in medicine to cure Huntington’s disease like the ones mentioned above. The research proposal proposes a number of ways through which one can address the gap. For instance, informed consent for any study of validation should be acquired whenever the specimen can be associated to the participant from whom it came.
In addition, it is unacceptable to intimidate or coerce families or individuals regarding their decisions about premarital or predictive genetic testing, it is essential to respect personal autonomy. Individuals being offered screening and testing must understand that it is on voluntary basis. Their informed consent, therefore, has to be obtained, and whatever their decision their care should not be different (Burris, Gostin& Tress, 2000). The proposal also points out that before the start of predictive genetic testing in a clinical setting, providers of health care have to describe and explain the features of genetic screening or testing, including possible consequences to potential patients. In most cases, the reason why individuals do not want to participate in genetic testing and screening is that they do not understand it(Benkendorf, Peshkin& Lerman, 2000).
The proposal also argues that the gap can be addressed if respect for the values and beliefs of individuals and couples is practiced concerning tests taken for decisions of assisted reproduction, and it should be maintained through the use of indirect stance through needing informed consent. Other proposals include refusing to take a genetic test on a child for a disease that starts in adulthood unless the test leads to a direct medical advantage or gain. Confidentially is another proposal the paper makes of information on patients and their results (Burris, Gostin& Tress, 2000). Health care providers also have to ensure that genetic testing does not lead to unfair discrimination by third parties such as insurers, educational institutions, and employers. In most cases, gaps in interventions and information happen because patients are worried about discriminatory behavior from their insurers and employers. Addressing this issue can be helpful in addressing the gaps that exist in interventions for Huntington’s disease. Another solution that might help address this gap is by allowing patients help in policy making (not necessarily in technical details) and associated decisions especially those regarding introduction, adoption, and use of predictive and premarital genetic testing and screening (Committee on Bioethics & American Academy of Pediatrics, 2001).
Furthermore, the formulation of an excellent and successful public health policy in relation to genetic screening and testing programs needs a continuous, evidence-based, systematic analysis of the risks, benefits, and costs of genetic testing and interventions involved in following- up(Khoury, Burke&Thomson, 2002). Multidisciplinary studies and perspectives from cultural anthropology, history, psychology, economics, and other disciplines might be useful in providing essential information to address these gaps. Given that, the harms of genetic screening and testing are mainly psychological, empirical research and evidence is required to assess whether the screens are justified or not, that is, whether the possible benefits outweigh the possible costs and harms. The possible benefits are different in different status conditions or genetic conditions, whether treatment or preventive measure is available, whether the available information is critical for making reproduction decisions (Committee on Bioethics & American Academy of Pediatrics, 2001).
To come up with more comprehensive recommendations and solutions on how to close this gap, the study will have to make use of number methodologies. First, literature reviews and analysis will participate in a major function in creating solutions mentioned in the research. There will be a number of literature that the research will consult including books, academic articles, and journals that highlight the issues discussed in this paper. In addition to carrying out a literature review, a number of interviews will be conducted to find out some of the gaps available today, their causes, and ways of addressing them. The interviews will be conducted with key health professionals including professors, doctors and other professionals in medicine. To illustrate the importance of the results of the paper, the proposal will have to refer to a number of statistics, which include the statistics of individuals who inherited Huntington’s disease from their parents, and the number of individuals currently suffering from the disorder. In addition to this, statistics of individuals who have consulted, are consulting or intend to consult the intervention methods mentioned in the research will also be referred to. Individuals not willing to seek these interventions will also be shown.
Statistics and research methodologies will have no meaning unless the study applies the appropriate ethical and legal ramifications as specified by the available policies. The research will observe legal and ethical policies that have to do with access to information, consent, issues with abortion and discrimination (Burris, Gostin& Tress, 2000).
Summary and Conclusion
The current state of Huntington’s disease is not as encouraging as it should be. This is because of the numerous gaps that exist between the current progression of the disease and the available intervention methods to treat and prevent the disease. The research proposal intends to highlight these gaps and a number of ways to address these gaps to increase the available knowledge, information and intervention methods available to Huntington’s disease patients. Because of this significant task, the proposal will serve as a critical foundation for solutions in public health to the prevention of genetic diseases such as HD at a number of intervention levels.
Benkendorf, J., Peshkin, B. & Lerman, C. (2000). Impact of genetic information and genetic counseling on public health. In Genetics and Public Health in the 21st Century, ed. Muin J. Khoury, Wylie Burke, and Elizabeth J. Thomson. New York: Oxford University.
Burris, S., Gostin, L.& Tress, D. (2000). Public health surveillance of genetic information: Ethical and legal responses to social risk. In Genetics and Public Health in the 21st Century, ed. Muin J. Khoury, Wylie Burke, and Elizabeth J. Thomson. New York: Oxford University Press.
Committee on Bioethics & American Academy of Pediatrics. (2001). Ethical Issues with Genetic Testing in Pediatrics. Pediatrics, 107 (6): 1451-1455.
Davis, D. (2000). Groups, Communities, and Contested Identities in Genetic Research. Hastings Center Report 30 (6): 38-45.
Doukas, D. &Berg, J. (2001). The Family Covenant and Genetic Testing.American Journal of Bioethics 1 (3): 2.
Green, S. (2006). Newborn screening: Complexities in universal genetic testing. Am J Public Health 96: 1955-59.
Haddad, M,S.& Cummings, L. (1997). Huntington’s disease. Psychiatry Clinics of North America 20:791-807. Mayo Clinic.
Harper P, S. & Morris M, (1991). Introduction: a historical background. In Huntington’s
Disease, W.B. Saunders, London.
Khoury, M., Burke, W. &Thomson, J. (2002). Genetics and public health: A framework for the integration of human genetics into public health practice in Genetics and Public Health in the 21st Century, ed. Muin J. Khoury, Wylie Burke, and Elizabeth J. Thomson. New York: Oxford University Press.
Motulsky, A. & Beutler, E. (2000). Population Screening in Hereditary Hemochromatosis. Annual Review of Public Health, 21 (1): 65-79.
Haddad, M,S.& Cummings J,L.( 1997). Huntington’s disease. Psychiatry Clinics of North America 20:791-807. Mayo Clinic.
Harper P, S. & Morris M,( 1991). Introduction: a historical background. In Huntington’s
Disease, W.B. Saunders, London.
Nuffield Council on Bioethics. (2006). Genetic screening: A supplement to the 1993 report by the Nuffield Council on Bioethics. Nuffield Council on Bioethics.
Prainsack, B. &Siegal, G. (2006). The rise of genetic couplehood? A comparative view of premarital genetic screening. BioSocieties 1: 17-36.
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