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Is Ageing Inevitably Associated with Disease - Report Example

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The paper "Is Ageing Inevitably Associated with Disease?" discusses the case of ageing, which is or not inevitably associated with the disease, including the use of in-depth examples of Alzheimer, Osteoarthritis and many other diseases, to discuss theories of ageing and how it impacts on health…
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Is Ageing Inevitably Associated with Disease
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Is ageing inevitably associated with disease? Is ageing inevitably associated with disease? Introduction: Phenomenon of aging is universally applicable and is well understood by most as a natural physiological process whereby changes take place in a human body that leads to ageing. To understand the pathological side of this process we should understand the normal physiological changes that take place over time in human body to compare and contrast the differences. As we normally see among human beings, age is mostly associated with diseases and ageing considerably affects the quality of life in most cases. Our body consists of a very organized system in which every organ plays a vital role to sustain life. The mechanical wear and tear in these organs over time is one factor among many that contributes to certain disease processes. Hormones also play a key role in maintaining and stabilizing the internal environment of our body. Therefore hormonal changes that take place during old age also results in degenerative changes. Interesting fact about a normal somatic human cell is that it can replicate for a fixed number of times before it lose its capability of division and enters a state of arrested growth known as replicative senescence. (Balducci et al 2005). Theories of Ageing: Various theories on the basis of ageing have been proposed by many scientists and researchers around the globe. These theories are mostly interlinked as one might support the other theory. (Bengtson et al 1999) Free radical theory was first introduced by Denham Harman in 1956 and according to this theory our body cells undergoes destruction due to interactions with these free radicals over time. (Farley et al 2010). These free radicals are unstable molecules which interact with stable molecules of our cells and also transform them into unstable free radicals. Therefore, it is a vicious cycle and many factors may contribute to excess production of these free radicals such as cigarette smoking, infections, exposure to x-rays or toxins (Chop et al 1999). This theory goes hand in hand with the mitochondrial decline theory. Mitochondria are the power house of human cell and are by far one of the most important organelle in the cell. Because of its property of handling chemical reactions that involves breaking down molecules make it a source of production for these free radicals. Therefore they damage the mitochondria and shut down the power house of cell eventually leading to death. It has been concluded that with age the mitochondrial machinery becomes rusty making it more likely to produce these free radicals. (Farage et al 2010). As I mentioned before many physiological changes during old age is attributed to hormonal changes. The neuro-endocrine theory (Dilman et al 1992) partially explains how these hormone deficiencies take place. This theory was first proposed by Vladimir Dilman and highlights the complex biochemical changes that correspond to decrease functioning of hypothalamus. Hypothalamus is a main regulator of hormones in our body and responds by various negative feedback mechanisms. But ageing can cause a disruption in its function and the most likely explanation for this dysfunction is cortisol accumulation. Cortisol is produced by adrenal gland is regarded as a stress hormone but it has also been associated with gradual destruction of hypothalamus. Hence with age, destruction reaches a certain limit where it affects the normal function of this gland thus indirectly interfering with other hormone production in a body. Cross linking or glycosylation theory of ageing also explains many diseases in old age. In the presence of oxygen, glucose can bind to different proteins, a process known as “glycosylation”. This additional structure on a protein can disrupt its shape and interfere with its function. The longer a person lives the greater the chance that glycosylation will take place. Therefore these glycoproteins accumulate in the body leading to various problems which I will discuss under the subsequent headings. These are only the few of many theories that explain the diseases of old age. Malignancies: Malignancies are among most devastating diseases and have been a focus of constant research over the years. The risk of most malignancies increase with age. So it is one the most important disease to address here. Let’s understand how cancer is associated with old age by incorporating certain theories discussed above. Theory of free radicals fits well in the pathophysiology of skin cancers. As we know that exposure to sunlight especially ultraviolet light is one the major risk factors in developing skin malignancies (Mackie 1989). Ultraviolet light is one the major source of free radical production. These free radicals in the skin cell can attack molecules of DNA as well. So any disruption in the gene regulating part of the DNA may result in the formation of Oncogenes which are independent of normal regulatory mechanisms of cell division. Thus a spontaneous or sporadic mutation in the skin cell due to free radical insult results in cancer. Moreover, in old age the repair mechanism of DNA following such insult is not very efficient increasing the likelihood of mutation in a cell. Other theory of cross linking or glycosylation also plays a part in cancer physiology. If we understand the structure of DNA, it is double helix of nucleic acids wind around a protein base. Thus glycosylation can also disrupt and damage the structure of DNA which may result in mutation and malignancies. One other important concept to understand here is that a single mutation or disruption in structure of DNA is very likely to result in cancer. In fact, an accumulation of many Oncogenes or suppression or deletions of tumor suppressor genes are required to trigger mutiny of that cell against restricted cell division. Therefore, it is more likely that these mutations will accumulate in an elderly person who has been long exposed to the associated factor responsible for such insult than a young person. Membrane Theory of Aging and Alzheimer Disease: Cell membrane is a lipid bilayer membrane that controls the flow of substances in and out of the cell. Membrane theory of aging was proposed by Imre Zs Nagi who highlighted the importance of partially permeable membrane and consequence of its deterioration by age (Colton et al 1996). According to this theory cell membrane loses its fluidity by losing lipids as cell grows old over time. This loses of water and mosaic nature of membrane hinders with the normal functioning of a cell membrane. This implies that important substance cannot be taken in and harmful toxic substances cannot be excreted out efficiently across the cell membrane. Thus, resulting in accumulation of toxins that can harm the cell eventually leading to death. Alzheimer disease is a most common cause of senile dementia affecting old people around the world. The pathophysiology of this disease can also be explained by this theory. The toxic product that accumulates inside the cell is called lipofuscin. Research showed that individuals with Alzheimer disease have an increase accumulation of lipofuscin in their brain cells as well in other parts of the body (Swaab 1986). Also the interference in the acetylcholine release can also be attributed to membrane impermeability. Menopause and Osteoporosis: In elderly females, the cessation of ovarian function and menstruation commence a difficult phase as it is associated with many symptoms and degenerative diseases. Decreased or no production of estrogen from the ovaries is the main culprit. This state of declined ovarian function and cessation of menses is defined as menopause. Many changes in the body results as a consequence but I will mainly discuss the one most significantly associated with old age. Old individuals especially females are more prone to bone fractures because their bone mass start to decrease as their age advances (Karasek 2006). The bones become brittle and fracture very easily, a condition called osteoporosis. In females, osteoporosis results mainly from estrogen deficiency. Calcium is the main constituent of bone that provides strength and flexibility. Estrogen is responsible for indirectly incorporating calcium in the bone so absence of estrogen cause depletion of calcium reserves resulting in weak and fracture prone bones (Currie 2006). Other symptoms of menopause include hot flushes, mood swings, joint pains etc. Conclusion: From all the above evidences we can conclude that ageing is inevitably associated with many diseases. Alzheimer, Parkinson, Osteoarthritis and many other diseases are more common in old age than otherwise. This in itself highlights the probability that old age is a main link in the development of these diseases. Furthermore, discussion of various ageing theories mentioned above and their mechanism complementing the pathogenesis of these diseases support my hypotheses. These diseases and other medical conditions severely affect quality of life and as it has a great impact on individual health and well being. Lot of research is underway to come up with a solution to these ageing problems. Many management plans and treatment regimes have been proposed but they are still under experimentation phase. Understanding of how ageing brings about changes in a human body gives us a fair chance to combat and resist those modifications. Reference: BENGTSON, V. L., & SCHAIE, K. W. (1999). Handbook of theories of aging. New York, Springer Pub. Co. KARASEK, M. (2006). Aging and age-related diseases: the basics. New York, Nova Biomedical. FARLEY, A., MCLAFFERTY, E., & HENDRY, C. (2010). The physiological effects of ageing. Oxford, Wiley-Blackwell. CHOP, W. C., & ROBNETT, R. H. (1999). Gerontology for the health care professional. Philadelphia, PA, F.A. Davis. FARAGE, M. A., MILLER, K. W., & MAIBACH, H. I. (2010). Textbook of aging skin. Berlin, Springer-Verlag. http://dx.doi.org/10.1007/978-3-540-89656-2. DILʹMAN, V. M., DEAN, W., FOWKES, S. W., & DILʹMAN, V. M. (1992). The neuroendocrine theory of aging and degenerative disease. Pensacola, Fla, Center for Bio-Gerontology. BALDUCCI, L., & EXTERMANN, M. (2005). Biological basis of geriatric oncology. New York, Springer. http://public.eblib.com/EBLPublic/PublicView.do?ptiID=226476. MACKIE, R. M. (1989). Skin cancer: an illustrated guide to the aetiology, clinical features, pathology and management of benign and malignant cutaneous tumours. London, M. Dunitz. COLTON, R. H., CASPER, J. K., & HIRANO, M. (1996). Understanding voice problems: a physiological perspective for diagnosis and treatment. Philadelphia, Lippincott Williams & Wilkins SWAAB, D. F. (1986). Aging of the brain and Alzheimers disease: proceedings of the 14th International Summer School of Brain Research, held at the Royal Netherlands Academy of Arts and Sciences, Amsterdam, the Netherlands, 26-30 August 1985. Amsterdam, Elsevier. CURRIE, H. (2006). Menopause. London, Class Health. SLUPIK, R., & GENTRY, L. (2003). The everything menopause book: reassuring advice and the latest information to keep you healthy and sane. Avon, MA, Adams Media Corp. Read More
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