Introduction
The aging population poses a huge challenge to the healthcare system, due to the increased risk of chronic diseases. As a matter of fact, the elderly are often seen as an economic burden due to increased government spending on pension, healthcare, and social benefits. To address the problem, some countries have initiated changes in retirement age, to ease the burden of public spending. While the government is concerned by the economic impact of aging, scientific researchers are intrigued by the ageing mechanism. This paper focuses on the pathophysiologic changes associated with aging. In particular, it argues that lifestyle factors and chronic illnesses contribute towards a significant poor quality of aging.
Pathophysiologic disruption in aging
Elderly persons, experience physiologic changes due to decreased functioning of various organ systems. Aging affects the cardiovascular system, hence reducing cardiac output, and increasing vascular resistance. Homeostatic regulation is also affected, elevating the rate of tissue damage, morbidity, and mortality. Typically, cells have several ways of maintaining the stability of their proteomes. However, this function is disrupted in the elderly, leading to the accumulation of the damaged cells, and inferring with the renewal of intracellular proteins. The altering of proteostatis in aged persons, increases the risk of age-related pathologies such as Alzheimer’s and Parkinson disease. The ageing process is also characterized by a regulatory change between cells, organs and systems. The integrity of cardiac, and muscle cells that are involved in involuntary control of heart, and vascular functions, are negatively impacted. As the cells lose their physiological capability, they age. The progressive aging of the cells, eventually leads to the disruption of trophic, and metabolic signaling pathways.
Genomic instability occurs during aging, due to increased DNA damage accumulation (Giachino, Orlando, & Turinetto, 2013). In young people, the body has the capacity, to repair the DNA. However, in the elderly persons, this function is challenged by agents, and endogenous threats. As a result, the elderly people get genetic lesions, which include mutations, translocations, chromosomal gains, and losses, telomere shortening, and gene disruption. Unfortunately, an aging body lacks the capacity to repair these genetic lesions, leading to genomic instability. The integrity of the mitochondrial DNA is also affected in aging persons. These lesions and the disruption of the nuclear architecture contribute to the aging process.
Another psychological disruption that occurs in aging persons is telomere attrition (Sui, Hu & Jin, 2016). The bodies of aged people loose the capacity to completely replicate the terminals ends of their DNA molecules. The integrity of the DNA is affected by telomere shortening. This happens in the absence of telomerase, which also increases the risk of pulmonary fibrosis, dyskeratosis congenital, and aplastic anemia. Telomerase deficiency and uncapping lead to the regenerative capacity of the tissues, hence accelerated aging.
Physiological disruption in aged population can be explained through the alteration of intercellular communication. Inflammaging eventually leads to increase production of IL-1ß, tumor necrosis factor and interferons (Titorenko, 2018). Defective inflammatory response in old people, is also associated with a high risk of obesity, and atherosclerosis. A study performed by flight (2011) found that inflammation also interferes with cell functions, and the immune system. The inhibition of the immune system contributes to the ageing process, as the clearance of infectious agents, and defective cells is delayed. On the other hand, He, Tu and Liu (2018) suggested that inflammatory and stress responses cause aging, by inhibiting the production of gonadotrophin-releasing hormone. The reduction in gonadotrophin-releasing hormone is responsible age-related changes such as bone fragility, muscle weakness, skin atrophy and reduced neurogenesis.
The other physiologic characteristic of aging is stem-cell exhaustion (Bugiani, 2011). Old people loose the regenerative potential of their tissues. Hematopoiesis, and diminished regenerative capacity, increases the risk of anemia, and myeloid malignancies in the elderly. The cell cycle activity in elderly people reduces, unlike in the younger persons. The disruption of this physiologic, correlates with the ambulation of DNA damage, leading to accelerated aging. Epigenetic alteration also responsible for pathophysiological changes in the elderly population. According to Srivastava (2017) epigenetic alterations involve the change of DNA methylation patterns, modification of histones, and chromatic remodeling. Other pathophysiologic changes include deregulated nutrient-sensing, mitochondrial dysfunction, and cellular senescence. Cellular senescence is very crucial in the ageing process, and it is triggered by telomere shortening, non-telomeric DNA damage, and repression of repression of the INK4/ARF locus (Titorenko, 2018).
Chronic illnesses, and poor quality of aging
Chronic conditions, have a negative impact on quality of life in seniors. According to Hwang (2010) chronic conditions affect, the elderly people’s physical, and functional ability. The presence of chronic conditions, also leads to emotional distress. The most degenerative diseases, which lead to poor quality of life, and aging include hypertension, cardiovascular disease, cancer, dementia, neurodegenerative diseases, obesity, arthritis, atherosclerosis, cardiovascular disease, and diabetes mellitus.
Hypertension
The elderly are more likely to be affected, if they suffer from hypertension. With aging, one loses viscoelastic properties of conduit vessels. There is also marked increase in atherosclerotic arterial diseases, hypertrophy and sclerosis Arterial stiffening leads to poor aging as it is associated with other adverse cardiovascular outcomes such as kidney diseases, myocardial infarction, and cognitive decline in health. The association of hypertension, and aging can be explained through increase in systolic blood pressure, and decrease in dialostic blood pressure (Fukutomi & Kario, 2010).
The role of hypertension in poor quality of aging can further be explained through metabolic syndrome (Logan, 2011). This condition is characterized by obesity, hypertension, dyslipidemia, insulin resistance, and hyperclycemia. As a result, the aged have abnormal carotid properties, and high blood pressure. There is also elastic degradation of collagen arteries, which could lead to early death of the elderly. Other known pathologies of hypertension in the elderly include inflammation, genes, and neurohumoral dysfunction.
Cardio vascular disease (COPD)
Chronic obstructive pulmonary disease leads to poor quality of life, through reduced breathing function. The effect of COP on quality of aging can be understood through telomere attrition (Chiu, Klein, Milton, Gensler, & Taylor, 2009). Elderly patients with COPD have shorter telomeres, due to cell senescence, and inflammation. The role of COPD in accelerated or poor quality of aging can also be examined through the mTOR pathway. The inhibition of the pathway in elderly patients with COPD, leads to accelerated aging due to dysregulated nutrient aging, and loss of proteostatis (Dimmelar & Nicotera, 2013). The decrease in proteasome activity in elderly COPD patients, also leads to loss in lung function. Another mechanism of age-related COPD is mitochondrial dysfunction. Other mechanisms include stem cell exhaustion, and oxidative stress.
Cancer
Cancer affects the quality of aging, among the elderly, according to Sidorova and Monnat (2015). As one ages, the probability of acquiring mutations, and having a cellular environment that favors carcinogenesis increases. In addition, with age, the body loses the ability of body repair, leading to chromosomal breaks, translocations, frequent mutations, DNA adduct formation, and DNA hypomethylation. On the other hand, the cellular microenvironment in elderly people encourages the expression of premalignant cells, and eventual transformation into malignant phenotype, Cancer affects the quality of aging, through the process of inflammaging. The process accelerates the aging process, as it encourages tumor progression. As a result, an elderly person with cancer has diminished cellular capabilities, than a peer who does not have this chronic condition. The presence of cancer in elderly patients, is complicated by lack of suitable treatment methods. This is because the effects of chemotherapy, are more toxic in elderly patients. Inefficient DNA repair, and decreased functioning of the liver, and nephron mass, leads to slow recovery. Sometimes, the treatment could lead to organ failure, comorbidities and polypharmacy. Cancer also affects the seniors’ quality of aging, because it impairs their homeostatic mechanisms, thus predisposing them to intraoperative haemodynamic instability.
Dementia
Dementia is characterized by the decline in memory, and other cognitive functions (Heese, 2015). As a result, an elderly becomes independent on others, and are unable to live fulfilling lives. Dementia is Caused the by accumulation of the protein beta-amyloid, and neurofibrillary tangles. The amyloid structures in the brain are affected leading to memory loss. The other mechanism that explains cognitive impairment is inadequate blood flow. The dementia is also characterized by the loss of motor ability. This incidence is attributed to the accumulation of Lewy bodies in the brain, causing a dopamine reduction.
Neurodegenerative diseases
The common neurodegenerative diseases among the elderly, include the Alzheimer’s disease, and Parkinson disease (PD). The neurodegenerative affect the quality of ageing due to memory impairment, orientation challenges, and problems in performing basic service functions (Biragyn, Aliseychik, & Rogaev, 2017). Alzheimer in elderly is a result of protein misfolding, and neuro-inflammation. Other mechanisms include oxidative stress, mitochondrial dysfunction, decreased proteasome activity, cellular senescence, and gut microbiota alterations (Yargin, Lupatov, & Kholodenko, 2015). The mechanisms of PD that impact negatively on the aging process include accumulation of senescent cells, inflammation, and propagation phenomena.
Other chronic illnesses
Obesity brings epigenetic changes in the human liver, thus accelerating aging by almost three years, for a 10-point increase in biomass index (Ghosh, Sinha, & Raghunath, 2019). The poor quality of aging in seniors with obesity is caused the presence of senescent cells, which cause inflammation. Obesity also activates IIS and mTor pathways, which are considered as the accelerators of the aging process. Other mechanisms that contributed to poor quality of aging in obese seniors include tolemere attribution, epigenetic alteration, mitochondrial dysfunction, deregulated nutrient sensing, altered intercellular communication, loss of proteostasis, and genomic instability. On the other hand, arthritis accelerates the aging process in the elderly by two years (Marloes, & Boonen, 2016). It contributes to poor quality of aging through immunosenescence, or the decline in T-cell function (Hohensinner, Goronzy, & Weyand-Cornelia, 2014).
Atherosclerosis is associated with premature biological aging due to advanced atherosclerotic plaque (Alique, Luna, & Ramirez, 2015). The other mechanism is cell senescence: replicative senescence, and stress-induced premature senescence. Replicative senescence causes telomere shortening, leading to lifespan reduction. Aside from the shortened telomeres, the accumulation of DNA damage also contributes to age-related atherosclerosis. The elderly are also an increased risk of cardiovascular diseases. Age-related cardiovascular diseases are associated with the following physiologic changes: hemodynamic disturbance, premature cellular senescence, synthesis impairment, and secretion of endothelium, derived vasoactive molecules.
Lifestyle factors, and poor quality of aging
Existing research shows that lifestyle factors exert important effects on physical aging (Halloran, 2012). One of such factors is diet which contributes to poor health, and greater mortality. Poor quality foods like trans fats increase the inflammation process. Another characteristic of poor quality of ageing attributable to poor dieting is the loss of skin integrity. Lack of a proper diet could also lead to loss of skeletal muscle mass, and function otherwise known as sacorpenia. In particular, lack of enough protein in the body, is a contributory factor to the loss of lean mass in the elderly. Poor nutrition could also reduce cell-mediated immune response, thus increasing the risk of infectious diseases. Besides poor diet, lack of enough sleep among the elderly, affects their physical, mental, and social wellbeing. Insufficient quality sleep is associated with neurocognitive impairments, end-organ dysfunction and increased mortality among the elderly (Paulose, Wang, O’Hara, & Cassone, 2019). Aging is also closely associated with obstructive sleep apnea, which is characterized by the collapse of pharyngeal airway.
Smoking is known to accelerate the aging process, among the elderly, through complex mechanisms (Yargin, Lupatov, & Kholodenko, 2015). Smoke has free radicals which are known to activate inflammatory cells, leading to oxidative damage. Oxidative stress in smokers is also caused by lower ethrocyte, and serum antioxidant vitamins. Another mechanism linking smoking to ageing is telomere shortening. Smoking not only affects the quality of life in the elderly, but is also associated with pathological conditions such as dementia, and osteoporosis.
Alcohol-drinking contributes to poor quality of ageing. Ageing is associated with loss of lean body mass, but alcohol consumption exacerbates the problem. Older people have lower levels of enzyme alcohol dehydrogenase, and as such, their bodies have reduced ability to break down alcohol. As a result, most of the alcohol reaches their bloodstream. In addition, alcohol consumption and exposure to elements accelerates extrinsic aging.
Stress affects the quality of aging in elderly population, by accelerating the process. Acute stress impact negatively on neuroendocrine function through the hypothalamic-pituitary-adrenal axis. Aging is associated with increased levels of inflammatory mediators such cytokines, and acute phase proteins. On the other hand, physical exercise is very important in the elderly population, as it reduces the risk of cardiovascular and metabolic diseases. Exercises induces cardiac autonomic balance, increases stroke volumes, and reduces resting, and submaximal heart rate, systolic blood pressure, and diastolic blood pressure (Hwang, 2010). Exercising is also likely to prevent age-related frailty. Typically, elderly people are likely to have higher body mass index, but smaller, and weaker muscles. Frailty impairs the elderly from engaging in daily activities, and affects the mental function. All the factors contribute to poor quality of aging due to premature death, and the inability to live a normal, fulfilling life.
Manifestations of aging and how to improve quality of aging.
Aging is characterized by the disappearance of the bone marrow, and reduction of reduction of calcium in the bones (Halloran, 2012). As a result, older people, have brittle bones, while their joints are stiff. They experience hair loss, graying, loss of height and teeth, and lesser muscle mass. They also have skin wrinkles, age spots, and their digestive system slows down. Aging is also associated with the changes in the brain, and nervous system. The brain, and spinal cord loses nerve cells, and weight, leading to memory loss, and reduction in sensation. Beside the loss of reflexes, and sensation, the elderly experience movement problems.
Aging is associated with telomere shortening, and reduced ability of the cells to divide. Waste products accumulate in the body, while connective tissues become stiffer. The functional capacity of the organs reduce, while heart, and blood vessels become less efficient. The deterioration of the circulatory system, makes it harder to control the temperature. In addition, the ability to sweat decreases, while the blood pressure drops. Other manifestations include thickening of the ear drums, thinning of retina, slow nail growth, stooped posture, overall decrease in energy, urinary incontinence, constipation, decrease in visual acuity, and hearing loss.
Poor quality of ageing in the elderly can be prevented through regular exercises. Research shows regular training improves the structure and function of cardiorespiratory, metabolic and musculoskeletal muscles (Halloran, 2012). Evidence further suggests that exercising reduces the mortality rate, and diseases such diabetes, and cardiovascular diseases (Karatzaferi, & Sakkas, 2012). Older people should perform exercise targeting the limb muscles to prevent sarcopenia, and muscle loss. They should also engage in resistance, and endurance training to reduce the risk of falling, and improve functional mobility, walking, and balance. In addition, they should stop smoking to reduce smoke-induced biological damage.
The elderly can achieve good quality by engaging in mental exercises, and prompt treatment. The elderly should be equipped with coping stress management tactics, to deal with negative experiences such as pain, hurt, fear, discomfort, emotional pain, and avoidance. They also need a supportive environment, influenza vaccination, and homecare services. The health of the elderly can also be optimized through geriatric, and gerontological services.
Conclusion
In sum, there are pathophysiologic changes that occur in elderly population, due to chronic illnesses, and lifestyle behaviors, leading to poor quality of life. Various mechanisms have been proposed to explain the functional impairment that occur in old age. Some of the age-associated changes can be alleviated though lifestyle change, or medical treatment. However, other physiological changes cannot be addressed as they characterize the normal aging process. To help the dearly population, the stakeholders should implement effective interventions, to maintain dependence, reduce morbidity, and increase quality of life in elderly persons.
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