Biological aging
Biological aging is the process by which changes occur in the body over time which in return leaves the body exposed to diseases and eventual death. It is a complex process that involves physical changes, exponential increase in mortality rate and also increased risk of attack by diseases. These changes are usually associated to the process of aging. They occur across all species of animals. The process is said to be under gene control. Although aging runs across all species, the life expectance differs depending on individual species. In America, over the last 100 years, the life expectancy has improved from 47.3 years in the year 1900 to about 77.3 in 2002.
Life expectancy
Life expectancy is the period of time that an animal is likely to live given ideal conditions. This is usually arrived at considering the number of years that previous species had lived. The human lifespan has been estimated to be 121 years. There has been an increase in the life expectancy of human beings through the twentieth century. This is partly due to better health facilities, improved hygiene and nutrition, control of some diseases through provision of clean water, antibiotics and vaccination which has been made possible through the numerous researches that are taking place. While most of the explicit factors that could cause diseases have been taken care of, implicit factors have remained which could be taken care of by healthy lifestyle among the people.
Senescence
All organisms that are multicellurar derive energy from the sun that they use in developing and maintaining their identity. When deterioration is more than what an organism is able to synthesize, it ages. Aging affects all individuals in all species. Many biologists suggest that aging is part of the development process in an animal while others think that it is a default state that comes after completion on natural selection process in an animal. After an animal has given birth to offspring and raised them, death comes. However, studies that have been done recently suggest that lifespan characteristics that are genetically determined can be controlled through gene alteration or change of diet (Caleb, p.1721).
Changes in the mammalian life span and those related to reproductive schedules are usually regulated by development. It is also possible that age related changes come due to mechanical senescence. For example in Alzheimers disease which affects human beings but it may not be related to the usual cognitive aging. It can be noted that longevity in humans may make us uniquely prone to Abeta toxicity. Due to this, there is a possibility that Alzheimers disease is a form of mechanical senescence despite the fact that some loci that are important in development of the disease enhance development (Denham, p. 7127).
Tooth erosion can also be used to demonstrate senescence together with mammal oocyte exhaustion, although they can be perceived to be caused by some intrinsic limitations in most mammals body plan. This can be attributed as an outcome of the developmental process. In female, senescence in reproduction comes as a result of loss of ovarian oocytes that is brought about by age. Some reptiles undergo oocyte regeneration during adulthood and as a result tend to appear not to age (Denham, p7127). During the earlier years of development of mammals, oocyte regeneration is not active until the earlier stages of development.
Hence reproductive senescence is perceived as an outcome of senescence blockage. Likewise, tooth erosion can be considered to be a limitation to mammal development whereby the development process comes to an end as a result of worn-out tooth not being able to be replaced. Dental development is usually slow in humans compared to other primates and also extinct hominids, suggesting that the on set of tooth erosion is affected by the pace at which dental development takes place. Hence, during mechanical senescence, age related changes can be perceived to be influenced by the timing of developmental mechanisms (Michael et al, p.4769).
Causes of aging
The death of cells and aging has been associated to be part of the ageing process. This is because the rate of cell production and the changes that occur are regulated by genes but they are also prone to environmental changes. When a cell is not able to perform its important functions, it dies. This is also true in the case of multicellular organisms and thereby the process of aging involves majority of body cells dying. Death of an animal occurs as a result of death of cells in vital body organs that are important in sustaining major body functions (Brakefield at al, p .435).
Because of the speculations around the aging process, people have tried to come up with some of the things that contribute to the process. Some of the suggestions include progressive breakdown in protein synthesis, encodement of Deoxyribonucleic acid in aging, damage brought about by free reaction, autoimmunity in higher organisms, and also cross linkage of macromolecules (Medvedev, p.377). Many theories have been formulated that try to explain the aging process.
The free radical theory is one of the theories and it is based on an assumption that aging is caused by a single cause that is modified by environmental and also genetic factors. According to it, free radical reactions are responsible for aging and age related disorders. The reactions are believed to come about due to exposure to ionizing radiations, non-enzymatic and also enzymatic ones particularly those involved in photosynthesis and oxygen regulation. This reactions cause oxidation to tissue which in return brings about aging programmed theories of aging (Conboy et al, p.761).
According to Holliday (p. 570), oxidative damage has also been linked to aging. According to this theory normal metabolism is one responsible for aging and that mutations are not a necessity. 2-3 of the oxygen taken by the mitochondria is reduced to a reactive oxygen species (ROS). ROS is composed of hydrogen peroxide, super oxide ions together with hydroxyl radicals which have a potential to oxidize and destroy cell membranes, nucleic acid and also proteins (Thomas, p.3779). This can be observed in drosophila which produces enzymes that destroy ROS and as a result its able to live longer than other wild-type flies. Other flies that mutate Methuselah gene, also live longer compared to other wild-type flies. This gene that they produce works by increasing resistance to paraquat which is a poison that generates ROS within cells. Through the examples above, it is evident that aging is genetically controlled and that ROS play a role in it (Qin etal, p. 4340).
In mammals, the role of ROS in aging is not clear although some studies tend to support it. Other studies have shown that caloric restriction in mammals can help in slowing the process of aging although it is said to have other effects also. Hence it is not yet certain that it works by preventing ROS synthesis. Other factors that prevent ROS synthesis include vitamins E and C. Studies have also indicated that when vitamin E is added to the diet of nematodes and flies, increases their longevity (Christoph, Jeen-Woo and Bruce, p 467).
Wear and tear is another theory that tries to account for aging. According to the theory, as an individual grows older, little traumas experienced by the body build up. There is an increase in point mutations and a decrease in efficiency of enzymes brought about by genes. Furthermore, large faulty proteins are made when there was a mutation in part of the protein synthesis material producing faulty DNA polymerases. Because DNA is vital in repair of worn-out tissues, individuals with faulty DNA will end up producing pre-mature aging syndromes. This may end up reducing their life span (Weindruch, Kayo, Lee, and Prolla, p.178).
Mitochondria genome damage is also thought to be the cause of aging. Because mitochondria mutates 10-20 times more fast than the DNA, its thought that if the mitochondria undergoes a mutation, it could affect a number of processes which include energy production in the cell, manufacture of ROS as a result of a faulty electron transport and it may also lead to apoptosis. Mitochondrion that has undergone mutation is thought to have greater replication frequency compared to wild-type mitochondria. As a result, the mutants outgrow the wild-type mitochondria and finally occupy majority of the cell. The mutants allow formation of ROS at the same time increasing the risk of mitochondrial DNA suffering damage from ROS (Michelle et al, p.471).
According to Hawkins and Lovett (p. 290), some genes have also been found to play a significant role in aging. Dormant mutant genes such as Hutchinson-Gilford progreria syndrome affect children and causes rapid growth and death during the early years of life. The victims are found to have the following symptoms hair loss, thin skin spotted with age spots, arteriosclerosis, and reabsorbed bone mass (Nijhout, P.166).
When an acid diet is taken in by an individual, the PH of blood and cytoplasm falls to acidic levels. In response to the fall in the level of acid, the body uses its bones to buffer the acid. This is achieved through activation of osteoclasts cells which produce inflammatory chemicals that in return break bones to produce minerals that it uses to buffer the acidic state. These minerals include Mg, Ca and K which are released into the blood cytoplasm to effect the change to aid in bone repair. When we also eat meals rich in alkali, osteoblasts are activated if the diet taken is relatively alkalizing, there is no need of production of these cells because of the minerals contained in the food. Acidifying diets lead to a constant flip flop which in return causes an increased rate of metabolism of osteoblasts and osteoclasts. An increase in metabolism leads to a faster cell turn over speeding up the shortening of telomeres hence the process of longevity is accelerated (Pamela p. 97).
Genetically regulated aging insulin pathway
The caenorhabditis elegans DAF-2 insulin like signaling path way not only has been found to regulate lifespan and increase stress resistance capability, but also has a significant resistance to bacteria pathogens. Resistance to a wide variety of bacteria pathogens and prolonged lifespan has also been noted in the loss of function daf-2 and age -1. This has increased the possibility that longevity and pathogen resistance in the insulin-like signaling pathway mutants could be using the same mechanism as daf-2 and age-1. Here, lifespan regulations and resistance to pathogens is found to link by a mechanism that resembles both genetically and contain a genetically distinguishable mechanism. Loss of germline proliferation is found to enhance resistance to pathogens and this in return requires daf-16 which is the same in lifespan regulation.
Contrary to that, regulation of pathogen resistance and lifespan is decoupled in the DAF-2 pathway. Wild-type resistance to pathogens is shown in long lived mutant of genes belonging to daf-2 like pdk-1 and also sgk-1. However, enhanced resistance to pathogen has been observed in akt-1 2 which also have individual modest effect on lifespan. However, pathogen resistance in insulin-like signaling pathway is connected to the increase of immunity gene expression during infection. Other factors that have an effect on an organisms longevity include Jun kinase signaling together with caloric restriction although they do not affect on bacterial pathogen resistance. The finding that insulin pathway affects the lifespan and metabolism showed a concordance with mammalian lifespan studies where by low calories in rat and mouse diets increase their lifespan by reduction of levels of insulin. Signaling of insulin in the nervous system has been found to be important in lifespan elongation (De Magalhaes, p.45).
Production of free radicals that have high insulin signaling in neurons may destroy them leading to a decline in hormonal signal towards the muscles and skin resulting in visible signs of aging in both humans and worms. Regulations of lifespan by hormones released from the brain depend upon regulation of other life stage events such as menopause together with puberty.
Promoting longevity
Aging is a process that cannot be avoided because no one has control over it. The only thing that can be done to prolong life is to alter the aging process through taking relevant measures. There are three factors that contribute largely to the aging process. They include the length of Telomere, replication rate and the rate of metabolism together with the free radicals in the system.
Telomeres resemble caps and are usually found at the edge of chromosomes. They protect the chromosomes from deteriorating. They get shortened every time there is division of cells. When the cell continues to divide, they eventually disappear leaving the cell without the capacity to replicate. The cells then age and eventually die and sometime they may become cancerous or temporarily immortal.
Replication rate is necessary for elimination of endogenous and exogenous toxins that are acquired from the environment. These toxins put older cells DNA at a higher risk of undergoing mutation which may result in cancer. However, when replication occurs too often, the length of telomere shortens prematurely exposing the cells to more risks (Weindruch, Kayo, Lee, and Prolla, p.178).
According to Vaux and Strasser (p. 243), metabolic rate and the free radical activity play an important role in cell breakdown and replication. The food that we consume and the activities that we engage in affect greatly these factors. When one engages in exercise, metabolism is increased temporarily leading to an increase in the number of free radicals in the body. This leads to a healthy and cleansing turnover of cells. When an individual thinks that heshe is starving, physiological processes reduce. This reduces the wastes products produced by cells and increases the levels of free radicals increasing the risk of acquiring cancer (Joseph et al, no.15).
The following measures can be helpful in ensuring that an individual enjoys longevity. They include
Making sure that antioxidant levels of your body are elevated. Oxidation is brought about by the chemical reactions that occur as a result of free radicals. This oxidation brings about oxidative stress to the body cells together with tissues. To take care of these oxidants, a daily assimilation of various nutrients is a necessity by use of strong antioxidant food supplements. This will ensure that the levels of radicals that are free in your body are kept at a low level and the adequate concentration of antioxidants is maintained. This will help strengthen the bodys immune system which will take care of infection and therefore preventing pre-mature deaths.
Through use of herbs, it can help in reducing the level of free radicals in the body. One of the best herbs that can be used as an antioxidant is Ganoderma Lucidum. This herb contains high levels of SOD. This enzyme is important in regulating the levels of free radicals present in the body at any particular time and therefore slowing the process of aging. Therefore, through long term consumption of Ganoderma, vitality together with longevity is promoted. Consumption has to be done over a long period of time to achieve the results.
Low levels of antioxidants are achieved by the body through the use of a natural anti oxidation system that is found in the body. The system is composed of natural enzymes such as Superoxide Dismutase (SOD), glutathione Peroxidase (GPX) and also Catalase enzymes. These are the ones responsible for eliminating free radicals in the body. However, these enzymes keep decreasing as one ages. The older one grows the less antioxidant enzymes you have. The levels of these enzymes in the body keep decreasing day after day. Other factors that contribute to the increased level of free radicals include prolonged periods of stress more so work related, irregular patterns of work and also anxiety (Robert et al, p.210).
Biological aging is a process that occurs naturally. It may occur earlier in some species and late in some depending on some of the factors such as genes and environmental conditions. Although aging is inevitable, one can prolong longevity by ensuring that the level of free radicals in the body is kept low through the use of the methods discussed above such as avoiding work related stress and avoiding situation s that may make someone exited.
Life expectancy
Life expectancy is the period of time that an animal is likely to live given ideal conditions. This is usually arrived at considering the number of years that previous species had lived. The human lifespan has been estimated to be 121 years. There has been an increase in the life expectancy of human beings through the twentieth century. This is partly due to better health facilities, improved hygiene and nutrition, control of some diseases through provision of clean water, antibiotics and vaccination which has been made possible through the numerous researches that are taking place. While most of the explicit factors that could cause diseases have been taken care of, implicit factors have remained which could be taken care of by healthy lifestyle among the people.
Senescence
All organisms that are multicellurar derive energy from the sun that they use in developing and maintaining their identity. When deterioration is more than what an organism is able to synthesize, it ages. Aging affects all individuals in all species. Many biologists suggest that aging is part of the development process in an animal while others think that it is a default state that comes after completion on natural selection process in an animal. After an animal has given birth to offspring and raised them, death comes. However, studies that have been done recently suggest that lifespan characteristics that are genetically determined can be controlled through gene alteration or change of diet (Caleb, p.1721).
Changes in the mammalian life span and those related to reproductive schedules are usually regulated by development. It is also possible that age related changes come due to mechanical senescence. For example in Alzheimers disease which affects human beings but it may not be related to the usual cognitive aging. It can be noted that longevity in humans may make us uniquely prone to Abeta toxicity. Due to this, there is a possibility that Alzheimers disease is a form of mechanical senescence despite the fact that some loci that are important in development of the disease enhance development (Denham, p. 7127).
Tooth erosion can also be used to demonstrate senescence together with mammal oocyte exhaustion, although they can be perceived to be caused by some intrinsic limitations in most mammals body plan. This can be attributed as an outcome of the developmental process. In female, senescence in reproduction comes as a result of loss of ovarian oocytes that is brought about by age. Some reptiles undergo oocyte regeneration during adulthood and as a result tend to appear not to age (Denham, p7127). During the earlier years of development of mammals, oocyte regeneration is not active until the earlier stages of development.
Hence reproductive senescence is perceived as an outcome of senescence blockage. Likewise, tooth erosion can be considered to be a limitation to mammal development whereby the development process comes to an end as a result of worn-out tooth not being able to be replaced. Dental development is usually slow in humans compared to other primates and also extinct hominids, suggesting that the on set of tooth erosion is affected by the pace at which dental development takes place. Hence, during mechanical senescence, age related changes can be perceived to be influenced by the timing of developmental mechanisms (Michael et al, p.4769).
Causes of aging
The death of cells and aging has been associated to be part of the ageing process. This is because the rate of cell production and the changes that occur are regulated by genes but they are also prone to environmental changes. When a cell is not able to perform its important functions, it dies. This is also true in the case of multicellular organisms and thereby the process of aging involves majority of body cells dying. Death of an animal occurs as a result of death of cells in vital body organs that are important in sustaining major body functions (Brakefield at al, p .435).
Because of the speculations around the aging process, people have tried to come up with some of the things that contribute to the process. Some of the suggestions include progressive breakdown in protein synthesis, encodement of Deoxyribonucleic acid in aging, damage brought about by free reaction, autoimmunity in higher organisms, and also cross linkage of macromolecules (Medvedev, p.377). Many theories have been formulated that try to explain the aging process.
The free radical theory is one of the theories and it is based on an assumption that aging is caused by a single cause that is modified by environmental and also genetic factors. According to it, free radical reactions are responsible for aging and age related disorders. The reactions are believed to come about due to exposure to ionizing radiations, non-enzymatic and also enzymatic ones particularly those involved in photosynthesis and oxygen regulation. This reactions cause oxidation to tissue which in return brings about aging programmed theories of aging (Conboy et al, p.761).
According to Holliday (p. 570), oxidative damage has also been linked to aging. According to this theory normal metabolism is one responsible for aging and that mutations are not a necessity. 2-3 of the oxygen taken by the mitochondria is reduced to a reactive oxygen species (ROS). ROS is composed of hydrogen peroxide, super oxide ions together with hydroxyl radicals which have a potential to oxidize and destroy cell membranes, nucleic acid and also proteins (Thomas, p.3779). This can be observed in drosophila which produces enzymes that destroy ROS and as a result its able to live longer than other wild-type flies. Other flies that mutate Methuselah gene, also live longer compared to other wild-type flies. This gene that they produce works by increasing resistance to paraquat which is a poison that generates ROS within cells. Through the examples above, it is evident that aging is genetically controlled and that ROS play a role in it (Qin etal, p. 4340).
In mammals, the role of ROS in aging is not clear although some studies tend to support it. Other studies have shown that caloric restriction in mammals can help in slowing the process of aging although it is said to have other effects also. Hence it is not yet certain that it works by preventing ROS synthesis. Other factors that prevent ROS synthesis include vitamins E and C. Studies have also indicated that when vitamin E is added to the diet of nematodes and flies, increases their longevity (Christoph, Jeen-Woo and Bruce, p 467).
Wear and tear is another theory that tries to account for aging. According to the theory, as an individual grows older, little traumas experienced by the body build up. There is an increase in point mutations and a decrease in efficiency of enzymes brought about by genes. Furthermore, large faulty proteins are made when there was a mutation in part of the protein synthesis material producing faulty DNA polymerases. Because DNA is vital in repair of worn-out tissues, individuals with faulty DNA will end up producing pre-mature aging syndromes. This may end up reducing their life span (Weindruch, Kayo, Lee, and Prolla, p.178).
Mitochondria genome damage is also thought to be the cause of aging. Because mitochondria mutates 10-20 times more fast than the DNA, its thought that if the mitochondria undergoes a mutation, it could affect a number of processes which include energy production in the cell, manufacture of ROS as a result of a faulty electron transport and it may also lead to apoptosis. Mitochondrion that has undergone mutation is thought to have greater replication frequency compared to wild-type mitochondria. As a result, the mutants outgrow the wild-type mitochondria and finally occupy majority of the cell. The mutants allow formation of ROS at the same time increasing the risk of mitochondrial DNA suffering damage from ROS (Michelle et al, p.471).
According to Hawkins and Lovett (p. 290), some genes have also been found to play a significant role in aging. Dormant mutant genes such as Hutchinson-Gilford progreria syndrome affect children and causes rapid growth and death during the early years of life. The victims are found to have the following symptoms hair loss, thin skin spotted with age spots, arteriosclerosis, and reabsorbed bone mass (Nijhout, P.166).
When an acid diet is taken in by an individual, the PH of blood and cytoplasm falls to acidic levels. In response to the fall in the level of acid, the body uses its bones to buffer the acid. This is achieved through activation of osteoclasts cells which produce inflammatory chemicals that in return break bones to produce minerals that it uses to buffer the acidic state. These minerals include Mg, Ca and K which are released into the blood cytoplasm to effect the change to aid in bone repair. When we also eat meals rich in alkali, osteoblasts are activated if the diet taken is relatively alkalizing, there is no need of production of these cells because of the minerals contained in the food. Acidifying diets lead to a constant flip flop which in return causes an increased rate of metabolism of osteoblasts and osteoclasts. An increase in metabolism leads to a faster cell turn over speeding up the shortening of telomeres hence the process of longevity is accelerated (Pamela p. 97).
Genetically regulated aging insulin pathway
The caenorhabditis elegans DAF-2 insulin like signaling path way not only has been found to regulate lifespan and increase stress resistance capability, but also has a significant resistance to bacteria pathogens. Resistance to a wide variety of bacteria pathogens and prolonged lifespan has also been noted in the loss of function daf-2 and age -1. This has increased the possibility that longevity and pathogen resistance in the insulin-like signaling pathway mutants could be using the same mechanism as daf-2 and age-1. Here, lifespan regulations and resistance to pathogens is found to link by a mechanism that resembles both genetically and contain a genetically distinguishable mechanism. Loss of germline proliferation is found to enhance resistance to pathogens and this in return requires daf-16 which is the same in lifespan regulation.
Contrary to that, regulation of pathogen resistance and lifespan is decoupled in the DAF-2 pathway. Wild-type resistance to pathogens is shown in long lived mutant of genes belonging to daf-2 like pdk-1 and also sgk-1. However, enhanced resistance to pathogen has been observed in akt-1 2 which also have individual modest effect on lifespan. However, pathogen resistance in insulin-like signaling pathway is connected to the increase of immunity gene expression during infection. Other factors that have an effect on an organisms longevity include Jun kinase signaling together with caloric restriction although they do not affect on bacterial pathogen resistance. The finding that insulin pathway affects the lifespan and metabolism showed a concordance with mammalian lifespan studies where by low calories in rat and mouse diets increase their lifespan by reduction of levels of insulin. Signaling of insulin in the nervous system has been found to be important in lifespan elongation (De Magalhaes, p.45).
Production of free radicals that have high insulin signaling in neurons may destroy them leading to a decline in hormonal signal towards the muscles and skin resulting in visible signs of aging in both humans and worms. Regulations of lifespan by hormones released from the brain depend upon regulation of other life stage events such as menopause together with puberty.
Promoting longevity
Aging is a process that cannot be avoided because no one has control over it. The only thing that can be done to prolong life is to alter the aging process through taking relevant measures. There are three factors that contribute largely to the aging process. They include the length of Telomere, replication rate and the rate of metabolism together with the free radicals in the system.
Telomeres resemble caps and are usually found at the edge of chromosomes. They protect the chromosomes from deteriorating. They get shortened every time there is division of cells. When the cell continues to divide, they eventually disappear leaving the cell without the capacity to replicate. The cells then age and eventually die and sometime they may become cancerous or temporarily immortal.
Replication rate is necessary for elimination of endogenous and exogenous toxins that are acquired from the environment. These toxins put older cells DNA at a higher risk of undergoing mutation which may result in cancer. However, when replication occurs too often, the length of telomere shortens prematurely exposing the cells to more risks (Weindruch, Kayo, Lee, and Prolla, p.178).
According to Vaux and Strasser (p. 243), metabolic rate and the free radical activity play an important role in cell breakdown and replication. The food that we consume and the activities that we engage in affect greatly these factors. When one engages in exercise, metabolism is increased temporarily leading to an increase in the number of free radicals in the body. This leads to a healthy and cleansing turnover of cells. When an individual thinks that heshe is starving, physiological processes reduce. This reduces the wastes products produced by cells and increases the levels of free radicals increasing the risk of acquiring cancer (Joseph et al, no.15).
The following measures can be helpful in ensuring that an individual enjoys longevity. They include
Making sure that antioxidant levels of your body are elevated. Oxidation is brought about by the chemical reactions that occur as a result of free radicals. This oxidation brings about oxidative stress to the body cells together with tissues. To take care of these oxidants, a daily assimilation of various nutrients is a necessity by use of strong antioxidant food supplements. This will ensure that the levels of radicals that are free in your body are kept at a low level and the adequate concentration of antioxidants is maintained. This will help strengthen the bodys immune system which will take care of infection and therefore preventing pre-mature deaths.
Through use of herbs, it can help in reducing the level of free radicals in the body. One of the best herbs that can be used as an antioxidant is Ganoderma Lucidum. This herb contains high levels of SOD. This enzyme is important in regulating the levels of free radicals present in the body at any particular time and therefore slowing the process of aging. Therefore, through long term consumption of Ganoderma, vitality together with longevity is promoted. Consumption has to be done over a long period of time to achieve the results.
Low levels of antioxidants are achieved by the body through the use of a natural anti oxidation system that is found in the body. The system is composed of natural enzymes such as Superoxide Dismutase (SOD), glutathione Peroxidase (GPX) and also Catalase enzymes. These are the ones responsible for eliminating free radicals in the body. However, these enzymes keep decreasing as one ages. The older one grows the less antioxidant enzymes you have. The levels of these enzymes in the body keep decreasing day after day. Other factors that contribute to the increased level of free radicals include prolonged periods of stress more so work related, irregular patterns of work and also anxiety (Robert et al, p.210).
Biological aging is a process that occurs naturally. It may occur earlier in some species and late in some depending on some of the factors such as genes and environmental conditions. Although aging is inevitable, one can prolong longevity by ensuring that the level of free radicals in the body is kept low through the use of the methods discussed above such as avoiding work related stress and avoiding situation s that may make someone exited.
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