1. De eeuwige jeugd...

Re: De eeuwige jeugd...

Dit is een aardige samenvatting van de verschillende theorieen voor het verouderingsproces (ageing):
Wel in het engels, voor mij makkelijk leesbaar maar dat zal niet voor iedereen gelden.
Theories of Aging - Introduction
We understand the physiological consequences of ageing. But what occurs at the molecular level? What cellular processes and events cause ageing? These questions are still being debated and many theories have been presented. Here we explain several prominent ageing theories and discuss how they reveal the molecular steps behind ageing.

Evolutionary Theories
Evolutionary theories of ageing describe how ageing could have evolved and thus explain why ageing occurs. Such knowledge is important in both understanding and investigating the complex cellular and molecular mechanisms underlying the ageing process. Currently, the most prominent evolutionary theories of ageing are the 'mutation accumulation', 'antagonistic pleiotropy', and 'disposable soma' theories. Although much controversy still exists, recent research has found increasing support for the 'disposable soma' theory. Use of model organisms has proved to be essential in all such experiments testing evolutionary theories. The most common and useful have been D. melanogaster and C. elegans.

Evolution of a non-adaptive process
From an evolutionary standpoint, the near universal existence of ageing in multicellular organisms presents an intriguing paradox. As favouring reproductive fitness is the underlying principle of natural selection, it compels us to wonder if the clearly detrimental phenomenon of ageing has actually evolved as an adaptive process, or if it is nothing more than an evolutionary consequence.

The earliest and simplest evolutionary explanation of ageing suggested that ageing is genetically programmed in order to limit population size and overcrowding (Weisman, 1891). A related idea is that ageing has been selected for to promote genetic diversity in changing environments. Since then, this concept of ageing as an adaptive process has re-surfaced repeatedly in various forms (Bowles, 2000; Zafon, 2003).

Prevailing consensus in the field however, has systematically rejected the adaptive nature of senescence based on two major criticisms (Kirkwood, 1997):
1) it is well known that the majority of animals die before they experience any ageing at all, thus there is little direct selection pressure for 'ageing genes'
2) ageing is clearly deleterious to the individual and mutations inactivating such genes should persist, thus it is difficult to see how 'ageing genes' could be selected for or maintained
Rather, since Medawar (1952) first proposed the 'mutation accumulation' theory, the idea of ageing as a non-adaptive process has been the dominant perspective in evolutionary theory. The 'mutation accumulation' theory postulates that ageing is largely outside the forces of evolution as ageing typically occurs after reproduction and only affect a minimal proportion of populations in the wild due to extrinsic mortality. Thus, any deleterious genes that act late in life could accumulate and persist as selection pressure against these genes is low.

In a somewhat similar vein, Williams (1957) proposed the concept of 'antagonistic pleiotropy', which suggested that genes that had positive beneficial effects would be selected for even if they had adverse affects late in life. Again, the plausibility of this theory rests on minimal survival to old age in the wild. However, this theory is peculiar as it seems highly unlikely that genes that cause such contrasting temporal effects can exist. Further, based on the nature of mutations, we should see much more early neutral and late detrimental genes (similar to the 'mutation accumulation' theory) than early beneficial and late detrimental (Bowles, 2000). Thus the influence of 'antagonistic pleiotropy' on ageing should be minor if at all.

The third major evolutionary theory, known as the 'disposable soma' theory, was developed by Kirkwood (1977). Kirkwood highlighted three fundamental points:
1) somatic cells exist only to allow transmission of genes to the following generation, and are thus 'disposable'
2) reproduction and cellular repair and maintenance both have a high energy cost
3) energy resources are scarce and so reproduction and cellular repair and maintenance compete for energy use
For Kirkwood then, ageing represents an optimal allocation or resources in a trade-off between somatic maintenance and reproduction. This theory suggests that investments in durability and maintenance of somatic tissues should only be sufficient for the normal expectation of reproductive life in the wild. Further, even with efficient maintenance systems, organisms die from external causes (hunger, cold, predators, accidents, etc.). Therefore, it is more beneficial to invest resources towards reproduction, albeit at the expense of less efficient maintenance systems that eventually lead to ageing and death.

These final three theories can be complementary with one another and are still being tested today. Nonetheless, it is seems clear that ageing is likely influenced by multiple genes through complex interactions.

Conclusion
Ultimately, knowing why ageing occurs is important to understanding how it occurs. Therefore, evolutionary theories aid in analysis of the complex cellular and molecular mechanisms underlying senescence. Present evidence most strongly supports the operative model to be the 'disposable soma' evolutionary theory of ageing, along with some contributions from the 'mutation accumulation' theory. Future research should involve further genetic techniques to specifically confirm these evolutionary theories. Towards this end, researchers should be confident using D. melanogaster and C. elegans.

The Neuroendocrine Theory
The neuroendocrine theory proposes that ageing is due to changes in neural and endocrine functions that are crucial for
1) coordinating communication and responsiveness of all body systems with the external environment;
2) programming physiological responses to environmental stimuli; and
3) maintaining an optimal functional state for reproduction and survival while responding to environmental demands.
(Weinert et al., 2003)

These changes often affect hormones and neurons that are involved in regulation of metabolism, reproduction, growth and development, as well as adaptation of stress. As a result, life span—one of the cyclic body functions regulated by “biological clocks,” would undergo a continuum or acceleration of sequential stages driven by nervous and endocrine signals. (Weinert et al., 2003)

mtDNA Mutation Theory
One of the prominent theories of aging is the DNA mutation theory. It postulates that mutations in DNA, both chromosomal and mitochondrial, accumulate to a point over the years after which repair becomes inadequate to sustain proper cell functioning. Gaining considerable popularity over the last few years is the mitochondrial DNA (mtDNA) theory which is part of the DNA mutation theory. This specialized theory states that mutations in the mitochondrial genome might lead to improper replication of the genome and functioning of the mitochondria, both of which impair the mitochondrion's ability to produce energy, and the latter of which may facilitate the leakage of reactive oxidative species into the surrounding cytosol.

The mitochondrial genome consists of a non-coding control region (D-loop) that contains the origin of replication as well as two hypervariable regions, and other coding sites for mitochondrial specific enzymes i.e. cytochromes, ATPases etc. (Wallace et al, 2004). It is 16569 bp in size. Recent work has shown that many mutations occur in the non-coding regions of the mitochondrial genome. It has been hypothesized that deleterious mutations in the coding regions of the genome are highly selected against and are, therefore, scarce. However, the evolutionary theories postulate that once an individual has reproduced, the selection pressure against deleterious mutations is alleviated somewhat (LeBourg, 2001). This may facilitate the expression of faulty enzymes or inefficient containment of reactive oxidative species.

The mechanisms underlying aging have been somewhat illusive thus far. It is highly probable that aging is brought on by several factors, all of which become apparent at certain stages in life. The potential for the leakage of reactive oxidative species by mitochondria can establish a causal role for mitochondria in aging, which makes the theory very promising. Since mitochondria are ubiquitously found in the body, and since they play such an instrumental role in cell sustenance and functioning, it is feasible to infer that they do play a role in aging.

The Oxidative Stress Theory
The oxidative stress theory of aging postulates that: the main causal factor underlying senescence-associated losses in physiological functions (i.e. aging) is the accrual of molecular oxidative damage (Melov, 2002; Finkel and Holbrook, 2000; Sohal et al., 2002). This damage is induced by a specific chemical species known as reactive oxygen species (ROS) (Sohal et al., 2002). An unavoidable by-product of respiration by the mitochondria of the cell and other internal metabolic systems (Finkel and Holbrook, 2000), ROS include: superoxide anions, hydroxyl radicals, and hydrogen peroxide (Melov, 2002; Finkel and Holbrook, 2000). Exogenously, ultraviolet light, radiation and environmental toxins can also lead to ROS production (Finkel and Holbrook, 2000).

While having a positive cellular role as signaling molecules for control mechanisms such as regulation, these ROS inevitably accumulate and cause damage to cellular lipids, proteins and nucleic acids, influencing cellular processes which may lead to ageing and age-related diseases (Finkel and Holbrook, 2000).

To defend against these ROS, eukaryotes have evolved combative defensive enzymes, or antioxidants, such as: superoxide dismutase (SOD), glutathione peroxidase, and catalase (Melov, 2002; Finkel and Holbrook, 2000). As well, vitamins A, C and E also play a role in antioxidant defense (Finkel and Holbrook, 2000).

Thus, the amount of oxidative stress an organism receives becomes a function of ROS generation, both endogenously and exogenously, and ROS removal, via antioxidants both natural and supplemented.

The Telomere Shortening Theory of Aging
The long and short on Telomeres
Courtesy of: The Genetic Science Learning Centre
Telomere shortening is one of the proposed molecular mechanisms responsible for the process of human aging. This mechanism coincides under the hypothesis that aging is explained by cell senescence (Kipling and Faragher, 1999). Cell senescence occurs when we reach a certain age and refers to the state where cells are no longer dividing (Weinberg, 1998). Telomeres are DNA sequences synthesized by the ribonucleoprotein enzyme telomerase during embryonic development (Lee et al, 1998). Telomerase activity is present in germ cells but repressed in many somatic cells such as fibroblasts. Due to the directional nature of DNA synthesis, each time DNA is replicated in cell division, the telomeres at the end of chromosomes are eroded (Rudolph et al, 1999). This is also known as the end-replication problem (Weinberg, 1998). Please refer to the diagram "The Long and Short of Telomeres" on the left of this page. Without telomerase, telomeres cannot be recovered and progressive telomere shortening results. It has been proposed that cells use this mechanism of telomere shortening as a clock to count the number of divisions that have occurred (Kipling and Faragher, 1999). After a certain number of cell divisions have been counted, the state of cell senescence begins. Under the theory that telomere length directs aging, we expect organisms with reduced telomere lengths to reach cell senescence and subsequently cell death more quickly while organisms with lengthened telomeres would have increased cell lifespans (Rudolph et al, 1999).
  • Dit is een aardige samenvatting van de verschillende theorieen voor het verouderingsproces (ageing):
    Wel in het engels, voor mij makkelijk leesbaar maar dat zal niet voor iedereen gelden.
    Theories of Aging - Introduction
    We understand the physiological consequences of ageing. But what occurs at the molecular level? What cellular processes and events cause ageing? These questions are still being debated and many theories have been presented. Here we explain several prominent ageing theories and discuss how they reveal the molecular steps behind ageing.

    Evolutionary Theories
    Evolutionary theories of ageing describe how ageing could have evolved and thus explain why ageing occurs. Such knowledge is important in both understanding and investigating the complex cellular and molecular mechanisms underlying the ageing process. Currently, the most prominent evolutionary theories of ageing are the 'mutation accumulation', 'antagonistic pleiotropy', and 'disposable soma' theories. Although much controversy still exists, recent research has found increasing support for the 'disposable soma' theory. Use of model organisms has proved to be essential in all such experiments testing evolutionary theories. The most common and useful have been D. melanogaster and C. elegans.

    Evolution of a non-adaptive process
    From an evolutionary standpoint, the near universal existence of ageing in multicellular organisms presents an intriguing paradox. As favouring reproductive fitness is the underlying principle of natural selection, it compels us to wonder if the clearly detrimental phenomenon of ageing has actually evolved as an adaptive process, or if it is nothing more than an evolutionary consequence.

    The earliest and simplest evolutionary explanation of ageing suggested that ageing is genetically programmed in order to limit population size and overcrowding (Weisman, 1891). A related idea is that ageing has been selected for to promote genetic diversity in changing environments. Since then, this concept of ageing as an adaptive process has re-surfaced repeatedly in various forms (Bowles, 2000; Zafon, 2003).

    Prevailing consensus in the field however, has systematically rejected the adaptive nature of senescence based on two major criticisms (Kirkwood, 1997):
    1) it is well known that the majority of animals die before they experience any ageing at all, thus there is little direct selection pressure for 'ageing genes'
    2) ageing is clearly deleterious to the individual and mutations inactivating such genes should persist, thus it is difficult to see how 'ageing genes' could be selected for or maintained
    Rather, since Medawar (1952) first proposed the 'mutation accumulation' theory, the idea of ageing as a non-adaptive process has been the dominant perspective in evolutionary theory. The 'mutation accumulation' theory postulates that ageing is largely outside the forces of evolution as ageing typically occurs after reproduction and only affect a minimal proportion of populations in the wild due to extrinsic mortality. Thus, any deleterious genes that act late in life could accumulate and persist as selection pressure against these genes is low.

    In a somewhat similar vein, Williams (1957) proposed the concept of 'antagonistic pleiotropy', which suggested that genes that had positive beneficial effects would be selected for even if they had adverse affects late in life. Again, the plausibility of this theory rests on minimal survival to old age in the wild. However, this theory is peculiar as it seems highly unlikely that genes that cause such contrasting temporal effects can exist. Further, based on the nature of mutations, we should see much more early neutral and late detrimental genes (similar to the 'mutation accumulation' theory) than early beneficial and late detrimental (Bowles, 2000). Thus the influence of 'antagonistic pleiotropy' on ageing should be minor if at all.

    The third major evolutionary theory, known as the 'disposable soma' theory, was developed by Kirkwood (1977). Kirkwood highlighted three fundamental points:
    1) somatic cells exist only to allow transmission of genes to the following generation, and are thus 'disposable'
    2) reproduction and cellular repair and maintenance both have a high energy cost
    3) energy resources are scarce and so reproduction and cellular repair and maintenance compete for energy use
    For Kirkwood then, ageing represents an optimal allocation or resources in a trade-off between somatic maintenance and reproduction. This theory suggests that investments in durability and maintenance of somatic tissues should only be sufficient for the normal expectation of reproductive life in the wild. Further, even with efficient maintenance systems, organisms die from external causes (hunger, cold, predators, accidents, etc.). Therefore, it is more beneficial to invest resources towards reproduction, albeit at the expense of less efficient maintenance systems that eventually lead to ageing and death.

    These final three theories can be complementary with one another and are still being tested today. Nonetheless, it is seems clear that ageing is likely influenced by multiple genes through complex interactions.

    Conclusion
    Ultimately, knowing why ageing occurs is important to understanding how it occurs. Therefore, evolutionary theories aid in analysis of the complex cellular and molecular mechanisms underlying senescence. Present evidence most strongly supports the operative model to be the 'disposable soma' evolutionary theory of ageing, along with some contributions from the 'mutation accumulation' theory. Future research should involve further genetic techniques to specifically confirm these evolutionary theories. Towards this end, researchers should be confident using D. melanogaster and C. elegans.

    The Neuroendocrine Theory
    The neuroendocrine theory proposes that ageing is due to changes in neural and endocrine functions that are crucial for
    1) coordinating communication and responsiveness of all body systems with the external environment;
    2) programming physiological responses to environmental stimuli; and
    3) maintaining an optimal functional state for reproduction and survival while responding to environmental demands.
    (Weinert et al., 2003)

    These changes often affect hormones and neurons that are involved in regulation of metabolism, reproduction, growth and development, as well as adaptation of stress. As a result, life span—one of the cyclic body functions regulated by “biological clocks,” would undergo a continuum or acceleration of sequential stages driven by nervous and endocrine signals. (Weinert et al., 2003)

    mtDNA Mutation Theory
    One of the prominent theories of aging is the DNA mutation theory. It postulates that mutations in DNA, both chromosomal and mitochondrial, accumulate to a point over the years after which repair becomes inadequate to sustain proper cell functioning. Gaining considerable popularity over the last few years is the mitochondrial DNA (mtDNA) theory which is part of the DNA mutation theory. This specialized theory states that mutations in the mitochondrial genome might lead to improper replication of the genome and functioning of the mitochondria, both of which impair the mitochondrion's ability to produce energy, and the latter of which may facilitate the leakage of reactive oxidative species into the surrounding cytosol.

    The mitochondrial genome consists of a non-coding control region (D-loop) that contains the origin of replication as well as two hypervariable regions, and other coding sites for mitochondrial specific enzymes i.e. cytochromes, ATPases etc. (Wallace et al, 2004). It is 16569 bp in size. Recent work has shown that many mutations occur in the non-coding regions of the mitochondrial genome. It has been hypothesized that deleterious mutations in the coding regions of the genome are highly selected against and are, therefore, scarce. However, the evolutionary theories postulate that once an individual has reproduced, the selection pressure against deleterious mutations is alleviated somewhat (LeBourg, 2001). This may facilitate the expression of faulty enzymes or inefficient containment of reactive oxidative species.

    The mechanisms underlying aging have been somewhat illusive thus far. It is highly probable that aging is brought on by several factors, all of which become apparent at certain stages in life. The potential for the leakage of reactive oxidative species by mitochondria can establish a causal role for mitochondria in aging, which makes the theory very promising. Since mitochondria are ubiquitously found in the body, and since they play such an instrumental role in cell sustenance and functioning, it is feasible to infer that they do play a role in aging.

    The Oxidative Stress Theory
    The oxidative stress theory of aging postulates that: the main causal factor underlying senescence-associated losses in physiological functions (i.e. aging) is the accrual of molecular oxidative damage (Melov, 2002; Finkel and Holbrook, 2000; Sohal et al., 2002). This damage is induced by a specific chemical species known as reactive oxygen species (ROS) (Sohal et al., 2002). An unavoidable by-product of respiration by the mitochondria of the cell and other internal metabolic systems (Finkel and Holbrook, 2000), ROS include: superoxide anions, hydroxyl radicals, and hydrogen peroxide (Melov, 2002; Finkel and Holbrook, 2000). Exogenously, ultraviolet light, radiation and environmental toxins can also lead to ROS production (Finkel and Holbrook, 2000).

    While having a positive cellular role as signaling molecules for control mechanisms such as regulation, these ROS inevitably accumulate and cause damage to cellular lipids, proteins and nucleic acids, influencing cellular processes which may lead to ageing and age-related diseases (Finkel and Holbrook, 2000).

    To defend against these ROS, eukaryotes have evolved combative defensive enzymes, or antioxidants, such as: superoxide dismutase (SOD), glutathione peroxidase, and catalase (Melov, 2002; Finkel and Holbrook, 2000). As well, vitamins A, C and E also play a role in antioxidant defense (Finkel and Holbrook, 2000).

    Thus, the amount of oxidative stress an organism receives becomes a function of ROS generation, both endogenously and exogenously, and ROS removal, via antioxidants both natural and supplemented.

    The Telomere Shortening Theory of Aging
    The long and short on Telomeres
    Courtesy of: The Genetic Science Learning Centre
    Telomere shortening is one of the proposed molecular mechanisms responsible for the process of human aging. This mechanism coincides under the hypothesis that aging is explained by cell senescence (Kipling and Faragher, 1999). Cell senescence occurs when we reach a certain age and refers to the state where cells are no longer dividing (Weinberg, 1998). Telomeres are DNA sequences synthesized by the ribonucleoprotein enzyme telomerase during embryonic development (Lee et al, 1998). Telomerase activity is present in germ cells but repressed in many somatic cells such as fibroblasts. Due to the directional nature of DNA synthesis, each time DNA is replicated in cell division, the telomeres at the end of chromosomes are eroded (Rudolph et al, 1999). This is also known as the end-replication problem (Weinberg, 1998). Please refer to the diagram "The Long and Short of Telomeres" on the left of this page. Without telomerase, telomeres cannot be recovered and progressive telomere shortening results. It has been proposed that cells use this mechanism of telomere shortening as a clock to count the number of divisions that have occurred (Kipling and Faragher, 1999). After a certain number of cell divisions have been counted, the state of cell senescence begins. Under the theory that telomere length directs aging, we expect organisms with reduced telomere lengths to reach cell senescence and subsequently cell death more quickly while organisms with lengthened telomeres would have increased cell lifespans (Rudolph et al, 1999).
  • tis btw ook zielig voor criminelen die levenslang krijgen… [écht levenslang…]
  • Prima is goed maar ik vond het wel iets toevoegen. Jij dus niet dus laat dan maar. En Miereneuker is geen scheldwoord. Je mag dat ook tegen politie agenten zeggen of wist je dat al?
  • Probeer anders een keer iets toe te voegen aan het onderwerp.

    Als je niks te zeggen hebt, zeg dan niks, ga niet posten om het posten.
  • Je hebt het nodig maar bij het metabolisch omzetten van zuurstof worden vrije radicalen gevormd, reactieve deeltjes die o.a. celmembranen en DNA kunnen beschadigen.
  • verouderd je lichaam,(dus ook de hersen cellen en) onderanderen niet door zuurstof, de meesten weten dit niet maar eigelijk is zuurstof een geiftige stof, dat is onderanderen waarom je er ouder uitgaatzien bijv rimpels

    iemand meer hier over==

    heh hoe kan dat zuurstof een giftige stof is als je het niet hebt ga je binnen 5 minuten dood en als je het wel hebt ga je bijnne 100 jaar ongeveer dood :S
  • verouderd je lichaam,(dus ook de hersen cellen en) onderanderen niet door zuurstof, de meesten weten dit niet maar eigelijk is zuurstof een geiftige stof, dat is onderanderen waarom je er ouder uitgaatzien bijv rimpels

    iemand meer hier over==
  • Ik zou best het eeuwige leven willen hebben als dat kan. Als ik alles zo'n beetje gezien heb kan ik altijd nog van een brug afspringen ofzo.
  • ja dat wel, maar ik bedoel, slecht horen / zien, niet meer kunnen lopen, etc.
    dus 1000 jaar zouden we mischien wel kunnen worden, maar dat kan niet

    haha dat wel of je bent half robo/ homosapien omdat je vel afzakt!
    half homo(sapien?) en alien ben je nu al ! :P
    ( ik ben niet de duivel hoor, gewoon een grapje)
  • daar komt het uiteindelijk op neer jah… En uiteindelijk zit alles veel te vol, behalve in de derde wereld, omdat de mensen daar te arm zijn :|
  • Mensen met geld gaan door, de armen die sterven.
  • Ik zou alleen eeuwig willen leven als ik me kan blijven gedragen als een 20-jarige.. en zo zou kunnen leven.

    moet er niet aan denken om 900 jaar gerimpeld en in een rolstoel zittend, 50 oorlogen mee te maken.

    maar ik moet er wel aan denken om nog 1000 jaar, me jong en onvolwassen te gedragen, doen wat ik wil.. niet te verrimpelen, en je helemaal uit kunnen leven.. 1000 jaar ballen o_0
  • ja dat wel, maar ik bedoel, slecht horen / zien, niet meer kunnen lopen, etc.
    dus 1000 jaar zouden we mischien wel kunnen worden, maar dat kan niet

    haha dat wel of je bent half robo/ homosapien omdat je vel afzakt!
  • ja dat wel, maar ik bedoel, slecht horen / zien, niet meer kunnen lopen, etc.
    dus 1000 jaar zouden we mischien wel kunnen worden, maar dat kan niet
  • Ja je draadje en je cellen raken op oud vel maar er is altijd nog de optie plastiche chirurgie toepasselijk!
  • ik denk dat eeuwig level wel kan, maar niet haalbaar is omdat als je oud word allemaal dingen krijgt, slecht zien etc.
  • quote: legend
    Verouderen komt neer op dat je lichaam cellen niet meer vernieuwd. Dat je lichaam hier mee ophoud is genetisch bepaald.

    dat bedoelde ik maar wist ff nie meer had zoiets op school gehoord met bio

    Dat heeft met je DNA te maken, dacht ik. Elke keer als cellen zich vermenigvuldigen, wordt het DNA ook gekopieerd. Dit DNA raakt echter constant beschadigd door allerlei externe oorzaken. Het lichaam repareert het DNA wel, maar de kwaliteit gaat toch langzaam achteruit, net als de kwaliteit van de nieuwe cellen. Uiteindelijk is de kwaliteit van de nieuwe cellen zo belabberd dat je lichaam niet meer goed kan functioneren en kwetsbaarder wordt voor ziektes zoals kanker (de celdeling slaat op hol).
  • Dit is het zelfde als mensen die zeggen dat ze onsterfelijk zijn.
    En 2 jaar later zijn ze in hun slaap gestorfen.
    Die man gaat zelf de pijp uit voor dat hij nog 120 word.
    Kijk langer leven gaat wel maar eeuwig leven gaat niet meer alles is versleten ik wil niet weten hoe je botten er uit zien als je 500 jaar hebt bewogen.
    We zijn later misschien wel in staat om 1000 te worden maar denk eens dat kan je lichaam niet meer aan of je moet honderden keren geopereerd worden en na 300 jaar dan is 2% van jou en die andere 98% zijn van andere mensen die jou in leven houden.
    Als je te oud word dan werken alleen je hersenen tog niet meer.
    Zie ook de paus die was eigenlijk al dagen dood hij kon niet eten niet drinken niet plassen dus al het urine kwam in zijn bloed terecht. Hij kon niet zelfstandig ademen en zijn hersenen waren amper actief Hij kon niks meer doen ze hielden hem letterlijk kunstmatig in leven ze wouden bijna zijn nieren gaan zuiveren zo dat hij nog 1 paar weken zou leven.
    Zo kom jij dan ook te liggen als je 1000 wilt worden.
    Dan word ik liever 90 en sterf ik in 1 keer.
    Zo heb je toch geen leven meer ik vind dat je het leven op zo,n manier niet moet gaan uitrekken operaties om dat je ziek bent ok maar je zal toch ooit dood moeten gaan je zal niet de eerste zijn en ook niet de laatste.
    Tenzij julius ceasar nog ergens verblijft in 1 bunker met 3 gladiatoren en wacht op het moment dat hij europa kan overmeesteren en ook de galliérs kan overmeesteren.
    Net zo als hitler nog leeft en een wo3 wilt starten mensen denken dat soms ook nog.
  • Discovery Channel :D

    Dat is de theorie die zegt dat je energieinname je leeftijd bepaalt. Kan er mee te maken hebben, maar het is zeker niet het enige.
  • kan het eigenlijk wel je lichaam is toch een keer op en uitgeput ik dnek nie dat et kan hoor

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