question: Why do things die of old age and why haven’t scientists figured out how to cure it?
comment: Cells die and and get copied and replaced. The copy isn't perfect and we see it as effects of aging.
passages: The idea that the human body can be repaired in old age to a more youthful state has gathered significant commercial interest over the past few years, including by companies such as Human Longevity Inc, Google Calico, and Elysium Health. In addition to these larger companies, many startups are currently developing therapeutics to tackle the 'ageing problem' using therapy. In 2015 a new class of drugs senolytics was announced (currently in pre-clinical development) designed specifically to combat the underlying biological causes of frailty.
  
  Section::::Philanthropy.
   Other research studies have been done with patients with heart disease, and, in these cases, the older patients were still less likely to receive further tests or treatments, independent of the severity of their health problems. Thus, the approach to the treatment of older people is concentrated on managing the disease rather than preventing or curing it. This is based on the stereotype that it is the natural process of aging for the quality of health to decrease, and, therefore, there is no point in attempting to prevent the inevitable decline of old age.
   About half of older adults suffer multimorbidity, that is, they have three or more chronic conditions. Medical advances have made it possible to "postpone death," but in many cases this postponement adds "prolonged sickness, dependence, pain, and suffering," a time that is costly in social, psychological, and economic terms.
   At present, researchers are only just beginning to understand the biological basis of ageing even in relatively simple and short-lived organisms such as yeast. Less still is known of mammalian ageing, in part due to the much longer lives of even small mammals such as the mouse (around 3 years). A model organism for studying of ageing is the nematode "C. elegans". Thanks to its short lifespan of 2–3 weeks, our ability to easily perform genetic manipulations or to suppress gene activity with RNA interference, or other factors. Most known mutations and RNA interference targets that extend lifespan were first discovered in "C. elegans".
   Senescence is the inevitable fate of all multicellular organisms with germ-soma separation, but it can be delayed. The discovery, in 1934, that calorie restriction can extend lifespan by 50% in rats, and the existence of species having negligible senescence and potentially immortal organisms such as "Hydra", have motivated research into delaying senescence and thus age-related diseases. Rare human mutations can cause accelerated aging diseases.
   BULLET::::- Some evidence is provided by oxygen-deprived bacterial cultures.
  
  BULLET::::- The theory would explain why the autosomal dominant disease, Huntington's disease, can persist even though it is inexorably lethal. Also, it has been suggested that some of the genetic variants that increase fertility in the young increase cancer risk in the old. Such variants occur in genes p53 and BRCA1.
   Health departments discourage listing old age as the cause of death because doing so does not benefit public health or medical research. Old age is not a scientifically recognized cause of death; there is always a more direct cause, although it may be unknown in certain cases and could be one of a number of aging-associated diseases. As an indirect or non-determinative factor, biological aging is the biggest contributor to deaths worldwide. It is estimated that of the roughly 150,000 people who die each day across the globe, about two thirds—100,000 per day—die of age-related causes. In industrialized nations the proportion is much higher, reaching 90%.
   A distinction can be made between "proximal ageing" (age-based effects that come about because of factors in the recent past) and "distal ageing" (age-based differences that can be traced to a cause in person's early life, such as childhood poliomyelitis).
  
  Ageing is among the greatest known risk factors for most human diseases. Of the roughly 150,000 people who die each day across the globe, about two thirds—100,000 per day—die from age-related causes. In industrialized nations, the proportion is higher, reaching 90%.
  
  Section::::Biological basis.
   Old people often have limited regenerative abilities and are more susceptible to disease, syndromes, injuries and sickness than younger adults. The organic process of ageing is called senescence, the medical study of the aging process is called gerontology, and the study of diseases that afflict the elderly is called geriatrics. The elderly also face other social issues around retirement, loneliness, and ageism.
   Aging (senescence) increases vulnerability to age-associated diseases, whereas genetics determines vulnerability or resistance between species and individuals within species. Some age-related changes (like graying hair) are said to be unrelated to an increase in mortality. But some biogerontologists believe that the same underlying changes that cause graying hair also increase mortality in other organ systems and that understanding the incidence of age-associated disease will advance knowledge of the biology of senescence just as knowledge of childhood diseases advanced knowledge of human development.
   Senescence refers to a scenario when a living being is able to survive all calamities, but eventually dies due to causes relating to old age. Animal and plant cells normally reproduce and function during the whole period of natural existence, but the aging process derives from deterioration of cellular activity and ruination of regular functioning. Aptitude of cells for gradual deterioration and mortality means that cells are naturally sentenced to stable and long-term loss of living capacities, even despite continuing metabolic reactions and viability. In the United Kingdom, for example, nine out of ten of all the deaths that occur on a daily basis relates to senescence, while around the world it accounts for two-thirds of 150,000 deaths that take place daily (Hayflick & Moody, 2003).
   It is estimated that of the roughly 150,000 people who die each day across the globe, about two thirds—100,000 per day—die of age-related causes. In industrialized nations the proportion is much higher, reaching 90 percent. Thus, albeit indirectly, biological aging (senescence) is by far the leading cause of death. Whether senescence as a biological process itself can be slowed down, halted, or even reversed is a subject of current scientific speculation and research.
  
  Section::::Worldwide.:2001 figures.
   With respect to specific types of chemical damage caused by metabolism, it is suggested that damage to long-lived biopolymers, such as structural proteins or DNA, caused by ubiquitous chemical agents in the body such as oxygen and sugars, are in part responsible for aging. The damage can include breakage of biopolymer chains, cross-linking of biopolymers, or chemical attachment of unnatural substituents (haptens) to biopolymers.
   BULLET::::- Those who believe in the idea that ageing is an unavoidable side effect of some necessary function (antagonistic pleiotropy or disposable soma theories) logically tend to believe that attempts to delay ageing would result in unacceptable side effects to the necessary functions. Altering ageing is therefore "impossible", and study of ageing mechanisms is of only academic interest.
  
  BULLET::::- Those believing in default theories of multiple maintenance mechanisms tend to believe that ways might be found to enhance the operation of some of those mechanisms. Perhaps they can be assisted by anti-oxidants or other agents.
   Examples of aging-associated diseases are atherosclerosis and cardiovascular disease, cancer, arthritis, cataracts, osteoporosis, type 2 diabetes, hypertension and Alzheimer's disease. The incidence of all of these diseases increases exponentially with age. 
  
  Of the roughly 150,000 people who die each day across the globe, about two thirds—100,000 per day—die of age-related causes. In industrialized nations, the proportion is higher, reaching 90%.
  
  Section::::Patterns of differences.
   Section::::Cancer versus cellular senescence tradeoff theory of aging.
  
  Senescent cells within a multicellular organism can be purged by competition between cells, but this increases the risk of cancer. This leads to an inescapable dilemma between two possibilities—the accumulation of physiologically useless senescent cells, and cancer—both of which lead to increasing rates of mortality with age.
  
  Section::::Chemical damage.
  
  One of the earliest aging theories was the "Rate of Living Hypothesis" described by Raymond Pearl in 1928 (based on earlier work by Max Rubner), which states that fast basal metabolic rate corresponds to short maximum life span.
   Before the surge in the over-65 population, accidents and disease claimed many people before they could attain old age, and health problems in those over 65 meant a quick death in most cases. If a person lived to an advanced age, it was due to genetic factors and/or a relatively easy lifestyle, since diseases of old age could not be treated before the 20th century.
   The causes of ageing are uncertain; current theories are assigned to the damage concept, whereby the accumulation of damage (such as DNA oxidation) may cause biological systems to fail, or to the programmed ageing concept, whereby internal processes (such as DNA methylation) may cause ageing. Programmed ageing should not be confused with programmed cell death (apoptosis).
  
  In 1934, it was discovered that calorie restriction can extend lifespan by 50% in rats and this has motivated research into delaying and preventing ageing .
  
  Section::::Ageing versus immortality.
   Section::::Types of aging damage and treatment schemes.:Intracellular junk—LysoSENS.
  
  Our cells are constantly breaking down proteins and other molecules that are no longer useful or which can be harmful. Those molecules which can’t be digested accumulate as junk inside our cells, which is detected in the form of lipofuscin granules. Atherosclerosis, macular degeneration, liver spots on the skin and all kinds of neurodegenerative diseases (such as Alzheimer's disease) are associated with this problem.
   The ultimate objective of SENS is the eventual elimination of age-related diseases and infirmity by repeatedly reducing the state of senescence in the organism. The SENS project consists in implementing a series of periodic medical interventions designed to repair, prevent or render irrelevant all the types of molecular and cellular damage that cause age-related pathology and degeneration, in order to avoid debilitation and death from age-related causes.
   While most people can afford to get resleeved at the end of their lives, they are unable to update their bodies and most go through the full aging process each time, which discourages most from resleeving more than once or twice. So while normal people can live indefinitely in theory, most choose not to. Only the wealthy are able to acquire replacement bodies on a continual basis. The long-lived are called Meths, a reference to the Biblical figure Methuselah. The very rich are also able to keep copies of their minds in remote storage, which they update regularly. This ensures that even if their stack is destroyed, they can be resleeved.
   Section::::Factors contributing to aging.
  
  Aging factors can be defined as irreparable damages to cellular components which ultimately contribute to the decreased fitness of the individual harbouring them. Putative aging factors include damaged DNA strands, old cell-surface material, and mis-folded or aggregated protein. The cell poles of replicating "E. coli" are often used as a proxy for aging factors as each bacterium inherits an old cell-pole (mother's pole) and a newly synthesized new cell-pole. Inclusion bodies, masses of aggregated damaged or mis-folded proteins, have recently been shown to contribute to the aging of cellular organisms.
   Disease is theoretically surmountable via technology. In short, it is an abnormal condition affecting the body of an organism, something the body shouldn't typically have to deal with its natural make up. Human understanding of genetics is leading to cures and treatments for a myriad of previously incurable diseases. The mechanisms by which other diseases do damage are becoming better understood. Sophisticated methods of detecting diseases early are being developed. Preventative medicine is becoming better understood. Neurodegenerative diseases like Parkinson's and Alzheimer's may soon be curable with the use of stem cells. Breakthroughs in cell biology and telomere research are leading to treatments for cancer. Vaccines are being researched for AIDS and tuberculosis. Genes associated with type 1 diabetes and certain types of cancer have been discovered, allowing for new therapies to be developed. Artificial devices attached directly to the nervous system may restore sight to the blind. Drugs are being developed to treat a myriad of other diseases and ailments.
   BULLET::::- “The End Of Ageing (Medical Documentary) - Real Stories” (2017-11-10)
  
  BULLET::::- BBC News documentary movie: “Can ageing be delayed, stopped or even reversed? BBC News” (2018-02-11)
  
  BULLET::::- “How we can finally win the fight against aging | Aubrey De Grey | TEDxMünchen” (2017-01-11)
  
  BULLET::::- How People Disappear by vSauce (Michael Stevens) (2013-09-25)
  
  BULLET::::- Why don't we all have cancer by vSauce (2014-05-19).
  
  BULLET::::- CGP Grey: “Why Die?”
  
  BULLET::::- Kurzgesagt – In a Nutshell:
  
  BULLET::::- Why Age? Should We End Aging Forever? (2017-10-20)
  
  BULLET::::- How to Cure Aging – During Your Lifetime? (2017-11-03)
   To achieve the more limited goal of halting the increase in mortality rate with age, a solution must be found to the fact that any intervention to remove senescent cells that creates competition among cells will increase age-related mortality from cancer.
  
  Section::::Immortalism and immortality as a movement.
  