Humanlifespan,or longevity,isdivided intotwoparts:meanlongevity(alsoknownaslifeexpectancy)and maximal longevity.Theaverageageof deathof all individualsina populationisreferred toasmeanlongevity.
Humanlifeexpectancyhasrisenthroughout history.
Biologyof Aging
Inthelateeighteenthcentury,for example,lifeexpectancyintheUnited Stateswasthirty-fiveyears.It hasrisen to 72 years by the final quarter of the twentieth century. Maximum longevity, the second component of life span,istheageat whichthemost long-lived individualsina group die.
In humans, this is difficult to calculate, however it is widely regarded to bebetween 110and 120years.The trend of increasing lifeexpectancyhasbeenlinked toadvancementsindiet,sanitation,and medical treatment.
Inreality,maximumlongevityappearstobeindependent of theseenvironmental influencesand isanabsolute limit,most likelyset bygeneactivity.
The genes that govern maximal lifespan are thought to be in charge of fixing faults in genetic information, mending errorsinproteinsynthesis,and determining themoment of death.
AgingChanges that OccurinHumans
The skin and its derivatives exhibit some of the most visible age-related changes in humans. These include pigment lossinthehair,skinwrinkling,pigment ncreaseintheskin,and nail thickening.
Other visible changes include a decrease in size due to muscle and bone mass loss, a decrease in muscle strength, a decrease in joint mobility, and a variety of neurological changes such as decreased sensory function (vision, hearing, smell, and taste), increased response time, and a decreased capacity for learning and memory.
Thelatter havebeenlinked toa decreaseof brainmass,whichhasbeenlinked toa lossof braincells.
Less obvious alterations include a drop in metabolic rate, impaired kidney, lung, and pancreatic function, cardiovascular disease, impaired immunological function, increased susceptibility to cancer, and a decline (in males) or cessation (in females) of reproductive function. All of these alterations have been linked to cellular eventsand processesexplained byvariousaging hypotheses.
Theories of Aging
It is well acknowledged that the aging process cannot be attributed to a single factor. A variety of deas have beenpresented toexplainthechangesthat occur aspeopleage.
The changes provided by the theory must match the following requirements in order to be a good contender for anexplanationof theaging process:
(1)theywill occur inall or most individuals (2)asa personages,thesechangeswill becomemoreprominent (3) the alterations will lead to cellular or organ malfunction, resulting in organ or systemfailure. The following arethemost widelyaccepted reasonsfor theaging process.
Free Radicals.
Freeradicals arehighly reactivechemical particles that contain an unpaired electron. Aerobicmetabolism, as well asradiationand other environmental factors,createthem.Their consequencesarefar-reaching.
They change or degrade the structure of many other molecules in the cell, impairing their activities. Proteins having enzymatic, structural, and regulatory roles react with free radicals. They create breaks in deoxyribonucleicacid (DNA),altering theinformationrequired for proteinsynthesis.
Theyinducelipidstoclump together,causing cell membranestodegrade.Their effectson carbshavereceived littleattention. Freeradicals aremost prevalent in mitochondria, which arecellular organelles whereoxidative processesoccur.
Mitochondrial damage, particularly mitochondrial DNA damage, has been hypothesized as a role in the aging process. Certain enzymes (superoxide dismutase and catalase) that disrupt the cycle of processes that generate free radical damage reduce their effects. Vitamins C and E, for example, defend against free radical damagebyquenching thereactions.
Crosslinkingof Proteins
Proteins can be transformed by the spontaneous and uncontrolled combining of protein molecules by glucose, in addition to the impacts of free radicals. The result of all of this glycosylation is that the proteins cling together.
The fibrous extracellular protein collagen, present in connective tissue, for example, stiffens as a result of this process,contributing toskinwrinkling and joint mobilityloss.
Events that have an impact on genetic material. Mutations, or alterations in DNA, are widespread and can causechangesinproteinstructureand function.
There are a variety of processes that can repair these mutations, but their efficiency may reduce with age sincetheyarecarried out byenzymeproteins,whicharedegraded bytheaging process.Another theoryisthat certaingenesareresponsiblefor thedemiseof individual cells.
It is also known that cells in tissue culture will only divide a fixed amount of times. This limit is roughly fifty cell divisionsinhumancells.
The increasing shortening of the telomere, the portion of each DNA molecule essential for starting DNA replication, has been proposed as a preliminary explanation for the so-called Hayflick limit (named for the scientist whooriginallydescribed it).
Asthetelomereshortens,anincreasing number of errorsdevelop intheduplicated DNA.
HormonalEffects
Normally, these chemical messengers have well-controlled effects on physiological tissues. Abnormally high levels of some hormones might alter tissue sensitivity to the hormones and promote the release of other hormones, the uncontrolled consequences of which could be harmful. Candidates for this process include insulin,growthhormone,glucocorticoid hormones,and reproductivehormones.
Immune SystemAlterations
This body's principal defensive system may undergo two types of changes, either of which may contribute to theaging process.
First, the immune system may progressively lose its capacity to differentiate between bodily cells and foreign cells,culminating inanimmunological attack onthebodyitself.
Second,theimmunesystemappearstobelesscapableof responding tomicroorganismsor foreign chemicals,making bodilycellsmorevulnerabletotheimpactsof thesenoxioussubstances.
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