Why Do We Age?

Kyle asks: Why do we get old?

agingGray hair, memory loss, wrinkles and brittle bones, sooner or later, each of us gets old (if we’re lucky). Yet scientists tell us that there is no evolutionary reason for us to age. So, why do we?

The Aging Process

Researchers do not agree as to the causes of aging. Some claim our genes are programmed to deteriorate, wither and die, while others believe accumulated damage is the root of our senescence. Muddying the waters further, many believe that a combination of several factors contributes to aging.

Cell Damage

Around since 1882 when biologist August Weismann first introduced it, at its fundamental level, the cell damage theory holds that the body succumbs to “wear and tear“: “Like components of an aging car, parts of the body eventually wear out from repeated use, killing them and then the body.”

Building on this fundamental idea, a number of researchers today are exploring particular physiological aspects to reveal where and how this “wear and tear” occurs.

Somatic DNA Damage

Focusing on the deterioration of DNA over a lifetime, according to this theory:

DNA damages occur continuously in cells . . . . While most of these damages are repaired, some accumulate . . . . [and] genetic mutations occur and accumulate with increasing age, causing cells to deteriorate and malfunction. In particular, damage to mitochondrial DNA might lead to . . . dysfunction. . . [where] aging results from damage to the genetic integrity of the body’s cells.

Mitochondrial DNA (mtDNA) mutate faster than DNA in a cell nucleus, so mtDNA create more damaging “free radicals” that are believed to induce aging. Given that mitochondria (the power plants of cells) work harder the more fuel (a.k.a. “food”) is available, the less an organism eats, the fewer free radicals are produced. As a result, some scientists have opined that calorie restriction (CR) can act as a fountain of youth: “A diet severely restricted in calories (about 30 percent below normal, but above starvation levels) can increase lifespan, lower rates of cancer, and slow declines in memory and movement.”

Others are more cautious when it comes to recommending a CR diet: “Restricted-diet animals grow more slowly, reproduce less, and have dampened immune systems . . . [because the] dietary restriction seems to switch the body into a survival mode in which growth and energy consumption are suppressed.”

In addition, detractors note that just because: “Lifespan extensions [were] seen in mice [this] may not be observed in large mammals like humans . . . [because unlike small animals] large mammals can migrate in times of famine . . . .”

Nonetheless, at least one study has shown that people on a CR diet will “lower blood cholesterol and insulin and . . . reduce[ the] risk of atherosclerosis,” all conditions that contribute to aging and mortality. 


Another branch of the cell damage theory focuses on “cross-linking,” a process whereby damaged and obsolete proteins, which would otherwise be broken down by enzymes (proteases), are protected from that action by making inappropriate attachments, allowing them to “stick around and . . . cause problems.” Over time: “An accumulation of cross-linked proteins damages cells and tissues, slowing down bodily processes . . . .”

This phenomenon has been identified in at least one sign of aging, and implicated in another:

Cross-linking of the skin protein collagen, for example, has proven at least partly responsible for wrinkling and other age-related dermal changes [and] . . . in the lens of the eye is also believed to play a role in age-related cataract formation. Researchers speculate that cross-linking of proteins in the walls of arteries or the filter systems of the kidney account for at least some of . . . atherosclerosis . . . .

Genetic Coding

Looking at the blueprints that drive organisms, each of these theories explores the idea that, at the cellular level, we are “programmed” for obsolescence.

Programmed Longevity

Many researchers believe that: “Aging is the result of a sequential switching on and off of certain genes, with senescence [old age] being defined as the time when age-associated deficits are manifested . . . .”

To support this theory, scientists have studied aging with the help of Caenorhabditis elegans: “The classic laboratory nematode . . . [which are] tiny, transparent worms . . . [that are] easy to manipulate genetically, and with a life span of just two weeks . . . provide a quick time-lapse view of the aging process . . . .”

In 1993, one group of researchers discovered that: “C. elegans with a specific single-gene mutation lived twice as long as members of the species that lacked [it. This] . . . led to a shift in thinking . . . that [as opposed to many genes] a single gene could dramatically regulate how long an organism lived . . . .”

This gene, daf-2, is a protein remarkably similar to our receptor protein insulin, and, at least in C. elegans, was shown in later research to be a very bossy gene: “Daf-2 normally controls many other genes . . . . For example, in their studies of C. Elegans, researchers have found a large set of genes that are either “turned on” or “turned off” in worms that carry two copies of the daf-2 mutation . . . .”

The types of genes that are regulated by daf-2 include stress resistance, development and metabolism. This is significant because these: “Various genes encode for proteins that extend life by acting as antioxidants, regulating metabolism and exerting an antibacterial effect . . . .”

Endocrine Theory

Other researchers ascribe to the theory that age-regulating genes carry: “Biological clocks [that] act through hormones to control the pace of aging [through] . . . the evolutionarily conserved insulin/IGF-1 signaling (IIS) pathway . . . .”

This signaling pathway is significant: “The IIS system is an ancient system that is highly conserved and coordinates growth, differentiation and metabolism in response to changing environmental conditions and nutrient availability . . .”

Thus, under this theory, individuals adapt at a cellular level, in response to environmental conditions, to foster the best outcome for continuation of the species: “In response to harsh environmental conditions . . . [cells adapt to produce] enhancement of cellular stress resistance and protection, suppression of low-grade inflammation and enhanced mitochondrial biogenesis [increased energy in the cell].”

Thus, in tough times the organism’s life is extended, at least long enough for it to fulfill its biological imperative to breed.

Immunological Theory

The third gene-coding proposal to explain aging provides that: “The immune system is programmed to decline over time, which leads to an increased vulnerability to infectious disease and thus aging and death.”

Proponents of this theory note that: “As one grows older, antibodies lose their effectiveness, and fewer new diseases can be combated effectively by the body, which causes cellular stress and eventual death.”

This last argument has been called into question by recent research that studied mortality and fertility across 46 different species (including humans), which produced remarkable results: “Although . . . most of the 46 species can be roughly classified along a continuum of senescence . . . [displaying] strong deterioration with age [other species demonstrated] negative deterioration, to negative senescence and improvement with age.”

This means that unlike people, some species: “Are the opposite of humans, becoming more likely to reproduce and less likely to die with each passing year.

In fact, there is so much diversity of aging across species that, even among those that age like us, there are some, such as the alpine swift, that become more fertile (likely to reproduce) as they approach their demise.

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  • No, no and no. All wrong. We age because God hates us.

    Well, He hates you. Me he’s just indifferent toward.

  • well actually, we age because of the way DNA replicates. Think if it this way- when you are born, you have a fresh code of DNA, and because it hasn’t replicated a lot yet, it is very “long.” Everytime DNA replicates, it gets smaller. Somatic and other cells will keep dividing until DNA is too short to divide correctly without problems. That point is ageing. Although we have enzymes that extend our DNA, such as trees have, this “fake” DNA only extends for replication, it is not viable coding for anything.

    • so if you can sequence a person’s DNA at a certain age, you can generate new stem cells with young DNA and prevent aging.

    • This is correct, I think that’s why this article talks about bad funtion of dna, iven they don’t say nothing about it here, but thats the reason of why in some point of a long life our organs don’t work right.

  • When we are young, we live the moment and we think that moment is our eternity and we will live forever (this helps!); when we get old, we miss those past moments and we think we have no more, we think that the current moment is the last one and that it is too short, and we will die soon.
    We are a machine that reconstructs itself every moment using food energy as the rebuilding blocks. With this hard work everyday, some mechanisms of that machine eventually breaks and becomes unable to reconstruct itself. It ages. If it is an important mechanism in the whole system, a dominoe effect is triggered and the whole body is comprimised. Take the heart, for instance. If it does not feed itself with oxigenated blood in the first place, it degrades quickly and takes the whole body away with it.
    I believe that thinking positively (as the young ones that think they will live forever) is a kind of fuel that helps to regenerate our bodies. Those who think negatively (like some elders) have a broken mechanism already (but they can fix it, if they wish).

    The only way to stop aging is by placing the reconstructing system outside the body. One part of this system is, in some way, outside the body and, currently, it is the only one we have at our disposal to help us to live longer: our mind. Try it.

  • Okay, how aging happens?

    Over the lifespan of an individual, human body cells have the ability to regenerate the tissues. The regenerative power of tissues and organs declines as we age. Adult stem cells are important as it keeps human tissues healthy by replacing old and damaged cells accumulated over time.This is because of the DNA at the end of chromosomes called telomeres that get shorter with each division. When they run out, the cell dies. As you can see, aging is mostly due to the short span of cells regenerative.

    The reasons of aging happens in our body?

    The number of stem cells reduces due to environmental factors, among others, mental depression and malnutrition. Decreasing number of stem cells also results in a number of age-related diseases. With Mesenchymal stem cells therapy, the new and young cells will repair and regenerate your body, thereby creating better health benefits.

    (Side Note: Mesenchymal stem cells (MSCs) are multipotent cells which have the unique ability of self-renewal. MSCs also divide and proliferate throughout the lifetime of an individual.)

    Wharton Jelly of the umbilical cord has been found to be rich in MSCs and it tends to be the most primitive stromal population in the human body. These attributes could potentially be harnessed to increase our body’s defence mechanism. They are also beneficial in terms of enhancement of immune system, prevention of diseases, better organ health and even anti-ageing process.

    These attributes also help divide and differentiate into a variety of mesenchymal tissues. The mesenchymal tissues include adipose tissues, tendons and ligaments, skeletal muscle tissues, bone and cartilage tissues and etc. Current stem cell research is generating strong evidences about how healthy stem cells, when under the right conditions or signals, could give rise to differentiated cells. It helps repair a host of ailments that occur because of tissue damage as people age.

  • Ageing is essential for organisms to continue to evolve over time in response to environmental change. If a species didn’t age then parents would normally out compete with their offspring because they would be better at finding food, shelter and avoiding predation. This would slow the small incremental changes that occur in populations over time due to evolution as a result of mutations. This is less of a disadvantage for populations living in a stable environment but if predators can evolve faster than some of their prey species then those slower evolving species may die out altogether.

    This is in the same way that animals that are large in size that may only have one offspring every one or two years can’t respond as quickly to environmental change as those species that produce larger numbers of offspring and as a result have a greater chance of favourable mutations.

  • We are supposed to live forever but we are dying because of sin. We are spiritual beings and there is a creator. God created everything for his purpose and glory. God created us in his image and likeness. He loves us so much that he does not want us to perish eternally because of sin. For God so loved the world that he gave his one and only son Jesus, for whoever so believes in Him shall not perish but have eternal life. Jesus says .. “I am the way, the truth, and the life. No one comes to the father except thru me”…God loves you and me. If we repent of our sins and accept Jesus as our Lord , we will live forever. Physically we will die because of sin but if we repent and trust in Jesus we will not spend eternity in Hell but in Heaven. There will come a time when we will have new bodies made for eternity. Don’t miss out on this gift that God offers you. Your choice …Heaven or Hell? God loves you and He wants you to be in Heaven , a better place. He does not want you to be in Hell. Don’t miss out on this….repent from your sin and trust and follow Jesus..this is the only answerbto what your searching for. You can explain all life forms or dna but God made all these, so don’t miss out on Jesus…