Aging is inevitable – unless you are Jennifer Aniston or Captain America. The hallmarks of aging, such as grey hair, weak knees and the inability to keep up with the latest social norms are conventionally associated with biology. Which is justified, as these macroscopic symptoms seem to be fruits of a myriad of biological processes associated with the most widely accepted cause of aging — cell death.
Sir Peter Medawar, in his groundbreaking book An Unsolved Problem of Biology, provides two explanations for aging. Medawar’s book, one of the most important texts on the modern study of aging, claims that aging is a result of either:
- Innate Senescence – a biological process or a necessity, to ensure death in order to make space for the young. It seems that evolution winds in us a master clock which comes with a number of calculated ticks that dictate aging and death.
- Wearing Out – where the physics of entropy determine the breakdown of cellular processes in a cell brought about by the accumulated effects of recurrent stress.
New research suggests that the latter is more convincing and is the underlying cause of cell death and, consequently, aging. Most importantly, it answers why our aging process might be inevitable, unlike the Cap.
Aging in the context of biology: Telomere Shortening
Digging deeper, biologists found that a cell is similar to a factory. The factory has a multitude of machines that metabolize food, repair DNA and dispose of garbage. The operators of these machines are the factory’s workers — proteins. The industry is powered by chemical energy, which is provided by the mitochondria. However, like any chemical power source, it leaves behind unwanted waste, and when that is not disposed of properly, it will accumulate and damage the industry’s functioning.
Fortunately, the industry comes with an efficient repair system that automatically repairs any faulty parts. Unfortunately, that repair is achieved by demolishing itself and then replicating or creating an exact copy to replace it from the body’s stem cell population. Replication occurs each time a cell appears to be damaged, but it is mandatory to possess a blueprint of the industry that is stored in the head office.
The blueprint is located in every cell nucleus on twisted, double-stranded molecules of DNA called chromosomes. On the end of chromosomes are stretches of DNA called telomeres. Just like the plastic ends on a shoelace, these telomeres prevent the ends from sticking together and scrambling genetic data.
The repair systems allow us to live longer than any mammal of comparable size and heart rate. However, each time cells divide and replicate, telomeres get clipped and are observed to become shorter. These telomeres are the embodiment of our “master” clock. As telomeres get even shorter, cells lose their ability to divide or replicate due to a disrupted blueprint, causing damaged or dead cells to accumulate in our body.
Telomere shortening and the consequent cell death can be increased by external causes, such as smoking or an unhealthy diet. That being said, critics argue that telomere shortening is a symptom, but not a direct cause of aging.
Aging in the context of physics: Free Radical Theory
In physicist Peter Hoffman’s bestseller Life’s Ratchet, he “was focused on how life can create and sustain highly ordered systems in the presence of the surrounding molecular chaos.” He also explains that molecular “ratchets” extract order from chaos to do this.
According to Hoffman, complex organisms harvest complex chemical energy to divide up and create order, while releasing heat in the process. The random bombardment of water molecules on proteins could be the source of thermal energy that they absorb to sustain their structure.
The Second Law of Thermodynamics directs the creation of an organism, representing a huge increase in local order and organization, which converts low-entropy concentrated chemical energy for its biological functioning into high-entropy heat. The most successful organisms are then those that use energy effectively and dissipate it quickly.
However, thermal motion also randomly breaks protein bonds, which leaves them open to being oxidized. Researchers have found that even a single event of oxidation within these proteins is sufficient to unfold its normally curled up structure. This is also called the free radical theory, as atoms with unpaired electrons are called free radicals.
These atoms are very reactive and produce a domino effect, promulgating the production of more free radicals and damaging more cells following every reaction. As more and more waste is accumulated, a cell’s key systems become damaged. This includes mitochondrial damage, which marks the failure of energy sources for the machines and their corresponding processes.
Additional losses due to interdependence lead to a cascade of failure. The scenario enacts a positive feedback loop, as the damaged functionality of machines prevents replication, so a cell dies without being replaced by a new one.
This coupled chemical and thermal degradation is popularly called inflammation and its apparent underlying cause – bond breaking – is linked to aging. Again, degradation can be further worsened by external causes, such as smoking or an unhealthy lifestyle.
Why the wearing out theory makes more sense?
The answer to why we age makes more sense in the context of physics, as it directly draws us a possible cause, rather than a correlation. Clipped telomeres are linked with cell death, but small-scale physics, which governs the formation of bonds, provides us with a sharp microscope and a scalpel that can pierce through the layers of the cell and shed light on its various internal wounds.
The link between thermal motion and aging becomes even more convincing when we consider an experiment on roundworms subjected to various internal temperatures.
The results showed an increased life span of worms subjected to lower temperatures than the lifespan of worms subjected to higher ones. Moreover, the exponential curve representing the relationship between bond breaking and increasing force scarcely resembles the “life” curve.
According to Leonard Hayflick, the original discoverer of cellular aging, “the common denominator that underlies all modern theories of aging is change in molecular structure and hence functioning.” He believes that the ultimate cause is “the increasing loss of molecular fidelity or increasing molecular disorder.”
So Why is it Inevitable?
We are bound to lose, because the game is played out under the rules of probability. It is erratically random and the collapse of bonds occurs at different times for different people. In other words, even if the technology catches up and immortality seems to be mouthwateringly close with the help of gene editing, nanotechnology or stem cell research, we still might fail miserably.
First, because it is an overwhelmingly complex prospect, and secondly, due to the probabilistic nature of molecular breakdown. The prevention of a particular molecular structure’s breakdown doesn’t necessarily prevent aging, as there are other structures that might fail instead.
The human lifespan has increased monumentally since the early 15th century, when the average person lived no more than 30 years. Today, our life span is almost 71 years. The major reason is our collective realization of polluted environments and the eradication of deadly diseases that they propagated. We improved sewer facilities, generated clean water, provided excellent medical facilities, designed great diets and optimized health care.
Even so, all these efforts might be in vain. Although life spans can be increased, death still seems inevitable. As Peter Hoffman says, “we will never defeat the laws of nature.”
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