Why do we age?

From the moment man realized his days on Earth were numbered, he has sought to prolong his life span in anyway possible. There is the legend of the philosopher’s stone, an elusive substance which, among other things, could be prepared as an elixir to prolong life indefinitely. Today, we have creams to rub out the lines in your face, Botox treatments, and plastic surgery to deflect the cosmetic effects of aging. We hook our loved ones up to machines that monitor their most basic vital signs and shoot them full of drugs to maintain the internal biological balances and processes that machines cannot monitor. At the end of our lives, in most cases our faces are lined, liver spots pepper our skin, the skin beneath the throat has collapsed into a fleshy pile, we are weak of hearing and sight, and we are victims of chronic diseases in every part of the body: heart disease, Alzheimer’s, osteoporosis, etc. We are no longer our once abundant, prolific, youthful selves. We have aged.

So what is aging? To paraphrase João Pedro de Magalhães, aging is a gradual decrease in physiological function that really begins after the peak of sexual fitness, which is around the age of 19 (1). Based on previous observations, the root cause of this deterioration seems to lie at the cellular level where, as we age, the mechanisms for the repair and maintenance functions of cells become damaged and cease to function as well as they once did. Scientists are split into two camps as to what actually causes this damage, or senescence: those who believe that in theories where mutations within the cell lead to the damage of biological mechanisms, or damage-based theories; and those who believe that environmental and evolutionary conditions led to the selection of certain genes within organisms that contribute to senescence, also known as programmed theories.

There are many different kinds of damage-based theories. The first we will examine has been formulated by a scientist named L. E. Orgel, who hypothesized that transcription errors within DNA could lead to damaged cells and, eventually, cells that would no longer function. To understand this, one must look at the cell cycle. The purpose of the cell cycle is to generate new cells through division of an old cell, creating two cells which are copies of the original cell. During the division, a cell transcribes information from its nucleus where the DNA (which contains the genetic blueprints for amino acids and therefore future blocks of DNA) is stored. The cell then copies this information into RNA, which creates the amino acids for a new DNA sequence which will be placed in the nuclei of the new cells. If in the transcription process an error is made, it is present in the new nuclei and will be present in all future divisions of that cell. If errors keep on being made, at some point at least “one of the processes necessary for the existence of [a] viable cell…[will become] critically inefficient” (2).

Another scientist, Dr. Denham Harmon, developed a second damage-based theory known as the Free Radical Theory of Aging. At the atomic level, circling the nucleus of all atoms is the electron cloud, and within the electron cloud electrons are grouped in pairs. When an atom loses an electron, the atom becomes a “free radical” (3). Free radicals will attack other stable, nearby atoms (those with an even number of electrons) and try to “grab” their electrons in order to achieve stability (3). When this happens, the once stable atoms become free radicals themselves and steal other electrons from other stable atoms, thus forming a continuous chain reaction that will eventually disrupt the processes of the living cell (3). These disruptions cause damage to the living tissue and the processes inside the cells, which is visible to us as age; in addition, the cells no longer work as correctly or as efficiently as they did before free radical damage. This damage can result not only death, but also in chronic diseases such as cancer and heart disease.

The second camp of theories, programmed theories, state that aging is built into the genes; that is, our genes are programmed to allow our cells to die, a concept also known as apoptosis (5). One programmed theory states that apoptosis is an evolutionary device to weed out the old; older people do not reproduce as much as others, cannot gather as much as others, and become feeble as time goes on. Therefore it is not a desirable characteristic or conducive to survival. Unfortunately, this theory is most likely incorrect because mortality among animals in the wild is so high from other factors that it is hard to find an animal that has reached a stage of senescence (6).

However, there is plenty of evidence that our genes play a role in how we age. For example, a study performed on mice in 2003 showed that the manipulation of a certain gene, p66shc, allowed the mice to live longer than their wild counterparts (5). Also important is that the cells of the mice in culture were “resistant to DNA damage-induced apoptosis” (5). The p66shc gene and other similar genes are involved in the body’s repair and maintenance processes (DNA transcription and replication, for example) within cells. Theoretically, instead of evolving to die past age 30, our bodies could have evolved repair and maintenance mechanisms designed only to work as well up until the expected date of mortality (6). However, in today’s contemporary, modern world where we have eliminated most natural predators and most diseases, our bodies are able to live much longer and way past the development of cellular senescence of our metabolic mechanisms. To conclude, in programming based theories, cellular senescence is not so much a result of programming as it is from a lack of programming.

All of these theories spell exciting news for man as he desperately attempts to prolong his life. For example, if the Free Radical Theory of Aging is correct, all we need to do to counteract cellular senescence is consume mass amounts of fruit and vegetables. The reason behind this is that fruits and vegetables contain vitamins such as C and E, also known as antioxidants. Antioxidants have stable atoms no matter if the number of the electrons is even or odd; therefore, they are free to donate electrons to free radicals without becoming free radicals themselves and continuing the damaging chain reaction (3). And if the programmed theories are correct, all we need to do is breed humans for optimal genes in the same way that Gregor Mendel once bred his peas for height and other inherited characteristics. Before long we will have a generation of super humans with better developed cells and superior genetic programming. Or, conversely, one could breed humans with stronger cells able to resist free radical damage more efficiently. In this way, chronic diseases could be cured. However, I think it highly unlikely that humanity will ever be able to shield itself completely from the detrimental effects of living out one’s life. Unfortunately, there will always be sunlight scorching our skin, or perhaps there will be water that is a little too hard for our stomach, or we will eat something spoiled at Burger King and give ourselves E. Coli, all of which contributes to the damage of tissue or the development of free radicals. There are unfortunately limits to our science, and there are certainly no limits to human error.

References

1) De Magalhães, João Pedro. "Why Do We Age? A Review of Theories of Aging."

senescence.info. 30 Sept. 2007 <http://senescence.info/>.

2) Orgel, L. E. "The Maintenance of the Accuracy of Protein Synthesis and Its

Relevance to Ageing."1963. 517-521. Rpt. in Proceedings of

the National Academy of Sciences of the United States of A. JSTOR. 30 Sept.

2007 <http://www.jstor.org/view/00278424/ap000575/00a00190/

0?frame=noframe&userID=a56af1cd@brynmawr.edu/01c054500e005019287&dpi=3&config=jst

or>.

3) “Understanding Free Radicals and Antioxidants." HealthCheck Systems. 30 Sept.

2007 <http://www.healthchecksystems.com/antioxid.htm>.

4) Loren, Karl. "The Ultimate Primer On Free Radicals -- Basic Cause Of Heart

Disease, Cancer and other Degenerative Ills." Oral Chelation – Vibrant Life

Home Page. 30 Sept. 2007 <http://www.chelationtherapyonline.com/

technical/p5.htm>.

5) Koubova, Jana, and Leonard Guarente. "Links Between CR, Aging, and Apoptosis."

Innovita Research. 30 Sept. 2007 <http://www.innovitaresearch.org/

news/03052001.html>.

6) Kirkwood, Tom, Professor. "Programmed for Survival: Why and How Do We Age?"

The Wellcome Trust. 30 Sept. 2007 <http://www.wellcome.ac.uk/>.