How and Why We Age

How our health deteriorates as we age is well known … but scientists are only beginning to unravel the reasons why we age and what we may or may not be able to do to slow down the onset of feeble old age. Here’s the state of play.

Aging and growing older are not the same thing.

Growing older refers to the onward march of time, the number of years we are clocking up. Aging is different.

Aging is the process by which we gradually weaken and lose function as we grow older; losing the energy, strength and resistance to disease we had when we were young.

As we age, the probability that we will develop heart disease, diabetes, deafness, blindness, incontinence, osteoporosis, arthritis, impotence, cancers, various forms of dementia and a host of other dreadful diseases of old age increases several fold.

All this is despite the fact that, throughout our lives, our bodies are constantly rebuilding and repairing themselves.

Chromosomes and cell division

Cells are the basic building blocks of our bodies.

Look at yourself in a mirror … what you see is about 10 trillion cells made up of about 200 differen­t types. Our muscles are made of muscle cells and our livers of liver cells. There are specialized types of cells that make the enamel for our teeth and the lenses in our eyes.

New cells are born every day while old cells die; ie, our bodies are constantly renewing themselves.

A chromosome is a tiny body contained within the nucleus of a cell. It consists of a threadlike structure made up of proteins and nucleic acids (mostly DNA).

Each chromosome has subunits called genes. Genes determine inherited traits. They are arranged in a line along the length of the chromosome. There can be thousands of genes on a single chromosome.

Chromosomes occur in pairs. The number of chromosomes in a cell varies between species. A body cell of a human being contains 46 chromosomes, or 23 pairs; that of a horse, 30 pairs.

Our bodies (like those of all other species) grow, develop and reproduce through cell division. Cell division is the process by which a parent cell divides into two or more daughter cells.

Here’s how this works.

First, the chromosomes in a cell duplicate themselves. Then, each set of chromosomes moves to opposite sides of the cell and the cell divides. Each new cell has a complete set of chromosomes which is identical to what was in the original cell.

In this way, our bodies are constantly renewing themselves.

Theoretically, as the old and new cells are identical, we should be immortal.

But we are not immortal. So, what kills us off?

The Hayflick Limit

In 1965, Dr Leonard Hayflick discovered that cells divide about 52 times on average, after which they stop producing daughter cells and die, ie their lives are finite.

Hayflick found that cells go through three phases. In the first, there is a rapid healthy division of cells. In the second phase cell division slows. In the third phase, cells undergo programmed cell death.

When a new cell is born from an older one through cell division, it begins its own lifespan.

Newly-made cells from an old person are readily recognisable as cells from an aging body. But when the nucleus of an old cell is removed and replaced with the nucleus of a young cell, the old cell takes on a new life.

The old cell’s life span is like that of a young cell … it divides most rapidly early on; then cell division slows as it ages, before it stops completely and dies.

This means that the key to the Hayflick limit is in the cell’s nucleus and that we are all basically programmed to die.

But how does this programming work?


This question was answered in 1978 when telomeres were discovered.

Telomeres are repetitive strings of DNA found at the ends of chromosome pairs within cells. Their purpose is to protect the chromosomes, similar to the way that the plastic ends of shoelaces keep the laces from fraying.

The problem is that each time a cell divides a portion of the telomere at the end of the chromosome is lost. Each new generation of cells has slightly shorter telomeres than its parents.

In fact, you can judge the age of a cell by measuring the length of its telomeres. When the telomere gets sufficiently short, the cell enters programmed cell death.

So a telomere serves as a count-down clock for a cell.

In addition, as the telomere shortens, the behaviour of the cell changes. Cells with shorter telomeres begin to slow down. The signals that control the output of hormones and the immune function become weaker. The cells start to act old.

As more and more cells start acting old, the body deteriorates. Eventually it can defend itself no longer and succumbs to disease.

In sum, your cells are dividing, your telomeres are shortening, and, as a result, you are aging. Your mortality seems to be assured.

Or is it?


In the mid-1980s telomerase was discovered. Telomerase is a protein that is capable of producing new telomeres on the ends of chromosomes in aging cells, ie it can prolong the lives of cells.

Telomerase is found in all cells. However in normal cells it is turned off, ie it does nothing.

But in abnormal cells, such as tumours, telomerase is active; busy increasing the length of telomeres at the ends of chromosomes and thus helping aging cancerous cells to continue growing and developing.

It would seem that should active telomerase be added to normal cells, these cells should continue to replicate beyond their Hayflick limit.

Indeed, researchers have reported that, in one study, cells to which they had introduced telomerase had replicated at least 20 more times than they normally would.

In another study, a group of men between the ages of 60 and 85 were given concentrated extracts of telomerase.

After six months the men showed remarkable changes with improved immune strength, significantly improved eyesight, better sex lives, and more youthful and radiant skin.

Of course, this is not to say that introducing telomerase can make cells immortal. Besides the shortening of telomeres, many more factors seem to be involved in programmed cell death.

However telomerase and the developing technologies needed to support its use do hold out the possibility that all the bad things we associate with aging … heart disease, arthritis, hearing loss, failing eyesight, dementia and so on … could become as rare in 70-year-olds as they are now in 35-year-olds.

People may not live longer but they should enjoy a healthier old age.

Author: Paul Kennedy

Paul D Kennedy is a qualified accountant and an international business consultant who used his skills as a researcher to uncover the mysteries of type 2 diabetes and gain control over his health and wellbeing.

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