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An Essay on Aging

Essay By: drStu
Health and fitness



An Essay on Aging explains why we age and explores the influence of diet on longevity


Submitted:Apr 12, 2012    Reads: 1,248    Comments: 0    Likes: 0   


An Essay on Aging

by Dr Stuart Mark Wilson

Copyright 2012 Stuart Wilson

With gratitude to Kenneth Wilson for help with typing and editing

Discover other titles at http://www.drstuartwilson.com

Follow me on twitter @drstuwilson

Foreword

There is no single elixir of life. However scientists have been working hard to understand aging and aging-related diseases. In 2011 there were more than 14,000 scientific studies conducted on aging. In The Handbook of Immortality I describe in everyday language what these scientists have found and how we can use that knowledge today in a practical way to help us all live long and healthy lives. First though, we must understand what aging is. In this Essay on Aging, I describe in simple terms the theories of aging and how what we eat affects aging and health.

CONTENTS

An introduction to aging

Car crashes on the road to immortality

Diet and aging

Science bites

The immortal cells of Henrieta Lacks

Cholesterol, good cop/bad cop

An introduction to aging

The record-breaking Wrinklies

The oldest known living inhabitant of our planet, Methuselah, lives on a wind-swept mountainside in the White Mountains of California. Methuselah is a gnarled Bristlecone pine that tree-ring studies have shown to be nearly 5000 years old. That is an impressive age, even for a tree and it is fifty times longer than many of us could expect to live. In our defence, trees are fairly simple life-forms when compared to the complexity of animals and humans. Trees don't have livers, kidneys, brains or a host of other complex organs that mammalian animals need for life. Methuselah has even lost a few limbs to the ravages of wind and time but I doubt if our planet's oldest inhabitant has even noticed.

Compared to Methuselah, mammals are much more complex and have much more fleeting lives. The oldest recorded mammal is that of a bowhead whale that was caught off the coast of Alaska in 2007. Embedded in the whale's neck was a harpoon tip of the type that had not been used in the region for over 130 years and has, in fact, been traced back to its manufacture in 1880. Scientists now believe that bowhead whales can live to be 200 years old. How does this compare to humans?

The record for the oldest human is Jeanne Calment of France, 1875-1997 at 122 years old. Though impressive, it is interesting to note that this record age is not much older than many of us might expect to live today. In fact, this record age is still only 50 years more than the mean life expectancy in the US and Europe. There is no doubt that we are living longer but this does not appear to be increasing the maximum lifespan that our species can achieve. If the maximum age that we could expect to live was in fact increasing year on year, then the record of Jeanne Calment, which has remained unbroken now for more than 15 years, would surely have already been broken and broken several times over. What explains this absolute age that we cannot live beyond? Why does our maximum lifespan appear to be capped?

We die because our selfish genes don't care.

In life, we may invest time and energy in our careers and hobbies but however fulfilling these are, it is not why we are here. Leaving aside the existence, or not, of a God or Gods or at least a sentient purpose to our existence, we exist in order to propagate. It is where we came from and it is where we are going or for those of us who are older, where we most likely have already been. We age because, in pure evolutionary terms, there has never been any selection pressure for our genes (the genetic information present in every one of our cells that makes us and our bodies who and what we are) to allow us to live beyond our reproductive years and the reproductive years of our children. Once we have fulfilled our roles as parents and grandparents which ensures that our genes have been passed safely on through our children and grandchildren there is no reason for our genes to keep us around. Our bodies slowly degenerate because they are not designed to do otherwise.

So we die through the casual neglect of our own selfish genes. Can anything be done about it? Many scientists now believe that we can tackle the age-related deterioration of our bodies but not by some magical elixir of life but by a basic scientific understanding of what has and what is going wrong and by correcting this with science and technology, some of which is already available to us. So what is going on? What is aging?

What is aging?

In order to be able to tackle aging, we must first know what aging is. As the years pass and we head for that age which most of us would call 'old age' a whole raft of changes occur so that our older bodies are vastly different from our youthful selves. So profound are these changes, that virtually no aspect of our bodies remain unaffected.

As we age, we lose muscle strength, our hair thins (in men and women), our brains shrink, our thyroids shrink, our bodies are less able to repair (cuts take longer to heal) and our body begins to attack itself (arthritis, for example), our skin becomes thinner and, along with our hearts, less elastic, our bones become brittle, we sleep badly, we develop cataracts, high blood pressure and have an increased risk of diseases such as cardiovascular disease, cancer, Alzheimer's Disease, diabetes, pneumonia, tuberculosis etc..

What is the root cause of all these changes? Is there even one single cause of aging? Perhaps not! Scientists have discovered that there may not be just one mechanism of aging and that there may be several problems that build up with time. Below, I discuss the main scientific theories of aging which reflect the fundamental processes of life: body growth, turnover and repair.

Theory of Aging One - the skipping rope effect

The cells which are the building blocks of our bodies and contain our genetic material need to constantly divide and multiply as part of the normal processes in the body but also to replace damaged and worn out tissues. For example, our skin is constantly being shed and renewed and when we cut ourselves the skin cells need to divide to repair the damage.

When we are young and vigorous, so are our youthful cells. The problem occurs as we get older. From the moment that we begin life as a fertilised egg, it appears that our cells are only able to divide a set number of times, a fact discovered by Leonard Hayflick in 1961. The number of times that a cell can divide is called the Hayflick Limit and it is surprisingly low. It appears that our cells can only divide tens of times, not hundreds or thousands as might be expected. Even this low number of divisions is enough to grow us to our youthful adult selves but as we get older, our cells run out of steam and can no longer divide. If our cells are no longer able to divide in order to replace the normal turnover of skin for example, or to repair damage, then our organs can struggle to do their job, our ability to fight off infection can be lessened and our skin can thin.

What causes this limit to the number of times that our cells can divide? Our genetic information or genes are contained in packages called chromosomes. These divide along with our cells to ensure that each new cell has all the information that is needed to do its job. At the ends of these chromosomes are special stretches of information called telomeres that orchestrate the division of our chromosomes. Unfortunately, as they do this important job these telomeres get shorter and shorter after each chromosome and cell division. Eventually, these telomeres, that are so crucial to cell division, are so short that they can no longer do their job and the cell can no longer divide. It is a bit like a long skipping rope that is cut in half again, again and again. Eventually, the rope will become too short to skip with.

Of course, the story is more complicated than this and some types of cells are special because they can restore the length of these crucial telomeres at the end of their chromosomes so that the cell can continue to divide forever and the skipping never stops. For example, in the production of sperm, the sperm cells can divide without limit which is useful if you want to create a new person from that sperm cell. It would be unfortunate if our children were born with our own shortened skipping ropes and with cells that could not divide more than a handful of times. In fact, if the cell of a fertilized egg could not divide more than a handful of times, how could it go on to build a completely new person? Stem cells (cells that are not yet programmed and can form any part of the body) can also maintain the length of their telomeres which is one of the reasons why they have the potential to rebuild damaged organs. So, why don't all of our cells have this special ability and why is it only given to the chosen few? If we think about cancer for a moment. Cancer is caused by cells that divide out of control but not only this, they can divide forever because they too have the special ability to restore the crucial telomere information at the end of their chromosomes. In fact, this is a crucial step in the progress of a normal cell turning into a cancerous cell. Without being able to do this, there would be no cancer. So perhaps the vast majority of our cells cannot divide forever in order to reduce the risk of our cells turning cancerous. Our bodies therefore have an inbuilt mechanism to try to protect us from cancer but in the longer term it leads to cells that can't divide and ultimately leads to old age.

If this theory is correct, what can we do avoid to aging? As I said, some special cells can divide forever because they restore that crucial telomere information at the end of their chromosomes and the skipping rope of life never becomes too short. If we could switch this special ability on in all our cells and restore the length of the telomeres, then all of our cells could carry on dividing and the ability of the body to function would not be impaired with age. Research by scientists has indeed shown that this ability to lengthen the telomeres can be switched on in normal cells and there is a substance available that does just that (see Astragalus at the root of aging). The worry might be though, that if we switch on this ability in normal cells, they might find it easier to become forever dividing cancer cells. However, if the drug only switches this ability for a short time but long enough to restore the telomeres to the length that they were when we were young and if when the drug is stopped, they again begin to shorten, it is possible that the risk of cancer may not have increased at all!

Science Bite. The Immortal Cells of Henrieta Lacks.

Under certain conditions, in some cells, the shortening of telomeres can be prevented. Scientists can actually do this with cells in the test tube. This immortalises the cells so that they can now grow and divide forever. This allows scientists to grow cells in the laboratory and not worry about them running out of steam midway through a vital experiment. The most famous and widely used immortalised cells are called HeLa cells. They were first taken from the cervical cancer of Henrieta Lacks in 1951 and are still happily growing in laboratories today. Most cancers have the ability to prevent the shortening of the telomeres which explains the immortality and the ability to divide forever of cancer cells in the test tube. Tragically Henrietta herself died from her cancer that same year but her descendant cells if all gathered together since that day would be enough for a thousand Henriettas

Theory of Aging Two - dysfunctional furnaces

Our cells need energy in order to do their jobs. For example, muscle cells need energy in order to shorten and contract. But where do our cells get that energy from? The cells get the energy from our food but food needs to be processed in order to release that energy. First the food is broken down into its chemical components, some of which, sugars for example, are used as fuel by the cells. The sugar fuel is taken up by the cells and 'burned' within the cells to release the energy. This burning is performed in special furnaces called mitochondria which can be found within all of our cells. In fact, each cell can have tens of mitochondria, lots of mini-furnaces to keep the cell supplied with energy.

How may our mitochondria be related to aging? When we are young and our mitochondria are young they are very efficient at releasing energy from sugars and making this available to the cell. The burning process, though, can damage the mitochondria and also the cell by oxidation through the production of toxic reactive oxygen species, (see the section below: Theory of Aging Three) and with time, this damage can build up. So in older bodies and in older cells, the mitochondria are damaged and are less efficient in burning sugars to release energy. It gets even worse than this, because this inefficient burning process itself can even damage the mitochondria further and harm the cell more. All of this means that our cells, tissues and organs can become progressively less efficient at using fuel and producing energy as we age. Luckily for our cells and our mitochondria mini-furnaces, there are substances that we can take that can keep our mitochondria in tip-top condition, minimise the production of toxic reactive oxygen and soak up any toxic reactive oxygen that might be produced.

Theory of Aging Three - we gunk up

Apart from the reduced ability of our cells to repair and replace damaged tissue and the malfunctioning of our mitochondria furnaces, as we age there is an accumulation of damage to the structure of our bodies. Oxygen, though essential to most forms of life on our planet, is actually very reactive and quite toxic. It is no coincidence that life on our planet started without it and much of the oxygen that we now breathe is produced as a waste product of photosynthesis by plants. This toxic oxygen and its more reactive forms, which, as we have seen, can be produced by defective mitochondria, can damage the building blocks of our cells and tissues by reacting with our genetic material and proteins and fats (lipids) that make up our cells. Normally, our bodies do have mechanisms to undo this damage but as we age the amount of damage can be so extensive that it becomes impossible to repair. To make it even worse, the damaged components of our bodies such as proteins can even cross-link together to form a structures that are very difficult to repair indeed. It is a bit like over-poaching an egg; in the hot water the egg stays nice and runny for a while but once it heats up and goes hard there is no going back. This cross-linking can be most apparent in the lack of elasticity of older skin. Use as much cream as you like, but eventually we all wrinkle up. Quite appropriately, these modified proteins are termed AGEs (advanced glycosylation end-products) and they are a measure of the amount of oxidative damage and aging that has occurred in our bodies. To make matters worse, these AGEs can also cause inflammation which can cause more damage and, with time, more AGEs. In this way there can be a vicious cycle of aging.

To address this type of age-related damage there are substances that we can take that act as antioxidants to mop up the toxic reactive oxygen and other substances that cause the AGEs and cross-linking. These substances can stop the cross-linking of our damaged proteins or even undo the cross-linking itself. Perhaps that over poached egg can be rescued after all!

Aging - the bottom line

In summary, it all sounds a heck of a mess but that is aging for you. Luckily, it is a mess that scientists are dissecting and analysing piece by piece. What is clear is that in order to increase longevity to a meaningful extent all of these problems of aging will have to be addressed. This leads us to suppose that there may not be a single cure-all to aging but there may have to be multiple therapies and substances that address every single one of the causes of the aging process.

Car crashes on the road to immortality

If we are all going to live forever, it is not only about tackling the aging processes of our bodies; we must also avoid our biggest killers. In Europe and North America, car accidents, cancer and heart disease are the biggest killers on the road to immortality. Each year cancer is responsible for half of our deaths, and heart disease for one quarter of all our deaths (The Office of National Statistics, 2010, www.ons.gov.uk). If we wish to achieve immortality, we must tackle both aging and the age-related diseases. In the Handbook of Immortality, some of the substances that I describe have been shown to have an effect on these age-related diseases; on cancer or Alzheimer's Disease, for example and give us a greater chance of remaining on the road to our immortality. As for car accidents, all that we can do is to ensure we drive safely.

Diet and aging

Science Bite. Cholesterol, good cop/bad cop

Cholesterol receives a bad press but not everyone realises that cholesterol is vital for the structure of our cells and we could not live without it. In fact, our bodies make a large amount of cholesterol each day with more coming from food, particularly from fats. Cholesterol is barely soluble in water and is transported in our blood in tiny fat droplets called low density lipoproteins. The problem is not with cholesterol as a whole but the amount of low density lipoproteins in the blood; often called 'bad cholesterol'. The more low density lipoproteins in the blood, the greater the chances of blood vessel blockage and heart problems especially if this low density lipoprotein has also been damaged by toxic reactive oxygen. So-called high density lipoproteins also carry cholesterol in the blood but this form of cholesterol is actually good for us and can help to repair damage to the blood vessel walls that has been caused by low density cholesterol; for this reason this is often called 'good cholesterol'. So, it is not the total amount of cholesterol in our blood which is an important indicator of the risk of heart problems but the amount of this cholesterol that is present in the bad low density lipoproteins compared to the good high density lipoproteins. Try discussing this with your medical practitioner!

You are what you eat - unfortunately. Before running out to buy vitamins or dietary supplements to improve our health, it is important to consider the role of diet in disease and aging.

It is clear from scientific studies that diet can have an influence on some of the diseases that might derail our ambitions for immortality. For example, it is often said that any man who lives long enough will eventually get prostate cancer and there seems to be some truth in this. When older men who had died of other causes were investigated for prostate cancer, the disease was found in eight out of ten of them (Haas et al 2009 The Worldwide epidemiology of prostate cancer: perspectives from autopsy studies. Con J Urol 15(1) 3866-3871). In the vast majority of cases these men would not have known that they were incubating the cancer. However, the incidence of prostate cancer is not spread equally around the globe. The highest levels are associated with a Western style diet and the lowest incidence is associated with a Japanese and Asian diet (Van Poppel et al 2011 Chemoprevention of prostate cancer with nutrients and supplements. Cancer management and research 3 91-100). In fact, the incidence of prostate cancer is now increasing in Japan as they adopt some aspects of the Western diet. It is bad news for those Japanese migrating to Western cultures and adopting Western diets as the incidence of prostate cancer in these men increases to a similar level of the indigenous population. The exact dietary causes of this difference in prostate cancer are unknown but the Western diet includes fried, high-fat, high-protein and low fibre diets whereas Japanese diets typically include steamed food with plenty of fish and vegetables. This difference in diet may also explain why a small island off the coast of Japan, Okinawa, has the greatest proportion of centenarians in the world.

Diet or at least food quantity can have a direct influence on lifespan. It is well known that animals on starvation rations have an increased lifespan. For example, rats on so-called calorie restricted diets lived longer than their fatty peers. A similar thing has been observed in a range of species and an on-going study on monkeys seems to confirm that calorie restriction can improve health and increase lifespan (Kemnitz 2011 Calorie restriction and ageing in non human primates ILARJ 52(1) 66-77). The reason for this is not completely understood but it is hypothesised (as scientists say) that a restricted diet reduces the 'burning' of food sugars in the mitochondria mini-furnaces which in turn reduces the amount of toxic reactive oxygen produced which reduces cross-linking of proteins and production of AGEs which also reduces inflammation.

Whatever the mechanism, some people have adopted this calorie restricted lifestyle but an effect on human lifespan has yet to be demonstrated.

If we do not want to spend a lifetime in starvation what else can we do, here and now, to ensure that we live a healthy long life? The Handbook of Immortality looks at the scientific evidence behind the most promising substances that are available for us to take and that may help us to achieve longevity.

First though, there is something that we should all do to improve quality of life. We all know that diet, and physical and mental exercise are important in healthy aging and this is backed up by numerous scientific studies. These studies have shown that exercising the brain and body slows mental decline in older years. So, get out there and do it!

Follow me on twitter @drstuwilson

Gat The Handbook of Immortality at http://www.drstuartwilson.com

The Handbook of Immortality is a practical guide to successful aging. In the handbook, the different theories of what causes aging and aging-related diseases such as Alzheimer's Disease, cancer, cardiovascular disease (heart attack), stroke and diabetes are explained. Scientists have been working hard to understand how the effects of aging and the risks of developing these aging-related diseases can be reduced. In 2011 there were more than 14,000 scientific studies on aging and related diseases which included the effects of carnosine, green tea, aspirin, melatonin, resveratrol, garlic and many more vitamins and substances. In the handbook, the scientific evidence of the possible benefits (or not) of these substances are explained in easy to digest, everyday language with a dash of humour.





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