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By Avi Roy, University of Buckingham and Anders Sandberg, University of Oxford

Men who are unemployed for more than two years show signs of faster ageing in their DNA, according to a study published today in the journal PLOS ONE.

Researchers at the University of Oulu, Finland and Imperial College, London arrived at this conclusion by studying blood samples collected from 5,620 men and women born in Northern Finland in 1966. The researchers measured the lengths of telomeres in their white blood cells, and compared them with the participants’ employment history for the prior three years, and found that extended unemployment (more than 500 days in three years) was associated with shorter telomere length.

Telomeres are repetitive DNA sequences at the ends of chromosomes, which protect the chromosomes from degrading. With every cell division, it appears that these telomeres get shorter. And the result of each shortening is that these cells degrade and age.

When cells are grown in a lab, their telomeres do indeed shorten each time the cells divide. This process can be used to find a cell’s “expiry date”, a prediction of when that cell will run out of telomeres and stop dividing. However, this does not seem to relate to the actual health of the cells.

In the new study, the researchers found that that on average, men who had been unemployed for more than two of the preceding three years were more than twice as likely to have short telomeres compared to men who were continuously employed. In women, there was no association between unemployment status and telomere length.

The researchers accounted for telomere length differences resulting from medical conditions, obesity, socio-economic status and early childhood environment.

Previous studies, noted by the study authors, have found a correlation between shorter telomeres and higher rates of age-related diseases like Type 2 diabetes and heart disease. The authors conclude that the reduction in these men’s telomeres may have been the result from the stress of long-term unemployment, adding to evidence of a direct connection between prolonged unemployment and poor health.

An abstract concept

Employment is something very abstract; an employed and unemployed body are apparently more or less the same. So it might seem surprising that such an abstract thing as employment can affect a body on the cellular level. But the same is true for how stimuli affect our brains: remote objects trigger electrochemical cascades in our visual system – and when we learn new things, gene expression in the brain changes. We are interactive creatures, with innumerable stimuli that are constantly shaping multiple processes in our bodies. In this sense, the hypothesis that employment experience has cellular effects is not surprising.

This was an association study, which means than under certain set of circumstances two variables are statistically linked. This study is therefore incapable of genuinely predicting whether unemployment is the cause, and short telomeres the effect. Perhaps the opposite is true: maybe people whose cells lose their telomeres also lose their jobs. More likely, an outside factor that shortens telomeres could have a limiting effect on success in the labour market. For example, such a factor might somehow contribute towards illness or pessimism.

Additionally, because the study was conducted in an isolated and genetically quite homogeneous population, the results of the study may be due to their genetic make-up as well as (or instead of) environmental effects.

In the end, we do not need a genetic study to know long-term unemployment is bad for people socially, medically and psychologically; there is plenty of evidence for that. Additionally, the bio-gerontology community (those who study the biological processes of ageing) recognises telomere attrition as one of the nine causes of the disease of ageing, including Type 2 diabetes and cardiovascular diseases.

Where this study does make a significant contribution is in recognising long-term, low-level stress as a major problem. In momentarily stressful situations, the instant fight-or-flight response stimulates us; but being under pressure for a long time with no relief wears us down. Prolonged stress is bad for memory and health, and could quite conceivably shorten telomeres – making an unemployed person significantly more unhealthy, with the effects persisting even after they get a job.

In the long run, what we really need to learn to slow or stop the ageing process is how to reduce or repair the damage done by stress.

The authors do not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article. They also have no relevant affiliations.

This article was originally published at The Conversation.
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By Avi Roy, University of Buckingham

In rich countries, more than 80% of the population today will survive past the age of 70. About 150 years ago, only 20% did. In all this while, though, only one person lived beyond the age of 120. This has led experts to believe that there may be a limit to how long humans can live.

Animals display an astounding variety of maximum lifespan ranging from mayflies and gastrotrichs, which live for 2 to 3 days, to giant tortoises and bowhead whales, which can live to 200 years. The record for the longest living animal belongs to the quahog clam, which can live for more than 400 years.

If we look beyond the animal kingdom, among plants the giant sequoia lives past 3000 years, and bristlecone pines reach 5000 years. The record for the longest living plant belongs to the Mediterranean tapeweed, which has been found in a flourishing colony estimated at 100,000 years old.

This jellyfish never dies. Michael W. May

Some animals like the hydra and a species of jellyfish may have found ways to cheat death, but further research is needed to validate this.

The natural laws of physics may dictate that most things must die. But that does not mean we cannot use nature’s templates to extend healthy human lifespan beyond 120 years.

Putting a lid on the can

Gerontologist Leonard Hayflick at the University of California thinks that humans have a definite expiry date. In 1961, he showed that human skin cells grown under laboratory conditions tend to divide approximately 50 times before becoming senescent, which means no longer able to divide. This phenomenon that any cell can multiply only a limited number of times is called the Hayflick limit.

Since then, Hayflick and others have successfully documented the Hayflick limits of cells from animals with varied life spans, including the long-lived Galapagos turtle (200 years) and the relatively short-lived laboratory mouse (3 years). The cells of a Galapagos turtle divide approximately 110 times before senescing, whereas mice cells become senescent within 15 divisions.

The Hayflick limit gained more support when Elizabeth Blackburn and colleagues discovered the ticking clock of the cell in the form of telomeres. Telomeres are repetitive DNA sequence at the end of chromosomes which protects the chromosomes from degrading. With every cell division, it seemed these telomeres get shorter. The result of each shortening was that these cells were more likely to become senescent.

Other scientists used census data and complex modelling methods to come to the same conclusion: that maximum human lifespan may be around 120 years. But no one has yet determined whether we can change the human Hayflick limit to become more like long-lived organisms such as the bowhead whales or the giant tortoise.

What gives more hope is that no one has actually proved that the Hayflick limit actually limits the lifespan of an organism. Correlation is not causation. For instance, despite having a very small Hayflick limit, mouse cells typically divide indefinitely when grown in standard laboratory conditions. They behave as if they have no Hayflick limit at all when grown in the concentration of oxygen that they experience in the living animal (3–5% versus 20%). They make enough telomerase, an enzyme that replaces degraded telomeres with new ones. So it might be that currently the Hayflick “limit” is more a the Hayflick “clock”, giving readout of the age of the cell rather than driving the cell to death.

The trouble with limits

Happy last few days? It doesn’t have to end this way. ptimat

The Hayflick limit may represent an organism’s maximal lifespan, but what is it that actually kills us in the end? To test the Hayflick limit’s ability to predict our mortality we can take cell samples from young and old people and grow them in the lab. If the Hayflick limit is the culprit, a 60-year-old person’s cells should divide far fewer times than a 20-year-old’s cells.

But this experiment fails time after time. The 60-year-old’s skin cells still divide approximately 50 times – just as many as the young person’s cells. But what about the telomeres: aren’t they the inbuilt biological clock? Well, it’s complicated.

When cells are grown in a lab their telomeres do indeed shorten with every cell division and can be used to find the cell’s “expiry date”. Unfortunately, this does not seem to relate to actual health of the cells.

It is true that as we get older our telomeres shorten, but only for certain cells and only during certain time. Most importantly, trusty lab mice have telomeres that are five times longer than ours but their lives are 40 times shorter. That is why the relationship between telomere length and lifespan is unclear.

Apparently using the Hayflick limit and telomere length to judge maximum human lifespan is akin to understanding the demise of the Roman empire by studying the material properties of the Colosseum. Rome did not fall because the Colosseum degraded; quite the opposite in fact, the Colosseum degraded because the Roman Empire fell.

Within the human body, most cells do not simply senesce. They are repaired, cleaned or replaced by stem cells. Your skin degrades as you age because your body cannot carry out its normal functions of repair and regeneration.

To infinity and beyond

If we could maintain our body’s ability to repair and regenerate itself, could we substantially increase our lifespans? This question is, unfortunately, vastly under-researched for us to be able to answer confidently. Most institutes on ageing promote research that delays onset of the diseases of ageing and not research that targets human life extension.

Those that look at extension study how diets like calorie restriction affect human health or the health impacts of molecules like resveratrol derived from red wine. Other research tries to understand the mechanisms underlying the beneficial effects of certain diets and foods with hopes of synthesising drugs that do the same. The tacit understanding in the field of gerontology seems to be that, if we can keep a person healthy longer, we may be able to modestly improve lifespan.

Living long and having good health are not mutually exclusive. On the contrary, you cannot have a long life without good health. Currently most ageing research is concentrated on improving “health”, not lifespan. If we are going to live substantially longer, we need to engineer our way out of the current 120-year-barrier.

Avi Roy does not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article, and has no relevant affiliations.

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After studying tables of current life expectancy (life expectancy increase per decade, in years, based upon United States National Vital Statistics) I found embedded a virtually perfect Fibonacci sequence. A Fibonacci sequence is a series of numbers as follows: 0, 1, 1, 2, 3, 5, 8, 13, 21, 34, 55, 89, 144, 233, …etc, where each number is the sum of the previous two. See here for more details on the Fibonacci sequence: http://www.mathacademy.com/pr/prime/articles/fibonac/index.asp
To my knowledge, this has not been described before. This is important because, based on my ideas regarding Global Brain acting as a catalyst for promoting extreme human lifespans (http://hplusmagazine.com/2011/03/04/indefinite-lifespans-a-natural-consequence-of-the-global-brain/), it may help us predict with some accuracy any dramatic increases in life expectancy. For example, the model predicts that the current maximum lifespan of 110-120 years will be increased to 175 in the next 20-30 years.

In simple terms, the fact that life expectancy increases in a certain manner, and this manner obeys deep-routed and universal natural laws, indicates that it may be possible to:
1. Predict life expectancy in the near future. Based on the Fibonacci sequence,
a 90 year old today, can expect to live another 5 years
a 95 year old can expect to live another 8 years
a 103 year old can expect to live another 13 years, then…
a 116 year old can expect to live another 21 years
a 137 year old would expect to live another 34 years
a 171 year old would expect to live another 55 years
a 236 year old would expect to live another 89 years
a 325 year old can expect to live another 144 years,
and so on.

2. Question the presence of ageing and death in an ever-evolving intellectually sophisticated human (who is a valuable component of the Global Brain). Based on current facts, the Fibonacci sequence with regards to life expectancy ends abruptly when lifespan reaches the limit of approximately 120 years. Why is this so? Why should a naturally extending lifespan deviate from universal natural laws? Life expectancy should continue to increase as an individual manages to survive to a certain age. The presence of ageing and death could therefore be considered unnatural.

3. Support the notion that ‘you need to live long enough to live forever’ (see Kurzweil
http://en.wikipedia.org/wiki/Fantastic_Voyage:_Live_Long_Enough_to_Live_Forever, and also De Grey’s ‘Longevity Escape Velocity’ suggestions http://www.ted.com/index.php/talks/aubrey_de_grey_says_we_can_avoid_aging.html).

Those who manage to survive to extreme age are more likely to see their life expectancy increase even further, and so on, recursively. Kurzweil believes that this scenario will be achieved through use of technology. De Grey believes that this will be achieved via biological developments. I think that this ‘live long enough to live forever’ scenario will happen naturally (with minor input both from technology and from biological research). Those individuals who fully integrate their activities within the Global Brain will experience a natural-driven ever-increasing life expectancy.

For more details see https://acrobat.com/#d=MAgyT1rkdwono-lQL6thBQ

Marios Kyriazis