Human World

Do unemployed people age faster?

By Avi Roy and Anders Sandberg

Men who are unemployed for more than two years show signs of faster aging in their DNA, according to a study published November 20, 2013 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.

Human chromosomes with their telomeres highlighted. Image via NASA
Human chromosomes with their telomeres highlighted. Image via NASA

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.

View larger. | Image via Flickr user jronaldlee.
View larger. | Image via Flickr user jronaldlee.

Employment is 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 aging) recognizes telomere attrition as one of the nine causes of the disease of aging, including Type 2 diabetes and cardiovascular diseases.

Where this study does make a significant contribution is in recognizing 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 aging process is how to reduce or repair the damage done by stress.

Anders Sandberg.
Anders Sandberg.
Avi Roy is a PhD student at the University of Buckingham in the UK, researching aging, mitochondria, and regenerative medicine; he is also an Ultimate (frisbee) enthusiast.
Avi Roy.

 

Anders Sandberg conducts research at the Future of Humanity Institute at the University of Oxford. His work centers on societal and ethical issues surrounding human enhancement and new technology.

Avi Roy is a PhD student at the University of Buckingham in the UK, researching aging, mitochondria, and regenerative medicine; he is also an Ultimate frisbee enthusiast.

Also by Avi Roy:

If you want to live longer, do nothing

Lust for life: Breaking the 120-year barrier in human aging

Is meat grown in labs the next logical step for food production?

Posted 
December 2, 2013
 in 
Human World

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