“We do not see the world as it is, we see the world as we are.”

The Talmud

The Big Picture

There are two modern biological theories of aging, namely: programmed theories and damage or error theories. The programmed theories are driven by biological timetables (changes in gene expression, physiological maintenance, repair and defense). Damage or error theories highlight environmental assaults, such as exposure to carcinogens, confounded by lifestyle choices (diet, exercise, etc.).

Here is video from Piled Higher and Deeper (PHD Comics)


Here are a few statistics from the World Data Bank

The older population—persons 65 years or older—numbered 46.2 million in 2014 (the latest year for which data is available). They represented 14.5% of the U.S. population, about one in every seven Americans.

Age is the main risk factor for the prevalent diseases of developed countries: cancer, cardiovascular disease and neurodegeneration.


World population (0-14)


World population (15-64)


World population (65+)


Population growth (Annual)

Also, there is the transposon theory of aging, in which elements of DNA break free in aging cells and are then incorporated elsewhere (transposed) in the genome, causing problems. This mostly happens in aging tissues.

Here is a video about transposons:

So what’s the update? 

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Activity with age: Fluorescence in the fat body of fruit flies tracks the activity of transposable elements of DNA. It increases markedly with age. Jason Wood/Brown University

A new study increases and strengthens the links that have led scientists to propose the “transposon theory of aging.” Transposons are rogue elements of DNA that break free in aging cells and rewrite themselves elsewhere in the genome, potentially creating lifespan-shortening chaos in the genetic makeups of tissues.

As cells get older, prior studies have shown, tightly wound heterochromatin wrapping that typically imprisons transposons becomes looser, allowing them to slip out of their positions in chromosomes and move to new ones, disrupting normal cell function. Meanwhile, scientists have shown that potentially related interventions, such as restricting calories or manipulating certain genes, can demonstrably lengthen lifespans in laboratory animals.

“In this report the big step forward is towards the possibility of a true causal relationship,” said Dr. Stephen Helfand, Brown University professor of biology and senior author of a new study in the Proceedings of the National Academy of Sciences. “So far there have been associations and suggestions that to all of us make sense, but the difference in science is that you need the data to back up your opinion.”

What’s the next step to understand the effects of transposon on aging?

While transposons appear to be a significant factor in aging, Helfand and Wood said, they are likely to be only part of a broader set of processes that undermine health over time.

The team will purposely encourage expression of transposable elements to see if that undermines health and lifespan. Another approach could be to use the powerful CRISPR gene editing technique to specifically disable the ability of transposable elements to mobilize within the genome. If that intervention affected lifespan, it would be telling as well, Helfand said.

A part of this post is reprinted from materials provided by Brown University.

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