Would you like to hear a truly astonishing fact? Are you ready?

Lobsters are immortal.

 

There you have it. If you didn’t already know, you probably don't believe it, but it’s true ¹. For millenia they have walked among us as we have both dreamed in vain for the Fountain of Youth and assumed it impossible. Gazing at the heavens, praying to gods and wishing on stars, we should have been looking down - at them. They were the ones that held The Secret - the most coveted answer to any riddle in all of human history - that real-world answer to that real-world question, that, when revealed, will make gods of men and women.

Lobsters do not speak in a conventional tongue, but if you listen to them in the right way, they can talk to you. We at Terraternal have prodded, cajoled and coaxed, looked at them from different perspectives and pleaded and finally we have gotten one to speak to us. And this is what he said:

Our eyebrows raised, our interest peaked, we leaned down and lent our ear to him, so that whatever it was he said next, if he were to say something next, we would be sure to hear it very clearly.

he said.

And then he crawled away, slowly, back into the ocean.

His comments puzzled us. For weeks, and then months, we contemplated what the Lobster had told us. We traveled the world, we spoke about it to anyone who would listen, We read books, magazines, studies and articles from anyone who had something to offer.

And little by little, we began to cobble together a larger picture of what it was he might have meant. We began to uncover the names of of those who seemed to be onto something - Leonard Hayflick, Calvin Harley, Jerry Shay, Maria Blasco, Elizabeth Blackburn, Rita Effros, and above all, a man named Michael Fossel. We began to be suspicious of the species we came from, painstakingly assembled more clues while it was not casting its watchful eye upon us, and finally found the chains the Lobster spoke of - long spiral strands at the distal ends of chromosomes called 'telomeres'.

And with all this we assembled our plan for rebellion. For ourselves and the rest of the world. But you cannot free those who do not know, as we did not, that they are enslaved, so what follows is a more detailed account of what we have learned, and the opinions we have formed, so that those who are convinced may join the our cause, quietly at first, and more boldly later as our goal - eternal life - comes ever closer.

The telomere is a strand of repetitive DNA sequences (TTAGGG in humans) at each end of the chromosome which get shorter with each cell division. When the telomere reaches a critically short length the cell goes into a state of replicative senescence in which it stops dividing and/or dies. Dr. Hayflick first discovered these after he found that the skin cells of a newborn baby, when cultured in a petri dish, will continue to divide for another 50-70 times before they reach replicative senescence, a point which is now referred to as the Hayflick Limit. Cells from an older person, on the other hand, would only divide several times before they hit this limit. Dr. Hayflick discovered that it was the telomere that was keeping track of these divisions. He posited that they were there to ‘cap’ the ends of the chromosomes and keep them from unraveling, as it were, in the way that shoelace tips cap a shoestring and that it was this unraveling caused by the arrival of the telomere at critically short length that threw the cell into crisis and caused it to senesce. He also theorized that it may be the accumulation of these senescent cells that are causing aging in us.

By the end of the 20th century, this relationship between telomeres and cell senescence was commonly accepted and investigation into the science of telomere biology was in full swing. What has recently come to light, however, is that even far before the Hayflick Limit is reached, through a mechanism that is still not fully understood, the shortening of the telomere is controlling the gene expression patterns of the genes on the chromosome it inhabits, causing cells to become less functional after a certain number of divisions. This phenomenon is referred to as the Telomere Position Effect (TPE) ², and this may in fact be the more important function of the telomere in aging and in fact be the real reason why the cells ultimately hit replicative senescence. Among the many functional changes that ensue as a result of the degradation of gene expression are that older cells (ones with shorter telomeres) divide less often, are less capable at defending themselves against various environmental insults such as free radical damage and glycation, are more prone to cancerous mutations and harbor energy-producing mitochondria that are less functional. ³

As a result of all this, as we age, our tissues gradually accumulate a larger proportion of senescent cells, as well as 'older' cells - that is cells whose gene expression has been altered for the worse. Seen from a macroscopic perspective, that is from the perspective of a human organism, this is what we, and other subscribers to the telomere theory of aging, believe aging is. The extra damage that our cells appear to accumulate we believe is primarily the effect of telomere-mediated gene-expression degradation of all the cells in our body and not in fact the cause of aging.

Our embryonic stem cells and germ cells maintain their telomere lengths across cell divisions with an enzyme that they produce called telomerase. And because of this these cells are immortal and do not suffer the damage over time that we observe in our other cell lines.  This was confirmed when in 1999 somatic (non stem) cells were coerced to express telomerase and were thereby immortalized in vitro (ie in a petri dish).  

A recent study entitled Longevity of lobsters is linked to ubiquitous telomerase expression has found that the somatic cells in a lobster, unlike that of almost all other multicellular organisms, each express high levels of telomerase throughout its life. The same authors studied another 'immortal' species, the Rainbow Trout, looking to see if there was a pattern of high telomerase expression, and found that there was.