We can see
how genetics play a role in how long we live. Looking at different species and
how long or short they live. But we do not know exactly how this works.
Alexander
Graham Bell, the inventor of the telephone, was more passionate about aging. In
1900s he found that people that lived long had long-lived children. Whether
this is due to genetics or to providing support to children, or both, remains undefined.
But the connection is there. Sometimes despite having the best genes, bad luck
just strikes. Take the example of Jeanne Louise Calment, who died at the age of
122 years in 1976. Despite having the best genes for longevity her family did
not enjoy these positive attributes. Sometimes bad luck negates good genes when
her daughter Yvonne, died at age 36 of pneumonia. Luckily, she left a son
Frederic, who became a physician. He lived with his grandmother in her
apartment. However, he also died early, in a motorbike accident, at the same age as
his mum 36 years old. Sometimes bad luck negates any genetic advantages.
Three classic
experiments define how a genetic advantage results in living longer. The first
experiment was conducted by Michael Rose who by allowing only eggs of older
flies to hatch he found that the next generation lived longer. The new
generation seemed to know that, similar to their parents, they need to live
longer in order to reproduce. We also find this among humans. The older your
mother was when she conceived you, the longer you will likely live. Unlike
human, there is no nurturing for flies, so this effect is predominantly genetic.
The second
type of experiment uses a naturally occurring disorder in a flatworm that
produces less growth hormone which stunts their growth but they end up living
much longer. Through a series of trial and errors Cynthia Kenyon at University
California San Francisco managed to chemically knock out one of these genes in
normal flatworms and in so doing nearly doubling their lifespan.
The third
type of genetic observation is seen with mice, in particular the work done by
Richard Miller and his infamous dwarf mouse called Yoda. Again, nature lead the
way in showing us about the longevity advantage of having less growth hormones.
In nature there are three types of dwarf mice that share this longevity characteristic:
Snell, Ames and Laron dwarf mice. These mice live about three times longer than
average.
By knocking
out a gene to stop growing larger we could all live longer. Somehow the body
knows that we need to live longer in order to be able to pass on its genes.
Fortunately, we also have examples among humans as well. In a southern Ecuador community
of 250 individuals that have Laron syndrome—causing a deficiency in primary
growth hormone—although protecting them against disease, especially cancer,
this apparent protection does not translate to living longer. This group
unfortunately engage in risk behaviors in particular alcoholism that negate
this genetic advantage.
No one wants
to have a stunted growth in order to live longer. But what about having older
parents to increased longevity? In biology, there is always a dark side—known
scientifically as antagonistic pleiotropy. This construct has plagued gerontological
research since it posits when one gene controls for more than one trait (e.g.
height) it is likely that one of these traits is beneficial (e.g. more
athletic) while another side is detrimental (e.g. heart disease) to the
individual later on in life.
The dark side
is that we know that women having children at much older ages increases the
risk of certain genetic problems. It has also been reported in 2018 by Boris
Rebolledo-Jaramillo with Nottingham-Trent University UK, and his colleagues
that children of older mothers face greater risk of developing diabetes,
dementia and heart disease. As for older fathers, their kids are more likely to
have dwarfism or Apert syndrome. Newer
research in 2012 by Augustine Kong at Reykjavik University, Iceland also
suggest that there is an increased risk for autism and schizophrenia. There is
a “goldilocks effect”, not too old and not too young, just right.
The
surprising result in genetic research is the finding that as we age we are also
changing our genes. It was always assumed that our genes unchanging and that
they are given to us exclusively by our parents, period. But we are learning
that we also add and modify our genes as we age. We acquire one percent of our
genes from bacteria, fungi, viruses and archae—single cell
micro-organisms. Specifically, there are
special molecules that reside in these cells that are there specifically to
develop antibodies. They are not part of the cell but act as independent
contractors. Known as “plasmids” they help us fight infections. If we are
constantly being infected, in order to help us develop immunity, they somehow insert
their antibodies-producing-genes into our DNA so we can develop this protection
ourselves. Sometimes our own genes change position in our chromosomes so they
gain higher priority. These genes are known as “jumping genes” or as “transposons.”
Such strange
genetic behavior was first discovered by Barbara McClintock in the 1940s who
was awarded the Nobel Prize for medicine in 1983. How plasmid and jumping genes
do this remains an absolute mystery. Her work provided evidence that the
composition of our genes—our genome—changes while we are living. The longer we
live, the more likely that these new genetic improvements are transmitted to
our children. So now we have figured out the method of how Michael Rose’s flies
create a time stamp on their genes. Plasmids are at work throughout the aging
process.
We develop
immunity from the day we are born and some of these biological adaptations end
up in our genes through the transfer of external genetic material. Our genes
are more permeable than we once thought. We get genes not just from our parents
but also from the environment. In addition, we also get genetic material from
our twins in the womb and mothers get genes from their children. We find male
chromosomes in mothers who had baby boys. We are a magnet for adaptive genetic
material from our environment.
Barbara
McClintock was also the first scientist to correctly speculate on the basic
concept of how some genes can be switched on and off—known as epigenetics, epi meaning
“above” controlling genes. Sometimes a defective gene (e.g. for diabetes or
Alzheimer’s disease) can be switched off—through diet, exercise and mild trauma.
As we age we pick up new genetic material and modify existing genes
(epigenetics) before we pass these genes on to our children. Our lives are
devoted to just this aim, making sure that our children are best prepared to
the new world they face. As for bad luck, we have Pandora’s last remaining
attribute: Hope.
© USA Copyrighted 2018 Mario D. Garrett
References
Bartke, A., Wright, J. C., Mattison, J. A., Ingram, D. K., Miller, R. A., & Roth, G. S. (2001). Longevity: extending the lifespan of long-lived mice. Nature, 414(6862), 412.
Garrett M (2017) Immortality With a Lifetime Guarantee. Createspace.
Kenyon, C., Chang, J., Gensch, E., Rudner, A., & Tabtiang, R. (1993). A C. elegans mutant that lives twice as long as wild type. Nature, 366(6454), 461.
McClintock, B. (1993). The significance of responses of the genome to challenge.
Accessed:https://www.nobelprize.org/nobel_prizes/medicine/laureates/1983/mcclintock-lecture.pdf
Rebolledo-Jaramillo, B., Su, M. S. W., Stoler, N., McElhoe, J. A., Dickins, B., Blankenberg, D., ... & Paul, I. M. (2014). Maternal age effect and severe germ-line bottleneck in the inheritance of human mitochondrial DNA. Proceedings of the National Academy of Sciences, 111(43), 15474-15479.
Rose, M. R. (1984). Laboratory evolution of postponed senescence in Drosophila melanogaster. Evolution, 38(5), 1004-1010.