the science of aging part 1: why we age



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“Live your questions now, and perhaps even without knowing it, you will live along some distant day into your answers.” Rainer Maria Rilke

It doesn’t matter if you are a biochemistry student, hollywood starlet or just an open mind: the question of why we aren’t immortal unites us. Let’s all thank the so-called ‘biogerontologists’, scientists who diligently search for an answer to this question. When you’re young you may think it is way too early to think about age at all but at the latest when you reach the twenty mark you are very likely to start to get conscious on this topic. Because that’s when the cosmetic industry reminds us that our collagen production decreases and we need to preserve what’s still left with sunscreen, innovative skincare etc. The average population thinks about starting a family and some might experience physiological changes which make them feel old. I spent the last years trying to understand what we already know about aging but it’s not very easy. Cell Biology is still a striving and exciting branch of science and you can be sure by the end of this sentence a few smart heads have already found another major piece of the puzzle, important enough to be mentioned here. To clear things up: I am not ‘anti’ aging in particular but I’ve always been a fan of preserving what you have and taking good care of it. At the end of this series on ‘aging’ I will focus on protective skin active ingredients, which are scientifically proven to keep skin young. Let’s start with the first theories made by early biogerontologists on why we age:

Rate-of-living theory
There are various popular theories about why we age and most of them add together to one explanation. 1908 Max Rubners introduced his “rate-of-living theory” after he observed the body temperature in relation to their body size of mammals and birds. He proposed that a slow metabolism increases an animal’s longevity and observation was that larger animals outlived smaller animals, and the metabolic rates of larger animals were slower per rate. Twenty years later Raymond Pearl expanded his theory with experiments on fruit flies (drosophila) which have shown that a decrease of environmental temperature go along with a increase of lifespan. But there was still one problem: it was not applicable between all species (source 1, 2, 3).

Mitochondrial theory of aging
1958 Denham Harman, a research chemist of Shell’s reaction kinetics department who was studying free radical reactions in petroleum products, completed a part of Pearl’s theory. He developed the idea of radical induced damages like replication- and translator errors, aswell as radiation and toxic substance induced changes can induce the senescence or death of a cell. All his studies showed that antioxidants increased the average lifespan, none really showed an increase in maximum life span. Decades of research later his conclusion was that mitochondria, the powerhouse of cells, were not affected by antioxidants that came from the outside. So he deduced that mitochondria determine lifespan. A new theory was born: the “mitochondrial theory of aging” (source 1, 2)

Telomere theory of aging and Hayflick limit
At the end of last century another theory popped up: the telomere theory of aging. Researchers found out that the cause for the shortening of chromosomal ends (telomers) in proliferated cells was the disability of dna-strings ends, for mechanical reasons, to be fully doubled after each replication round. To prevent genetic damage, cells developed telomers, repetitive nucleotid sequences. According to Leonard Hayflick, with each round of dna replication and increasing age they shorten until finally the prior protected part of the dna is damaged, which weakens the stability of chromosomes altogether and leads to apoptose- the cell death. Basically it means you can tell by the length of the telomere how often the cell can replicate until it suddenly stops. Hayflick demonstrated normal human cells in vitro divide about 52 times until they automatically enter the senescence phase. Telomere shortening happens mainly with proliferating cells, while for example stemcells and cancerous cells produce an enzyme called telomerase which prolongs the telormers again after a replication round (Source 1, 2, 3, 4).

Negligible Senescence in nature and SENS
In the last years several genes and their proteins entered the limelight of gerontology; lots of them regulate stress resistance and repair of dna-damage, with transport functions or antioxidant effects. It appeared to be that aging is a programmed species- and cell specific process. Imagine a car that wears out over time. It isn’t very different. So if you think like there’s nothing you could do about the aging process you should look how Aubrey de Grey feels about it. Some might think the Cambridge researcher with a tremendous beard is more of a dreamer than a scientist but I like his fervor. He basically breaks down the types of Aging Damage to 7 and there is a TED video that shows his enthusiasm quite well and is actually very funny (see here). Read more here 1, 2, 3, 4, 5

I really hope this small biogerontology journey didn’t confuse you too much and made you as excited about this topic as I am. It’s crazy how many researchers work together to encipher the mystery of aging and are looking for the molecular fountain of youth. Consider this a humble overview! Next week we’ll see some examples of the ‘immortality gene’ in animals like the hydra. Best, Ea Birkkam


today: Eve from Only Lovers Left Alive (2013)