Cracking the Aging Code by Josh Mitteldorf was an amazing read on the science of aging. This book really enhanced my understanding of the aging process as well as evolutionary biology. Unfortunately, there are very little practical takeaways for the reader to utilize to slow down aging. Nonetheless, I would recommend this book to anybody who has an interest in understanding evolution.
Notes
- The Age-1 gene found in nature was the one that gave the worm a short life span… AGE-1 looked not like a selfish gene but an aging gene. It was just the kind of gene that natural selection ought to eliminate handily… there are now hundreds of “killer” genes that lengthen life span when they are deleted. When present, these genes have the effect of shortening life span (1) – 6
- At low levels, net life span is increased by radation exposure… Rats have been forced to slog through freezing cold water for hours and the result is that hey live longer… Mice raised in a sterile evinorment free of bcateria and viruses don’t live as long as mice that are exposed to disease pathogens in a sterile environment. Shocking worms with a short term exposure to heat that is not quite sufficient to kill them actually makes them live longer… Hormesis is an important clue about the evolutionary meaning of aging. It tells us that when the environment is rough, and many individuals are succumbing to starvation or disease, then aging relaxes its grip so that fewer animals die of old age. This suggests that aging serves to level the death rate in good times and in bad. – 141-142
- In ciliates, reproduction is by cloning, and gene-sharing is by a process called conjugation. The two processes are metabolically independent, so there would be nothing to stop a successful individual paramecium from eating and cloning until its descendants took over the colony in a monoculture. So natural selection has erected a barrier against this. Each time the paramecium reproduces, it loses a little bit of DNA from the tail of its chromosomes, called a telomere. With each division the telomere shortens until the chromosome becomes unstable and can’t function. The cure for this malady is an enzyme called telomerase. It acts as an antidote to death, restoring the telomere. Evolution has prevented the paramecium from getting telomerase except when it has sex. The result is that any line can go on reproducing for a few hundred generations, but then it runs out of telomere and the whole line will die out unless they share their genes. This is the earliest known form of aging. In retrospect, we may say that aging evolved for the purpose of protecting the community, enforcing the imperative that selfish individuals must share their genes – 155-156
- Diseases of old age in which apoptosis is implicated include Alzheimer’s, Parkinson’s, ALS, sarcopenia, osteoporosis, and Huntnigton’s disease – 177
- For the predator, aging helps to level out the death rate in good times and in bad so that the population is less likel to overshoot its sustainable carrying capacity and come crashing dowm from starvation or epdicemic. For the prey, aging helspt o assure that the weakest members fo the community are not he youngest but the oldest. The weakest and slowest are the ones predators grab first, and feeding the old and inform to the predators allows the young ones a better chance of growing to adulthood. For any animal subject to microbial infection, aging helsp to promote population turnover, keeping the population diverse so that theire is bettere resistance to disease and epidcems cannt kill everyone at once. The fatser turnover also helsp the species evoling new defense mechianism against micbornes that evolve rapidlybecause they reproduce rapidly. If the old have waekend immune systems, they will be the first to die of an infection, ad the rest of the population has a chance to develop immunity – 222
- Albatrosses and naked mole rats remain completely healthy through their lives and then die at a predetermined time… thrare animals capable of reverting from thir adult stage back to larval form… When teir bodes sense that the envinroemnt is so hostile that it was a mistake to grow up , they erevrse the process and become larvae once more… Once a clam outgows the arms of a starfish, it can eep gorwing indeifniet.y Giant clams, up to 750 pounds, live the same lifestyle of their smaller relatives. Like gianlobsters, the giant clams provide eggs for a whole community… Every conceivable combination of aging trajectories is possible, with rapid aging and no aging and backward aging, paired with life spans of weeks or years or cenutires… low mortality that rises suddenly at the ndo of the lfie sspan is experienced by humans and lab worms and guppie fish… For most trees, tortoises, clams, and sharks, the older an individual is, the less their risk of death… there are fewer dying old than dying young… Once an octopus delivers her young, she refrains from eating and dies within a few days… This is controlled by optic glands. If these optic clands are surgically removed, the ocopus can live up to forty weeks more… Non-aging is much more common in plants than in aniamls. Aging evolved to help prevent famines, and only animlas but not plants have to worry about famine… Planaria and Turritopsis nutricula jellyfish regress back to a earlier stage and live without any apparent signs of aging… Carrion beetles can regress back to larva, grow, and regress again repeatedly without aging… Worker bees live a few weeks and then die of old age, while queen beas, who have identical genes, can live and lay for years and sometimes for decades without aging. The queen dies only after runniny out of sperm she received during nuptial flight – 65-78
- An older, “retitred”segment of the population that is alive but no longer reproductive can help keep the population stale over scycles of feat and famine. When times rae good, they eat the excess ood andprevent population overshoot. When food is cscare, they are the first to die – page 79
References
- Increased lifespan of age-1 mutants in caenorhabditis elgans and lower gmpertz rate of aging, COmparing mutants selective breeding and transgencics in the dissection of aging processes of caeonorhabditis elegans, Genetic pathways that regualte aging in model organisms
- A brief review of radiation hormesis, Toxioclogical awakenings the rebirth of hormesis as a central pillar of toxicology
- Cracking the aging code, sex and the origons of death, A means to an end: the biolgocai basis of aging and death
- Skeletal muscle apoptosis, sarcopenia and frailty at old age, Apoptosis and alzheimers disease
- Cracking the aging code
- Diversity of aging across the tree of life, Cracking the aging code
- Cracking the aging code