Your body wasn’t built to last: Math of human mortality (2009)
gravityandlevity.wordpress.com
gravityandlevity.wordpress.com
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Recent advances in computational epigenetics https://www.dovepress.com/recent-advances-in-computational-e...
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End-to-end guide design for CRISPR/Cas9 with machine learning https://www.microsoft.com/en-us/research/project/crispr/
Will require new math.
Death is really scary shit and I get that someone with the money and connectionts of Kurzweil can convince himself that it won't happen to him, but we must all realise that, at this point, that's just a pipe dream.
What I'm not happy is so many folks calling him a prophet and jumping this magic-nanothech-30year-singularity bandwagon.
https://doi.org/10.1006/jtbi.2001.2430
"Reliability theory is a general theory about systems failure. It allows researchers to predict the age-related failure kinetics for a system of given architecture (reliability structure) and given reliability of its components. Reliability theory predicts that even those systems that are entirely composed of non-aging elements (with a constant failure rate) will nevertheless deteriorate (fail more often) with age, if these systems are redundant in irreplaceable elements. Aging, therefore, is a direct consequence of systems redundancy. The theory explains why mortality rates increase exponentially with age (the Gompertz law) in many species, by taking into account the initial flaws (defects) in newly formed systems."
https://doi.org/10.1073/pnas.1714478115
"For many cancer types, incidence rises rapidly with age as an apparent power law, supporting the idea that cancer is caused by a gradual accumulation of genetic mutations. Similarly, the incidence of many infectious diseases strongly increases with age. Here, combining data from immunology and epidemiology, we show that many of these dramatic age-related increases in incidence can be modeled based on immune system decline, rather than mutation accumulation. In humans, the thymus atrophies from infancy, resulting in an exponential decline in T cell production with a half-life of ∼16 years, which we use as the basis for a minimal mathematical model of disease incidence. Our model outperforms the power law model with the same number of fitting parameters in describing cancer incidence data across a wide spectrum of different cancers, and provides excellent fits to infectious disease data. This framework provides mechanistic insight into cancer emergence, suggesting that age-related decline in T cell output is a major risk factor."
And of course the SENS synthesis of the compelling evidence for aging to be the consequence of accumulated damage of various sorts:
http://www.sens.org/research/introduction-to-sens-research
"Many things go wrong with aging bodies, but at the root of them all is the burden of decades of unrepaired damage to the cellular and molecular structures that make up the functional units of our tissues. As each essential microscopic structure fails, tissue function becomes progressively compromised – imperceptibly at first, but ending in the slide into the diseases and disabilities of aging. Decades of research in aging people and experimental animals has established that there are no more than seven major classes of such cellular and molecular damage, shown in the table below. We can be confident that this list is complete, first and foremost because of the fact that scientists have not discovered any new kinds of aging damage in nearly a generation of research, despite the increasing number of centers and scientists dedicated to studying the matter, and the use of increasingly powerful tools to examine the aging body. In its own way, each of these kinds of damage make our bodies frail, and contribute to the rising frailty and ill-health that appears in our sixth decade of life and accelerates thereafter."
"Please respond to the strongest plausible interpretation of what someone says, not a weaker one that's easier to criticize."
That principle applies as well to articles as to persons, and there's clearly more in this piece than you reduced it to. But even if you were right, the combination of an empty comment and an acidic pH makes for a sourer website, and the internet is hostile enough already.
The nature of this connection can be different. This is what discussed in the article.
> Notice that the article doesn't even offer new facts, only statistical observations.
Statistical observations are facts.
This age might keep increasing because those who try too late won't reproduce. So it's passive selection for longevity.
Maybe immortal humans give you a better bang for the buck.
New humans allow for changes in DNA to fit a changing environment (immortality doesn’t - hey, you get my drift)
Thinking of the people’s throughout history who shrunk to be smaller due to poor nutrition or unstable food source let’s the human race adapt pretty well to a whole host of issues. Immortality (unless it’s accompanied by some pretty impressive technology from the future) doesn’t.
https://doi.org/10.18632/aging.100640
"Why do humans live longer than other higher primates? Why do women live longer than men? What is the significance of the menopause? Answers to these questions may be sought by reference to the mechanisms by which human aging might have evolved. Here, an evolutionary hypothesis is presented that could answer all three questions, based on the following suppositions. First, that the evolution of increased human longevity was driven by increased late-life reproduction by men in polygynous primordial societies. Second, that the lack of a corresponding increase in female reproductive lifespan reflects evolutionary constraint on late-life oocyte production. Third, that antagonistic pleiotropy acting on androgen-generated secondary sexual characteristics in men increased reproductive success earlier in life, but shortened lifespan."
https://arxiv.org/abs/1103.4649
"Understanding why we age is a long-lived open problem in evolutionary biology. Aging is prejudicial to the individual and evolutionary forces should prevent it, but many species show signs of senescence as individuals age. Here, I will propose a model for aging based on assumptions that are compatible with evolutionary theory: i) competition is between individuals; ii) there is some degree of locality, so quite often competition will between parents and their progeny; iii) optimal conditions are not stationary, mutation helps each species to keep competitive. When conditions change, a senescent species can drive immortal competitors to extinction. This counter-intuitive result arises from the pruning caused by the death of elder individuals. When there is change and mutation, each generation is slightly better adapted to the new conditions, but some older individuals survive by random chance. Senescence can eliminate those from the genetic pool. Even though individual selection forces always win over group selection ones, it is not exactly the individual that is selected, but its lineage. While senescence damages the individuals and has an evolutionary cost, it has a benefit of its own. It allows each lineage to adapt faster to changing conditions. We age because the world changes."
https://www.demogr.mpg.de/en/news_press/news/press/forever_y...
“A long-term experiment with the freshwater polyp Hydra, a microscopic animal: observing many hundreds of them for almost ten years, researchers calculated that Hydra’s mortality permanently stays constant and extremely low. For most species, including humans, the probability of dying within a specific year rises with age. Scientists regard this as an indicator of the decay of the aging body. For Hydra, evolution seems to have found a way to escape the mechanisms of the physical deterioration of getting older. Hydra apparently manages to keep its body young because it does not senesce by accumulating damages and mutations, as most other living beings do. Hydra are probably able to follow a special self-preservation strategy, as its body and cellular processes are rather simple. For instance, Hydra are capable of completely replacing parts of the body that are damaged or are somehow lost. It can even fully regenerate if its body is destroyed almost completely thanks to a high number of stem cells. Stem cells are capable of developing into any part of the body at any time. Additionally, as Hydra replaces all of their cells within only four weeks, it regularly and quickly expels all cells that have been changed genetically by mutations. Thus, damages have little chance to accumulate."
If life expectancy for men and women was found to be similar when controlling for height, it would suggest that aging is more a result of increasing disorder than of a characteristic of either sex.