Theory of Aging

 Unlike. any normal human, A scientist, to me, is one who keeps his religion strictly out of the propounded theory. It can not matter what their belief system is, I only believe in empirical theory everywhere, It matters not what he divines for his beliefs from empirical theories. God is NOR dead but irrelevant to my science. This means empirical facts remain independent of their theories. You have to prove everything from empirically constructed theories. Next is personal despite excellent folks who believe otherwise, they remain meta-morons and vulnerable to sophisticated thugs exploiting their stupidity.

The aging theory has been the essential goal for 4000 years since the dawn of written language in Mesopotamia through empirical novels of Gilgamesh. Since that time many fraus have arisen. How can you decide I am not one too? Because I only state this story on empirical proofs by Dr. Sinclair at Harvard. Any mistakes are mine and will be corrected once pointed out.

How can one provide proof empirically for any theory of aging? First, you have to accept evolution. Then you demonstrate the correctness of your theory on mice, doable much faster given their small lifespan. Also, it is ethical to sacrifice mice.

The mice have their optic nerve destroyed by crushing. Next, mice in this experiment prove mice have gone blind. How in mice? Mice stare at lines. If not blind, then their throat moves their head to the side the lines move. All crushed optic nerve mice prove they have become blind, Now the NAD+ boost is done. All the mice so treated get back eye-sight after treatment. Their eyes act like genuine eyes for the rest of their life. Note that I skip over treatment which is done by triggering genes.

So aging is understood in mice. Same works in other animals. By evolution, also applies to humans. The experiment has a human analog, for whatever reason, people end up with diseased optic nerve and become blind. They can be cured with an analog NAD+ boost.

A full life of the human-animal?

A human or any sexual evolution animal starts from a single cell called a zygote that fuses the mother and father DNA halves. The DNA of the zygote divides repeatedly over the birth intervals. The DNA has an epigenomic layer that modifies the cell by context. Eventually, the birth-human is produced. It keeps growing till adulthood. This happens with a continued division of stem cells. The body is repeatedly attacked by useful microbes and pathogens. There is a full-fledged immune system for inbuilt and adaptive immunity.

Humans and similar animals have 3 classes of enzymes that control the stem cells. The stems do not wither away. They stop their growth activity as a consequence of chemical signals. They are needed badly in wound repair till death!

The classes are Sirtuins, AMPk, and mTOR  Keeping them occupied is how aging will be intervened in Singularity 1.0. There are 7 Sirtuins, which only Sirt1 will be focused on. AMPk and NAD+ improvements are sought. mTOR signals abundance and increases with proteins signaling body no longer be in an alert state, shutting down repair machinery deployed for fears of starvation. This is counteracted by fasting, exercise, low sugars, low proteins, etc. These are excellent ways to fool the body which responds by hunkering down for adversity!

Roughly, NAD+ boosters (sirt1), metformin (AMPk), and low dosage rapamycin (mTOR) affect the growth genes. One has no dangers of body growth because the stem cells are halted by independent chemicals.

Very brief cell biology required to understand Aging and mRNA vaccines?

A cell has many compartments. Interest to us are

1. Nucleolus sack containing the DNA

2. zero plus mitochondria sub-cells

3. Ribosomes

How does a cell work? Two top important processes are making a protein and making energy.

To make a protein, it is somehow included as query protein, which enters the nucleolus and matches the short-chain in DNA which produces mRNA with one new sugar, enough to mark the molecule as mRNA that now exits the nucleolus. Once in the cell, it unites with a ribosome and makes the needed protein. The mRNA is still there and can not reenter the nucleolus. It dies as programmed to die quickly. Sometimes it exits the cell but is then eaten by an immune cell.

Or the signal might make energy, then ends up in a mitochondria subcell. They have their own small DNA. In any case, the signal causes production from ATP by Krebs using NAD+.

Why does NAD+ decline and what if it does?

NAD+ catalyzes many Krebs subcycles. It is basic to convert to energy, autophagy, and apoptosis. NAD+ is slowly, and with difficulty made from vitamin B3 in each cell, and is used in many sub-cycles in the Krebs cycle in so many animals and human cells. Its loss hurts by lack of energy, weakened immunity, more cancers, and many chronic diseases.

It declines because it bothers dead senescent cells which accumulate because of autophagy and apoptosis decline. To adulthood and near beyond, bad cells are garbage collected and replaced by new daughter cells from division. But that does not happen with age. The dead cells accumulate. They take to producing SASP. Some make neighbor cells senescent too. Others simply neutralize NAD+ which bothers dead cells. Each dead cell not removed is a big problem.

Hallmarks of Aging?

Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contribution to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging with minimal side effects.

The next page talks about interventions.