A Guide to Slowing Down Aging (Part 2)

Aside from the low-tech approaches mentioned in Part 1, which include healthy nutrition, exercise, and a variety of other lifestyle changes, many researchers all over the world are developing innovative therapies that can significantly slow down and even moderately roll back aging.

The idea that aging is the root cause of all aging-related diseases like heart disease, Alzheimer's disease, osteoporosis, and macular degeneration is gaining ground. People are realizing – and science is proving – that tackling aging addresses the root cause of all of these diseases. Managing aging would necessitate far more effective and improved treatments to prevent, slow, or even reverse aging-related diseases.

Consider heart diseases. Imagine if we could successfully treat and prevent all heart diseases and heart attacks, your average lifespan increases only by 2.9 years!

That is not much. People would die from another aging-related disease rather than heart disease a few years later. As a result, rather than focusing on specific diseases, it is crucial to concentrate on aging.

Heart disease is an excellent illustration of why treating the causes of aging rather than the disease itself is far beneficial. Many doctors will tell you that heart disease is caused by cholesterol buildup and inflammation in the blood vessel walls. They will state specifically that white blood cells stuffed with cholesterol accumulate in blood vessel walls causes artery narrowing.

However, these processes are caused by underlying aging mechanisms. Because white blood cells' lysosomes are incapable of properly breaking down cholesterol, it accumulates. Lysosomal dysfunction is an aging symptom.

Many other mechanisms contribute to atherosclerosis, such as senescent cells in the blood vessel walls, dysfunctional stem cells in the blood vessel walls, and other cells damaged by mitochondrial dysfunction, protein accumulation, cross-linking, epigenetic dysregulation, and so on. All of these are aging mechanisms that contribute to atherosclerosis and other age-related diseases.

What are some of the technologies aimed at slowing or even reversing the aging process?

Mitochondrial renewal

Mitochondria are our cells' powerhouses. As we age, they become more dysfunctional, contributing to the aging process.

The deterioration of mitochondrial DNA is a major cause of mitochondrial dysfunction. This is worrisome because mitochondrial DNA contains blueprints for the construction and maintenance of mitochondria.

There are numerous methods for reinvigorating mitochondria. One method is to introduce new, undamaged mitochondrial DNA, which contains the building instructions for mitochondrial proteins, into the mitochondria. This is accomplished by injecting tagged mitochondrial DNA intravenously, which automatically travels to the mitochondria.

Other methods include injecting specific peptides that improve mitochondrial health, moving mitochondrial genes from the mitochondria into the cell nucleus, where they are better protected from damage, or using new and safer mitochondrial decoupling agents, or even injecting whole young and healthy mitochondria in animals, a procedure known as mitotherapy.

All of these treatments will take time to develop. In the meantime, natural compounds like fisetin, glycine, calcium alpha-ketoglutarate, nicotinamide mononucleotide (NMN), and pterostilbene have been shown to optimize mitochondrial health.

Reprogramming of the epigenome

The epigenome is the intricate molecular machinery that surrounds DNA and regulates which genes are active and which are not. The epigenome serves as a switch for our genes.

As we age, our epigenome becomes dysregulated, with some genes turning on when they should be turned off and vice versa. Cancer and inflammation-promoting genes, for example, are activated, increasing our chances of developing cancer and inflammatory diseases.

Scientists were able to reverse some of the effects of aging in mice by reprogramming their epigenome. They rejuvenated old mice by temporarily increasing Yamanaka factors in their cells. Many scientists are studying epigenetic reprogramming to rejuvenate cells and organisms.

Calcium alpha-ketoglutarate, vitamin C, lithium, nicotinamide mononucleotide (NMN), and glycine are examples of natural substances that can improve epigenetic health.

Clearing up the protein mess

As we age, proteins accumulate both inside and outside of our cells. Protein buildup in the brain is a major contributor to Alzheimer's disease. Protein accumulation in the heart plays a role in aging-related heart dysfunction. Protein accumulation in blood vessel walls makes them more prone to tearing or clogging.

Protein accumulation can be slowed or reversed in a variety of ways. With the help of a protein vaccine or by infusing antibodies that latch onto and clear up specific proteins that accumulate during aging, the immune system can be induced to clear up specific proteins.

Another option is to inject lysosomal enzymes. Lysosomes act as incinerators for the cell, breaking down protein and other cellular waste. Lysosomes become less efficient as we age. Lysosomal enzymes injected into the bloodstream can travel to aged lysosomes and help them break down proteins. This has already been used to treat previously fatal lysosomal storage diseases with success. Some researchers try to enhance lysosomal function by attempting to make the lysosomes more acidic so that they can more efficaciously "digest" cellular waste.

Another approach to addressing protein accumulation is to improve autophagy, the process by which the cell digests or breaks down its own protein waste. Because autophagy declines with age, reactivating this system may be beneficial in the fight against aging.

Glucosamine, lithium, glycine, and acetyl-glucosamine are examples of natural substances that can help with protein homeostasis (a building block of hyaluronic acid, which also improves skin health).

Stem cell therapy

Stem cells are cells that generate new cells and aid in the proper functioning of our tissues and organs. Our bodies' stem cells become dysfunctional or die off as we age.

To replenish depleted stem cell pools or to revitalize existing stem cell populations, stem cells can be injected into the human body.

However, stem cell therapy is fraught with difficulties. For example, stem cells may be rejected by the immune system (as with "allogeneic" stem cells derived from other people), or they may be old and damaged (this is the case for autologous stem cells, which come from your own, aged body).

Many companies offer stem cell therapies to treat aging and diseases associated with aging, but  almost all of them promote improper treatments. These stem cell therapies are ineffective and may be dangerous. Stem cell injection, for example, can result in clots in the lungs, or the stem cell infusion can be contaminated with bacteria.

Moreover, scientists are increasingly convinced that the health benefits of stem cell infusion are caused not by the stem cells grafting and creating new cells, but by the stem cells briefly secreting substances that can reinvigorate the body before dying off or being eliminated. For example, calcium alpha-ketoglutarate has been shown to improve stem cell health.

Heterochronic parabiosis and young blood

According to research, giving young blood to old mice can make them younger in some ways. Certain substances found in young blood appear to rejuvenate elderly mice. Specific substances found in old blood, on the other hand, have the ability to either accelerate or maintain the aging process.

Various biotechnology companies and research organizations are attempting to identify the rejuvenating substances in young blood so that they can be administered to humans in order to improve health and slow or even partially reverse aging.

Telomere lengthening

Telomeres are the caps that protect the ends of our DNA strands from unraveling, similar to the plastic caps on shoelaces. Telomeres become shorter as cells divide, which is bad.

Telomeres are the subject of numerous myths. Telomere length does not appear to be strongly related to aging. As a result, many people believe telomeres have no effect on aging. The rate of telomere lengthening (or shortening) is, however, related to life expectancy.

Mice, for example, have significantly longer telomeres than humans (while having much shorter lifespans). However, when compared to humans, mice's telomeres shorten much faster.

Scientists are looking into new ways to deliver the enzyme (telomerase) that lengthens telomeres . Despite popular belief, short-term telomere lengthening does not significantly raise cancer risk.

Telomerase, an enzyme that lengthens telomeres, is active in cancer cells, allowing them to divide indefinitely and become immortal. As a result, many people believe that increasing the length of telomeres in normal cells makes them more prone to cancer. This is possible if telomerase has been active in organisms since birth (these organisms get more cancer). However, studies show that upregulating telomerase infrequently ("facultatively") does not increase the risk of cancer.

In fact, having too short telomeres causes genetic instability, which increases the risk of cancer.

Another popular misconception is that because some cells (such as brain cells) rarely divide, their telomeres do not shorten, but these cells still age. The cells that surround the rarely dividing brain cells, on the other hand, divide rapidly, and their dysfunction contributes to the aging of the brain cells.

Getting rid of senescent cells

Senescent cells are "zombie" cells because they are damaged and should die as a result of this damage, but they continue to live by secreting various substances that "infect" neighboring cells, resulting in more "zombified" senescent cells.

Senescent cells arise from healthy cells that have been damaged by aging and have stopped dividing. They do not die, but instead remain in the tissues, secreting substances that harm healthy cells.

Wrinkles are caused by senescent skin cells, atherosclerosis is caused by senescent blood vessel walls, and osteoarthritis is caused by senescent cartilage cells.

According to studies, senescent cells can be removed from animals. Small molecules found in nature, such as fisetin or peptides, can eliminate senescent cells, leading to longer lifespans and fewer aging symptoms and diseases in these animals.