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Can Aging Be Reversed?

Can Aging Be Reversed?

Aging is the inevitable consequence of living, but what if we could defy this fate? Science is on the verge of discovering how to manipulate our biological clocks and reverse the signs of aging. 

The aging process is not fixed; it’s a challenge we’re trying to overcome. This vision of a future without the limitations of age is attracting considerable attention and funding. The question is: can the potential of age reversal research live up to the expectations? Can we slow down, or even stop, the aging process? The field has progressed from wishful thinking to realistic possibilities. 

If we succeed in slowing aging, we could prevent or delay its related diseases, such as Alzheimer’s, diabetes, and cardiovascular disease. This would enhance our well-being and quality of life. However, there is also a trade-off: increased lifespan. Some people around us already live longer than average, even beyond one hundred years. These individuals are not only long-lived; they are also healthy and active. The identification of longevity genes in these exceptional individuals provides clues to their secrets. By mimicking their genetic benefits, we could develop strategies, such as drugs or gene therapies, to extend our lifespan.

The Disposable Soma Theory 

Aging is the gradual deterioration of our bodies over time, leading us closer to death. Why do we age? One possible answer is the Disposable Soma Theory, which proposes a trade-off between self-maintenance and reproduction. According to this theory, organisms face many threats in the natural world, so they invest more in reproducing early and less in keeping their bodies in good shape. As a result, the body becomes more vulnerable to damage and disease with age.

The evidence for this theory is striking: an adult human’s risk of dying doubles every eight years. At 30, the chance of dying within a year is less than 0.1%; at 60, it rises to 1%; and by 90, it reaches over 15%. However, this pattern is not universal. Some animals can live much longer and healthier than others, and some can even manipulate their aging process.

One of the first discoveries that challenged the idea that aging is inevitable was made by Clive McKay, a scientist at Cornell University in New York state, in the 1930s. He found that by restricting the food intake of rats to near-starvation levels, he could extend their lifespan by up to 33 percent. This was the first demonstration that aging could be slowed down, and it has been replicated in many other animals, from yeast to dogs. This seems paradoxical, but it makes sense from an evolutionary perspective. When food is scarce, reproduction is not a priority, so the body switches to survival mode and activates mechanisms that delay aging and preserve health. This way, the animal can wait for better conditions to reproduce. The goal is not to suffer in old age, but to enjoy a healthy old age.

However, living on a very low-calorie diet is not a desirable way to achieve longevity. The challenge is to trick the body into thinking it’s starving when it’s not, and the key to that may be in our genes. In the 1990s, Cynthia Kenyon’s groundbreaking work with roundworms showed that genes can influence aging. She changed a gene called daf-2 and doubled the lifespan of the worm, while also keeping it young and active for longer. Since then, scientists have modified various genes in roundworms, creating mutants that can live up to ten times longer than normal. The reason these gene changes slow down aging is that they activate a system of resilience that protects the animals from infections, DNA damage, and other stressors. These are the same changes that happen in animals that eat very little, except that these animals can eat as much as they want because their genes have been fooled into thinking they’re starving.

These findings suggest that aging is not fixed, but flexible. We may be able to manipulate our biological clocks and reverse the signs of aging. This would not only extend our lifespan, but also improve our quality of life. Imagine a future where we can stay young and healthy for as long as we want. Science is getting closer to making this a reality.

Genes may affect how long we live, but we don’t know how. Changing genes in people is permanent, so a better way to slow aging might be to change how genes are read. This is done by modifying the epigenome, a layer of information on the DNA. The epigenome tells genes when to turn on and off. A new therapy called epigenetic reprogramming can turn back a cell’s biological clock by changing the epigenome. This is done by using four proteins called Yamanaka factors. These factors make old cells younger.

Epigenetic treatments are very promising and attract a lot of research and investment. They aim to modify the epigenome to slow down aging. This is possible because the epigenome is shaped by enzymes that can be reversed. If we can target the right enzymes and make the epigenome young again, then we can use epigenetics as a way to fight aging. While a drug that can do this is still far from reality, there are other ways to reverse aging.

One way is to dilute the bad factors of old animals by mixing them with the good factors of young animals. This can be done by transferring blood or feces from young animals to old animals. This can extend their lifespan. We don’t know why this works, but it may have to do with the microbiome, the bacteria in the gut. The microbiome changes with age and adapts to the host. If we can change the microbiome to a younger state, we may be able to increase longevity through the gut.

Drugs That SLow Down Your Aging

Some drugs can slow down aging, and you might already know some of them. These drugs are not meant to cure specific diseases, but rather to delay or prevent the onset of multiple age-related conditions by modulating the cellular and molecular processes that drive aging.

Some of these drugs are already approved for other purposes, such as treating cancer, diabetes, or organ rejection. However, they have also shown potential to extend lifespan and health span in various animal models and human studies. Here are some examples of these drugs and how they work:

Dasatinib is a drug that inhibits a protein called BCR-ABL, which is involved in the development of chronic myeloid leukemia. However, dasatinib also has the ability to kill senescent cells, which are cells that stop dividing and secrete harmful substances that cause inflammation and tissue damage. Senescent cells accumulate with age and contribute to many age-related diseases, such as arthritis, atherosclerosis, and Alzheimer’s disease. By eliminating senescent cells, dasatinib can improve the health and function of various organs and tissues, such as the heart, lungs, kidneys, and skin. Dasatinib has been shown to extend the lifespan of mice by 10-36% and reduce age-related symptoms. It is currently being tested in clinical trials for treating age-related diseases, such as idiopathic pulmonary fibrosis and osteoarthritis.

Metformin is a drug that lowers blood sugar levels and is widely used to treat type 2 diabetes. However, metformin also has anti-aging effects, such as activating a protein called AMPK, which regulates cellular energy and metabolism. AMPK can improve insulin sensitivity, reduce oxidative stress, and enhance autophagy, which is the process of recycling damaged cellular components. Metformin can also modulate the activity of other proteins and pathways involved in aging, such as mTOR, SIRT1, and NF-kB4. Metformin has been shown to extend the lifespan of worms, flies, and mice by 5-40% and protect against age-related diseases, such as cancer, cardiovascular disease, and neurodegeneration56. It is currently being tested in a large-scale clinical trial called TAME (Targeting Aging with Metformin), which aims to evaluate the effects of metformin on aging and age-related diseases in humans.

Rapamycin is a drug that suppresses the immune system and is used to prevent organ rejection after transplantation. However, rapamycin also has anti-aging effects, such as inhibiting a protein complex called mTOR, which regulates cell growth and proliferation. mTOR can sense and respond to nutrients, hormones, and stress signals, and modulate various cellular and molecular processes that affect aging, such as protein synthesis, autophagy, inflammation, and stem cell function. Rapamycin can also influence the expression and activity of other proteins and pathways involved in aging, such as SIRT1, FOXO, and IGF-1. Rapamycin has been shown to extend the lifespan of yeast, worms, flies, and mice by 9-60% and protect against age-related diseases, such as cancer, diabetes, and neurodegeneration . It is currently being tested in clinical trials for treating age-related diseases, such as Alzheimer’s disease and progeria.

These drugs are examples of repurposed drugs, which are drugs that are already approved for other indications but have potential to treat aging and age-related diseases. Repurposed drugs have the advantage of being relatively safe, cheap, and accessible, as they have already undergone extensive testing and clinical use. However, they also have some limitations, such as side effects, interactions, and dosage issues, which need to be carefully monitored and optimized for each individual and condition.

Another approach to develop anti-aging drugs is to design new compounds that specifically target the epigenome, which is the set of chemical modifications on the DNA and histones that regulate gene expression. The epigenome can change over time and in response to environmental factors, such as diet, stress, and toxins. These changes can alter the activity of genes that are involved in aging and age-related diseases, such as DNA repair, cell cycle, inflammation, and stem cell function.

By manipulating the epigenome, it may be possible to reverse or prevent some of the detrimental effects of aging and restore the youthful function of cells and tissues. For example, a drug called JQ1 can inhibit a protein called BRD4, which is involved in the regulation of gene expression and inflammation. JQ1 can reverse the epigenetic changes and improve the function of senescent cells, which are normally resistant to conventional drugs. Another drug called OSKM can activate four genes that are involved in the reprogramming of cells to a pluripotent state, which is the ability to differentiate into any cell type. OSKM can rejuvenate the cells and tissues of old mice and extend their lifespan by 30%.

These drugs are examples of epigenetic drugs, which are drugs that modulate the epigenome and gene expression. Epigenetic drugs have the potential to be more specific, effective, and reversible than conventional drugs, as they can target the root cause of aging and disease. However, they also have some challenges, such as delivery, stability, and safety, which need to be overcome before they can be widely used in humans.

Anti-aging treatments are needed more than ever, because we have more old people and fewer young people. The global population is aging rapidly, and the proportion of people over 60 years old is expected to increase from 12% in 2015 to 22% in 2050. This poses a huge burden on the health care system and the economy, as older people tend to have more chronic diseases and disabilities, and require more medical and social services.

We want our old people to be healthy and productive, and we want that for ourselves and our loved ones too. A future where we grow old without aging would help billions of people and the economy. It’s worth trillions of dollars. People who live to 100 spend much less on health care than people who die at 70. If we can live longer and healthier, we can save money and lives.

Therefore, investing in anti-aging research and development is not only a scientific and medical endeavor, but also a social and ethical responsibility. By finding and testing drugs that can slow down or reverse aging, we can improve the quality and quantity of life for everyone.

The true costs of ageing

The wealthy world is aging fast. In 1950, around 1 in every 12 people in high-income countries was over 65. By 2050, it's expected to be more like one in four, and it's storing up a big problem. It is a feat that we can live longer and that we can enjoy being alive for longer, but it's expensive. 

When people retire, they start to cost society more money, and the costs will soon be unsustainable. What's becoming increasingly clear is that the three-stage model of life, where you educate, you work, you retire, is fundamentally broken. Current approaches to care for the elderly are a massive drain on society's resources. If you look at it from an economical perspective, we are spending too much money on doing the wrong things, and these mistakes cost more than just money. So, how can societies provide high-quality but affordable care for their growing elderly populations, both today and into the future?

Japan is the oldest nation on earth with the highest proportion of elderly people in its population. The changing shape of societies in the developed world is clearly shown by UN population data. In 1950, there were more than double the number of people in their 20s compared with those in their 60s, but today the number in their 60s has nearly tripled. The number of children and retirees relative to those of working age is known as the dependency ratio. When this changes, it can mean there are fewer workers to support the elderly, which has serious economic consequences. An aging population of course brings lots of good and exciting things, but it’s expensive. The cost of pensions, the cost of health care which is largely spent on people in their last years of life, it’s very costly. When people retire in their 60s, they tend to spend less, pay less in taxes, and cost society more. A shrinking workforce can also cause GDP growth and investment to slow, which threatens economic stagnation. Some countries, such as France, have made repeated attempts to shake up their pension systems, including by raising the retirement age, but this has led to fierce protests.

There are other ways to reduce the dependency ratio, such as encouraging immigration of skilled workers and improving child care provision to encourage more women to work, but these aren’t enough. A lot of this is about tweaking around the edges, and if you really think of the magnitude of the challenge here, the more fruitful thinking lies in a really quite fundamental shift in how we think about different life stages.

Aging populations threaten societies with shrinking workforces, economic stagnation, and crippling costs for pensions and care. Simply throwing more money at the issue is not going to be enough. From a societal perspective, I think we’re missing the huge opportunity we have to help people age better, to live better lives. Dealing with aging is an opportunity but also a problem that keeps getting kicked down the road. We can’t just keep postponing actually dealing with it or wishfully thinking that tweaking around the edges around the retirement age will fix it. It needs a much, much bigger, more fundamental rethink.

Sayed Hasan Al Manzur
Author

Sayed Hasan Al Manzur

Editor-In-Chief

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