Sharing my learnings from the book, Lifespan by David Sinclair & Matthew LaPlante
Lifespan by David Sinclair & Matthew LaPlante
As cells age, they become larger and less capable of reproduction, undergoing changes that eventually result in the loss of cellular identity. For years, scientists have argued about why these changes occur, but popular opinion has coalesced around nine “hallmarks of aging.” But are these hallmarks a cause or a symptom?
In his new book, Lifespan, David Sinclair has proposed a radical new theory of aging, suggesting that the aging hallmarks are symptoms of epigenetic changes that occur over time, but that the original genetic code remains very much intact.
If we can reset the code, can we slow, stop or even reverse aging? Sinclair believes we can.
- we are moving closer to a world in which aging will be optional. A world in which it will be up to us, and not the processes of aging, to determine the limits of our lifespans. Soon, we’ll be able to live healthy lives for far longer.
- Recent breakthroughs in genetics show that aging actually is a disease. Not only that, it’s a disease that’s potentially curable, and eliminating it would add years to our lifespans. Without the symptoms of aging to deal with, the quality of our newly extended lives would be improved immensely.
- The freshwater polyp Hydra vulgaris – a small water-dwelling organism – has long fascinated geneticists. Why? It’s evolved to resist biological senescence. This is the slow deterioration of function that occurs when cells that have stopped dividing accumulate in an organism. It’s also, essentially, the cause of aging.
- Humans now exhibit a more evolved version of this survival circuit, but its basic function is the same: to repair DNA and prevent the loss of genetic information that causes cells to stop replicating, become senescent and contribute to the aging process. In this sense, we’re hardwired to avoid senescence. So, why aren’t we immortal? The answer to this question lies in that very same survival circuit.
- longevity genes” like sirtuin genes are tremendously important in the fight against aging. The flip side is that when they don’t function correctly, they can also cause aging. That’s because when sirtuins are mobilized to respond to emergencies, they don’t always find their way back to their rightful place inside their cell. They can turn into unregulated agents, switching off genes that should be switched on, and vice versa. When sirtuins go rogue, they contribute to the loss of cellular information that causes aging.
- Thanks to the Information Theory of Aging, researchers are not only grasping the root cause of aging. They’re also coming closer to developing an effective cure
- You can help your longevity genes fight aging.
- Plant-based proteins deliver just enough amino acids to maintain healthy bodily functions while still keeping the body in a state of desirable stress: cells are under enough stress that the survival instinct to repair and preserve DNA stays active without reaching a state of emergency where overall health and function is compromised.
- fasting is another simple way to create the desirable stress that mobilizes the longevity genes without sending them into overdrive.
- A cure for aging may be closer than we think.
- One potential cure has its origins in Rapa Nui, the island off the coast of Chile, more commonly known in the West as Easter Island. In the 1960s, a team of scientists discovered a new type of bacteria in the soil under one of the island’s famous head statues. It was found to contain an antifungal compound which was subsequently named rapamycin. Initially used as an immune suppressor that prevented the bodies of organ-transplant recipients from rejecting their new organs, rapamycin has since been discovered to have life-extending potential.
- there’s another anti-aging wonder drug that’s already being prescribed, albeit as a treatment for diabetes rather than an antidote for aging. It’s called metformin, and it’s derived from goat’s rue, a type of wildflower. Studies have found that metformin activates AMPK, an enzyme which in turn restores mitochondrial activity. The mitochondria are tiny organelles in the cell that transform nutrients into energy.
- In the meantime, researchers are also waging war against aging on a different front – by targeting senescent cells, or as they’re also known; zombie cells. What’s the solution to this plague of zombie cells? It’s complicated. We need to terminate the senescent cells without damaging the remainder of our delicate cellular ecosystems. Senolytics, an emergent class of pharmaceuticals, might be up to the task.
- There is an aging reset button! Thanks to experiments in cloning, we now also know that not only is this original information locked somewhere inside our DNA, it can also potentially be unlocked. Japanese scientist Shinya Yamanaka may have already discovered the key. Yamanaka has isolated four genes that can be induced to transform into pluripotent stem cells, or young cells that haven’t yet been assigned a function by the epigenome. These four genes, now known as Yamanaka factors, can be reset to perform any function in the body – and researchers at Harvard say they’ve already seen promising results from reprogramming Yamanaka genes in mice.
- Of the 100 billion humans who have at one time lived on our planet, only one is recorded to have lived past the age of 120 – Jeanne Calment of France. So while Jeanne Calment is regarded as an outlier today, it may soon be commonplace for humans to survive to 122 and beyond.