Aging and its cure

Health is one of the most valuable and important things we have in life, but we tend to forget that until we lose it. We are living longer than ever before, which is great, but an unforeseen consequence of this is that we also spend a larger and larger portion of our lives being sick.


Getting old soon means that to spend more time in pain. So, the scientist is making try to shift the attention of the medical community from optimizing lifespans to healthspans, the part of our lives during which we’re disease free.

To do this we had to attack the root cause of almost all bodily defects: aging itself. Unbeknown to most people, the science of aging has enormous progress in the last few years, with human trails about to begin in the near future.

Let’s look at three examples of discoveries that might benefit people who are alive right now:-


Your cell has an expiration date. Each time one of the cells divide, it copies its chromosomes. Because of the way this works, they lose a tiny bit of DNA at the end of cell division. This could be catastrophic, so to protect themselves we have a long segment of DNA called telomeres that sort of act like the stiff bits at the end of shoelaces, but they shrink with every cell division.

In some cells, after a number of a division, the telomere is gone, and the cell becomes a zombie, a senescent cell. Senescent cells stay around and don’t die. The older you get the more of the senescent cells are inside you. The senescent cells harmed tissue around them and are linked to many diseases that accompany old age like diabetes and kidney failure.

But what if you kill them off? Scientist genetically engineered mice so that they could destroy their senescent cells as they pleased. Older mice without senescent cells are more active. Their heart and kidney worked better, and they were loss-prone and cancer. Overall they live 30% longer and in better health than average mice.

Since we can’t genetically engineer all the cells in the human body, we need to find another way to get rid of our senescent cells. But how do we kill them without harming healthy cells? The most cells in the body commit a programmed cell suicide when they are damaged, but senescent cells don’t. It turns out that they underproduce a protein that tells them when it’s time to die.

So in late 2016 study, mice were given an injection of the protein. It killed 80% of their senescent cells while causing almost no harm to healthy cells. The treated mouse became generally healthier and even regrow lost hair. As a result, there are a number of new companies looking at treatment involving senescent cells and the first human trials will start soon.


Cells are made of hundreds of million parts. They are structures, machine, messages, and the catalysts that make the reaction happen. All these part constantly need to be destroyed, cleaned up, and rebuilt. As we age, this process less effective and so parts became crumpled, bunched up, or are removed slower, or they are no longer produced in the quantities we need.

One of these parts is NAD+, a coenzyme that tells ourselves to look after themselves. At age 50, we only have about half as much in our bodies as we do at age 20. Low amount of it is linked to a whole bunch of disease from skin cancer to Alzheimer’s, cardiovascular disease, and multiple sclerosis. But NAD+ can’t enter cells directly so we can’t get it as a pill. But scientist notice that other more flexible substance could enter cells and would then turn into an NAD+ inside. In 206, multiple trails on mice showed that they boosted the multiplication of skin, brain, and muscle stem cells.

They were rejuvenated, had a higher ability to repair their damaged DNA, and had a slightly increased lifespan. This even got NASA interested, which are looking for a way to minimize the DNA damage to the astronauts, who would be exposed to from cosmic radiation on Mars missions. There are human trails being planned right now, but it too soon to say if this will boost our healthspan or even lifespan. But NAD+ is a serious candidate and could become the first human anti-aging pill.


Stem cells are like the blueprint of cells that sit at various places in the body and copy themselves to produce a steady flow of fresh young cells, but they decline as we age and so we decline too. Without new parts, human body break. In mice, the scientist observed that as the stem cells in their brain disappeared, they started to develop diseases.

So they took stem cells from baby mice brain and injected them directly into the brain of middle-aged mice, more specifically the hypothalamus, a polyp that’s involved in regulating a lot of bodily functions. The first stem cells reinvigorated older brain cells by secreting micro RNAs that regulated their metabolism. After four months, the brain and muscles work better than those of untreated mice and on average, they lived ten percent longer.

Another study took stem cells from mice embryos and injected them directly into the hearts of older mice. As a consequence, they had improved heart function, could exercise 20% longer, and weirdly enough their hair regrew faster.


What all of this tells us is that there is not a single magic bullet with which to cure aging. It requires a complex array of different therapies. We can kill off senescent cells to clear away the junk, give ourselves fresh new stem cells to fill the gap, all while regulating the metabolism of the other cells using medication.

This article comes with a big caveat. After all, these studies have been carried out on mice. There is no guarantee the same therapies would work in us to the same extent, but they are proof of concepts. To learn more about how we can modify our own healthspan, we need human trails. We’ve only covered a tiny part of the research that’s being done right now, and only scratched the surface of these ideas.

The field of healthspan extension needs more attention and funding. If it gets it, all of us might enjoy growing old without pain.

Review Date
Reviewed Item
Aging and its cure
Author Rating


Leave a Reply

Your email address will not be published. Required fields are marked *

CommentLuv badge